{"_id":"b86b3305-5593-448a-9b64-aba20f651484","text":"LCMV infections can occur after exposure to fresh urine, droppings, saliva, or nesting materials from infected rodents.  Transmission may also occur when these materials are directly introduced into broken skin, the nose, the eyes, or the mouth, or presumably, via the bite of an infected rodent. Person-to-person transmission has not been reported, with the exception of vertical transmission from infected mother to fetus, and rarely, through organ transplantation."}
{"_id":"73542b96-2b6a-4571-bc12-e7e747e82b20","text":"LCMV is most commonly recognized as causing neurological disease, as its name implies, though infection without symptoms or mild febrile illnesses are more common clinical manifestations. \n                \nFor infected persons who do become ill, onset of symptoms usually occurs 8-13 days after exposure to the virus as part of a biphasic febrile illness. This initial phase, which may last as long as a week, typically begins with any or all of the following symptoms: fever, malaise, lack of appetite, muscle aches, headache, nausea, and vomiting. Other symptoms appearing less frequently include sore throat, cough, joint pain, chest pain, testicular pain, and parotid (salivary gland) pain. \n                \nFollowing a few days of recovery, a second phase of illness may occur. Symptoms may consist of meningitis (fever, headache, stiff neck, etc.), encephalitis (drowsiness, confusion, sensory disturbances, and\/or motor abnormalities, such as paralysis), or meningoencephalitis (inflammation of both the brain and meninges). LCMV has also been known to cause acute hydrocephalus (increased fluid on the brain), which often requires surgical shunting to relieve increased intracranial pressure. In rare instances, infection results in myelitis (inflammation of the spinal cord) and presents with symptoms such as muscle weakness, paralysis, or changes in body sensation. An association between LCMV infection and myocarditis (inflammation of the heart muscles) has been suggested. \n                \nPrevious observations show that most patients who develop aseptic meningitis or encephalitis due to LCMV survive. No chronic infection has been described in humans, and after the acute phase of illness, the virus is cleared from the body. However, as in all infections of the central nervous system, particularly encephalitis, temporary or permanent neurological damage is possible. Nerve deafness and arthritis have been reported. \n                \nWomen who become infected with LCMV during pregnancy may pass the infection on to the fetus. Infections occurring during the first trimester may result in fetal death and pregnancy termination, while in the second and third trimesters, birth defects can develop. Infants infected In utero can have many serious and permanent birth defects, including vision problems, mental retardation, and hydrocephaly (water on the brain). Pregnant women may recall a flu-like illness during pregnancy, or may not recall any illness. \n                \nLCM is usually not fatal. In general, mortality is less than 1%."}
{"_id":"c3a82ddb-4685-48e7-9db4-6d234890e893","text":"Individuals of all ages who come into contact with urine, feces, saliva, or blood of wild mice are potentially at risk for infection. Owners of pet mice or hamsters may be at risk for infection if these animals originate from colonies that were contaminated with LCMV, or if their animals are infected from other wild mice. Human fetuses are at risk of acquiring infection vertically from an infected mother. \n                \nLaboratory workers who work with the virus or handle infected animals are also at risk. However, this risk can be minimized by utilizing animals from sources that regularly test for the virus, wearing proper protective laboratory gear, and following appropriate safety precautions."}
{"_id":"cc2309b1-d68c-4fa9-8b16-8598e7669c5f","text":"During the first phase of the disease, the most common laboratory abnormalities are a low white blood cell count (leukopenia) and a low platelet count (thrombocytopenia). Liver enzymes in the serum may also be mildly elevated. After the onset of neurological disease during the second phase, an increase in protein levels, an increase in the number of white blood cells or a decrease in the glucose levels in the cerebrospinal fluid (CSF) is usually found. \n   \nLaboratory diagnosis is usually made by detecting IgM and IgG antibodies in the CSF and serum. Virus can be detected by PCR or virus isolation in the CSF at during the acute stage of illness."}
{"_id":"bb168206-a1a4-4217-9905-f03944c3be46","text":"Aseptic meningitis, encephalitis, or meningoencephalitis requires hospitalization and supportive treatment based on severity. Anti-inflammatory drugs, such as corticosteroids, may be considered under specific circumstances. Although studies have shown that ribavirin, a drug used to treat several other viral diseases, is effective against LCMV in vitro, there is no established evidence to support its routine use for treatment of LCM in humans."}
{"_id":"76389084-331a-4541-b80a-f3024522c092","text":"LCMV infection can be prevented by avoiding contact with wild mice and taking precautions when handling pet rodents (i.e. mice, hamsters, or guinea pigs). \n                \nRarely, pet rodents may become infected with LCMV from wild rodents. Breeders, pet stores, and pet owners should take measures to prevent infestations of wild rodents. Pet rodents should not come into contact with wild rodents. If you have a pet rodent, wash your hands with soap and water (or waterless alcohol-based hand rubs when soap is not available and hands are not visibly soiled) after handling rodents or their cages and bedding. \n                \nIf you have a rodent infestation in and around your home, take the following precautions to reduce the risk of LCMV infection: \n \n - Seal up rodent entry holes or gaps with steel wool, lath metal, or caulk. \n - Trap rats and mice by using an appropriate snap trap. \n - Clean up rodent food sources and nesting sites and take precautions when cleaning rodent-infected areas: \n   \n   - Use cross-ventilation when entering a previously unventilated enclosed room or dwelling prior to cleanup. \n   - Put on rubber, latex, vinyl or nitrile gloves. \n   - Do not stir up dust by vacuuming, sweeping, or any other means. \n   - Thoroughly wet contaminated areas with a bleach solution or household disinfectant. \n   - Hypochlorite (bleach) solution: Mix 1 and 1\/2 cups of household bleach in 1 gallon of water. \n   - Once everything is wet, take up contaminated materials with damp towel and then mop or sponge the area with bleach solution or household disinfectant. \n   - Spray dead rodents with disinfectant and then double-bag along with all cleaning materials and throw bag out in an appropriate waste disposal system. \n   - Remove the gloves and thoroughly wash your hands with soap and water (or waterless alcohol-based hand rubs when soap is not available and hands are not visibly soiled). \n    \n \n                \nThe geographic distributions of the rodent hosts are widespread both domestically and abroad. However, infrequent recognition and diagnosis, and historic underreporting of LCM, have limited scientists' ability to estimate incidence rates and prevalence of disease among humans. Understanding the epidemiology of LCM and LCMV infections will help to further delineate risk factors for infection and develop effective preventive strategies. Increasing physician awareness will improve disease recognition and reporting, which may lead to better characterization of the natural history and the underlying immunopathological mechanisms of disease, and stimulate future therapeutic research and development."}
{"_id":"b2ede095-793a-4140-8bae-f71e9be6a986","text":"Cysticercosis is an infection caused by the larvae of the parasite Taenia solium.  This infection occurs after a person swallows tapeworm eggs. The larvae get into tissues such as muscle and brain, and form cysts there (these are called cysticerci). When cysts are found in the brain, the condition is called neurocysticercosis."}
{"_id":"6ba103c8-f47e-49e7-a486-0253c7e17ae7","text":"Cysticercosis is an infection caused by the larvae of the tapeworm, Taenia solium. A person with an adult tapeworm, which lives in the person\u2019s gut, sheds eggs in the stool.  The infection with the adult tapeworm is called taeniasis.  A pig then eats the eggs in the stool.  The eggs develop into larvae inside the pig and form cysts (called cysticerci) in the pig's muscles or other tissues. The infection with the cysts is called cysticercosis. Humans who eat undercooked or raw infected pork swallow the cysts in the meat. The larvae then come out of their cysts in the human gut and develop into adult tapeworms, completing the cycle.\n    \nPeople get cysticercosis when they swallow eggs that are excreted in the stool of people with the adult tapeworm. This may happen when people\n    \n     - Drink water or eat food contaminated with tapeworm eggs\n     - Put contaminated fingers in their mouth\n    \n    \nCysticercosis is not spread by eating undercooked meat. However, people get infected with tapeworms (taeniasis) by eating undercooked infected pork. People who have tapeworm infections can infect themselves with the eggs and develop cysticercosis (this is called autoinfection). They can also infect other people if they have poor hygiene and contaminate food or water that other people swallow. People who live with someone who has a tapeworm infection in their intestines have a much higher risk of getting cysticercosis than other people.\n    \nHuman cysticercosis is found worldwide, especially in areas where pig cysticercosis is common. Both taeniasis and cysticercosis are most often found in rural areas of developing countries with poor sanitation, where pigs roam freely and eat human feces. Taeniasis and cysticercosis are rare among persons who live in countries where pigs are not raised and in countries where pigs do not have contact with human feces. Although uncommon, cysticercosis can occur in people who have never traveled outside of the United States if they are exposed to tapeworm eggs.\n    \nMore on: Taeniasis"}
{"_id":"c4d825ac-fdfd-4705-a493-847cd25e98b4","text":"If you think that you may have cysticercosis, please see your health care provider. Your health care provider will ask you about your symptoms, where you have travelled, and what kinds of foods you eat. The diagnosis of neurocysticercosis usually requires MRI or CT brain scans. Blood tests may be useful to help diagnose an infection, but they may not always be positive in light infections.\n  \nIf you have been diagnosed with cysticercosis, you and your family members should be tested for intestinal tapeworm infection. See the taeniasis section for more information on intestinal tapeworm infections.  \n  \nMore on: Taeniasis\n  \nMore on: Resources for Health Professionals: Diagnosis"}
{"_id":"3824ba34-f8e8-48af-95a4-336ba642ba6b","text":"Some people with cysticercosis do not need to be treated. There are medications available to treat cysticercosis for those who do need treatment. Sometimes surgery may be needed. Your doctor will advise you on which treatment is best for you.\n    \nMore on: Resources for Health Professionals: Treatment\n    \nMore on: Taeniasis"}
{"_id":"5a694a27-33de-456e-a7c8-59f861411792","text":"To prevent cysticercosis, the following precautions should be taken:\n    \n     - Wash your hands with soap and warm water after using the toilet, changing diapers, and before handling food\n     - Teach children the importance of washing hands to prevent infection\n     - Wash and peel all raw vegetables and fruits before eating\n     - Use good food and water safety practices while traveling in developing countries such as: \n      \n       - Drink only bottled or boiled (1 minute) water or carbonated (bubbly) drinks in cans or bottles\n       - Filter unsafe water through an \"absolute 1 micron or less\" filter AND dissolve iodine tablets in the filtered water; \"absolute 1 micron\" filters can be found in camping and outdoor supply stores\n      \n    \n    \nMore on: Handwashing\n    \nMore on: Food and Water Safety"}
{"_id":"0e4d7ead-1024-486e-a5a4-d2ade7d5a5b3","text":"Whipworm (Trichuris trichiura) is an intestinal parasite of humans. The larvae and adult worms live in the intestine of humans and can cause intestinal disease. The name is derived from the worm\u2019s distinctive whip-like shape."}
{"_id":"c03947bf-b4cf-49c7-a590-265af5d8233b","text":"Whipworm is a soil-transmitted helminth (STH) and is the third most common roundworm of humans. Whipworm causes an infection called trichuriasis and often occurs in areas where human feces is used as fertilizer or where defecation onto soil happens. The worms are spread from person to person by fecal-oral transmission or through feces-contaminated food.\n    Geographic Distribution\nWorldwide, infection occurs more frequently in areas with tropical weather and poor sanitation practices, and among children. In 2002, the estimated number of persons infected with whipworm was 1 billion. Trichuriasis also occurs in the southern United States."}
{"_id":"aba5dc53-4ca4-4dab-91fa-3c4f3f55bfb1","text":"The standard method for diagnosing the presence of whipworm is by microscopically identifying whipworm eggs in a stool sample. Because eggs may be difficult to find in light infections, a concentration procedure is recommended."}
{"_id":"5c83292e-1c4e-4099-8b9a-f2e25a5b8de2","text":"Anthelminthic medications (drugs that rid the body of parasitic worms), such as albendazole and mebendazole, are the drugs of choice for treatment. Infections are generally treated for 3 days. The recommended medications are effective. Health care providers may decide to repeat a stool exam after treatment. Iron supplements may also be prescribed if the infected person suffers from anemia.\n    \nMore on: Resources for Health Professionals: Treatment"}
{"_id":"524fb143-20b3-4b5b-b866-36a70295002e","text":"The best way to prevent whipworm infection is to always:\n    \n     - Avoid ingesting soil that may be contaminated with human feces, including where human fecal matter (\"night soil\") or wastewater is used to fertilize crops.\n     - Wash your hands with soap and warm water before handling food.\n     - Teach children the importance of washing hands to prevent infection.\n     - Wash, peel, or cook all raw vegetables and fruits before eating, particularly those that have been grown in soil that has been fertilized with manure.\n    \n    \nMore on: Handwashing\n    \nTransmission of infection to others can be prevented by\n    \n     - Not defecating outdoors.\n     - Effective sewage disposal systems."}
{"_id":"bc6a5056-be4f-4811-aa1e-c36c635783c0","text":"Marine toxins are naturally occurring chemicals that can contaminate certain seafood. The seafood contaminated with these chemicals frequently looks, smells, and tastes normal. When humans eat such seafood, disease can result."}
{"_id":"d22613d5-d00e-40a4-8cec-14f135aef8f8","text":"Diagnosis of marine toxin poisoning is generally based on symptoms and a history of recently eating a particular kind of seafood. Laboratory testing for the specific toxin in patient samples is generally not necessary because this requires special techniques and equipment available in only specialized laboratories. If suspect, leftover fish or shellfish are available, they can be tested for the presence of the toxin more easily. Identification of the specific toxin is not usually necessary for treating patients because there is no specific treatment."}
{"_id":"9ba41b91-7035-4f5f-b316-7541babe864c","text":"Other than supportive care there are few specific treatments for ciguatera poisoning, paralytic shellfish poisoning, neurotoxic shellfish poisoning, or amnesic shellfish poisoning. Antihistamines and epinephrine, however, may sometimes be useful in treating the symptoms of scombrotoxic fish poisoning. Intravenous mannitol has been suggested for the treatment of severe ciguatera poisoning."}
{"_id":"08abfcbb-99d0-49af-a476-9d671e053aea","text":"Every year, approximately 30 cases of poisoning by marine toxins are reported in the United States. Because healthcare providers are not required to report these illnesses and because many milder cases are not diagnosed or reported, the actual number of poisonings may be much greater. Toxic seafood poisonings are more common in the summer than winter because dinoflagelates grow well in warmer seasons. It is estimated from cases with available data that one person dies every 4 years from toxic seafood poisonings."}
{"_id":"103d9bce-eda5-47d2-8db0-d014fbb78493","text":"General guidelines for safe seafood consumption:"}
{"_id":"6857a064-8e64-497b-afff-68284ca9ab10","text":"Some health departments test shellfish harvested within their jurisdiction to monitor the level of dinoflagellate toxins and asses the risk for contamination. Based on the results of such testing, recreational and commercial seafood harvesting may be prohibited locally during periods of risk. State and federal regulatory agencies monitor reported cases of marine toxin poisoning, and health departments investigate possible outbreaks and devise control measures. The Centers for Disease Control and Prevention (CDC) provides support to investigators as needed."}
{"_id":"a914cc97-904d-4dd3-9ac5-8ebe8e7510c2","text":"It is important to notify public health departments about even one person with marine toxin poisoning. Public health departments can then investigate to determine if a restaurant, oyster bed, or fishing area has a problem. This prevents other illnesses. In any food poisoning occurrence, consumers should note foods eaten and freeze any uneaten portions in case they need to be tested. A commercial test has been developed in Hawaii to allow persons to test sport caught fish for ciguatoxins."}
{"_id":"03988d3e-b35f-40f8-bfdd-866614bc992f","text":"If you continue to live or travel in yellow fever-endemic areas, you should receive a booster dose of yellow fever vaccine after 10 years.\n                \nAfter receiving the vaccine, you should receive an International Certificate of Vaccination (yellow card) that has been validated by the vaccination center. This Certificate becomes valid 10 days after vaccination and lasts for 10 years. You will need this card as proof of vaccination to enter certain countries."}
{"_id":"0a5efd1a-1bb8-4728-b9db-a6235bbfa502","text":"Schistosomiasis, also known as bilharzia, is a disease caused by parasitic worms. Infection with Schistosoma mansoni, S. haematobium, and S. japonicum causes illness in humans; less commonly, S. mekongi and S. intercalatum can cause disease. Although the worms that cause schistosomiasis are not found in the United States, more than 200 million people are infected worldwide."}
{"_id":"f666e111-9ba0-46d0-b226-2677395a21e0","text":"Schistosomiasis is an important cause of disease in many parts of the world, most commonly in places with poor sanitation. School-age children who live in these areas are often most at risk because they tend to spend time swimming or bathing in water containing infectious cercariae.\nIf you live in, or travel to, areas where schistosomiasis is found and are exposed to contaminated freshwater, you are at risk.\n   \nAreas where human schistosomiasis is found include:\n   \n    - Schistosoma mansoni \n     \n      - distributed throughout Africa: There is risk of infection in freshwater in southern and sub-Saharan Africa\u2013including the great lakes and rivers as well as smaller bodies of water. Transmission also occurs in the Nile River valley in Sudan and Egypt\n      - South America: including Brazil, Suriname, Venezuela\n      - Caribbean (risk is low): Dominican Republic, Guadeloupe, Martinique, and Saint Lucia.\n     \n    - S. haematobium \n     \n      - distributed throughout Africa: There is risk of infection in freshwater in southern and sub-Saharan Africa\u2013including the great lakes and rivers as well as smaller bodies of water. Transmission also occurs in the Nile River valley in Egypt and the Mahgreb region of North Africa.\n      - found in areas of the Middle East\n     \n    - S. japonicum \n     \n      - found in Indonesia and parts of China and Southeast Asia\n     \n    - S. mekongi \n     \n      - found in Cambodia and Laos\n     \n    - S. intercalatum \n     \n      - found in parts of Central and West Africa."}
{"_id":"c138e35d-014b-49a7-9436-a8b01fdb1109","text":"Stool or urine samples can be examined microscopically for parasite eggs (stool for S. mansoni or S. japonicum eggs and urine for S. haematobium eggs). The eggs tend to be passed intermittently and in small amounts and may not be detected, so it may be necessary to perform a blood (serologic) test.\n    \nMore on: Resources for Health Professionals: Diagnosis"}
{"_id":"ba6e2ab0-bfd2-40ef-8511-b3e18cacf09b","text":"Safe and effective medication is available for treatment of both urinary and intestinal schistosomiasis. Praziquantel, a prescription medication, is taken for 1-2 days to treat infections caused by all Schistosoma species.\n    \nMore on: Resources for Health Professionals: Treatment"}
{"_id":"ef0d0bf1-e61b-40f5-bb05-6ac117ec1133","text":"Prevention\n    \nNo vaccine is available.\n    \nThe best way to prevent schistosomiasis is to take the following steps if you are visiting or live in an area where schistosomiasis is transmitted:\n    \n     - Avoid swimming or wading in freshwater when you are in countries in which schistosomiasis occurs. Swimming in the ocean and in chlorinated swimming pools is safe.\n     - Drink safe water. Although schistosomiasis is not transmitted by swallowing contaminated water, if your mouth or lips come in contact with water containing the parasites, you could become infected. Because water coming directly from canals, lakes, rivers, streams, or springs may be contaminated with a variety of infectious organisms, you should either bring your water to a rolling boil for 1 minute or filter water before drinking it. Bring your water to a rolling boil for at least 1 minute will kill any harmful parasites, bacteria, or viruses present. Iodine treatment alone WILL NOT GUARANTEE that water is safe and free of all parasites.\n     - Water used for bathing should be brought to a rolling boil for 1 minute to kill any cercariae, and then cooled before bathing to avoid scalding. Water held in a storage tank for at least 1 - 2 days should be safe for bathing.\n     - Vigorous towel drying after an accidental, very brief water exposure may help to prevent the Schistosoma parasite from penetrating the skin. However, do not rely on vigorous towel drying alone to prevent schistosomiasis.\n    \n    \nThose who have had contact with potentially contaminated water overseas should see their health care provider after returning from travel to discuss testing.\n    \nMore on: Schistosomiasis in Travelers\n   \n  \n  \n   Control\n   \nIn countries where schistosomiasis causes significant disease, control efforts usually focus on:\n   \n    - reducing the number of infections in people and\/or\n    - eliminating the snails that are required to maintain the parasite\u2019s life cycle.\n   \n   \nFor all species that cause schistosomiasis, improved sanitation could reduce or eliminate transmission of this disease. In some areas with lower transmission levels, elimination of schistosomiasis is considered a \"winnable battle\" by public health officials.\n   \nControl measures can include mass drug treatment of entire communities and targeted treatment of school-age children. Some of the problems with control of schistosomiasis include:\n   \n    - Chemicals used to eliminate snails in freshwater sources may harm other species of animals in the water and, if treatment is not sustained, the snails may return to those sites afterwards.\n    - For certain species of the parasite, such as S. japonicum, animals such as cows or water buffalo can also be infected. Runoff from pastures (if the cows are infected) can contaminate freshwater sources."}
{"_id":"07d1b249-2b73-4562-959c-c702beea18ae","text":"The head louse, or Pediculus humanus capitis, is a parasitic insect that can be found on the head, eyebrows, and eyelashes of people. Head lice feed on human blood several times a day and live close to the human scalp. Head lice are not known to spread disease."}
{"_id":"5e659878-4ac0-410b-ba66-9212ee0815aa","text":"In the United States, infestation with head lice (Pediculus humanus capitis) is most common among preschool- and elementary school-age children and their household members and caretakers. Head lice are not known to transmit disease; however, secondary bacterial infection of the skin resulting from scratching can occur with any lice infestation.\n    \nGetting head lice is not related to cleanliness of the person or his or her environment.\n    \nHead lice are mainly spread by direct contact with the hair of an infested person. The most common way to get head lice is by head-to-head contact with a person who already has head lice. Such contact can be common among children during play at:\n    \n     - school,\n     - home, and\n     - elsewhere (e.g., sports activities, playgrounds, camp, and slumber parties).\n    \n    \nUncommonly, transmission may occur by:\n    \n     - wearing clothing, such as hats, scarves, coats, sports uniforms, or hair ribbons worn by an infested person;\n     - using infested combs, brushes or towels; or\n     - lying on a bed, couch, pillow, carpet, or stuffed animal that has recently been in contact with an infested person.\n    \n    \nReliable data on how many people get head lice each year in the United States are not available; however, an estimated 6 million to 12 million infestations occur each year in the United States among children 3 to 11 years of age. Some studies suggest that girls get head lice more often than boys, probably due to more frequent head-to-head contact.\n    \nIn the United States, infestation with head lice is much less common among African-Americans than among persons of other races. The head louse found most frequently in the United States may have claws that are better adapted for grasping the shape and width of some types of hair but not others."}
{"_id":"3d68eb07-edc8-4d66-b195-1c33068089d3","text":"Misdiagnosis of head lice infestation is common. The diagnosis of head lice infestation is best made by finding a live nymph or adult louse on the scalp or hair of a person.\n    \nBecause adult and nymph lice are very small, move quickly, and avoid light, they may be difficult to find. Use of a fine-toothed louse comb may facilitate identification of live lice.\n    \nIf crawling lice are not seen, finding nits attached firmly within \u00bc inch of the base of hair shafts suggests, but does not confirm, the person is infested. Nits frequently are seen on hair behind the ears and near the back of the neck. Nits that are attached more than \u00bc inch from the base of the hair shaft are almost always non-viable (hatched or dead). Head lice and nits can be visible with the naked eye, although use of a magnifying lens may be necessary to find crawling lice or to identify a developing nymph inside a viable nit. Nits are often confused with other particles found in hair such as dandruff, hair spray droplets, and dirt particles.\n    \nIf no nymphs or adults are seen, and the only nits found are more than \u00bc inch from the scalp, then the infestation is probably old and no longer active \u2014 and does not need to be treated."}
{"_id":"6af7000d-12ec-4a43-828f-2f966e16e286","text":"General Guidelines \n   \nTreatment for head lice is recommended for persons diagnosed with an active infestation. All household members and other close contacts should be checked; those persons with evidence of an active infestation should be treated. Some experts believe prophylactic treatment is prudent for persons who share the same bed with actively-infested individuals. All infested persons (household members and close contacts) and their bedmates should be treated at the same time. \n   \nSome pediculicides (medicines that kill lice) have an ovicidal effect (kill eggs). For pediculicides that are only weakly ovicidal or not ovicidal, routine retreatment is recommended. For those that are more strongly ovicidal, retreatment is recommended only if live (crawling) lice are still present several days after treatment (see recommendation for each medication). To be most effective, retreatment should occur after all eggs have hatched but before new eggs are produced. \n   \nWhen treating head lice, supplemental measures can be combined with recommended medicine (pharmacologic treatment); however, such additional (non-pharmacologic) measures generally are not required to eliminate a head lice infestation. For example, hats, scarves, pillow cases, bedding, clothing, and towels worn or used by the infested person in the 2-day period just before treatment is started can be machine washed and dried using the hot water and hot air cycles because lice and eggs are killed by exposure for 5 minutes to temperatures greater than 53.5\u00b0C (128.3\u00b0F). Items that cannot be laundered may be dry-cleaned or sealed in a plastic bag for two weeks. Items such as hats, grooming aids, and towels that come in contact with the hair of an infested person should not be shared. Vacuuming furniture and floors can remove an infested person's hairs that might have viable nits attached. \n     \n   \nTreatment of the infested person(s): Requires using an Over-the-counter (OTC) or prescription medication. Follow these treatment steps: \n    \n    - Before applying treatment, it may be helpful to remove clothing that can become wet or stained during treatment. \n    - Apply lice medicine, also called pediculicide, according to the instructions contained in the box or printed on the label. If the infested person has very long hair (longer than shoulder length), it may be necessary to use a second bottle. Pay special attention to instructions on the label or in the box regarding how long the medication should be left on the hair and how it should be washed out.\n \n       \n       \n        \n       \n       \n    - Have the infested person put on clean clothing after treatment. \n    - If a few live lice are still found 8\u201312 hours after treatment, but are moving more slowly than before, do not retreat. The medicine may take longer to kill all the lice. Comb dead and any remaining live lice out of the hair using a fine\u2013toothed nit comb. \n    - If, after 8\u201312 hours of treatment, no dead lice are found and lice seem as active as before, the medicine may not be working. Do not retreat until speaking with your health care provider; a different pediculicide may be necessary. If your health care provider recommends a different pediculicide, carefully follow the treatment instructions contained in the box or printed on the label. \n    - Nit (head lice egg) combs, often found in lice medicine packages, should be used to comb nits and lice from the hair shaft. Many flea combs made for cats and dogs are also effective. \n    - After each treatment, checking the hair and combing with a nit comb to remove nits and lice every 2\u20133 days may decrease the chance of self\u2013reinfestation. Continue to check for 2\u20133 weeks to be sure all lice and nits are gone. Nit removal is not needed when treating with spinosad topical suspension. \n    - Retreatment is meant to kill any surviving hatched lice before they produce new eggs. For some drugs, retreatment is recommended routinely about a week after the first treatment (7\u20139 days, depending on the drug) and for others only if crawling lice are seen during this period. Retreatment with lindane shampoo is not recommended. \n    \n     \n   \nSupplemental Measures: Head lice do not survive long if they fall off a person and cannot feed. You don't need to spend a lot of time or money on housecleaning activities. Follow these steps to help avoid re\u2013infestation by lice that have recently fallen off the hair or crawled onto clothing or furniture. \n    \n    -  \nMachine wash and dry clothing, bed linens, and other items that the infested person wore or used during the 2 days before treatment using the hot water (130\u00b0F) laundry cycle and the high heat drying cycle. Clothing and items that are not washable can be dry\u2013cleaned \nOR \nsealed in a plastic bag and stored for 2 weeks.  \n    - Soak combs and brushes in hot water (at least 130\u00b0F) for 5\u201310 minutes. \n    - Vacuum the floor and furniture, particularly where the infested person sat or lay. However, the risk of getting infested by a louse that has fallen onto a rug or carpet or furniture is very low. Head lice survive less than 1\u20132 days if they fall off a person and cannot feed; nits cannot hatch and usually die within a week if they are not kept at the same temperature as that found close to the human scalp. Spending much time and money on housecleaning activities is not necessary to avoid reinfestation by lice or nits that may have fallen off the head or crawled onto furniture or clothing. \n    - Do not use fumigant sprays; they can be toxic if inhaled or absorbed through the skin. \n    \n   \n \n     \n   \nPrevent Reinfestation: \n   \nMore on: Prevention & Control \n   \n \n     \n   Over-the-counter Medications \n   \nMany head lice medications are available \"over-the-counter\" without a prescription at a local drug store or pharmacy. Each over-the-counter product approved by the FDA for the treatment of head lice contains one of the following active ingredients. If crawling lice are still seen after a full course of treatment contact your health care provider. \n    \n    -  \nPyrethrins combined with piperonyl butoxide;\n Brand name products: A\u2013200*, Pronto*, R&C*, Rid*, Triple X*, Licide* \nPyrethrins are naturally occurring pyrethroid extracts from the chrysanthemum flower. Pyrethrins are safe and effective when used as directed. Pyrethrins can only kill live lice, not unhatched eggs (nits). A second treatment is recommended 9 to 10 days after the first treatment to kill any newly hatched lice before they can produce new eggs. Pyrethrins generally should not be used by persons who are allergic to chrysanthemums or ragweed. Pyrethrin is approved for use on children 2 years of age and older.  \n    -  \nPermethrin lotion, 1%;\n Brand name product: Nix*. \nPermethrin is a synthetic pyrethroid similar to naturally occurring pyrethrins. Permethrin lotion 1% is approved by the FDA for the treatment of head lice. Permethrin is safe and effective when used as directed. Permethrin kills live lice but not unhatched eggs. Permethrin may continue to kill newly hatched lice for several days after treatment. A second treatment often is necessary on day 9 to kill any newly hatched lice before they can produce new eggs. Permethrin is approved for use on children 2 months of age and older.  \n    \n   \n \n     \n   Prescription Medications \n   \nThe following medications, in alphabetical order, approved by the U.S. Food and Drug Administration (FDA) for the treatment of head lice are available only by prescription. If crawling lice are still seen after a full course of treatment, contact your health care provider. \n    \n    -  \nBenzyl alcohol lotion, 5%;\n Brand name product: Ulesfia lotion* \nBenzyl alcohol is an aromatic alcohol. Benzyl alcohol lotion, 5% has been approved by the FDA for the treatment of head lice and is considered safe and effective when used as directed. It kills lice but it is not ovicidal(i.e., does not kill lice eggs). A second treatment is needed 9 days after the first treatment to kill any newly hatched lice before they can produce new eggs. Benzyl alcohol lotion is intended for use on persons who are 6 months of age and older and its safety in persons aged more 60 years has not been established. It can be irritating to the skin.  \n    -  \nIvermectin lotion, 0.5%;\n Brand name product: Sklice* \nIvermectin lotion, 0.5% was approved by the FDA in 2012 for treatment of head lice in persons 6 months of age and older. It is not ovicidal, but appears to prevent nymphs (newly hatched lice) from surviving. It is effective in most patients when given as a single application on dry hair without nit combing. It should not be used for retreatment without talking to a healthcare provider. \nGiven as a tablet in mass drug administrations, oral ivermectin has been used extensively and safely for over two decades in many countries to treat filarial worm infections. Although not FDA-approved for the treatment of lice, ivermectin tablets given in a single oral dose of 200 micrograms\/kg repeated in 10 days or 400 micrograms\/kg repeated in 7 days has been shown effective against head lice. It should not be used in children weighing less than 15 kg or in pregnant women.   \n    -  \nSpinosad 0.9% topical suspension;\n Brand name product: Natroba* \nSpinosad is derived from soil bacteria. Spinosad topical suspension, 0.9%, was approved by the FDA in 2011. Since it kills live lice as well as unhatched eggs, retreatment is usually not needed. Nit combing is not required. Spinosad topical suspension is approved for the treatment of children 6 months of age and older. It is safe and effective when used as directed. Repeat treatment should be given only if live (crawling) lice are seen 7 days after the first treatment.  \n    \n   \nFor second\u2013line treatment only: \n    \n    -  \nLindane shampoo 1%;\n Brand name products: None available \nLindane is an organochloride. The American Academy of Pediatrics (AAP) no longer recommends it as a pediculocide. Although lindane shampoo 1% is approved by the FDA for the treatment of head lice, it is not recommended as a first\u2013line treatment. Overuse, misuse, or accidentally swallowing lindane can be toxic to the brain and other parts of the nervous system; its use should be restricted to patients for whom prior treatments have failed or who cannot tolerate other medications that pose less risk. Lindane should not be used to treat premature infants, persons with HIV, a seizure disorder, women who are pregnant or breast\u2013feeding, persons who have very irritated skin or sores where the lindane will be applied, infants, children, the elderly, and persons who weigh less than 110 pounds. Retreatment should be avoided.  \n    \n   \n \n   \nWhen treating head lice \n    \n    - Do not use extra amounts of any lice medication unless instructed to do so by your physician or pharmacist. The drugs used to treat lice are insecticides and can be dangerous if they are misused or overused. \n    - All the medications listed above should be kept out of the eyes. If they get onto the eyes, they should be immediately flushed away. \n    - Do not treat an infested person more than 2\u20133 times with the same medication if it does not seem to be working. This may be caused by using the medicine incorrectly or by resistance to the medicine. Always seek the advice of your health care provider if this should happen. He\/she may recommend an alternative medication. \n    - Do not use different head lice drugs at the same time unless instructed to do so by your physician or pharmacist. \n    \n   \n \n   \n*Use of trade names is for identification purposes only and does not imply endorsement by the Public Health Service or by the U.S. Department of Health and Human Services."}
{"_id":"cfa469d7-cb5e-4a5d-a05d-08b1f92c7d5d","text":"Head lice are spread most commonly by direct head-to-head (hair-to-hair) contact. However, much less frequently they are spread by sharing clothing or belongings onto which lice have crawled or nits attached to shed hairs may have fallen. The risk of getting infested by a louse that has fallen onto a carpet or furniture is very small. Head lice survive less than 1\u20132 days if they fall off a person and cannot feed; nits cannot hatch and usually die within a week if they are not kept at the same temperature as that found close to the scalp.\n    \nThe following are steps that can be taken to help prevent and control the spread of head lice:\n    \n     - Avoid head-to-head (hair-to-hair) contact during play and other activities at home, school, and elsewhere (sports activities, playground, slumber parties, camp).\n     - Do not share clothing such as hats, scarves, coats, sports uniforms, hair ribbons, or barrettes.\n     - Do not share combs, brushes, or towels. Disinfest combs and brushes used by an infested person by soaking them in hot water (at least 130\u00b0F) for 5\u201310 minutes.\n     - Do not lie on beds, couches, pillows, carpets, or stuffed animals that have recently been in contact with an infested person.\n     - Machine wash and dry clothing, bed linens, and other items that an infested person wore or used during the 2 days before treatment using the hot water (130\u00b0F) laundry cycle and the high heat drying cycle. Clothing and items that are not washable can be dry-cleaned OR sealed in a plastic bag and stored for 2 weeks.\n     - Vacuum the floor and furniture, particularly where the infested person sat or lay. However, spending much time and money on housecleaning activities is not necessary to avoid reinfestation by lice or nits that may have fallen off the head or crawled onto furniture or clothing.\n     - Do not use fumigant sprays or fogs; they are not necessary to control head lice and can be toxic if inhaled or absorbed through the skin.\n    \n    \nTo help control a head lice outbreak in a community, school, or camp, children can be taught to avoid activities that may spread head lice."}
{"_id":"5a548a13-241a-4506-89f3-2ad0331cc0c0","text":"Body lice are parasitic insects that live on clothing and bedding used by infested persons. Body lice frequently lay their eggs on or near the seams of clothing. Body lice must feed on blood and usually only move to the skin to feed. Body lice exist worldwide and infest people of all races. Body lice infestations can spread rapidly under crowded living conditions where hygiene is poor (the homeless, refugees, victims of war or natural disasters). In the United States, body lice infestations are found only in homeless transient populations who do not have access to bathing and regular changes of clean clothes. Infestation is unlikely to persist on anyone who bathes regularly and who has at least weekly access to freshly laundered clothing and bedding."}
{"_id":"7498f84a-3b8a-4cfc-a9da-ad296964b16d","text":"Body lice infestation is found worldwide but generally is limited to persons who live under conditions of crowding and poor hygiene who do not have access to regular bathing and changes of clean clothes, such as:\n    \n     - the homeless,\n     - refugees,\n     - survivors of war or natural disasters.\n    \n    \nInfestations can spread rapidly under such conditions. Body lice infestation can occur in people of all races.\n    \nBody lice are spread through direct contact with a person who has body lice or through contact with articles such as clothing, beds, bed linens, or towels that have been in contact with an infested person. However, in the United States, actual infestation with body lice tends to be occur only in homeless, transient persons who do not have access to regular bathing and changes of clean clothes.\n    \nBody lice can transmit disease. Epidemics of typhus and louse-borne relapsing fever have been caused by body lice (typically in areas where climate, poverty, and social customs or war and social upheaval prevent regular changes and laundering of clothing)."}
{"_id":"1c439352-5046-4061-8857-b3c7cfd9a406","text":"Body lice infestation is diagnosed by finding eggs and crawling lice in the seams of clothing. Sometimes a body louse can be seen crawling or feeding on the skin.\n    \nAlthough body lice and nits can be large enough to be seen with the naked eye, a magnifying lens may be necessary to find crawling lice or eggs."}
{"_id":"3cb8c49b-9da7-4b41-b6f5-f04508cf03c3","text":"A body lice infestation is treated by improving the personal hygiene of the infested person, including assuring a regular (at least weekly) change of clean clothes. Clothing, bedding, and towels used by the infested person should be laundered using hot water (at least 130\u00b0F) and machine dried using the hot cycle.\n    \nSometimes the infested person also is treated with a pediculicide, a medicine that can kill lice; however, a pediculicide generally is not necessary if hygiene is maintained and items are laundered appropriately at least once a week. A pediculicide should be applied exactly as directed on the bottle or by your physician.\n    \nIf you choose to treat, guidelines for the choice of the pediculicide are the same as for head lice.\n    \nMore on: Head Lice Treatment"}
{"_id":"31abf7ca-bab8-43bc-9417-03d6173a1a7b","text":"Body lice are spread most commonly by direct contact with an infested person or an infested person\u2019s clothing or bedding. Body lice usually infest persons who do not launder and change their clothes regularly.\n    \nThe following are steps that can be taken to help prevent and control the spread of body lice:\n    \n     - Bathe regularly and change into properly laundered clothes at least once a week; launder infested clothing at least once a week.\n     - Machine wash and dry infested clothing and bedding using the hot water (at least 130\u00b0F) laundry cycle and the high heat drying cycle. Clothing and items that are not washable can be dry-cleaned OR sealed in a plastic bag and stored for 2 weeks.\n     - Do not share clothing, beds, bedding, and towels used by an infested person.\n     - Fumigation or dusting with chemical insecticides sometimes is necessary to control and prevent the spread of body lice for certain diseases (epidemic typhus)."}
{"_id":"7bcbad7a-0fce-4111-a6ec-2cebf0d3fc1a","text":"There is no vaccine against La Crosse encephalitis virus (LACV). Reducing exposure to mosquito bites is the best defense against getting infected with LACV or other mosquito-borne viruses. There are several approaches you and your family can use to prevent and control mosquito-borne diseases. \n \n - Use repellent: When outdoors, use insect repellent containing DEET, picaridin, IR3535 or oil of lemon eucalyptus on exposed skin as well as on clothing (mosquitoes will bite through thin cloth). \n   \n   - Permethrin is a repellent\/insecticide that can be applied to clothing and will provide excellent protection through multiple washes. You can treat clothing yourself (always follow the directions on the package!) or purchase pre-treated clothing. For best protection it is still necessary to apply other repellent to exposed skin.  \n    \n - Wear protective clothing: Wear long sleeves, pants and socks when weather permits. \n - Avoid peak biting hours: Avoid outdoor activity or use protective measures when mosquitoes are active (Aedes triseriatus mosquitoes are most active during daytime\u2014from dawn until dusk). \n - Install and repair screens: Have secure, intact screens on windows and doors to keep mosquitoes out.  \n - Keep mosquitoes from laying eggs near you: Mosquitoes can lay eggs even in small amounts of standing water. While Aedes triseriatus prefers treeholes, it will also lay eggs in artificial containers. You can fill treeholes in\/around your yard with soil. Get rid of mosquito breeding sites by emptying standing water from flower pots, buckets, barrels, and tires. Change the water in pet dishes and replace the water in bird baths weekly. Drill holes in tire swings so water drains out. Empty children's wading pools and store on their side after use.  \n"}
{"_id":"2d531a00-86e2-4d36-a478-a45c285d779a","text":"Frequently Asked Questions (FAQs)\n    \n    \n                \n    Fact Sheets"}
{"_id":"df34290b-b109-4979-96e9-63d3aada24d7","text":"Infected dogs and cats shed Toxocara eggs in their feces into the environment. Once in the environment, it takes 2 to 4 weeks for Toxocara larvae to develop and for the eggs to become infectious. Humans or other animals can be infected by accidentally ingesting Toxocara eggs. For example, humans can become infected if they work with dirt and accidentally ingest dirt containing Toxocara eggs. Although rare, people can be infected by eating undercooked or raw meat from an infected animal such as a lamb or rabbit. Because dogs and cats are frequently found where people live, there may be large numbers of infected eggs in the environment. Once in the body, the Toxocara eggs hatch and roundworm larvae can travel in the bloodstream to different parts of the body, including the liver, heart, lungs, brain, muscles, or eyes. Most infected people do not have any symptoms. However, in some people, the Toxocara larvae can cause damage to these tissues and organs. The symptoms of toxocariasis, the disease caused by these migrating larvae, include fever, coughing, inflammation of the liver, or eye problems.\n    \nA U.S. study in 1996 showed that 30% of dogs younger than 6 months deposit Toxocara eggs in their feces; other studies have shown that almost all puppies are born already infected with Toxocara canis. Research also suggests that 25% of all cats are infected with Toxocara cati. Infection rates are higher for dogs and cats that are left outside for more time and allowed to eat other animals. In humans, it has been found that almost 14% of the U.S. population has been infected with Toxocara. Globally, toxocariasis is found in many countries, and prevalence rates can reach as high as 40% or more in parts of the world. There are several factors that have been associated with higher rates of infection with Toxocara. People are more likely to be infected with Toxocara if they own a dog. Children and adolescents under the age of 20 are more likely to test positive for Toxocara infection. This may be because children are more likely to eat dirt and play in outdoor environments, such as sandboxes, where dog and cat feces can be found. This infection is more common in people living in poverty. Geographic location plays a role as well, because Toxocara is more prevalent in hot, humid regions where eggs are kept viable in the soil."}
{"_id":"be36997c-5f5e-4358-a3cb-88b2f8a04dda","text":"If you think you or your child may have toxocariasis, you should see your health care provider to discuss the possibility of infection and, if necessary, to be examined. Toxocariasis can be difficult to diagnose because the symptoms of toxocariasis are similar to the symptoms of other infections. A blood test is available that looks for evidence of infection with Toxocara larvae. In addition to the blood test, diagnosis of toxocariasis includes identifying the presence of typical clinical signs of VT or OT and a history of exposure to cats and dogs."}
{"_id":"bb1813a6-1f0e-4367-8207-7be8f32fcd0d","text":"Visceral toxocariasis can be treated with antiparasitic drugs such as albendazole or mebendazole. Treatment of ocular toxocariasis is more difficult and usually consists of measures to prevent progressive damage to the eye.\n    \nMore on: Resources For Health Professionals: Treatment"}
{"_id":"7d4e92e9-7d82-49f1-80c5-617a7748fdd0","text":"Controlling Toxocara infection in dogs and cats will reduce the number of infectious eggs in the environment and reduce the risk of infection for people. Have your veterinarian treat your dogs and cats, especially young animals, regularly for worms. This is especially important if your pets spend time outdoors and may become infected again.\n    \nThere are several things that you can do around your home to make you and your pets safer:\n    \n     - Clean your pet\u2019s living area at least once a week. Feces should be either buried or bagged and disposed of in the trash. Wash your hands after handling pet waste.\n     - Do not allow children to play in areas that are soiled with pet or other animal feces and cover sandboxes when not in use to make sure that animals do not get inside and contaminate them.\n     - Wash your hands with soap and warm water after playing with your pets or other animals, after outdoor activities, and before handling food.\n     - Teach children the importance of washing hands to prevent infection.\n     - Teach children that it is dangerous to eat dirt or soil.\n    \n    \nMore on: Handwashing\n    \nToxocara eggs have a strong protective layer which makes the eggs able to survive in the environment for months or even years under the right conditions. Many common disinfectants are not effective against Toxocara eggs but extreme heat has been shown to kill the eggs. Prompt removal of animal feces can help prevent infection since the eggs require 2 to 4 weeks to become infective once they are out of the animal."}
{"_id":"c7679b08-ee61-4e34-85dc-25ade428e30c","text":"Acanthamoeba is a microscopic, free-living ameba (single-celled living organism) commonly found in the environment that can cause rare, but severe, illness. Acanthamoeba causes three main types of illness involving the eye (Acanthamoeba keratitis), the brain and spinal cord (Granulomatous Encephalitis), and infections that can spread throughout the entire body (disseminated infection)."}
{"_id":"5d273bd0-1898-4cf4-87fe-2230110e664c","text":"Acanthamoeba keratitis\n  \n   \nAcanthamoeba keratitis is a rare disease that can affect anyone, but is most common in individuals who wear contact lenses. In the United States, an estimated 85% of cases occur in contact lens users. The incidence of the disease in developed countries is approximately one to 33 cases per million contact lens wearers.\n   \nFor people who wear contact lenses, certain practices can increase the risk of getting Acanthamoeba keratitis:\n   \n    - Storing and handling lenses improperly\n    - Disinfecting lenses improperly (such as using tap water or topping off solutions when cleaning the lenses or lens case)\n    - Swimming, using a hot tub, or showering while wearing lenses\n    - Coming into contact with contaminated water\n    - Having a history of trauma to the cornea\n   \n   \nContact lens wearers who practice proper lens care and non-contact lens wearers can still develop the infection. For additional information on contact lens care and prevention of Acanthamoeba keratitis visit CDC\u2019s web page on Prevention and Control.\n   \nThere have been no reports of Acanthamoeba keratitis being spread from one person to another.\n   Granulomatous Amebic Encephalitis (GAE)\n   \nGranulomatous Amebic Encephalitis (GAE) and disseminated infection are very rare forms of Acanthamoeba infection and primarily affect people with compromised immune systems. While unusual, disseminated infection can also affect healthy children and adults. Conditions that may increase a patient\u2019s risk for GAE and disseminated infection include:\n   \n    - AIDS\n    - Organ\/Tissue transplant\n    - Steroids or excessive use of antibiotics\n    - Diabetes Mellitus\n    - Cancer\n    - Disorders in which white blood cells in the lymphatic tissue are over-produced or abnormal\n    - Disorders in which blood cells or blood clotting mechanisms do not function properly or are abnormal\n    - Liver cirrhosis\n    - Lupus"}
{"_id":"f08137f3-040b-4327-bf4e-632991ca2a0f","text":"Early diagnosis is essential for effective treatment of Acanthamoeba keratitis. The infection is usually diagnosed by an eye specialist based on symptoms, growth of the ameba from a scraping of the eye, and\/or seeing the ameba by a process called confocal microscopy.\n    \nGranulomatous Amebic Encephalitis (GAE) and disseminated infection are more difficult to diagnose and are often at advanced stages when they are diagnosed. Tests useful in the diagnosis of GAE include brain scans, biopsies, or spinal taps. In disseminated disease, biopsy of the involved sites (e.g. , skin, sinuses) can be useful in diagnosis."}
{"_id":"783f2d89-a97d-4382-94e0-c808377728d6","text":"Early diagnosis is essential for effective treatment of Acanthamoeba keratitis. Several prescription eye medications are available for treatment. However, the infection can be difficult to treat. The best treatment regimen for each patient should be determined by an eye doctor. If you suspect your eye may be infected with Acanthamoeba, see an eye doctor immediately.\n    \nSkin infections that are caused by Acanthamoeba but have not spread to the central nervous system can be successfully treated. Because this is a serious infection and the people affected typically have weakened immune systems, early diagnosis offers the best chance at cure.\n    \nMost cases of brain and spinal cord infection with Acanthamoeba (Granulomatous Amebic Encephalitis) are fatal."}
{"_id":"0e8d3655-6419-4d81-bffb-92689324f193","text":"Topics"}
{"_id":"0048ede1-193e-4739-8a9e-ba270b160359","text":"Scabies is an infestation of the skin by the human itch mite (Sarcoptes scabiei var. hominis). The microscopic scabies mite burrows into the upper layer of the skin where it lives and lays its eggs. The most common symptoms of scabies are intense itching and a pimple-like skin rash. The scabies mite usually is spread by direct, prolonged, skin-to-skin contact with a person who has scabies.\nScabies is found worldwide and affects people of all races and social classes. Scabies can spread rapidly under crowded conditions where close body and skin contact is frequent. Institutions such as nursing homes, extended-care facilities, and prisons are often sites of scabies outbreaks. Child care facilities also are a common site of scabies infestations."}
{"_id":"ed7a01d1-4cd1-487f-a959-782cbc3c9b2f","text":"Transmission\n    \nHuman scabies is caused by an infestation of the skin by the human itch mite (Sarcoptes scabiei var. hominis). The adult female scabies mites burrow into the upper layer of the skin (epidermis) where they live and deposit their eggs. The microscopic scabies mite almost always is passed by direct, prolonged, skin-to-skin contact with a person who already is infested. An infested person can spread scabies even if he or she has no symptoms. Humans are the source of infestation; animals do not spread human scabies.\n    Persons At Risk\n    \nScabies can be passed easily by an infested person to his or her household members and sexual partners. Scabies in adults frequently is sexually acquired.\n    \nScabies is a common condition found worldwide; it affects people of all races and social classes. Scabies can spread easily under crowded conditions where close body and skin contact is common. Institutions such as nursing homes, extended-care facilities, and prisons are often sites of scabies outbreaks. Child care facilities also are a common site of scabies infestations.\n    Crusted (Norwegian) Scabies\n    \nSome immunocompromised, elderly, disabled, or debilitated persons are at risk for a severe form of scabies called crusted, or Norwegian, scabies. Persons with crusted scabies have thick crusts of skin that contain large numbers of scabies mites and eggs. The mites in crusted scabies are not more virulent than in non-crusted scabies; however, they are much more numerous (up to 2 million per patient). Because they are infested with such large numbers of mites, persons with crusted scabies are very contagious to other persons. In addition to spreading scabies through brief direct skin-to-skin contact, persons with crusted scabies can transmit scabies indirectly by shedding mites that contaminate items such as their clothing, bedding, and furniture. Persons with crusted scabies should receive quick and aggressive medical treatment for their infestation to prevent outbreaks of scabies."}
{"_id":"faca4e72-d273-4657-88a1-93c7253f816b","text":"Diagnosis of a scabies infestation usually is made based upon the customary appearance and distribution of the the rash and the presence of burrows.\n    \nWhenever possible, the diagnosis of scabies should be confirmed by identifying the mite or mite eggs or fecal matter (scybala). This can be done by carefully removing the mite from the end of its burrow using the tip of a needle or by obtaining a skin scraping to examine under a microscope for mites, eggs, or mite fecal matter (scybala). However, a person can still be infested even if mites, eggs, or fecal matter cannot be found; fewer then 10-15 mites may be present on an infested person who is otherwise healthy."}
{"_id":"5d629f40-ba2e-4a07-a10b-b458935f0d3e","text":"Suggested General Guidelines \n  \n    \n   \n  \nIt is important to remember that the first time a person gets scabies they usually have no symptoms during the first 2 to 6 weeks they are infested; however they can still spread scabies during this time. \n  \nTreatment should be given to both the infested person and to household members and sexual contacts, particularly those who have had prolonged direct skin-to-skin contact with the infested person. Both sexual and close personal contacts who have had direct prolonged skin-to-skin contact with an infested person within the preceding month should be examined and treated. All persons should be treated at the same time to prevent reinfestation. Scabies may sometimes be sexually-acquired in adults, but is rarely sexually-acquired in children. \n  \nBedding, clothing, and towels used by infested persons or their household, sexual, and close contacts (as defined above) anytime during the three days before treatment should be decontaminated by washing in hot water and drying in a hot dryer, by dry-cleaning, or by sealing in a plastic bag for at least 72 hours. Scabies mites generally do not survive more than 2 to 3 days away from human skin. \n  \nUse of insecticide sprays and fumigants is not recommended. \n    \n  Medications Used to Treat Scabies \n  \n    \n   \n  \nProducts used to treat scabies are called scabicides because they kill scabies mites; some also kill mite eggs. Scabicides used to treat human scabies are available only with a doctor\u2019s prescription. No \u201cover-the-counter\u201d (non-prescription) products have been tested and approved to treat scabies. \n  \nScabicide should be applied to all areas of the body from the neck down to the feet and toes. In addition, when treating infants and young children, scabicide also should be applied to their entire head and neck because scabies can affect their face, scalp, and neck, as well as the rest of their body. The scabicide should be applied to a clean body and left on for the recommended time before washing it off. Clean clothing should be worn after treatment. \n  \nThe instructions contained in the box or printed on the label always should be followed carefully. Always contact a doctor or pharmacist if unsure how to use a particular medicine. \n  \nBecause the symptoms of scabies are due to a hypersensitivity reaction (allergy) to mites and their feces (scybala), itching still may continue for several weeks after treatment even if all the mites and eggs are killed. If itching still is present more than 2 to 4 weeks after treatment or if new burrows or pimple-like rash lesions continue to appear, retreatment may be necessary. \n  \nSkin sores that become infected should be treated with an appropriate antibiotic prescribed by a doctor."}
{"_id":"6bbf9d19-4212-40c3-8fa4-11b030ff20e9","text":"When a person is infested with scabies mites the first time, symptoms may not appear for up to two months after being infested. However, an infested person can transmit scabies, even if they do not have symptoms. Scabies usually is passed by direct, prolonged skin-to-skin contact with an infested person. However, a person with crusted (Norwegian) scabies can spread the infestation by brief skin-to-skin contact or by exposure to bedding, clothing, or even furniture that he\/she has used.\n    \nScabies is prevented by avoiding direct skin-to-skin contact with an infested person or with items such as clothing or bedding used by an infested person. Scabies treatment usually is recommended for members of the same household, particularly for those who have had prolonged skin-to-skin contact. All household members and other potentially exposed persons should be treated at the same time as the infested person to prevent possible reexposure and reinfestation. Bedding and clothing worn or used next to the skin anytime during the 3 days before treatment should be machine washed and dried using the hot water and hot dryer cycles or be dry-cleaned. Items that cannot be dry-cleaned or laundered can be disinfested by storing in a closed plastic bag for several days to a week. Scabies mites generally do not survive more than 2 to 3 days away from human skin. Children and adults usually can return to child care, school, or work the day after treatment.\n    \nPersons with crusted scabies and their close contacts, including household members, should be treated rapidly and aggressively to avoid outbreaks. Institutional outbreaks can be difficult to control and require a rapid, aggressive, and sustained response.\n    \nRooms used by a patient with crusted scabies should be thoroughly cleaned and vacuumed after use. Environmental disinfestation using pesticide sprays or fogs generally is unnecessary and is discouraged."}
{"_id":"d5b0f996-1373-4d3b-804b-ded7bd0f1529","text":"Transmission of AHFV is not well understood. AHFV is a zoonotic virus, and its described tick hosts (the soft tick Ornithodoros savignyi and the hard tick Hyalomma dromedari) are widely distributed. People can become infected through a tick bite or when crushing infected ticks. Epidemiologic studies indicate that contact with domestic animals or livestock may increase the risk of human infection. No human-to-human transmission of AHF has been documented. \n \nAlthough livestock animals may provide blood meals for ticks, it is thought that they play a minor role in transmitting AHFV to humans. No transmission through non-pasteurized milk has been described, although other tick-borne flaviviruses have been transmitted to humans through this route."}
{"_id":"bed0f07e-0f14-454f-8e8f-5244ed2ac2ba","text":"Based on limited information, after an incubation period that could be as short as 2-4 days, the disease presents initially with non-specific flu-like symptoms, including fever, anorexia (loss of appetite), general malaise, diarrhea, and vomiting; a second phase has appeared in some patients, and includes neurologic and hemorrhagic symptoms in severe form. Multi-organ failure precedes fatal outcomes. No repeated or chronic symptoms have been reported following recovery. Evidence suggests that a milder form may exist, where hospitalization is not required. \n                \nThrombocytopenia, leukopenia, and elevated liver enzymes are nearly always observed in patients who have been hospitalized."}
{"_id":"a7fda042-e7b2-42a7-af72-253ce404646d","text":"Contact with  livestock with tick exposure are risk factors for humans, as is contact with infected ticks, whether through crushing the infected tick with unprotected fingers or by a bite from an infected tick. Slaughtering of animals which may acutely but asymptomatically infected may also be a risk factor, as it is possible that infected animals develop a viremia without obvious clinical signs."}
{"_id":"dfbdf6f3-358b-41ab-a214-8996872548af","text":"Clinical diagnosis could be difficult due to similarities between AVHF, Crimean-Congo Hemorrhagic fever (CCHF), and Rift Valley fever (RVF), which occur in similar geographic areas. Laboratory diagnosis of AHF can be made in the early stage of the illness by molecular detection by PCR or virus isolation from blood. Later, serologic testing using enzyme-linked immunosorbent serologic assay (ELISA) can be performed."}
{"_id":"8cabda06-988a-4c13-ac3e-fb803dd73f32","text":"There is no standard specific treatment for the disease. Patients receive supportive therapy, which consists of balancing the patient\u2019s fluid and electrolytes, maintaining oxygen status and blood pressure, and treatment for any complications. Mortality in hospitalized patients ranges from 1-20%."}
{"_id":"88ce916d-b543-4667-9704-0c8912d54f90","text":"Given that no treatment or specific prophylaxis is presently available, prevention and increased awareness of AHFV are the only recommended measures. Complete control of ticks and interruption of the virus life cycle is impractical; in endemic regions, it is important to avoid tick-infested areas and to limit contact with livestock and domestic animals.  \n                \nIndividuals should use tick repellants on skin and clothes and check skin for attached ticks, removing them as soon as possible. Tick collars are available for domestic animals, and dipping in acaricides is effective in killing ticks on livestock. People working with animals or animal products in farms or slaughterhouses should avoid unprotected contact with the blood, fluids, or tissues of any potentially infected or viremic animals."}
{"_id":"5027db73-88ed-4161-a934-792f1a39916f","text":"Taeniasis in humans is a parasitic infection caused by the tapeworm species Taenia saginata (beef tapeworm), Taenia solium (pork tapeworm), and Taenia asiatica (Asian tapeworm). Humans can become infected with these tapeworms by eating raw or undercooked beef (T. saginata) or pork (T. solium and T. asiatica). People with taeniasis may not know they have a tapeworm infection because symptoms are usually mild or nonexistent.\n\nT. solium tapeworm infections can lead to cysticercosis, which is a disease that can cause seizures, so it is important seek treatment."}
{"_id":"a5b196cd-854c-4445-8561-6aca16fb8da5","text":"The tapeworms that cause taeniasis (Taenia saginata, T. solium, and T. asiatica) are found worldwide. Eating raw or undercooked beef or pork is the primary risk factor for acquiring taeniasis. Persons who don't eat raw or undercooked beef or pork are not likely to get taeniasis.\n    \nInfections with T. saginata occur wherever contaminated raw beef is eaten, particularly in Eastern Europe, Russia, eastern Africa and Latin America. Taeniasis due to T. saginata is rare in the United States, except in places where cattle and people are concentrated and sanitation is poor, such as around feed lots when cattle can be exposed to human feces. Tapeworm infections due to T. solium are more prevalent in under-developed communities with poor sanitation and where people eat raw or undercooked pork. Higher rates of illness have been seen in people in Latin America, Eastern Europe, sub-Saharan Africa, India, and Asia. Taenia solium taeniasis is seen in the United States, typically among Latin American immigrants. Taenia asiatica is limited to Asia and is seen mostly in the Republic of Korea, China, Taiwan, Indonesia, and Thailand.\n    \nA disease called cysticercosis can occur when T. solium tapeworm eggs are ingested. For example, people with poor hygiene who have taeniasis -- with or without symptoms -- will shed tapeworm eggs in their feces and might accidentally contaminate their environment. This can lead to transmission of cysticercosis to themselves or others.\n    \nMore on: Cysticercosis"}
{"_id":"a7b585fd-0e76-4495-b4c8-66f4cdde228e","text":"Diagnosis of Taenia tapeworm infections is made by examination of stool samples; individuals should also be asked if they have passed tapeworm segments. Stool specimens should be collected on three different days and examined in the lab for Taenia eggs using a microscope. Tapeworm eggs can be detected in the stool 2 to 3 months after the tapeworm infection is established.\n    \nTapeworm eggs of T. solium can also infect humans, causing cysticercosis. It is important to diagnose and treat all tapeworm infections.\n    \nMore on: cysticercosis"}
{"_id":"65521fc8-e447-46d1-a65a-c32cdcf8688e","text":"Treatment is available after accurate diagnosis. Your doctor will provide prescription medication, either praziquantel or niclosamide, which is taken by mouth. The medication is also available in a children\u2019s dosage. Work with your health care provider for proper treatment options for you and your family.\n    \nMore on: Resources For Health Professionals: Treatment"}
{"_id":"b46e67a9-955f-4918-8ead-2661a913acfd","text":"One way to prevent taeniasis is to cook meat to safe temperatures. A food thermometer should be used to measure the internal temperature of cooked meat. Do not sample meat until it is cooked. USDA recommends the following for meat preparation.\n   \n    - For Whole Cuts of Meat (excluding poultry) \n     \n      - Cook to at least 145\u00b0 F (63\u00b0 C) as measured with a food thermometer placed in the thickest part of the meat, then allow the meat to rest* for three minutes before carving or consuming.\n     \n    - For Ground Meat (excluding poultry) \n     \n      - Cook to at least 160\u00b0 F (71\u00b0 C); ground meats do not require a rest* time.\n     \n   \n   \n*According to USDA, \"A 'rest time' is the amount of time the product remains at the final temperature, after it has been removed from a grill, oven, or other heat source. During the three minutes after meat is removed from the heat source, its temperature remains constant or continues to rise, which destroys pathogens.\"\n   \nMore on: Fight BAC: Safe Food Handling"}
{"_id":"eb24b068-5f18-4628-af7f-546327a62361","text":"Baylisascaris worms are intestinal parasites found in a wide variety of animals. Different species of Baylisascaris are associated with different animal hosts. For example, Baylisascaris procyonis is found in raccoons and Baylisascaris columnaris is an intestinal parasite found in skunks. Cases of Baylisascaris infection in people are not frequently reported, but can be severe. Baylisascaris procyonis is thought to pose the greatest risk to humans because of the often close association of raccoons to human dwellings."}
{"_id":"5256e2b2-462d-47c3-87fb-2b86e58889f9","text":"Raccoons are the primary, or definitive, host of Baylisascaris procyonis, a roundworm. Raccoons become infected with Baylisascaris in one of two ways:\n    \n     - Young raccoons become infected by eating eggs during foraging, feeding, and grooming.\n     - Adult raccoons acquire the infection by eating rodents, rabbits, and birds infected with the larvae of Baylisascaris.\n    \n    \nInfected raccoons have been found throughout the United States, mainly in the Midwest, Northeast, Middle Atlantic, and West Coast.\n    \nRaccoons are peridomestic animals, which means they live in or around areas where people live. Roundworm eggs are passed in the feces of infected raccoons. Raccoons defecate in communal sites, called latrines. Raccoon latrines are often found at bases of trees, unsealed attics, or on flat surfaces such as logs, tree stumps, rocks, decks, and rooftops. As more raccoons move into populated areas, the number and density of their latrines will increase.\n    \nWhile raccoons are the roundworm's primary host, other types of animals can become infected. Birds and small mammals, such as rodents and rabbits, are susceptible to the parasite. Unlike raccoons, these animals sometimes show signs of infection, such as muscle spasms, tremors, and progressive weakness; infection can lead to death. Predator animals, including dogs, may become infected by eating an animal that has been infected with Baylisascaris. In some dogs, Baylisascaris may develop to adult worms and pass eggs in the dogs' feces.\n    \nThe worms develop to maturity in the raccoon intestine, where they produce millions of eggs that are passed in the feces. Eggs that are excreted by raccoons are not immediately infectious. These eggs must develop in the environment for 2 to 4 weeks, after which the eggs are able to cause infection. The eggs are resistant to most environmental conditions and with adequate moisture, can survive for years.\n    \n     \n    \n    \nHumans become infected by ingesting embryonated (fertile) eggs. Anyone who is exposed to environments where raccoons frequent is potentially at risk. Young children or developmentally disabled persons are at highest risk for infection as they may be more likely to put contaminated fingers, soil, or objects into their mouths.\n    \nHunters, trappers, taxidermists, and wildlife handlers may also be at increased risk if they have contact with raccoons or raccoon habitats.\n    \nFewer than 25 cases of Baylisascaris disease have been documented in the United States. However, it is possible that some cases are incorrectly diagnosed as other infections or go undiagnosed. Cases that are diagnosed tend to be severe.\n    \nCases have been reported in California, Illinois, Louisiana, Massachusetts, Michigan, Minnesota, Missouri, New York, Oregon, and Pennsylvania. As of 2012, there were 16 published human neurological cases in the US; six of the infected persons died."}
{"_id":"a17c9c06-f538-46b5-bb50-e7f9e35324d4","text":"If you suspect you have been infected, consult your health care provider immediately. Be sure to tell your health care provider if you have recently been exposed to raccoons or their feces.\n    \nDiagnosis is difficult because symptoms depend on the number of infecting larvae and location in the body. Ocular larva migrans, when the larvae migrate to the eye, can cause sensitivity to light, inflammation of the eye, and blindness. Symptoms of visceral larva migrans, when the larvae travel to organs, depend on which organs are affected. For example, an invasion of the liver may cause hepatomegaly (inflammation and enlargement of the liver), while an invasion of the lung may cause pulmonary symptoms such as cough or chest pain. Larvae rarely end up in the nervous system but the most severe cases are neural larva migrans, when the larvae migrate into the brain and cause it to swell (encephalitis). There is no commercially available test for Baylisascaris infection. A health care provider may test blood, cerebrospinal fluid (CSF), and tissue to determine if an individual is infected. Eye examinations may reveal a migrating larva or lesions and are often the most significant clue to infection with Baylisascaris.\n    \nDiagnosis often is made by ruling out other infections that cause similar symptoms. Information on diagnosis and testing can be obtained through your local or state health department or CDC.\n    \nMore on: Resources for Health Professionals: Diagnosis"}
{"_id":"8e0fef0d-642c-4438-870a-467d2c71fd66","text":"No drugs have been shown to be totally effective for the treatment of Baylisascaris infection. Albendazole, a broad spectrum anthelmintic, has been recommended for specific cases.\n    \nEarly treatment might reduce serious damage caused by the infection. Should you suspect you may have ingested raccoon feces, seek immediate medical attention.\n    \nMore on: Resources for Health Professionals: Treatment"}
{"_id":"dab91bb3-01eb-4fec-8a0a-ac5777a3d24f","text":"Baylisascaris infection can be prevented by avoiding contact with raccoons and their feces. Washing your hands after working or playing outdoors is good practice for preventing a number of diseases.\n    \nDo not keep, feed, or adopt wild animals, including raccoons, as pets. Infection rarely causes symptoms in raccoons, so you cannot tell if a raccoon is infected by observing its behavior. Roundworm eggs passed in the feces of infected raccoons are not visible to the naked eye. Eggs can only be seen using a microscope.\n    \n     \n    \n    \nYou may discourage raccoons from living in and around your home or parks by taking these steps:\n    \n     - prevent access to food\n     - keep trash containers tightly closed\n     - close off access to attics and basements\n     - keep sandboxes covered when not in use (raccoons may use sandboxes as a latrine)\n     - remove fish ponds -- they eat the fish and drink the water\n     - eliminate water sources\n     - remove bird feeders\n     - clear brush so raccoons are not likely to make a den on your property\n    \n    \nStay away from areas and materials that might be contaminated by raccoon feces. Raccoons typically defecate at the base of or in raised forks of trees, or on raised horizontal surfaces such as fallen logs, stumps, or large rocks. Raccoon feces also can be found on woodpiles, decks, rooftops, and in attics, garages, and haylofts. Feces usually are dark and tubular, have a pungent odor (usually worse than dog or cat feces), and often contain undigested seeds or other food items.\n    \nIf you have found a raccoon latrine near your home, cleaning the area may prevent possible infection. Newly deposited eggs take at least 2-4 weeks to become infective. Prompt removal and destruction of raccoon feces will reduce risk for exposure and possible infection.\n    \nMore on: Raccoon Latrine Clean-up [PDF, 111 KB, 1 page]\n    \n     \n    \n    \nIf you choose to clean the site yourself, care should be taken to avoid contaminating hands and clothes.\n    \n     - Wear disposable gloves to help prevent cross contamination.\n     - Wear a N95-rated respirator if working in a confined space to prevent accidental ingestion of eggs or other harmful materials.\n     - Avoid stirring up dust and debris- you can lightly mist the latrine area with a little water from a spray bottle to reduce the amount of dust.\n     - Wear rubber boots that can be scrubbed or cover your shoes with disposable booties that can be thrown away, so that you do not bring eggs into your household.\n     - Feces and material contaminated with raccoon feces should be removed and burned, buried, or sent to a landfill.\n     - Most chemicals do not kill roundworm eggs; however, heat kills the eggs instantly.\n     - Treat feces-soiled decks, patios, and other surfaces with boiling water or a propane torch (please contact your local fire department for regulations and safety practices).\n    \n    \nTo help further reduce the risk of possible infection, wash your hands well with soap and warm running water. Clean\/launder your clothes thoroughly with hot water and detergent.\n    \nMore on: Handwashing\n    \nIf you are cleaning an indoor raccoon latrine and are not able to use a propane torch, use a damp (but not wet) sponge to wipe the area with hot soapy water. Rinse your sponge frequently. After you are finished, flush dirty water down the toilet. Place the sponge in a plastic bag and put the plastic bag in the garbage.\n    \nContact your local animal control office for additional assistance.\n    Dogs\n    \nDogs may be infected with adult B. procyonis roundworms, but may not show symptoms. Have all pets de-wormed under a veterinarian's supervision and take precautions to avoid contact with their feces.\n    Exotic pets\n    \nRaccoons and dogs are not the only hosts of Baylisascaris. B. procyonis infection has also been documented in kinkajous. Other animals such as coatis may be susceptible. When wild animals are kept as pets, there can be a risk of disease transmission to humans."}
{"_id":"80d10b4c-af61-4018-9314-bd06df264447","text":"Babesiosis is caused by microscopic parasites that infect red blood cells. Most human cases of Babesia infection in the United States are caused by the parasite Babesia microti. Occasional cases caused by other species (types) of Babesia have been detected. Babesia microti is spread in nature by Ixodes scapularis ticks (also called blacklegged ticks or deer ticks). Tickborne transmission is most common in particular regions and seasons: it mainly occurs in parts of the Northeast and upper Midwest; and it usually peaks during the warm months. Babesia infection can range in severity from asymptomatic to life threatening. The infection is both treatable and preventable.\n    Frequently Asked Questions (FAQs)\n    \n    Podcasts"}
{"_id":"e722ed05-97d4-4f35-aba5-11899752e94e","text":"People can get infected with Babesia parasites in several ways:\n    \n     - The main way is through the bite of an infected tick\u2014during outdoor activities in areas where babesiosis is found (see below).\n     - A less common way is by getting a transfusion from a blood donor who has a Babesia infection but does not have any symptoms. (No tests have been licensed yet for screening blood donors for Babesia.)\n     - Rare cases of congenital transmission\u2014from an infected mother to her baby (during pregnancy or delivery)\u2014have been reported.\n    \n    \nBabesia parasites are not transmitted from person-to-person like the flu or the common cold.\n    \nMany different species (types) of Babesia parasites have been found in animals, only a few of which have been found in people. Babesia microti\u2014which usually infects white-footed mice and other small mammals\u2014is the main species that has been found in people in the United States. Occasional (sporadic) cases of babesiosis caused by other Babesia species have been detected.\n    \n     \n    \n    \nBabesia microti is transmitted in nature by Ixodes scapularis ticks (also called blacklegged ticks or deer ticks).\n    \n     - Tickborne transmission primarily occurs in the Northeast and upper Midwest, especially in parts of New England, New York state, New Jersey, Wisconsin, and Minnesota.\n     - The parasite typically is spread by the young nymph stage of the tick, which is most apt to be found (seeking or \"questing\" for a blood meal) during warm months (spring and summer), in areas with woods, brush, or grass.\n     - Infected people might not recall a tick bite because I. scapularis nymphs are very small (about the size of a poppy seed)."}
{"_id":"8e6256a5-d273-4cbc-973b-d3e1cd9b8f42","text":"In symptomatic people, babesiosis usually is diagnosed by examining blood specimens under a microscope and seeing Babesia parasites inside red blood cells.\n    \nTo be sure the diagnosis is correct, your health care provider might have specimens of your blood tested by a specialized reference laboratory (such as at CDC or a health department).\n    \nMore on: Resources for Health Professionals: Diagnosis"}
{"_id":"78695f3a-951a-4ffa-b3a1-02b8339d00ad","text":"Effective treatments are available. People who do not have any symptoms or signs of babesiosis usually do not need to be treated.\n    \nBefore considering treatment, the first step is to make sure the diagnosis is correct.\n    \nFor more information, people should talk to their health care provider.\n    \nMore on: Resources for Health Professionals: Treatment"}
{"_id":"a8a78e27-e720-466c-a732-f69d43609a72","text":"Steps can be taken to reduce the risk for babesiosis and other tickborne infections. The use of prevention measures is especially important for people at increased risk for severe babesiosis (for example, people who do not have a spleen). Avoiding exposure to tick habitats is the best defense.\n   \nBabesia microti is spread by Ixodes scapularis ticks, which are mostly found in wooded, brushy, or grassy areas, in certain regions and seasons. No vaccine is available to protect people against babesiosis. However, people who live, work, or travel in tick-infested areas can take simple steps to help protect themselves against tick bites and tickborne infections.\n   \n    \n   \n   \nDuring outdoor activities in tick habitats, take precautions to keep ticks off the skin.\n   \n    - Walk on cleared trails and stay in the center of the trail, to minimize contact with leaf litter, brush, and overgrown grasses, where ticks are most likely to be found.\n    - Minimize the amount of exposed skin, by wearing socks, long pants, and a long-sleeved shirt. Tuck the pant legs into the socks, so ticks cannot crawl up the inside of the pants. Wear light-colored clothing, to make it easier to see and remove ticks before they attach to skin.\n    - Apply repellents to skin and clothing. Follow the instructions on the product label. \n     \n      - Products that contain DEET (N,N-diethylmetatoluamide) can be directly applied to exposed skin and to clothing, to help keep ticks away (by repelling them). The product label includes details about how and where to apply the repellent, how often to reapply it, and how to use it safely on children.\n      - Permethrin products can be applied to clothing\/boots (not to skin), actually kill ticks that come in contact with the treated clothing, and usually stay effective through several washings.\n     \n   \n   \n    \n   \n   \nAfter outdoor activities, conduct daily tick checks and promptly remove any ticks that are found. Thorough, daily tick checks are very important. The I. scapularis nymphs that typically spread B. microti are so small (about the size of a poppy seed) that they are easily overlooked. But they usually must stay attached to a person for more than 36-48 hours to be able to transmit the parasite.\n   \n    - Remove ticks from clothing and pets before going indoors.\n    - Conduct a full-body exam for ticks. Use a hand-held or full-length mirror to view all parts of the body. Be sure to check behind the knees, between the legs (groin\/thighs), between the toes, under the arms (armpits), around the waist, inside the belly button, the back of the neck, behind and in the ears, as well as in and around the scalp, hairline, and hair. Remember to check children and pets, too.\n   \n   \nRemove ticks that are attached to the skin as soon as possible, preferably by using pointed (fine-tipped) tweezers. Grab the tick\u2019s mouth parts close to the skin, and slowly pull the tick straight out (with steady outward pressure), until the tick lets go.\n   \nMore on: Removing Ticks\n   \nMore on: Ticks"}
{"_id":"5852c5f3-3e46-4e43-88a7-509795d486e7","text":"The first symptoms of rabies may be very similar to those of the flu including general weakness or discomfort, fever, or headache. These symptoms may last for days.\n                \nThere may be also discomfort or a prickling or itching sensation at the site of bite, progressing within days to symptoms of cerebral dysfunction, anxiety, confusion, agitation. As the disease progresses, the person may experience delirium, abnormal behavior, hallucinations, and insomnia.\n                \nThe acute period of disease typically ends after 2 to 10 days. Once clinical signs of rabies appear, the disease is nearly always fatal, and treatment is typically supportive.\n                \nDisease prevention includes administration of both passive antibody, through an injection of human immune globulin and a round of injections with rabies vaccine.\n                \nOnce a person begins to exhibit signs of the disease, survival is rare. To date less than 10 documented cases of human survival from clinical rabies have been reported and only two have not had a history of pre- or postexposure prophylaxis."}
{"_id":"6c365787-e5ca-4d82-99d8-f2971d929622","text":"Any animal bitten or scratched by either a wild, carnivorous mammal or a bat that is not available for testing should be regarded as having been exposed to rabies.\n  \nUnvaccinated dogs, cats, and ferrets exposed to a rabid animal should be euthanized immediately. If the owner is unwilling to have this done, the animal should be placed in strict isolation for 6 months and vaccinated 1 month before being released.\n  \nAnimals with expired vaccinations need to be evaluated on a case-by-case basis. Dogs and cats that are currently vaccinated are kept under observation for 45 days.\n  \nSmall mammals such as squirrels, rats, mice, hamsters, guinea pigs, gerbils, chipmunks, rabbits, and hares are almost never found to be infected with rabies and have not been known to cause rabies among humans in the United States. Bites by these animals are usually not considered a risk of rabies unless the animal was sick or behaving in any unusual manner and rabies is widespread in your area.\n  \nHowever, from 1985 through 1994, woodchucks accounted for 86% of the 368 cases of rabies among rodents reported to CDC. Woodchucks or groundhogs (Marmota monax) are the only rodents that may be frequently submitted to state health department because of a suspicion of rabies. In all cases involving rodents, the state or local health department should be consulted before a decision is made to initiate postexposure prophylaxis (PEP).\n  Is there rabies in my area?\n  \nEach state collects specific information about rabies, and is the best source for information on rabies in your area. In addition, the CDC publishes rabies surveillance data every year for the United States. The report, entitled Rabies Surveillance in the United States, contains information about the number of cases of rabies reported to CDC during the year, the animals reported rabid, maps showing where cases were reported for wild and domestic animals, and distribution maps showing outbreaks of rabies associated with specific animals."}
{"_id":"eafd0739-4a74-4750-817b-7ed377179cce","text":"In animals, rabies is diagnosed using the direct fluorescent antibody (DFA) test, which looks for the presence of rabies virus antigens in brain tissue. In humans, several tests are required.\n \nRapid and accurate laboratory diagnosis of rabies in humans and other animals is essential for timely administration of postexposure prophylaxis. Within a few hours, a diagnostic laboratory can determine whether or not an animal is rabid and inform the responsible medical personnel. The laboratory results may save a patient from unnecessary physical and psychological trauma, and financial burdens, if the animal is not rabid.\n \nIn addition, laboratory identification of positive rabies cases may aid in defining current epidemiologic patterns of disease and provide appropriate information for the development of rabies control programs.\n \nThe nature of rabies disease dictates that laboratory tests be standardized, rapid, sensitive, specific, economical, and reliable."}
{"_id":"45c7bda3-850b-439f-926c-18b34a4b216d","text":"Botulism is a rare but serious paralytic illness caused by a nerve toxin that is produced by the bacterium Clostridium botulinum and sometimes by strains of Clostridium butyricum and Clostridium baratii. There are five main kinds of botulism. Foodborne botulism is caused by eating foods that contain the botulinum toxin. Wound botulism is caused by toxin produced from a wound infected with Clostridium botulinum. Infant botulism is caused by consuming the spores of the botulinum bacteria, which then grow in the intestines and release toxin. Adult intestinal toxemia (adult intestinal colonization) botulism is a very rare kind of botulism that occurs among adults by the same route as infant botulism. Lastly, iatrogenic botulism can occur from accidental overdose of botulinum toxin. All forms of botulism can be fatal and are considered medical emergencies. Foodborne botulism is a public health emergency because many people can be poisoned by eating a contaminated food."}
{"_id":"2a71f05d-a07c-428c-aae7-d35d0fed7591","text":"In the United States, an average of 145 cases are reported each year.Of these, approximately 15% are foodborne, 65% are infant botulism, and 20% are wound. Adult intestinal colonization and iatrogenic botulism also occur, but rarely. Outbreaks of foodborne botulism involving two or more persons occur most years and are usually caused by home-canned foods. Most wound botulism cases are associated with black-tar heroin injection, especially in California."}
{"_id":"81b774f8-5982-4eb5-b006-d1c1d02d2acd","text":"The classic symptoms of botulism include double vision, blurred vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness. Infants with botulism appear lethargic, feed poorly, are constipated, and have a weak cry and poor muscle tone. These are all symptoms of the muscle paralysis caused by the bacterial toxin. If untreated, these symptoms may progress to cause paralysis of the respiratory muscles, arms, legs, and trunk. In foodborne botulism, symptoms generally begin 18 to 36 hours after eating a contaminated food, but they can occur as early as 6 hours or as late as 10 days."}
{"_id":"be1b0c75-1981-49f6-b2b2-2c44abbe7a7d","text":"Physicians may consider the diagnosis if the patient's history and physical examination suggest botulism. However, these clues are usually not enough to allow a diagnosis of botulism. Other diseases such as Guillain-Barr\u00e9 syndrome, stroke, and myasthenia gravis can appear similar to botulism, and special tests may be needed to exclude these other conditions. These tests may include a brain scan, spinal fluid examination, nerve conduction test (electromyography, or EMG), and a tensilon test for myasthenia gravis. Tests for botulinum toxin and for bacteria that cause botulism can be performed at some state health department laboratories and at CDC."}
{"_id":"29cbfb16-6072-4ef4-9b4e-820eeea58559","text":"The respiratory failure and paralysis that occur with severe botulism may require a patient to be on a breathing machine (ventilator) for weeks or months, plus intensive medical and nursing care. The paralysis slowly improves. Botulism can be treated with an antitoxin which blocks the action of toxin circulating in the blood. Antitoxin for infants is available from the California Department of Public Health, and antitoxin for older children and adults is available through CDC.If given before paralysis is complete, antitoxin can prevent worsening and shorten recovery time. Physicians may try to remove contaminated food still in the gut by inducing vomiting or by using enemas. Wounds should be treated, usually surgically, to remove the source of the toxin-producing bacteria followed by administration of appropriate antibiotics. Good supportive care in a hospital is the mainstay of therapy for all forms of botulism."}
{"_id":"08ac0aba-23f6-42ac-886a-80c473e0f362","text":"Botulism can result in death due to respiratory failure. However, in the past 50 years the proportion of patients with botulism who die has fallen from about 50% to 3-5%. A patient with severe botulism may require a breathing machine as well as intensive medical and nursing care for several months, and some patients die from infections or other problems related to remaining paralyzed for weeks or months. Patients who survive an episode of botulism poisoning may have fatigue and shortness of breath for years and long-term therapy may be needed to aid recovery."}
{"_id":"ab93aa80-6224-40ff-8e41-ab73581aff0a","text":"Many cases of botulism are preventable. Foodborne botulism has often been from home-canned foods with low acid content, such as asparagus, green beans, beets and corn and is caused by failure to follow proper canning methods. However, seemingly unlikely or unusual sources are found every decade, with the common problem of improper handling during manufacture, at retail, or by consumers; some examples are chopped garlic in oil, canned cheese sauce, chile peppers, tomatoes, carrot juice, and baked potatoes wrapped in foil. In Alaska, foodborne botulism is caused by fermented fish and other aquatic game foods. Persons who do home canning should follow strict hygienic procedures to reduce contamination of foods, and carefully follow instructions on safe home canning including the use of pressure canners\/cookers as recommended through county extension services or from the US Department of Agriculture. Oils infused with garlic or herbs should be refrigerated. Potatoes which have been baked while wrapped in aluminum foil should be kept hot until served or refrigerated. Because the botulinum toxin is destroyed by high temperatures, persons who eat home-canned foods should consider boiling the food for 10 minutes before eating it to ensure safety. Wound botulism can be prevented by promptly seeking medical care for infected wounds and by not using injectable street drugs. Most infant botulism cases cannot be prevented because the bacteria that causes this disease is in soil and dust.  The bacteria can be found inside homes on floors, carpet, and countertops even after cleaning.  Honey can contain the bacteria that causes infant botulism so, children less than 12 months old should not be fed honey. Honey is safe for persons 1 year of age and older."}
{"_id":"5eb55afb-ec5c-4ad6-9aef-bb4937437a89","text":"Public education about botulism prevention is an ongoing activity. Information about safe canning is widely available for consumers. Persons in state health departments and at CDC are knowledgeable about botulism and available to consult with physicians 24 hours a day. If antitoxin is needed to treat a patient, it can be quickly delivered to a physician anywhere in the country. Suspected outbreaks of botulism are quickly investigated, and if they involve a commercial product, the appropriate control measures are coordinated among public health and regulatory agencies. Physicians should immediately report suspected cases of botulism to their state health department.\n                \nFor information and quidelines on canning foods at home: USDA Home Canning Guide"}
{"_id":"c58d0fb0-5d59-473e-8934-afc53521a676","text":"It is unknown how Marburg virus first transmits from its animal host to humans; however, for the 2 cases in tourists visiting Uganda in 2008, unprotected contact with infected bat feces or aerosols are the most likely routes of infection. \n  \nAfter this initial crossover of virus from host animal to humans, transmission occurs through person-to-person contact. This may happen in several ways: direct contact to droplets of body fluids from infected persons, or contact with equipment and other objects contaminated with infectious blood or tissues. \n  \nIn previous outbreaks, persons who have handled infected non-human primates or have come in direct contact with their fluids or cell cultures have become infected. Spread of the virus between humans has occurred in close environments and direct contacts. A common example is through caregivers in the home or in a hospital (nosocomial transmission)."}
{"_id":"70a6fd4e-5355-4db7-88b8-649880003038","text":"After an incubation period of 5-10 days, symptom onset is sudden and marked by fever, chills, headache, and myalgia. Around the fifth day after the onset of symptoms, a maculopapular rash, most prominent on the trunk (chest, back, stomach), may occur. Nausea, vomiting, chest pain, a sore throat, abdominal pain, and diarrhea may then appear. Symptoms become increasingly severe and can include jaundice, inflammation of the pancreas, severe weight loss, delirium, shock, liver failure, massive hemorrhaging, and multi-organ dysfunction. \n \nBecause many of the signs and symptoms of Marburg hemorrhagic fever are similar to those of other infectious diseases such as malaria or typhoid fever, clinical diagnosis of the disease can be difficult, especially if only a single case is involved. \n \nThe case-fatality rate for Marburg hemorrhagic fever is between 23-90%. For a complete listing of the case fatality rates for previous outbreaks, please see the History of Outbreaks table"}
{"_id":"054a7930-8eae-4d67-a76c-5d9a625d3fcd","text":"People who have close contact with African fruit bats, humans patients, or non-human primates infected with Marburg virus are at risk. \n                \nHistorically, the people at highest risk include family members and hospital staff who care for patients infected with Marburg virus and have not used proper barrier nursing techniques. Particular occupations, such as veterinarians and laboratory or quarantine facility workers who handle non-human primates from Africa, may also be at increased risk of exposure to Marburg virus. \n                \nExposure risk can be higher for travelers visiting endemic regions in Africa, including Uganda and other parts of central Africa, and have contact with fruit bats, or enter caves or mines inhabited by fruit bats."}
{"_id":"a82c7ee4-cd83-45ed-ab29-490ebb7670db","text":"Many of the signs and symptoms of Marburg hemorrhagic fever are similar to those of other more frequent infectious diseases, such as malaria or typhoid fever, making diagnosis of the disease difficult. This is especially true if only a single case is involved. \n \nHowever, if a person has the early symptoms of Marburg HF and there is reason to believe that Marburg HF should be considered, the patient should be isolated and public health professionals notified. Samples from the patient can then be collected and tested to confirm infection. \n \nAntigen-capture enzyme-linked immunosorbent assay (ELISA) testing, polymerase chain reaction (PCR), and IgM-capture ELISA can be used to confirm a case of Marburg HF within a few days of symptom onset. Virus isolation may also be performed but should only be done in a high containment laboratory with good laboratory practices. The IgG-capture ELISA is appropriate for testing persons later in the course of disease or after recovery. In deceased patients, immunohistochemistry, virus isolation, or PCR of blood or tissue specimens may be used to diagnose Marburg HF retrospectively."}
{"_id":"63a8c1bc-aedd-4afd-90a0-da410653863f","text":"There is no specific treatment for Marburg hemorrhagic fever. Supportive hospital therapy should be utilized, which includes balancing the patient's fluids and electrolytes, maintaining oxygen status and blood pressure, replacing lost blood and clotting factors, and treatment for any complicating infections. \n \nExperimental treatments are validated in non-human primates models, but have never been tried in humans."}
{"_id":"5cd6638d-4454-46c7-a32c-9095826c35b6","text":"Preventive measures against Marburg virus infection are not well defined, as transmission from wildlife to humans remains an area of ongoing research. However, avoiding fruit bats, and sick non-human primates in central Africa, is one way to protect against infection. \n \nMeasures for prevention of secondary, or person-to-person, transmission are similar to those used for other hemorrhagic fevers. If a patient is either suspected or confirmed to have Marburg hemorrhagic fever, barrier nursing techniques should be used to prevent direct physical contact with the patient. These precautions include wearing of protective gowns, gloves, and masks; placing the infected individual in strict isolation; and sterilization or proper disposal of needles, equipment, and patient excretions. \n \nIn conjunction with the World Health Organization, CDC has developed practical, hospital-based guidelines, titled: Infection Control for Viral Haemorrhagic Fevers In the African Health Care Setting. The manual can help health-care facilities recognize cases and prevent further hospital-based disease transmission using locally available materials and few financial resources. \n \nMarburg hemorrhagic fever is a very rare human disease. However, when it occurs, it has the potential to spread to other people, especially health care staff and family members who care for the patient. Therefore, increasing awareness in communities and among health-care providers of the clinical symptoms of patients with Marburg hemorrhagic fever is critical. Better awareness can lead to earlier and stronger precautions against the spread of Marburg virus in both family members and health-care providers. Improving the use of diagnostic tools is another priority. With modern means of transportation that give access even to remote areas, it is possible to obtain rapid testing of samples in disease control centers equipped with Biosafety Level 4 laboratories in order to confirm or rule out Marburg virus infection."}
{"_id":"e21229c5-7a8e-46f4-9d38-860096f8e3c0","text":"Leishmaniasis is a parasitic disease that is found in parts of the tropics, subtropics, and southern Europe. Leishmaniasis is caused by infection with Leishmania parasites, which are spread by the bite of infected sand flies. There are several different forms of leishmaniasis in people. The most common forms are cutaneous leishmaniasis, which causes skin sores, and visceral leishmaniasis, which affects several internal organs (usually spleen, liver, and bone marrow)."}
{"_id":"2957bc82-0f16-4809-8be0-b447a3f503fc","text":"Leishmaniasis is found in people in focal areas of more than 90 countries in the tropics, subtropics, and southern Europe. The ecologic settings range from rain forests to deserts. Leishmaniasis usually is more common in rural than in urban areas, but it is found in the outskirts of some cities. Climate and other environmental changes have the potential to expand the geographic range of the sand fly vectors and the areas in the world where leishmaniasis is found.\n    \nLeishmaniasis is found on every continent except Australia and Antarctica.\n    \n     - In the Old World (the Eastern Hemisphere), leishmaniasis is found in some parts of Asia, the Middle East, Africa (particularly in the tropical region and North Africa, with some cases elsewhere), and southern Europe. It is not found in Australia or the Pacific islands.\n     - In the New World (the Western Hemisphere), it is found in some parts of Mexico, Central America, and South America. It is not found in Chile or Uruguay. Occasional cases of cutaneous leishmaniasis have been acquired in Texas and Oklahoma.\n    \n    \nThe number of new cases per year is not known with certainty. For cutaneous leishmaniasis, estimates of the number of cases range from approximately 0.7 million (700,000) to 1.2 million (1,200,000). For visceral leishmaniasis, estimates of the number of cases range from approximately 0.2 million (200,000) to 0.4 million (400,000). The cases of leishmaniasis evaluated in the United States reflect travel and immigration patterns. For example, many of the cases of cutaneous leishmaniasis in U.S. civilian travelers have been acquired in common tourist destinations in Latin America, such as in Costa Rica.\n    \nOverall, infection in people is caused by more than 20 species (types) of Leishmania parasites, which are spread by about 30 species of phlebotomine sand flies; particular species of the parasite are spread by particular sand flies. The sand fly vectors generally are the most active during twilight, evening, and night-time hours (from dusk to dawn).\n    \nIn many geographic areas where leishmaniasis is found in people, infected people are not needed to maintain the transmission cycle of the parasite in nature; infected animals (such as rodents or dogs), along with sand flies, maintain the cycle. However, in some parts of the world, infected people are needed to maintain the cycle; this type of transmission (human\u2014sand fly\u2014human) is called anthroponotic. In areas with anthroponotic transmission, effective treatment of individual patients can help control the spread of the parasite."}
{"_id":"30c62ed5-dddf-4c2d-ab30-7e11b83db500","text":"Various laboratory methods can be used to diagnose leishmaniasis\u2014to detect the parasite as well as to identify the Leishmania species (type). Some of the methods are available only in reference laboratories. In the United States, CDC staff can assist with the testing for leishmaniasis.\n    \nTissue specimens\u2014such as from skin sores (for cutaneous leishmaniasis) or from bone marrow (for visceral leishmaniasis)\u2014can be examined for the parasite under a microscope, in special cultures, and in other ways. Blood tests that detect antibody (an immune response) to the parasite can be helpful for cases of visceral leishmaniasis; tests to look for the parasite itself usually also are done.\n    \nMore on: Resources for Health Professionals: Diagnosis"}
{"_id":"de859d0d-664b-42e5-98dc-64eacc154a59","text":"Before considering treatment, the first step is to make sure the diagnosis is correct.\n    \nTreatment decisions should be individualized. Health care providers may consult CDC staff about the relative merits of various approaches. Examples of factors to consider include the form of leishmaniasis, the Leishmania species that caused it, the potential severity of the case, and the patient's underlying health.\n    \nThe skin sores of cutaneous leishmaniasis usually heal on their own, even without treatment. But this can take months or even years, and the sores can leave ugly scars. Another potential concern applies to some (not all) types of the parasite found in parts of Latin America: certain types might spread from the skin and cause sores in the mucous membranes of the nose (most common location), mouth, or throat (mucosal leishmaniasis). Mucosal leishmaniasis might not be noticed until years after the original sores healed. The best way to prevent mucosal leishmaniasis is to ensure adequate treatment of the cutaneous infection.\n    \nIf not treated, severe (advanced) cases of visceral leishmaniasis typically are fatal.\n    \nMore on: Resources for Health Professionals: Treatment"}
{"_id":"bf16a95c-506d-42fb-81ea-c3e10004cedd","text":"No vaccines or drugs to prevent infection are available. The best way for travelers to prevent infection is to protect themselves from sand fly bites. To decrease the risk of being bitten, follow these preventive measures:\n    \nAvoid outdoor activities, especially from dusk to dawn, when sand flies generally are the most active.\n    \nWhen outdoors (or in unprotected quarters):\n    \n     - Minimize the amount of exposed (uncovered) skin. To the extent that is tolerable in the climate, wear long-sleeved shirts, long pants, and socks; and tuck your shirt into your pants. (See below about wearing insecticide-treated clothing.)\n     - Apply insect repellent to exposed skin and under the ends of sleeves and pant legs. Follow the instructions on the label of the repellent. The most effective repellents generally are those that contain the chemical DEET (N,N-diethylmetatoluamide).\n    \n    \n     \n       \n       \n        \n         \n          \n         \n        \n        \n        \n      \n     \n    \n    \nWhen indoors:\n    \n     - Stay in well-screened or air-conditioned areas.\n     - Keep in mind that sand flies are much smaller than mosquitoes and therefore can get through smaller holes.\n     - Spray living\/sleeping areas with an insecticide to kill insects.\n     - If you are not sleeping in a well-screened or air-conditioned area, use a bed net and tuck it under your mattress. If possible, use a bed net that has been soaked in or sprayed with a pyrethroid-containing insecticide. The same treatment can be applied to screens, curtains, sheets, and clothing (clothing should be retreated after five washings).\n    \n    \nMore on: Insect Bite Prevention"}
{"_id":"dda734dd-de28-4b4a-ab7b-74d5de16e98a","text":"A single-celled parasite called Toxoplasma gondii causes a disease known as toxoplasmosis. While the parasite is found throughout the world, more than 60 million people in the United States may be infected with the Toxoplasma parasite. Of those who are infected, very few have symptoms because a healthy person\u2019s immune system usually keeps the parasite from causing illness. However, pregnant women and individuals who have compromised immune systems should be cautious; for them, a Toxoplasma infection could cause serious health problems."}
{"_id":"73c4fd4f-80a2-410a-859a-d7d2b5ee1c1a","text":"Toxoplasmosis is caused by the protozoan parasite Toxoplasma gondii. In the United States it is estimated that 22.5% of the population 12 years and older have been infected with Toxoplasma. In various places throughout the world, it has been shown that up to 95% of some populations have been infected with Toxoplasma. Infection is often highest in areas of the world that have hot, humid climates and lower altitudes. \n    \nToxoplasmosis is not passed from person-to-person, except in instances of mother-to-child (congenital) transmission and blood transfusion or organ transplantation. People typically become infected by three principal routes of transmission. \n         \n     \n     \n       \n      \n     \n    \n      \n    Foodborne transmission \n    \nThe tissue form of the parasite (a microscopic cyst consisting of bradyzoites) can be transmitted to humans by food. People become infected by: \n     \n     - Eating undercooked, contaminated meat (especially pork, lamb, and venison) \n     - Accidental ingestion of undercooked, contaminated meat after handling it and not washing hands thoroughly (Toxoplasma cannot be absorbed through intact skin) \n     - Eating food that was contaminated by knives, utensils, cutting boards, or other foods that had contact with raw, contaminated meat \n     \n    \n      \n    Animal-to-human (zoonotic) transmission \n    \nCats play an important role in the spread of toxoplasmosis. They become infected by eating infected rodents, birds, or other small animals. The parasite is then passed in the cat's feces in an oocyst form, which is microscopic. \n    \nKittens and cats can shed millions of oocysts in their feces for as long as 3 weeks after infection. Mature cats are less likely to shed Toxoplasma if they have been previously infected. A Toxoplasma-infected cat that is shedding the parasite in its feces contaminates the litter box. If the cat is allowed outside, it can contaminate the soil or water in the environment as well. \n     \n       \n      \n     \n    \nPeople can accidentally swallow the oocyst form of the parasite. People can be infected by: \n     \n     - Accidental ingestion of oocysts after cleaning a cat's litter box when the cat has shed Toxoplasma in its feces \n     - Accidental ingestion of oocysts after touching or ingesting anything that has come into contact with a cat's feces that contain Toxoplasma \n     - Accidental ingestion of oocysts in contaminated soil (e.g., not washing hands after gardening or eating unwashed fruits or vegetables from a garden) \n     - Drinking water contaminated with the Toxoplasma parasite \n     \n    \n      \n    Mother-to-child (congenital) transmission \n    \nA woman who is newly infected with Toxoplasma during pregnancy can pass the infection to her unborn child (congenital infection). The woman may not have symptoms, but there can be severe consequences for the unborn child, such as diseases of the nervous system and eyes. \n    \n      \n    Rare instances of transmission \n    \nOrgan transplant recipients can become infected by receiving an organ from a Toxoplasma-positive donor. Rarely, people can also become infected by receiving infected blood via transfusion. Laboratory workers who handle infected blood can also acquire infection through accidental inoculation."}
{"_id":"496bbac2-e056-4956-b07d-0feaadc1200e","text":"The diagnosis of toxoplasmosis is typically made by serologic testing. A test that measures immunoglobulin G (IgG) is used to determine if a person has been infected. If it is necessary to try to estimate the time of infection, which is of particular importance for pregnant women, a test which measures immunoglobulin M (IgM) is also used along with other tests such as an avidity test.\n    \nDiagnosis can be made by direct observation of the parasite in stained tissue sections, cerebrospinal fluid (CSF), or other biopsy material. These techniques are used less frequently because of the difficulty of obtaining these specimens.\n    \nParasites can also be isolated from blood or other body fluids (for example, CSF) but this process can be difficult and requires considerable time.\n    \nMolecular techniques that can detect the parasite's DNA in the amniotic fluid can be useful in cases of possible mother-to-child (congenital) transmission.\n    \nOcular disease is diagnosed based on the appearance of the lesions in the eye, symptoms, course of disease, and often serologic testing."}
{"_id":"2e5a6db3-6ed3-41cc-b01c-b153fa342f0e","text":"Healthy people (nonpregnant)\n    \nMost healthy people recover from toxoplasmosis without treatment. Persons who are ill can be treated with a combination of drugs such as pyrimethamine and sulfadiazine, plus folinic acid.\n    \n     \n    Pregnant women, newborns, and infants\n    \nPregnant women, newborns, and infants can be treated, although the parasite is not eliminated completely. The parasites can remain within tissue cells in a less active phase; their location makes it difficult for the medication to completely eliminate them.\n    \n     \n    Persons with ocular disease\n    \nPersons with ocular toxoplasmosis are sometimes prescribed medicine to treat active disease by their ophthalmologist. Whether or not medication is recommended depends on the size of the eye lesion, the location, and the characteristics of the lesion (acute active, versus chronic not progressing).\n    \n     \n    Persons with compromised immune systems\n    \nPersons with compromised immune systems need to be treated until they have improvement in their condition. For AIDS patients, continuation of medication for the rest of their lives may be necessary, or for as long as they are immunosuppressed.\n    \nMore on: Resources for Health Professionals: Treatment"}
{"_id":"441dd1b9-4e32-47db-a59d-13d21f8e3dd9","text":"People who are healthy should follow the guidelines below to reduce risk of toxoplasmosis. If you have a weakened immune system, please see guidelines for Immunocompromised Persons.\n   Reduce Risk from Food\n   \nTo prevent risk of toxoplasmosis and other infections from food:\n   \n    - Freeze meat for several days at sub-zero (0\u00b0 F) temperatures before cooking to greatly reduce chance of infection.\n    - Peel or wash fruits and vegetables thoroughly before eating. \n     \n      \n     \n    - Wash cutting boards, dishes, counters, utensils, and hands with hot soapy water after contact with raw meat, poultry, seafood, or unwashed fruits or vegetables.\n   \n   \nMore on: Handwashing\n   \nThe U.S. Government and the meat industry continue their efforts to reduce T. gondii in meat.\n   Reduce Risk from the Environment\n   \nTo prevent risk of toxoplasmosis from the environment:\n   \n    - Avoid drinking untreated drinking water.\n    - Wear gloves when gardening and during any contact with soil or sand because it might be contaminated with cat feces that contain Toxoplasma. Wash hands with soap and warm water after gardening or contact with soil or sand.\n    - Teach children the importance of washing hands to prevent infection.\n    - Keep outdoor sandboxes covered. \n     \n      \n     \n    - Feed cats only canned or dried commercial food or well-cooked table food, not raw or undercooked meats.\n    - Change the litter box daily if you own a cat. The Toxoplasma parasite does not become infectious until 1 to 5 days after it is shed in a cat's feces. If you are pregnant or immunocompromised: \n     \n      - Avoid changing cat litter if possible. If no one else can perform the task, wear disposable gloves and wash your hands with soap and warm water afterwards.\n      - Keep cats indoors.\n      - Do not adopt or handle stray cats, especially kittens. Do not get a new cat while you are pregnant."}
{"_id":"929ce3d4-d267-4101-93d2-c491d163cc44","text":"Hookworm is an intestinal parasite of humans. The larvae and adult worms live in the small intestine can cause intestinal disease. The two main species of hookworm infecting humans are Ancylostoma duodenale and Necator americanus."}
{"_id":"72691c0f-a29a-4b07-a95f-b31912175a48","text":"Hookworm is a soil-transmitted helminth (STH) and is one of the most common roundworm of humans. Infection is caused by the nematode parasites Necator americanus and Ancylostoma duodenale. Hookworm infections often occur in areas where human feces are used as fertilizer or where defecation onto soil happens.\n    Geographic Distribution\n    \nThe geographic distributions of the hookworm species that are intestinal parasites in human, Ancylostoma duodenale and Necator americanus, are worldwide in areas with warm, moist climates and are widely overlapping. Necator americanus was widespread in the Southeastern United States until the early 20th century."}
{"_id":"66129d47-37db-47fb-b4b1-a7074a78f7d9","text":"The standard method for diagnosing the presence of hookworm is by identifying hookworm eggs in a stool sample using a microscope. Because eggs may be difficult to find in light infections, a concentration procedure is recommended."}
{"_id":"1381b017-ebdd-4447-9b5f-6996ceba1b07","text":"Anthelminthic medications (drugs that rid the body of parasitic worms), such as albendazole and mebendazole, are the drugs of choice for treatment of hookworm infections. Infections are generally treated for 1-3 days. The recommended medications are effective and appear to have few side effects. Iron supplements may also be prescribed if the infected person has anemia.\n    \nMore on: Resources for Health Professionals: Treatment"}
{"_id":"8fef9ae5-26b1-49a3-8c58-bf071d693639","text":"The best way to avoid hookworm infection is not to walk barefoot in areas where hookworm is common and where there may be human fecal contamination of the soil. Also, avoid other skin contact with such soil and avoid ingesting it.\n    \nInfection can also be prevented by not defecating outdoors and by effective sewage disposal systems."}
{"_id":"97d82288-6847-4f90-b33a-87dd1717cf28","text":"Chagas disease is caused by the parasite Trypanosoma cruzi, which is transmitted to animals and people by insect vectors that are found only in the Americas (mainly, in rural areas of Latin America where poverty is widespread). Chagas disease (T. cruzi infection) is also referred to as American trypanosomiasis.\nIt is estimated that as many as 8 million people in Mexico, Central America, and South America have Chagas disease, most of whom do not know they are infected. If untreated, infection is lifelong and can be life threatening.\nThe impact of Chagas disease is not limited to the rural areas in Latin America in which vectorborne transmission occurs. Large-scale population movements from rural to urban areas of Latin America and to other regions of the world have increased the geographic distribution and changed the epidemiology of Chagas disease. In the United States and in other regions where Chagas disease is now found but is not endemic, control strategies should focus on preventing transmission from blood transfusion, organ transplantation, and mother-to-baby (congenital transmission)."}
{"_id":"d2734669-13e1-4b43-830e-f7ce4aaec87b","text":"Chagas disease, or American trypanosomiasis, is caused by the parasite Trypanosoma cruzi. Infection is most commonly acquired through contact with the feces of an infected triatomine bug (or \"kissing bug\"), a blood-sucking insect that feeds on humans and animals.\n    \nInfection can also occur from:\n    \n     - mother-to-baby (congenital),\n     - contaminated blood products (transfusions),\n     - an organ transplanted from an infected donor,\n     - laboratory accident, or\n     - contaminated food or drink (rare)\n    \n    \nChagas disease is endemic throughout much of Mexico, Central America, and South America where an estimated 8 million people are infected. The triatomine bug thrives under poor housing conditions (for example, mud walls, thatched roofs), so in endemic countries, people living in rural areas are at greatest risk for acquiring infection. Public health efforts aimed at preventing transmission have decreased the number of newly infected people and completely halted vectorborne transmission in some areas. Infection acquired from blood products, organ transplantation, or congenital transmission continues to pose a threat.\n    \nBy applying published seroprevalence figures to immigrant populations, CDC estimates that more than 300,000 persons with Trypanosoma cruzi infection live in the United States. Most people with Chagas disease in the United States acquired their infections in endemic countries. Although there are triatomine bugs in the U.S. , only rare vectorborne cases of Chagas disease have been documented.\n    \nMore on: Triatomine Bugs"}
{"_id":"56bb8f51-4abd-47ec-b6da-8ba6ce5f06e9","text":"The diagnosis of Chagas disease can be made by observation of the parasite in a blood smear by microscopic examination. A thick and thin blood smear are made and stained for visualization of parasites. However, a blood smear works well only in the acute phase of infection when parasites are seen circulating in blood.\n    \nDiagnosis of chronic Chagas disease is made after consideration of the patient's clinical findings, as well as by the likelihood of being infected, such as having lived in an endemic country. Diagnosis is generally made by testing with at least two different serologic tests."}
{"_id":"c95e6b84-3e47-4a69-b0b0-da178d155881","text":"Treatment for Chagas disease is recommended for all people diagnosed with an acute infection, congenital infection, and for those with suppressed immune systems, and for all children with chronic infection. Adults with chronic infection may also benefit from treatment.\n    \nFor cardiac or gastrointestinal problems resulting from Chagas disease, symptomatic treatment may be helpful. Patients should consult with their primary health care provider. Some patients may be referred to a specialist, such as a cardiologist, gastroenterologist, or infectious disease specialist.\n    \nIn the U.S., medication for Chagas is available only through CDC. Your health care provider can talk with CDC staff about whether and how you should be treated.\n    \nMore on: Resources for Health Professionals: Antiparasitic Treatment"}
{"_id":"d88be55f-9473-498d-9c94-f0f78386d1fa","text":"In endemic areas of Mexico, Central America, and South America improved housing and spraying insecticide inside housing to eliminate triatomine bugs has significantly decreased the spread of Chagas disease. Further, screening of blood donations for Chagas is another important public health tool in helping to prevent transfusion-acquired disease. Early detection and treatment of new cases, including mother-to-baby (congenital) cases, will also help reduce the burden of disease.\n    \nIn the United States and in other regions where Chagas disease is now found but is not endemic, control strategies are focused on preventing transmission from blood transfusion, organ transplantation, and mother-to-baby."}
{"_id":"9b03b3fc-f5cc-4787-a64b-176f58b6d959","text":"The bacteria that cause nocardiosis are commonly found in soil and water.\n    \nYou could become sick with nocardiosis if:\n    \n     - You inhale (breathe in) the bacteria\n     - Bacteria gets into an open wound or cut\n    \n    \nIn rare cases, infection can occur during surgical procedures.\n    \nFortunately, nocardiosis is not spread person to person, so being around someone who has the disease will not make you sick."}
{"_id":"a84b9a83-d22a-4d73-ad81-78608730bc64","text":"People with very weak immune (body defense) systems are at risk for getting nocardiosis. \n    \nSeveral diseases and circumstances can cause the immune system to be weak. These include:\n    \n     - Diabetes\n     - Cancer\n     - HIV\/AIDS\n     - Pulmonary alveolar proteinosis (an illness that causes the air sacs of the lungs to become plugged)\n     - Connective tissue disorder (a disease that affects the tissue that connects and supports different parts of the body)\n     - Alcoholism\n     - Having a bone marrow or solid organ transplant\n     - Taking high doses of drugs called corticosteroids\n    \n    \nIn the United States, it has been estimated that 500-1,000 new cases of nocardiosis infection occur every year. Approximately 60% of nocardiosis cases are associated with pre-existing immune compromise. \n    \nIn addition, men have a greater risk of getting the infection than women; for every female who gets sick with nocardiosis, there are about 3 males who get the disease."}
{"_id":"acc9d023-feed-4bc4-9911-bfbe7453d684","text":"The symptoms of nocardiosis vary depending on which part of your body is affected.\n    \nNocardiosis infection most commonly occurs in the lung. If your lungs are infected, you can experience:\n    \n     - Fever\n     - Weight loss\n     - Night sweats\n     - Cough\n     - Chest pain\n     - Pneumonia\n    \n    \nWhen lung infections occur, the infection commonly spreads to the brain. If your central nervous system (brain and spinal cord) is infected, you can experience:\n    \n     - Headache\n     - Weakness\n     - Confusion\n     - Seizures (sudden, abnormal electrical activity in the brain)\n    \n    \nSkin infections can occur when open wounds or cuts come into contact with contaminated soil. If your skin is affected, you can experience:\n    \n     - Ulcers\n     - Nodules sometimes draining and spreading along lymph nodes"}
{"_id":"877f258b-9b65-4b98-85db-ce2894942661","text":"If you think you might be sick with nocardiosis, talk to your doctor.\n    \nHe or she can help find out if you have the disease by performing tests that can identify the bacteria that causes nocardiosis.\n    \nTesting may involve taking tissue samples from the part of the body that is infected. Tissue samples may include the:\n    \n     - Brain\n     - Skin\n     - Lungs (or other parts of the lower airways)\n     - Mucus from the lower airways"}
{"_id":"fbab3c86-3f4c-4aab-baea-3503e5d6202f","text":"Like all arenaviruses, Chapare virus has a rodent host as its reservoir. Humans can contract CHHF through contact with an infected rodent. Contact can be direct or through inhalation of aerosolized Chapare virus from the urine or feces of infected rodents. \n \nAlthough arenaviruses have been isolated from insects, neither they nor any other intermediary host appear to spread CHHF. \n \nPerson-to-person transmission of arenaviruses through aerosolization, although possible, is rare. From the only observed cluster of cases of CHHF, there was no evidence of person-to-person transmission. \n \nTransmission, if it can occur with CHHF, is most likely the result of direct contact with an infected person."}
{"_id":"453ae517-0768-4dee-86b7-cf512872d6f0","text":"The symptoms of CHHF, as reported in the only described patient, resemble those of other South American hemorrhagic fevers, such as Argentine HF or Bolivian HF. The incubation period is unknown, but for Argentine hemorrhagic fever (AHF) is 6 to 16 days. \n   \nThe CHHF clinical course included: \n    \n    - fever \n    - headache \n    - articulation and muscle pain \n    - vomiting \n    \n   \nThese symptoms were followed by deterioration with multiple hemorrhagic signs. The only described CHHF patient died 14 days after onset of symptoms. \n   \nSince Arenaviruses may enter the fetus through infection of the mother, and anecdotal evidence suggests that infected pregnant women may suffer miscarriages, it is reasonable to assume that both infection of the fetus and miscarriage may be associated with CHHF infection in the mother."}
{"_id":"73c47460-2223-46d3-9163-075a90d44456","text":"CHHF occurs in the Cochabamba region of Bolivia. \nField workers \n                \nField workers are at greatest risk because of increased human contact with the reservoir rodent population. Sexual partners of field workers may be at greater risk as well. Laboratory infections have been frequently described with Arenaviruses and Chapare virus can certainly be transmitted to laboratory workers during manipulation of the virus especially during experimental infections of rodents."}
{"_id":"d5988499-6950-47c3-9a74-60ce5aab063a","text":"CHHF virus has been successfully isolated from both blood and serum during the acute febrile phase of illness. Although not undertaken at the time of the initial cluster, virus can certainly be isolated from tissue obtained post-mortem if available. A subsequent complete genomic analysis of Chapare virus facilitated the development of specific molecular detection (RT-PCR) assays. \n   \nSerologic diagnosis of CHHF can be made by indirect immunofluorescent assay and ELISA. However, individuals from endemic areas who show fever, dizziness, and myalgia, accompanied by laboratory findings of low white blood cell and platelet counts and excess protein in the urine, should be suspected of having one of the South American hemorrhagic fever viruses. Clinical specimens should be tested using specific assays."}
{"_id":"7dd01d62-2e5d-4a6e-8ae3-0fc6711595e2","text":"Supportive therapy is important in CHHF. This includes: \n    \n    - maintenance of hydration \n    - management of shock \n    - sedation \n    - pain relief \n    - usual precautions for patients with bleeding disorders \n    - transfusions (when necessary) \n    \n   \nUse of convalescent plasma therapy for treatment of AHF reduces mortality significantly and anecdotal evidence shows that the antiviral drug ribavirin may also hold promise for treating AHF. Ribavirin has also been considered for preventing development of disease in people exposed to other arenaviruses. \n   Recovery \n   \nThe precise mortality of CHHF is unknown and the only described case was fatal. \n   \nPatients who have suffered from other arenaviruses may continue to excrete virus in urine or semen for weeks after recovery. For this reason, these fluids should be monitored for infectivity, since convalescent patients have the potential to infect others (particularly sexual partners) via these fluids."}
{"_id":"f77ce26d-8d16-4f45-9ea1-5f090c7248d7","text":"Although rodent control would be desirable, it will not be a successful strategy for preventing Chapare hemorrhagic fever cases caused by exposures outdoors. \n   \nAs for other hemorrhagic fevers, full barrier nursing procedures should be implemented during management of suspected or confirmed CHHF cases."}
{"_id":"016cdc43-c976-4840-b05a-45900c6fac8d","text":"Yersiniosis is an infectious disease caused by a bacterium of the genus Yersinia. In the United States, most human illness is caused by one species, Y. enterocolitica. Infection with Y. enterocolitica can cause a variety of symptoms depending on the age of the person infected. Infection with Y. enterocolitica occurs most often in young children. Common symptoms in children are fever, abdominal pain, and diarrhea, which is often bloody. Symptoms typically develop 4 to 7 days after exposure and may last 1 to 3 weeks or longer. In older children and adults, right-sided abdominal pain and fever may be the predominant symptoms, and may be confused with appendicitis. In a small proportion of cases, complications such as skin rash, joint pains, or spread of bacteria to the bloodstream can occur."}
{"_id":"3906002a-0b60-4998-9e5c-3e1af77c98d2","text":"Y. enterocolitica is a relatively infrequent cause of diarrhea and abdominal pain. Based on data from the Foodborne Diseases Active Surveillance Network (FoodNet), which measures the burden and sources of specific diseases over time, approximately one culture-confirmed Y. enterocolitica infection per 100,000 persons occurs each year. Children are infected more often than adults, and the infection is more common in the winter."}
{"_id":"25cdf3c8-8bd2-4e05-be86-0bcb708bd028","text":"Y. enterocolitica infections are generally diagnosed by detecting the organism in the stools. Many laboratories do not routinely test for Y. enterocolitica,so it is important to notify laboratory personnel when infection with this bacterium is suspected so that special tests can be done. The organism can also be recovered from other sites, including the throat, lymph nodes, joint fluid, urine, bile, and blood."}
{"_id":"cee42857-e901-44f8-85b3-403a83965b9b","text":"Uncomplicated cases of diarrhea due to Y. enterocolitica usually resolve on their own without antibiotic treatment. However, in more severe or complicated infections, antibiotics such as aminoglycosides, doxycycline, trimethoprim-sulfamethoxazole, or fluoroquinolones may be useful."}
{"_id":"812088c1-24cd-4120-91bf-1a5d15adb03a","text":"The Centers for Disease Control and Prevention (CDC) monitors the frequency of Y. enterocolitica infections through the foodborne disease active surveillance network (FoodNet). In addition, CDC conducts investigations of outbreaks of yersiniosis to control them and to learn more about how to prevent these infections. CDC has collaborated in an educational campaign to increase public awareness about prevention of Y. enterocolitica infections. The U.S. Food and Drug Administration inspects imported foods and milk pasteurization plants and promotes better food preparation techniques in restaurants and food processing plants. The U.S. Department of Agriculture monitors the health of food animals and is responsible for the quality of slaughtered and processed meat. The U.S. Environmental Protection Agency regulates and monitors the safety of our drinking water supplies."}
{"_id":"8f372d1a-7b18-4271-bec8-c61a3b28a5b3","text":"Frequently Asked Questions (FAQs)\n    \n    Vector Information"}
{"_id":"c49ecf0e-dbf2-477e-921e-1e05a1a29c46","text":"There are three different filarial species that can cause lymphatic filariasis in humans. Most of the infections worldwide are caused by Wuchereria bancrofti. In Asia, the disease can also be caused by Brugia malayi and Brugia timori.\n    \nThe infection spreads from person to person by mosquito bites. The adult worm lives in the human lymph vessels, mates, and produces millions of microscopic worms, also known as microfilariae. Microfilariae circulate in the person's blood and infect the mosquito when it bites a person who is infected. Microfilariae grow and develop in the mosquito. When the mosquito bites another person, the larval worms pass from the mosquito into the human skin, and travel to the lymph vessels. They grow into adult worms, a process that takes 6 months or more. An adult worm lives for about 5\u20137 years. The adult worms mate and release millions of microfilariae into the blood. People with microfilariae in their blood can serve as a source of infection to others.\n    \n     \n    \n    \nA wide range of mosquitoes can transmit the parasite, depending on the geographic area. In Africa, the most common vector is Anopheles and in the Americas, it is Culex quinquefasciatus. Aedes and Mansonia can transmit the infection in the Pacific and in Asia.\n    \nMany mosquito bites over several months to years are needed to get lymphatic filariasis. People living for a long time in tropical or sub-tropical areas where the disease is common are at the greatest risk for infection. Short-term tourists have a very low risk.\n    \nPrograms to eliminate lymphatic filariasis are under way in more than 50 countries. These programs are reducing transmission of the filarial parasites and decreasing the risk of infection for people living in or visiting these communities.\n    Geographic distribution\n    \n     \n    \n    \nLymphatic filariasis affects over 120 million people in 73 countries throughout the tropics and sub-tropics of Asia, Africa, the Western Pacific, and parts of the Caribbean and South America.\n    \nIn the Americas, only four countries are currently known to be endemic: Haiti, the Dominican Republic, Guyana and Brazil.\n    \nIn the United States, Charleston, South Carolina, was the last known place with lymphatic filariasis. The infection disappeared early in the 20th century. Currently, you cannot get infected in the U.S."}
{"_id":"1ea38300-d03c-4081-9db1-22b17b7c5e62","text":"The standard method for diagnosing active infection is the identification of microfilariae in a blood smear by microscopic examination. The microfilariae that cause lymphatic filariasis circulate in the blood at night (called nocturnal periodicity). Blood collection should be done at night to coincide with the appearance of the microfilariae, and a thick smear should be made and stained with Giemsa or hematoxylin and eosin. For increased sensitivity, concentration techniques can be used.\n    \nSerologic techniques provide an alternative to microscopic detection of microfilariae for the diagnosis of lymphatic filariasis. Patients with active filarial infection typically have elevated levels of antifilarial IgG4 in the blood and these can be detected using routine assays.\n    \nBecause lymphedema may develop many years after infection, lab tests are most likely to be negative with these patients."}
{"_id":"4243c940-ca62-480c-b0b7-b2622e99a409","text":"Patients currently infected with the parasite\n    \nDiethylcarbamazine (DEC) is the drug of choice in the United States. The drug kills the microfilaria and some of the adult worms. DEC has been used world-wide for more than 50 years. Because this infection is rare in the U.S., the drug is no longer approved by the Food and Drug Administration (FDA) and cannot be sold in the U.S. Physicians can obtain the medication from CDC after confirmed positive lab results. CDC gives the physicians the choice between 1 or 12-day treatment of DEC (6 mg\/kg\/day). One day treatment is generally as effective as the 12-day regimen. DEC is generally well tolerated. Side effects are in general limited and depend on the number of microfilariae in the blood. The most common side effects are dizziness, nausea, fever, headache, or pain in muscles or joints.\n    \nDEC should not be administered to patients who may also have onchocerciasis as  DEC can worsen onchocercal eye disease.  In patients with loiasis, DEC can cause serious adverse reactions, including encephalopathy and death. The risk and severity of the adverse reactions are related to Loa loa microfilarial density.\nThe drug ivermectin kills only the microfilariae, but not the adult worm; the adult worm is responsible for the pathology of lymphedema and hydrocele.\n    \nSome studies have shown adult worm killing with treatment with doxycycline (200mg\/day for 4\u20136 weeks).  \n    Patients with clinical symptoms\n    \nLymphedema and elephantiasis are not indications for DEC treatment because most people with lymphedema are not actively infected with the filarial parasite.\n    \nTo prevent the lymphedema from getting worse, patients should ask their physician for a referral to a lymphedema therapist so they can be informed about some basic principles of care such as hygiene, exercise and treatment of wounds.\n    \nPatients with hydrocele may have evidence of active infection, but typically do not improve clinically following treatment with DEC. The treatment for hydrocele is surgery.\n    \nMore on: Resources for Health Professionals: Treatment"}
{"_id":"377feb15-9a60-4d17-aa5b-0209b09fe231","text":"The best way to prevent lymphatic filariasis is to avoid mosquito bites. The mosquitoes that carry the microscopic worms usually bite between the hours of dusk and dawn. If you live in an area with lymphatic filariasis:\n   \n    - at night \n     \n      - sleep in an air-conditioned room or\n      - sleep under a mosquito net\n     \n    - between dusk and dawn \n     \n      - wear long sleeves and trousers and\n      - use mosquito repellent on exposed skin.\n     \n   \n   \nAnother approach to prevention includes giving entire communities medicine that kills the microscopic worms -- and controlling mosquitoes. Annual mass treatment reduces the level of microfilariae in the blood and thus, diminishes transmission of infection. This is the basis of the global campaign to eliminate lymphatic filariasis.\n   \nExperts consider that lymphatic filariasis, a neglected tropical disease (NTD), can be eradicated and a global campaign to eliminate lymphatic filariasis as a public health problem is under way. The elimination strategy is based on annual treatment of whole communities with combinations of drugs that kill the microfilariae. As a result of the generous contributions of these drugs by the companies that make them, tens of millions of people are being treated each year. Since these drugs also reduce levels of infection with intestinal worms, benefits of treatment extend beyond lymphatic filariasis. Successful campaigns to eliminate lymphatic filariasis have taken place in China and other countries.\n   \nMore on: Insect Bite Prevention"}
{"_id":"71e2b072-657a-4788-a2bd-99bb02e5d3bd","text":"Loiasis is an infection caused by the parasitic worm Loa loa."}
{"_id":"5bf6ab2f-d7d5-4776-ab26-fd81c3fabb7b","text":"Loa loa parasites are found in West and Central Africa. Ten countries have areas where there are high rates of infection (i.e., where more than 40% of the people who live in that area report that they have had eye worm in the past). An estimated 14.4 million people live in these areas of high rates of infection. Another 15.2 live in areas where 20\u201340% of people report that they have had eye worm in the past.\n    \nMore on: Where Loa Loa is Prevelant [WHO Map]\n    \nThe people most at risk for loiasis are those who live in the certain rain forests in West and Central Africa. The deerflies that pass the parasite to humans usually bite during the day and are more common during the rainy season. They are attracted by the movement of people and by smoke from wood fires. Rubber plantations are areas where more deerflies may be found. The flies do not typically enter homes, but they might be attracted to homes that are well lit.\n    \nTravelers are more likely to become infected if they are in areas where they are bitten by deerflies for many months, though occasionally they get infected even if they are in an affected area for less than 30 days.\n    \nYour risk of infection depends on the number of bites received, the number of infected deerflies in the area you visit, and the length of your stay in the area."}
{"_id":"be9ef71e-6f1b-4ba9-98d9-a63a85c776cf","text":"In people who have been bitten by the flies that carry Loa loa in areas where Loa loa is known to exist, the diagnosis can be made in the following ways:\n  \n   - Identification of the adult worm by a microbiologist or pathologist after its removal from under the skin or eye\n   - Identification of an adult worm in the eye by a health care provider\n   - Identification of the microfilariae on a blood smear made from blood taken from the patient between 10AM and 2PM\n   - Identification of antibodies against L. loa on specialized blood test\n  \n  \nDiagnosis of loiasis can be difficult, especially in light infections where there are very few microfilariae in the blood. The specialized blood test is not widely available in the United States. A positive antibody blood test in someone with no symptoms means only that the person was infected sometime in his\/her life. It does not mean that the person still has living parasites in his\/her body."}
{"_id":"0df0a845-44fb-4559-b0d3-d3fc6509bbf6","text":"Decisions about treatment of loiasis can be difficult and often require advice from an expert in infectious diseases or tropical medicine. Although surgical removal of adult worms moving under the skin or across the eye can be done to relieve anxiety, loiasis is not cured by surgery alone. There are two medications that can be used to treat the infection and manage the symptoms. The treatment of choice is diethylcarbamazine (DEC), which kills the microfilariae and adult worms. Albendazole is sometimes used in patients who are not cured with multiple DEC treatments. It is thought to kill adult worms. Certain people with heavy infections are at risk of brain inflammation when treated with DEC. This can cause coma or sometimes death. People with heavy infections need to be treated by experienced specialists.  Sometimes, other medical conditions need to be addressed first in order to make it safer to use DEC. Sometimes treatment is not recommended.\n    \nMore on: Resources for Health Professionals: Treatment"}
{"_id":"17a124f6-f5bc-40eb-b249-c00e19f34806","text":"There are no programs to control or eliminate loiasis in affected areas. Your risk of infection may be less in areas where communities receive regular treatment for onchocerciasis or lymphatic filariasis.\n    \nThere are no vaccines that protect you from loiasis. If you are going to be in an area with loiasis for a long period of time, diethylcarbamazine (DEC)\u2014300mg taken once a week\u2014can reduce your risk of infection. Avoiding areas where the deerflies are found, such as muddy, shaded areas along rivers or around wood fires, may also reduce your risk of infection. You may reduce your risk of bites by using insect repellants that contain DEET (N,N-Diethyl-meta-toluamide) and wearing long sleeves and long pants during the day, which is when deerflies bite. Treating your clothes with permethrin may also help. For a description of CDC's information for preventing insect bites, see CDC's Yellow Book.\n    \nMore on: Insect Bite Prevention"}
{"_id":"a84840d1-ca9c-4cba-b013-767f6d3057c3","text":"Humans can become infected through tick bites or through contact with the blood, feces, or urine of an infected, sick, or dead animal \u2013 most commonly, rodents. Occupational and recreational activities such as hunting or trapping may increase human risk of infection. \n \nTransmission may also occur with no direct tick or rodent exposure as OHFV appears to be extremely stable in different environments. It has been isolated from aquatic animals and water and there is even evidence that OHFV can be transmitted through the milk of infected goats or sheep to humans. \n \nNo human-to-human transmission of OHFV has been documented but infections due to lab contamination have been described."}
{"_id":"f1ef17f4-4b9c-4d4c-b4fe-9a0388c53c89","text":"After an incubation period of 3-8 days, the symptoms of OHF begin suddenly with chills, fever, headache, and severe muscle pain with vomiting, gastrointestinal symptoms and bleeding problems occurring 3-4 days after initial symptom onset. Patients may experience abnormally low blood pressure and low platelet, red blood cell, and white blood cell counts.  \n                \nAfter 1-2 weeks of symptoms, some patients recover without complication. However, the illness is biphasic for a subset of patients who experience a second wave of symptoms at the beginning of the third week. These symptoms include fever and encephalitis (inflammation of the brain). \n                \nThe case fatality rate of OHF is low (0.5% to 3%)."}
{"_id":"53c34683-dadc-40d5-a5f4-989e684bb534","text":"In areas where rodent reservoirs and tick species are prevalent, people with recreational or occupational exposure to rural or outdoor settings (e.g., hunters, campers, forest workers, farmers) are potentially at increased risk for OHF by contact with infected ticks and animals. Furthermore, those in Siberia who hunt and trap muskrats specifically are at higher risk for OHF. \n                \nExposure may also occur in the laboratory environment."}
{"_id":"fcc86695-81bc-440e-abe0-5691c0b54cb4","text":"OHF virus may be detected in blood samples by virus isolation in cell culture or using molecular techniques such as PCR. Blood samples can also be tested for antibody presence using enzyme-linked immunosorbent seologic assay (ELISA)."}
{"_id":"cae47e94-efa5-4a5e-986c-be4d837d3b37","text":"There is no specific treatment for OHF, but supportive therapy is important. Supportive therapy includes the maintenance of hydration and the usual precautions for patients with bleeding disorders. \n                \nThough rare, OHF can cause hearing loss, hair loss, and behavioral or psychological difficulties associated with neurological conditions and long term supportive case may be needed."}
{"_id":"d9bf9f35-8ec1-4223-a33d-aebddc25ab41","text":"There is no vaccine currently available for OHF, but vaccines for tick-borne encephalitis disease (TBE) have been shown to confer some immunity and may be used for high-risk groups. \n                \nAdditionally, utilizing insect repellents and wearing protective clothing in areas where ticks are endemic is recommended."}
{"_id":"c8d49feb-59b6-48a8-a1f7-cd7422ee5a51","text":"A pinworm (\"threadworm\") is a small, thin, white roundworm (nematode) called Enterobius vermicularis that sometimes lives in the colon and rectum of humans. Pinworms are about the length of a staple. While an infected person sleeps, female pinworms leave the intestine through the anus and deposit their eggs on the surrounding skin."}
{"_id":"9e9a36d1-c5a6-42ed-8abe-a3013ae016c7","text":"Risk Factors\n    \nThe people most likely to be infected with pinworm are children under 18, people who take care of infected children and people who are institutionalized. In these groups, the prevalence can reach 50%.\n    \nPinworm is the most common worm infection in the United States. Humans are the only species that can transfer this parasite. Household pets like dogs and cats cannot become infected with human pinworms. Pinworm eggs can survive in the indoor environment for 2 to 3 weeks.\n    Epidemiology\n    \nPinworm infections are more common within families with school-aged children, in primary caregivers of infected children, and in institutionalized children.\n    \nA person is infected with pinworms by ingesting pinworm eggs either directly or indirectly. These eggs are deposited around the anus by the worm and can be carried to common surfaces such as hands, toys, bedding, clothing, and toilet seats. By putting anyone\u2019s contaminated hands (including one\u2019s own) around the mouth area or putting one\u2019s mouth on common contaminated surfaces, a person can ingest pinworm eggs and become infected with the pinworm parasite. Since pinworm eggs are so small, it is possible to ingest them while breathing.\n    \nOnce someone has ingested pinworm eggs, there is an incubation period of 1 to 2 months or longer for the adult gravid female to mature in the small intestine. Once mature, the adult female worm migrates to the colon and lays eggs around the anus at night, when many of their hosts are asleep. People who are infected with pinworm can transfer the parasite to others for as long as there is a female pinworm depositing eggs on the perianal skin. A person can also re-infect themselves, or be re-infected by eggs from another person."}
{"_id":"637d1bd2-288f-477b-bb28-099318b947bf","text":"A person infected with pinworm is often asymptomatic, but itching around the anus is a common symptom. Diagnosis of pinworm can be reached from three simple techniques. The first option is to look for the worms in the perianal reqion 2 to 3 hours after the infected person is asleep. The second option is to touch the perianal skin with transparent tape to collect possible pinworm eggs around the anus first thing in the morning. If a person is infected, the eggs on the tape will be visible under a microscope. The tape method should be conducted on 3 consecutive mornings right after the infected person wakes up and before he\/she does any washing. Since anal itching is a common symptom of pinworm, the third option for diagnosis is analyzing samples from under fingernails under a microscope. An infected person who has scratched the anal area may have picked up some pinworm eggs under the nails that could be used for diagnosis.\n    \nSince pinworm eggs and worms are often sparse in stool, examining stool samples is not recommended. Serologic tests are not available for diagnosing pinworm infections."}
{"_id":"1d908c58-aa56-4c33-b095-afeaeaaa9387","text":"The medications used for the treatment of pinworm are mebendazole, pyrantel pamoate, and albendazole. All three of these drugs are to be given in 1 dose at first and then another single dose 2 weeks later. Pyrantel pamoate is available without prescription. The medication does not reliably kill pinworm eggs. Therefore, the second dose is to prevent re-infection by adult worms that hatch from any eggs not killed by the first treatment.Health practitioners and parents should weigh the health risks and benefits of these drugs for patients under 2 years of age.\n    \nRepeated infections should be treated by the same method as the first infection. In households where more than one member is infected or where repeated, symptomatic infections occur, it is recommended that all household members be treated at the same time. In institutions, mass and simultaneous treatment, repeated in 2 weeks, can be effective."}
{"_id":"d7538adb-8e5d-4820-9342-d5dcff1172f1","text":"Washing your hands with soap and warm water after using the toilet, changing diapers, and before handling food is the most successful way to prevent pinworm infection. In order to stop the spread of pinworm and possible re-infection, people who are infected should bathe every morning to help remove a large amount of the eggs on the skin. Showering is a better method than taking a bath, because showering avoids potentially contaminating the bath water with pinworm eggs. Infected people should not co-bathe with others during their time of infection.\n    \nAlso, infected people should comply with good hygiene practices such as washing their hands with soap and warm water after using the toilet, changing diapers, and before handling food. They should also cut fingernails regularly, and avoid biting the nails and scratching around the anus. Frequent changing of underclothes and bed linens first thing in the morning is a great way to prevent possible transmission of eggs in the environment and risk of reinfection. These items should not be shaken and carefully placed into a washer and laundered in hot water followed by a hot dryer to kill any eggs that may be there.\n    \nIn institutions, day care centers, and schools, control of pinworm can be difficult, but mass drug administration during an outbreak can be successful. Teach children the importance of washing hands to prevent infection.\n    \nMore on: Handwashing"}
{"_id":"a0944975-3ca9-442f-98f1-5a6fb2c84303","text":"Diagnosing HPS\n  \nDiagnosing HPS in an individual who has only been infected a few days is difficult, because early symptoms such as fever, muscle aches, and fatigue are easily confused with influenza. However, if the individual is experiencing fever and fatigue and has a history of potential rural rodent exposure, together with shortness of breath, would be strongly suggestive of HPS. If the individual is experiencing these symptoms they should see their physician immediately and mention their potential rodent exposure.\n  Treating HPS\n  \n    \n      \n     \n   \n  \n  \nThere is no specific treatment, cure, or vaccine for hantavirus infection. However, we do know that if infected individuals are recognized early and receive medical care in an intensive care unit, they may do better. In intensive care, patients are intubated and given oxygen therapy to help them through the period of severe respiratory distress.\n  \nThe earlier the patient is brought in to intensive care, the better. If a patient is experiencing full distress, it is less likely the treatment will be effective.\n  \nTherefore, if you have been around rodents and have symptoms of fever, deep muscle aches, and severe shortness of breath, see your doctor immediately. Be sure to tell your doctor that you have been around rodents\u2014this will alert your physician to look closely for any rodent-carried disease, such as HPS."}
{"_id":"547fd80f-3311-4a02-8f5c-869fbc34db7c","text":"Due to the small number of HPS cases, the \"incubation time\" is not positively known. However, on the basis of limited information, it appears that symptoms may develop between 1 and 5 weeks after exposure to fresh urine, droppings, or saliva of infected rodents.\n  Early Symptoms\n  \n    \n   \nEarly symptoms include fatigue, fever and muscle aches, especially in the large muscle groups\u2014thighs, hips, back, and sometimes shoulders. These symptoms are universal.\n   \nThere may also be headaches, dizziness, chills, and abdominal problems, such as nausea, vomiting, diarrhea, and abdominal pain. About half of all HPS patients experience these symptoms.\n  \n  Late Symptoms\n  \n    \n   \nFour to 10 days after the initial phase of illness, the late symptoms of HPS appear. These include coughing and shortness of breath, with the sensation of, as one survivor put it, a \"...tight band around my chest and a pillow over my face\" as the lungs fill with fluid.\n  \n  Is the Disease Fatal?\n  \nYes. HPS can be fatal. It has a mortality rate of 38%."}
{"_id":"41beea74-eac4-490f-9f16-7dc34c093eed","text":"Eliminate or minimize contact with rodents in your home, workplace, or campsite. If rodents don't find that where you are is a good place for them to be, then you're less likely to come into contact with them. Seal up holes and gaps in your home or garage. Place traps in and around your home to decrease rodent infestation. Clean up any easy-to-get food.\n  \nRecent research results show that many people who became ill with HPS developed the disease after having been in frequent contact with rodents and\/or their droppings around a home or a workplace. On the other hand, many people who became ill reported that they had not seen rodents or rodent droppings at all. Therefore, if you live in an area where the carrier rodents are known to live, try to keep your home, vacation place, workplace, or campsite clean.\n  \nFor more information on how you can prevent rodent infestations, the following information is available on the CDC Rodents site:"}
{"_id":"8b5546c4-cbef-4bda-9a46-c03cacd0a3e0","text":"The \"First\"Outbreak\n  \nIn May 1993, an outbreak of an unexplained pulmonary illness occurred in the southwestern United States, in an area shared by Arizona, New Mexico, Colorado and Utah known as \"The Four Corners\". A young, physically fit Navajo man suffering from shortness of breath was rushed to a hospital in New Mexico and died very rapidly.\n   \n  \nWhile reviewing the results of the case, medical personnel discovered that the young man's fianc\u00e9e had died a few days before after showing similar symptoms, a piece of information that proved key to discovering the disease. As Dr. James Cheek of the Indian Health Service (IHS) noted, \"I think if it hadn't been for that initial pair of people that became sick within a week of each other, we never would have discovered the illness at all\".\n  \nAn investigation combing the entire Four Corners region was launched by the New Mexico Office of Medical Investigations (OMI) to find any other people who had a similar case history. Within a few hours, Dr. Bruce Tempest of IHS, working with OMI, had located five young, healthy people who had all died after acute respiratory failure.\n  \nA series of laboratory tests had failed to identify any of the deaths as caused by a known disease, such as bubonic plague. At this point, the CDC Special Pathogens Branch was notified. CDC, the state health departments of New Mexico, Colorado and Utah, the Indian Health Service, the Navajo Nation, and the University of New Mexico all joined together to confront the outbreak.\n   \n  \nDuring the next few weeks, as additional cases of the disease were reported in the Four Corners area, physicians and other scientific experts worked intensively to narrow down the list of possible causes. The particular mixture of symptoms and clinical findings pointed researchers away from possible causes, such as exposure to a herbicide or a new type of influenza, and toward some type of virus. Samples of tissue from patients who had gotten the disease were sent to CDC for exhaustive analysis. Virologists at CDC used several tests, including new methods to pinpoint virus genes at the molecular level, and were able to link the pulmonary syndrome with a virus, in particular a previously unknown type of hantavirus.\n  Researchers Launch Investigations to Pin Down the Carrier of the New Virus\n   \n  \nResearchers knew that all other known hantaviruses were transmitted to people by rodents, such as mice and rats. Therefore, an important part of their mission was to trap as many different species of rodents living in the Four Corners region as possible to find the particular type of rodent that carried the virus. From June through mid-August of 1993, all types of rodents were trapped inside and outside homes where people who had hantavirus pulmonary syndrome had lived, as well as in pi\u00f1on groves and summer sheep camps where they had worked. Additional rodents were trapped for comparison in and around nearby households as well. Taking a calculated risk, researchers decided not to wear protective clothing or masks during the trapping process. \"We didn't want to go in wearing respirators, scaring...everybody\", John Sarisky, an Indian Health Service environmental disease specialist said. However, when the almost 1,700 rodents trapped were dissected to prepare samples for analysis at CDC, protective clothing and respirators were worn.\n  \nAmong rodents trapped, the deer mouse (Peromyscus maniculatus) was found to be the main host to a previously unknown type of hantavirus. Since the deer mouse often lives near people in rural and semi-rural areas\u2014in barns and outbuildings, woodpiles, and inside people's homes\u2014researchers suspected that the deer mouse might be transmitting the virus to humans. About 30% of the deer mice tested showed evidence of infection with hantavirus. Tests also showed that several other types of rodents were infected, although in lesser numbers.\n  \nThe next step was to pin down the connection between the infected deer mice and households where people who had gotten the disease lived. Therefore, investigators launched a case-control investigation. They compared \"case\" households, where people who had gotten the disease lived, with nearby \"control\" households. Control households were similar to those where the case-patients lived, except for one factor: no one in the control households had gotten the disease.\n  \nThe results? First, investigators trapped more rodents in case households than in control households, so more rodents may have been living in close contact with people in case households. Second, people in case households were more likely than those in control households to do cleaning around the house or to plant in or hand-plow soil outdoors in fields or gardens. However, it was unclear if the risk for contracting HPS was due to performing these tasks, or with entering closed-up rooms or closets to get tools needed for these tasks.\n  \nIn November 1993, the specific hantavirus that caused the Four Corners outbreak was isolated. The Special Pathogens Branch at CDC used tissue from a deer mouse that had been trapped near the New Mexico home of a person who had gotten the disease and grew the virus from it in the laboratory. Shortly afterwards and independently, the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) also grew the virus, from a person in New Mexico who had gotten the disease as well as from a mouse trapped in California.\n   \n  \nThe new virus was called Muerto Canyon virus \u2014 later changed to Sin Nombre virus (SNV) \u2014 and the new disease caused by the virus was named hantavirus pulmonary syndrome, or HPS.\n  \nThe isolation of the virus in a matter of months was remarkable. This success was based on close cooperation of all the agencies and individuals involved in investigating the outbreak, years of basic research on other hantaviruses that had been conducted at CDC and USAMRIID, and on the continuing development of modern molecular virologic tests. To put the rapid isolation of the Sin Nombre virus in perspective, it took several decades for the first hantavirus discovered, the Hantaan virus, to be isolated.\n  \n                \n  HPS Not Really a New Disease\n  \nAs part of the effort to locate the source of the virus, researchers located and examined stored samples of lung tissue from people who had died of unexplained lung disease. Some of these samples showed evidence of previous infection with Sin Nombre virus\u2014indicating that the disease had existed before the \"first\" known outbreak\u2014it simply had not been recognized!\n  \nOther early cases of HPS have been discovered by examining samples of tissue belonging to people who had died of unexplained adult respiratory distress syndrome. By this method, the earliest known case of HPS that has been confirmed has been the case of a 38-year-old Utah man in 1959.\n  \nInterestingly, while HPS was not known to the epidemiologic and medical communities, there is evidence that it was recognized elsewhere. The Navajo Indians, a number of whom contracted HPS during the 1993 outbreak, recognize a similar disease in their medical traditions, and actually associate its occurrence with mice. As strikingly, Navajo medical beliefs concur with public health recommendations for preventing the disease.\n  \n                \n  Why Did the Outbreak Occur in the Four Corners Area?\n  \nBut why this sudden cluster of cases? The key answer to this question is that, during this period, there were suddenly many more mice than usual. The Four Corners area had been in a drought for several years. Then, in early 1993, heavy snows and rainfall helped drought-stricken plants and animals to revive and grow in larger-than-usual numbers. The area's deer mice had plenty to eat, and as a result they reproduced so rapidly that there were ten times more mice in May 1993 than there had been in May of 1992. With so many mice, it was more likely that mice and humans would come into contact with one another, and thus more likely that the hantavirus carried by the mice would be transmitted to humans.\n  \n                \n  Person-to-Person Spread of HPS Decided Unlikely\n  \n\"Although person-to-person spread [of HPS] has not been documented with any of the other known hantaviruses, we were concerned [during this outbreak] because we were dealing with a new agent\", said Charles Vitek, a CDC medical investigator.\n  \nResearchers and clinicians investigating the ongoing outbreak were not the only groups concerned about the disease. Shortly after the first few HPS patients died and it became clear that a new disease was affecting people in the area, and that no one knew how it was transmitted, the news media began extensive reporting on the outbreak. Widespread concern among the public ensued.\n  \nUnfortunately, the first victims of the outbreak were Navajo. News reports focused on this fact, and the misperception grew that the unknown disease was somehow linked to Navajos. As a consequence, Navajos found themselves at the center of intense media attention and the objects of the some people's fears.\n  \nBy later in the summer of 1993, the media frenzy had quieted somewhat, and the source of the disease was pinpointed. Researchers determined that, like other hantaviruses, the virus that causes HPS is not transmitted from person to person the way other infections, such as the common cold, may be. The exception to this is an outbreak of HPS in Argentina in 1996. Evidence from this outbreak suggests that strains of hantaviruses in South America may be transmissable from person to person.\n  \nTo date, no cases of HPS have been reported in the United States in which the virus was transmitted from one person to another. In fact, in a study of health care workers who were exposed to either patients or specimens infected with related types of hantaviruses (which cause a different disease in humans), none of the workers showed evidence of infection or illness.\n  \n                \n  HPS Since the First Outbreak\n  \nAfter the initial outbreak, the medical community nationwide was asked to report any cases of illness with symptoms similar to those of HPS that could not be explained by any other cause. As a result, additional cases have been reported.\n  \nSince 1993, researchers have discovered that there is not just one hantavirus that causes HPS, but several. In June 1993, a Louisiana bridge inspector who had not traveled to the Four Corners area developed HPS. An investigation was begun. The patient's tissues were tested for the presence of antibodies to hantavirus. The results led to the discovery of another hantavirus, named Bayou virus, which was linked to a carrier, the rice rat (Oryzomys palustris). In late 1993, a 33-year-old Florida man came down with HPS symptoms; he later recovered. This person also had not traveled to the Four Corners area. A similar investigation revealed yet another hantavirus, named the Black Creek Canal virus, and its carrier, the cotton rat (Sigmodon hispidus). Another case occurred in New York. This time, the Sin Nombre-like virus was named New York-1, and the white-footed mouse (Peromyscus leucopus), was implicated as the carrier.\n  \nMore recently, cases of HPS stemming from related hantaviruses have been documented in Argentina, Brazil, Canada, Chile, Paraguay, and Uruguay, making HPS a pan-hemispheric disease.\n  \n                \n  References\n  \nInformation for this page was developed using the CDC video Preventing Hantavirus Disease and resource articles listed in the bibliography."}
{"_id":"9fba7919-c8fb-499a-b49d-90ec221b7272","text":"Q fever can cause acute or chronic illness in humans, who usually acquire infection after contact with infected animals or exposure to contaminated environments. The acute symptoms caused by infection with Coxiella burnetii usually develop within 2-3 weeks of exposure, although as many as half of humans infected withC. burnetii do not show symptoms. \n \nThe following is a list of symptoms commonly seen with acute Q fever. However, it is important to note that the combination of symptoms varies greatly from person to person. \n  \n  - high fevers (up to 104-105\u00b0F)  \n  - severe headache  \n  - general malaise  \n  - myalgia  \n  - chills and\/or sweats  \n  - non-productive cough  \n  - nausea  \n  - vomiting  \n  - diarrhea  \n  - abdominal pain  \n  - chest pain  \n  \n \nAlthough most persons with acute Q fever infection recover, others may experience serious illness with complications that may include pneumonia, granulomatous hepatitis (inflammation of the liver), myocarditis (inflammation of the heart tissue) and central nervous system complications. Pregnant women who are infected may be at risk for pre-term delivery or miscarriage. The estimated case fatality rate (i.e. the proportion of persons who die as a result of their infection) is low,  at < 2% of hospitalized patients. Treatment with the correct antibiotic may shorten the course of illness for acute Q fever.  \n \nChronic Q fever is a severe disease occurring in <5% of acutely infected patients. It may present soon (within 6 weeks) after an acute infection, or may manifest years later.  The three groups at highest risk for chronic Q fever are pregnant women, immunosuppressed persons and patients with a pre-existing heart valve defects. Endocarditis is the major form of chronic disease, comprising 60-70% of all reported cases. The estimated case fatality rate in untreated patients with endocarditis is 25-60%. Patients with endocarditis require early diagnosis and long-term antibiotic treatment (at least 18 months) for a successful outcome.   Other forms of chronic Q fever include aortic aneurysms and infections of the bone, liver or reproductive organs, such as the testes in males. \n \nCoxiella burnetii has the ability to persist for long periods of time in the host after infection. Although the majority of people with acute Q fever recover completely, a post-Q fever fatigue syndrome has been reported to occur in 10-25% of some acute patients. This syndrome is characterized by constant or recurring fatigue, night sweats, severe headaches, photophobia (eye sensitivity to light), pain in muscles and joints, mood changes, and difficulty sleeping.  \n \n \n Physician Diagnosis \n \nThere are several aspects of Q fever that make it challenging for healthcare providers to diagnose and treat.  The symptoms vary from patient to patient and can be difficult to distinguish from other diseases.  Treatment is more likely to be effective if started in the first three days of symptoms. Diagnostic tests based on the detection of antibodies will frequently appear negative in the first 7-10 days of illness.  For this reason, healthcare providers must use their judgment to treat patients based on clinical suspicion alone. Healthcare providers may find important information in the patient\u2019s history and physical examination that may aid clinical diagnosis. Information such as recent travel to rural or agricultural communities where infected livestock may be present, or employment in high risk occupations such as veterinarians or farmers can be helpful in making the diagnosis.  Chronic Q fever is a risk for anyone with a history of acute Q fever illness, particularly those persons with valvular disease, blood vessel abnormalities, immunosuppressed persons, and women who were pregnant when they became infected.  \n \nThe healthcare provider should also look at routine blood tests, such as a complete blood cell count or a chemistry panel. Clues such as a prolonged fever with low platelet count, normal leukocyte count, and elevated liver enzymes are suggestive of acute Q fever infection, but may not be present in all patients.  After a suspect diagnosis is made based on clinical suspicion and treatment has begun, specialized laboratory testing should be used to confirm the diagnosis of Q fever. \n \nSuspect diagnosis of Q fever is made based on signs and symptoms and a high index of clinical suspicion.  Diagnosis can later be confirmed using specialized confirmatory laboratory tests. Treatment should never be delayed pending the receipt of laboratory test results, or be withheld on the basis of an initial negative laboratory result. \n \n  \n \n \n Laboratory Confirmation \n \nDuring the acute phase of illness, a sample of whole blood can be tested by polymerase chain reaction (PCR) assay to determine if a patient has Q fever. This method is most sensitive in the first week of illness, and rapidly decreases in sensitivity following the administration of appropriate antibiotics. PCR or immunohistochemistry of biopsy specimens has also been used to diagnose Q fever. These tests may be appropriate for endocarditis patients undergoing valve replacement surgery or patients with hepatitis. Although a positive PCR result is helpful, a negative result does not rule out the diagnosis, and treatment should not be withheld due to a negative result. Culture isolation of C. burnetii is only available at specialized laboratories; routine hospital blood cultures cannot detect the organism.  \n \nWhen a person develops Q fever, their immune system produces antibodies to C. burnetii, with detectable antibody titers usually observed by 7-10 days after illness onset.  It is important to note that a negative test during the first week of illness does not rule out Q fever as a cause of illness. There are two distinct antigenic phases to which humans develop antibody responses. In acute infection, an antibody response to C. burnetii Phase II antigen is predominant and is higher than Phase I antibody response; the reverse is true in chronic infection which is associated with a rising Phase I IgG titer (according to current U.S. case definitions >1:800) that is often much higher than Phase II IgG.  The gold standard serologic test for diagnosis of acute Q fever is the indirect immunofluorescence assay (IFA) using C. burnetii antigen, performed on paired serum samples to demonstrate a significant (four-fold) rise in antibody titers. The first sample should be taken as early in the disease as possible, preferably in the first week of symptoms, and the second sample should be taken 2 to 4 weeks later. In most cases of Q fever, the first IgG IFA titer is typically low, or \u201cnegative,\u201d and the second typically shows a significant (four-fold) increase in IgG antibody levels. IgM antibodies usually rise at the same time as IgG near the end of the first week of illness and remain elevated for months or longer.  Also, IgM antibodies are less specific than IgG antibodies and more likely to result in a false positive.  For these reasons, physicians should request both Phase I and Phase II IgG and IgM serologic titers for diagnostic confirmation of acute and chronic Q fever.  Antibodies to C. burnetii may remain elevated for months or longer after the disease has resolved, or may be detected in persons who were previously exposed to antigenically related organisms.  Approximately 3% of currently healthy people in the U.S. general population and up to 20% of people in high-risk professions (veterinarians, ranchers, etc.) have elevated antibody titers due to past exposure to C. burnetii. Therefore, if only one sample is tested it can be difficult to interpret the findings.  \n \nPaired samples taken 2-3 weeks apart demonstrating a significant (four-fold) rise in antibody titer provides the best evidence for a correct diagnosis of acute Q fever. Diagnosis of chronic Q fever is confirmed by elevated Phase I IgG antibody (according to current U.S. case definitions >1:800 and higher than Phase II IgG) and an identifiable persistent focus of infection (e.g. endocarditis).  Elevated Phase I titers alone do not confirm a chronic Q fever diagnosis and would not warrant treatment in a clinically normal patient. Because chronic Q fever involves lengthy persistence of the organism in the body, the antibody levels are often quite high and you will not see a rising titer between paired serum specimens. \n \nFor more in-depth information about the diagnosis of Q fever, please visit http:\/\/www.bt.cdc.gov\/agent\/qfever\/clinicians\/diagnosis.asp \n \n \n Treatment \n \nDoxycycline is the first line treatment for all adults, and for children with severe illness. Treatment should be initiated immediately whenever Q fever is suspected. \n \nUse of antibiotics other than doxycycline or other tetracyclines is associated with a higher risk of severe illness. Doxycycline is most effective at preventing severe complications from developing if it is started early in the course of disease. Therefore, treatment must be based on clinical suspicion alone and should always begin before laboratory results return. \n \nIf the patient is treated within the first 3 days of the disease, fever generally subsides within 72 hours.  In fact, failure to respond to doxycycline suggests that the patient\u2019s condition might not be due to Q fever. Severely ill patients may require longer periods before their fever resolves. Resistance to doxcycline has not been documented.  \n \nThere is no role for prophylactic antimicrobial agents in preventing Q fever after a known exposure and prior to symptom onset; attempts at prophylaxis will likely extend the incubation period by several days but will not prevent infection from occurring.  \n \nRecommended Dosage for Acute Q fever\n Doxycycline is the first line treatment for children with severe illness of all ages and adults: \n  \n  - Adults: 100 mg every 12 hours  \n  - Children under 45 kg (100 lbs): 2.2 mg\/kg body weight given twice a day  \n  \n \nPatients should be treated for at least 3 days after the fever subsides and until there is evidence of clinical improvement. Standard duration of treatment is 2-3 weeks.  \n \nRecommended Dosage for Chronic Q fever \n  \n  - Adults: Doxycycline 100 mg every 12 hours and hydroxychloroquine 200 mg every 8 hours. \n  \n \nStandard duration of treatment is 18 months. \n \n \n Treating children \n \nThe use of doxycycline is recommended to treat Q fever in children of all ages who are hospitalized or are severely ill. Unlike older generations of tetracyclines, doxycycline has not been shown to cause staining of permanent teeth, and most experts consider the benefit of doxycycline in treating Q fever in children younger than 8 years of age with severe illness or who are hospitalized greater than the potential risk of dental staining.  Children with mild illness who are less than 8 years of age may be treated with co-trimoxazole, but therapy should be switched to doxycycline if their course of illness worsens. \n \n \n Other Treatments \n \nIn cases of life threatening allergies to doxycycline and in pregnant patients, physicians may need to consider alternate antibiotics. Treatment of pregnant women diagnosed with acute Q fever with once daily co-trimoxazole throughout pregnancy has been shown to significantly decrease the risk of adverse consequences for the fetus."}
{"_id":"220ef6b0-3351-4d40-a51c-36496da44502","text":"More detailed information on the diagnosis, management, and treatment of Q fever is available in other sections of this web site and in the materials referenced in the section titled \u201cFurther Reading\u201d.  \n How to Contact the Rickettsial Zoonoses Branch at CDC \n \nThe general public and healthcare providers should first call 1-800-CDC-INFO (1-800-232-4636) for questions regarding Q fever. If a consultation with a CDC scientist specializing in Q fever is advised, your call will be appropriately forwarded. \n Case Definitions \n \nAs of January 1, 2009, Q fever infections are reported under distinct reporting categories described in the 2009 Q fever surveillance case definition.\n2009 Q Fever Case Definition \n Case Report Forms \n \nFor confirmed and probable cases of Q fever that have been identified and reported through the National Notifiable Disease Surveillance System, states are also encouraged to submit additional information using the CDC Case Report Form (CRF). This form collects additional important information that routine electronic reporting does not, such as information on how the diagnosis was made, and whether the patient was hospitalized or died. If a different state-specific form is already used to collect this information, this information may be submitted to CDC in lieu of a CRF. \n   \n   \n    \n   \n  \n How to Submit Specimens to CDC for Q FeverTesting \n \nPrivate citizens may not directly submit specimens to CDC for testing. If you feel that diagnostic testing is necessary, consult your healthcare provider or state health department. Laboratory testing is available at many commercial laboratories. \n State Health Departments \n \nSpecimens may be submitted to CDC for reference testing for Q fever. To coordinate specimen submission, please call 404-639-1075 during business hours (8:00 - 4:30 ET).  \n U.S. Healthcare Providers \n \nQ fever laboratory testing is available at many commercial laboratories. U.S. healthcare providers should not submit specimens for testing directly to CDC. CDC policy requires that specimens for testing be submitted through or with the approval of the state health department. Please contact your state health department and request assistance with specimen submission and reporting of infection. For general questions about Q fever, please call 1-800-CDC-INFO (1-800-232-4636). If you have questions about a suspect Q fever case, please first consult your state health department. Healthcare providers requiring an epidemiologic or laboratory consultation on Q fever may also call 404-639-1075 during business hours (8:00 - 4:30 ET). Or 770-488-7100 after hours.  \n Non-U.S. Healthcare Providers \n \nNon-U.S. healthcare providers should consult CDC prior to submitting specimens for testing. For general questions about Q fever, please call 1-800-CDC-INFO (1-800-232-4636). If you would like to discuss a suspect Q fever case with CDC, please call 404-639-1075 during business hours (8:00 - 4:30 ET), or 770-488-7100 after hours."}
{"_id":"85628296-bbbe-4dcf-8657-c3ed865ea4e6","text":"In the United States, Q fever outbreaks have resulted mainly from occupational exposure involving veterinarians, meat processing plant workers, sheep and dairy workers, livestock farmers, and researchers at facilities housing sheep. Prevention and control efforts should be directed primarily toward these groups and environments. \n \nThe following measures should be used in the prevention and control of Q fever: \n  \n  - Educate the public on sources of infection.  \n  - Appropriately dispose of placenta, birth products, fetal membranes, and aborted fetuses at facilities housing sheep and goats.  \n  - Restrict access to barns and laboratories used in housing potentially infected animals.   \n  - Use appropriate procedures for bagging, autoclaving, and washing of laboratory clothing.  \n  - Vaccinate (where possible) individuals engaged in research with pregnant sheep or live C. burnetii.  \n  - Quarantine imported animals.  \n  - Ensure that holding facilities for sheep should be located away from populated areas. Animals should be routinely tested for antibodies to C. burnetii, and measures should be implemented to prevent airflow to other occupied areas.  \n  - Counsel persons at highest risk for developing chronic Q fever, especially persons with pre-existing cardiac valvular disease or individuals with vascular grafts.  \n  \n \nA vaccine for Q fever has been developed and has successfully protected humans in occupational settings in Australia. However, this vaccine is not commercially available in the United States. Persons wishing to be vaccinated should first have a skin test to determine a history of previous exposure. Individuals who have previously been exposed to C. burnetii should not receive the vaccine because severe reactions, localized to the area of the injected vaccine, may occur. A vaccine for use in animals has also been developed, but it is not available in the United States. \n Significance for Bioterrorism \n \nCoxiella burnetii is a highly infectious agent that is rather resistant to heat and drying. It can become airborne and inhaled by humans. A single C. burnetii organism may cause disease in a susceptible person. This agent has a past history of being developed for use in biological warfare and is considered a potential terrorist threat."}
{"_id":"bcc79635-b8e3-45f2-91f5-9e9e90a73691","text":"Transmission of Hendra virus to humans can occur after exposure to body fluids and tissues or excretions of horses infected with Hendra virus. \n \nHorses may be infected after exposure to virus in the urine of infected flying foxes. \n \nTo date, no human-to-human transmission has been documented."}
{"_id":"e80bf60b-b610-4329-94d9-25790542e1ef","text":"After an incubation of 9-16 days, infection with Hendra virus can lead to respiratory illness with severe flu-like signs and symptoms. In some cases, illness may progress to encephalitis. \n                \nAlthough infection with Hendra virus is rare, the case fatality is high: 4\/7 (57%)."}
{"_id":"4b278171-7a64-4bbc-aed7-b9ba53619970","text":"Australia\u2019s \u201cFlying fox\u201d bats (genus Pteropus) are the natural reservoir of Hendra virus. Serologic evidence for HeV infection have been found in all fours species of Australian flying foxes, but spillover of the virus in horses is limited to coastal and forested regions in Australia (Queensland and New South Wales states)  (see Henipavirus Distribution Map). \n                \nPeople at highest risk are those living within the distribution of the flying foxes and with occupational or recreational exposure to horses that have had potential contact with flying foxes in Australia."}
{"_id":"c8e0e702-17df-4d60-a57f-9b1f4a55b583","text":"Laboratory tests that are used to diagnose Hendra virus (HV) and Nipah virus (NV) include detection of antibody by ELISA (IgG and IgM), real time polymerase chain reaction (RT-PCR), and virus isolation attempts.  In most countries, handling Hendra virus needs to be done in high containment laboratories. Laboratory diagnosis of a patient with a clinical history of HV or NV can be made during the acute and convalescent phase of the disease by using a combination of tests including detection of antibody in the serum or the cerebrospinal fluid (CSF), viral RNA detection (RT-PCR) in the serum, CSF, or throat swabs, and virus isolation from the CSF or throat swabs."}
{"_id":"60d3a835-5157-4040-962c-158ac1079de9","text":"The drug ribavirin has been shown to be effective against the viruses in vitro, but the clinical usefulness of this drug is uncertain. \n                \nA post-exposure therapy with a Nipah\/Hendra neutralizing antibody, efficacious in animal models is in human preclinical development stages in Australia."}
{"_id":"bbeb985f-67c8-4195-805e-4ffb69560ca9","text":"The occurrence of the disease in humans has been associated only with infection of an intermediate species such as horses.  Early recognition of the disease in the intermediate animal host is probably the most crucial means of limiting future human cases.  \n                \nHendra virus infection can be prevented by avoiding horses that are ill or may be infected with HeV and using appropriate personal protective equipment when contact is necessary, as in veterinary procedures. \n                \nA commercial vaccine has been recently licensed in Australia for horses and could be beneficial for other animal species and eventually humans."}
{"_id":"a63c75ec-4a4c-49bd-ab82-364c9e90711f","text":"There are many different species of hookworms, some are human parasites and some are animal parasites. People can be infected by larvae of animal hookworms, usually dog and cat hookworms. The most common result of animal hookworm infection is a skin condition called cutaneous larva migrans."}
{"_id":"a4ecd595-7125-44ef-9a18-e0e0a2b6224e","text":"Dog and cat hookworms are found throughout the world, especially in warmer climates. In the United States, zoonotic hookworms are found everywhere but more commonly along the East Coast than the West Coast. Worldwide, zoonotic hookworms are found in tropical and subtropical regions where the parasite is better able to survive because of environmental conditions. However, there is one type of dog and cat hookworm that is more commonly found in cooler climates.\n    \nThe global burden of zoonotic hookworm in dogs and cats is not known; also, the amount of disease in people caused by these parasites is also unknown. Cutaneous larva migrans (CLM) is most often reported by returning travelers to tropical regions who have had soil and\/or sand exposures in places where dogs and cats are likely to have hookworms. However, CLM is likely causing significant problems for the people who live in less developed parts of the world, even though the disease is not reported regularly. In less developed areas of the world, dogs and cats are often free-ranging and have high rates of infection with hookworm which leads to widespread contamination of sand and soil. In a survey of a rural population in Brazil, the prevalence of CLM during the rainy season was 14.9% among children less than 5 years old and 0.7% among adults aged 20 years and older."}
{"_id":"7be6770e-6ade-4f1c-a376-77fc69567725","text":"Cutaneous larva migrans (CLM) is a clinical diagnosis based on the presence of the characteristic signs and symptoms, and exposure history to zoonotic hookworm. For example, the diagnosis can be made based on finding red, raised tracks in the skin that are very itchy. This is usually found on the feet or lower part of the legs on persons who have recently traveled to tropical areas and spent time at the beach. There is no blood test for zoonotic hookworm infection. Persons who think they have CLM should consult their health care provider for accurate diagnosis."}
{"_id":"710d729d-c907-41ef-8017-d1236ed6f143","text":"The zoonotic hookworm larvae that cause cutaneous larva migrans (CLM) usually do not survive more than 5 \u2013 6 weeks in the human host. In most patients with CLM, the signs and symptoms resolve without medical treatment. However, treatment may help control symptoms and help prevent secondary bacterial infections. Antiparasitic treatments may be prescribed by your health care provider.\n    \nMore on: Resources For Health Professionals: Treatment"}
{"_id":"6c8fa1b0-bb21-4f5b-99c2-9dea45bea101","text":"Wearing shoes and taking other protective measures to avoid skin contact with sand or soil will prevent infection with zoonotic hookworms. Travelers to tropical and subtropical climates, especially where beach exposures are likely, should be advised to wear shoes and use protective mats or other coverings to prevent direct skin contact with sand or soil. Routine veterinary care of dogs and cats, including regular deworming, will reduce environmental contamination with zoonotic hookworm eggs and larvae. Prompt disposal of animal feces prevents eggs from hatching and contaminating soil -- which makes it important for control of this parasitic infection."}
{"_id":"3521469e-eda9-47db-8576-a572799429e2","text":"Chronic fatigue syndrome, or CFS, is a devastating and complex disorder. People with CFS have overwhelming fatigue and a host of other symptoms that are not improved by bed rest and that can get worse after physical activity or mental exertion. They often function at a substantially lower level of activity than they were capable of before they became ill.\n  \nBesides severe fatigue, other symptoms include muscle pain, impaired memory or mental concentration, insomnia, and post-exertion malaise lasting more than 24 hours. In some cases, CFS can persist for years.\n  \nResearchers have not yet identified what causes CFS, and there are no tests to diagnose CFS. Moreover, because many illnesses have fatigue as a symptom, doctors need to take care to rule out other conditions, which may be treatable."}
{"_id":"2f9caa2d-106f-4b4e-a429-6e302a94335c","text":"Despite a vigorous search, scientists have not yet identified what causes CFS. While a single cause for CFS may yet be identified, another possibility is that CFS has multiple causes. Conditions that have been studied to determine if they cause or trigger the development of CFS include infections, immune disorders, stress, trauma, and toxins.\n  Infection\n  \nVarious types of infections have been studied to determine if they might cause or trigger CFS:\n  \n   - Candida albicans, a fungus that causes yeast infections\n   - Mycoplasma, a cause of atypical pneumonia\n   - Ross River virus, which causes Ross River Fever, a mosquito-borne tropical disease\n  \n  Could One Type of Infection Lead to CFS?\n  \nResearchers from around the world have studied if a single type of infection might be the cause of CFS, analyzed the data, and not yet found any association between CFS and infection. Researchers are still analyzing samples from CFS patients using the latest molecular methods to search for previously unknown infections (pathogen discovery). To date, these studies suggest that no one infection or pathogen causes CFS and that the illness may be triggered by a variety of illnesses or conditions. In fact, infection with Epstein-Barr virus, Ross River virus, and Coxiella burnetti will lead to a post-infective condition that meets the criteria for CFS in approximately 10-12% of cases. People who had severe symptoms when they became infected were more likely than those with mild symptoms to later develop CFS symptoms. The possibility remains that there may be a variety of different ways in which patients can develop CFS.\n  Immune System and Allergies\n  \nStudies have looked to see if changes in a person's immune system might lead to CFS. The findings have been mixed. Similarities in symptoms from immune responses to infection and CFS lead to hypotheses that CFS may be caused by stress or a viral infection, which may lead to the chronic production of cytokines and then to CFS.\n  \nAntibodies against normal parts of the body (auto-antibodies) and immune complexes have been seen in some CFS patients. However, no associated tissue damage typical of autoimmune disease has been described in CFS patients. The opportunistic infections or increased risk for cancer observed in persons with immunodeficiency diseases or in immunosuppressed individuals is also not observed in CFS.\n  \nT-cell activation markers have been reported to be different between groups of CFS patients and healthy persons, but not all investigators have consistently observed these differences.\n  \nAllergic diseases and secondary illnesses such as sinusitis could be one predisposing factor for CFS, but not all CFS patients have allergies. Many patients do, however, report intolerances for certain substances that may be found in foods or over-the-counter medications, such as alcohol.\n  \n                \n  Hypothalamic-Pituitary Adrenal (HPA) Axis\n  \nThe central nervous system plays an important role in CFS. Physical or emotional stress, which is commonly reported as a pre-onset condition in CFS patients, alters the activity of the hypothalamic-pituitary-adrenal axis, or HPA axis, leading to altered release of corticotrophin-releasing hormone (CRH), cortisol, and other hormones. These hormones can influence the immune system and many other body systems.\n  \nSome CFS patients produce lower levels of cortisol than do healthy people. Similar hormonal abnormalities have also been observed among CFS patients and in persons with related disorders like fibromyalgia. Cortisol suppresses inflammation and cellular immune activation, and reduced levels might relax constraints on inflammatory processes and immune cell activation. Even though CFS patients had lower levels of cortisol than healthy individuals, their cortisol levels were still within the acceptable range of what is considered normal. Therefore, doctors cannot use cortisol levels as a way to diagnose CFS.\n  \n                \n  Abnormally Low Blood Pressure and Lightheadedness (Neurally Mediated Hypotension)\n  \nDisturbances in the autonomic regulation of blood pressure and pulse have been found in CFS patients. This problem with maintaining blood pressure can be diagnosed by using tilt table testing, which involves laying the patient horizontally on a table and then tilting the table upright to 70 degrees for 45 minutes while monitoring blood pressure and heart rate. Persons with neurally mediated hypotension (NMH) or postural orthostatic tachycardia (POTS) will develop lower blood pressure under these conditions, as well as other characteristic symptoms, such as lightheadedness, visual dimming, or a slow response to verbal stimuli. Others may develop an unusually rapid heart rate also associated with the symptoms of the syndrome. Many CFS patients experience lightheadedness or worsened fatigue when they stand for prolonged periods or when in warm places, such as in a hot shower -- all circumstances that are known to trigger NMH or POTS.\n  \nNMH and\/or POTS share some of the symptoms of CFS. They should be considered in a CFS patients whose symptoms are worsened with changes in position, after eating, following unusual amounts of or inadequate fluid intake, or increases in activity. Not all patients with CFS will have these conditions, however.\n  \n                \n  Nutritional Deficiency\n  \nThere is no published scientific evidence that CFS is caused by a nutritional deficiency. While evidence is currently lacking for nutritional defects in CFS patients, it should also be added that a balanced diet can be favorable to better health in general and would be expected to benefit a person with any chronic illness."}
{"_id":"ba8e23b8-6dac-485f-bb50-997a491eeff5","text":"Diagnostic Challenges\n  \nFor doctors, diagnosing chronic fatigue syndrome (CFS) can be complicated by a number of factors:\n  \n   - There's no lab test or biomarker for CFS.\n   - Fatigue and other symptoms of CFS are common to many illnesses.\n   - For some CFS patients, it may not be obvious to doctors that they are ill.\n   - The illness has a pattern of remission and relapse.\n   - Symptoms vary from person to person in type, number, and severity.\n  \n  \nThese factors have contributed to a low diagnosis rate. Of the one to four million Americans who have CFS, less than 20% have been diagnosed.\n  Exams and Screening Tests for CFS\n  \nBecause there is no blood test, brain scan, or other lab test to diagnose CFS, the doctor should first rule out other possible causes.\n  \nIf a patient has had 6 or more consecutive months of severe fatigue that is reported to be unrelieved by sufficient bed rest and that is accompanied by nonspecific symptoms, including flu-like symptoms, generalized pain, and memory problems, the doctor should consider the possibility that the patient may have CFS. Further exams and tests are needed before a diagnosis can be made:\n  \n   - A detailed medical history will be needed and should include a review of medications that could be causing the fatigue and symptoms\n   - A thorough physical and mental status examination will also be needed\n   - A battery of laboratory screening tests will be needed to help identify or rule out other possible causes of the symptoms that could be treated\n   - The doctor may also order additional tests to follow up on results of the initial screening tests\n  \n  \nA CFS diagnosis requires that the patient has been fatigued for 6 months or more and has 4 of the 8 symptoms for CFS for 6 months or more. If, however, the patient has been fatigued for 6 months or more but does not have four of the eight symptoms, the diagnosis may be idiopathic fatigue.\n  \nThe complete process for diagnosing CFS can be found here.\n  \nAdditional information for healthcare professionals on use of tests can be found here."}
{"_id":"917d799d-b6f3-4ce8-868c-cbde1d520df4","text":"Chronic fatigue syndrome can be misdiagnosed or overlooked because its symptoms are similar to so many other illnesses. Fatigue, for instance, can be a symptom for hundreds of illnesses. Looking closer at the nature of the symptoms though, can help a doctor distinguish CFS from other illnesses.\n  Primary Symptoms\n  \nAs the name chronic fatigue syndrome suggests, fatigue is one part of this illness. With CFS, however, the fatigue is accompanied by other symptoms. In addition, the fatigue is not the kind you might feel after a particularly busy day or week, after a sleepless night, or after a single stressful event. It's a severe, incapacitating fatigue that isn't improved by bed rest and that is often worsened by physical activity or mental exertion. It's an all-encompassing fatigue that can dramatically reduce a person's activity level and stamina.\n  \nPeople with CFS function at a significantly lower level of activity than they were capable of before they became ill. The illness results in a substantial reduction in work-related, personal, social, and educational activities.\n  \nThe fatigue of CFS is accompanied by characteristic illness symptoms lasting at least 6 months. These symptoms include:\n  \n   - increased malaise (extreme exhaustion and sickness) following physical activity or mental exertion\n   - problems with sleep\n   - difficulties with memory and concentration\n   - persistent muscle pain\n   - joint pain (without redness or swelling)\n   - headache\n   - tender lymph nodes in the neck or armpit\n   - sore throat\n  \n  Other Symptoms\n  \nThe symptoms listed above are the symptoms used to diagnose CFS. However, many CFS patients and patients in general may experience other symptoms, including:\n  \n   - brain fog (feeling like you're in a mental fog)\n   - difficulty maintaining an upright position, dizziness, balance problems or fainting\n   - allergies or sensitivities to foods, odors, chemicals, medications, or noise\n   - irritable bowel\n   - chills and night sweats\n   - visual disturbances (sensitivity to light, blurring, eye pain)\n   - depression or mood problems (irritability, mood swings, anxiety, panic attacks)\n  \n  \nIt's important to tell your health care professional if you're experiencing any of these symptoms. You might have CFS, or you might have another treatable disorder. Only a health care professional can diagnose CFS.\n  What's the Clinical Course of CFS?\n  \nThe severity of CFS varies from patient to patient. Some people can maintain fairly active lives. For most patients, however, CFS significantly limits their work, school, and family activities for periods of time.\n  \nWhile symptoms vary from person to person in number, type, and severity, all CFS patients are limited in what they can do to some degree. CDC studies show that CFS can be as disabling as multiple sclerosis, lupus, rheumatoid arthritis, heart disease, end-stage renal disease, chronic obstructive pulmonary disease (COPD), and similar chronic conditions.\n  \nCFS often affects patients in cycles: Patients will have periods of illness followed by periods of relative well-being. For some patients, symptoms may diminish or even go into complete remission; however, they often recur at a later point in time. This pattern of remission and relapse makes CFS especially hard for patients to manage. Patients who are in remission may be tempted to overdo activities when they're feeling better, but this overexertion may actually contribute to a relapse.\n  \nThe percentage of CFS patients who recover is unknown, but there is some evidence to indicate that patients benefit when accompanying conditions are identified and treated and when symptoms are managed. High-quality health care is important."}
{"_id":"6653cc9b-3616-4ffe-946c-177f5495cd0a","text":"Introduction\n  \nManaging chronic fatigue syndrome can be as complex as the illness itself. There is no cure, no prescription drugs have been developed specifically for CFS, and symptoms can vary a lot over time. Thus, people with CFS should closely monitor their health and let their doctor know of any changes; and doctors should regularly monitor their patients' conditions and change treatment strategies as needed.\n  \nA team approach that involves doctors and patients is one key to successfully managing CFS. Patients and their doctors can work together to create an individualized treatment program that best meets the needs of the patient with CFS. This program should be based on a combination of therapies that address symptoms, coping techniques, and managing normal daily activities.\n  \nCFS affects patients in different ways, and the treatment plan should be tailored to address symptoms that are most disruptive or disabling for each patient. Helping the patient get relief from symptoms is the main goal of treatment. However, expecting a patient to return to usual activities should not be the immediate goal because the physical and mental exertion needed to try to reach that goal may aggravate the illness.\n  \nBecause CFS is a complicated illness, its management may require input from a variety of medical professionals. Primary care providers can develop effective treatment plans based on their experience in treating other illnesses. Patients benefit when they can work in collaboration with a team of doctors and other health care professionals, who might also include rehabilitation specialists, mental health professionals, and physical or exercise therapists.\n  Difficulties of Living with CFS\n  \nLiving with chronic fatigue syndrome can be difficult. Like other debilitating chronic illnesses, CFS can have a devastating impact on patients' daily lives and require them to make major lifestyle changes to adapt to many new limitations.\n  \nCommon difficulties for CFS patients include problems coping with:\n  \n   - the changing and unpredictable symptoms\n   - a decrease in stamina that interferes with activities of daily life\n   - memory and concentration problems that seriously hurt work or school performance\n   - loss of independence, livelihood, and economic security\n   - alterations in relationships with partners, family members, and friends\n   - worries about raising children\n  \n  \nFeelings of anger, guilt, anxiety, isolation and abandonment are common in CFS patients. While it's OK to have such feelings, unresolved emotions and stress can make symptoms worse, interfere with prescription drug therapies, and make recovery harder."}
{"_id":"e2d4dd42-0b60-4b30-aa3b-1635b4de249d","text":"The first symptoms of Rocky Mountain spotted fever (RMSF) typically begin 2-14 days after the bite of an infected tick. A tick bite is usually painless and about half of the people who develop RMSF do not remember being bitten. The disease frequently begins as a sudden onset of fever and headache and most people visit a healthcare provider during the first few days of symptoms. Because early symptoms may be non-specific, several visits may occur before the diagnosis of RMSF is made and correct treatment begins. The following is a list of symptoms commonly seen with this disease, however, it is important to note that few people with the disease will develop all symptoms, and the number and combination of symptoms varies greatly from person to person. \n \n - Fever  \n - Rash (occurs 2-5 days after fever, may be absent in some cases; see below) \n - Headache  \n - Nausea  \n - Vomiting  \n - Abdominal pain (may mimic appendicitis or other causes of acute abdominal pain)  \n - Muscle pain  \n - Lack of appetite  \n - Conjunctival injection (red eyes)  \n \n                \nRMSF is a serious illness that can be fatal in the first eight days of symptoms if not treated correctly, even in previously healthy people. The progression of the disease varies greatly. Patients who are treated early may recover quickly on outpatient medication, while those who experience a more severe course may require intravenous antibiotics, prolonged hospitalization or intensive care. \n                \n \nRash \n                \nWhile most people with RMSF (90%) have some type of rash during the course of illness, some people do not develop the rash until late in the disease process, after treatment should have already begun.  Approximately 10% of RMSF patients never develop a rash. It is important for physicians to consider RMSF if other signs and symptoms support a diagnosis, even if a rash is not present. \n                \nA classic case of RMSF involves a rash that first appears 2-5 days after the onset of fever as small, flat, pink, non-itchy spots (macules) on the wrists, forearms, and ankles and spreads to include the trunk and sometimes the palms and soles.  Often the rash varies from this description and people who fail to develop a rash, or develop an atypical rash, are at increased risk of being misdiagnosed. \n                \nThe red to purple, spotted (petechial) rash of RMSF is usually not seen until the sixth day or later after onset of symptoms and occurs in 35-60% of patients with the infection. This is a sign of progression to severe disease, and every attempt should be made to begin treatment before petechiae develop. \n                \nFigure 1a and 1b: Examples of an early-stage rash in an RMSF patient. \n \n  \n   \n     \n    \n   \n  \n  \n   \n     \n    \n   \n  \n \n \n   \n  \n \n                \n  \n \n                \n \nLong-term Health Problems \n                \nPatients who had a particularly severe infection requiring prolonged hospitalization may have long-term health problems caused by this disease. Rickettsia rickettsii infects the endothelial cells that line the blood vessels. The damage that occurs in the blood vessels results in a disease process called a \"vasculitis\", and bleeding or clotting in the brain or other vital organs may occur. Loss of fluid from damaged vessels can result in loss of circulation to the extremities and damaged fingers, toes or even limbs may ultimately need to be amputated. Patients who suffer this kind of severe vasculitis in the first two weeks of illness may also be left with permanent long-term health problems such as profound neurological deficits, or damage to internal organs. Those who do not have this kind of vascular damage in the initial stages of the disease typically recover fully within several days to months. \n                \n \nInfection in Children \n                \nChildren with RMSF infection may experience nausea, vomiting, and loss of appetite. Children are less likely to report a headache, but more likely to develop an early rash than adults. Other frequently observed signs and symptoms in children with RMSF are abdominal pain, altered mental status, and conjunctival injection. Occasionally, symptoms like cough, sore throat, and diarrhea may be seen, and can lead to misdiagnosis. \n                \nFor more in-depth information about signs and symptoms of RMSF, please visit http:\/\/www.cdc.gov\/mmwr\/preview\/mmwrhtml\/rr5504a1.htm \n                \n \nPhysician Diagnosis \n                \nThere are several aspects of RMSF that make it challenging for healthcare providers to diagnose and treat. The symptoms of RMSF vary from patient to patient and can easily resemble other, more common diseases. Treatment for this disease is most effective at preventing death if started in the first five days of symptoms. Diagnostic tests for this disease, especially tests based on the detection of antibodies, will frequently appear negative in the first 7-10 days of illness. Due to the complexities of this disease and the limitations of currently available diagnostic tests, there is no test available at this time that can provide a conclusive result in time to make important decisions about treatment. \n                \nFor this reason, healthcare providers must use their judgment to treat patients based on clinical suspicion alone. Healthcare providers may find important information in the patient\u2019s history and physical examination that may aid clinical suspicion. Information such as recent tick bites, exposure to high grass and tick-infested areas, contact with dogs, similar illnesses in family members or pets, or history of recent travel to areas of high incidence can be helpful in making the diagnosis. Also, information about the presence of symptoms such as fever and rash may be helpful. The healthcare provider may also look at routine blood tests, such as a complete blood cell count or a chemistry panel. Clues such as a low platelet count (thrombocytopenia), low sodium levels (hyponatremia), or elevated liver enzyme levels are often helpful predictors of RMSF but may not be present in all patients. After a suspect diagnosis is made on clinical suspicion and treatment has begun, specialized laboratory testing should be used to confirm the diagnosis of RMSF. \n  \n  \n   \n  \n \n                \n \nLaboratory Confirmation \n                \nR. rickettsii infects the endothelial cells that line blood vessels, and does not circulate in large numbers in the blood unless the patient has progressed to a very severe phase of infection. For this reason, blood specimens (whole blood, serum) are not always useful for detection of the organism through polymerase chain reaction (PCR) or culture. If the patient has a rash, PCR or immunohistochemical (IHC) staining can be performed on a skin biopsy taken from the rash site. This test can often deliver a rapid result. These tests have good sensitivity (70%) when applied to tissue specimens collected during the acute phase of illness and before antibiotic treatment has been started, but a negative result should not be used to guide treatment decisions. PCR, culture, and IHC can also be applied to autopsy specimens (liver, spleen, kidney, etc) collected after a patient dies. Culture of R. rickettsii is only available at specialized laboratories; routine hospital blood cultures cannot detect R. rickettsii. \n                \nDuring RMSF infection, a patient\u2019s immune system develops antibodies to R. rickettsii, with detectable antibody titers usually observed by 7-10 days after illness onset. It is important to note that antibodies are not detectable in the first week of illness in 85% of patients, and a negative test during this time does not rule out RMSF as a cause of illness. \n                \nThe gold standard serologic test for diagnosis of RMSF is the indirect immunofluorescence assay (IFA) with R. rickettsii antigen, performed on two paired serum samples to demonstrate a significant (four-fold) rise in antibody titers. The first sample should be taken as early in the disease as possible, preferably in the first week of symptoms, and the second sample should be taken 2 to 4 weeks later. In most RMSF cases, the first IgG IFA titer is typically low or negative, and the second typically shows a significant (fourfold) increase in IgG antibody levels. IgM antibodies usually rise at the same time as IgG near the end of the first week of illness and remain elevated for months or even years. Also, IgM antibodies are less specific than IgG antibodies and more likely to result in a false positive. For these reasons, physicians requesting IgM serologic titers should also request a concurrent IgG titer. \n                \nBoth IgM and IgG levels may remain elevated for months or longer after the disease has resolved, or may be detected in persons who were previously exposed to antigenically related organisms. Up to 10% of currently healthy people in some areas may have elevated antibody titers due to past exposure to R. rickettsii or similar organisms. Therefore, if only one sample is tested it can be difficult to interpret, whereas two paired samples taken weeks apart demonstrating a significant (four-fold) rise in antibody titer provide the best evidence for a correct diagnosis of RMSF. For more in-depth information about testing, please visit http:\/\/www.cdc.gov\/mmwr\/preview\/mmwrhtml\/rr5504a1.htm \n                \n \nTreatment \n                \nDoxycycline is the first line treatment for adults and children of all ages and should be initiated immediately whenever RMSF is suspected.  \n                \nUse of antibiotics other than doxycycline is associated with a higher risk of fatal outcome. Treatment is most effective at preventing death if doxycycline is started in the first 5 days of symptoms. Therefore, treatment must be based on clinical suspicion alone and should always begin before laboratory results return or symptoms of severe disease, such as petechiae, develop. \n                \nIf the patient is treated within the first 5 days of the disease, fever generally subsides within 24-72 hours. In fact, failure to respond to doxycycline suggests that the patient\u2019s condition might not be RMSF. Severely ill patients may require longer periods before their fever resolves, especially if they have experienced damage to multiple organ systems. Resistance to doxcycline or relapses in symptoms after the completion of the recommended course of treatment have not been documented. \n                \nRecommended Dosage\nDoxycycline is the first line treatment for adults and children of all ages: \n \n - Adults: 100 mg every 12 hours \n - Children under 45 kg (100 lbs): 2.2 mg\/kg body weight given twice a day \n \n                \nPatients should be treated for at least 3 days after the fever subsides and until there is evidence of clinical improvement. Standard duration of treatment is 7-14 days. \nTreating Children \n                \nThe use of doxycycline to treat suspected RMSF in children is standard practice recommended by both CDC and the AAP Committee on Infectious Diseases. Use of antibiotics other than doxycycline increases the risk of patient death. Unlike older tetracyclines, the recommended dose and duration of medication needed to treat RMSF has not been shown to cause staining of permanent teeth, even when five courses are given before the age of eight. Healthcare providers should use doxycycline as the first-line treatment for suspected Rocky Mountain spotted fever in patients of all ages. \nOther Treatments \n                \nIn cases of life threatening allergies to doxycycline and in some pregnant patients for whom the clinical course of RMSF appears mild, chloramphenicol may be considered as an alternative antibiotic. Oral forumulations of chloramphenicol are not available in the United States, and use of this drug carries the potential for other adverse risks, such as aplastic anemia and Grey baby syndrome. Furthermore, the risk for fatal outcome is elevated in patients who are treated with chloramphenicol compared to those treated with doxycycline. Other antibiotics, including broad spectrum antibiotics are not effective against R. rickettsii, and the use of sulfa drugs may worsen infection. \nProphylaxis (Preventive Treatment) \n                \nAntibiotic treatment following a tick bite is not recommended as a means to prevent RMSF. There is no evidence this practice is effective, and may simply delay onset of disease. Instead, persons who experience a tick bite should be alert for symptoms suggestive of tickborne illness and consult a physician if fever, rash, or other symptoms of concern develop. \n                \nFor more in-depth information about treatment, please visit http:\/\/www.cdc.gov\/mmwr\/preview\/mmwrhtml\/rr5504a1.htm \n                \n \nOther Considerations \n                \nThe clinical presentation for RMSF can also resemble other tickborne diseases, such as ehrlichiosis and anaplasmosis. Similar to RMSF, these infections respond well to treatment with doxycycline. Healthcare providers should order diagnostic tests for additional agents if the clinical history and geographic association warrant. For more in-depth about other similar tickborne diseases, please visit http:\/\/www.cdc.gov\/mmwr\/preview\/mmwrhtml\/rr5504a1.htm"}
{"_id":"89f08077-7f05-44e0-9bea-27ffbc2c9c4e","text":"More detailed information on the diagnosis, management, and treatment of tickborne rickettsial diseases is available in Diagnosis and Management of Tickborne Rickettsial Diseases: Rocky Mountain Spotted Fever, Ehrlichioses, and Anaplasmosis \u2013 United States.\n*Case definitions have been updated since publication \nHow to Contact the Rickettsial Zoonoses Branch at CDC \n                \nThe general public and healthcare providers should first call 1-800-CDC-INFO (1-800-232-4636) for questions regarding RMSF and other rickettsial diseases. If a consultation with a CDC scientist specializing in rickettsial diseases is advised, your call will be appropriately forwarded. \nCase Definitions \n                \nAs of January 1, 2010, cases of RMSF are reported under a new category called Spotted Fever Rickettsiosis (including Rocky Mountain spotted fever). \n  \n \nCase Report Forms \n                \nFor confirmed and probable cases of RMSF that have been identified and reported through the National Notifiable Disease Surveillance System, states are also encouraged to submit additional information using CDC Case Report Forms (CRFs). These forms collect additional important information that routine electronic reporting does not, such as information on how the diagnosis was made, and whether the patient was hospitalized or died. If a different state-specific form is already used to collect this information, this information may be submitted to CDC in lieu of CRFs.  \n  \n \nHow to Submit Specimens to CDC for RMSF Testing \n                \nPrivate citizens may not directly submit specimens to CDC for testing. If you feel that diagnostic testing is necessary, consult your healthcare provider or state health department. \nState Health Departments \n                \nSpecimens may be submitted to CDC for testing for rickettsial diseases, including RMSF. To coordinate specimen submission, please call 404 639 1075 during business hours (8:00 - 4:30 ET).  \nU.S. Healthcare Providers \n                \nU.S. healthcare providers should not submit specimens for testing directly to CDC. CDC policy requires that specimens for testing be submitted through or with the approval of the state health department. Please contact your state health department, who will assist you with specimen submission and reporting of an infected patient. For general questions about RMSF, please call 1-800-CDC-INFO (1-800-232-4636). If you have questions about a suspect RMSF case, please first consult your state health department. Healthcare providers requiring an epidemiologic consultation on rickettsial diseases may also call 404-639-1075 during business hours (8:00 - 4:30 ET). Or 770-488-7100 after hours.  \nNon-U.S. Healthcare Providers \n                \nNon-U.S. healthcare providers should consult CDC prior to submitting specimens for testing. For general questions about RMSF, please call 1-800-CDC-INFO (1-800-232-4636). If you would like to discuss a suspect rickettsial case with CDC, please call 404-639-1075 during business hours (8:00 - 4:30 ET), or 770-488-7100 after hours."}
{"_id":"6d6ee51c-e249-48c3-b063-4932e196fcb8","text":"Frequently Asked Queestions (FAQs)"}
{"_id":"6d8b2fff-ae06-453b-b1c1-64fa1d09ae0d","text":"There are two subspecies of the parasite Trypanosoma brucei that cause disease in humans. The clinical features of the infection depend on the subspecies involved. The two subspecies are found in different regions of Africa. At present, there is no overlap in their geographic distribution.\n    \nT. b. rhodesiense (East African sleeping sickness) is found in focal areas of eastern and southeastern Africa. Each year a few hundred cases are reported to the World Health Organization. Over 95% of the cases of human infection occur in Tanzania, Uganda, Malawi, and Zambia. Animals are the primary reservoir of infection. Cattle have been implicated in the spread of the disease to new areas and in local outbreaks. A wild animal reservoir is thought to be responsible for sporadic transmission to hunters and visitors to game parks. Infection of international travelers is rare, but it occasionally occurs. In the U.S., one case per year, on average, is diagnosed. Most cases of sleeping sickness imported into the U.S. have been in travelers who were on safari in East Africa.\n    \nT. b. gambiense (West African sleeping sickness) is found predominantly in central Africa and in limited areas of West Africa. Most of the sleeping sickness in Africa is caused by this form of the parasite. Epidemics of sleeping sickness have been a significant public health problem in the past, but the disease is reasonably well-controlled at present, with 7,000-10,000 cases reported annually in recent years. Over 95% of the cases of human infection are found in Democratic Republic of Congo, Angola, Sudan, Central African Republic, Chad, and northern Uganda. Humans are the important reservoir of infection, although the parasite can sometimes be found in domestic animals (e.g., pigs, dogs, goats). Imported infection in the U.S. is extremely rare, and most cases have occurred in African nationals who have immigrated rather than in returning U.S. travelers.\n    \n     \n    \n    \nBoth forms of sleeping sickness are transmitted by the bite of the tsetse fly (Glossina species). Tsetse flies inhabit rural areas, living in the woodlands and thickets that dot the East African savannah. In central and West Africa, they live in the forests and vegetation along streams. Tsetse flies bite during daylight hours. Both male and female flies can transmit the infection, but even in areas where the disease is endemic, only a very small percentage of flies are infected. Although the vast majority of infections are transmitted by the tsetse fly, other modes of transmission are possible. Occasionally, a pregnant woman can pass the infection to her unborn baby. In theory, the infection can also be transmitted by blood transfusion or sexual contact, but such cases have rarely been documented.\n   \n  \n  \n  \nThis information is not meant to be used for self-diagnosis or as a substitute for consultation with a health care provider. If you have any questions about the parasites described above or think that you may have a parasitic infection, consult a health care provider."}
{"_id":"aed74f71-14d9-485e-b207-12975983460b","text":"The diagnosis of African Trypanosomiasis is made through laboratory methods, because the clinical features of infection are not sufficiently specific. The diagnosis rests on finding the parasite in body fluid or tissue by microscopy. The parasite load in T. b. rhodesiense infection is substantially higher than the level in T. b. gambiense infection.\n    \nT. b. rhodesiense parasites can easily be found in blood. They can also be found in lymph node fluid or in fluid or biopsy of a chancre. Serologic testing is not widely available and is not used in the diagnosis, since microscopic detection of the parasite is straightforward.\n    \nThe classic method for diagnosing T. b. gambiense infection is by microscopic examination of lymph node aspirate, usually from a posterior cervical node. It is often difficult to detect T. b. gambiense in blood. Concentration techniques and serial examinations are frequently needed. Serologic testing is available outside the U.S. for T. b. gambiense; however, it normally is used for screening purposes only and the definitive diagnosis rests on microscopic observation of the parasite.\n    \nAll patients diagnosed with African trypanosomiasis must have their cerebrospinal fluid examined to determine whether there is involvement of the central nervous system, since the choice of treatment drug(s) will depend on the disease stage. The World Health Organization criteria for central nervous system involvement include increased protein in cerebrospinal fluid and a white cell count of more than 5. Trypanosomes can often be observed in cerebrospinal fluid in persons with second stage infection.\n    \nMore on: Resources for Health Professionals: Diagnosis"}
{"_id":"b5be96d3-3b38-4603-8b67-ed6194acca8c","text":"All persons diagnosed with African Trypanosomiasis should receive treatment. The specific drug and treatment course will depend on the type of infection (T. b. gambiense or T. b. rhodesiense) and the disease stage (i.e. whether the central nervous system has been invaded by the parasite). Pentamidine, which is the recommended drug for first stage T. b. gambiense infection, is widely available in the U.S. The other drugs (suramin, melarsoprol, eflornithine, and nifurtimox) used to treat African trypanosomiasis are available in the U.S. only from the CDC. Physicians can consult with CDC staff for advice on diagnosis and management and to obtain otherwise unavailable treatment drug.\n    \nThere is no test of cure for African trypanosomiasis. After treatment patients need to have serial examinations of their cerebrospinal fluid for 2 years, so that relapse can be detected if it occurs.\n    \nMore on: Resources for Health Professionals: Treatment"}
{"_id":"6bf5ed76-f8a9-44f0-ae97-12c6403d7b94","text":"There is no vaccine or drug for prophylaxis against African trypanosomiasis. Preventive measures are aimed at minimizing contact with tsetse flies. Local residents are usually aware of the areas that are heavily infested and they can provide advice about places to avoid. Other helpful measures include:\n    \n     - Wear long-sleeved shirts and pants of medium-weight material in neutral colors that blend with the background environment. Tsetse flies are attracted to bright or dark colors, and they can bite through lightweight clothing.\n     - Inspect vehicles before entering. The flies are attracted to the motion and dust from moving vehicles.\n     - Avoid bushes. The tsetse fly is less active during the hottest part of the day but will bite if disturbed.\n     - Use insect repellent. Permethrin-impregnated clothing and insect repellent have not been proved to be particularly effective against tsetse flies, but they will prevent other insect bites that can cause illness.\n    \n    \nControl of African trypanosomiasis rests on two strategies: reducing the disease reservoir and controlling the tsetse fly vector. Because humans are the significant disease reservoir for T. b. gambiense, the main control strategy for this subspecies is active case-finding through population screening, followed by treatment of the infected persons that are identified. Tsetse fly traps are sometimes used as an adjunct. Reducing the reservoir of infection is more difficult for T. b. rhodesiense, since there are a variety of animal hosts. Vector control is the primary strategy in use. This is usually done with traps or screens, in combination with insecticides and odors that attract the flies."}
{"_id":"339a13f7-e3da-40cc-9e34-763b9da61633","text":"At a Glance \n \nVaccine-preventable disease levels are at or near record lows. Even though most infants and toddlers have received all recommended vaccines by age 2, many under-immunized children remain, leaving the potential for outbreaks of disease. Many adolescents and adults are under-immunized as well, missing opportunities to protect themselves against diseases such as Hepatitis B, influenza, and pneumococcal disease. CDC works closely with public health agencies and private partners to improve and sustain immunization coverage and to monitor the safety of vaccines so that this public health success story can be maintained and expanded in the century to come.  \n  \n Vaccine Shortages & Delays \n  \n   \n   \n \n   \n  \n  \n   \n   \nThe latest national information about vaccine supplies and guidance for healthcare providers who are facing vaccine shortages or delays \n     \n    \n   \n  \n  \n \n  \n  \n  \n Potential New Vaccines \n  \n   \n   \n \n   \n  \n  \n   \n   \nResources for finding information on potential vaccines, research and development status, licensure status, etc. \n       \n    \n   \n  \n  \n \n  \n  \n  \n Vaccines: The Basics \n  \n   \n   \n \n   \n  \n  \n   \n   \nWithout vaccines, epidemics of many preventable diseases could return, resulting in increased \u2013 and unnecessary \u2013 illness, disability, and death. \n          \n    \n   \n  \n  \n \n  \n  \n  \n FAQ about Vaccines & Diseases they Prevent \n  \n   \n   \n \n   \n  \n  \n   \n          \n    \n   \n  \n  \n \n  \n  \n   \n  \n                \n \n                \n \n \n \n                \n  \n \n  \n  \nImages and logos on this website which are trademarked\/copyrighted or used with permission of the trademark\/copyright or logo holder are not in the public domain. These images and logos have been licensed for or used with permission in the materials provided on this website. The materials in the form presented on this website may be used without seeking further permission. Any other use of trademarked\/copyrighted images or logos requires permission from the trademark\/copyright holder...more \n  \n  \n  \n  This graphic notice means that you are leaving an HHS Web site. For more information, please see the Exit Notification and Disclaimer policy."}
{"_id":"b05d4325-0017-4cf9-8df3-ea10aab05258","text":"Fascioliasis is an infectious disease caused by Fasciola parasites, which are flat worms referred to as liver flukes. The adult (mature) flukes are found in the bile ducts and liver of infected people and animals, such as sheep and cattle. In general, fascioliasis is more common in livestock and other animals than in people.\nTwo Fasciola species (types) infect people. The main species is Fasciola hepatica, which is also known as \"the common liver fluke\" and \"the sheep liver fluke.\" A related species, Fasciola gigantica, also can infect people."}
{"_id":"e3a6eca0-efbb-4c21-88a9-03d6e0f672e1","text":"Fascioliasis occurs in many areas of the world and usually is caused by F. hepatica, which is a common liver fluke of sheep and cattle. In general, fascioliasis is more common and widespread in animals than in people. Even so, the number of infected people in the world is thought to exceed 2 million.\n    \nFasciola hepatica is found in more than 50 countries, in all continents except Antarctica. It is found in parts of Latin America, the Caribbean, Europe, the Middle East, Africa, Asia, and Oceania. Fasciola gigantica is less widespread. Human cases have been reported in the tropics, in parts of Africa and Asia, and also in Hawaii.\n    \nIn some areas where fascioliasis is found, human cases are uncommon (sporadic). In other areas, human fascioliasis is very common (hyperendemic). For example, the areas with the highest known rates of human infection are in the Andean highlands of Bolivia and Peru.\n    \nSpecial conditions are needed for fascioliasis to be present in an area, and its geographic distribution is very patchy (focal). The eggs passed in the stool of infected mammals have to develop (mature) in a suitable aquatic snail host to be able to infect another mammalian host. Requirements include sufficient moisture and favorable temperatures (above 50\u00b0F) that allow the development of miracidia, reproduction of snails, and larval development within the snails. These factors also contribute to both the prevalence and level (intensity) of infection. Prevalence is highest in areas where climatic conditions promote development of cercariae.\n    \nMore on: Biology\n    \nInfective Fasciola larvae (metacercariae) are found in contaminated water, either stuck to (encysted on) water plants or floating in the water, often in marshy areas, ponds, or flooded pastures. People (and animals) typically become infected by eating raw watercress or other contaminated water plants. The plants may be eaten as a snack or in salads or sandwiches. People also can get infected by ingesting contaminated water, such as by drinking it or by eating vegetables that were washed or irrigated with contaminated water. Infection also can result from eating undercooked sheep or goat livers that contain immature forms of the parasite.\n    \nThe possibility of becoming infected in the United States should be considered, despite the fact that few locally acquired cases have been documented. The prerequisites for the Fasciola life cycle exist in some parts of the United States. In addition, transmission because of imported contaminated produce could occur, as has been documented in Europe."}
{"_id":"92ffae93-16f8-4eea-9b40-6b4c98755a1a","text":"The standard way to be sure a person is infected with Fasciola is by seeing the parasite. This is usually done by finding Fasciola eggs in stool (fecal) specimens examined under a microscope. More than one specimen may need to be examined to find the parasite. Sometimes eggs are found by examining duodenal contents or bile.\n    \nInfected people don't start passing eggs until they have been infected for several months; people don't pass eggs during the acute phase of the infection. Therefore, early on, the infection has to be diagnosed in other ways than by examining stool. Even during the chronic phase of infection, it can be difficult to find eggs in stool specimens from people who have light infections.\n    \nCertain types of blood tests can be helpful for diagnosing Fasciola infection, including routine blood work and tests that detect antibodies (an immune response) to the parasite.\n    \nMore on: Resources for Health Professionals: Diagnosis"}
{"_id":"7848439e-4a49-4e49-94a2-22e1d68ef128","text":"The first step is to make sure the diagnosis is correct. For more information, patients should consult their health care provider. Health care providers may consult with CDC staff about the diagnosis and treatment of fascioliasis.\n    \nThe drug of choice is triclabendazole. In the United States, this drug is available through CDC, under a special (investigational) protocol. The drug is given by mouth, usually in one or two doses. Most people respond well to the treatment.\n    \nMore on: Resources for Health Professionals: Treatment"}
{"_id":"84368690-286e-4a23-8d70-2ab8ca15cb6d","text":"No vaccine is available to protect people against Fasciola infection.\n    \nIn some areas of the world where fascioliasis is found (endemic), special control programs are in place or are planned. The types of control measures depend on the setting (such as epidemiologic, ecologic, and cultural factors). Strict control of the growth and sale of watercress and other edible water plants is important.\n    \nIndividual people can protect themselves by not eating raw watercress and other water plants, especially from endemic grazing areas. As always, travelers to areas with poor sanitation should avoid food and water that might be contaminated (tainted). Vegetables grown in fields that might have been irrigated with polluted water should be thoroughly cooked, as should viscera from potentially infected animals."}
{"_id":"43ca0f3b-21ed-42c1-9e9c-d4b0f2bb0da4","text":"Anaplasmosis is a disease caused by the bacterium Anaplasma phagocytophilium. This pathogen is transmitted to humans by the bite of an infected tick. The black-legged tick (Ixodes scapularis) is the vector of A. phagocytophilum in the northeast and upper midwestern United States. The western black-legged tick (Ixodes pacificus) is the primary vector in Northern California. The first symptoms of anaplasmosis typically begin within 1-2 weeks after the bite of an infected tick. A tick bite is usually painless, and some patients who develop anaplasmosis do not remember being bitten. The following is a list of symptoms commonly seen with this disease. However, it is important to note that few people with the disease will develop all symptoms, and the number and combination of symptoms varies greatly from person to person. \n  \n  - Fever \n  - Headache \n  - Muscle pain \n  - Malaise \n  - Chills \n  - Nausea \/ Abdominal pain \n  - Cough \n  - Confusion \n  - Rash (rare with anaplasmosis) \n  \n \nAnaplasmosis can be a serious illness that can be fatal if not treated correctly, even in previously healthy people.  Severe clinical presentations may include difficulty breathing, hemorrhage, renal failure or neurological problems. The estimated case fatality rate (i.e., the proportion of persons who die as a result of their infection) is less than 1%. Patients who are treated early may recover quickly on outpatient medication, while those who experience a more severe course may require intravenous antibiotics, prolonged hospitalization or intensive care. \n \n \n Rash \n \nRash is rarely reported in patients with anaplasmosis and the presence of a rash may signify that the patient has a coinfection with the pathogen that causes Lyme disease or another tickborne disease, such as Rocky Mountain Spotted Fever . \n \n \n Immune-compromised Individuals \n \nThe severity of anaplasmosis may depend in part on the immune status of the patient. Persons with compromised immunity caused by immunosuppressive therapies (e.g., corticosteroids, cancer chemotherapy, or longterm immunosuppressive therapy following organ transplant), HIV infection, or splenectomy appear to develop more severe disease, and case-fatality rates for these individuals are characteristically higher than case-fatality rates reported for the general population. \n \n \n Blood Transfusion and Organ Transplant Risks Associated with Anaplasma species \n \nBecause A. phagocytophilum infects the white blood cells and circulates in the blood stream, this pathogen may pose a risk to be transmitted through blood transfusions. Anaplasma phagocytophilum has been shown to survive for more than a week in refrigerated blood. Several cases of anaplasmosis have been reported associated with the transfusion of packed red blood cells donated from asymptomatic or acutely infected donors. Patients who develop anaplasmosis within a month of receiving a blood transfusion or solid organ transplant should be reported to state health officials for prompt investigation. Use of leukoreduced blood products may theoretically decrease the risk of transfusion-associated transmission of these pathogens.  However, the filtration process does not remove all leukocytes or bacteria not associated with leukocytes from leukoreduced blood. Therefore, while this process may reduce the risk of transmission, it does not eliminate it completely. \n \n \n Physician Diagnosis \n \nThere are several aspects of anaplasmosis that make it challenging for healthcare providers to diagnose and treat.  The symptoms vary from patient to patient and can be difficult to distinguish from other diseases.  Treatment is more likely to be effective if started early in the course of disease. Diagnostic tests based on the detection of antibodies will frequently appear negative in the first 7-10 days of illness. \n \nFor this reason, healthcare providers must use their judgment to treat patients based on clinical suspicion alone. Healthcare providers may find important information in the patient\u2019s history and physical examination that may aid clinical diagnosis. Information such as recent tick bites, exposure to areas where ticks are likely to be found, or history of recent travel to areas where anaplasmosis is endemic can be helpful in making the diagnosis.  The healthcare provider should also look at routine blood tests, such as a complete blood cell count or a chemistry panel. Clues such as a low platelet count (thrombocytopenia), low white blood cell count (leukopenia), or elevated liver enzyme levels are helpful predictors of anaplasmosis, but may not be present in all patients.   After a suspect diagnosis is made on clinical suspicion and treatment has begun, specialized laboratory testing should be used to confirm the diagnosis of anaplasmosis. \n   \n   \n    \n   \n  \n \n \n Laboratory Detection \n \nDuring the acute phase of illness, a sample of whole blood can be tested by polymerase chain reaction (PCR) assay to determine if a patient has anaplasmosis. This method is most sensitive in the first week of illness, and rapidly decreases in sensitivity following the administration of appropriate antibiotics. Although a positive PCR result is helpful, a negative result does not completely rule out the diagnosis, and treatment should not be with held due to a negative result. \n \nDuring the first week of illness a microscopic examination of blood smears (known as a peripheral blood smear) may reveal morulae (microcolonies of anaplasma) in the cytoplasm of white blood cells in up to 20% of patients.  During A. phagocytophilum infection, morulae are most frequently observed in granulocytes. However, the observance of morulae in a particular cell type cannot conclusively identify the infecting species. Culture isolation of A. phagocytophilum is only available at specialized laboratories; routine hospital blood cultures cannot detect the organism. \n Figure 1: Morulae detected in a granulocyte on a peripheral blood smear, associated with A. phagocytophilum infection. \n  \n   \n     \n    \n   \n  \n \nWhen a person develops anaplasmosis, their immune system produces antibodies to A. phagocytophilum, with detectable antibody titers usually observed by 7-10 days after illness onset.  It is important to note that a negative test during the first week of illness does not rule out anaplasmosis as a cause of illness.  \n \nThe gold standard serologic test for diagnosis of anaplasmosis is the indirect immunofluorescence assay (IFA) using A. phagocytophilum antigen, performed on paired serum samples to demonstrate a significant (four-fold) rise in antibody titers.  The first sample should be taken as early in the disease as possible, preferably in the first week of symptoms, and the second sample should be taken 2 to 4 weeks later. In most cases of anaplasmosis, the first IgG IFA titer is typically low, or \u201cnegative,\u201d and the second typically shows a significant (four-fold) increase in IgG antibody levels. IgM antibodies usually rise at the same time as IgG near the end of the first week of illness and remain elevated for months or longer.  Also, IgM antibodies are less specific than IgG antibodies and more likely to result in a false positive.  For these reasons, physicians requesting IgM serologic titers should also request a concurrent IgG titer. \n \nSerologic tests based on enzyme immunoassay (EIA) technology are available from some commercial laboratories. However, EIA tests are qualitative rather than quantitative, meaning they only provide a positive\/negative result, and are less useful to measure changes in antibody titers between paired specimens. Furthermore, some EIA assays rely on the evaluation of IgM antibody alone, which may have a higher frequency of false positive results. \n \nAntibodies to A. phagocytophilum may remain elevated for months or longer after the disease has resolved, or may be detected in persons who were previously exposed to antigenically related organisms.  Between 5-10% of currently healthy people in some areas may have elevated antibody titers due to past exposure to A. phagocytophilum or similar organisms. Therefore, if only one sample is tested it can be difficult to interpret, while paired samples taken weeks apart demonstrating a significant (four-fold) rise in antibody titer provides the best evidence for a correct diagnosis of anaplasmosis. \n \nFor more in-depth information about the diagnosis of anaplasmosis, please visit http:\/\/www.cdc.gov\/mmwr\/preview\/mmwrhtml\/rr5504a1.htm \n \n \n Treatment \n \nDoxycycline is the first line treatment for adults and children of all ages and should be initiated immediately whenever anaplasmosis is suspected.  \n \nUse of antibiotics other than doxycycline or other tetracyclines has been associated with a higher risk of fatal outcome for some rickettsial infections. Doxycycline is most effective at preventing severe complications from developing if it is started early in the course of disease. Therefore, treatment must be based on clinical suspicion alone and should always begin before laboratory results return. \n \nIf the patient is treated within the first 5 days of the disease, fever generally subsides within 24-72 hours.  In fact, failure to respond to doxycycline suggests that the patient\u2019s condition might not be due to anaplasmosis. Severely ill patients may require longer periods before their fever resolves. Resistance to doxcycline or relapses in symptoms after the completion of the recommended course have not been documented.  \n \nRecommended Dosage\nDoxycycline is the first line treatment for adults and children of all ages: \n  \n  - Adults: 100 mg every 12 hours \n  - Children under 45 kg (100 lbs): 2.2 mg\/kg body weight given twice a day \n  \n \nPatients should be treated for at least 3 days after the fever subsides and until there is evidence of clinical improvement. Standard duration of treatment is 7 to 14 days. Some patients may continue to experience headache, weakness and malaise for weeks after adequate treatment. \n Treating children \n \nThe use of doxycycline to treat suspected anaplasmosis in children is standard practice recommended by both CDC and the AAP Committee on Infectious Diseases. Unlike older generations of tetracyclines, the recommended dose and duration of medication needed to treat anaplasmosis has not been shown to cause staining of permanent teeth, even when five courses are given before the age of eight.  Healthcare providers should use doxycycline as the first-line treatment for suspected anaplasmosis in patients of all ages.  \n Other Treatments \n \nIn cases of life threatening allergies to doxycycline and in some pregnant patients for whom the clinical course of anaplasmosis appears mild, physicians may need to consider alternate antibiotics. Although recommended as a second-line therapeutic alternative to treat Rocky Mountain Spotted Fever , chloramphenicol is not recommended for the treatment of anaplasmosis, as studies have shown a lack of efficacy. Rifampin has been used successfully in several pregnant women with anaplasmosis, and studies suggest that this drug appears effective against Anaplasma species. However, rifampin is not effective in treating RMSF, a disease that may be confused with anaplasmosis. Healthcare providers should be cautious when exploring treatments other than doxycycline, which is highly effective in treating both. Other antibiotics, including broad spectrum antibiotics are not considered highly effective against A. phagocytophilum, and the use of sulfa drugs during acute illness may worsen the severity of infection.  \n Prophylaxis (Preventive Treatment) \n \nAntibiotic treatment following a tick bite is not recommended as a means to prevent anaplasmosis. There is no evidence this practice is effective, and this may simply delay onset of disease. Instead, persons who experience a tick bite should be alert for symptoms suggestive of tickborne illness and consult a physician if fever, rash, or other symptoms of concern develop.  \n \nFor more in-depth information about treatment, please visit http:\/\/www.cdc.gov\/mmwr\/preview\/mmwrhtml\/rr5504a1.htm \n \n \n Other Considerations \n \nThe clinical presentation for anaplasmosis can resemble other tickborne diseases, such as Rocky Mountain Spotted Fever and ehrlichiosis. Similar to anaplasmosis, these infections respond well to treatment with doxycycline. Healthcare providers should order diagnostic tests for additional agents if the clinical history and geographic association warrant. For more in-depth about other similar tickborne diseases, please visit http:\/\/www.cdc.gov\/mmwr\/preview\/mmwrhtml\/rr5504a1.htm ."}
{"_id":"e4fc26ee-dc61-4924-95bb-82612330a2ce","text":"More detailed information on the diagnosis, management, and treatment of anaplasmosis is available in Diagnosis and Management of Tickborne Rickettsial Diseases: Rocky Mountain Spotted Fever, Ehrlichioses, and Anaplasmosis \u2013 United States.\n*Case definitions have been updated since publication \n How to Contact the Rickettsial Zoonoses Branch at CDC \n \nThe general public and healthcare providers should first call 1-800-CDC-INFO (1-800-232-4636) for questions regarding RMSF and other rickettsial diseases. If a consultation with a CDC scientist specializing in rickettsial diseases is advised, your call will be appropriately forwarded. \n Case Definitions \n \n2008 Case Definition \n Case Report Forms \n \nFor confirmed and probable cases of anaplasmosis that have been identified and reported through the National Notifiable Disease Surveillance System, states are also encouraged to submit additional information using the CDC Case Report Form (CRF). This form collects additional important information that routine electronic reporting does not, such as information on how the diagnosis was made, and whether the patient was hospitalized or died. If a different state-specific form is already used to collect this information, this information may be submitted to CDC in lieu of a CRF. \n \n2010 CDC Case Report Form: Tickborne Rickettsial Diseases (2010 version) [PDF \u2013 3 pages] \n How to Submit Specimens to CDC for RMSF Testing \n \nPrivate citizens may not directly submit specimens to CDC for testing. If you feel that diagnostic testing is necessary, consult your healthcare provider or state health department. \n State Health Departments \n \nSpecimens may be submitted to CDC for testing for anaplasmosis. To coordinate specimen submission, please call 404-639-1075 during business hours (8:00 - 4:30 ET). \n U.S. Healthcare Providers: \n \nU.S. healthcare providers should not submit specimens for testing directly to CDC. CDC policy requires that specimens for testing be submitted through or with the approval of the state health department. Please contact your state health department, who will assist you with specimen submission and reporting of infection. For general questions about anaplasmosis, please call 1-800-CDC-INFO (1-800-232-4636). If you have questions about a suspect ehrlichiosis case, please first consult your state health department. Healthcare providers requiring an epidemiologic or laboratory consultation on anaplasmosis may also call 404-639-1075 during business hours (8:00 - 4:30 ET). Or 770-488-7100 after hours. \n Non U.S. Healthcare Providers: \n \nNon-U.S. healthcare providers should consult CDC prior to submitting specimens for testing. For general questions about anaplasmosis, please call 1-800-CDC-INFO (1-800-232-4636). If you would like to discuss a suspect anaplasmosis case with CDC, please call 404-639-1075 during business hours (8:00 - 4:30 ET), or 770-488-7100 after hours."}
{"_id":"977759a6-cd60-43e4-9b84-56e86da89c1a","text":"Frequently Asked Questions (FAQs)\n    \nCystic echinococcosis (CE) disease results from being infected with the larval stage of Echinococcus granulosus, a tiny tapeworm (~2-7 millimeters in length) found in dogs (definitive host), sheep, cattle, goats, foxes, and pigs, amongst others (intermediate hosts). Most infections in humans are asymptomatic, but CE, also known as hydatid disease, causes slowly enlarging masses, most commonly in the liver and the lungs. Treatment can involve both medication and surgery.\n    \nMore on: Cystic Echinococcosis (CE) FAQs\n    \nAlveolar echinococcosis (AE) disease results from being infected with the larval stage of Echinococcus multilocularis, a tiny tapeworm (~1-4 millimeters in length) found in foxes, coyotes, dogs, and cats (definitive hosts). Although human cases are rare, infection in humans causes parasitic tumors to form in the liver, and, less commonly, the lungs, brain, and other organs. If left untreated, infection with AE can be fatal.\n    \nMore on: Alveolar Echinococcosis (AE) FAQs"}
{"_id":"24366c47-e237-46f9-8f1b-acaa99a57d48","text":"Cystic echinococcosis (CE) is caused by infection with the larval stage of Echinococcus granulosus. CE is found in Africa, Europe, Asia, the Middle East, Central and South America, and in rare cases, North America. The parasite is transmitted to dogs when they ingest the organs of other animals that contain hydatid cysts. The cysts develop into adult tapeworms in the dog. Infected dogs shed tapeworm eggs in their feces which contaminate the ground. Sheep, cattle, goats, and pigs ingest tapeworm eggs in the contaminated ground; once ingested, the eggs hatch and develop into cysts in the internal organs. The most common mode of transmission to humans is by the accidental consumption of soil, water, or food that has been contaminated by the fecal matter of an infected dog. Echinococcus eggs that have been deposited in soil can stay viable for up to a year. The disease is most commonly found in people involved in raising sheep, as a result of the sheep's role as an intermediate host of the parasite and the presence of working dogs that are allowed to eat the offal of infected sheep.\n    \nAlveolar echinococcosis (AE) is caused by infection with the larval stage of Echinococcus multilocularis. AE is found across the globe and is especially prevalent in the northern latitudes of Europe, Asia, and North America. The adult tapeworm is normally found in foxes, coyotes, and dogs. Infection with the larval stages is transmitted to people through ingestion of food or water contaminated with tapeworm eggs."}
{"_id":"f5402e6c-849a-4c5f-876e-ff452db9488b","text":"The presence of a cyst-like mass in a person with a history of exposure to sheepdogs in an area where E. granulosus is endemic suggests a diagnosis of cystic echinococcosis. Imaging techniques, such as CT scans, ultrasonography, and MRIs, are used to detect cysts. After a cyst has been detected, serologic tests may be used to confirm the diagnosis.\n    \nAlveolar echinococcosis is typically found in older people. Imaging techniques such as CT scans are used to visually confirm the parasitic vesicles and cyst-like structures and serologic tests can confirm the parasitic infection."}
{"_id":"93ffd9eb-8548-4848-912f-b42c08224467","text":"In the past, surgery was the only treatment for cystic echinococcal cysts. Chemotherapy, cyst puncture, and PAIR (percutaneous aspiration, injection of chemicals and reaspiration) have been used to replace surgery as effective treatments for cystic echinococcosis. However, surgery remains the most effective treatment to remove the cyst and can lead to a complete cure. Some cysts are not causing any symptoms and are inactive; those cysts often go away without any treatment.\n    \nThe treatment of alveolar echinococcosis is more difficult than cystic echinococcosis and usually requires radical surgery, long-term chemotherapy, or both.\n    \nMore on: Resources for Health Professionals: Treatment"}
{"_id":"1d24e1fe-28a1-4303-bbc3-e04e6687ade4","text":"Cystic echinococcosis is controlled by preventing transmission of the parasite. Prevention measures include limiting the areas where dogs are allowed and preventing animals from consuming meat infected with cysts.\n    \n     - Prevent dogs from feeding on the carcasses of infected sheep.\n     - Control stray dog populations.\n     - Restrict home slaughter of sheep and other livestock.\n     - Do not consume any food or water that may have been contaminated by fecal matter from dogs.\n     - Wash your hands with soap and warm water after handling dogs, and before handling food.\n     - Teach children the importance of washing hands to prevent infection.\n    \n    \nAlveolar echinococcosis can be prevented by avoiding contact with wild animals such as foxes, coyotes, and dogs and their fecal matter and by limiting the interactions between dogs and rodent populations.\n    \n     - Do not allow dogs to feed on rodents and other wild animals.\n     - Avoid contact with wild animals such as foxes, coyotes and stray dogs.\n     - Do not encourage wild animals to come close to your home or keep them as pets.\n     - Wash your hands with soap and warm water after handling dogs or cats, and before handling food.\n     - Teach children the importance of washing hands to prevent infection.\n    \n    \nMore on: Handwashing"}
{"_id":"97ec17b1-d8a4-456f-ad07-06bec3ebf513","text":"Angiostrongylus cantonensis is a parasitic worm of rats. It is also called the rat lungworm. The adult form of the parasite is found only in rodents. Infected rats pass larvae of the parasite in their feces. Snails and slugs get infected by ingesting the larvae. These larvae mature in snails and slugs but do not become adult worms. The life cycle is completed when rats eat infected snails or slugs and the larvae further mature to become adult worms."}
{"_id":"edc6c739-71b6-4574-a3cd-0bad85c4f177","text":"Angiostrongylus cantonensis\n    \nAngiostrongylus cantonensis, also known as the rat lungworm, is a parasitic nematode (worm) that is transmitted between rats and mollusks (such as slugs or snails) in its natural life cycle. Other animals that become infected such as freshwater shrimp, land crabs, frogs, and planarians of the genus Platydemus, are transport hosts that are not required for reproduction of the parasite but might be able to transmit infection to humans if eaten raw or undercooked. Humans are accidental hosts who do not transmit infection to others. Most cases of infection are diagnosed in Southeast Asia and the Pacific Basin, but the parasite has also been found in Australia, some areas of Africa, the Caribbean, Hawaii and Louisiana. Outbreaks of human angiostrongyliasis have involved a few to hundreds of persons; over 2,800 cases have been reported in the literature from approximately 30 countries. It is likely that the parasite has been spread by rats transported on ships and by the introduction of mollusks such as the giant African land snail (Achatina fulica). In addition, the semi-slug, Parmarion martensi (native of Southeast Asia)has spread in regions of Hawaii and is found to often be infected with A. cantonensis, and the freshwater snail Pomacea canaliculata (native of South America) has been introduced into Taiwan and China and has been implicated in outbreaks of disease in those countries.\n    \nRisk factors for infection with A. cantonensis include the ingestion of raw or undercooked infected snails or slugs; or pieces of snails and slugs accidentally chopped up in vegetables, vegetable juices, or salads; or foods contaminated by the slime of infected snails or slugs. It is possible that ingestion of raw or undercooked transport hosts (freshwater shrimp, land crabs, frogs, etc. ) can result in human infection, though this is less certain. In addition, contamination of the hands during the preparation of uncooked infected snails or slugs could lead to ingestion of the parasite.\n    \n     \n    Angiostrongylus costaricensis\n    \nAngiostrongylus costaricensis is a parasitic nematode (worm) that resides in rodents and uses mollusks, such as slugs, as an intermediate host. Rats, such as the cotton rat, transmit the larvae through their feces. Slugs then ingest the larvae. Humans are accidental hosts of the parasite. The parasite is not able to complete its life cycle in humans and eventually dies in the abdomen. Human infection principally occurs in Latin America and the Caribbean, with a few cases suspected in the United States and in the Republic of Congo. The organism is also found in animals in the Southern U.S. (Texas).\n    \nRisk factors for infection with A. costaricensis are not well established but are likely to be ingestion of infected slugs or raw vegetables or vegetable juices contaminated with slugs or their slime, which can contain A. costaricensis larvae. The infection of transport hosts, which are not essential to the lifecycle of the parasite, has not been identified and any role in human infection is not known, in contrast to A. cantonensis. Some reports have shown the case rate to be higher in children 6 to 12 years of age, males, and in persons of higher socioeconomic status. There has been one food-related outbreak in Guatemala that affected primarily adults."}
{"_id":"93d7ca28-688d-4d2b-8d14-c700eeae2e56","text":"Angiostrongylus cantonensis\n    \nDiagnosing A. cantonensis infections can be difficult, in part because there are no readily available blood tests. Important clues that could lead to the diagnosis of infection are a history of travel to where the parasite is known to be found and ingestion of raw or undercooked snails, slugs, or possibly transport hosts (such as frogs, fresh water shrimp or land crabs) in those areas. A high level of eosinophils, a blood cell that can be elevated in the presence of a parasite, in the blood or in the fluid that surrounds the brain can be another important clue. Persons worried that they might be infected should consult their health care provider.\n    \n     \n    Angiostrongylus costaricensis\n    \nDiagnosing A. costaricensis infections can be difficult, in part because there are no readily available blood tests. Important clues that could lead to the diagnosis of infection are a history of travel to where the parasite is known to be found and ingestion of raw or undercooked slugs or food contaminated by infected slugs or their slime. A high blood level of eosinophils, a blood cell that can be elevated in the presence of a parasite, can be another important clue. Persons worried that they might be infected should consult their health care provider."}
{"_id":"a288057a-1009-4eca-bc65-832d10873235","text":"Angiostrongylus cantonensis\n    \nThere is no specific treatment for A. cantonensis infection. There is some evidence that certain supportive treatments may reduce the severity of headache and the duration of symptoms. Persons with symptoms should consult their health care provider for more information.\n    Angiostrongylus costaricensis\n    \nThere is no specific treatment for A. costaricensis infections. Most infections resolve spontaneously though sometime surgical treatment is necessary to removed portions of inflamed intestine. Persons with symptoms should consult their health care provider for more information."}
{"_id":"b396bc9b-8eb5-47f6-ae02-afa8a7a96a81","text":"Angiostrongylus cantonensis\n    \nPrevention of A. cantonensis infections involves educating persons residing in or traveling to areas where the parasite is found about not ingesting raw or undercooked snails and slugs, freshwater shrimp, land crabs, frogs, and monitor lizards, or potentially contaminated vegetables, or vegetable juice. Removing snails, slugs, and rats found near houses and gardens should also help reduce risk. Thoroughly washing hands and utensils after preparing raw snails or slugs is also recommended. Vegetables should be thoroughly washed if eaten raw.\n    Angiostrongylus costaricensis\n    \nPrevention of A. costaricensis infections involves educating persons residing in and traveling to areas where the parasite is known to be found about not ingesting raw or undercooked slugs or potentially contaminated vegetables or vegetable juices. Removing slugs and rats found near houses and gardens should help reduce risk. Thoroughly washing hands and utensils after preparing raw slugs is also recommended. Vegetables should be thoroughly washed if eaten raw."}
{"_id":"e3bb405a-98c6-4c1f-a8e9-a21b3f9a585e","text":"Persons with typhoid fever usually have a sustained fever as high as 103\u00b0 to 104\u00b0 F (39\u00b0 to 40\u00b0 C). They may also feel weak, or have stomach pains, headache, or loss of appetite. In some cases, patients have a rash of flat, rose-colored spots. The only way to know for sure if an illness is typhoid fever is to have samples of stool or blood tested for the presence of Salmonella Typhi.\n\nTyphoid fever\u2019s danger doesn\u2019t end when symptoms disappear: \n\nEven if your symptoms seem to go away, you may still be carrying Salmonella Typhi. If so, the illness could return, or you could pass the disease to other people. In fact, if you work at a job where you handle food or care for small children, you may be barred legally from going back to work until a doctor has determined that you no longer carry any typhoid bacteria.\n                \nIf you are being treated for typhoid fever, it is important to do the following:\n                \nKeep taking the prescribed antibiotics for as long as the doctor has asked you to take them.\n                \nWash your hands carefully with soap and water after using the bathroom, and do not prepare or serve food for other people. This will lower the chance that you will pass the infection on to someone else.\n                \nHave your doctor perform a series of stool cultures to ensure that no Salmonella Typhi bacteria remain in your body."}
{"_id":"69e5f053-ff4a-4b96-8516-fcc3c78d1a54","text":"Ascaris is an intestinal parasite of humans. It is the most common human worm infection. The larvae and adult worms live in the small intestine and can cause intestinal disease."}
{"_id":"1267d4a0-6ca7-41e5-b7a0-0c3c61dafa7e","text":"Ascaris infection is one of the most common intestinal worm infections. It is found in association with poor personal hygiene, poor sanitation, and in places where human feces are used as fertilizer.\n    Geographic Distribution\n    \nThe geographic distributions of Ascaris are worldwide in areas with warm, moist climates and are widely overlapping. Infection occurs worldwide and is most common in tropical and subtropical areas where sanitation and hygiene are poor."}
{"_id":"3335ddc0-7c49-4ccd-a23c-b6610f2a6b89","text":"The standard method for diagnosing ascariasis is by identifying Ascaris eggs in a stool sample using a microscope. Because eggs may be difficult to find in light infections, a concentration procedure is recommended."}
{"_id":"ed0e0f5b-4ae0-41d0-b589-40822eaa378e","text":"Anthelminthic medications (drugs that rid the body of parasitic worms), such as albendazole and mebendazole, are the drugs of choice for treatment of Ascaris infections. Infections are generally treated for 1-3 days. The drugs are effective and appear to have few side effects.\n    \nMore on: Resources for Health Professionals: Treatment"}
{"_id":"c66fad0e-83da-4693-b5f9-8276f1a55180","text":"The best way to prevent ascariasis is to always:\n    \n     - Avoid ingesting soil that may be contaminated with human feces, including where human fecal matter (\"night soil\") or wastewater is used to fertilize crops.\n     - Wash your hands with soap and warm water before handling food.\n     - Teach children the importance of washing hands to prevent infection.\n     - Wash, peel, or cook all raw vegetables and fruits before eating, particularly those that have been grown in soil that has been fertilized with manure.\n    \n    \nMore on: Handwashing\n    \nTransmission of infection to others can be prevented by\n    \n     - Not defecating outdoors.\n     - Effective sewage disposal systems.\n    \n    \nMore on: Handwashing"}
{"_id":"f4f13f4e-ae1b-4c2b-9c57-7e4bac453879","text":"Content on this page was developed during the 2009-2010 H1N1 pandemic and has not been updated. \n    \n    - The H1N1 virus that caused that pandemic is now a regular human flu virus and continues to circulate seasonally worldwide. \n    - The English language content on this website is being archived for historic and reference purposes only.  \n    \n    \n  General Information \n    \n   \n  Information for Health Care Professionals"}
{"_id":"d0ab1d47-dab3-4fc8-bf1f-5b94da6298ac","text":"Content on this page was developed during the 2009-2010 H1N1 pandemic and has not been updated. \n    \n    - The H1N1 virus that caused that pandemic is now a regular human flu virus and continues to circulate seasonally worldwide. \n    - The English language content on this website is being archived for historic and reference purposes only.  \n    \n    \n   \n  General Information \n   \n  \nQuick Facts for the Public on Antiviral Treatments for 2009 H1N1 (NEW) Nov 23 \n  \n2009 H1N1 and Seasonal Flu: What You Should Know About Flu Antiviral Drugs (PDF Version) Oct 13 \n  \nQuestions & Answers: Antiviral Drugs, 2009-2010 Flu Season \n  \nQuestions & Answers: Opening and Mixing Tamiflu\u00ae Capsules with Liquids if Child Cannot Swallow Capsules  Nov 16 \n  \n Podcast: Take Three Actions to Fight Flu \n  Information for Health Care Professionals \n  \nQuick Facts for Clinicians on Antiviral Treatments for 2009 H1N1 Nov 4 \n  \nAntiviral Recommendations Oct 16 \n  \nIntravenous Peramivir Oct 24 \n  \nCDC Podcast: Antiviral Drugs for the 2009-2010 Influenza Season Oct 19 \n  \nAntiviral Safety Information Nov 3 \n  \nPediatric Supplement Recommendations Dec 1 \n  \n Information for Pharmacists (including information related to supply of antiviral drugs) Nov 25 \n  \n Emergency Use Authorization (EUA) of Medical Products and Devices (including antiviral drugs) \n  \nRecommendations for Obstetric Health Care Providers Oct 28 \n  \n(Video Blog) 2009 H1N1: Who Should Receive Antiviral Therapy? Dec 1 \n  \nFrontline Questions and Expert Opinion Answers Dec 9"}
{"_id":"9e48f8f7-f267-45ed-b5da-482f5251b709","text":"On this Page General Information about VISA\/VRSA What is Staphylococcus aureus? How do VISA and VRSA get their names? What should a patient do if they suspect they have a Staph, MRSA, VISA, or VRSA infection? Are VISA and VRSA infections treatable? How can the spread of VISA and VRSA be prevented? What should a person do if a family member or close friend has VISA or VRSA? What is CDC doing to address VISA and VRSA? Recommendations and Guidelines General Information about VISA\/VRSA For more images of this bacterium, search the Public Health Image Library Vancomycin [van\u2212k\u014d\u2212m\u012b\u2212sin]-intermediate Staphylococcus aureus [staff\u2212u\u2212lu\u2212kaw\u2212kus  aw\u2212ree\u2212us] (also called VISA) and Vancomycin-resistant Staphylococcus aureus (also called VRSA) are specific types of antimicrobial-resistant bacteria. However, as of October 2010, all VISA and VRSA isolates have been susceptible to other Food and Drug Administration (FDA)-approved drugs. Persons who develop this type of staph infection may have underlying health conditions (such as diabetes and kidney disease), tubes going into their bodies (such as catheters), previous infections with methicillin-resistant Staphylococcus aureus (MRSA), and recent exposure to vancomycin and other antimicrobial agents. What is Staphylococcus aureus? Staphylococcus aureus is a bacterium commonly found on the skin and in the nose of about 30% of individuals. Most of the time, staph does not cause any harm. These infections can look like pimples, boils, or other skin conditions and most are able to be treated. Sometimes staph bacteria can get into the bloodstream and cause serious infections which can be fatal, including: Bacteremia or sepsis when bacteria spread to the bloodstream usually as a result of using catheters or having surgery. Pneumonia which predominantly affects people with underlying lung disease including those on mechanical ventilators. Endocarditis (infection of the heart valves) which can lead to heart failure. Osteomyelitis (bone infection) which can be caused by staph bacteria traveling in the bloodstream or put there by direct contact such as following trauma (puncture wound of foot or intravenous (IV) drug abuse). Top of page How do VISA and VRSA get their names? Staph bacteria are classified as VISA or VRSA based on laboratory tests. Laboratories perform tests to determine if staph bacteria are resistant to antimicrobial agents that might be used for treatment of infections. For vancomycin and other antimicrobial agents, laboratories determine how much of the agent it requires to inhibit the growth of the organism in a test tube. The result of the test is usually expressed as a minimum inhibitory concentration (MIC) or the minimum amount of antimicrobial agent that inhibits bacterial growth in the test tube. Therefore, staph bacteria are classified as VISA if the MIC for vancomycin is 4-8\u00b5g\/ml, and classified as VRSA if the vancomycin MIC is \u226516\u00b5g\/ml. Top of page What should a patient do if they suspect they have a staph, MRSA, VISA, or VRSA infection? See a healthcare provider. Top of page Are VISA and VRSA infections treatable? Yes. As of October 2010, all VISA and VRSA isolates have been susceptible to several Food and Drug Administration (FDA)-approved drugs. Top of page How can the spread of VISA and VRSA be prevented? Use of appropriate infection control practices (such as wearing gloves before and after contact with infectious body substances and adherence to hand hygiene) by healthcare personnel can reduce the spread of VISA and VRSA. Top of page What should a person do if a family member or close friend has VISA or VRSA? VISA and VRSA are types of antibiotic-resistant staph bacteria. Therefore, as with all staph bacteria, spread occurs among people having close physical contact with infected patients or contaminated material, such as bandages. Persons having close physical contact with infected patients while they are outside of the healthcare setting should: (1) keep their hands clean by washing thoroughly with soap and water, and (2) avoid contact with other people's wounds or material contaminated from wounds. If they go to the hospital to visit a friend or family member who is infected with VISA or VRSA , they must follow the hospital's recommended precautions. Top of page What is CDC doing to address VISA and VRSA? In addition to providing guidance for clinicians and infection control personnel, CDC is also working with state and local health agencies, healthcare facilities, and clinical microbiology laboratories to ensure that laboratories are using proper methods to detect VISA and VRSA. Top of page Recommendations and Guidelines CDC issued a Clinical Reminder, in 2010, which serves as a reminder about the important role of clinical laboratories in the diagnosis of VRSA cases to ensure prompt recognition, isolation, and management by infection control personnel. Investigation and Control of Vancomycin-Resistant Staphylococcus aureus (VRSA) [PDF - 300 KB] - This document is a guide to conducting a public health investigation of patients from whom vancomycin-resistant Staphylococcus aureus (VRSA, vancomycin MIC \u2265 16 \u00b5g\/ml) has been isolated. The information reflects the experience gained from field investigations of the first fourteen VRSA identified in the United States. Top of page"}
{"_id":"99f61358-06c7-43ee-9f35-536f80653c4a","text":"On this Page General Information about VISA\/VRSA What is Staphylococcus aureus? How do VISA and VRSA get their names? What should a patient do if they suspect they have a Staph, MRSA, VISA, or VRSA infection? Are VISA and VRSA infections treatable? How can the spread of VISA and VRSA be prevented? What should a person do if a family member or close friend has VISA or VRSA? What is CDC doing to address VISA and VRSA? Recommendations and Guidelines General Information about VISA\/VRSA For more images of this bacterium, search the Public Health Image Library Vancomycin [van\u2212k\u014d\u2212m\u012b\u2212sin]-intermediate Staphylococcus aureus [staff\u2212u\u2212lu\u2212kaw\u2212kus  aw\u2212ree\u2212us] (also called VISA) and Vancomycin-resistant Staphylococcus aureus (also called VRSA) are specific types of antimicrobial-resistant bacteria. However, as of October 2010, all VISA and VRSA isolates have been susceptible to other Food and Drug Administration (FDA)-approved drugs. Persons who develop this type of staph infection may have underlying health conditions (such as diabetes and kidney disease), tubes going into their bodies (such as catheters), previous infections with methicillin-resistant Staphylococcus aureus (MRSA), and recent exposure to vancomycin and other antimicrobial agents. What is Staphylococcus aureus? Staphylococcus aureus is a bacterium commonly found on the skin and in the nose of about 30% of individuals. Most of the time, staph does not cause any harm. These infections can look like pimples, boils, or other skin conditions and most are able to be treated. Sometimes staph bacteria can get into the bloodstream and cause serious infections which can be fatal, including: Bacteremia or sepsis when bacteria spread to the bloodstream usually as a result of using catheters or having surgery. Pneumonia which predominantly affects people with underlying lung disease including those on mechanical ventilators. Endocarditis (infection of the heart valves) which can lead to heart failure. Osteomyelitis (bone infection) which can be caused by staph bacteria traveling in the bloodstream or put there by direct contact such as following trauma (puncture wound of foot or intravenous (IV) drug abuse). Top of page How do VISA and VRSA get their names? Staph bacteria are classified as VISA or VRSA based on laboratory tests. Laboratories perform tests to determine if staph bacteria are resistant to antimicrobial agents that might be used for treatment of infections. For vancomycin and other antimicrobial agents, laboratories determine how much of the agent it requires to inhibit the growth of the organism in a test tube. The result of the test is usually expressed as a minimum inhibitory concentration (MIC) or the minimum amount of antimicrobial agent that inhibits bacterial growth in the test tube. Therefore, staph bacteria are classified as VISA if the MIC for vancomycin is 4-8\u00b5g\/ml, and classified as VRSA if the vancomycin MIC is \u226516\u00b5g\/ml. Top of page What should a patient do if they suspect they have a staph, MRSA, VISA, or VRSA infection? See a healthcare provider. Top of page Are VISA and VRSA infections treatable? Yes. As of October 2010, all VISA and VRSA isolates have been susceptible to several Food and Drug Administration (FDA)-approved drugs. Top of page How can the spread of VISA and VRSA be prevented? Use of appropriate infection control practices (such as wearing gloves before and after contact with infectious body substances and adherence to hand hygiene) by healthcare personnel can reduce the spread of VISA and VRSA. Top of page What should a person do if a family member or close friend has VISA or VRSA? VISA and VRSA are types of antibiotic-resistant staph bacteria. Therefore, as with all staph bacteria, spread occurs among people having close physical contact with infected patients or contaminated material, such as bandages. Persons having close physical contact with infected patients while they are outside of the healthcare setting should: (1) keep their hands clean by washing thoroughly with soap and water, and (2) avoid contact with other people's wounds or material contaminated from wounds. If they go to the hospital to visit a friend or family member who is infected with VISA or VRSA , they must follow the hospital's recommended precautions. Top of page What is CDC doing to address VISA and VRSA? In addition to providing guidance for clinicians and infection control personnel, CDC is also working with state and local health agencies, healthcare facilities, and clinical microbiology laboratories to ensure that laboratories are using proper methods to detect VISA and VRSA. Top of page Recommendations and Guidelines CDC issued a Clinical Reminder, in 2010, which serves as a reminder about the important role of clinical laboratories in the diagnosis of VRSA cases to ensure prompt recognition, isolation, and management by infection control personnel. Investigation and Control of Vancomycin-Resistant Staphylococcus aureus (VRSA) [PDF - 300 KB] - This document is a guide to conducting a public health investigation of patients from whom vancomycin-resistant Staphylococcus aureus (VRSA, vancomycin MIC \u2265 16 \u00b5g\/ml) has been isolated. The information reflects the experience gained from field investigations of the first fourteen VRSA identified in the United States. Top of page"}
{"_id":"883372e8-3988-4098-b0bd-e1477d519886","text":"On this Page General Information about VISA\/VRSA What is Staphylococcus aureus? How do VISA and VRSA get their names? What should a patient do if they suspect they have a Staph, MRSA, VISA, or VRSA infection? Are VISA and VRSA infections treatable? How can the spread of VISA and VRSA be prevented? What should a person do if a family member or close friend has VISA or VRSA? What is CDC doing to address VISA and VRSA? Recommendations and Guidelines General Information about VISA\/VRSA For more images of this bacterium, search the Public Health Image Library Vancomycin [van\u2212k\u014d\u2212m\u012b\u2212sin]-intermediate Staphylococcus aureus [staff\u2212u\u2212lu\u2212kaw\u2212kus  aw\u2212ree\u2212us] (also called VISA) and Vancomycin-resistant Staphylococcus aureus (also called VRSA) are specific types of antimicrobial-resistant bacteria. However, as of October 2010, all VISA and VRSA isolates have been susceptible to other Food and Drug Administration (FDA)-approved drugs. Persons who develop this type of staph infection may have underlying health conditions (such as diabetes and kidney disease), tubes going into their bodies (such as catheters), previous infections with methicillin-resistant Staphylococcus aureus (MRSA), and recent exposure to vancomycin and other antimicrobial agents. What is Staphylococcus aureus? Staphylococcus aureus is a bacterium commonly found on the skin and in the nose of about 30% of individuals. Most of the time, staph does not cause any harm. These infections can look like pimples, boils, or other skin conditions and most are able to be treated. Sometimes staph bacteria can get into the bloodstream and cause serious infections which can be fatal, including: Bacteremia or sepsis when bacteria spread to the bloodstream usually as a result of using catheters or having surgery. Pneumonia which predominantly affects people with underlying lung disease including those on mechanical ventilators. Endocarditis (infection of the heart valves) which can lead to heart failure. Osteomyelitis (bone infection) which can be caused by staph bacteria traveling in the bloodstream or put there by direct contact such as following trauma (puncture wound of foot or intravenous (IV) drug abuse). Top of page How do VISA and VRSA get their names? Staph bacteria are classified as VISA or VRSA based on laboratory tests. Laboratories perform tests to determine if staph bacteria are resistant to antimicrobial agents that might be used for treatment of infections. For vancomycin and other antimicrobial agents, laboratories determine how much of the agent it requires to inhibit the growth of the organism in a test tube. The result of the test is usually expressed as a minimum inhibitory concentration (MIC) or the minimum amount of antimicrobial agent that inhibits bacterial growth in the test tube. Therefore, staph bacteria are classified as VISA if the MIC for vancomycin is 4-8\u00b5g\/ml, and classified as VRSA if the vancomycin MIC is \u226516\u00b5g\/ml. Top of page What should a patient do if they suspect they have a staph, MRSA, VISA, or VRSA infection? See a healthcare provider. Top of page Are VISA and VRSA infections treatable? Yes. As of October 2010, all VISA and VRSA isolates have been susceptible to several Food and Drug Administration (FDA)-approved drugs. Top of page How can the spread of VISA and VRSA be prevented? Use of appropriate infection control practices (such as wearing gloves before and after contact with infectious body substances and adherence to hand hygiene) by healthcare personnel can reduce the spread of VISA and VRSA. Top of page What should a person do if a family member or close friend has VISA or VRSA? VISA and VRSA are types of antibiotic-resistant staph bacteria. Therefore, as with all staph bacteria, spread occurs among people having close physical contact with infected patients or contaminated material, such as bandages. Persons having close physical contact with infected patients while they are outside of the healthcare setting should: (1) keep their hands clean by washing thoroughly with soap and water, and (2) avoid contact with other people's wounds or material contaminated from wounds. If they go to the hospital to visit a friend or family member who is infected with VISA or VRSA , they must follow the hospital's recommended precautions. Top of page What is CDC doing to address VISA and VRSA? In addition to providing guidance for clinicians and infection control personnel, CDC is also working with state and local health agencies, healthcare facilities, and clinical microbiology laboratories to ensure that laboratories are using proper methods to detect VISA and VRSA. Top of page Recommendations and Guidelines CDC issued a Clinical Reminder, in 2010, which serves as a reminder about the important role of clinical laboratories in the diagnosis of VRSA cases to ensure prompt recognition, isolation, and management by infection control personnel. Investigation and Control of Vancomycin-Resistant Staphylococcus aureus (VRSA) [PDF - 300 KB] - This document is a guide to conducting a public health investigation of patients from whom vancomycin-resistant Staphylococcus aureus (VRSA, vancomycin MIC \u2265 16 \u00b5g\/ml) has been isolated. The information reflects the experience gained from field investigations of the first fourteen VRSA identified in the United States. Top of page"}
{"_id":"bb0c2ff2-684b-40b5-872a-9d26d1690331","text":"On this Page General Information about VISA\/VRSA What is Staphylococcus aureus? How do VISA and VRSA get their names? What should a patient do if they suspect they have a Staph, MRSA, VISA, or VRSA infection? Are VISA and VRSA infections treatable? How can the spread of VISA and VRSA be prevented? What should a person do if a family member or close friend has VISA or VRSA? What is CDC doing to address VISA and VRSA? Recommendations and Guidelines General Information about VISA\/VRSA For more images of this bacterium, search the Public Health Image Library Vancomycin [van\u2212k\u014d\u2212m\u012b\u2212sin]-intermediate Staphylococcus aureus [staff\u2212u\u2212lu\u2212kaw\u2212kus  aw\u2212ree\u2212us] (also called VISA) and Vancomycin-resistant Staphylococcus aureus (also called VRSA) are specific types of antimicrobial-resistant bacteria. However, as of October 2010, all VISA and VRSA isolates have been susceptible to other Food and Drug Administration (FDA)-approved drugs. Persons who develop this type of staph infection may have underlying health conditions (such as diabetes and kidney disease), tubes going into their bodies (such as catheters), previous infections with methicillin-resistant Staphylococcus aureus (MRSA), and recent exposure to vancomycin and other antimicrobial agents. What is Staphylococcus aureus? Staphylococcus aureus is a bacterium commonly found on the skin and in the nose of about 30% of individuals. Most of the time, staph does not cause any harm. These infections can look like pimples, boils, or other skin conditions and most are able to be treated. Sometimes staph bacteria can get into the bloodstream and cause serious infections which can be fatal, including: Bacteremia or sepsis when bacteria spread to the bloodstream usually as a result of using catheters or having surgery. Pneumonia which predominantly affects people with underlying lung disease including those on mechanical ventilators. Endocarditis (infection of the heart valves) which can lead to heart failure. Osteomyelitis (bone infection) which can be caused by staph bacteria traveling in the bloodstream or put there by direct contact such as following trauma (puncture wound of foot or intravenous (IV) drug abuse). Top of page How do VISA and VRSA get their names? Staph bacteria are classified as VISA or VRSA based on laboratory tests. Laboratories perform tests to determine if staph bacteria are resistant to antimicrobial agents that might be used for treatment of infections. For vancomycin and other antimicrobial agents, laboratories determine how much of the agent it requires to inhibit the growth of the organism in a test tube. The result of the test is usually expressed as a minimum inhibitory concentration (MIC) or the minimum amount of antimicrobial agent that inhibits bacterial growth in the test tube. Therefore, staph bacteria are classified as VISA if the MIC for vancomycin is 4-8\u00b5g\/ml, and classified as VRSA if the vancomycin MIC is \u226516\u00b5g\/ml. Top of page What should a patient do if they suspect they have a staph, MRSA, VISA, or VRSA infection? See a healthcare provider. Top of page Are VISA and VRSA infections treatable? Yes. As of October 2010, all VISA and VRSA isolates have been susceptible to several Food and Drug Administration (FDA)-approved drugs. Top of page How can the spread of VISA and VRSA be prevented? Use of appropriate infection control practices (such as wearing gloves before and after contact with infectious body substances and adherence to hand hygiene) by healthcare personnel can reduce the spread of VISA and VRSA. Top of page What should a person do if a family member or close friend has VISA or VRSA? VISA and VRSA are types of antibiotic-resistant staph bacteria. Therefore, as with all staph bacteria, spread occurs among people having close physical contact with infected patients or contaminated material, such as bandages. Persons having close physical contact with infected patients while they are outside of the healthcare setting should: (1) keep their hands clean by washing thoroughly with soap and water, and (2) avoid contact with other people's wounds or material contaminated from wounds. If they go to the hospital to visit a friend or family member who is infected with VISA or VRSA , they must follow the hospital's recommended precautions. Top of page What is CDC doing to address VISA and VRSA? In addition to providing guidance for clinicians and infection control personnel, CDC is also working with state and local health agencies, healthcare facilities, and clinical microbiology laboratories to ensure that laboratories are using proper methods to detect VISA and VRSA. Top of page Recommendations and Guidelines CDC issued a Clinical Reminder, in 2010, which serves as a reminder about the important role of clinical laboratories in the diagnosis of VRSA cases to ensure prompt recognition, isolation, and management by infection control personnel. Investigation and Control of Vancomycin-Resistant Staphylococcus aureus (VRSA) [PDF - 300 KB] - This document is a guide to conducting a public health investigation of patients from whom vancomycin-resistant Staphylococcus aureus (VRSA, vancomycin MIC \u2265 16 \u00b5g\/ml) has been isolated. The information reflects the experience gained from field investigations of the first fourteen VRSA identified in the United States. Top of page"}
{"_id":"071b1d4f-b242-4c72-8edf-34607ea4b9b6","text":"Ixodid (hard) ticks, especially those of the genus, Hyalomma, are both a reservoir and a vector for the CCHF virus. Numerous wild and domestic animals, such as cattle, goats, sheep and hares, serve as amplifying hosts for the virus. Transmission to humans occurs through contact with infected ticks or animal blood. CCHF can be transmitted from one infected human to another by contact with infectious blood or body fluids. Documented spread of CCHF has also occurred in hospitals due to improper sterilization of medical equipment, reuse of injection needles, and contamination of medical supplies."}
{"_id":"81b50595-b24e-44da-9706-5ce2b68c9edf","text":"The onset of CCHF is sudden, with initial signs and symptoms including headache, high fever, back pain, joint pain, stomach pain, and vomiting. Red eyes, a flushed face, a red throat, and petechiae (red spots) on the palate are common. Symptoms may also include jaundice, and in severe cases, changes in mood and sensory perception. \n                \nAs the illness progresses, large areas of severe bruising, severe nosebleeds, and uncontrolled bleeding at injection sites can be seen, beginning on about the fourth day of illness and lasting for about two weeks. In documented outbreaks of CCHF, fatality rates in hospitalized patients have ranged from 9% to as high as 50%. \n                \nThe long-term effects of CCHF infection have not been studied well enough in survivors to determine whether or not specific complications exist. However, recovery is slow."}
{"_id":"49b99e25-57af-4854-a330-6dda1f307a28","text":"Animal herders, livestock workers, and slaughterhouse workers in endemic areas are at risk of CCHF. Healthcare workers in endemic areas are at risk of infection through unprotected contact with infectious blood and body fluids. Individuals and international travelers with contact to livestock in endemic regions may also be exposed."}
{"_id":"4a4c79df-221a-40ff-82cd-a4f485065e62","text":"Laboratory tests that are used to diagnose CCHF include antigen-capture enzyme-linked immunosorbent assay (ELISA), real time polymerase chain reaction (RT-PCR), virus isolation attempts, and detection of antibody by ELISA (IgG and IgM). Laboratory diagnosis of a patient with a clinical history compatible with CCHF can be made during the acute phase of the disease by using the combination of detection of the viral antigen (ELISA antigen capture), viral RNA sequence (RT-PCR) in the blood or in tissues collected from a fatal case and virus isolation. Immunohistochemical staining can also show evidence of viral antigen in formalin-fixed tissues. Later in the course of the disease, in people surviving, antibodies can be found in the blood. But antigen, viral RNA and virus are no more present and detectable"}
{"_id":"338564bd-1e4f-4308-845f-bd13a101b80c","text":"Treatment for CCHF is primarily supportive. Care should include careful attention to fluid balance and correction of electrolyte abnormalities, oxygenation and hemodynamic support, and appropriate treatment of secondary infections. The virus is sensitive in vitro to the antiviral drug ribavirin. It has been used in the treatment of CCHF patients reportedly with some benefit. \nRecovery \n                \nThe long-term effects of CCHF infection have not been studied well enough in survivors to determine whether or not specific complications exist. However, recovery is slow."}
{"_id":"731991be-45c8-48f6-af5b-b046f77c253a","text":"Agricultural workers and others working with animals should use insect repellent on exposed skin and clothing. Insect repellants containing DEET (N, N-diethyl-m-toluamide) are the most effective in warding off ticks. Wearing gloves and other protective clothing is recommended. Individuals should also avoid contact with the blood and body fluids of livestock or humans who show symptoms of infection. It is important for healthcare workers to use proper infection control precautions to prevent occupational exposure. \n                \nAn inactivated, mouse-brain derived vaccine against CCHF has been developed and is used on a small scale in Eastern Europe. However, there is no safe and effective vaccine currently available for human use. Further research is needed to develop these potential vaccines as well as determine the efficacy of different treatment options including ribavirin and other antiviral drugs."}
{"_id":"9e7928cb-4de7-4fe8-b918-dedda20d5f42","text":"There is no vaccine against Eastern equine encephalitis virus (EEEV) for humans. Reducing exposure to mosquitoes is the best defense against infection with EEEV and other mosquito-borne viruses. There are several approaches you and your family can use to prevent and control mosquito-borne diseases. \n   \n   -  Use repellent: When outdoors, use insect repellent containing DEET, picaridin, IR3535 or oil of lemon eucalyptus on exposed skin and\/or clothing. The repellent\/insecticide permethrin can be used on clothing to protect through several washes. Always follow the directions on the package.  \n   -  Wear protective clothing: Wear long sleeves and pants when weather permits.  \n   -  Install and repair screens: Have secure, intact screens on windows and doors to keep mosquitoes out.  \n   -  Keep mosquitoes from laying eggs near you: Mosquitoes can lay eggs even in small amounts of standing water. Get rid of mosquito breeding sites by emptying standing water from flower pots, buckets, barrels, and tires. Change the water in pet dishes and replace the water in bird baths weekly. Drill holes in tire swings so water drains out. Empty children's wading pools and store on their side after use.  \n"}
{"_id":"f621f759-bc43-4b7b-9f91-0aeff55be23f","text":"Like all arenaviruses, Lujo virus has a rodent host as its reservoir. Humans can contract LUHF through contact with an infected rodent. Contact can be direct or through inhalation of aerosolized Lujo virus from the urine or feces of infected rodents. \n \nPerson-to-person transmission of Lujo virus was observed in the small, nosocomial cluster of hemorrhagic disease which resulted in the discovery of the Lujo virus. \n \nTransmission of arenaviruses, and Lujo virus in particular, is most likely the result of direct contact with the body fluids of an infected person, in the absence of infection control precautions."}
{"_id":"cbd4e161-e7b2-4463-be95-ae32936cd2d0","text":"The symptoms of Lujo hemorrhagic fever, as described in the five patients in the original cluster outbreak, resemble those of severe Lassa Fever. After an incubation period of 7 to 13 days, the clinical course started by a non-specific febrile illness accompanied by headache and muscle pain. \n                \nThe disease increases in severity, with: \n \n - a morbilliform rash of the face and trunk \n - face and neck swelling \n - pharyngitis (sore throat) \n - diarrhea \n \n                \nBleeding was not a prominent feature during the illness. \n                \nIn the fatal cases (4\/5 patients), a transient improvement was followed by: \n \n - rapid deterioration with respiratory distress \n - neurological signs and circulatory collapse \n \n                \nDeath occurred 10 to 13 days after onset. \n                \nLow blood platelets, low white blood cell count (at the onset, rising later on) and elevated liver function values were present in all patients. \n                \nSince Arenaviruses may enter the fetus through infection of the mother, and anectodal evidence suggests that infected pregnant women may suffer miscarriages, it is reasonable to assume that both infection of the fetus and miscarriage may be associated with Lujo infection in the mother."}
{"_id":"134d6734-9ccf-4862-ab3f-d0ca48d35904","text":"Lujo hemorrhagic fever (LUHF) occurs in southern Africa. The initial case was certainly infected in Zambia. \n   Field workers \n   \nField workers are at greatest risk because of increased human contact with the reservoir rodent population. Sexual partners of field workers may be at greater risk as well. In addition to nosocomial infection in healthcare workers already described, laboratory infections have been frequently described with Arenaviruses and Lujo virus can certainly be transmitted to laboratory workers during manipulation of the virus, especially during experimental infections of rodents."}
{"_id":"078037a1-fd54-4e33-8ab2-5de675a39a69","text":"During the acute febrile phase, Lujo virus was isolated from blood from days 2 to 13 after onset. Virus was also isolated from liver tissue obtained post-mortem. A subsequent complete genomic analysis of Lujo virus facilitated the development of specific molecular detection (RT-PCR) assays. \n   \nSerologic diagnosis of Lujo hemorrhagic fever can be made by indirect immunofluorescent assay and ELISA. However, individuals from endemic areas displaying fever, rash, pharyngitis, accompanied by laboratory findings of low platelet counts and elevated liver enzymes, should be suspected of having a hemorrhagic fever virus infection. Clinical specimens should be tested using specific assays."}
{"_id":"60247f49-50ce-4db1-b708-148e80fec610","text":"Supportive therapy is important in Lujo hemorrhagic fever. This includes: \n    \n    - maintenance of hydration \n    - management of shock \n    - sedation \n    - pain relief \n    - usual precautions for patients with bleeding disorders \n    - transfusions (when necessary) \n    \n   \nTreatment of arenavirus hemorrhagic fevers with convalescent plasma therapy reduces mortality significantly and anectodal evidence from the only surviving Lujo patient shows that the antiviral drug ribavirin may hold promise in the treatment of LUHF. Ribavirin has been considered for preventing development of disease in people exposed to other arenaviruses. \n   Recovery \n   \nThe precise mortality of LUHF is unknown, but 4 of 5 described cases were fatal. \n   \nPatients who have suffered from other arenaviruses may excrete virus in urine or semen for weeks after recovery. For this reason, these fluids should be monitored for infectivity, since convalescent patients have the potential to infect others (particularly sexual partners) via these fluids."}
{"_id":"bf6dde59-efa8-426f-a633-2ff181430f4a","text":"Although rodent control would be desirable, it will not be a successful strategy for preventing Lujo hemorrhagic fever cases caused by exposures outdoors. \n   \nAs for other hemorrhagic fevers, full barrier nursing procedures should be implemented during management of suspected or confirmed LUHF cases (no infection occurred after their implementation in South Africa)."}
{"_id":"2e99c894-1f8e-45dc-b4f2-01a184902c33","text":"Why Are Childhood Vaccines So Important? It is always better to prevent a disease than to treat it after it occurs. Diseases that used to be common in this country and around the world, including polio, measles, diphtheria, pertussis (whooping cough), rubella (German measles), mumps, tetanus, rotavirus and Haemophilus influenzae type b (Hib) can now be prevented by vaccination. Thanks to a vaccine, one of the most terrible diseases in history \u2013 smallpox \u2013 no longer exists outside the laboratory. Over the years vaccines have prevented countless cases of disease and saved millions of lives. Immunity Protects us From Disease Immunity is the body\u2019s way of preventing disease.  Children are born with an immune system composed of cells, glands, organs, and fluids located throughout the body. The immune system recognizes germs that enter the body as \"foreign invaders\u201d (called antigens) and produces proteins called antibodies to fight them. The first time a child is infected with a specific antigen (say measles virus), the immune system produces antibodies designed to fight it. This takes time . . . usually the immune system can\u2019t work fast enough to prevent the antigen from causing disease, so the child still gets sick.  However, the immune system \u201cremembers\u201d that antigen. If it ever enters the body again, even after many years, the immune system can produce antibodies fast enough to keep it from causing disease a second time. This protection is called immunity. It would be nice if there were a way to give children immunity to a disease without their having to get sick first. In fact there is: Vaccines contain the same antigens (or parts of antigens) that cause diseases. For example, measles vaccine contains measles virus. But the antigens in vaccines are either killed, or weakened to the point that they don\u2019t cause disease. However, they are strong enough to make the immune system produce antibodies that lead to immunity. In other words, a vaccine is a safer substitute for a child\u2019s first exposure to a disease. The child gets protection without having to get sick. Through vaccination, children can develop immunity without suffering from the actual diseases that vaccines prevent. Top of Page More Facts Newborn babies are immune to many diseases because they have antibodies they got from their mothers. However, this immunity goes away during the first year of life. If an unvaccinated child is exposed to a disease germ, the child's body may not be strong enough to fight the disease. Before vaccines, many children died from diseases that vaccines now prevent, such as whooping cough, measles, and polio. Those same germs exist today, but because babies are protected by vaccines, we don\u2019t see these diseases nearly as often. Immunizing individual children also helps to protect the health of our community, especially those people who cannot be immunized (children who are too young to be vaccinated, or those who can\u2019t receive certain vaccines for medical reasons), and the small proportion of people who don\u2019t respond to a particular vaccine. Vaccine-preventable diseases have a costly impact, resulting in doctor's visits, hospitalizations, and premature deaths. Sick children can also cause parents to lose time from work.   Related Pages Why Immunize? Vaccines: A Safe Choice Parents Guide to Immunizations For Parents: How Vaccines Prevent Diseases Top of Page   Images and logos on this website which are trademarked\/copyrighted or used with permission of the trademark\/copyright or logo holder are not in the public domain. These images and logos have been licensed for or used with permission in the materials provided on this website. The materials in the form presented on this website may be used without seeking further permission. Any other use of trademarked\/copyrighted images or logos requires permission from the trademark\/copyright holder...more This graphic notice means that you are leaving an HHS Web site. For more information, please see the Exit Notification and Disclaimer policy."}
{"_id":"f608f4f8-9915-4d63-a7da-1f2c17b9bca3","text":"Measles: Make Sure Your Child Is Protected with MMR Vaccine Measles starts with a fever. Soon after, it causes a cough, runny nose, and red eyes. Then a rash of tiny, red spots breaks out. Measles can be serious for young children. Learn about protecting your child from measles with MMR vaccine. Protect your child at every age. Click on your child's age group for vaccine information. View or print age-specific vaccine information [252 KB, 27 pages] Records & Requirements Recording immunizations Finding immunization records Interpreting abbreviations on records Immunization requirements for child care and schools Making the Vaccine Decision How vaccines prevent diseases Vaccine side effects\/risks Vaccine ingredients Ensuring vaccine safety Vaccines and your child\u2019s immune system Learn More About Preteen and Teen Vaccines The Vaccines For Children program has helped prevent diseases and save lives\u2026big time! [enlarged view] Watch The Immunization Baby Book Learn what vaccines your child needs, when they are needed, and why it is so important to follow the CDC\u2019s recommended immunization schedule as you flip through this video baby book (4:04 mins) on CDC-TV or on YouTube. Who & When (Immunization Schedules) Birth through 6 Years Schedule [2 pages] Create a schedule for your child 7 through 18 Years Schedule [2 pages] 19 Years and Older Schedule [2 pages] Learn more about how CDC sets the immunization schedule for your family Knowing the childhood vaccination rates in your community is important. More Diseases and the Vaccines that Prevent Them Learn more about the 16 diseases that can be prevented with vaccines, as well as the benefits and risks of vaccination. Learn More About... Adoption and Vaccines Pregnancy Help Paying for Vaccines Evaluating Information on the Web"}
{"_id":"7ce39338-ee3d-4114-bb83-ebbf2764e677","text":"Vaccines and Preventable Diseases On this Page Vaccine Shortages & Delays Potential New Vaccines Vaccines: The Basics FAQ about Vaccines & Diseases they Prevent   VACCINE-PREVENTABLE DISEASES OR, find it by Vaccine Anthrax Cervical Cancer Diphtheria Hepatitis A Hepatitis B Haemophilus influenzae type b (Hib) Human Papillomavirus (HPV) H1N1 Flu (Swine Flu) Influenza (Seasonal Flu) Japanese Encephalitis (JE) Measles Meningococcal Mumps Pertussis (Whooping Cough) Pneumococcal Poliomyelitis (Polio) Rabies Rotavirus Rubella (German Measles) Shingles (Herpes Zoster) Smallpox Tetanus (Lockjaw) Tuberculosis Typhoid Fever Varicella (Chickenpox) Yellow Fever At a Glance Vaccine-preventable disease levels are at or near record lows. Even though most infants and toddlers have received all recommended vaccines by age 2, many under-immunized children remain, leaving the potential for outbreaks of disease. Many adolescents and adults are under-immunized as well, missing opportunities to protect themselves against diseases such as Hepatitis B, influenza, and pneumococcal disease. CDC works closely with public health agencies and private partners to improve and sustain immunization coverage and to monitor the safety of vaccines so that this public health success story can be maintained and expanded in the century to come. Vaccine Shortages & Delays The latest national information about vaccine supplies and guidance for healthcare providers who are facing vaccine shortages or delays Chart of shortages & delays   Potential New Vaccines Resources for finding information on potential vaccines, research and development status, licensure status, etc. New Vaccine Surveillance Network Program evaluates impact of new vaccines and vaccine policies through a network of 6 US sites Status of Licensure and Recs for New Vaccines American Academy of Pediatrics (AAP) Potential New Vaccines Immunization Action Coalition (IAC)   Vaccines: The Basics Without vaccines, epidemics of many preventable diseases could return, resulting in increased \u2013 and unnecessary \u2013 illness, disability, and death. All about vaccines How vaccines prevent disease List of all vaccine-preventable diseases List of all vaccines used in United States Photos of vaccine-preventable diseases and\/or people affected by them View all...   FAQ about Vaccines & Diseases they Prevent What are the ingredients in vaccines? What vaccines do adults need? What vaccines do children need? What vaccines are used in the United States? What diseases do vaccines prevent? View all...   Related Pages Basics and Common Questions Who Should NOT Get These Vaccines? Unprotected Stories Top of Page   Images and logos on this website which are trademarked\/copyrighted or used with permission of the trademark\/copyright or logo holder are not in the public domain. These images and logos have been licensed for or used with permission in the materials provided on this website. The materials in the form presented on this website may be used without seeking further permission. Any other use of trademarked\/copyrighted images or logos requires permission from the trademark\/copyright holder...more This graphic notice means that you are leaving an HHS Web site. For more information, please see the Exit Notification and Disclaimer policy."}
{"_id":"0dee3b56-eef7-425e-aa1f-518838b02f91","text":"List of Vaccine-Preventable Diseases The following links will lead you to the main page that describes both the disease and the vaccine(s). Vaccines are available for all of the following vaccine-preventable diseases (unless otherwise noted): Anthrax Cervical Cancer (Human Papillomavirus) Diphtheria Hepatitis A Hepatitis B Haemophilus influenzae type b (Hib) Human Papillomavirus (HPV) Influenza (Flu) Japanese encephalitis (JE) Measles Meningococcal Mumps Pertussis Pneumococcal Polio Rabies Rotavirus Rubella Shingles (Herpes Zoster) Smallpox Tetanus Typhoid Tuberculosis (TB) Varicella (Chickenpox) Yellow Fever Related Pages For Parents: What You Need to Know List of Vaccines Used in U.S. Photos of diseases Top of Page   Images and logos on this website which are trademarked\/copyrighted or used with permission of the trademark\/copyright or logo holder are not in the public domain. These images and logos have been licensed for or used with permission in the materials provided on this website. The materials in the form presented on this website may be used without seeking further permission. Any other use of trademarked\/copyrighted images or logos requires permission from the trademark\/copyright holder...more This graphic notice means that you are leaving an HHS Web site. For more information, please see the Exit Notification and Disclaimer policy."}
{"_id":"4db8700d-666b-4634-947f-39272df6a6e0","text":"Symptoms  \n                \nIn the United States, the term \u201cehrlichiosis\u201d may be broadly applied to several different infections. Ehrlichia chaffeensis and Ehrlichia ewingii are transmitted by the lonestar tick in the southeastern and southcentral United States. In addition, a third Ehrlichia species provisionally called Ehrlichia muris-like (EML) has been identified in a small number of patients residing in or traveling to Minnesota and Wisconsin; a tick vector for the EML organism has not yet been established. The symptoms caused by infection with these Ehrlichia species usually develop 1-2 weeks after being bitten by an infected tick.  The tick bite is usually painless, and about half of the people who develop ehrlichiosis may not even remember being bitten by a tick.  \n                \n The following is a list of symptoms commonly seen with this disease, however, it is important to note that the combination of symptoms varies greatly from person to person. \n \n - Fever \n - Headache \n - Chills \n - Malaise \n - Muscle pain \n - Nausea \/ Vomiting \/ Diarrhea \n - Confusion \n - Conjunctival injection (red eyes) \n - Rash (in up to 60% of children, less than 30% of adults) \n \n                \nEhrlichiosis is a serious illness that can be fatal if not treated correctly, even in previously healthy people.  Severe clinical presentations may include difficulty breathing, or bleeding disorders. The estimated case fatality rate (i.e. the proportion of persons who die as a result of their infection) is 1.8%. Patients who are treated early may recover quickly on outpatient medication, while those who experience a more severe course may require intravenous antibiotics, prolonged hospitalization or intensive care.  \n                \n \nRash \n                \nSkin rash is not considered a common feature of ehrlichiosis, and should not be used to rule in or rule out an infection. Ehrlichia chaffeensis infection can cause a rash in up to 60% of children, but is reported in fewer than 30% of adults. Rash is not commonly reported in patients infected with Ehrlichia ewingii or the Ehrlichia muris-like organism.  The rash associated with Ehrlichia chaffeensis infection may range from maculopapular to petechial in nature, and is usually not pruritic (itchy). The rash usually spares the face, but in some cases may spread to the palms and soles.  A type of rash called erythroderma may develop in some patients.  Erythroderma is a type of rash that resembles a sunburn and consists of widespread reddening of the skin that may peel after several days.  Some patients may develop a rash that resembles the rash of Rocky Mountain spotted fever making these two diseases difficult to differentiate on the basis of clinical signs alone. \n                \n \nImmune-compromised Individuals \n                \nThe severity of ehrlichiosis may depend in part on the immune status of the patient. Persons with compromised immunity caused by immunosuppressive therapies (e.g., corticosteroids , cancer chemotherapy, or longterm immunosuppressive therapy following organ transplant), HIV infection, or splenectomy appear to develop more severe disease, and may also have higher case-fatality rates (i.e. the proportion of patients that die from infection.)   \n                \n \nBlood Transfusion and Organ Transplant Risks Associated with Ehrlichia species \n                \nBecause Ehrlichia organisms infect the white blood cells and circulate in the blood stream, these pathogens may pose a risk to be transmitted through blood transfusions. Ehrlichia chaffeensis has been shown to survive for more than a week in refrigerated blood. Several instances of suspected E. chaffeensis transmission through solid organ transplant have been investigated, although to date no cases have been confirmed that can be attributed to this route of transmission. Patients who develop ehrlichiosis within a month of receiving a blood transfusion or solid organ transplant should be reported to state health officials for prompt investigation. Use of leukoreduced blood products may theoretically decrease the risk of transfusion-associated transmission of these pathogens. However, the filtration process does not remove all leukocytes or bacteria not associated with leukocytes from leukoreduced blood; therefore, this process may not eliminate the risk completely. \n                \nFor more in-depth information about signs and symptoms of ehrlichiosis, please visit http:\/\/www.cdc.gov\/mmwr\/preview\/mmwrhtml\/rr5504a1.htm \n                \n \nDiagnosis \n                \n  \n                \nThe diagnosis of ehrlichiosis must be made based on clinical signs and symptoms, and can later be confirmed using specialized confirmatory laboratory tests.  Treatment should never be delayed pending the receipt of laboratory test results, or be withheld on the basis of an initial negative laboratory result.  \nPhysician Diagnosis \n                \nThere are several aspects of ehrlichiosis that make it challenging for healthcare providers to diagnose and treat.  The symptoms vary from patient to patient and can be difficult to distinguish from other diseases.  Treatment is more likely to be effective if started early in the course of disease. Diagnostic tests based on the detection of antibodies will frequently be negative in the first 7-10 days of illness. \n                \nFor this reason, healthcare providers must use their judgment to treat patients based on clinical suspicion alone. Healthcare providers may find important information in the patient\u2019s history and physical examination that may aid clinical suspicion. Information such as recent tick bites, exposure to areas where ticks are likely to be found, or history of recent travel to areas where ehrlichiosis is endemic can be helpful in making the diagnosis.  The healthcare provider should also look at routine blood tests, such as a complete blood cell count or a chemistry panel. Clues such as a low platelet count (thrombocytopenia), low white blood cell count (leukopenia), or elevated liver enzyme levels are helpful predictors of ehrlichiosis, but may not be present in all patients depending on the course of the disease.   After a suspect diagnosis is made on clinical suspicion and treatment has begun, specialized laboratory testing should be used to confirm the diagnosis of ehrlichiosis. \n                \n \nLaboratory Detection \n                \nDuring the acute phase of illness, a sample of whole blood can be tested by polymerase chain reaction (PCR) assay to determine if a patient has ehrlichiosis. This method is most sensitive in the first week of illness, and quickly decreases in sensitivity following the administration of appropriate antibiotics. Although a positive PCR result is helpful, a negative result does not completely rule out the diagnosis. \n                \nDuring the first week of illness a microscopic examination of blood smears (known as a peripheral blood smear) may reveal morulae (microcolonies of ehrlichiae) in the cytoplasm of white blood cells in up to 20% of patients. \n \n   \n  \n \n                \nThe type of blood cell in which morulae are observed may provide insight into the infecting species: E. chaffeensis most commonly infects monocytes, whereas E. ewingii more commonly infect granulocytes. However, the observance of morulae in a particular cell type cannot conclusively identify the infecting species. Culture isolation of Ehrlichia is only available at specialized laboratories; routine hospital blood cultures cannot detect Ehrlichia. \n                \nWhen a person develops ehrlichiosis, their immune system produces antibodies to the Ehrlichia, with detectable antibody titers usually observed by 7-10 days after illness onset.  It is important to note that antibodies are not detectable in the first week of illness in 85% of patients, and a negative test during this time does not rule out ehrlichiosis as a cause of illness.  \n                \nThe gold standard serologic test for diagnosis of ehrlichiosis is the indirect immunofluorescence assay (IFA) using E. chaffeensis antigen, performed on paired serum samples to demonstrate a significant (four-fold) rise in antibody titers.  The first sample should be taken as early in the disease as possible, preferably in the first week of symptoms, and the second sample should be taken 2 to 4 weeks later. In most cases of ehrlichiosis, the first IgG IFA titer is typically low, or \u201cnegative,\u201d and the second typically shows a significant (four-fold) increase in IgG antibody levels. IgM antibodies usually rise at the same time as IgG near the end of the first week of illness and remain elevated for months or longer.  Also, IgM antibodies are less specific than IgG antibodies and more likely to result in a false positive.  For these reasons, physicians requesting IgM serologic titers should also request a concurrent IgG titer. \n                \nSerologic tests based on enzyme immunoassay (EIA) technology are available from some commercial laboratories. However, EIA tests are qualitative rather than quantitative, meaning they only provide a positive\/negative result, and are less useful to measure changes in antibody titers between paired specimens. Furthermore, some EIA assays rely on the evaluation of IgM antibody alone, which may have a higher frequency of false positive results.  \n                \nAntibodies to E. chaffeensis may remain elevated for months or longer after the disease has resolved, or may be detected in persons who were previously exposed to antigenically related organisms.  Up to 12% of currently healthy people in some areas may have elevated antibody titers due to past exposure to Ehrlichia species or similar organisms. Therefore, if only one sample is tested it can be difficult to interpret, while paired samples taken weeks apart demonstrating a significant (four-fold) rise in antibody titer provides the best evidence for a correct diagnosis of ehrlichiosis.  \n                \nFor more in-depth information about the diagnosis of ehrlichiosis, please visit http:\/\/www.cdc.gov\/mmwr\/preview\/mmwrhtml\/rr5504a1.htm \n                \n \nTreatment \n                \nDoxycycline is the first line treatment for adults and children of all ages and should be initiated immediately whenever ehrlichiosis is suspected.  \n                \nUse of antibiotics other than doxycycline and other tetracyclines is associated with a higher risk of fatal outcome for some rickettsial infections. Doxycycline is most effective at preventing severe complications from developing if it is started early in the course of disease. Therefore, treatment must be based on clinical suspicion alone and should always begin before laboratory results return. \n                \nIf the patient is treated within the first 5 days of the disease, fever generally subsides within 24-72 hours.  In fact, failure to respond to doxycycline suggests that the patient\u2019s condition might not be due to ehrlichiosis. Severely ill patients may require longer periods before their fever resolves. Resistance to doxcycline or relapses in symptoms after the completion of the recommended course have not been documented.  \n                \nRecommended Dosage \n                \nDoxycycline is the first line treatment for adults and children of all ages: \n \n - Adults: 100 mg every 12 hours \n - Children under 45 kg (100 lbs): 2.2 mg\/kg body weight given twice a day \n \n                \nPatients should be treated for at least 3 days after the fever subsides and until there is evidence of clinical improvement. Standard duration of treatment is 7 to 14 days.  Some patients may continue to experience headache, weakness and malaise for weeks after adequate treatment. \n                \n \nTreating children \n                \nThe use of doxycycline to treat suspected ehrlichiosis in children is standard practice recommended by both CDC and the AAP Committee on Infectious Diseases. Unlike older generations of tetracyclines, the recommended dose and duration of medication needed to treat ehrlichiosis has not been shown to cause staining of permanent teeth, even when five courses are given before the age of eight.  Healthcare providers should use doxycycline as the first-line treatment for suspected ehrlichiosis in patients of all ages.  \n                \n \nOther Treatments \n                \nIn cases of life threatening allergies to doxycycline and in some pregnant patients for whom the clinical course of ehrlichiosis appears mild, physicians may need to consider alternate antibiotics. Although recommended as a second-line therapeutic alternative to treat Rocky Mountain spotted fever (RMSF), chloramphenicol is not recommended for the treatment of either ehrlichiosis or anaplasmosis, as studies have shown a lack of efficacy. Rifampin appears effective against Ehrlichia in laboratory settings. However, rifampin is not effective in treating RMSF, a disease that may be confused with ehrlichiosis. Healthcare providers should be cautious when exploring treatments other than doxycycline, which is highly effective in treating both. Other antibiotics, including broad spectrum antibiotics are not considered highly effective against ehrlichiosis, and the use of sulfa drugs during acute illness may worsen the severity of infection.  \n                \n \nProphylaxis (Preventive Treatment) \n                \nAntibiotic treatment following a tick bite is not recommended as a means to prevent ehrlichiosis. There is no evidence this practice is effective, and this may simply delay onset of disease. Instead, persons who experience a tick bite should be alert for symptoms suggestive of tickborne illness and consult a physician if fever, rash, or other symptoms of concern develop.  \n                \nFor more in-depth information about treatment, please visit http:\/\/www.cdc.gov\/mmwr\/preview\/mmwrhtml\/rr5504a1.htm \n                \n \nOther Considerations \n                \nThe clinical presentation for ehrlichiosis can resemble other tickborne diseases, such as Rocky Mountain spotted fever and anaplasmosis. Similar to ehrlichiosis, these infections respond well to treatment with doxycycline. Healthcare providers should order diagnostic tests for additional agents if the clinical history and geographic association warrant. For more in-depth about other similar tickborne diseases, please visit http:\/\/www.cdc.gov\/mmwr\/preview\/mmwrhtml\/rr5504a1.htm"}
{"_id":"5defcbe3-7ca9-40e7-812d-37b3c50c3c36","text":"More detailed information on the diagnosis, management, and treatment of ehrlichiosis is available in Diagnosis and Management of Tickborne Rickettsial Diseases: Rocky Mountain Spotted Fever, Ehrlichioses, and Anaplasmosis \u2013 United States. \n                \n*Case definitions have been updated since publication \nHow to Contact the Rickettsial Zoonoses Branch at CDC \n                \nThe general public and healthcare providers should first call 1-800-CDC-INFO (1-800-232-4636) for questions regarding ehrlichiosis. If a consultation with a CDC scientist specializing in ehrlichiosis is advised, your call will be appropriately forwarded. \n                \n \nCase Definitions \n                \nAs of January 1, 2008, E. chaffeensis and E. ewingii infections are reported under distinct reporting categories. \n                \n2008 Case Definition \n                \n \nCase Report Forms \n                \nFor confirmed and probable cases of ehrlichiosis that have been identified and reported through the National Notifiable Disease Surveillance System, states are also encouraged to submit additional information using the CDC Case Report Form (CRF). This form collects additional important information that routine electronic reporting does not, such as information on how the diagnosis was made, and whether the patient was hospitalized or died. If a different state-specific form is already used to collect this information, this information may be submitted to CDC in lieu of a CRF. \n                \n2010 CDC Case Report Form: Tickborne Rickettsial Diseases (2010 version)  (PDF \u2013 982kb; 3 pages) \n                \n \nHow to Submit Specimens to CDC for Ehrlichiosis Testing \n                \nPrivate citizens may not directly submit specimens to CDC for testing. If you feel that diagnostic testing is necessary, consult your healthcare provider or state health department. \nState Health Departments: \n                \nSpecimens may be submitted to CDC for testing for ehrlichiosis. To coordinate specimen submission, please call 404-639-1075 during business hours (8:00 - 4:30 ET). \n                \n  \nU.S. Healthcare Providers: \n                \nU.S. healthcare providers should not submit specimens for testing directly to CDC. CDC policy requires that specimens for testing be submitted through or with the approval of the state health department. Please contact your state health department, who will assist you with specimen submission and reporting of infection. For general questions about ehrlichiosis, please call 1-800-CDC-INFO (1-800-232-4636). If you have questions about a suspect ehrlichiosis case, please first consult your state health department. Healthcare providers requiring an epidemiologic or laboratory consultation on ehrlichiosis may also call 404-639-1075 during business hours (8:00 - 4:30 ET). Or 770-488-7100 after hours. \nNon U.S. Healthcare Providers: \n                \nNon-U.S. healthcare providers should consult CDC prior to submitting specimens for testing. For general questions about ehrlichiosis, please call 1-800-CDC-INFO (1-800-232-4636). If you would like to discuss a suspect ehrlichiosis case with CDC, please call 404-639-1075 during business hours (8:00 - 4:30 ET), or 770-488-7100 after hours."}
{"_id":"d3fcd36d-ca75-4fa7-85eb-1795090032f1","text":"Acinetobacter [asz\u2212in\u2212\u00e9e\u2212toe\u2013back\u2212ter] is a group of bacteria commonly found in soil and water. While there are many types or \u201cspecies\u201d of Acinetobacter and all can cause human disease, Acinetobacter baumannii [asz\u2212in\u2212\u00e9e\u2212toe\u2013back\u2212ter   boe-maa-nee-ie] accounts for about 80% of reported infections.\n                \nOutbreaks of Acinetobacter infections typically occur in intensive care units and healthcare settings housing very ill patients. Acinetobacter infections rarely occur outside of healthcare settings."}
{"_id":"697d90fc-7e7e-4638-838b-f311fbc54753","text":"Acinetobacter causes a variety of diseases, ranging from pneumonia to serious blood or wound infections, and the symptoms vary depending on the disease. Acinetobacter may also \u201ccolonize\u201d or live in a patient without causing infection or symptoms, especially in tracheostomy sites or open wounds."}
{"_id":"7ada3e3e-a9dd-49c4-a38b-e7130b21ac1a","text":"Acinetobacter poses very little risk to healthy people. However, people who have weakened immune systems, chronic lung disease, or diabetes may be more susceptible to infections with Acinetobacter. Hospitalized patients, especially very ill patients on a ventilator, those with a prolonged hospital stay, those who have open wounds, or any person with invasive devices like urinary catheters are also at greater risk for Acinetobacter infection. Acinetobacter can be spread to susceptible persons by person-to-person contact or contact with contaminated surfaces."}
{"_id":"0797882a-e9db-4131-bd15-16e092705e9d","text":"Acinetobacter can live on the skin and may survive in the environment for several days. Careful attention to infection control procedures, such as hand hygiene and environmental cleaning, can reduce the risk of transmission."}
{"_id":"0cae55bf-9634-4b94-9444-3f440e4be3be","text":"Acinetobacter is often resistant to many commonly prescribed antibiotics. Decisions on treatment of infections with Acinetobacter should be made on a case-by-case basis by a healthcare provider. Acinetobacter infection typically occurs in ill patients and can either cause or contribute to death in these patients."}
{"_id":"942731ff-1c81-4ab2-8cc6-438d1667078a","text":"Tuberculosis (TB) is a disease that is spread through the air from one person to another. There are two kinds of tests that are used to determine if a person has been infected with TB bacteria: the tuberculin skin test and TB blood tests. \n  \nA positive TB skin test or TB blood test only tells that a person has been infected with TB bacteria. It does not tell whether the person has latent TB infection (LTBI) or has progressed to TB disease. Other tests, such as a chest x-ray and a sample of sputum, are needed to see whether the person has TB disease. \n  \nTuberculin skin test: The TB skin test (also called the Mantoux tuberculin skin test) is performed by injecting a small amount of fluid (called tuberculin) into the skin in the lower part of the arm. A person given the tuberculin skin test must return within 48 to 72 hours to have a trained health care worker look for a reaction on the arm. The health care worker will look for a raised, hard area or swelling, and if present, measure its size using a ruler. Redness by itself is not considered part of the reaction. \n  \nThe skin test result depends on the size of the raised, hard area or swelling. It also depends on the person\u2019s risk of being infected with TB bacteria and the progression to TB disease if infected. \n   \n   - Positive skin test: This \n     means the person\u2019s body was infected with TB bacteria. Additional tests are needed to determine if the person has latent TB infection or TB disease. A health care worker will then provide treatment as needed. \n   - Negative skin test: This means the person\u2019s body did not react to the test, and that latent TB infection or TB disease is not likely. \n   \n  \n \n     TB blood tests: \n    TB blood tests (also called interferon-gamma release assays or IGRAs) measure how the immune system reacts to the bacteria that cause TB. An IGRA measures how strong a person\u2019s immune system reacts to TB bacteria by testing the person\u2019s blood in a laboratory. \n  \nTwo IGRAs are approved by the U.S. Food and Drug Administration (FDA) and are available in the United States: \n   \n   - QuantiFERON\u00ae\u2013TB Gold In-Tube test (QFT-GIT) \n   - T-SPOT\u00ae.TB test (T-Spot) \n   \n   \n   - Positive IGRA: This means that the person has been infected with TB bacteria. Additional tests are needed to determine if the person has latent TB infection or TB disease. A health care worker will then provide treatment as needed. \n   - Negative IGRA: This means that the person\u2019s blood did not react to the test and that latent TB infection or TB disease is not likely. \n   \n  \nIGRAs are the preferred method of TB infection testing for the following: \n    \n   - People who have a difficult time returning for a second appointment to look for a reaction to the TST. \n   \n  \nThere is no problem with repeated IGRAs. \n    \n   \n   \n     Testing for TB in BCG-Vaccinated Persons \n  \nMany people born outside of the United States have been BCG-vaccinated. \n  \nPeople who have had a previous BCG vaccine may receive a TB skin test. In some people, BCG may cause a positive skin test when they are not infected with TB bacteria. If a TB skin test is positive, additional tests are needed. \n  \nIGRAs, unlike the TB skin tests, are not affected by prior BCG vaccination and are not expected to give a false-positive result in people who have received BCG. \n   \n     Choosing a TB Test \n  \nThe person\u2019s health care provider should choose which TB test to use. Factors in selecting which test to use include the reason for testing, test availability, and cost. Generally, it is not recommended to test a person with both a TST and an IGRA. \n   \n     Diagnosis of Latent TB Infection or TB Disease \n  \nIf a person is found to be infected with TB bacteria, other tests are needed to see if the person has TB disease. \n  \nTB disease can be diagnosed by medical history, physical examination, chest x-ray, and other laboratory tests. TB disease is treated by taking several drugs as recommended by a health care provider. \n  \nIf a person does not have TB disease, but has TB bacteria in the body, then latent TB infection is diagnosed. The decision about treatment for latent TB infection will be based on a person\u2019s chances of developing TB disease. \n   \n     Diagnosis of TB Disease \n  \nPeople suspected of having TB disease should be referred for a medical evaluation, which will include \n   \n   - Medical history, \n   - Physical examination, \n   - Test for TB infection (TB skin test or TB blood test), \n   - Chest radiograph (X-ray), and \n   - Appropriate laboratory tests \n   \n  \nSee Diagnosis of TB (Fact sheet) for more information about TB diagnosis. \n   \n    \n      Related Links \n     \n    \n   For Patients \n        \n    \n   For Health Care Providers"}
{"_id":"3f9d0a8d-83a0-4642-8054-f5699f62765f","text":"Infection Control in Health Care Settings\n  \nTuberculosis (TB) transmission has been documented in health care settings where health care workers and patients come in contact with people who have TB disease.\n  \nPeople who work or receive care in health care settings are at higher risk for becoming infected with TB; therefore, it is necessary to have a TB infection control plan as part of a general infection control program designed to ensure the following:\n  \n   - prompt detection of infectious patients,\n   - airborne precautions, and\n   - treatment of people who have suspected or confirmed TB disease.\n  \n  \nIn order to be effective, the primary emphasis of a TB infection control program should be on achieving these three goals.\n  \nIn all health care settings, particularly those in which people are at high risk for exposure to TB, policies and procedures for TB control should be developed, reviewed periodically, and evaluated for effectiveness to determine the actions necessary to minimize the risk for transmission of TB.\n  \nThe TB infection control program should be based on a three-level hierarchy of control measures and include:\n  \n   - Administrative measures\n   - Environmental controls\n   - Use of respiratory protective equipment\n  \n  \nThe first and most important level of the hierarchy, administrative measures, impacts the largest number of people. It is intended primarily to reduce the risk of uninfected people who are exposed to people who have TB disease.\n  \nThe second level of the hierarchy is the use of environmental controls to reduce the amount of TB in the air. The first two control levels of the hierarchy also minimize the number of areas in the health care setting where exposure to TB may occur.\n  \nThe third level of the hierarchy is the use of respiratory protective equipment in situations that pose a high risk of exposure to TB. Use of respiratory protection equipment can further reduce the risk for exposure of health care workers.\n  \nMore: Information about Infection Control in Health Care Settings\n  \n     TB Prevention\n  \nPreventing Exposure to TB Disease While Traveling Abroad\nTravelers should avoid close contact or prolonged time with known TB patients in crowded, enclosed environments (for example, clinics, hospitals, prisons, or homeless shelters).\n  \nTravelers who will be working in clinics, hospitals, or other health care settings where TB patients are likely to be encountered should consult infection control or occupational health experts. They should ask about administrative and environmental procedures for preventing exposure to TB. Once those procedures are implemented, additional measures could include using personal respiratory protective devices.\n  \nTravelers who anticipate possible prolonged exposure to people with TB (for example, those who expect to come in contact routinely with clinic, hospital, prison, or homeless shelter populations) should have a tuberculin skin test (TST) or interferon-gamma release assay (IGRA) test before leaving the United States. If the test reaction is negative, they should have a repeat test 8 to 10 weeks after returning to the United States. Additionally, annual testing may be recommended for those who anticipate repeated or prolonged exposure or an extended stay over a period of years. Because people with HIV infection are more likely to have an impaired response to both the TST and IGRA, travelers who are HIV positive should tell their physicians about their HIV infection status.\n  \nMore: Tuberculosis Information for International Travelers\n  \n     What to Do If You Have Been Exposed to TB\n  \nIf you think you have been exposed to someone with TB disease, contact your health care provider or local health department to see if you should be tested for TB. Be sure to tell the doctor or nurse when you spent time with someone who has TB disease.\n  \nMore: What to Do If You Have Been Exposed to TB\n  \n     Preventing Latent TB Infection from Progressing to TB Disease\n  \nMany people who have latent TB infection never develop TB disease. But some people who have latent TB infection are more likely to develop TB disease than others. Those at high risk for developing TB disease include:\n  \n   - People with HIV infection\n   - People who became infected with TB bacteria in the last 2 years\n   - Babies and young children\n   - People who inject illegal drugs\n   - People who are sick with other diseases that weaken the immune system\n   - Elderly people\n   - People who were not treated correctly for TB in the past\n  \n  \nIf you have latent TB infection and you are in one of these high-risk groups, you should take medicine to keep from developing TB disease. There are several treatment options for latent TB infection. You and your health care provider must decide which treatment is best for you. If you take your medicine as instructed, it can keep you from developing TB disease. Because there are less bacteria, treatment for latent TB infection is much easier than treatment for TB disease. A person with TB disease has a large amount of TB bacteria in the body. Several drugs are needed to treat TB disease."}
{"_id":"d4791d5e-fb79-4d65-a941-3d831f115280","text":"Tuberculosis (TB) is caused by a bacterium called Mycobacterium tuberculosis. The bacteria usually attack the lungs, but TB bacteria can attack any part of the body such as the kidney, spine, and brain. If not treated properly, TB disease can be fatal.\n  \nNot everyone infected with TB bacteria becomes sick. As a result, two TB-related conditions exist: latent TB infection and TB disease. Both latent TB infection and TB disease can be treated. Learn more about the difference between latent TB infection and TB disease.\n  \n     Treatment for Latent TB Infection\n  \nPeople with latent TB infection have TB bacteria in their bodies, but they are not sick because the bacteria are not active. People with latent TB infection do not have symptoms, and they cannot spread TB bacteria to others. However, if TB bacteria become active in the body and multiply, the person will go from having latent TB infection to being sick with TB disease. For this reason, people with latent TB infection are often prescribed treatment to prevent them from developing TB disease. Treatment of latent TB infection is essential for controlling and eliminating TB in the United States.\n  \nBecause there are less bacteria in a person with latent TB infection, treatment is much easier. Four regimens are approved for the treatment of latent TB infection. The medications used to treat latent TB infection include:\n  \n   - isoniazid (INH)\n   - rifampin (RIF)\n   - rifapentine (RPT)\n  \n  \nCertain groups of people (such as people with weakened immune systems) are at very high risk of developing TB disease once infected with TB bacteria. Every effort should be made to begin appropriate treatment and to ensure completion of the entire course of treatment for latent TB infection.\n  \nMore: Treatment for Latent TB Infection\n  \n     Treatment for TB Disease\n  \nTB bacteria become active (multiplying in the body) if the immune system can't stop them from growing. When TB bacteria are active, this is called TB disease. TB disease will make a person sick. People with TB disease may spread the bacteria to people with whom they spend many hours.\n  \nTB disease can be treated by taking several drugs for 6 to 9 months. There are 10 drugs currently approved by the U.S. Food and Drug Administration (FDA) for treating TB. Of the approved drugs, the first-line anti-TB agents that form the core of treatment regimens include:\n  \n   - isoniazid (INH)\n   - rifampin (RIF)\n   - ethambutol (EMB)\n   - pyrazinamide (PZA)\n  \n  \nRegimens for treating TB disease have an initial phase of 2 months, followed by a choice of several options for the continuation phase of either 4 or 7 months (total of 6 to 9 months for treatment). Learn more about the continuation phase of treatment.\n  \nIt is very important that people who have TB disease finish the medicine, taking the drugs exactly as prescribed. If they stop taking the drugs too soon, they can become sick again; if they do not take the drugs correctly, the TB bacteria that are still alive may become resistant to those drugs. TB that is resistant to drugs is harder and more expensive to treat.\n  \nMore: Treatment for TB Disease\n  \n     Treatment Completion\n  \nTreatment completion is determined by the number of doses ingested over a given period of time. Although basic TB regimens are broadly applicable, there are modifications that should be made under special circumstances (such as people with HIV infection, drug resistance, pregnancy, or treatment of children)."}
{"_id":"b07d750e-41f3-46a6-b3b4-3279b34fba48","text":"The Division of Tuberculosis Elimination (DTBE) Laboratory Branch (LB) provides services for the following tests on mycobacterial cultures. Any local health department, licensed physician's office, licensed laboratory or licensed health care facility may submit cultures for testing but they must be routed through either their state health department or other authorized facility.\n  Genotyping\n  State or local TB control programs\n  \nA genotyping laboratory, in Michigan  is under contract with CDC to provide genotyping services to TB programs in the United States. Three genotyping methods to identify TB strains:\n  \n   - Spoligotyping\n   - Mycobacterial interspersed repetitive unit (MIRU) analysis\n   - IS6110-based restriction fragment length polymorphism (RFLP) analysis\n  \n  \nFor more information, view the Guide to the Application of Genotyping to Tuberculosis Prevention and Control.\n  \nDTBE epidemiologic investigations and surveillance activities\n  \n   - The LB provides support for DTBE epidemiologic investigations and surveillance activities. TB genotyping results, when combined with epidemiologic data, help to distinguish TB patients who are involved in the same chain of recent transmission.\n  \n  Drug susceptibility testing\n  \nThe LB performs drug susceptibility testing for selected Mycobacterium species referred from state or other authorized health facilities. Cultures of mycobacteria are tested by the indirect proportion method with antituberculosis drugs incorporated into 7H10 agar plates.\n  \n  Additional Resources"}
{"_id":"cda10311-d1dd-4200-96f8-7c7767ad8941","text":"TB Epidemiologic Studies Consortium\n  \n The TB Epidemiologic Studies Consortium (TBESC) was established to strengthen, focus, and coordinate tuberculosis (TB) research. The TBESC is designed to build the scientific research capacities of state and metropolitan TB control programs, participating laboratories, academic institutions, hospitals, and both non- and for-profit organizations.\n                \n  TB Trials Consortium\n  \n The TB Trials Consortium (TBTC) is a collaboration of North American and international clinical investigators whose mission is to conduct programmatically relevant research concerning the diagnosis, clinical management, and prevention of TB infection and disease.\n  Behavioral and Social Science Research\n  Behavioral and social science research has the potential to make a tremendous impact on TB elimination efforts. This research is needed to 1) understand how behaviors of both patients and providers affect TB-related care seeking, diagnosis, treatment success, and prevention; and 2) understand how other social, cultural, and environmental influences affect health seeking and treatment outcomes related to TB."}
{"_id":"029aae96-f57f-4def-ab0a-a06ce4a748a8","text":"Also called crab lice or \"crabs,\" pubic lice are parasitic insects found primarily in the pubic or genital area of humans. Pubic lice infestation is found worldwide and occurs in all races, ethnic groups, and levels of society."}
{"_id":"c037e8a2-d620-4e40-b7fa-491ef9cc5fee","text":"Pubic (\"crab\") lice infestation is found worldwide and occurs in all races and ethnic groups and in all levels of society. Pubic lice usually are spread through sexual contact and are most common in adults. Occasionally pubic lice may be spread by close personal contact or contact with articles such as clothing, bed linens, and towels that have been used by an infested person. Pubic lice found on the head or eyelashes of children may be an indication of sexual exposure or abuse.\n    \nPubic lice do not transmit disease; however, secondary bacterial infection can occur from scratching of the skin."}
{"_id":"a5fd0ec2-8695-410b-ae5e-8dac0ed2e885","text":"Pubic lice are short and crab-like and appear very different from head and body lice. Pubic lice infestation is diagnosed by finding a \u201ccrab\u201d louse or eggs on hair in the pubic region or, less commonly, elsewhere on the body (eyebrows, eyelashes, beard, mustache, armpit, perianal area, groin, trunk, scalp). Although pubic lice and nits can be large enough to be seen with the naked eye, a magnifying lens may be necessary to find lice or eggs."}
{"_id":"46074e82-6bad-4781-8e95-cbbf7db996c9","text":"A lice-killing lotion containing 1% permethrin or a mousse containing pyrethrins and piperonyl butoxide can be used to treat pubic (\"crab\") lice. These products are available over-the-counter without a prescription at a local drug store or pharmacy. These medications are safe and effective when used exactly according to the instructions in the package or on the label. \n    \nLindane shampoo is a prescription medication that can kill lice and lice eggs. However, lindane is not recommended as a first-line therapy. Lindane can be toxic to the brain and other parts of the nervous system; its use should be restricted to patients who have failed treatment with or cannot tolerate other medications that pose less risk. Lindane should not be used to treat premature infants, persons with a seizure disorder, women who are pregnant or breast-feeding, persons who have very irritated skin or sores where the lindane will be applied, infants, children, the elderly, and persons who weigh less than 110 pounds. \n    \nMalathion* lotion 0.5% (Ovide*) is a prescription medication that can kill lice and some lice eggs; however, malathion lotion (Ovide*) currently has not been approved by the U.S. Food and Drug Administration (FDA) for treatment of pubic (\"crab\") lice. \n    \nBoth topical and oral ivermectin have been used successfully to treat lice; however, only topical ivermectin lotion currently is approved by the U.S. Food and Drug Administration (FDA) for treatment of lice. Oral ivermectin is not FDA-approved for treatment of lice. \n    \nHow to treat pubic lice infestations: (Warning: See special instructions for treatment of lice and nits on eyebrows or eyelashes. The lice medications described in this section should not be used near the eyes.) \n    \n   \n   \n    \n    - Wash the infested area; towel dry. \n    - Carefully follow the instructions in the package or on the label. Thoroughly saturate the pubic hair and other infested areas with lice medication. Leave medication on hair for the time recommended in the instructions. After waiting the recommended time, remove the medication by following carefully the instructions on the label or in the box. \n    - Following treatment, most nits will still be attached to hair shafts. Nits may be removed with fingernails or by using a fine-toothed comb. \n    - Put on clean underwear and clothing after treatment. \n    - To kill any lice or nits remaining on clothing, towels, or bedding, machine-wash and machine-dry those items that the infested person used during the 2\u20133 days before treatment. Use hot water (at least 130\u00b0F) and the hot dryer cycle. \n    - Items that cannot be laundered can be dry-cleaned or stored in a sealed plastic bag for 2 weeks. \n    - All sex partners from within the previous month should be informed that they are at risk for infestation and should be treated. \n    - Persons should avoid sexual contact with their sex partner(s) until both they and their partners have been successfully treated and reevaluated to rule out persistent infestation. \n    - Repeat treatment in 9\u201310 days if live lice are still found. \n    - Persons with pubic lice should be evaluated for other sexually transmitted diseases (STDs). \n    \n   \nSpecial instructions for treatment of lice and nits found on eyebrows or eyelashes: \n    \n    - If only a few live lice and nits are present, it may be possible to remove these with fingernails or a nit comb. \n    - If additional treatment is needed for lice or nits on the eyelashes, careful application of ophthalmic-grade petrolatum ointment (only available by prescription) to the eyelid margins 2\u20134 times a day for 10 days is effective. Regular petrolatum (e.g., Vaseline)* should not be used because it can irritate the eyes if applied. \n    \n   \n*Use of trade names is for identification purposes only and does not imply endorsement by the Public Health Service or by the U.S. Department of Health and Human Services. \n    \n   \nThis information is not meant to be used for self-diagnosis or as a substitute for consultation with a health care provider. If you have any questions about the parasites described above or think that you may have a parasitic infection, consult a health care provider."}
{"_id":"8f447a36-be7a-4584-b92c-4989f917d945","text":"Pubic (\"crab\") lice most commonly are spread directly from person to person by sexual contact. Pubic lice very rarely may be spread by clothing, bedding, or a toilet seat.\n    \nThe following are steps that can be taken to help prevent and control the spread of pubic (\"crab\") lice:\n    \n     - All sexual contacts of the infested person should be examined. All those who are infested should be treated.\n     - Sexual contact between the infested person(s)s and their sexual partner(s) should be avoided until all have been examined, treated as necessary, and reevaluated to rule out persistent infestation.\n     - Machine wash and dry clothing worn and bedding used by the infested person in the hot water (at least 130\u00b0F) laundry cycle and the high heat drying cycle. Clothing and items that are not washable can be dry-cleaned OR sealed in a plastic bag and stored for 2 weeks.\n     - Do not share clothing, bedding, and towels used by an infested person.\n     - Do not use fumigant sprays or fogs; they are not necessary to control pubic (\"crab\") lice and can be toxic if inhaled or absorbed through the skin.\n    \n    \nPersons with pubic lice should be examined and treated for any other sexually transmitted diseases (STDs) that may be present."}
{"_id":"62e8be95-840c-49b4-8cbc-f6d94c4003b8","text":"Frequently Asked Queestions (FAQs)"}
{"_id":"e9723bfe-b520-47a8-a14a-4d0c054f27fd","text":"Several species of Paragonimus cause most infections; the most important is P. westermani, which occurs primarily in Asia including China, the Philippines, Japan, Vietnam, South Korea, Taiwan, and Thailand. P. africanus causes infection in Africa, and P. mexicanus in Central and South America. Specialty dishes in which shellfish are consumed raw or prepared only in vinegar, brine, or wine without cooking play a key role in the transmission of paragonimiasis. Raw crabs or crayfish are also used in traditional medicine practices in Korea, Japan, and some parts of Africa.\n    \nAlthough rare, human paragonimiasis from P. kellicotti has been acquired in the United States, with multiple cases from the Midwest. Several cases have been associated with ingestion of uncooked crawfish during river raft float trips in Missouri."}
{"_id":"da7d2836-0df9-4ad8-bf13-8be5023c66ab","text":"The infection is usually diagnosed by identification of Paragonimus eggs in sputum. The eggs are sometimes found in stool samples (coughed-up eggs are swallowed). A tissue biopsy is sometimes performed to look for eggs in a tissue specimen.\n    \nSpecific and sensitive antibody tests based on P. westermani antigens are available through CDC, and serologic tests using a variety of techniques are available through commercial laboratories.\n    \nMore on: Resources for Health Professionals: Diagnosis\n    \nMore on: DPDx: Paragonimus"}
{"_id":"476b2f05-1a23-4f79-9c06-a5b8c5a4d1ec","text":"Paragonimus infections are treatable by your health care provider. Prescription medications are available.\n    \nMore on: Resources for Health Professionals: Treatment"}
{"_id":"96113a4b-566f-4c72-ad37-4d8859209357","text":"Never eat raw freshwater crabs or crayfish. Cook crabs and crayfish for to at least 145\u00b0F (~63\u00b0C). Travelers should be advised to avoid traditional meals containing undercooked freshwater crustaceans.\n    \nMore on: Fight BAC: Safe Food Handling"}
{"_id":"09ebd88d-f65e-432a-bfcc-7f10ec7b3918","text":"On this Page General Information What is vancomycin-resistant enterococci? What types of infections does vancomycin-resistant enterococci cause? Are certain people at risk of getting vancomycin-resistant enterococci? What is the treatment for vancomycin-resistant enterococci? How is vancomycin-resistant enterococci spread? How can patients prevent the spread of vancomycin-resistant enterococci? What should a patient do if they think they have vancomycin-resistant enterococci? Recommendations and Guidelines General Information For more images of this bacterium, search the Public Health Image Library What is vancomycin-resistant enterococci? Enteroccocci are bacteria that are normally present in the human intestines and in the female genital tract and are often found in the environment. These bacteria can sometimes cause infections. Vancomycin is an antibiotic that is used to treat some drug-resistant infections caused by enterococci. In some instances, enterococci have become resistant to this drug and thus are called vancomycin-resistant enterococci (VRE). Most VRE infections occur in hospitals. Top of page What types of infections does VRE cause? VRE can live in the human intestines and female genital tract without causing disease (often called colonization). However, sometimes it can cause infections of the urinary tract, the bloodstream, or of wounds associated with catheters or surgical procedures. Top of page Are certain people at risk of getting VRE? The following persons are at increased risk becoming infected with VRE: People who have been previously treated with the antibiotic vancomycin or other antibiotics for long periods of time. People who are hospitalized, particularly when they receive antibiotic treatment for long periods of time. People with weakened immune systems such as patients in intensive care units, or in cancer or transplant wards. People who have undergone surgical procedures such as abdominal or chest surgery. People with medical devices that stay in for some time such as urinary catheters or central intravenous (IV) catheters. People who are colonized with VRE. Top of page What is the treatment for VRE? People with colonized VRE (bacteria are present, but have no symptoms of an infection)  do not need treatment. Most VRE infections can be treated with antibiotics other than vancomycin. Laboratory testing of the VRE can determine which antibiotics will work. For people who get VRE infections in their bladder and have urinary catheters, removal of the catheter when it is no longer needed can also help get rid of the infection. Top of page How is VRE spread? VRE is often passed from person to person by the contaminated hands of caregivers. VRE can get onto a caregiver's hands after they have contact with other people with VRE or after contact with contaminated surfaces. VRE can also be spread directly to people after they touch surfaces that are contaminated with VRE. VRE is not spread through the air by coughing or sneezing. Top of page How can patients prevent the spread of VRE? If a patient or someone in their household has VRE, the following are some things they can do to prevent the spread of VRE: Keep their hands clean. Always wash their hands thoroughly after using the bathroom and before preparing food. Clean their hands after contact with persons who have VRE. Wash with soap and water (particularly when visibly soiled) or use alcohol-based hand rubs. Frequently clean areas of the home, such as bathrooms, that may become contaminated with VRE. Wear gloves if hands may come in contact with body fluids that may contain VRE, such as stool or bandages from infected wounds. Always wash their hands after removing gloves. If someone has VRE, be sure to tell healthcare providers so that they are aware of the infection. Healthcare facilities use special precautions to help prevent the spread of VRE to others. Top of page What should patients do if they think they have vancomycin-resistant enterococci (VRE)? Anyone who thinks they have VRE must talk with their healthcare provider. Top of page Recommendations and Guidelines For more information about prevention and treatment of HAIs, see the resources below: Siegel JD, Rhinehart E, Jackson M, et al. The Healthcare Infection Control Practices Advisory Committee (HICPAC). Management of Multidrug-Resistant Organisms In Healthcare Settings, 2006"}
{"_id":"42bd64b7-1d20-439b-8ab0-281886ee25a9","text":"On this Page General Information What is vancomycin-resistant enterococci? What types of infections does vancomycin-resistant enterococci cause? Are certain people at risk of getting vancomycin-resistant enterococci? What is the treatment for vancomycin-resistant enterococci? How is vancomycin-resistant enterococci spread? How can patients prevent the spread of vancomycin-resistant enterococci? What should a patient do if they think they have vancomycin-resistant enterococci? Recommendations and Guidelines General Information For more images of this bacterium, search the Public Health Image Library What is vancomycin-resistant enterococci? Enteroccocci are bacteria that are normally present in the human intestines and in the female genital tract and are often found in the environment. These bacteria can sometimes cause infections. Vancomycin is an antibiotic that is used to treat some drug-resistant infections caused by enterococci. In some instances, enterococci have become resistant to this drug and thus are called vancomycin-resistant enterococci (VRE). Most VRE infections occur in hospitals. Top of page What types of infections does VRE cause? VRE can live in the human intestines and female genital tract without causing disease (often called colonization). However, sometimes it can cause infections of the urinary tract, the bloodstream, or of wounds associated with catheters or surgical procedures. Top of page Are certain people at risk of getting VRE? The following persons are at increased risk becoming infected with VRE: People who have been previously treated with the antibiotic vancomycin or other antibiotics for long periods of time. People who are hospitalized, particularly when they receive antibiotic treatment for long periods of time. People with weakened immune systems such as patients in intensive care units, or in cancer or transplant wards. People who have undergone surgical procedures such as abdominal or chest surgery. People with medical devices that stay in for some time such as urinary catheters or central intravenous (IV) catheters. People who are colonized with VRE. Top of page What is the treatment for VRE? People with colonized VRE (bacteria are present, but have no symptoms of an infection)  do not need treatment. Most VRE infections can be treated with antibiotics other than vancomycin. Laboratory testing of the VRE can determine which antibiotics will work. For people who get VRE infections in their bladder and have urinary catheters, removal of the catheter when it is no longer needed can also help get rid of the infection. Top of page How is VRE spread? VRE is often passed from person to person by the contaminated hands of caregivers. VRE can get onto a caregiver's hands after they have contact with other people with VRE or after contact with contaminated surfaces. VRE can also be spread directly to people after they touch surfaces that are contaminated with VRE. VRE is not spread through the air by coughing or sneezing. Top of page How can patients prevent the spread of VRE? If a patient or someone in their household has VRE, the following are some things they can do to prevent the spread of VRE: Keep their hands clean. Always wash their hands thoroughly after using the bathroom and before preparing food. Clean their hands after contact with persons who have VRE. Wash with soap and water (particularly when visibly soiled) or use alcohol-based hand rubs. Frequently clean areas of the home, such as bathrooms, that may become contaminated with VRE. Wear gloves if hands may come in contact with body fluids that may contain VRE, such as stool or bandages from infected wounds. Always wash their hands after removing gloves. If someone has VRE, be sure to tell healthcare providers so that they are aware of the infection. Healthcare facilities use special precautions to help prevent the spread of VRE to others. Top of page What should patients do if they think they have vancomycin-resistant enterococci (VRE)? Anyone who thinks they have VRE must talk with their healthcare provider. Top of page Recommendations and Guidelines For more information about prevention and treatment of HAIs, see the resources below: Siegel JD, Rhinehart E, Jackson M, et al. The Healthcare Infection Control Practices Advisory Committee (HICPAC). Management of Multidrug-Resistant Organisms In Healthcare Settings, 2006"}
{"_id":"6f3c4af3-47ca-4d23-8c3a-308a915dcae7","text":"On this Page General Information What is vancomycin-resistant enterococci? What types of infections does vancomycin-resistant enterococci cause? Are certain people at risk of getting vancomycin-resistant enterococci? What is the treatment for vancomycin-resistant enterococci? How is vancomycin-resistant enterococci spread? How can patients prevent the spread of vancomycin-resistant enterococci? What should a patient do if they think they have vancomycin-resistant enterococci? Recommendations and Guidelines General Information For more images of this bacterium, search the Public Health Image Library What is vancomycin-resistant enterococci? Enteroccocci are bacteria that are normally present in the human intestines and in the female genital tract and are often found in the environment. These bacteria can sometimes cause infections. Vancomycin is an antibiotic that is used to treat some drug-resistant infections caused by enterococci. In some instances, enterococci have become resistant to this drug and thus are called vancomycin-resistant enterococci (VRE). Most VRE infections occur in hospitals. Top of page What types of infections does VRE cause? VRE can live in the human intestines and female genital tract without causing disease (often called colonization). However, sometimes it can cause infections of the urinary tract, the bloodstream, or of wounds associated with catheters or surgical procedures. Top of page Are certain people at risk of getting VRE? The following persons are at increased risk becoming infected with VRE: People who have been previously treated with the antibiotic vancomycin or other antibiotics for long periods of time. People who are hospitalized, particularly when they receive antibiotic treatment for long periods of time. People with weakened immune systems such as patients in intensive care units, or in cancer or transplant wards. People who have undergone surgical procedures such as abdominal or chest surgery. People with medical devices that stay in for some time such as urinary catheters or central intravenous (IV) catheters. People who are colonized with VRE. Top of page What is the treatment for VRE? People with colonized VRE (bacteria are present, but have no symptoms of an infection)  do not need treatment. Most VRE infections can be treated with antibiotics other than vancomycin. Laboratory testing of the VRE can determine which antibiotics will work. For people who get VRE infections in their bladder and have urinary catheters, removal of the catheter when it is no longer needed can also help get rid of the infection. Top of page How is VRE spread? VRE is often passed from person to person by the contaminated hands of caregivers. VRE can get onto a caregiver's hands after they have contact with other people with VRE or after contact with contaminated surfaces. VRE can also be spread directly to people after they touch surfaces that are contaminated with VRE. VRE is not spread through the air by coughing or sneezing. Top of page How can patients prevent the spread of VRE? If a patient or someone in their household has VRE, the following are some things they can do to prevent the spread of VRE: Keep their hands clean. Always wash their hands thoroughly after using the bathroom and before preparing food. Clean their hands after contact with persons who have VRE. Wash with soap and water (particularly when visibly soiled) or use alcohol-based hand rubs. Frequently clean areas of the home, such as bathrooms, that may become contaminated with VRE. Wear gloves if hands may come in contact with body fluids that may contain VRE, such as stool or bandages from infected wounds. Always wash their hands after removing gloves. If someone has VRE, be sure to tell healthcare providers so that they are aware of the infection. Healthcare facilities use special precautions to help prevent the spread of VRE to others. Top of page What should patients do if they think they have vancomycin-resistant enterococci (VRE)? Anyone who thinks they have VRE must talk with their healthcare provider. Top of page Recommendations and Guidelines For more information about prevention and treatment of HAIs, see the resources below: Siegel JD, Rhinehart E, Jackson M, et al. The Healthcare Infection Control Practices Advisory Committee (HICPAC). Management of Multidrug-Resistant Organisms In Healthcare Settings, 2006"}
{"_id":"833f8dd0-ed0c-43e3-83a8-731fdc2bcfe7","text":"On this Page General Information What is vancomycin-resistant enterococci? What types of infections does vancomycin-resistant enterococci cause? Are certain people at risk of getting vancomycin-resistant enterococci? What is the treatment for vancomycin-resistant enterococci? How is vancomycin-resistant enterococci spread? How can patients prevent the spread of vancomycin-resistant enterococci? What should a patient do if they think they have vancomycin-resistant enterococci? Recommendations and Guidelines General Information For more images of this bacterium, search the Public Health Image Library What is vancomycin-resistant enterococci? Enteroccocci are bacteria that are normally present in the human intestines and in the female genital tract and are often found in the environment. These bacteria can sometimes cause infections. Vancomycin is an antibiotic that is used to treat some drug-resistant infections caused by enterococci. In some instances, enterococci have become resistant to this drug and thus are called vancomycin-resistant enterococci (VRE). Most VRE infections occur in hospitals. Top of page What types of infections does VRE cause? VRE can live in the human intestines and female genital tract without causing disease (often called colonization). However, sometimes it can cause infections of the urinary tract, the bloodstream, or of wounds associated with catheters or surgical procedures. Top of page Are certain people at risk of getting VRE? The following persons are at increased risk becoming infected with VRE: People who have been previously treated with the antibiotic vancomycin or other antibiotics for long periods of time. People who are hospitalized, particularly when they receive antibiotic treatment for long periods of time. People with weakened immune systems such as patients in intensive care units, or in cancer or transplant wards. People who have undergone surgical procedures such as abdominal or chest surgery. People with medical devices that stay in for some time such as urinary catheters or central intravenous (IV) catheters. People who are colonized with VRE. Top of page What is the treatment for VRE? People with colonized VRE (bacteria are present, but have no symptoms of an infection)  do not need treatment. Most VRE infections can be treated with antibiotics other than vancomycin. Laboratory testing of the VRE can determine which antibiotics will work. For people who get VRE infections in their bladder and have urinary catheters, removal of the catheter when it is no longer needed can also help get rid of the infection. Top of page How is VRE spread? VRE is often passed from person to person by the contaminated hands of caregivers. VRE can get onto a caregiver's hands after they have contact with other people with VRE or after contact with contaminated surfaces. VRE can also be spread directly to people after they touch surfaces that are contaminated with VRE. VRE is not spread through the air by coughing or sneezing. Top of page How can patients prevent the spread of VRE? If a patient or someone in their household has VRE, the following are some things they can do to prevent the spread of VRE: Keep their hands clean. Always wash their hands thoroughly after using the bathroom and before preparing food. Clean their hands after contact with persons who have VRE. Wash with soap and water (particularly when visibly soiled) or use alcohol-based hand rubs. Frequently clean areas of the home, such as bathrooms, that may become contaminated with VRE. Wear gloves if hands may come in contact with body fluids that may contain VRE, such as stool or bandages from infected wounds. Always wash their hands after removing gloves. If someone has VRE, be sure to tell healthcare providers so that they are aware of the infection. Healthcare facilities use special precautions to help prevent the spread of VRE to others. Top of page What should patients do if they think they have vancomycin-resistant enterococci (VRE)? Anyone who thinks they have VRE must talk with their healthcare provider. Top of page Recommendations and Guidelines For more information about prevention and treatment of HAIs, see the resources below: Siegel JD, Rhinehart E, Jackson M, et al. The Healthcare Infection Control Practices Advisory Committee (HICPAC). Management of Multidrug-Resistant Organisms In Healthcare Settings, 2006"}
{"_id":"205c7a7f-c4c0-482c-b530-9b7a783dafb4","text":"On this Page General Information What is vancomycin-resistant enterococci? What types of infections does vancomycin-resistant enterococci cause? Are certain people at risk of getting vancomycin-resistant enterococci? What is the treatment for vancomycin-resistant enterococci? How is vancomycin-resistant enterococci spread? How can patients prevent the spread of vancomycin-resistant enterococci? What should a patient do if they think they have vancomycin-resistant enterococci? Recommendations and Guidelines General Information For more images of this bacterium, search the Public Health Image Library What is vancomycin-resistant enterococci? Enteroccocci are bacteria that are normally present in the human intestines and in the female genital tract and are often found in the environment. These bacteria can sometimes cause infections. Vancomycin is an antibiotic that is used to treat some drug-resistant infections caused by enterococci. In some instances, enterococci have become resistant to this drug and thus are called vancomycin-resistant enterococci (VRE). Most VRE infections occur in hospitals. Top of page What types of infections does VRE cause? VRE can live in the human intestines and female genital tract without causing disease (often called colonization). However, sometimes it can cause infections of the urinary tract, the bloodstream, or of wounds associated with catheters or surgical procedures. Top of page Are certain people at risk of getting VRE? The following persons are at increased risk becoming infected with VRE: People who have been previously treated with the antibiotic vancomycin or other antibiotics for long periods of time. People who are hospitalized, particularly when they receive antibiotic treatment for long periods of time. People with weakened immune systems such as patients in intensive care units, or in cancer or transplant wards. People who have undergone surgical procedures such as abdominal or chest surgery. People with medical devices that stay in for some time such as urinary catheters or central intravenous (IV) catheters. People who are colonized with VRE. Top of page What is the treatment for VRE? People with colonized VRE (bacteria are present, but have no symptoms of an infection)  do not need treatment. Most VRE infections can be treated with antibiotics other than vancomycin. Laboratory testing of the VRE can determine which antibiotics will work. For people who get VRE infections in their bladder and have urinary catheters, removal of the catheter when it is no longer needed can also help get rid of the infection. Top of page How is VRE spread? VRE is often passed from person to person by the contaminated hands of caregivers. VRE can get onto a caregiver's hands after they have contact with other people with VRE or after contact with contaminated surfaces. VRE can also be spread directly to people after they touch surfaces that are contaminated with VRE. VRE is not spread through the air by coughing or sneezing. Top of page How can patients prevent the spread of VRE? If a patient or someone in their household has VRE, the following are some things they can do to prevent the spread of VRE: Keep their hands clean. Always wash their hands thoroughly after using the bathroom and before preparing food. Clean their hands after contact with persons who have VRE. Wash with soap and water (particularly when visibly soiled) or use alcohol-based hand rubs. Frequently clean areas of the home, such as bathrooms, that may become contaminated with VRE. Wear gloves if hands may come in contact with body fluids that may contain VRE, such as stool or bandages from infected wounds. Always wash their hands after removing gloves. If someone has VRE, be sure to tell healthcare providers so that they are aware of the infection. Healthcare facilities use special precautions to help prevent the spread of VRE to others. Top of page What should patients do if they think they have vancomycin-resistant enterococci (VRE)? Anyone who thinks they have VRE must talk with their healthcare provider. Top of page Recommendations and Guidelines For more information about prevention and treatment of HAIs, see the resources below: Siegel JD, Rhinehart E, Jackson M, et al. The Healthcare Infection Control Practices Advisory Committee (HICPAC). Management of Multidrug-Resistant Organisms In Healthcare Settings, 2006"}
{"_id":"f97c8bb3-5de4-495f-b71e-cdb834d21536","text":"On this Page General Information What is vancomycin-resistant enterococci? What types of infections does vancomycin-resistant enterococci cause? Are certain people at risk of getting vancomycin-resistant enterococci? What is the treatment for vancomycin-resistant enterococci? How is vancomycin-resistant enterococci spread? How can patients prevent the spread of vancomycin-resistant enterococci? What should a patient do if they think they have vancomycin-resistant enterococci? Recommendations and Guidelines General Information For more images of this bacterium, search the Public Health Image Library What is vancomycin-resistant enterococci? Enteroccocci are bacteria that are normally present in the human intestines and in the female genital tract and are often found in the environment. These bacteria can sometimes cause infections. Vancomycin is an antibiotic that is used to treat some drug-resistant infections caused by enterococci. In some instances, enterococci have become resistant to this drug and thus are called vancomycin-resistant enterococci (VRE). Most VRE infections occur in hospitals. Top of page What types of infections does VRE cause? VRE can live in the human intestines and female genital tract without causing disease (often called colonization). However, sometimes it can cause infections of the urinary tract, the bloodstream, or of wounds associated with catheters or surgical procedures. Top of page Are certain people at risk of getting VRE? The following persons are at increased risk becoming infected with VRE: People who have been previously treated with the antibiotic vancomycin or other antibiotics for long periods of time. People who are hospitalized, particularly when they receive antibiotic treatment for long periods of time. People with weakened immune systems such as patients in intensive care units, or in cancer or transplant wards. People who have undergone surgical procedures such as abdominal or chest surgery. People with medical devices that stay in for some time such as urinary catheters or central intravenous (IV) catheters. People who are colonized with VRE. Top of page What is the treatment for VRE? People with colonized VRE (bacteria are present, but have no symptoms of an infection)  do not need treatment. Most VRE infections can be treated with antibiotics other than vancomycin. Laboratory testing of the VRE can determine which antibiotics will work. For people who get VRE infections in their bladder and have urinary catheters, removal of the catheter when it is no longer needed can also help get rid of the infection. Top of page How is VRE spread? VRE is often passed from person to person by the contaminated hands of caregivers. VRE can get onto a caregiver's hands after they have contact with other people with VRE or after contact with contaminated surfaces. VRE can also be spread directly to people after they touch surfaces that are contaminated with VRE. VRE is not spread through the air by coughing or sneezing. Top of page How can patients prevent the spread of VRE? If a patient or someone in their household has VRE, the following are some things they can do to prevent the spread of VRE: Keep their hands clean. Always wash their hands thoroughly after using the bathroom and before preparing food. Clean their hands after contact with persons who have VRE. Wash with soap and water (particularly when visibly soiled) or use alcohol-based hand rubs. Frequently clean areas of the home, such as bathrooms, that may become contaminated with VRE. Wear gloves if hands may come in contact with body fluids that may contain VRE, such as stool or bandages from infected wounds. Always wash their hands after removing gloves. If someone has VRE, be sure to tell healthcare providers so that they are aware of the infection. Healthcare facilities use special precautions to help prevent the spread of VRE to others. Top of page What should patients do if they think they have vancomycin-resistant enterococci (VRE)? Anyone who thinks they have VRE must talk with their healthcare provider. Top of page Recommendations and Guidelines For more information about prevention and treatment of HAIs, see the resources below: Siegel JD, Rhinehart E, Jackson M, et al. The Healthcare Infection Control Practices Advisory Committee (HICPAC). Management of Multidrug-Resistant Organisms In Healthcare Settings, 2006"}
{"_id":"fa17263a-c526-4c70-835f-b17389027d92","text":"Transmission to humans may occur after a tick bite or contact with an infected animal, most importantly a sick or recently dead monkey. No person-to-person transmission has been described. \n \nLarge animals such as goats, cows, and sheep may become infected with KFD but play a limited role in the transmission of the disease. These animals provide the blood meals for ticks and it is possible for infected animals with viremia to infect other ticks, but transmission of KFDV to humans from these larger animals is extremely rare. Furthermore, there is no evidence of disease transmission via the unpasteurized milk of any of these animals."}
{"_id":"89cbc4ed-4ab1-418b-8267-bf951c1f0d87","text":"After an incubation period of 3-8 days, the symptoms of KFD begin suddenly with chills, fever, and headache. Severe muscle pain with vomiting, gastrointestinal symptoms and bleeding problems may occur 3-4 days after initial symptom onset. Patients may experience abnormally low blood pressure, and low platelet, red blood cell, and white blood cell counts. \n                \nAfter 1-2 weeks of symptoms, some patients recover without complication. However, the illness is biphasic for a subset of patients (10-20%) who experience a second wave of symptoms at the beginning of the third week. These symptoms include fever and signs of neurological manifestations, such as severe headache, mental disturbances, tremors, and vision deficits. \n                \nThe estimated case-fatality rate is from 3 to 5% for KFD."}
{"_id":"c4560df3-3f80-420f-8363-b15fd5c850a2","text":"KFD has historically been limited to the western and central districts of Karnataka State, India. However, in November 2012, samples from humans and monkeys tested positive for KFDV in the southernmost district of the State which neighbors Tamil Nadu State and Kerala State, indicating the possibility of wider distribution of KFDV. Additionally, a virus very similar to KFD virus (Alkhurma hemorrhagic fever virus) has been described in Saudi Arabia. \n                \nPeople with recreational or occupational exposure to rural or outdoor settings (e.g., hunters, herders, forest workers, farmers) within Karnataka State are potentially at risk for infection by contact with infected ticks. Seasonality is another important risk factor as more cases are reported during the dry season, from November through June."}
{"_id":"c9dfaf6b-4791-4224-9f58-1297010b3a72","text":"Diagnosis can be made in the early stage of illness by molecular detection by PCR or virus isolation from blood. Later, serologic testing using enzyme-linked immunosorbent serologic assay (ELISA) can be performed."}
{"_id":"07bac4cf-160f-4d57-b009-1e8fe62487a3","text":"There is no specific treatment for KFD, but early hospitalization and supportive therapy is important. Supportive therapy includes the maintenance of hydration and the usual precautions for patients with bleeding disorders."}
{"_id":"6b0a677b-0fac-417e-bcf5-3a44600cb5f3","text":"A vaccine does exist for KFD and is used in endemic areas of India. Additional preventative measures include insect repellents and wearing protective clothing in areas where ticks are endemic."}
{"_id":"957f53f2-b27a-4e0a-9123-5816b9cc47e3","text":"Cyclospora cayetanensis is a parasite composed of one cell, too small to be seen without a microscope. This parasite causes an intestinal infection called cyclosporiasis."}
{"_id":"8057c474-9189-4b79-bf98-da6b9f12878a","text":"People become infected with Cyclospora by ingesting sporulated oocysts, which are the infective form of the parasite. This most commonly occurs when food or water contaminated with feces is consumed. An infected person sheds unsporulated (immature, non-infective) Cyclospora oocysts in the feces. The oocysts are thought to require days to weeks in favorable environmental conditions to sporulate (become infective). Therefore, direct person-to-person transmission is unlikely, as is transmission via ingestion of newly contaminated food or water.\n    \nMore on: Cyclospora Biology\n    Geographic Distribution\n    \nCyclosporiasis occurs in many countries, but it seems to be most common in tropical and subtropical regions. In areas where cyclosporiasis has been studied, the risk for infection is seasonal. However, no consistent pattern has been identified regarding the time of year or the environmental conditions, such as temperature or rainfall.\n    \nIn the United States, foodborne outbreaks of cyclosporiasis since the mid-1990s have been linked to various types of imported fresh produce, including raspberries, basil, snow peas, and mesclun lettuce; no commercially frozen or canned produce has been implicated.\n    \nU.S. cases of infection also have occurred in persons who traveled to Cyclospora-endemic areas. To reduce the risk for infection, travelers should take precautions, such as those recommended in CDC's Health Information for International Travel (Yellow Book). Travelers also should be aware that treatment of water or food with chlorine or iodine is unlikely to kill Cyclospora oocysts."}
{"_id":"3944c84e-d837-4277-bb09-e75a3ae615d3","text":"Clinical Diagnosis\n    \nHealth care providers should consider Cyclospora as a potential cause of prolonged diarrheal illness, particularly in patients with a history of recent travel to Cyclospora-endemic areas. Testing for Cyclospora is not routinely done in most U.S. laboratories, even when stool is tested for parasites. Therefore, if indicated, health care providers should specifically request testing for Cyclospora.\n    \nMore on: Resources for Health Professionals: Diagnosis\n    Laboratory Diagnosis\n    \nCyclospora infection is diagnosed by examining stool specimens. Diagnosis can be difficult in part because even persons who are symptomatic might not shed enough oocysts in their stool to be readily detectable by laboratory examinations. Therefore, patients might need to submit several specimens collected on different days.\n    \nSpecial techniques, such as acid-fast staining, are often used to make Cyclospora oocysts more visible under the microscope. In addition, Cyclospora oocysts are autofluorescent, meaning that when stool containing the parasite is viewed under an ultraviolet (UV) fluorescence microscope the parasite appears blue or green against a black background. Molecular diagnostic methods, such as polymerase chain reaction (PCR) analysis, are used to look for the parasite's DNA in the stool.\n    \nMore on: Key points for the laboratory diagnosis of cyclosporiasis"}
{"_id":"16e8b9c7-f819-4e82-8b0d-d9dc5d7ad5a2","text":"Trimethoprim\/sulfamethoxazole (TMP\/SMX), sold under the trade names Bactrim*, Septra*, and Cotrim*, is the usual therapy for Cyclospora infection. No highly effective alternative antibiotic regimen has been identified yet for patients who do not respond to the standard treatment or have a sulfa allergy.\n    \nMore on: Resources for Health Professionals: Treatment\n    \nMost people who have healthy immune systems will recover without treatment. If not treated, the illness may last for a few days to a month or longer. Symptoms may seem to go away and then return one or more times (relapse). Anti-diarrheal medicine may help reduce diarrhea, but a health care provider should be consulted before such medicine is taken. People who are in poor health or who have weakened immune systems may be at higher risk for severe or prolonged illness.\n    \nMore on: Resources for Health Professionals FAQs\n    \n* Use of trade names is for identification only and does not imply endorsement by the Public Health Service or by the U.S. Department of Health and Human Services."}
{"_id":"2c8ab7ac-9733-4bce-834b-a137a06ef267","text":"On the basis of the currently available information, avoiding food or water that may have been contaminated with feces is the best way to prevent cyclosporiasis. Treatment with chlorine or iodine is unlikely to kill Cyclospora oocysts. No vaccine for cyclosporiasis is available.\n    \nThe U.S. Food and Drug Administration's (FDA) Center for Food Safety and Applied Nutrition (CFSAN) publishes detailed food safety recommendations for growers and suppliers. In its Guide to Minimize Microbial Food Safety Hazards for Fresh Fruits and Vegetables, CFSAN describes good agricultural practices (GAPs) and good manufacturing practices (GMPs) for fresh fruits and vegetables. The guidelines address the growing, harvesting, sorting, packaging, and storage processes; following the guidelines can help reduce the overall risk for microbial contamination during these processes. The precise ways that food and water become contaminated with Cyclospora oocysts are not fully understood.\n    \nCDC monitors the occurrence of cyclosporiasis in the United States and helps state health departments identify and investigate cyclosporiasis outbreaks to prevent additional cases of illness.\n    \nMore on: Surveillance and Outbreak Response"}
{"_id":"b822cc94-589e-46d4-8129-005b8f2bf97c","text":"Trichinellosis, also called trichinosis, is caused by eating raw or undercooked meat of animals infected with the larvae of a species of worm called Trichinella. Infection occurs commonly in certain wild carnivorous (meat-eating) animals such as bear or cougar, or omnivorous (meat and plant-eating) animals such as domestic pigs or wild boar."}
{"_id":"75f16dfa-73aa-4989-8c9e-bb621102e32f","text":"People acquire trichinellosis by consuming raw or undercooked meat infected with the Trichinella parasite, particularly wild game meat or pork. Even tasting very small amounts of undercooked meat during preparation or cooking puts you at risk for infection. Outbreaks occur in settings where multiple people consume the same Trichinella-infected meat.\nWorldwide, an estimated 10,000 cases of trichinellosis occur every year. Several different species of Trichinella can cause human disease; the most common species is Trichinella spiralis, which has a global distribution and is the species most commonly found in pigs. Other Trichinella species are less commonly reported as the cause of human disease and may be found in different parts of the world, usually infecting wild animals.\nIn the United States, trichinellosis cases are reported to CDC much less commonly now than in the past (Figure 1). During the late 1940s, when the U.S. Public Health Service began counting cases of trichinellosis, 400 cases in the United States were recorded each year on average. During 2008-2010, 20 cases were reported to CDC each year on average. The overall number of cases reported has decreased because of improved pig-raising practices in the pork industry, commercial and home freezing of pork, and public awareness of the danger of eating raw or undercooked meat products. The number of cases associated with raw or undercooked wild game meats has remained relatively constant over time (Figure 2). Over the past 40 years, few cases of trichinellosis have been reported in the United States, and the risk of trichinellosis from commercially raised and properly prepared pork is very low. However, eating undercooked wild game, particularly bear meat, puts one at risk for acquiring this disease."}
{"_id":"0c34eee1-b704-4384-8e99-1e8b2a734a0f","text":"A diagnosis of trichinellosis is made in patients whose signs and symptoms are compatible with trichinellosis, have a positive laboratory test for Trichinella, and who can recall eating raw or undercooked pork or wild game meat.\n    \nLaboratory diagnosis of Trichinella infection is most often made by a Trichinella antibody test. In some cases a muscle biopsy may be performed.\n    \nMore on: Resources for Health Professionals: Diagnosis"}
{"_id":"affa7bf9-9611-49a5-93c1-282d884dd6fa","text":"Safe and effective prescription drugs are available to treat both Trichinella infection and the symptoms that occur as a result of infection. Treatment should begin as soon as possible; a doctor will make the decision to treat based upon symptoms, exposure to raw or undercooked meat, and laboratory test results.\n    \nMore on: Resources For Health Professionals: Treatment"}
{"_id":"a330f3f8-9947-4ce0-a958-0cf06d998907","text":"- Wash your hands with warm water and soap after handling raw meat.\n    - Curing (salting), drying, smoking, or microwaving meat alone does not consistently kill infective worms; homemade jerky and sausage were the cause of many cases of trichinellosis reported to CDC in recent years.\n    - Freeze pork less than 6 inches thick for 20 days at 5\u00b0F (-15\u00b0C) to kill any worms.\n    - Freezing wild game meats, unlike freezing pork products, may not effectively kill all worms because some worm species that infect wild game animals are freeze-resistant.\n    - Clean meat grinders thoroughly after each use.\n   \n   \nTo help prevent Trichinella infection in animal populations, do not allow pigs or wild animals to eat uncooked meat, scraps, or carcasses of any animals, including rats, which may be infected with Trichinella."}
{"_id":"b729a76e-6b2e-438f-83bd-066c13cad426","text":"Striatonigral degeneration is a neurological disorder caused by a disruption in the connection between two areas of the brain-the striatum and the substantia nigra. These two areas work together to enable balance and movement. Striatonigral degeneration is a type of multiple system atrophy (MSA). Symptoms of the disorder resemble some of those seen in Parkinson's disease, including rigidity, instability, impaired speech, and slow movements."}
{"_id":"607100f2-2245-42f2-9a88-995476496bc5","text":"There is no cure for striatonigral degeneration, and treatments for the disorder have variable success. Treatments used for Parkinson's disease are recommended. However, unlike Parkinson's disease, striatonigral degeneration is not responsive to levodopa. Dopamine and anticholinergics provide some benefit. Generally, treatment is reevaluated as the disorder progresses."}
{"_id":"4ecba8c1-385b-4a86-ae2b-4f6ef472b4eb","text":"Striatonigral degeneration progresses slowly. Some patients have normal life expectancy."}
{"_id":"9c904fa6-d388-400d-b952-f956ad2a0ef7","text":"The NINDS supports and conducts research on disorders of the brain and nervous system such as striatonigral degeneration. This research focuses on finding ways to prevent and treat these disorders."}
{"_id":"88d0a80c-b47c-499f-bf7f-15cbefadd686","text":"Empty Sella Syndrome (ESS) is a disorder that involves the sella turcica, a bony structure at the base of the brain that surrounds and protects the pituitary gland. ESS is often discovered during radiological imaging tests for pituitary disorders. ESS occurs n up to 25 percent of the population.An individual with ESS may have no symptoms or may have symptoms resulting from partial or complete loss of pituitary function (including headaches, low sex drive, and impotence).There are two types of ESS: primary and secondary. Primary ESS happens when a small anatomical defect above the pituitary gland allows spinal fluid to partially or completely fill the sella turcica. This causes the gland to flatten out along the interior walls of the sella turcica cavity. Individuals with primary ESS may have high levels of the hormone prolactin, which can interfere with the normal function of the testicles and ovaries. Primary ESS is most common in adults and women, and is often associated with obesity and high blood pressure. In some instances the pituitary gland may be smaller than usual; this may be due to a condition called pseudotumor cerebri (which means \"false brain tumor,\" brought on by high pressure within the skull), In rare instances this high fluid pressure can be associated with drainage of spinal fluid through the nose. Secondary ESS is the result of the pituitary gland regressing within the cavity after an injury, surgery, or radiation therapy. Individuals with secondary ESS can sometimes have symptoms that reflect the loss of pituitary functions, such as the ceasing of menstrual periods, infertility, fatigue, and intolerance to stress and infection. In children, ESS may be associated with early onset of puberty, growth hormone deficiency, pituitary tumors, or pituitary gland dysfunction. Magnetic resonance imaging (MRI) scans are useful in evaluating ESS and for identifying underlying disorders that may be the cause of high fluid pressure."}
{"_id":"35da6b46-8664-4395-95c4-a39247ceca98","text":"Unless the syndrome results in other medical problems, treatment for endocrine dysfunction associated with pituitary malfunction is symptomatic and supportive. Individuals with primary ESS who have high levels of prolactin may be given bromocriptine. In some cases, particularly when spinal fluid drainage is observed, surgery may be needed."}
{"_id":"7b8e7ef4-c71b-441b-9784-9b700af89003","text":"ESS is not a life-threatening condition. Most often, and particularly among those with primary ESS, the disorder does not cause health problems and does not affect life expectancy."}
{"_id":"61651d56-86d3-446b-8d62-010977459cb9","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. The NINDS supports and conducts fundamental studies that explore the complex mechanisms of normal brain development and to better understand neurological conditions such as ESS. The knowledge gained from these fundamental studies helps researchers understand neurodevelopment and provides opportunities to more effectively treat and perhaps even prevent, such disorders."}
{"_id":"7cff5e3e-d1fa-4a07-b976-f23e45efd6d1","text":"Primary lateral sclerosis (PLS) is a rare neuromuscular disease with slowly progressive weakness in voluntary muscle movement. PLS belongs to a group of disorders known as motor neuron diseases. PLS affects the upper motor neurons (also called corticospinal neurons) in the arms, legs, and face. It occurs when nerve cells in the motor regions of the cerebral cortex (the thin layer of cells covering the brain which is responsible for most higher level mental functions) gradually degenerate, causing movements to be slow and effortful. The disorder often affects the legs first, followed by the body, trunk, arms and hands, and, finally the bulbar muscles (muscles that control speech, swallowing, and chewing). Symptoms include weakness, muscle stiffness and spasticity, clumsiness, slowing of movement, and problems with balance and speech. PLS is more common in men than in women, with a varied gradual onset that generally occurs between ages 40 and 60. PLS progresses gradually over a number of years, or even decades. Scientists do not believe PLS has a simple hereditary cause. The diagnosis of PLS requires extensive testing to exclude other diseases. When symptoms begin, PLS may be mistaken for amyotrophic lateral sclerosis (ALS) or spastic paraplegia. Most neurologists follow an affected individual's clinical course for at least 3 to 4 years before making a diagnosis of PLS.."}
{"_id":"0ba99234-111f-46d3-a273-f12708bba4cc","text":"Treatment for individuals with PLS is symptomatic. Muscle relaxants such as baclofen, tizanidine, and the benzodiazepines may reduce spasticity. Other drugs may relieve pain and antidepressants can help treat depression. Physical therapy, occupational therapy, and rehabilitation may prevent joint immobility and slow muscle weakness and atrophy. Assistive devices such as supports or braces, speech synthesizers, and wheelchairs ma help some people retain independence.. Speech therapy may be useful for those with involvement of the facial muscles."}
{"_id":"3532ba51-103a-490a-a299-0dd61716eb0d","text":"PLS is not fatal. There is no cure and the progression of symptoms varies. Some people may retain the ability to walk without assistance, but others eventually require wheelchairs, canes, or other assistive devices."}
{"_id":"19b05a8e-e225-4b1e-bc67-44bfc0a86a77","text":"The NINDS conducts a broad range of research on neuromuscular disorders such as PLS. This research is aimed at developing techniques to diagnose, treat, prevent, and ultimately cure these devastating diseases."}
{"_id":"fb60593b-cbd2-4c9a-9d53-c3beae8be159","text":"The dystonias are movement disorders in which sustained muscle contractions cause twisting and repetitive movements or abnormal postures. The movements, which are involuntary and sometimes painful, may affect a single muscle; a group of muscles such as those in the arms, legs, or neck; or the entire body. Early symptoms may include deterioration in handwriting, foot cramps, or a dragging foot after running or walking some distance. Other possible symptoms are tremor and voice or speech difficulties. About half the cases of dystonia have no connection to disease or injury and are called primary or idiopathic dystonia. Of the primary dystonias, many cases appear to be inherited. Dystonias can also be symptoms of other diseases, some of which may be hereditary. Dystonia can occur at any age, but is often described as either early, or childhood, onset versus adult onset."}
{"_id":"9fc57c0a-619d-4d24-bc89-1dcd9e169ca9","text":"No one treatment has been found to be universally effective. Instead, doctors use a variety of therapies (medications, surgery, and other treatments such as physical therapy, splinting, stress management, and biofeedback) aimed at reducing or eliminating muscle spasms and pain. Since response to drugs varies among individuals and even in the same person over time, the most effective therapy is often individualized."}
{"_id":"cb13ef5f-bda3-4c5a-9456-20c698ff4e02","text":"The initial symptoms can be very mild and may be noticeable only after prolonged exertion, stress, or fatigue. Dystonias often progress through various stages. Initially, dystonic movements are intermittent and appear only during voluntary movements or stress. Later, individuals may show dystonic postures and movements while walking and ultimately even while they are relaxed. Dystonic motions may lead to permanent physical deformities by causing tendons to shorten."}
{"_id":"5f219bd8-2ac0-4fb0-879f-da6387f25c9f","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to dystonia in its laboratories at the National Institutes of Health (NIH) and also supports additional dystonia research through grants to major research institutions across the country. Scientists at other NIH Institutes (National institute on Deafness and Other Communications Disorders, National Eye Institute, and Eunice Kennnedy Shriver National Institute on Child Health and Human Development) also support research that may benefit individuals with dystonia. Investigators believe that the dystonias result from an abnormality in an area of the brain called the basal ganglia, where some of the messages that initiate muscle contractions are processed. Scientists at the NINDS laboratories have conducted detailed investigations of the pattern of muscle activity in persons with dystonias. Studies using EEG analysis and neuroimaging are probing brain activity. The search for the gene or genes responsible for some forms of dominantly inherited dystonias continues."}
{"_id":"ce1b6c96-d08c-43d6-8b32-9edec1376843","text":"Farbers disease, also known as Farber's lipogranulomatosis, describes a group of inherited metabolic disorders called lipid storage diseases, in which excess amounts of lipids (oils, fatty acids, and related compounds) build up to harmful levels in the joints, tissues, and central nervous system. The liver, heart, and kidneys may also be affected. Disease onset is typically seen in early infancy but may occur later in life. Symptoms of the classic form may have moderately impaired mental ability and difficulty with swallowing. Other symptoms may include chronic shortening of muscles or tendons around joints. arthritis, swollen lymph nodes and joints, hoarseness, nodules under the skin (and sometimes in the lungs and other parts of the body), and vomiting. Affected persons may require the insertion of a breathing tube. In severe cases, the liver and spleen are enlarged. Farber's disease is caused by a deficiency of the enzyme ceramidase. The disease occurs when both parents carry and pass on the defective gene that regulates the protein sphingomyelin. Children born to these parents have a 25 percent chance of inheriting the disorder and a 50 percent chance of carrying the faulty gene. The disorder affects both males and females."}
{"_id":"fbb47524-8fbd-4fee-a28c-34329c55d1f2","text":"Currently there is no specific treatment for Farbers disease. Corticosteroids may help relieve pain. Bone marrow transplants may improve granulomas (small masses of inflamed tissue) on individuals with little or no lung or nervous system complications. Older persons may have granulomas surgically reduced or removed."}
{"_id":"0b442981-f362-4714-afa4-81e06f304e86","text":"Most children with the classic form of Farbers disease die by age 2, usually from lung disease. Children born with the most severe form of the disease usually die within 6 months, while individuals having a milder form of the disease may live into their teenage years or young adulthood."}
{"_id":"ef426c59-120a-4116-b47f-a46032ddc306","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. Research funded by the NINDS focuses on better understanding of how neurological deficits arise in lipid storage diseases and on the development of new treatments targeting disease mechanisms, including gene therapies, cell-based therapies and pharmacological approaches. The NINDS, along with other Institutes and Centers at the National Institutes of Health, supports the Lysosomal Disease network of centers that addresses some of the major challenges in the diagnosis, management, and therapy of rare diseases, including the lipid storage diseases.Research on lipid storage diseases within the Network includes longitudinal studies of the natural history and\/or treatment of these disorders. Additional studies will emphasize the quantitative analysis of the central nervous system structure and function, and develop biomarkers (signs that can indicate the diagnosis or progression of a disease) for these disorders."}
{"_id":"5afa3ebc-bb3f-4d86-9f80-7650707723fc","text":"Familial periodic paralyses are a group of inherited neurological disorders caused by mutations in genes that regulate sodium and calcium channels in nerve cells. They are characterized by episodes in which the affected muscles become slack, weak, and unable to contract. Between attacks, the affected muscles usually work as normal.\n                \nThe two most common types of periodic paralyses are: Hypokalemic periodic paralysis is characterized by a fall in potassium levels in the blood. In individuals with this mutation attacks often begin in adolescence and are triggered by strenuous exercise, high carbohydrate meals, or by injection of insulin, glucose, or epinephrine. Weakness may be mild and limited to certain muscle groups, or more severe and affect the arms and legs. Attacks may last for a few hours or persist for several days. Some patients may develop chronic muscle weakness later in life. Hyperkalemic periodic paralysis is characterized by a rise in potassium levels in the blood. Attacks often begin in infancy or early childhood and are precipitated by rest after exercise or by fasting. Attacks are usually shorter, more frequent, and less severe than the hypokalemic form. Muscle spasms are common."}
{"_id":"b3ab9dc9-45ce-4589-801f-addb31b71a47","text":"Treatment of the periodic paralyses focuses on preventing further attacks and relieving acute symptoms. Avoiding carbohydrate-rich meals and strenuous exercise, and taking acetazolamide daily may prevent hypokalemic attacks. Attacks can be managed by drinking a potassium chloride oral solution. Eating carbohydrate-rich, low-potassium foods, and avoiding strenuous exercise and fasting, can help prevent hyperkalemic attacks. Dichorphenamide may prevent attacks."}
{"_id":"410c91b0-1ed3-4c00-be1e-3f23f8377fd5","text":"The prognosis for the familial periodic paralyses varies. Chronic attacks may result in progressive weakness that persists between attacks. Some cases respond well to treatment, which can prevent or reverse progressive muscle weakness."}
{"_id":"ee31a07b-b846-4b1e-8939-4e7dd6f08677","text":"The NINDS conducts and supports research on neuromuscular disorders such as the familial periodic paralyses. These studies are aimed at increasing knowledge about these disorders and finding ways to prevent, treat, and cure them."}
{"_id":"5d13b1f8-6528-4db1-a519-712a8a562ca9","text":"A spinal cord injury usually begins with a sudden, traumatic blow to the spine that fractures or dislocates vertebrae. The damage begins at the moment of injury when displaced bone fragments, disc material, or ligaments bruise or tear into spinal cord tissue. Most injuries to the spinal cord don't completely sever it. Instead, an injury is more likely to cause fractures and compression of the vertebrae, which then crush and destroy axons -- extensions of nerve cells that carry signals up and down the spinal cord between the brain and the rest of the body. An injury to the spinal cord can damage a few, many, or almost all of these axons. Some injuries will allow almost complete recovery. Others will result in complete paralysis."}
{"_id":"3b1fc35c-0395-46e9-833d-c52be31be1d7","text":"Improved emergency care for people with spinal cord injuries and aggressive treatment and rehabilitation can minimize damage to the nervous system and even restore limited abilities. Respiratory complications are often an indication of the severity of spinal cord injury About one-third of those with injury to the neck area will need help with breathing and require respiratory support. The steroid drug methylprednisolone appears to reduce the damage to nerve cells if it is given within the first 8 hours after injury. Rehabilitation programs combine physical therapies with skill-building activities and counseling to provide social and emotional support.Electrical simulation of nerves by neural prosthetic devices may restore specific functions, including bladder, breathing, cough, and arm or leg movements, though eligibility for use of these devices depends on the level and type of the spinal cord injury."}
{"_id":"02b7d656-aec2-44bb-af3e-c841fcc71987","text":"Spinal cord injuries are classified as either complete or incomplete. An incomplete injury means that the ability of the spinal cord to convey messages to or from the brain is not completely lost. People with incomplete injuries retain some motor or sensory function below the injury. A complete injury is indicated by a total lack of sensory and motor function below the level of injury. People who survive a spinal cord injury will most likely have medical complications such as chronic pain and bladder and bowel dysfunction, along with an increased susceptibility to respiratory and heart problems. Successful recovery depends upon how well these chronic conditions are handled day to day.\n                \nSurgery to relieve compression of the spinal tissue by surrounding bones broken or dislocated by the injury is often necessary, through timing of such surgery may vary widely. A recent prospective multicenter trial called STASCIS is exploring whether performing decompression surgery early (less than 24 hours following injury) can improve outcomes for patients with bone fragments or other tissues pressing on the spinal cord."}
{"_id":"6c0b5bb6-8acd-4a1d-85c9-a0bfc2908ad6","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts spinal cord research in its laboratories at the National Institutes of Health (NIH) and also supports additional research through grants to major research institutions across the country. Advances in research are giving doctors and patients hope that repairing injured spinal cords is a reachable goal. Advances in basic research are also being matched by progress in clinical research, especially in understanding the kinds of physical rehabilitation that work best to restore function. Some of the more promising rehabilitation techniques are helping spinal cord injury patients become more mobile."}
{"_id":"1a0692fe-05e7-48ff-8b9b-44ec1376ebab","text":"Todd's paralysis is a neurological condition experienced by individuals with epilepsy, in which a seizure is followed by a brief period of temporary paralysis. The paralysis may be partial or complete but usually occurs on just one side of the body. The paralysis can last from half an hour to 36 hours, with an average of 15 hours, at which point it resolves completely. Todd's paralysis may also affect speech and vision. Scientists don't know what causes Todd's paralysis. Current theories propose biological processes in the brain that involve a slow down in either the energy output of neurons or in the motor centers of the brain. It is important to distinguish Todd's paralysis from a stroke, which it can resemble, because a stroke requires completely different treatment."}
{"_id":"97bafd48-0d63-4e28-80b6-a0ffc0ca1161","text":"There is no treatment for Todd's paralysis. Individuals must rest as comfortably as possible until the paralysis disappears."}
{"_id":"211e29d2-9607-4409-900e-37b6adef0e9f","text":"Todd's paralysis is an indication that an individual has had an epileptic seizure. The outcome depends on the effects of the seizure and the subsequent treatment of the epilepsy."}
{"_id":"914db1b5-1fe7-4e62-ad43-7d81ef82e201","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to Todd's paralysis in its clinics and laboratories at The National Institutes of Health (NIH), and supports additional research through grants to major medical institutions across the country. Much of this research focuses on finding successful methods to prevent Todd's paralysis in individuals with epilepsy."}
{"_id":"5fbeb7a5-3193-4f1b-80e8-3e70b7ee1308","text":"Syncope is a medical term used to describe a temporary loss of consciousness due to the sudden decline of blood flow to the brain. Syncope is commonly called fainting or passing out. If an individual is about to faint, he or she will feel dizzy, lightheaded, or nauseous and their field of vision may white out or black out. The skin may be cold and clammy. The person drops to the floor as he or she loses consciousness. After fainting, an individual may be unconscious for a minute or two, but will revive and slowly return to normal. Syncope can occur in otherwise healthy people and affects all age groups, but occurs more often in the elderly.\n                \nVasovagal\n                \nCarotid sinus\n                \nSituational"}
{"_id":"6230693a-1b4e-44ca-84e6-68e94e4d9f8c","text":"The immediate treatment for an individual who has fainted involves checking first to see if their airway is open and they are breathing. The person should remain lying down for at least 10-15 minutes, preferably in a cool and quiet space. If this isnt possible, have the individual sit forward and lower their head below their shoulders and between their knees. Ice or cold water in a cup is refreshing. For individuals who have problems with chronic fainting spells, therapy should focus on recognizing the triggers and learning techniques to keep from fainting. At the appearance of warning signs such as lightheadedness, nausea, or cold and clammy skin, counter-pressure maneuvers that involve gripping fingers into a fist, tensing the arms, and crossing the legs or squeezing the thighs together can be used to ward off a fainting spell. If fainting spells occur often without a triggering event, syncope may be a sign of an underlying heart disease."}
{"_id":"91694e10-7a45-42b9-8160-5c3493842dcd","text":"Syncope is a dramatic event and can be life-threatening if not treated properly. Generally, however, people recover completely within minutes to hours. If syncope is symptomatic of an underlying condition, then the prognosis will reflect the course of the disorder."}
{"_id":"073d73a4-edbd-46a4-997b-85291839302e","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to syncope in laboratories at the NIH and support additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent and treat syncope."}
{"_id":"efd1be4b-43dc-4461-a161-5ba5a2e14fe8","text":"The term cerebral palsy refers to a group of neurological disorders that appear in infancy or early childhood and permanently affect body movement, muscle coordination, and balance.CP affects the part of the brain that controls muscle movements. The majority of children with cerebral palsy are born with it, although it may not be detected until months or years later.The early signs of cerebral palsy usually appear before a child reaches 3 years of age.The most common are a lack of muscle coordination when performing voluntary movements (ataxia); stiff or tight muscles and exaggerated reflexes (spasticity); walking with one foot or leg dragging; walking on the toes, a crouched gait, or a scissored gait; and muscle tone that is either too stiff or too floppy.Other neurological symptoms that commonly occur in individuals with CP include seizures, hearing loss and impaired vision, bladder and bowel control issues, and pain and abnormal sensations. A small number of children have CP as the result of brain damage in the first few months or years of life, brain infections such as bacterial meningitis or viral encephalitis, or head injury from a motor vehicle accident, a fall, or child abuse. The disorder isn't progressive, meaning that the brain damage typically doesn't get worse over time. Risk factors associated with CP do not cause the disorder but can increase a child's chance of being born with the disorder.CP is not hereditary."}
{"_id":"8ff52570-f102-4cf4-8ace-8be7eaa0f26f","text":"Cerebral palsy cant be cured, but treatment will often improve a child's capabilities. In general, the earlier treatment begins the better chance children have of overcoming developmental disabilities or learning new ways to accomplish the tasks that challenge them.Early intervention, supportive treatments, medications, and surgery can help many individuals improve their muscle control. Treatment may include physical and occupational therapy, speech therapy, drugs to control seizures, relax muscle spasms, and alleviate pain; surgery to correct anatomical abnormalities or release tight muscles; braces and other orthotic devices; wheelchairs and rolling walkers; and communication aids such as computers with attached voice synthesizers."}
{"_id":"46d84603-423e-4b62-b479-2fad37671fa5","text":"Cerebral palsy doesnt always cause profound disabilities and for most people with CP the disorder does not affect life expectancy. Many children with CP have average to above average intelligence and attend the same schools as other children their age. Supportive treatments, medications, and surgery can help many individuals improve their motor skills and ability to communicate with the world..While one child with CP might not require special assistance, a child with severe CP might be unable to walk and need extensive, lifelong care."}
{"_id":"49ddf13c-d23c-4090-83d3-fc4b320e3a83","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease.The NINDS is a component of the National Institutes of Health, the leading supporter of biomedical research in the world. Researchers supported by the NINDS are investigating the roles of mishaps early in brain development, including genetic defects, which are sometimes responsible for the brain malformations and abnormalities that result in cerebral palsy.Scientists are also looking at traumatic events in newborn babies brains, such as bleeding, epileptic seizures, and breathing and circulation problems, which can cause the abnormal release of chemicals that trigger the kind of damage that causes cerebral palsy. NINDS-supported researchers also hope to find ways to prevent white matter disease, the most common cause of cerebral palsy. To make sure children are getting the right kinds of therapies, studies are also being done that evaluate both experimental treatments and treatments already in use so that physicians and parents have valid information to help them choose the best therapy."}
{"_id":"2f90407d-1ac3-44ac-9cdb-4fa53058fede","text":"Tuberous sclerosis (TSC) is a rare genetic disease that causes benign tumors to grow in the brain and on other vital organs such as the kidneys, heart, eyes, lungs, and skin. It usually affects the central nervous system. In addition to the benign tumors that frequently occur in TSC, other common symptoms include seizures,impaired intellectual development, behavior problems, and skin abnormalities. TSC may be present at birth, but signs of the disorder can be subtle and full symptoms may take some time to develop. Three types of brain tumors are associated with TSC: cortical tubers, which generally form on the surface of the brain; subependymal nodules, which form in the walls of the ventricles (the fluid-filled cavities of the brain); and giant-cell astrocytomas, a type of tumor that can block the flow of fluids within the brain."}
{"_id":"54c93c95-c6b8-448e-a0dc-3a80958ea1b1","text":"There is no cure for TSC, although treatment is available for a number of the symptoms. Rapamycin and related drugs are not yet approved by the U.S. Food and Drug Administration (FDA) for any purpose in individuals with TSC. The FDA has approved the drug everolimus (Afinitor) to treat subependymal giant cell astrocytomas (SEGA brain tumors) and angiomyolipoma kidney tumors. Antiepileptic drugs such as vigabatrin may be used to control seizures and medications may be prescribed for behavior problems. Intervention programs, including special schooling and occupational therapy, may benefit individuals with special needs and developmental issues. Surgery, including dermabrasion and laser treatment, may be useful for treatment of skin lesions. Because TSC is a lifelong condition, individuals need to be regularly monitored by a doctor. Due to the many varied symptoms of TSC, care by a clinician experienced with the disorder is recommended."}
{"_id":"7eb7ef51-6a24-4e66-acd5-3ff61c7f9247","text":"The prognosis for individuals with TSC depends on the severity of symptoms. Individuals with mild symptoms generally do well and live long productive lives, while individuals with the more severe form may have serious disabilities. In rare cases, seizures, infections, or tumors in vital organs such as the kidneys and brain can lead to severe complications and even death. However, with appropriate medical care, most individuals with the disorder can look forward to normal life expectancy."}
{"_id":"1368601f-dbc7-464c-aaa0-f3ba4876f35f","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts TSC research in its laboratories at the National Institutes of Health (NIH) and also supports TSC research through grants to major medical institutions across the country. Scientists in one study are learning more about the genes that can cause TSC and the function of the proteins those genes produce. Another study focuses on two major brain disorders --autism and epilepsy -- that occur in children with TSC. Other scientists are trying to determine what causes skin tumors to develop in individuals with TSC and to find the molecular basis of these tumors. Scientists hope knowledge gained from their current research will improve the genetic test for TSC and lead to new avenues of treatment, methods of prevention, and, ultimately, a cure."}
{"_id":"6ecfd957-d97b-4e8b-9bde-1e70e6d8289f","text":"Batten disease is a fatal, inherited disorder of the nervous system that begins in childhood. In some cases, the early signs are subtle, taking the form of personality and behavior changes, slow learning, clumsiness, or stumbling. Symptoms of Batten disease are linked to a buildup of substances called lipopigments in the body's tissues. Lipopigments are made up of fats and proteins. Because vision loss is often an early sign, Batten disease may be first suspected during an eye exam. Often, an eye specialist or other physician may refer the child to a neurologist. Diagnostic tests for Batten disease include blood or urine tests, skin or tissue sampling, an electroencephalogram (EEG), electrical studies of the eyes, and brain scans."}
{"_id":"a935095d-27b4-4fa9-ad84-55c06dc1fc0f","text":"As yet, no specific treatment is known that can halt or reverse the symptoms of Batten disease. However, seizures can sometimes be reduced or controlled with anticonvulsant drugs, and other medical problems can be treated appropriately as they arise. Physical therapy and occupational therapy may help patients retain functioning as long as possible."}
{"_id":"07982901-a9c3-46db-8e9e-3d8073f9db70","text":"Over time, affected children suffer cognitive impairment, worsening seizures, and progressive loss of sight and motor skills. Eventually, children with Batten disease become blind, bedridden, and demented. Batten disease is often fatal by the late teens or twenties."}
{"_id":"e4e78ca4-3bb6-41c8-bc42-14122fe6cbe7","text":"The biochemical defects that underlie several NCLs have recently been discovered. An enzyme called palmitoyl-protein thioesterase has been shown to be insufficiently active in the infantile form of Batten disease (this condition is now referred to as CLN1). In the late infantile form (CLN2), a deficiency of an acid protease, an enzyme that hydrolyzes proteins, has been found as the cause of this condition. A mutated gene has been identified in juvenile Batten disease (CLN3), but the protein for which this gene codes has not been identified. In addition, research scientists are working with NCL animal models to improve understanding and treatment of these disorders. One research team, for example, is testing the usefulness of bone marrow transplantation in a sheep model, while other investigators are working to develop mouse models. Mouse models will make it easier for scientists to study the genetics of these diseases."}
{"_id":"70969d78-92d8-47ba-910d-64d09ff5aa75","text":"Holoprosencephaly is a disorder caused by the failure of the prosencephalon (the embryonic forebrain) to sufficiently divide into the double lobes of the cerebral hemispheres. The result is a single-lobed brain structure and severe skull and facial defects. In most cases of holoprosencephaly, the malformations are so severe that babies die before birth. In less severe cases, babies are born with normal or near-normal brain development and facial deformities that may affect the eyes, nose, and upper lip.\n                \nThere are three classifications of holoprosencephaly. Alobar, in which the brain has not divided at all, is usually associated with severe facial deformities. Semilobar, in which the brain's hemispheres have somewhat divided, causes an intermediate form of the disorder. Lobar, in which there is considerable evidence of separate brain hemispheres, is the least severe form. In some cases of lobar holoprosencephaly the baby's brain may be nearly normal.\n                \nThe least severe of the facial anomalies is the median cleft lip (premaxillary agenesis). The most severe is cyclopia, an abnormality characterized by a single eye located in the area normally occupied by the root of the nose, and a missing nose or a proboscis (a tubular-shaped nose) located above the eye. The least common facial anomaly is ethmocephaly, in which a proboscis separates closely-set eyes. Cebocephaly, another facial anomaly, is characterized by a small, flattened nose with a single nostril situated below incomplete or underdeveloped closely-set eyes."}
{"_id":"2e27bf26-8132-438f-b081-17a3f1432478","text":"There is no standard course of treatment for holoprosencephaly. Treatment is symptomatic and supportive."}
{"_id":"ee59fddd-2842-4e07-97aa-1af50ada5a45","text":"The prognosis for individuals with the disorder depends on the severity of the brain and facial deformities."}
{"_id":"75a670e8-6898-4105-aa04-796b7c4082e4","text":"The NINDS supports and conducts a wide range of studies that focus on identifying and learning more about the factors involved in normal brain development. Recent research has identified specific genes that cause holoprosencephaly. The knowledge gained from these fundamental studies provides the foundation for understanding how to develop new ways to treat, and potentially prevent, this disorder."}
{"_id":"d0dd0d29-feaf-470e-af02-8820c4a8c579","text":"Bell's palsy is a form of temporary facial paralysis resulting from damage or trauma to the 7th cranial nerve, one of the facial nerves. It is the most common cause of facial paralysis. Generally, Bell's palsy affects only one side of the face, however, in rare cases, it can affect both sides. Symptoms usually begin suddenly and reach their peak within 72 hours, and can range in severity from mild weakness to total paralysis. Symptoms vary among individuals and include sudden weakness on one side of the face, drooping eyelid or corner of the mouth, drooling, dry eye or mouth, altered taste, and excessive tearing in the eye. Bells palsy can cause significant facial distortion. The exact cause of Bell's palsy isn't known, but many scientists believe that reactivation of a dormant viral infection can cause the facial nerve to swell and becomes inflamed. Several other conditions can cause facial paralysis that might be diagnosed as Bell's palsy.."}
{"_id":"cf40dc14-e741-44e0-853a-e1c3f2077e22","text":"Steroids such as prednisone -- used to reduce inflammation and swelling -- are an effective treatment for Bell's palsy. Antiviral drugs may have some benefit in shortening the course of the disease. Analgesics such as aspirin, acetaminophen, or ibuprofen may relieve pain. Because of possible drug interactions, individuals should always talk to their doctors before taking any over-the-counter medicines. Keeping the eye moist and protecting it from debris and injury, especially at night, is important. Lubricating eye drops can help. Other therapies such as physical therapy, facial massage or acupuncture may provide a potential small improvement in facial nerve function and pain.."}
{"_id":"27c1eb80-a624-413a-a262-01ad6907d3e5","text":"The prognosis for individuals with Bell's palsy is generally very good. The extent of nerve damage determines the extent of recovery. With or without treatment, most individuals begin to get better within 2 weeks after the initial onset of symptoms and recover some or all facial function within 3 to 6 months."}
{"_id":"17065622-9872-42f1-ad86-f48cdaa9f097","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS conducts and supports an extensive research program of basic science to increase understanding of how the nervous system works and circumstances that lead to nerve damage. Knowledge gained from this research may help scientists find the definitive cause of Bell's palsy, leading to the discovery of new effective treatments for the disorder. Other NINDS-supported research is aimed at developing methods to repair damaged nerves and restore full use and strength to injured areas, and finding ways to prevent nerve damage and injuries from occurring."}
{"_id":"c8c0c895-3fb5-4a14-90fa-8e3417970354","text":"Multiple system atrophy (MSA) is a progressive neurodegenerative disorder characterized by symptoms of autonomic nervous system failure such as fainting spells and bladder control problems, combined with motor control symptoms such as tremor, rigidity, and loss of muscle coordination. MSA affects both men and women primarily in their 50s. Although what causes MSA is unknown, the disorder's symptoms reflect the loss of nerve cells in several different areas in the brain and spinal cord that control the autonomic nervous system and coordinate muscle movements. The loss of nerve cells may be due to the buildup of a protein called alpha-synuclein in the cells that support nerve cells in the brain."}
{"_id":"2900e1b9-d856-4c1c-a270-2de68707b2f0","text":"There is no cure for MSA. Currently, there are no treatments to delay the progress of neurodegeneration in the brain. But there are treatments available to help people cope with some of the more disabling symptoms of MSA. In some individuals, levodopa may improve motor function, but the benefit may not continue as the disease progresses."}
{"_id":"e4541d66-8b30-454e-b4b7-67d2f2b72e0a","text":"The disease tends to advance rapidly over the course of 5 to 10 years, with progressive loss of motor skills, eventual confinement to bed, and death. There is no remission from the disease. There is currently no cure."}
{"_id":"84fc9d8f-0a68-4a9b-ace2-308432807cc5","text":"The NINDS supports research about MSA through grants to major medical institutions across the country. Researchers hope to learn why alpha-synuclein buildup occurs in MSA and Parkinsons disease, and how to prevent it. Drugs that reduce the abnormal alpha-synuclein buildup may be promising treatments for MSA"}
{"_id":"fb9bdbab-2ee3-42b9-87ff-29e2c44e3acc","text":"Giant axonal neuropathy (GAN) is a rare inherited genetic disorder that affects both the central and peripheral nervous systems. The majority of children with GAN will begin to show symptoms of the disease sometime before five years of age. Signs of GAN usually begin in the peripheral nervous system, which controls movement and sensation in the arms, legs, and other parts of the body. The typical symptoms of GAN are clumsiness and muscle weakness that progresses from a waddling gait to a pronounced difficulty in walking. Additional symptoms include numbness or lack of feeling in the arms and legs, seizures, nystagmus (rapid back and forth movement of the eyes), and impaired cognitive development. A characteristic sign of the disease is dull, tightly curled hair that is markedly different from the parents in color and texture.\n                \nResearchers have discovered more than 20 different mutations associated with GAN in a gene, GAN1, which makes a protein called gigaxonin. These mutations disrupt the regulation or production of gigaxonin in the nervous system. As a result, axons, which are the long tails of neurons that allow them to communicate with other nerve cells, swell up with tangled filaments and become abnormally large. Eventually these axons deteriorate and cause problems with movement and sensation since neurons are no longer able to communicate with each other.\n                \nDoctors diagnose GAN by using several tests, including one that measures nerve conduction velocity, a brain MRI, and a peripheral nerve biopsy (in which a bit of tissue from a peripheral nerve is removed and examined to look for swollen axons). A definitive diagnosis using genetic testing is available on a research basis only.\n                \nGAN is inherited in an autosomal recessive pattern, which means that both parents of a child with GAN have to carry a copy of the mutated gene. Parents, typically, will show no signs of the disease."}
{"_id":"37c003eb-6c9f-4f1f-a3ad-627605d7b06a","text":"Treatment is symptomatic. Children with GAN and their families usually work with a medical team that includes a pediatric neurologist, orthopedic surgeon, physiotherapist, psychologist, and speech and occupational therapists. The major goals of treatment are to maximize intellectual and physical development and minimize their deterioration as time passes. Many children with GAN begin with normal intellectual development and are able to attend a regular school program. Children should be monitored at least once a year to assess their intellectual abilities and to look for the presence of neurological deterioration."}
{"_id":"462ae9c9-d20a-4a99-aa55-5dea37adb1df","text":"GAN generally progresses slowly as neurons degenerate and die. Most children have problems with walking in the early stages of the disorder. Later they may lose sensation, coordination, strength, and reflexes in their arms and legs. As time goes on, the brain and spinal cord may become involved, causing a gradual decline in mental function, loss of control of body movement, and seizures. Most children become wheelchair dependent in the second decade of life. Some children may survive into early adulthood."}
{"_id":"8858a031-16bd-446f-8c05-a48d32c13b24","text":"The National Institute of Neurological Disorders and Stroke (NINDS) supports research related to GAN through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure inherited neurological disorders such as GAN."}
{"_id":"a87a9835-4fd7-4dd2-b201-677127a47f43","text":"TOS is an umbrella term that encompasses three related syndromes that involve compression of the nerves, arteries, and veins in the lower neck and upper chest area and cause pain in the arm, shoulder, and neck. Most doctors agree that TOS is caused by compression of the brachial plexus or subclavian vessels as they pass through narrow passageways leading from the base of the neck to the armpit and arm, but there is considerable disagreement about its diagnosis and treatment. Making the diagnosis of TOS even more difficult is that a number of disorders feature symptoms similar to those of TOS, including rotator cuff injuries, cervical disc disorders, fibromyalgia, multiple sclerosis, complex regional pain syndrome, and tumors of the syrinx or spinal cord. The disorder can sometimes be diagnosed in a physical exam by tenderness in the supraclavicular area, weakness and\/or a \"pins and needles\" feeling when elevating the hands, weakness in the fifth (\"little\") finger, and paleness in the palm of one or both hands when the individual raises them above the shoulders, with the fingers pointing to the ceiling. Symptoms of TOS vary depending on the type.  Neurogenic TOS has a characteristic sign, called the Gilliatt-Sumner hand, in which there is severe wasting in the fleshy base of the thumb. Other symptoms include paresthesias (pins and needles sensation or numbness) in the fingers and hand, change in hand color, hand coldness, or dull aching pain in the neck, shoulder, and armpit.  Venous TOS features pallor, a weak or absent pulse in the affected arm, which also may be cool to the touch and appear paler than the unaffected arm. Symptoms may include numbness, tingling, aching, swelling of the extremity and fingers, and weakness of the neck or arm..  Arterial TOS most prominently features change in color and cold sensitivity in the hands and fingers, swelling, heaviness, paresthesias and poor blood circulation in the arms, hands, and fingers..\n                \nThere are many causes of TOS, including physical trauma, anatomical defects, tumors that press on nerves, poor posture that causes nerve compression, pregnancy, and repetitive arm and shoulder movements and activity, such as from playing certain sports.  TOS is more common in women. The onset of symptoms usually occurs between 20 and 50 years of age. Doctors usually recommend nerve conduction studies, electromyography, or imaging studies to confirm or rule out a diagnosis of TOS."}
{"_id":"64172eb4-fc99-4d08-996b-a1eec59fa4d4","text":"Treatment begins with exercise programs and physical therapy to strengthen chest muscles, restore normal posture, and relieve compression by increasing the space of the area the nerve passes through. Doctors will often prescribe non-steroidal anti-inflammatory drugs (such as naproxen or ibuprofen) for pain. Other medicines include thromobolytics to break up blood clots and anticoagulants to prevent clots. If this doesn't relieve pain, a doctor may recommend thoracic outlet decompression surgery to release or remove the structures causing compression of the nerve or artery."}
{"_id":"bfc9a2d0-70e3-4c01-a645-251b0e5ca620","text":"The outcome for individuals with TOS varies according to type. The majority of individuals with TOS will improve with exercise and physical therapy. Vascular TOS, and true neurogenic TOS often require surgery to relieve pressure on the affected vessel or nerve."}
{"_id":"f8818cd9-3ba9-4465-a468-61cbd8c28ed2","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes at the National Institutes of Health support research in TOS through grants to major medical research institutions across the country. Much of this research focuses on finding better ways to diagnose and treat TOS."}
{"_id":"f2d3eaf7-2848-401d-95ac-b31f87bfebd6","text":"Angelman syndrome is a genetic disorder that causes developmental delay and neurological problems. The physician Harry Angelman first delineated the syndrome in 1965, when he described several children in his practice as having \"flat heads, jerky movements, protruding tongues, and bouts of laughter.\" Infants with Angelman syndrome appear normal at birth, but often have feeding problems in the first months of life and exhibit noticeable developmental delays by 6 to 12 months. Seizures often begin between 2 and 3 years of age. Speech impairment is pronounced, with little to no use of words. Individuals with this syndrome often display hyperactivity, small head size, sleep disorders, and movement and balance disorders that can cause severe functional deficits. Angelman syndrome results from absence of a functional copy of the UBE3A gene inherited from the mother."}
{"_id":"ee01b49a-6e57-48f3-8937-a616c6af50dc","text":"There is no specific therapy for Angelman syndrome. Medical therapy for seizures is usually necessary. Physical and occupational therapies, communication therapy, and behavioral therapies are important in allowing individuals with Angelman syndrome to reach their maximum developmental potential."}
{"_id":"b3b56610-f228-4185-a282-694771f5c3b4","text":"Most individuals with Angelman syndrome will have severe developmental delays, speech limitations, and motor difficulties. However, individuals with Angelman syndrome can have normal life spans and generally do not show developmental regression as they age. Early diagnosis and tailored interventions and therapies help improve quality of life."}
{"_id":"3210ffa7-8766-411e-ba51-e1dfd236f858","text":"The NINDS supports and conducts research on neurogenetic disorders such as Angelman syndrome, to develop techniques to diagnose, treat, prevent, and ultimately cure them."}
{"_id":"edac5340-c81a-42c3-86ff-e92deab8116f","text":"Inclusion body myositis (IBM) is one of a group of muscle diseases known as the inflammatory myopathies, which are characterized by chronic, progressive muscle inflammation accompanied by muscle weakness. The onset of muscle weakness in IBM is generally gradual (over months or years) and affects both proximal (close to the trunk of the body) and distal (further away from the trunk) muscles. Muscle weakness may affect only one side of the body. Falling and tripping are usually the first noticeable symptoms of IBM. For some individuals, the disorder begins with weakness in the wrists and fingers that causes difficulty with pinching, buttoning, and gripping objects. There may be weakness of the wrist and finger muscles and atrophy (thinning or loss of muscle bulk) of the forearm muscles and quadricep muscles in the legs. Difficulty swallowing occurs in approximately half of IBM cases. Symptoms of the disease usually begin after the age of 50, although the disease can occur earlier. IBM occurs more frequently in men than in women."}
{"_id":"44dfb909-e807-4f04-a678-502f1794b420","text":"There is no cure for IBM, nor is there a standard course of treatment. The disease is generally unresponsive to corticosteroids and immunosuppressive drugs. Some evidence suggests that intravenous immunoglobulin may have a slight, but short-lasting, beneficial effect in a small number of cases. Physical therapy may be helpful in maintaining mobility. Other therapy is symptomatic and supportive."}
{"_id":"6c9d2016-c61c-47c5-9b25-b2e7c8701350","text":"IBM is generally resistant to all therapies and its rate of progression appears to be unaffected by currently available treatments."}
{"_id":"1bdef21a-9d89-441b-ad5f-d1043f9bd121","text":"The National Institute of Neurological Disorders and Stroke (NINDS), National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institute of Environmental Health Sciences (NIEHS) and other institutes of the National Institutes of Health (NIH) conduct research relating to IBM in laboratories at the NIH and support additional research through grants to major medical institutions across the country. Currently funded research is exploring patterns of gene expression among the inflammatory myopathies, the role of viral infection as a precursor to the disorders, and the safety and efficacy of various treatment regimens."}
{"_id":"14c0e68f-011e-490a-a9de-26577a0e3e9c","text":"Subacute sclerosing panencephalitis (SSPE) is a progressive neurological disorder of children and young adults that affects the central nervous system (CNS). It is a slow, but persistent, viral infection caused by defective measles virus. SSPE has been reported from all parts of the world, but it is considered a rare disease in developed countries, with fewer than 10 cases per year reported in the United States. The incidence of SSPE declined by at least 90 percent in countries that have practiced widespread immunization with measles vaccine. The incidence of SSPE is still high in developing countries such as India and Eastern Europe. There is a higher incidence among males than females (male\/female: 3\/1). Most youngsters with SSPE have a history of measles infection at an early age, usually younger than 2 years, followed by a latent period of 6 to 8 years before neurological symptoms begin. Despite the long interval between the measles infection and the onset of SSPE, researchers think that the infection of the brain occurs soon after the primary bout with measles and progresses slowly. Why it persists and progresses still isn't clear. The initial symptoms of SSPE are subtle and include mild mental deterioration (such as memory loss) and changes in behavior (such as irritability) followed by disturbances in motor function, including uncontrollable involuntary jerking movements of the head, trunk or limbs called myoclonic jerks. Seizures may also occur. Some people may become blind. In advanced stages of the disease, individuals may lose the ability to walk, as their muscles stiffen or spasm. There is progressive deterioration to a comatose state, and then to a persistent vegetative state. Death is usually the result of fever, heart failure, or the brain's inability to continue controlling the autonomic nervous system."}
{"_id":"686dbea4-172f-4701-a17c-b5ebbb5d07b7","text":"Currently, there is no cure for SSPE. Clinical trials of antiviral (isoprinosine and ribavirin) and immunomodulatory (interferon alpha) drugs have suggested that these types of therapies given alone or in combination halt the progression of the disease and can prolong life, but their long-term effects on individuals, and eventual outcome, are unknown. Good nursing care is the most important aspect of treatment for SSPE, along with anticonvulsant and antispasmodic drugs when needed."}
{"_id":"9444d7ab-a609-478b-8288-cb012801228a","text":"Most individuals with SSPE will die within 1 to 3 years of diagnosis. In a small percentage of people, the disease will progress rapidly, leading to death over a short course within three months of diagnosis. Another small group will have a chronic, slowly progressive form, some with relapses and remissions. A very small number (approximately 5 percent) may experience spontaneous long term improvement and regain lost function. Prevention, in the form of measles vaccination, is the only real \"cure\" for SSPE."}
{"_id":"ff2dbe47-0ec9-45da-9530-d2250456fe09","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes at the National Institutes of Health conduct research related to SSPE in their clinics and laboratories and support additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat and ultimately cure SSPE."}
{"_id":"a148d4ca-51d7-45e6-885d-d4c1bf5f85ab","text":"Hemifacial spasm is a neuromuscular disorder characterized by frequent involuntary contractions (spasms) of the muscles on one side (hemi-) of the face (facial). The disorder occurs in both men and women, although it more frequently affects middle-aged or elderly women. It is much more common in the Asian population. The first symptom is usually an intermittent twitching of the eyelid muscle that can lead to forced closure of the eye. The spasm may then gradually spread to involve the muscles of the lower face, which may cause the mouth to be pulled to one side. Eventually the spasms involve all of the muscles on one side of the face almost continuously. The condition may be caused by a facial nerve injury, or a tumor, or it may have no apparent cause. Rarely, doctors see individuals with spasm on both sides of the face. Most often hemifacial spasm is caused by a blood vessel pressing on the facial nerve at the place where it exits the brainstem."}
{"_id":"0a637ac8-f419-4500-a0da-a9783b7cb833","text":"Surgical treatment in the form of microvascular decompression, which relieves pressure on the facial nerve, will relieve hemifacial spasm in many cases. This intervention has significant potential side-effects, so risks and benefits have to be carefully balanced. Other treatments include injections of botulinum toxin into the affected areas, which is the most effective therapy and the only one used in most cases. Drug therapy is generally not effective."}
{"_id":"b14128d6-c2ec-4592-860a-40c8e0d490e0","text":"The prognosis for an individual with hemifacial spasm depends on the treatment and their response. Some individuals will become relatively free from symptoms with injection therapy. Some may require surgery. In most cases, a balance can be achieved, with tolerable residual symptoms."}
{"_id":"02dededa-b1d7-454c-80d1-9579290fc8f2","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts and supports research related to hemifacial spams through grants to major research institutions across the country. Much of this research focuses on better ways to prevent, treat, and ultimately cure neurological disorders, such as hemifacial spasm."}
{"_id":"4e50921f-6b43-4237-95dd-e85c2c2837f6","text":"Olivopontocerebellar atrophy (OPCA) is a term that describes the degeneration of neurons in specific areas of the brain  the cerebellum, pons, and inferior olives. OPCA is present in several neurodegenerative syndromes, including inherited and non-inherited forms of ataxia (such as the hereditary spinocerebellar ataxia known as Machado-Joseph disease) and multiple system atrophy (MSA), with which it is primarily associated. http:\/\/www.ninds.nih.gov\/disorders\/msa\/msa.htm\n                \nOPCA may also be found in the brains of individuals with prion disorders and inherited metabolic diseases. The characteristic areas of brain damage that indicate OPCA can be seen by imaging the brain using CT scans or MRI studies."}
{"_id":"f804a056-65d4-4929-b777-2edba34c1597","text":"There is no specific treatmentfor OPCA. Physicians may try different medications to treat the ataxia, tremor, and rigidity that are associated with the disorder. Other treatments are directed at specific symptoms. Stiffness, spasms, sleep disorders, depression, and tremor may be improved with medication. A physical therapist may be helpful in establishing a routine of exercise and stretching, and in obtaining devices or appliances to assist in walking and other daily activities."}
{"_id":"75db6dae-3cae-4a3b-b28d-56dc1d464382","text":"There is no cure for OPCA. The disorder is slowly progressive with death usually occurring approximately 20 years after onset."}
{"_id":"83581387-65d5-4cc8-b50e-ec42d64acdf2","text":"The NINDS supports and conducts a broad range of basic and clinical research on cerebellar degeneration, including work aimed at finding the cause(s) of OPCA and ways to treat, cure, and, ultimately, prevent the disease. There has been great progress recently since the genes for several of the hereditary forms of OPCA have been found."}
{"_id":"7f3ff99c-1241-4b39-badc-02c6bfd6e8f8","text":"Multifocal motor neuropathy is a progressive muscle disorder characterized by muscle weakness in the hands, with differences from one side of the body to the other in the specific muscles involved. It affects men much more than women. Symptoms also include muscle wasting, cramping, and involuntary contractions or twitching of the leg muscles. The disorder is sometimes mistaken for amyotrophic laterial sclerosis (ALS, or Lou Gehrig's disease) but unlike ALS, it is treatable. An early and accurate diagnosis allows patients to recover quickly."}
{"_id":"ab9f655e-f305-41cb-9788-a927ca07b941","text":"Treatment for multifocal motor neuropathy varies. Some individuals experience only mild, modest symptoms and require no treatment. For others, treatment generally consists of intravenous immunoglobulin (IVIg) or immunosuppressive therapy with cyclophosphamide."}
{"_id":"812aed9d-39db-4089-a121-f4b895cde391","text":"Improvement in muscle strength usually begins within 3 to 6 weeks after treatment is started. Most patients who receive treatment early experience little, if any, disability. However, there is evidence of slow progression over many years."}
{"_id":"a7f146b1-fa33-440b-b5fc-601ae4fbedbd","text":"The NINDS supports a broad range of research on neuromuscular disorders with the goal of finding ways to prevent, treat, and, ultimately, cure them."}
{"_id":"f8c8fef9-6043-4b7b-b666-42e06fb366ab","text":"Occipital neuralgia is a distinct type of headache characterized by piercing, throbbing, or electric-shock-like chronic pain in the upper neck, back of the head, and behind the ears, usually on one side of the head. Typically, the pain of occipital neuralgia begins in the neck and then spreads upwards. Some individuals will also experience pain in the scalp, forehead, and behind the eyes. Their scalp may also be tender to the touch, and their eyes especially sensitive to light. The location of pain is related to the areas supplied by the greater and lesser occipital nerves, which run from the area where the spinal column meets the neck, up to the scalp at the back of the head. The pain is caused by irritation or injury to the nerves, which can be the result of trauma to the back of the head, pinching of the nerves by overly tight neck muscles, compression of the nerve as it leaves the spine due to osteoarthritis, or tumors or other types of lesions in the neck. Localized inflammation or infection, gout, diabetes, blood vessel inflammation (vasculitis), and frequent lengthy periods of keeping the head in a downward and forward position are also associated with occipital neuralgia. In many cases, however, no cause can be found. A positive response (relief from pain) after an anesthetic nerve block will confirm the diagnosis."}
{"_id":"41c989a4-e77a-4020-a0ef-e38fc4f08d07","text":"Treatment is generally symptomatic and includes massage and rest. In some cases, antidepressants may be used when the pain is particularly severe. Other treatments may include local nerve blocks and injections of steroids directly into the affected area."}
{"_id":"cacb8951-6efd-46cd-ad24-97702b69bd31","text":"Occipital neuralgia is not a life-threatening condition. Many individuals will improve with therapy involving heat, rest, anti-inflammatory medications, and muscle relaxants. Recovery is usually complete after the bout of pain has ended and the nerve damage repaired or lessened."}
{"_id":"3706b699-a643-4d26-b8c3-a59ce82b271b","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes at the National Institutes of Health conduct research related to pain and occipital neuralgia in their clinics and laboratories and support additional research through grants to major medical institutions across the country. Much of this research focuses on understanding the basic mechanisms of pain and testing treatments in order to find better ways to treat occipital neuralgia."}
{"_id":"73256490-b5d4-4515-95f1-11da39e399dc","text":"Arachnoiditis describes a pain disorder caused by the inflammation of the arachnoid, one of the membranes that surround and protect the nerves of the spinal cord. The arachnoid can become inflamed because of an irritation from chemicals, infection from bacteria or viruses, as the result of direct injury to the spine, chronic compression of spinal nerves, or complications from spinal surgery or other invasive spinal procedures. Inflammation can sometimes lead to the formation of scar tissue and adhesions, which cause the spinal nerves to stick together. If arachnoiditis begins to interfere with the function of one or more of these nerves, it can cause a number of symptoms, including numbness, tingling, and a characteristic stinging and burning pain in the lower back or legs. Some people with arachnoiditis will have debilitating muscle cramps, twitches, or spasms. It may also affect bladder, bowel, and sexual function. In severe cases, arachnoiditis may cause paralysis of the lower limbs."}
{"_id":"1c6e82a4-f5b0-424b-8099-d74175654306","text":"Arachnoiditis remains a difficult condition to treat, and long-term outcomes are unpredictable. Most treatments for arachnoiditis are focused on pain relief and the improvement of symptoms that impair daily function. A regimen of pain management, physiotheraphy, exercise, and psychotheraphy is often recommended. Surgical intervention is controversial since the outcomes are generally poor and provide only short-term relief."}
{"_id":"919a1085-2ea4-4bac-8ba9-7a512e921a23","text":"Arachnoiditis is adisorder that causes chronic pain and neurological deficits and does not improve significantly with treatment.Surgery may only provide temporary relief. The outlook for someone witharachnoiditis iscomplicated by the fact that the disorder has no predictable pattern or severity of symptoms."}
{"_id":"6381f199-871e-4d1f-9f14-dc950a7fab7b","text":"Within the NINDS research programs, arachnoiditis is addressed primarily through studies associated with pain research. NINDS vigorously pursues a research program seeking new treatments for pain and nerve damage with the ultimate goal of reversing debilitating conditions such as arachnoiditis."}
{"_id":"b5d999ef-922e-4ab4-899c-1472a4f1372c","text":"Craniosynostosis is a birth defect of the skull characterized by the premature closure of one or more of the fibrous joints between the bones of the skull (called the cranial sutures) before brain growth is complete. Closure of a single suture is most common. Normally the skull expands uniformly to accommodate the growth of the brain; premature closure of a single suture restricts the growth in that part of the skull and promotes growth in other parts of the skull where sutures remain open. This results in a misshapen skull but does not prevent the brain from expanding to a normal volume. However, when many sutures close prematurely, the skull cannot expand to accommodate the growing brain, which leads to increased pressure within the skull and impaired development of the brain. Craniosynostosis can be gene-linked or caused by metabolic diseases (such as rickets )or an overactive thyroid. Some cases are associated with other disorders such as microcephaly (abnormally small head) and hydrocephalus (excessive accumulation of cerebrospinal fluid in the brain). The first sign of craniosynostosis is an abnormally shaped skull. Other features can include signs of increased intracranial pressure, developmental delays, or impaired cognitive development, which are caused by constriction of the growing brain. Seizures and blindness may also occur."}
{"_id":"0a59283c-85fa-41a6-b9d5-f823e6785b4c","text":"Treatment for craniosynostosis generally consists of surgery to improve the symmetry and appearance of the head and to relieve pressure on the brain and the cranial nerves. For some children with less severe problems, cranial molds can reshape the skull to accommodate brain growth and improve the appearance of the head."}
{"_id":"3298f550-8460-44a6-b585-2f524d4bebcf","text":"The prognosis for craniosynostosis varies depending on whether single or multiple cranial sutures are involved or other abnormalities are present. The prognosis is better for those with single suture involvement and no associated abnormalities."}
{"_id":"14508415-4617-4dcf-9ec4-b03c52e146a4","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. The NINDS conducts and supports a wide range of studies that explore the complex mechanisms of brain development. The knowledge gained from these fundamental studies provides the foundation for understanding how this process can change and offers hope for new ways to treat and prevent birth defects that can prevent normal brain development, such as craniosynostosis."}
{"_id":"33649cae-f06f-4e48-b71c-288f9c03cac5","text":"Cerebral cavernous malformations (CCMs) are vascular lesions comprised of clusters of tightly packed, abnormally thin-walled small blood vessels (capillaries) that displace normal neurological tissue in the brain or spinal cord. The vessels are filled with slow-moving or stagnant blood that is usually clotted or in a state of decomposition. Cavernous malformations can occur in the brain, spinal cord, and some other body regions. In the brain and spinal cord these cavernous lesions are quite fragile and are prone to bleeding, causing hemorrhagic strokes (bleeding into the brain), seizures, and neurological deficits. CCMs can range in size from a few fractions of an inch to several inches in diameter, depending on the number of blood vessels involved. Some people develop multiple lesions while others never experience related medical problems. Hereditary forms of CCM are caused by mutations in one of three CCM disease genes: CCM1, CCM2, and CCM3. A large population with hereditary CCM disease is found in New Mexico and the Southwestern United States, in which the disease is caused by mutations in the gene CCM1 (or KRIT1)."}
{"_id":"0b52bf3f-76cd-4d35-b555-b39d1ca708b8","text":"The primary treatment option for a CCM is surgical removal. Radiation therapy has not been shown to be effective. The decision to operate is made based upon the risk of approaching the lesion. For example, symptomatic lesions close to the brain surface in non eloquent brain (areas for example, those areas not involved with motor function, speech, vision, hearing, memory, and learning) are very likely to be candidates for removal. On the other hand, lesions located in deep brain areas are associated with higher surgical risk and are often not candidates for surgery until the lesion has bled multiple times. Medications can often lessen general symptoms such as headache, back pain, and seizures."}
{"_id":"bd03f3be-4cb1-4651-bb60-342a8a9bc1d2","text":"Rebleeding from a cavernous angioma is common, it is not predictable, and individuals frequently have multiple CCMs found via magnetic resonance imaging. Individuals with CCM are faced with a diagnosis that imparts risk of multiple future hemorrhages that occur seemingly at random and without any preventative therapy except surgical removal."}
{"_id":"732dc6ae-1b6b-4cb5-8338-888bc92d1059","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. Studies of cerebral cavernous malformations (CCMs) show that alterations in the function of structural proteins may also give rise to vascular malformations. Currently there is no therapy to prevent the development or progression of CCMs. NINDS-funded scientists have developed an animal model that studies two of the familial genes related to the development of CCMs. Research shows that the protein signaling pathway Rhoa\/ROCK, which allows cells to communicate regarding the formation of cell structure, is involved in blood vessel activity\/ and the flow of molecules and cells into and out of blood vessels. These scientists hypothesize that blocking ROCK activity will inhibit CCM development and hemorrhage, and possibly create a therapy for these malformations."}
{"_id":"dcfe659a-7ae7-4565-8b2e-a6b70673837b","text":"Locked-in syndrome is a rare neurological disorder characterized by complete paralysis of voluntary muscles in all parts of the body except for those that control eye movement. It may result from traumatic brain injury, diseases of the circulatory system, diseases that destroy the myelin sheath surrounding nerve cells, or medication overdose. Individuals with locked-in syndrome are conscious and can think and reason, but are unable to speak or move. The disorder leaves individuals completely mute and paralyzed. Communication may be possible with blinking eye movements"}
{"_id":"44c06698-94e7-44f9-a0b3-c5622fcfd7f2","text":"There is no cure for locked-in syndrome, nor is there a standard course of treatment. A therapy called functional neuromuscular stimulation, which uses electrodes to stimulate muscle reflexes, may help activate some paralyzed muscles. Several devices to help communication are available. Other treatment is symptomatic and supportive."}
{"_id":"0d647786-5299-4f8a-ad10-e34fddf5f1b4","text":"While in rare cases some patients may regain certain functions, the chances for motor recovery are very limited."}
{"_id":"e5515b02-5104-4b11-b794-83752c67961e","text":"The NINDS supports research on neurological disorders that can cause locked-in syndrome. The goals of this research are to find ways to prevent, treat, and cure these disorders."}
{"_id":"042f1101-3d6f-4e27-b934-01800e36e68a","text":"Lyme disease is caused by a bacterial organism that is transmitted to humans via the bite of an infected tick. Most people with Lyme disease develop a characteristic skin rash around the area of the bite. The rash may feel hot to the touch, and vary in size, shape, and color, but it will often have a \"bull's eye\" appearance (a red ring with a clear center). However, there are those who will not develop the rash, which can make Lyme disease hard to diagnose because its symptoms and signs mimic those of many other diseases.\n                \nAnywhere from 7 to 14 days (or in some cases, 30 days) following an infected tick's bite, the first stage of Lyme disease may begin with flu-like symptoms such as fever, chills, swollen lymph nodes, headaches, fatigue, muscle aches, and joint pain.\n                \nNeurological complications most often occur in the second stage of Lyme disease, with numbness, pain, weakness, Bell's palsy (paralysis of the facial muscles), visual disturbances, and meningitis symptoms such as fever, stiff neck, and severe headache. Other problems, which may not appear until weeks, months, or years after a tick bite, include decreased concentration, irritability, memory and sleep disorders, and nerve damage in the arms and legs."}
{"_id":"5a9a7fbd-2fd3-4eb4-83bf-f0d33ea9d051","text":"Lyme disease is treated with antibiotics under the supervision of a physician."}
{"_id":"77386de3-dbda-4b1b-8b25-f4f33af3edc7","text":"Most individuals with Lyme disease respond well to antibiotics and have full recovery. In a small percentage of individuals, symptoms may continue or recur, requiring additional antibiotic treatment. Varying degrees of permanent joint or nervous system damage may develop in individuals with late-stage Lyme disease."}
{"_id":"fb6f98ae-6a7a-4306-947a-66d4f2f88cb5","text":"The NINDS supports research on Lyme disease. Current areas of interest include improving diagnostic tests and developing more effective treatments. The National Institute of Allergy and Infectious Diseases (NIAID), the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), and the National Center for Research Resources (NCRR), all parts of the National Institutes of Health (NIH), also support research on Lyme disease."}
{"_id":"68ba8185-80d2-46de-9afa-727d332a1e36","text":"Acid lipase disease or deficiency occurs when the enzyme needed to break down certain fats that are normally digested by the body is lacking or missing, resulting in the toxic buildup of these fats in the bodys cells and tissues. These fatty substances, called lipids, include fatty acids, oils, and cholesterol. Two rare lipid storage diseases are caused by the deficiency of the enzyme lysosomal acid lipase:\n                \nWolmans disease (also known as acid lipase deficiency) is an autosomal recessive disorder marked by the buildup of cholesteryl esters (normally a tranport form of cholesterol that brings nutrients into the cells and carries out waste) and triglycerides (a chemical form in which fats exist in the body). Infants with the disorder appear normal at birth but quickly develop progressive mental deterioration, low muscle tone,enlarged liver and grossly enlarged spleen, gastrointestinal problems including an excessive amount of fats in the stools, jaundice, anemia, vomiting, and calcium deposits in the adrenal glands, which causes them to harden. Both male and female infants are affected by the disorder.\n                \nCholesteryl ester storage disease (CESD) is an extremely rare disorder that results from storage of cholesteryl esters and triglycerides in cells in the blood and lymph and lymphoid tissue. Children develop an enlarged liver, leading to cirrhosis and chronic liver failure before adulthood. Children may also develop calcium deposits in the adrenal glands and jaundice. Onset varies, and the disorder may not be diagnosed until adulthood."}
{"_id":"4dc02b1c-4d28-49c3-843e-e130bbc8ab90","text":"Enzyme replacement therapy for both Wolman's and cholesteryl ester storage disease is currently under investigation. Certain drugs may be given to help with adrenal gland production, and children may need to be fed intravenously. Individuals with CESD may benefit from a low cholesterol diet."}
{"_id":"07e3b75d-b762-4501-8417-458e48146812","text":"Wolmans disease is usually fatal by age 1. The onset and course of cholesteryl ester storage disease varies, and individuals may live into adulthood."}
{"_id":"aab2c870-a659-480a-be10-19165336346c","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge abut the brain and nervous system, and to use that knowledge to reduce the burden of neurological diseaset. The NINDS conducts and supports research to understand lipid storage diseases such as acid lipase deficiency. Additional research studies hope to identify biomarkers (signs that may indicate risk of a disease and improve diagnosis) for thee lipid storage diseases that will speed the development of novel therapeutics for these disorders. Other investigators hope to establish an international disease registry designed to collect longitudinal data that would be used to improve the care and treatment of individuals with lysosomal acid lipase deficiency.\n                \nThe National Library of Medicine (NLM), a part of the National Institutes of Health (NIH) within the U.S. Department of Health and Human Services, offers free searches of biomedical literature through an Internet service called PubMed. To search, go to: http:\/\/www.ncbi.nlm.nih.gov\/PubMed . The NLM also offers extensive health information from NIH and other trusted sources. To research your condition, go to: http:\/\/www.medlineplus.gov ."}
{"_id":"1ac77f12-5b2c-4caa-b515-95d56a336275","text":"Agenesis of the corpus callosum (ACC) is one of several disorders of the corpus callosum, the structure that connects the two hemispheres (left and right) of the brain. In ACC the corpus callosum is partially or completely absent. It is caused by a disruption of brain cell migration during fetal development. ACC can occur as an isolated condition or in combination with other cerebral abnormalities, including Arnold-Chiari malformation, Dandy-Walker syndrome, schizencephaly (clefts or deep divisions in brain tissue), and holoprosencephaly (failure of the forebrain to divide into lobes.) Girls may have a gender-specific condition called Aicardi syndrome, which causes severe cognitive impairment and developmental delays, seizures, abnormalities in the vertebra of the spine, and lesions on the retina of the eye. ACC can also be associated with malformations in other parts of the body, such as midline facial defects. The effects of the disorder range from subtle or mild to severe, depending on associated brain abnormalities. Children with the most severe brain malformations may have intellectual impairment, seizures, hydrocephalus, and spasticity. Other disorders of the corpus callosum include dysgenesis, in which the corpus callosum is developed in a malformed or incomplete way, and hypoplasia, in which the corpus callosum is thinner than usual. Individuals with these disorders have a higher risk of hearing deficits and cardiac abnormalities than individuals with the normal structure. It is estimated that at lease one in 4,000 individuals has a disorder of the corpus callosum."}
{"_id":"0dd0ebb5-0d15-49db-9886-70e99825d464","text":"There is no standard course of treatment for ACC. Treatment usually involves management of symptoms and seizures if they occur. Associated difficulties are much more manageable with early recognition and therapy, especially therapies focusing on left\/right coordination. Early diagnosis and interventions are currently the best treatments to improve social and developmental outcomes."}
{"_id":"15f90702-1fc3-4f9a-b801-ae81737b5e3b","text":"Prognosis depends on the extent and severity of malformations. Intellectual impairment does not worsen. Individuals with a disorder of the corpus callosum typically have delays in attaining developmental milestones such as walking, talking, or reading; challenges with social interactions; clumsiness and poor motor coordination, particularly on skills that require coordination of left and right hands and feet (such as swimming, bicycle riding, and driving; and mental and social processing problems that become more apparent with age, with problems particularly evident from junior high school into adulthood."}
{"_id":"31d182fd-8bef-4d3d-9f3c-8e3c43d6fd2e","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS conducts and supports a wide range of studies that explore the complex mechanisms of normal brain development. NINDS-funded research includes studies to understand the genetic causes of ACC, as well as to understand how magnetic resonance imaging findings may help predict outcome and response to therapy."}
{"_id":"f9a69f81-f5d7-4dc0-8227-5612255b220a","text":"Trigeminal neuralgia (TN), also called tic douloureux, is a chronic pain condition that causes extreme, sporadic, sudden burning or shock-like face pain. The painseldomlasts more than a few seconds or a minute or twoper episode. The intensity of pain can be physically and mentally incapacitating. TN pain is typically felt on one side of the jaw or cheek. Episodes can last for days, weeks, or months at a time and then disappear for months or years. In the days before an episode begins, some patients may experience a tingling or numbing sensation or a somewhat constant and aching pain. The attacks often worsen over time, with fewer and shorter pain-free periods before they recur. The intense flashes of pain can be triggered by vibration or contact with the cheek (such as when shaving, washing the face, or applying makeup), brushing teeth, eating, drinking, talking, or being exposed to the wind. TN occurs most often in people over age 50, but it can occur at any age, and is more common in women than in men. There is some evidence that the disorder runs in families, perhaps because of an inherited pattern of blood vessel formation. Although sometimes debilitating, the disorder is not life-threatening.\n                \nThe presumed cause of TN is a blood vessel pressing on the trigeminal nerve in the head as it exits the brainstem. TN may be part of the normal aging process but in some cases it is the associated with another disorder, such as multiple sclerosis or other disorders characterized by damage to the myelin sheath that covers certain nerves."}
{"_id":"c20d5ada-12f8-4867-aec1-2e55a105d06c","text":"Because there are a large number of conditions that can cause facial pain, TN can be difficult to diagnose. But finding the cause of the pain is important as the treatments for different types of pain may differ. Treatment options include medicines such as anticonvulsants and tricyclic antidepressants, surgery, and complementary approaches. Typical analgesics and opioids are not usually helpful in treating the sharp, recurring pain caused by TN. If medication fails to relieve pain or produces intolerable side effects such as excess fatigue, surgical treatment may be recommended. Several neurosurgical procedures are available. Some are done on an outpatient basis, while others are more complex and require hospitalization. Some patients choose to manage TN using complementary techniques, usually in combination with drug treatment. These techniques include acupuncture, biofeedback, vitamin therapy, nutritional therapy, and electrical stimulation of the nerves."}
{"_id":"95f5c539-5635-4613-b159-f93cf6334780","text":"The disorder is characterized by recurrences and remissions, and successive recurrences may incapacitate the patient. Due to the intensity of the pain, even the fear of an impending attack may prevent activity. Trigeminal neuralgia is not fatal."}
{"_id":"6ab34f14-3cd7-4e11-9431-95d1320f0a95","text":"Within the NINDS research programs, trigeminal neuralgia is addressed primarily through studies associated with pain research. NINDS vigorously pursues a research program seeking new treatments for pain and nerve damage with the ultimate goal of reversing debilitating conditions such as trigeminal neuralgia. NINDS has notified research investigators that it is seeking grant applications both in basic and clinical pain research."}
{"_id":"9bb9e0ce-6969-43d5-b9ef-2c3eef3af00f","text":"Neuronal migration disorders (NMDs) are a group of birth defects caused by the abnormal migration of neurons in the developing brain and nervous system. In the developing brain, neurons must migrate from the areas where they are born to the areas where they will settle into their proper neural circuits. Neuronal migration, which occurs as early as the second month of gestation, is controlled by a complex assortment of chemical guides and signals. When these signals are absent or incorrect, neurons do not end up where they belong. This can result in structurally abnormal or missing areas of the brain in the cerebral hemispheres, cerebellum, brainstem, or hippocampus. The structural abnormalities found in NMDs include schizencephaly, porencephaly, lissencephaly, agyria, macrogyria, polymicrogyria, pachygyria, microgyria, micropolygyria, neuronal heterotopias (including band heterotopia), agenesis of the corpus callosum, and agenesis of the cranial nerves. Symptoms vary according to the abnormality, but often feature poor muscle tone and motor function, seizures, developmental delays, impaired cognitive development, failure to grow and thrive, difficulties with feeding, swelling in the extremities, and a smaller than normal head. Most infants with an NMD appear normal, but some disorders have characteristic facial or skull features that can be recognized by a neurologist. Several genetic abnormalities in children with NMDs have been identified. Defects in genes that are involved in neuronal migration have been associated with NMDs, but the role they play in the development of these disorders is not yet well-understood. More than 25 syndromes resulting from abnormal neuronal migration have been described. Among them are syndromes with several different patterns of inheritance; genetic counseling thus differs greatly between syndromes."}
{"_id":"28f49f36-ea02-44f0-ada1-9c98ffce3840","text":"Treatment is symptomatic, and may include anti-seizure medication and special or supplemental education consisting of physical, occupational, and speech therapies."}
{"_id":"ab5ba21e-3047-4c96-b65a-8a0d6edc88a2","text":"The prognosis for children with NMDs varies depending on the specific disorder and the degree of brain abnormality and subsequent neurological signs and symptoms."}
{"_id":"2b85e5ab-4d53-4462-81b6-ebf3b82216f4","text":"The NINDS conducts and supports a wide range of studies that explore the complex systems of brain development. These studies include the identification of the mechanism of action of the known causes of NMD as well as studies to identify further causes of disease. NIH-funded researchers work closely with parental support groups to bring research discoveries directly to patients. The knowledge gained from these studies provides the foundation for understanding abnormal development and offers hope for new ways to treat and prevent NMDs."}
{"_id":"27d73889-c8df-49d9-b3f4-fa38c9da1d61","text":"Autistic disorder (sometimes called autism or classical ASD) is the most common condition in a group of developmental disorders known as the autism spectrum disorders (ASDs).\n                \nAutistic children have difficulties with social interaction, display problems with verbal and nonverbal communication, and exhibit repetitive behaviors or narrow, obsessive interests. These behaviors can range in impact from mild to disabling. Autism varies widely in its severity and symptoms and may go unrecognized, especially in mildly affected children or when more debilitating handicaps mask it. Scientists arent certain what causes autism, but its likely that both genetics and environment play a role."}
{"_id":"7ad2dadc-5142-41ef-903e-d364866de22e","text":"There is no cure for autism. Therapies and behavioral interventions are designed to remedy specific symptoms and can bring about substantial improvement. The ideal treatment plan coordinates therapies and interventions that meet the specific needs of individual children. Treatment options include educational\/bahavioral interventions, medications, and other therapies. Most professionals agree that the earlier the intervention, the better."}
{"_id":"e30c74f5-eb26-4661-8505-7db2bc17f693","text":"For many children, autism symptoms improve with treatment and with age. Some children with autism grow up to lead normal or near-normal lives. Children whose language skills regress early in life, usually before the age of 3, appear to be at risk of developing epilepsy or seizure-like brain activity. During adolescence, some children with autism may become depressed or experience behavioral problems. Parents of these children should be ready to adjust treatment for their child as needed. People with an ASD usually continue to need services and support as they get older but many are able to work successfully and live independently or within a supportive environment."}
{"_id":"6eec9dda-0654-4dc7-8745-12a421490f09","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research in its laboratories at the National Institutes of Health (NIH) and also supports additional research through grants to major medical institutions across the country. As part of the Childrens Health Act of 2000, the NINDS and three sister institutes have formed the NIH Autism Coordinating Committee to expand, intensify, and coordinate NIHs autism research. As part of the Childrens Health Act of 2000, the NINDS and three sister institutes have formed the NIH Autism Coordinating Committee to expand, intensify, and coordinate NIHs autism research. Eight dedicated research centers across the country have been established as Centers of Excellence in Autism Research to bring together researchers and the resources they need.  The Centers are conducting basic and clinical research, including investigations into causes, diagnosis, early detection, prevention, and treatment of autism."}
{"_id":"cc8065f8-f820-45f1-a8ae-6e1d0cb8796d","text":"Meningitis is an infection of the meninges, the membranes that surround the brain and spinal cord. Encephalitis is inflammation of the brain itself. Causes of encephalitis and meningitis include viruses, bacteria, fungus, and parasites. Anyone can get encephalitis or meningitis.Inflammation from encephalitis and meningitis produce a wide range of symptoms. Symptoms of encephalitis include sudden fever, headache, vomiting, heightened sensitivity to light, stiff neck and back, confusion and impaired judgment, drowsiness, weak muscles, a clumsy and unsteady gait, and irritability. In more severe cases, people may have problems with speech or hearing, vision problems, and hallucinations. Symptoms that might require emergency treatment include loss of consciousness, seizures, muscle weakness, or sudden severe dementia.\n                \nSymptoms of meningitis, which may appear suddenly, often include high fever, severe and persistent headache, stiff neck, nausea, sensitivity to bright light, and vomiting. Changes in behavior such as confusion, sleepiness, and difficulty waking up may also occur. In infants, symptoms of meningitis or encephalitis may include fever, vomiting, lethargy, body stiffness, unexplained irritability, and a full or bulging fontanel (the soft spot on the top of the head). Anyone experiencing symptoms of meningitis or encephalitis should see a doctor immediately."}
{"_id":"843111f2-e1b5-453c-aa32-b5393d4395c1","text":"Anyone experiencing symptoms of meningitis or encephalitis should see a doctor immediately. Antibiotics for most types of meningitis can greatly reduce the risk of dying from the disease. Antiviral medications may be prescribed for viral encephalitis or other severe viral infections.Anticonvulsants are used to prevent or treat seizures. Corticosteroidd rugs can reduce brain swelling and inflammation. Over-the-counter medications may be used for fever and headache. Individuals with encephalitis or bacterial meningitis are usually hospitalized for treatment. Affected individuals with breathing difficulties may require artificial respiration."}
{"_id":"78477380-464d-4460-9e84-4350e817d885","text":"The prognosis for for people with encephalitis or meningitis varies. Some cases are mild, short and relatively benign and individuals have full recovery, although the process may be slow. Individuals who experience mild symptoms may recover in 2-4 weeks. Other cases are severe, and permanent impairment or death is possible. The acute phase of encephalitis may last for 1 to 2 weeks, with gradual or sudden resolution of fever and neurological symptoms. Individuals treated for bacterial meningitis typically show some relief within 48-72 hours. Neurological symptoms may require many months before full recovery. With early diagnosis and prompt treatment, most individuals recover from meningitis. However, in some cases, the disease progresses so rapidly that death occurs during the first 48 hours, despite early treatment."}
{"_id":"a51b5aee-e4a4-44a5-bec0-f4819ce5cddf","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS is a component of the National Institutes of Health, the leading supporter of biomedical research in the world. Current research efforts include gaining a better understanding of how the central nervous system responds to inflammation in the brain, as well as to better understand the molecular mechanisms involved in the protection and disruption of the blood-brain barrier, which could lead to the development of new treatments for several neuroinflammatory diseases such as meningitis and encephalitis."}
{"_id":"1f6c963a-c23e-4a6e-8f81-1d963a0e9496","text":"SUNCT-Short-lasting, Unilateral, Neuralgiform headache attacks with Conjunctival injection and Tearing-is a rare form of headache that is most common in men after age 50. The disorder is marked by bursts of moderate to severe burning, piercing, or throbbing pain, usually on one side of the head and around the eye or temple. The pain usually peaks within seconds of onset and may follow a pattern of increasing and decreasing intensity. Attacks typically occur in daytime hours and last from 5 seconds to 4 minutes per episode. Individuals generally have five to six attacks per hour.\n                \nAutonomic nervous system responses include watery eyes, reddish or bloodshot eyes caused by dilation of blood vessels (conjunctival injection), nasal congestion, runny nose, sweaty forehead, swelling of the eyelids, and increased pressure within the eye on the affected side of head. Systolic blood pressure may rise during the attacks. Movement of the neck may trigger these headaches. SUNCT may be a form of trigeminal neuralgia and is considered one of the trigeminal autonomic cephalgias, or TACs."}
{"_id":"95e8aaf8-9403-4992-ac5c-4a6eb592fb3c","text":"These headaches are generally non-responsive to usual treatment for other short-lasting headaches. Corticosteroids and the anti-epileptic drugs gabapentin, lamotrigine, and carbamazepine may help relieve some symptoms in some patients. Studies have shown that injections of glycerol to block nerve signaling along the trigeminal nerve may provide temporary relief in some severe cases, but the headaches recurred in about 40 percent of individuals studied."}
{"_id":"4652fbbf-e701-4f5d-a6db-13bf7b6ab713","text":"There is no cure for these headaches. The disorder is not fatal but can cause considerable discomfort."}
{"_id":"7d44626d-809b-4fb5-bd2a-07c9083127de","text":"The NINDS conducts a wide range of research on headache disorders. This research aims to discover ways to better diagnose, treat, and ultimately, prevent these disorders."}
{"_id":"05ab299a-55a3-49d3-bfe7-23837bbc97ba","text":"Dyslexia is a brain-based type of learning disability that specifically impairs a person's ability to read. These individuals typically read at levels significantly lower than expected despite having normal intelligence. Although the disorder varies from person to person, common characteristics among people with dyslexia are difficulty with phonological processing (the manipulation of sounds), spelling, and\/or rapid visual-verbal responding. In individuals with adult onset of dyslexia, it usually occurs as a result of brain injury or in the context of dementia; this contrasts with individuals with dyslexia who simply were never identified as children or adolescents. Dyslexia can be inherited in some families, and recent studies have identified a number of genes that may predispose an individual to developing dyslexia."}
{"_id":"2cceb141-472d-48b6-9739-b965c1352da3","text":"The main focus of treatment should be on the specific learning problems of affected individuals. The usual course is to modify teaching methods and the educational environment to meet the specific needs of the individual with dyslexia."}
{"_id":"057ca837-bb9f-41fe-a572-0af03cc9bf2a","text":"For those with dyslexia, the prognosis is mixed. The disability affects such a wide range of people and produces such different symptoms and varying degrees of severity that predictions are hard to make. The prognosis is generally good, however, for individuals whose dyslexia is identified early, who have supportive family and friends and a strong self-image, and who are involved in a proper remediation program."}
{"_id":"57e64ca0-d968-4b15-8437-7461e08c1ac5","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) support dyslexia research through grants to major research institutions across the country. Current research avenues focus on developing techniques to diagnose and treat dyslexia and other learning disabilities, increasing the understanding of the biological and possible genetic bases of learning disabilities, and exploring the relationship between neurophysiological processes and cognitive functions with regard to reading ability."}
{"_id":"da47182b-e232-432a-8413-74516e391de1","text":"Aphasia is a neurological disorder caused by damage to the portions of the brain that are responsible for language production or processing. It may occur suddenly or progressively, depending on the type and location of brain tissue involved. Primary signs of the disorder include difficulty in expressing oneself when speaking, trouble understanding speech, and difficulty with reading and writing. Aphasia is not a disease, but a symptom of brain damage. Although it is primarily seen in individuals who have suffered a stroke, aphasia can also result from a brain tumor, infection, inflammation, head injury, or dementia that affect language-associated regions of the brain. It is estimated that about 1 million people in the United States today suffer from aphasia. The type and severity of language dysfunction depends on the precise location and extent of the damaged brain tissue.\n                \nGenerally, aphasia can be divided into four broad categories: (1) Expressive aphasia (also called Broca's aphasia) involves difficulty in conveying thoughts through speech or writing. The person knows what she\/he wants to say, but cannot find the words he needs. (2) Receptive aphasia (Wernicke's aphasia) involves difficulty understanding spoken or written language. The individual hears the voice or sees the print but cannot make sense of the words. (3) Global aphasia results from severe and extensive damage to the language areas of the brain. People lose almost all language function, both comprehension and expression. They cannot speak or understand speech, nor can they read or write. (4) Indiivfduals with anomic or amnesia aphasia, the least severe form of aphasia, have difficulty in using the correct names for particular objects, people, places, or events."}
{"_id":"1819bb04-e33a-430e-b3b1-ea28cf4316f8","text":"In some instances, an individual will completely recover from aphasia without treatment. In most cases, however, language therapy should begin as soon as possible and be tailored to the individual needs of the person. Rehabilitation with a speech pathologist involves extensive exercises in which individuals read, write, follow directions, and repeat what they hear. Computer-aided therapy may supplement standard language therapy."}
{"_id":"0f84267d-38d7-4975-856f-6913929afc80","text":"The outcome of aphasia is difficult to predict given the wide range of variability of the condition. Generally, people who are younger or have less extensive brain damage fare better. The location of the injury is also important and is another clue to prognosis. In general, people tend to recover skills in language comprehension more completely than those skills involving expression."}
{"_id":"cc52ce08-925d-4bcf-8cc8-74b4a7753f4b","text":"The National Institute of Neurological Disorders and Stroke and the National Institute on Deafness and Other Communication Disorders conduct and support a broad range of scientific investigations to increase our understanding of aphasia, find better treatments, and discover improved methods to restore lost function to people who have aphasia."}
{"_id":"a892f487-4802-4fd5-a94a-dfaedae46258","text":"Colpocephaly is a congenital brain abnormality in which the occipital horns - the posterior or rear portion of the lateral ventricles (cavities) of the brain -- are larger than normal because white matter in the posterior cerebrum has failed to develop or thicken. Colpocephaly, one of a group of structural brain disorders known as cephalic disorders, is characterized by microcephaly (an abnormally small head) and impaired intellect. Other features may include movement abnormalities, muscle spasms, and seizures. Although the cause of colpocephaly is unknown, researchers believe that the disorder results from some kind of disturbance in the fetal environment that occurs between the second and sixth months of pregnancy. Colpocephaly may be diagnosed late in pregnancy, although it is often misdiagnosed as hydrocephalus (excessive accumulation of cerebrospinal fluid in the brain). It may be more accurately diagnosed after birth when signs of impaired intellect, microcephaly, and seizures are present."}
{"_id":"5781113e-b74c-42fd-8e02-777187adfedc","text":"There is no definitive treatment for colpocephaly. Anticonvulsant medications are often prescribed to prevent seizures, and doctors rely on exercise therapies and orthopedic appliances to reduce shrinkage or shortening of muscles."}
{"_id":"871b4bfb-0b31-403e-b282-8f8aacfe14e0","text":"The prognosis for individuals with colpocephaly depends on the severity of the associated conditions and the degree of abnormal brain development. Some children benefit from special education."}
{"_id":"04d19ec7-64fc-4403-a867-234e6e4c45f7","text":"The National Institute of Neurological Disorders and Stroke (NINDS), and other institutes of the National Institutes of Health (NIH), conduct research related to colpocephaly and other cephalic disorders in laboratories at the NIH, and also support additional research through grants to major medical institutions across the country. Much of this research focuses on finding ways to prevent brain abnormalities such as colpocephaly."}
{"_id":"e8ccff00-85c9-43a3-88cb-fac4b6a5af43","text":"Benign essential blepharospasm (BEB) is a progressive neurological disorder characterized by involuntary muscle contractions and spasms of the eyelid muscles. It is a form of dystonia, a movement disorder in which muscle contractions cause sustained eyelid closure, twitching or repetitive movements. BEB begins gradually with increased frequency of eye blinking often associated with eye irritation. Other symptoms may include increasing difficulty in keeping the eyes open, and light sensitivity. Generally, the spasms occur during the day, disappear in sleep, and reappear after waking. As the condition progresses, the spasms may intensify, forcing the eyelids to remain closed for long periods of time, and thereby causing substantial visual disturbance or functional blindness. It is important to note that the blindness is caused solely by the uncontrollable closing of the eyelids and not by a dysfunction of the eyes. BEB occurs in both men and women, although it is especially common in middle-aged and elderly women."}
{"_id":"b33c61c4-d7cb-4f4b-88cf-0e80f28aab4a","text":"In most cases of BEB the treatment of choice is botulinum toxin injections which relax the muscles and stop the spasms. Other treatment options include medications (drug therapy) or surgery--either local surgery of the eye muscles or deep brain stimulation surgery."}
{"_id":"c2690f1e-e16d-43d5-af26-5b539bf35af2","text":"With botulinum toxin treatment most individuals with BEB have substantial relief of symptoms. Although some may experience side effects such as drooping eyelids, blurred or double vision, and eye dryness, these side effects are usually only temporary. The condition may worsen or expand to surrounding muscles; remain the same for many years; and, in rare cases, improve spontaneously."}
{"_id":"bc4e0100-cf66-4373-9747-b37b0d990260","text":"The NINDS supports a broad program of research on disorders of the nervous system, including BEB. Much of this research is aimed at increasing understanding of these disorders and finding ways to prevent, treat, and cure them."}
{"_id":"404ba216-dd8d-4a97-86f1-6d7969842a55","text":"Traumatic brain injury (TBI), a form ofacquired brain injury, occurs when a sudden trauma causes damage to the brain. TBI can result when the head suddenly and violently hits an object, or when an object pierces the skull and enters brain tissue.Symptoms of a TBI can be mild, moderate, or severe, depending on the extent of the damage to the brain. A person with a mild TBI may remain conscious or may experience a loss of consciousness for a few seconds or minutes. Other symptoms of mild TBI include headache, confusion, lightheadedness, dizziness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue or lethargy, a change in sleep patterns, behavioral or mood changes, and trouble with memory, concentration, attention, or thinking. A person with a moderate or severe TBI may show these same symptoms, but may also have a headache that gets worse or does not go away, repeated vomiting or nausea, convulsions or seizures, an inability to awaken from sleep, dilation of one or both pupils of the eyes, slurred speech, weakness or numbness in the extremities, loss of coordination, and increased confusion, restlessness, or agitation."}
{"_id":"224aa72f-2386-413a-9bd4-4916c19268a3","text":"Anyone with signs of moderate or severe TBI should receive medical attention as soon as possible. Because little can be done to reverse the initial brain damage caused by trauma, medical personnel try to stabilize an individual with TBI and focus on preventing further injury. Primary concerns include insuring proper oxygen supply to the brain and the rest of the body, maintaining adequate blood flow, and controlling blood pressure. Imaging tests help in determining the diagnosis and prognosis of a TBI patient. Patients with mild to moderate injuries may receive skull and neck X-rays to check for bone fractures or spinal instability. For moderate to severe cases, the imaging test is a computed tomography (CT) scan. Moderately to severely injured patients receive rehabilitation that involves individually tailored treatment programs in the areas of physical therapy, occupational therapy, speech\/language therapy, physiatry (physical medicine), psychology\/psychiatry, and social support."}
{"_id":"1e114820-56ac-412c-a53d-e987858950d0","text":"Approximately half of severely head-injured patients will need surgery to remove or repair hematomas (ruptured blood vessels) or contusions (bruised brain tissue). Disabilities resulting from a TBI depend upon the severity of the injury, the location of the injury, and the age and general health of the individual. Some common disabilities include problems with cognition (thinking, memory, and reasoning), sensory processing (sight, hearing, touch, taste, and smell), communication (expression and understanding), and behavior or mental health (depression, anxiety, personality changes, aggression, acting out, and social inappropriateness). More serious head injuries may result in stupor, an unresponsive state, but one in which an individual can be aroused briefly by a strong stimulus, such as sharp pain; coma, a state in which an individual is totally unconscious, unresponsive, unaware, and unarousable; vegetative state, in which an individual is unconscious and unaware of his or her surroundings, but continues to have a sleep-wake cycle and periods of alertness; and a persistent vegetative state (PVS), in which an individual stays in a vegetative state for more than a month."}
{"_id":"6b1d4bf1-7275-49d4-a976-4cf7a8925273","text":"The National Institute of Neurological Disorders and Stroke (NINDS) supports TBI research through grants to major medical institutions across the country and conducts TBI research in its intramural laboratories and Clinical Center at the National Institutes of Health (NIH) in Bethesda,Maryland. The Center for Neuroscience and Regenerative Medicine (CNRM) is a TBI research collaboration between intramural NIH and the Uniformed Services University for the Health Sciences (USUHS). NINDS-funded research involves studies in the laboratory and in clinical settings to better understand TBI and the biological mechanisms underlying damage to the brain. This research will allow scientists to develop strategies and interventions to limit the primary and secondary brain damage that occurs within days of a head trauma, and to devise therapies to treat brain injury and improve long-term recovery of function.\n                \nMore information about Traumatic Brain Injury (TBI) Research is available at: http:\/\/www.ninds.nih.gov\/research\/tbi\/index.htm\n                \nMore information about CNRM clinical studies is available at: http:\/\/cnrmstudies.org\/"}
{"_id":"ab0342cc-35d0-4a21-b945-18272543f067","text":"Polymyositis is one of a group of muscle diseases known as the inflammatory myopathies, which are characterized by chronic muscle inflammation accompanied by muscle weakness. Polymyositis affects skeletal muscles (those involved with making movement) on both sides of the body. It is rarely seen in persons under age 18; most cases are in adults between the ages of 31 and 60. Progressive muscle weakness starts in the proximal muscles (muscles closest to the trunk of the body) which eventually leads to difficulties climbing stairs, rising from a seated position, lifting objects, or reaching overhead. People with polymyositis may also experience arthritis, shortness of breath, difficulty swallowing and speaking, and heart arrhythmias. In some cases of polymyositis, distal muscles (muscles further away from the trunk of the body, such as those in the forearms and around the ankles and wrists) may be affected as the disease progresses. Polymyositis may be associated with collagen-vascular or autoimmune diseases, such as lupus. Polymyositis may also be associated with infectious disorders, such as HIV-AIDS."}
{"_id":"1f1a54e7-85f9-4e5c-9110-33ac52ae963d","text":"There is no cure for polymyositis, but the symptoms can be treated. Options include medication, physical therapy, exercise, heat therapy (including microwave and ultrasound), orthotics and assistive devices, and rest. The standard treatment for polymyositis is a corticosteroid drug, given either in pill form or intravenously. Immunosuppressant drugs, such as azathioprine and methotrexate, may reduce inflammation in people who do not respond well to prednisone. Periodic treatment using intravenous immunoglobulin can also improve recovery. Other immunosuppressive agents used to treat the inflammation associated with polymyositis include cyclosporine A, cyclophosphamide, and tacrolimus. Physical therapy is usually recommended to prevent muscle atrophy and to regain muscle strength and range of motion."}
{"_id":"9aa48131-f3ab-41fe-a827-9613b1b45f32","text":"The prognosis for polymyositis varies. Most people respond fairly well to therapy, but some have a more severe disease that does not respond adequately to therapies and are left with significant disability. In rare cases individuals with severe and progressive muscle weakness will develop respiratory failure or pneumonia. Difficulty swallowing may cause weight loss and malnutrition."}
{"_id":"a4617543-ec28-424e-aa38-d114fcba82ef","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research relating to polymyositis in laboratories at the NIH and support additional research through grants to major medical institutions across the country. Currently funded research is exploring patterns of gene expression among the inflammatory myopathies, the role of viral infection as a precursor to the disorders, and the safety and efficacy of various treatment regimens."}
{"_id":"299e4140-6165-4807-bb67-2112792a7e4b","text":"Wallenbergs syndrome is a neurological condition caused by a stroke in the vertebral or posterior inferior cerebellar artery of the brain stem. Symptoms include difficulties with swallowing, hoarseness, dizziness, nausea and vomiting, rapid involuntary movements of the eyes (nystagmus), and problems with balance and gait coordination. Some individuals will experience a lack of pain and temperature sensation on only one side of the face, or a pattern of symptoms on opposite sides of the body  such as paralysis or numbness in the right side of the face, with weak or numb limbs on the left side. Uncontrollable hiccups may also occur, and some individuals will lose their sense of taste on one side of the tongue, while preserving taste sensations on the other side. Some people with Wallenbergs syndrome report that the world seems to be tilted in an unsettling way, which makes it difficult to keep their balance when they walk."}
{"_id":"79876ebe-8384-4b4f-a351-4cc222ee7908","text":"Treatment for Wallenberg's syndrome is symptomatic. A feeding tube may be necessary if swallowing is very difficult. Speech\/swallowing therapy may be beneficial. In some cases, medication may be used to reduce or eliminate pain. Some doctors report that the anti-epileptic drug gabapentin appears to be an effective medication for individuals with chronic pain."}
{"_id":"acd4dfa8-2072-4046-96bd-2376d89e3465","text":"The outlook for someone with Wallenbergs syndrome depends upon the size and location of the area of the brain stem damaged by the stroke. Some individuals may see a decrease in their symptoms within weeks or months. Others may be left with significant neurological disabilities for years after the initial symptoms appeared."}
{"_id":"d05e15ac-719f-4c6c-b37d-392b2de0399e","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to Wallenbergs syndrome in its laboratories at the National Institutes of Health (NIH), and also supports additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders such as Wallenbergs syndrome."}
{"_id":"44338a44-f0de-4ca6-b259-a597d26d43d4","text":"Monomelic amyotrophy (MMA) is characterized by progressive degeneration and loss of motor neurons, the nerve cells in the brain and spinal cord that are responsible for controlling voluntary muscles. It is characterized by weakness and wasting in a single limb, usually an arm and hand rather than a foot and leg. There is no pain associated with MMA. While some physicians contend that mild sensory loss may be associated with this disease, many experts suggest that such symptoms actually indicate a cause other than MMA. MMA occurs in males between the ages of 15 and 25. Onset and progression are slow. MMA is seen most frequently in Asia, particularly in Japan and India; it is much less common in North America. In most cases, the cause is unknown, although there have been a few published reports linking MMA to traumatic or radiation injury. There are also familial forms of MMA. Diagnosis is made by physical exam and medical history. Electromyography (EMG), a special recording technique that detects electrical activity in muscles, shows a loss of the nerve supply, or denervation, in the affected limb; MRI and CT scans may show muscle atrophy. People believed to have MMA should be followed by a neuromuscular disease specialist for a number of months to make certain that no signs of other motor neuron diseases develop."}
{"_id":"a087621c-6d8f-4a01-b801-0a1629181c96","text":"There is no cure for MMA. Treatment consists of muscle strengthening exercises and training in hand coordination"}
{"_id":"0a680f14-27df-4246-9094-0f81b68bd7c9","text":"The symptoms of MMA usually progress slowly for one to two years before reaching a plateau, and then remain stable for many years. Disability is generally slight. Rarely, the weakness progresses to the opposite limb. There is also a slowly progressive variant of MMA known as O'Sullivan-McLeod syndrome, which only affects the small muscles of the hand and forearm and has a slowly progressive course."}
{"_id":"fd2525c7-d7b5-413d-a977-023a8ccfdccf","text":"The NINDS conducts and supports a broad range of research on motor neuron diseases. The goals of these studies are to increase understanding of these disorders and to find ways to treat, prevent, and ultimately cure them."}
{"_id":"01221a4a-e474-45f3-93fd-2938d27f9187","text":"Gerstmann's syndrome is a cognitive impairment that results from damage to a specific area of the brain -- the left parietal lobe in the region of the angular gyrus. It may occur after a stroke or in association with damage to the parietal lobe. It is characterized by four primary symptoms: a writing disability (agraphia or dysgraphia), a lack of understanding of the rules for calculation or arithmetic (acalculia or dyscalculia), an inability to distinguish right from left, and an inability to identify fingers (finger agnosia). The disorder should not be confused with Gerstmann-Strussler-Scheinker disease, a type of transmissible spongiform encephalopathy.\n                \nIn addition to exhibiting the above symptoms, many adults also experience aphasia, (difficulty in expressing oneself when speaking, in understanding speech, or in reading and writing).\n                \nThere are few reports of the syndrome, sometimes called developmental Gerstmann's syndrome, in children. The cause is not known. Most cases are identified when children reach school age, a time when they are challenged with writing and math exercises. Generally, children with the disorder exhibit poor handwriting and spelling skills, and difficulty with math functions, including adding, subtracting, multiplying, and dividing. An inability to differentiate right from left and to discriminate among individual fingers may also be apparent. In addition to the four primary symptoms, many children also suffer from constructional apraxia, an inability to copy simple drawings. Frequently, there is also an impairment in reading. Children with a high level of intellectual functioning as well as those with brain damage may be affected with the disorder."}
{"_id":"ca57e930-05d1-45cb-9aa1-c43a74f4e73b","text":"There is no cure for Gerstmann's syndrome. Treatment is symptomatic and supportive. Occupational and speech therapies may help diminish the dysgraphia and apraxia. In addition, calculators and word processors may help school children cope with the symptoms of the disorder."}
{"_id":"31542624-5893-4401-a59c-54e8574d9ec3","text":"In adults, many of the symptoms diminish over time. Although it has been suggested that in children symptoms may diminish over time, it appears likely that most children probably do not overcome their deficits, but learn to adjust to them."}
{"_id":"135ba6a8-b65c-48dd-918f-a7438fea82a6","text":"The NINDS supports research on disorders that result from damage to the brain such as dysgraphia. The NINDS and other components of the National Institutes of Health also support research on learning disabilities. Current research avenues focus on developing techniques to diagnose and treat learning disabilities and increase understanding of the biological basis of them."}
{"_id":"a0ebfb24-a635-430c-89ba-d097f98b4fed","text":"Whiplash-a soft tissue injury to the neck-is also called neck sprain or neck strain. It is characterized by a collection of symptoms that occur following damage to the neck, usually because of sudden extension and flexion. The disorder commonly occurs as the result of an automobile accident and may include injury to intervertebral joints, discs, and ligaments, cervical muscles, and nerve roots. Symptoms such as neck pain may be present directly after the injury or may be delayed for several days. In addition to neck pain, other symptoms may include neck stiffness, injuries to the muscles and ligaments (myofascial injuries), headache, dizziness, abnormal sensations such as burning or prickling (paresthesias), or shoulder or back pain. In addition, some people experience cognitive, somatic, or psychological conditions such as memory loss, concentration impairment, nervousness\/irritability, sleep disturbances, fatigue, or depression."}
{"_id":"3ad58e32-a097-4363-8c3a-8f09d9629a2b","text":"Treatment for individuals with whiplash may include pain medications, nonsteroidal anti-inflammatory drugs, antidepressants, muscle relaxants, and a cervical collar (usually worn for 2 to 3 weeks). Range of motion exercises, physical therapy, and cervical traction may also be prescribed. Supplemental heat application may relieve muscle tension."}
{"_id":"c6fbf44c-869e-40f2-b499-001ac25498e2","text":"Generally, prognosis for individuals with whiplash is good. The neck and head pain clears within a few days or weeks. Most patients recover within 3 months after the injury, however, some may continue to have residual neck pain and headaches."}
{"_id":"cdd2886f-8da8-4779-84be-de2384c0b64e","text":"The NINDS conducts and supports research on trauma-related disorders such as whiplash. Much of this research focuses on increasing scientific understanding of these disorders and finding ways to prevent and treat them."}
{"_id":"bf75cf60-187b-4426-8ec2-689a808f0f82","text":"Tardive dyskinesia is a neurological syndrome caused by the long-term use of neuroleptic drugs. Neuroleptic drugs are generally prescribed for psychiatric disorders, as well as for some gastrointestinal and neurological disorders. Tardive dyskinesia is characterized by repetitive, involuntary, purposeless movements. Features of the disorder may include grimacing, tongue protrusion, lip smacking, puckering and pursing, and rapid eye blinking. Rapid movements of the arms, legs, and trunk may also occur. Involuntary movements of the fingers may be present."}
{"_id":"533e6c90-ef6e-4aea-8ca8-f76feb825b97","text":"Treatment is highly individualized. The first step is generally to stop or minimize the use of the neuroleptic drug, but this can be done only under close supervision of the physician.. However, for patients with a severe underlying condition this may not be a feasible option. Replacing the neuroleptic drug with substitute drugs may help some individuals. The only approved drug treatment for tardive dyskenesia is tetrabenazine, which is usually effective but can have side effects that need to be discussed prior to starting therapy. Other drugs such as benzodiazepines, clozapine, or botulinum toxin injections also may be tried."}
{"_id":"d60dd97b-89f0-4b47-bb77-9bcf648b205c","text":"Symptoms of tardive dyskinesia may remain long after discontinuation of neuroleptic drugs. In many cases, the symptoms stop spontaneously, but in some cases they may persist indefinitely."}
{"_id":"7829a529-8a4d-4ce7-ac40-bb189917dca6","text":"The NINDS conducts and supports a broad range of research on movement disorders including tardive dyskinesia. The goals of this research are to improve understanding of these disorders and to discover ways to treat, prevent, and, ultimately, cure them."}
{"_id":"8662017b-aa6a-44fc-ad31-e8514e24ec1f","text":"Issacs' syndrome (also known as neuromyotonia, Isaacs-Mertens syndrome, continuous muscle fiber activity syndrome, and quantal squander syndrome) is a rare neuromuscular disorder caused by hyperexcitability and continuous firing of the peripheral nerve axons that activate muscle fibers. Symptoms, which include progressive muscle stiffness, continuously contracting or twitching muscles (myokymia), cramping, increased sweating, and delayed muscle relaxation, occur even during sleep or when individuals are under general anesthesia. Many people also develop weakened reflexes and muscle pain, but numbness is relatively uncommon. In most people with Issacs' syndrome, stiffness is most prominent in limb and trunk muscles, although symptoms can be limited to cranial muscles. Speech and breathing may be affected if pharyngeal or laryngeal muscles are involved. Onset is between ages 15 and 60, with most individuals experiencing symptoms before age 40. There are hereditary and acquired (occurring from unknown causes) forms of the disorder. The acquired form occasionally develops in association with peripheral neuropathies or after radiation treatment, but more often is caused by an autoimmune condition. Autoimmune-mediated Issacs' syndrome is typically caused by antibodies that bind to potassium channels on the motor nerve. Issacs' syndrome is only one of several neurological conditions that can be caused by potassium channel antibodies."}
{"_id":"4fbb962d-ba06-40a1-aaa7-e3faf5cb033c","text":"Anticonvulsants, including phenytoin and carbamazepine, usually provide significant relief from the stiffness, muscle spasms, and pain associated with Isaacs' syndrome. Plasma exchange may provide short-term relief for individuals with some forms of the acquired disorder."}
{"_id":"a6c0b7f3-0a96-4940-839b-b97d507b21d7","text":"There is no cure for Isaacs' syndrome. The long-term prognosis for individuals with the disorder is uncertain."}
{"_id":"0ce1cfe1-e3f4-43ec-aa22-7568967eea2b","text":"The NINDS supports an extensive research program of basic studies to increase understanding of diseases that affect the brain, spinal cord, muscles, and nerves. This research examines the genetics, symptoms, progression, and psychological and behavioral impact of diseases, with the goal of improving ways to diagnose, treat, and, ultimately, cure these disorders."}
{"_id":"6c24040f-ee55-4432-97e6-fed465b4eab5","text":"Learning disabilities are disorders that affect the ability to understand or use spoken or written language, do mathematical calculations, coordinate movements, or direct attention. Although learning disabilities occur in very young children, the disorders are usually not recognized until the child reaches school age. Research shows that 8 to 10 percent of American children under 18 years of age have some type of learning disability."}
{"_id":"98a6e6d1-646f-4023-ae75-da8e66de6840","text":"The most common treatment for learning disabilities is special education. Specially trained educators may perform a diagnostic educational evaluation assessing the child's academic and intellectual potential and level of academic performance. Once the evaluation is complete, the basic approach is to teach learning skills by building on the child's abilities and strengths while correcting and compensating for disabilities and weaknesses. Other professionals such as speech and language therapists also may be involved. Some medications may be effective in helping the child learn by enhancing attention and concentration. Psychological therapies may also be used."}
{"_id":"9bf71396-d73d-40d6-81c8-432d320df863","text":"Learning disabilities can be lifelong conditions. In some people, several overlapping learning disabilities may be apparent. Other people may have a single, isolated learning problem that has little impact on their lives."}
{"_id":"77521e66-804c-4c03-b52e-3e54be3411cd","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other Institutes of the National Institutes of Health (NIH) support research learning disabilities through grants to major research institutions across the country. Current research avenues focus on developing techniques to diagnose and treat learning disabilities and increase understanding of their biological basis."}
{"_id":"4dc3465a-490e-4bef-a321-9187d222da34","text":"Spasticity is a condition in which there is an abnormal increase in muscle tone or stiffness of muscle, which might interfere with movement, speech, or be associated with discomfort or pain. Spasticity is usually caused by damage to nerve pathways within the brain or spinal cord that control muscle movement. It may occur in association with spinal cord injury, multiple sclerosis, cerebral palsy, stroke, brain or head trauma, amyotrophic lateral sclerosis, hereditary spastic paraplegias, and metabolic diseases such as adrenoleukodystrophy, phenylketonuria, and Krabbe disease. Symptoms may include hypertonicity (increased muscle tone), clonus (a series of rapid muscle contractions), exaggerated deep tendon reflexes, muscle spasms, scissoring (involuntary crossing of the legs), and fixed joints (contractures). The degree of spasticity varies from mild muscle stiffness to severe, painful, and uncontrollable muscle spasms. Spasticity can interfere with rehabilitation in patients with certain disorders, and often interferes with daily activities."}
{"_id":"dbbbb325-ca32-4afb-a859-34731ce56fc1","text":"Treatment may include such medications as baclofen, diazepam, tizanidine or clonazepam. Physical therapy regimens may include muscle stretching and range of motion exercises to help prevent shrinkage or shortening of muscles and to reduce the severity of symptoms. Targeted injection of botulinum toxin into muscles with the most tome can help to selectively weaken these muscles to improve range of motion and function. Surgery may be recommended for tendon release or to sever the nerve-muscle pathway."}
{"_id":"ce9324b6-623f-4c4b-83a5-c2662326b1c8","text":"The prognosis for those with spasticity depends on the severity of the spasticity and the associated disorder(s)."}
{"_id":"ab44b0f0-003e-48be-a67b-700756bd95ae","text":"The NINDS supports research on brain and spinal cord disorders that can cause spasticity. The goals of this research are to increase scientific understanding about these disorders and to find ways to prevent, treat, and cure them."}
{"_id":"ffb2c0f0-709e-4196-a043-f83b5713d158","text":"Prosopagnosia is a neurological disorder characterized by the inability to recognize faces. Prosopagnosia is also known as face blindness or facial agnosia. The term prosopagnosia comes from the Greek words for face and lack of knowledge. Depending upon the degree of impairment, some people with prosopagnosia may only have difficulty recognizing a familiar face; others will be unable to discriminate between unknown faces, while still others may not even be able to distinguish a face as being different from an object. Some people with the disorder are unable to recognize their own face. Prosopagnosia is not related to memory dysfunction, memory loss, impaired vision, or learning disabilities. Prosopagnosia is thought to be the result of abnormalities, damage, or impairment in the right fusiform gyrus, a fold in the brain that appears to coordinate the neural systems that control facial perception and memory. Prosopagnosia can result from stroke, traumatic brain injury, or certain neurodegenerative diseases. In some cases it is a congenital disorder, present at birth in the absence of any brain damage. Congenital prosopagnosia appears to run in families, which makes it likely to be the result of a genetic mutation or deletion. Some degree of prosopagnosia is often present in children with autism and Aspergers syndrome, and may be the cause of their impaired social development."}
{"_id":"5b388260-314d-4a6b-96e0-0792b815c435","text":"The focus of any treatment should be to help the individual with prosopagnosia develop compensatory strategies. Adults who have the condition as a result of stroke or brain trauma can be retrained to use other clues to identify individuals."}
{"_id":"056a7020-c068-4f60-8474-1e8817181f09","text":"Prosopagnosia can be socially crippling. Individuals with the disorder often have difficulty recognizing family members and close friends. They often use other ways to identify people, such as relying on voice, clothing, or unique physical attributes, but these are not as effective as recognizing a face. Children with congenital prosopagnosia are born with the disability and have never had a time when they could recognize faces. Greater awareness of autism, and the autism spectrum disorders, which involve communication impairments such as prosopagnosia, is likely to make the disorder less overlooked in the future."}
{"_id":"772843ae-92b9-426d-ac6e-facdb256b451","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to prosopagnosia in its laboratories at the National Institutes of Health (NIH), and also supports additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders, such as prosopagnosia."}
{"_id":"e6c2fa3e-a5a6-4739-bd5c-f14dfe4a7559","text":"Lesch-Nyhan syndrome (LNS) is a rare, inherited disorder caused by a deficiency of the enzyme hypoxanthine-guanine phosphoribosyltransferase (HPRT). LNS is an X-linked recessive disease-- the gene is carried by the mother and passed on to her son. LNS is present at birth in baby boys. The lack of HPRT causes a build-up of uric acid in all body fluids, and leads to symptoms such as severe gout, poor muscle control, and moderate retardation, which appear in the first year of life. A striking feature of LNS is self-mutilating behaviors  characterized by lip and finger biting  that begin in the second year of life. Abnormally high uric acid levels can cause sodium urate crystals to form in the joints, kidneys, central nervous system, and other tissues of the body, leading to gout-like swelling in the joints and severe kidney problems. Neurological symptoms include facial grimacing, involuntary writhing, and repetitive movements of the arms and legs similar to those seen in Huntingtons disease. Because a lack of HPRT causes the body to poorly utilize vitamin B12, some boys may develop a rare disorder called megaloblastic anemia."}
{"_id":"db19cbd6-c3b9-4614-9ed2-a3fee960b97d","text":"Treatment for LNS is symptomatic. Gout can be treated with allopurinol to control excessive amounts of uric acid. Kidney stones may be treated with lithotripsy, a technique for breaking up kidney stones using shock waves or laser beams. There is no standard treatment for the neurological symptoms of LNS. Some may be relieved with the drugs carbidopa\/levodopa, diazepam, phenobarbital, or haloperidol."}
{"_id":"768aee3f-5366-4a49-bf27-bee6562985d8","text":"The prognosis for individuals with LNS is poor. Death is usually due to renal failure in the first or second decade of life."}
{"_id":"5b75eb31-3b23-42bd-9e91-1957aebb18a3","text":"The gene associated with LNS is known. The NINDS supports and conducts research on genetic disorders such as LNS in an effort to find ways to prevent and treat these disorders."}
{"_id":"6530c8a3-1e05-4e2f-bb50-6362ba8757c6","text":"Deep brain stimulation (DBS) is a surgical procedure used to treat several disabling neurological symptomsmost commonly the debilitating motor symptoms of Parkinsons disease (PD), such as tremor, rigidity, stiffness, slowed movement, and walking problems. The procedure is also used to treat essential tremor and dystonia. At present, the procedure is used only for individuals whose symptoms cannot be adequately controlled with medications. However, only individuals who improve to some degree after taking medication for Parkinsons benefit from DBS. A variety of conditions may mimic PD but do not respond to medications or DBS. DBS uses a surgically implanted, battery-operated medical device called an implantable pulse generator (IPG) - similar to a heart pacemaker and approximately the size of a stopwatch to - deliver electrical stimulation to specific areas in the brain that control movement, thus blocking the abnormal nerve signals that cause PD symptoms.\n                \nBefore the procedure, a neurosurgeon uses magnetic resonance imaging (MRI) or computed tomography (CT) scanning to identify and locate the exact target within the brain for surgical intervention. Some surgeons may use microelectrode recording - which involves a small wire that monitors the activity of nerve cells in the target area - to more specifically identify the precise brain area that will be stimulated. Generally, these areas are the thalamus, subthalamic nucleus, and globus pallidus. There is a low chance that placement of the stimulator may cause bleeding or infection in the brain.\n                \nThe DBS system consists of three components: the lead, the extension, and the IPG. The lead (also called an electrode)a thin, insulated wireis inserted through a small opening in the skull and implanted in the brain. The tip of the electrode is positioned within the specific brain area. \n                \nThe extension is an insulated wire that is passed under the skin of the head, neck, and shoulder, connecting the lead to the implantable pulse generator. The IPG (the \"battery pack\") is the third component and is usually implanted under the skin near the collarbone. In some cases it may be implanted lower in the chest or under the skin over the abdomen.\n                \nOnce the system is in place, electrical impulses are sent from the IPG up along the extension wire and the lead and into the brain. These impulses block abnormal electrical signals and alleviate PD motor symptoms."}
{"_id":"e06ef279-ae99-4ada-b44c-b631b05fface","text":"Unlike previous surgeries for PD, DBS involves minimal permanent surgical changes to the brain. Instead, the procedure uses electrical stimulation to regulate electrical signals in neural circuits to and from identified areas in the brain to improve PD symptoms. Thus, if DBS causes unwanted side effects or newer, more promising treatments develop in the future, the implantable pulse generator can be removed, and the DBS procedure can be halted. Also, stimulation from the IPG is easily adjustablewithout further surgeryif the persons condition changes. Some people describe the pulse generator adjustments as \"programming.\""}
{"_id":"46084ba3-46dc-4a01-8fda-097cb598fc8b","text":"Although most individuals still need to take medication after undergoing DBS, many people with Parkinsons disease experience considerable reduction of their motor symptoms and are able to reduce their medications. The amount of reduction varies but can be considerably reduced in most individuals, and can lead to a significant improvement in side effects such as dyskinesias (involuntary movements caused by long-term use of levodopa). In some cases, the stimulation itself can suppress dyskinesias without a reduction in medication. DBS does not improve cognitive symptoms in PD and indeed may worsen them, so it is not generally used if there are signs of dementia. DBS changes the brain firing pattern but does not slow the progression of the neurodegeneration."}
{"_id":"109c9c03-3710-49fe-856b-32c2ae8dcaae","text":"The National Institute of Neurological Disorders and Stroke (NINDS), a part of the National institutes of Health (NIH), supports research on DBS to determine its safety, reliability, and effectiveness as a treatment for PD. NINDS supported research on brain circuitry was critical to the development of DBS.\n                \nResearchers are continuing to study DBS and to develop ways of improving it. A two-part study funded by the NINDS and the Department of Veterans Affairs first compared bilateral DBS to best medical therapy, including medication adjustment and physical therapy. Bilateral DBS showed overall superiority to best medical therapy at improving motor symptoms and quality of life. The second part of the study, involving nearly 300 patients, compared subthalamic nucleus (STN) DBS to globus pallidus interna (GPI) DBS. The two groups reported similar improvements in motor control and quality of life in scores on the Unified Parkinsons Disease Rating Scale. On a variety of neuropsychological tests, there were no significant differences between the two groups. However, the STN DBS group experienced a greater decline on a test of visuomotor processing speed, which measures how quickly someone thinks and acts on information. Also, the STN DBS group had slight worsening on a standard assessment of depression, while the GPI DBS group had slight improvement on the same test. The importance of these two differences is not clear, and will be scrutinized in follow-up research.\n                \nIn addition, NINDS-supported researchers are developing and testing improved implantable pulse generators, and conducting studies to better understand the therapeutic effect of neurostimulation on neural circuitry and brain regions affected in PD. For more information about current studies on brain stimulation and Parkinsons disease, see www.clinicaltrials.gov and search for deep brain stimulation AND Parkinson AND NINDS. For information about NINDS-and NIH-supported research studies in this area, see the NIH RePORTER (Research Portfolio Online Reporting Tools) at http:\/\/projectreporter.nih.gov and search for deep brain stimulation AND Parkinson.\n                \nThe Brain Initiative for Advancing Innovative Neurotechnologies (BRAIN) initiative, announced in 2013, offers unprecedented opportunities to unlock the mysteries of the brain and accelerate the development of research and technologies to treat disorders such as Parkinsons disease. For more information about the BRAIN initiative, see www.nih.gov\/science\/brain."}
{"_id":"c4928452-30fa-4799-8702-7efa4590d2ff","text":"Lambert-Eaton myasthenic syndrome (LEMS) is a disorder of the neuromuscular junction-the site where nerve cells meet muscle cells and help activate the muscles. It is caused by a disruption of electrical impulses between these nerve and muscle cells. LEMS is an autoimmune condition; in such disorders the immune system, which normally protects the body from foreign organisms, mistakenly attacks the body's own tissues. The disruption of electrical impulses is associated with antibodies produced as a consequence of this autoimmunity. Symptoms include muscle weakness, a tingling sensation in the affected areas, fatigue, and dry mouth. LEMS is closely associated with cancer, in particular small cell lung cancer. More than half the individuals diagnosed with LEMS also develop small cell lung cancer. LEMS may appear up to 3 years before cancer is diagnosed."}
{"_id":"cd553314-48b1-47cf-b158-055b6d10feb5","text":"There is no cure for LEMS. Treatment is directed at decreasing the autoimmune response (through the use of steroids, plasmapheresis, or high-dose intravenous immunoglobulin) or improving the transmission of the disrupted electrical impulses by giving drugs such as di-amino pyridine or pyridostigmine bromide (Mestinon). For patients with small cell lung cancer, treatment of the cancer is the first priority."}
{"_id":"e919673a-bfca-4245-b31b-b4e793fa715d","text":"The prognosis for individuals with LEMS varies. Those with LEMS not associated with malignancy have a benign overall prognosis. Generally the presence of cancer determines the prognosis."}
{"_id":"0824c47c-0ab9-4f2a-aa32-66a00200aee6","text":"The NINDS supports research on neuromuscular disorders such as LEMS with the ultimate goal of finding ways to treat, prevent, and cure them."}
{"_id":"29514dfe-8ca9-4283-92df-90141424e619","text":"Having trouble swallowing (dysphagia) is a symptom that accompanies a number of neurological disorders. The problem can occur at any stage of the normal swallowing process as food and liquid move from the mouth, down the back of the throat, through the esophagus and into the stomach. Difficulties can range from a total inability to swallow, to coughing or choking because the food or liquid is entering the windpipe, which is referred to as aspiration. When aspiration is frequent a person can be at risk of developing pneumonia. Food may get \"stuck\" in the throat or individuals may drool because they cannot swallow their saliva. Neurological conditions that can cause swallowing difficulties are: stroke (the most common cause of dysphagia); traumatic brain injury; cerebral palsy; Parkinson disease and other degenerative neurological disorders such as amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig's disease), multiple sclerosis, progressive supranuclear palsy, Huntington disease, and myasthenia gravis. Muscular dystrophy and myotonic dystrophy are accompanied by dysphagia, which is also the cardinal symptom of oculopharyngeal muscular dystrophy, a rare, progressive genetic disorder."}
{"_id":"637c9edd-6ee4-4773-b61e-67303d74a665","text":"Changing a person's diet by adding thickeners helps many people, as does learning different ways to eat and chew that reduce the risk for aspiration. Occasionally drug therapy that helps the neurological disorder can also help dysphagia. In a few persons, botulinum toxin injections can help when food or liquid cannot enter the esophagus to get to the stomach. More severely disabled individuals may require surgery or the insertion of feeding tubes."}
{"_id":"a3e0e5dd-4567-4521-bcdb-db29cb4b25b0","text":"The prognosis depends upon the type of swallowing problem and the course of the neurological disorder that produces it. In some cases, dysphagia can be partially or completely corrected using diet manipulation or non-invasive methods. In others, especially when the dysphagia is causing aspiration and preventing adequate nutrition and causing weight loss, it may require aggressive intervention such as a feeding tube. For those with progressive degenerative neurological disorders, dysphagia will be only one in a cluster of symptoms and disabilities that have to be treated."}
{"_id":"6497fb25-4c9b-4ee2-bfcf-e775e49abd54","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes at the National Institutes of Health conduct research related to dysphagia in their clinics and laboratories and support additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to treat dysphagia."}
{"_id":"b7ed1ed1-3f2a-47b4-82b5-d22d1cb2421e","text":"Post-polio syndrome (PPS) is a condition that affects polio survivors many years after recovery from an initial attack of the poliomyelitis virus. PPS is characterized by a further weakening of muscles that were previously affected by the polio infection. The most common symptoms include slowly progressive muscle weakness, fatigue (both general and muscular), and a decrease in muscle size (muscular atrophy). Pain from joint deterioration and increasing skeletal deformities such as scoliosis are common. Some individuals experience only minor symptoms, while others develop more visible muscle weakness and atrophy. PPS is rarely life-threatening but the symptoms can interfere significantly with the individual's capacity to function independently. While polio is contagious, PPS is not transmissible. Only a polio survivor can develop PPS."}
{"_id":"91c01c3e-dbfe-46af-9aba-a75f7d34b02a","text":"Presently, no prevention has been found that can stop deterioration or reverse the deficits caused by the syndrome A number of controlled studies have demonstrated that nonfatiguing exercises may improve muscle strength and reduce tiredness. Doctors recommend that polio survivors follow standard healthy lifestyle practices: consuming a well-balanced diet, exercising judiciously (preferably under the supervision of an experienced health professional), and visiting a doctor regularly. There has been much debate about whether to encourage or discourage exercise for polio survivors or individuals who already have PPS. A commonsense approach, in which people use individual tolerance as their limit, is currently recommended. Preliminary studies indicate that intravenous immunoglobulin therapy may reduce pain, increase quality of life, and improve strength modestly."}
{"_id":"3c862862-d70e-4470-a6dc-de3d078860e0","text":"PPS is a very slowly progressing condition marked by long periods of stability. The severity of PPS depends on the degree of the residual weakness and disability an individual has after the original polio attack. People who had only minimal symptoms from the original attack and subsequently develop PPS will most likely experience only mild PPS symptoms. People originally hit hard by the polio virus, who were left with severe residual weakness, may develop a more severe case of PPS with a greater loss of muscle function, difficulty in swallowing, and more periods of fatigue."}
{"_id":"259bd58b-5c5f-4e3c-b6ee-3c0f34badd80","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to PPS in laboratories at the NIH, and also support additional PPS research through grants to major medical institutions across the country."}
{"_id":"bdaf94c4-2390-454b-8af5-4ea3a921ed79","text":"The septum pellucidum (SP) is a thin membrane located at the midline of the brain between the two cerebral hemispheres, or halves of the brain.. It is connected to the corpus callosum -- a collection of nerve fibers that connect the cerebral hemispherers. This rare abnormality accompanies various malformations of the brain that affect intelligence, behavior, and the neurodevelopmental process, and seizures may occur. Children who are born without this membrane and also have other abnormalities--pituitary deficiencies and abnormal development of the optic disk--have a disorder known as septo-optic dysplasia. More information about this condition can be located at the NINDS Septo-Optic Dysplasia Information Page."}
{"_id":"b7a96f0c-c77b-4130-9542-f07273119275","text":"Absence of the SP alone is not a disorder but is instead a characteristic noted in children with septo-optic dysplasia or other developmental anomalies."}
{"_id":"04ffb011-7fd0-48cd-a656-d94a75767f58","text":"When the absence of the septum pellucidum is part of septo-optic dysplasia, the prognosis varies according to the presence and severity of associated symptoms. By itself, absence of the septum pellucidum is not life-threatening."}
{"_id":"a30dc04f-c650-47bc-8cb4-d1522a9c91ff","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system ad to use that knowledge to reduce the burden of neurological disease. The NINDS conducts and supports a wide range of studies that explore the complex mechanisms of normal brain development. The knowledge gained from these fundamental studies provides the foundation for understanding how this process can go awry and offers hope for new means to treat and prevent developmental brain disorders."}
{"_id":"f0172137-b05c-47d3-ab87-c4bf02b94656","text":"Peripheral neuropathy describes damage to the peripheral nervous system, which transmits information from the brain and spinal cord to every other part of the body.\n                \nMore than 100 types of peripheral neuropathy have been identified, each with its own characteristic set of symptoms, pattern of development, and prognosis. Impaired function and symptoms depend on the type of nerves -- motor, sensory, or autonomic -- that are damaged. Some people may experience temporary numbness, tingling, and pricking sensations, sensitivity to touch, or muscle weakness. Others may suffer more extreme symptoms, including burning pain (especially at night), muscle wasting, paralysis, or organ or gland dysfunction. Peripheral neuropathy may be either inherited or acquired. Causes of acquired peripheral neuropathy include physical injury (trauma) to a nerve, tumors, toxins, autoimmune responses, nutritional deficiencies, alcoholism, medical procedures, and vascular and metabolic disorders. Acquired peripheral neuropathies are caused by systemic disease, trauma from external agents, or infections or autoimmune disorders affecting nerve tissue. Inherited forms of peripheral neuropathy are caused by inborn mistakes in the genetic code or by new genetic mutations."}
{"_id":"c4d1f432-e528-4ac1-848b-df5b4d666b37","text":"No medical treatments exist that can cure inherited peripheral neuropathy. However, there are therapies for many other forms. In general, adopting healthy habits -- such as maintaining optimal weight, avoiding exposure to toxins, following a physician-supervised exercise program, eating a balanced diet, correcting vitamin deficiencies, and limiting or avoiding alcohol consumption -- can reduce the physical and emotional effects of peripheral neuropathy. Systemic diseases frequently require more complex treatments."}
{"_id":"e7a2c3bc-421e-4b7a-b1e6-21b7f5d215f0","text":"In acute neuropathies, such as Guillain-Barr syndrome, symptoms appear suddenly, progress rapidly, and resolve slowly as damaged nerves heal. In chronic forms, symptoms begin subtly and progress slowly. Some people may have periods of relief followed by relapse. Others may reach a plateau stage where symptoms stay the same for many months or years. Some chronic neuropathies worsen over time, but very few forms prove fatal unless complicated by other diseases. Occasionally the neuropathy is a symptom of another disorder."}
{"_id":"e86a7aa6-c800-44c0-b04e-7c7af26bf7bf","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to peripheral neuropathies in laboratories at the NIH and also support additional research through grants to major medical institutions across the country. Current research projects funded by the NINDS involve investigations of genetic factors associated with hereditary neuropathies, studies of biological mechanisms involved in diabetes-associated neuropathies, and investigations exploring how the immune system contributes to peripheral nerve damage. Neuropathic pain is a primary target of NINDS-sponsored studies aimed at developing more effective therapies for symptoms of peripheral neuropathy. Some scientists hope to identify substances that will block the brain chemicals that generate pain signals, while others are investigating the pathways by which pain signals reach the brain."}
{"_id":"49a9973c-5251-4740-8ade-b5cb31a73823","text":"Microcephaly is a medical condition in which the circumference of the head is smaller than normal because the brain has not developed properly or has stopped growing. Microcephaly can be present at birth or it may develop in the first few years of life. It is most often caused by genetic abnormalities that interfere with the growth of the cerebral cortex during the early months of fetal development. Babies may also be born with microcephaly if, during pregnancy, their mother abused drugs or alcohol; became infected with a cytomegalovirus, rubella (German measles), varicella (chicken pox) virus, or possibly Zika virus; was exposed to certain toxic chemicals; or had untreated phenylketonuria (PKU, a harmful buildup of the amino acid phenylalanine in the blood). Microcephaly is associated with Downs syndrome, chromosomal syndromes, and neurometabolic syndromes.\n                \nWith viral-induced brain injury, such as with the Zika virus, there is often widespread tissue and cell death leading to brain shrinkage rather than simply impaired growth. The Zika virus is also associated with retinal lesions in about a third of cases, often leading to blindness.\n                \nDepending on the severity of the accompanying syndrome, children with microcephaly may have impaired cognitive development, delayed motor functions and speech, facial distortions, dwarfism or short stature, hyperactivity, seizures, difficulties with coordination and balance, and other brain or neurological abnormalities."}
{"_id":"535f51b2-7bca-49da-9a63-e7a695187775","text":"There is no treatment for microcephaly that can return a childs head to a normal size or shape. Treatment focuses on ways to decrease the impact of the associated deformities and neurological disabilities. Children with microcephaly and developmental delays are usually evaluated by a pediatric neurologist and followed by a medical management team. Early childhood intervention programs that involve physical, speech, and occupational therapists help to maximize abilities and minimize dysfunction. Medications are often used to control seizures, hyperactivity, and neuromuscular symptoms. Genetic counseling may help families understand the risk for microcephaly in subsequent pregnancies."}
{"_id":"33a71ccd-e0c7-49d4-b11c-094a9d3df9f1","text":"Some children with microcephaly will have normal intelligence and a head that will grow bigger, but they may track below the normal growth curves for head circumference. Some children may have only mild disability, while those with more severe cases may face significant learning disabilities, cognitive delays, or develop other neurological disorders. Many, if not most, cases if Zika microcephaly will be very severe, possibly requiring lifelong intensive care."}
{"_id":"b5a175ca-eb47-430b-85af-24095f683266","text":"The National Institute of Neurological Disorders and Stroke (NINDS), one of several institutes of the National Institutes of Health (NIH), conducts and funds research aimed at understanding normal brain development, as well as disease-related disorders of the brain and nervous system. Other NIH institutes and centers also support research on disorders that may affect development. Among several projects, scientists are studying genetic mechanisms and identifying novel genes involved with brain development. Animal models are helping scientists to better understand the pathology of human disease, and to discover how the sizes of tissues and organs are impacted by developmental variability. Other researchers hope to gain a better understanding of normal brain development and the molecular and cellular mechanisms of microcephaly."}
{"_id":"7c0a7e1a-d279-478c-a5b4-6b420a7981b5","text":"The brachial plexus is a network of nerves that conducts signals from the spine to the shoulder, arm, and hand. Brachial plexus injuries are caused by damage to those nerves. Erb-Duchenne (Erb's) palsy refers to paralysis of the upper brachial plexus. Dejerine-Klumpke (Klumpke's) palsy refers to paralysis of the lower brachial plexus. Although injuries can occur at any time, many brachial plexus injuries happen when a baby's shoulders become impacted during delivery and the brachial plexus nerves stretch or tear. There are four types of brachial plexus injuries: avulsion, the most severe type, in which the nerve is torn from the spine; rupture, in which the nerve is torn but not at the spinal attachment; neuroma, in which the nerve has torn and healed but scar tissue puts pressure on the injured nerve and prevents it from conducting signals to the muscles; and neuropraxia or stretch, in which the nerve has been damaged but not torn. Neuropraxia is the most common type of brachial plexus injury. Symptoms of brachial plexus injury may include a limp or paralyzed arm; lack of muscle control in the arm, hand, or wrist; and lack of feeling or sensation in the arm or hand."}
{"_id":"e1d2eae0-e8b7-4aca-aa66-f18dfb00f9b2","text":"Some brachial plexus injuries may heal without treatment. Many children who are injured during birth improve or recover by 3 to 4 months of age. Treatment for brachial plexus injuries includes physical therapy and, in some cases, surgery."}
{"_id":"1711932e-dea4-4736-9d37-d8d078c981ab","text":"The site and type of brachial plexus injury determines the prognosis. For avulsion and rupture injuries, there is no potential for recovery unless surgical reconnection is made in a timely manner. The potential for recovery varies for neuroma and neuropraxia injuries. Most individuals with neuropraxia injuries recover spontaneously with a 90-100 percent return of function."}
{"_id":"55c409c6-490d-4d60-bbaa-ae39662301b4","text":"The NINDS conducts and supports research on injuries to the nervous system such as brachial plexus injuries. Much of this research is aimed at finding ways to prevent and treat these disorders."}
{"_id":"31e7ff95-4149-4835-b117-5187a39c7666","text":"Dementia with Lewy bodies (DLB) is one of the most common types of progressive dementia. The central features of DLB include progressive cognitive decline, fluctuations in alertness and attention, visual hallucinations, and parkinsonian motor symptoms, such as slowness of movement, difficulty walking, or rigidity. People may also suffer from depression. The symptoms of DLB are caused by the build-up of Lewy bodies  accumulated bits of alpha-synuclein protein -- inside the nuclei of neurons in areas of the brain that control particular aspects of memory and motor control. Researchers dont know exactly why alpha-synuclein accumulates into Lewy bodies or how Lewy bodies cause the symptoms of DLB, but they do know that alpha-synuclein accumulation is also linked to Parkinson's disease, multiple system atrophy, and several other disorders, which are referred to as the \"synucleinopathies.\" The similarity of symptoms between DLB and Parkinsons disease, and between DLB and Alzheimers disease, can often make it difficult for a doctor to make a definitive diagnosis. In addition, Lewy bodies are often also found in the brains of people with Parkinson's and Alzheimers diseases. These findings suggest that either DLB is related to these other causes of dementia or that an individual can have both diseases at the same time. DLB usually occurs sporadically, in people with no known family history of the disease. However, rare familial cases have occasionally been reported."}
{"_id":"8bd89c65-a253-473b-8d1a-48657de596ba","text":"There is no cure for DLB. Treatments are aimed at controlling the cognitive, psychiatric, and motor symptoms of the disorder. Acetylcholinesterase inhibitors, such as donepezil and rivastigmine, are primarily used to treat the cognitive symptoms of DLB, but they may also be of some benefit in reducing the psychiatric and motor symptoms. Doctors tend to avoid prescribing antipsychotics for hallucinatory symptoms of DLB because of the risk that neuroleptic sensitivity could worsen the motor symptoms. Some individuals with DLB may benefit from the use of levodopa for their rigidity and loss of spontaneous movement."}
{"_id":"6187b611-0517-4f05-b1bc-6431f92ab5b2","text":"Like Alzheimers disease and Parkinsons disease, DLB is a neurodegenerative disorder that results in progressive intellectual and functional deterioration. There are no known therapies to stop or slow the progression of DLB. Average survival after the time of diagnosis is similar to that in Alzheimers disease, about 8 years, with progressively increasing disability."}
{"_id":"68d843c4-83ea-4b9b-93d2-02c528e594a5","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health conduct research related to DLB in laboratories at the NIH and support additional research through grants to major medical institutions across the country. Much of this research focuses on searching for the genetic roots of DLB, exploring the molecular mechanisms of alpha-synuclein accumulation, and discovering how Lewy bodies cause the particular symptoms of DLB and the other synucleinopathies. The goal of NINDS research is to find better ways to prevent, treat, and ultimately cure disorders such as DLB."}
{"_id":"82d09535-2923-4655-8d25-0e8a5e81a7a9","text":"Encephalitis lethargica is a disease characterized by high fever, headache, double vision, delayed physical and mental response, and lethargy. In acute cases, patients may enter coma. Patients may also experience abnormal eye movements, upper body weakness, muscular pains, tremors, neck rigidity, and behavioral changes including psychosis. The cause of encephalitis lethargica is unknown. Between 1917 to 1928, an epidemic of encephalitis lethargica spread throughout the world, but no recurrence of the epidemic has since been reported. Postencephalitic Parkinson's disease may develop after a bout of encephalitis-sometimes as long as a year after the illness."}
{"_id":"8b240d16-1c1e-4938-92e2-ea83b1f6b0a5","text":"Treatment for encephalitis lethargica is symptomatic. Levodopa and other antiparkinson drugs often produce dramatic responses."}
{"_id":"c560bcf7-e3e7-4594-ad79-710cc6a242b2","text":"The course of encephalitis lethargica varies depending upon complications or accompanying disorders."}
{"_id":"cde5455c-6423-40bb-ae1d-8d921daecd16","text":"The NINDS supports research on disorders that affect the brain, such as encephalitis lethargica, with the goal of finding ways to prevent and treat them. (The disease was the subject of the book and film, \"Awakenings.\")"}
{"_id":"7a946604-0297-4a11-a95a-632bbca2142c","text":"Cephalic disorders are congenital conditions that stem from damage to or abnormal development of the budding nervous system. Most cephalic disorders are caused by a disturbance that occurs very early in the development of the fetal nervous system. Damage to the developing nervous system is a major cause of chronic, disabling disorders, and sometimes death in infants, children, and even adults. Cephalic disorders may be influenced by hereditary or genetic conditions or by environmental exposures during pregnancy (e.g., medication taken by the mother, maternal infection, exposure to radiation). Some cephalic disorders occur when the cranial sutures (the fibrous joints that connect the bones of the skull) join prematurely. Understanding the normal development of the human nervous system may lead to a better understanding of cephalic disorders."}
{"_id":"3bde76e4-48de-4dea-9612-96df0706e8f8","text":"Treatments for cephalic disorders depend upon the particular type of disorder. For most cephalic disorders, treatment is only symptomatic and supportive. In some cases, anticonvulsant medications shunts, or physical therapy are appropriate."}
{"_id":"23f67804-ae84-4935-84fd-41f4efb44b3a","text":"The degree to which damage to the developing nervous system harms the mind and body varies enormously. Many disabilities are mild enough to allow those afflicted to eventually function independently in society. Others are not. Some infants, children, and adults die; others remain totally disabled; and an even larger population is partially disabled, functioning well below normal capacity."}
{"_id":"a6aadd72-21ec-4dd7-b21e-a7fc5bed629f","text":"Scientists are rapidly learning how harmful insults, a critical nutritional deficiency, or exposure to an environmental insult at various stages of pregnancy can lead to developmental disorders. Research projects currently underway include a study to evaluate increased risk of neural tube defects and various other congenital malformations in association with environmental and occupational exposure to pesticides. Scientists are also concentrating their efforts on understanding the complex processes responsible for normal early development of the brain and nervous system and how the disruption of any of these processes results in congenital anomalies such as cephalic disorders. Currently, researchers are examining the mechanisms involved in neurulation -- the process of forming the neural tube. Investigators are also conducting a variety of genetic studies. Understanding how genes control brain cell migration, proliferation, differentiation, and death, and how radiation, drugs, toxins, infections, and other factors disrupt these processes will aid in preventing many congenital neurological disorders. Recent studies have shown that the addition of folic acid to the diet of women of child-bearing age may significantly reduce the incidence of neural tube defects. Therefore, it is recommended that all women of child-bearing age consume 0.4 mg of folic acid daily."}
{"_id":"11615bd6-1043-4269-afed-56df0f940580","text":"Multi-infarct dementia (MID) is a common cause of memory loss in the elderly. MID is caused by multiple strokes (disruption of blood flow to the brain). Disruption of blood flow leads to damaged brain tissue. Some of these strokes may occur without noticeable clinical symptoms. Doctors refer to these as silent strokes. An individual having asilent stroke may not even know it is happening, but over time, as more areas of the brain are damaged and more small blood vessels are blocked, the symptoms of MID begin to appear. MID can be diagnosed by an MRI or CT of the brain, along with a neurological examination. Symptoms include confusion or problems with short-term memory; wandering, or getting lost in familiar places; walking with rapid, shuffling steps; losing bladder or bowel control; laughing or crying inappropriately; having difficulty following instructions; and having problems counting money and making monetary transactions. MID, which typically begins between the ages of 60 and 75, affects men more often than women. Because the symptoms of MID are so similar to Alzheimers disease, it can be difficult for a doctor to make a firm diagnosis. Since the diseases often occur together, making a single diagnosis of one or the other is even more problematic."}
{"_id":"7357ac11-7f49-49af-8134-dadade9df057","text":"There is no treatment available to reverse brain damage that has been caused by a stroke. Treatment focuses on preventing future strokes by controlling or avoiding the diseases and medical conditions that put people at high risk for stroke: high blood pressure, diabetes, high cholesterol, and cardiovascular disease. The best treatment for MID is prevention early in life  eating a healthy diet, exercising, not smoking, moderately using alcohol, and maintaining a healthy weight."}
{"_id":"7b549df2-55f0-4d44-b8d5-26b1f40b4410","text":"The prognosis for individuals with MID is generally poor. The symptoms of the disorder may begin suddenly, often in a step-wise pattern after each small stroke. Some people with MID may even appear to improve for short periods of time, then decline after having more silent strokes. The disorder generally takes a downward course with intermittent periods of rapid deterioration. Death may occur from stroke, heart disease, pneumonia, or other infection."}
{"_id":"b461a76a-f108-4743-8cc9-bf987181c2a7","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to MID in its laboratories at the National Institutes of Health (NIH), and also supports additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure the vascular dementias, such as MID."}
{"_id":"9228d066-686c-4c85-99bf-c96d37b3796e","text":"Febrile seizures are convulsions or seizures in infants or small children that are brought on by a fever. Most often during a febrile seizure, a child loses consciousness and shakes uncontrollably. Less commonly, a child becomes rigid or has twitches in only a portion of the body. Most febrile seizures last a minute or two; some can be as brief as a few seconds, while others may last for more than 15 minutes. Approximately one in every 25 children will have at least one febrile seizure. Febrile seizures usually occur in children between the ages of 6 months and 5 years, with the risk peaking in the second year of life. The older a child is when the first febrile seizure occurs, the less likely that child is to have more. A few factors appear to boost a child's risk of having recurrent febrile seizures, including young age (less than 18 months) during the first seizures and having immediate family members with a history of febrile seizures."}
{"_id":"5d93dd99-bd46-4dcc-92be-924e8da62b21","text":"A child who has a febrile seizure usually doesn't need to be hospitalized. If the seizure is prolonged or is accompanied by a serious infection, or if the source of the infection cannot be determined, a doctor may recommend that the child be hospitalized for observation. Prolonged daily use of anti-seizure medicines is usually not recommended because of their potential for harmful side effects. Children especially prone to febrile seizures may be treated with medication when they have a fever to lower the risk of having another febrile seizure."}
{"_id":"4bda2977-a4e2-4c1b-9921-339745e9ce24","text":"The vast majority of febrile seizures are short and harmless. There is no evidence that short febrile seizures cause brain damage. Multiple or prolonged seizures are a risk factor for epilepsy but most children who experience febrile seizures do not go on to develop the reoccurring seizures that re characteristic of epilepsy. Certain children who have febrile seizures face an increased risk of developing epilepsy. These children include those who have a febrile seizure that lasts longer than 10 minutes, who have febrile seizures that are lengthy or affect only one part of the body, or experience seizures that reoccur within 24 hours.."}
{"_id":"bd4b1811-820e-4bec-a051-83476fb39fa0","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research on seizures at its research center in Bethesda, Maryland, and through grants to major medical institutions across the country. NINDS-supported scientists are exploring environmental, biological, and genetic risk factors that might make children susceptible to febrile seizures. Investigators continue to monitor the long-term impact that febrile seizures might have on intelligence, behavior, school achievement, and the development of epilepsy. Investigators also continue to explore which drugs can effectively treat or prevent febrile seizures, and to identify factors that may cause a child who has prolonged febrile seizures to develop temporal lobe epilepsy."}
{"_id":"61af9de7-9485-4b26-91a4-269a532099a4","text":"Normal pressure hydrocephalus (NPH) is an abnormal buildup of cerebrospinal fluid (CSF) in the brain's ventricles, or cavities. It occurs if the normal flow of CSF throughout the brain and spinal cord is blocked in some way. This causes the ventricles to enlarge, putting pressure on the brain. Normal pressure hydrocephalus can occur in people of any age, but it is most common in the elderly. It may result from a subarachnoid hemorrhage, head trauma, infection, tumor, or complications of surgery. However, many people develop NPH even when none of these factors are present. In these cases the cause of the disorder is unknown.\n                \nSymptoms of NPH include progressive mental impairment and dementia, problems with walking, and impaired bladder control. The person also may have a general slowing of movements or may complain that his or her feet feel \"stuck.\" Because these symptoms are similar to those of other disorders such as Alzheimer's disease, Parkinson's disease, and Creutzfeldt-Jakob disease, the disorder is often misdiagnosed. Many cases go unrecognized and are never properly treated. Doctors may use a variety of tests, including brain scans (CT and\/or MRI), a spinal tap or lumbar catheter, intracranial pressure monitoring, and neuropsychological tests, to help them diagnose NPH and rule out other conditions."}
{"_id":"2ce51def-ca57-4068-8b09-b4de79992b31","text":"Treatment for NPH involves surgical placement of a shunt in the brain to drain excess CSF into the abdomen where it can be absorbed as part of the normal circulatory process. This allows the brain ventricles to return to their normal size. Regular follow-up care by a physician is important in order to identify subtle changes that might indicate problems with the shunt."}
{"_id":"8a0fc70f-9788-4ee2-9e4f-f9cfa9de62b4","text":"The symptoms of NPH usually get worse over time if the condition is not treated, although some people may experience temporary improvements. While the success of treatment with shunts varies from person to person, some people recover almost completely after treatment and have a good quality of life. Early diagnosis and treatment improves the chance of a good recovery. Without treatment, symptoms may worsen and cause death."}
{"_id":"f4990b88-1abc-4909-9925-db07353f2302","text":"The NINDS conducts and supports research on neurological disorders, including normal pressure hydrocephalus. Research on disorders such as normal pressure hydrocephalus focuses on increasing knowledge and understanding of the disorder, improving diagnostic techniques and neuroimaging, and finding improved treatments and preventions."}
{"_id":"6cc3816b-1ef4-4270-bbd6-a05a1e201b80","text":"Miller Fisher syndrome is a rare, acquired nerve disease that is considered to be a variant of Guillain-Barr syndrome. It is characterized by abnormal muscle coordination, paralysis of the eye muscles, and absence of the tendon reflexes. Like Guillain-Barr syndrome, symptoms may be preceded by a viral illness. Additional symptoms include generalized muscle weakness and respiratory failure. The majority of individuals with Miller Fisher syndrome have a unique antibody that characterizes the disorder."}
{"_id":"2a401d1e-ab9a-43cb-88bc-376ec1ad5155","text":"Treatment for Miller Fisher syndrome is identical to treatment for Guillain-Barr syndrome: intravenous immunoglobulin (IVIg) or plasmapheresis (a procedure in which antibodies are removed from the blood) and supportive care."}
{"_id":"ac9514ba-a7c4-44fb-9696-4838d75b60c7","text":"The prognosis for most individuals with Miller Fisher syndrome is good. In most cases, recovery begins within 2 to 4 weeks of the onset of symptoms, and may be almost complete within 6 months. Some individuals are left with residual deficits. Relapses may occur rarely (in less than 3 percent of cases)."}
{"_id":"2b40ef7c-4ab8-4bce-a665-e01f7cbbe79b","text":"The NINDS supports research aimed at discovering new ways to diagnose, treat, and, ultimately, cure neuropathies such as Miller Fisher syndrome."}
{"_id":"01c20bb6-bebf-472c-8c26-0af2484fdb8a","text":"While acute pain is a normal sensation triggered in the nervous system to alert you to possible injury and the need to take care of yourself, chronic pain is different. Chronic pain persists. Pain signals keep firing in the nervous system for weeks, months, even years. There may have been an initial mishap -- sprained back, serious infection, or there may be an ongoing cause of pain -- arthritis, cancer, ear infection, but some people suffer chronic pain in the absence of any past injury or evidence of body damage. Many chronic pain conditions affect older adults. Common chronic pain complaints include headache, low back pain, cancer pain, arthritis pain, neurogenic pain (pain resulting from damage to the peripheral nerves or to the central nervous system itself), psychogenic pain (pain not due to past disease or injury or any visible sign of damage inside or outside the nervous system). A person may have two or more co-existing chronic pain conditions. Such conditions can include chronic fatigue syndrome, endometriosis, fibromyalgia, inflammatory bowel disease, interstitial cystitis, temporomandibular joint dysfunction, and vulvodynia. It is not known whether these disorders share a common cause."}
{"_id":"75769f30-ef80-48a9-bca7-2133e8c3b54e","text":"Medications, acupuncture, local electrical stimulation, and brain stimulation, as well as surgery, are some treatments for chronic pain. Some physicians use placebos, which in some cases has resulted in a lessening or elimination of pain. Psychotherapy, relaxation and medication therapies, biofeedback, and behavior modification may also be employed to treat chronic pain."}
{"_id":"d0daf29b-0d85-4ea3-897b-8c170016fabd","text":"Many people with chronic pain can be helped if they understand all the causes of pain and the many and varied steps that can be taken to undo what chronic pain has done. Scientists believe that advances in neuroscience will lead to more and better treatments for chronic pain in the years to come."}
{"_id":"0aa2745e-79bd-453b-a13b-f8bc79926bcb","text":"Clinical investigators have tested chronic pain patients and found that they often have lower-than-normal levels of endorphins in their spinal fluid. Investigations of acupuncture include wiring the needles to stimulate nerve endings electrically (electroacupuncture), which some researchers believe activates endorphin systems. Other experiments with acupuncture have shown that there are higher levels of endorphins in cerebrospinal fluid following acupuncture. Investigators are studying the effect of stress on the experience of chronic pain. Chemists are synthesizing new analgesics and discovering painkilling virtues in drugs not normally prescribed for pain."}
{"_id":"3990f6ae-a38f-4d1a-b52a-ad12dec7def4","text":"X-linked Adrenoleukodystrophy (ALD) is one of a group of genetic disorders called the leukodystrophies that cause damage to the myelin sheath, an insulating membrane that surrounds nerve cells in the brain. Women have two X chromosomes and are the carriers of the disease, but since men only have one X chromosome and lack the protective effect of the extra X chromosome, they are more severely affected. People with X-ALD accumulate high levels of saturated, very long chain fatty acids (VLCFA) in the brain and adrenal cortex. The loss of myelin and the progressive dysfunction of the adrenal gland are the primary characteristics of X-ALD. While nearly all patients with X-ALD suffer from adrenal insufficiency, also known as Addison's disease, the neurological symptoms can begin either in childhood or in adulthood. The childhood cerebral form is the most severe, with onset between ages 4 and 10. The most common symptoms are usually behavioral changes such as abnormal withdrawal or aggression, poor memory, and poor school performance. Other symptoms include visual loss, learning disabilities, seizures, poorly articulated speech, difficulty swallowing, deafness, disturbances of gait and coordination, fatigue, intermittent vomiting, increased skin pigmentation, and progressive dementia. The milder adult-onset form is also known as adrenomyeloneuropathy (AMN), which typically begins between ages 21 and 35. Symptoms may include progressive stiffness, weakness or paralysis of the lower limbs, and ataxia. Although adult-onset ALD progresses more slowly than the classic childhood form, it can also result in deterioration of brain function. Almost half the women who are carriers of X-ALS will develop a milder form of AMN but almost never will develop symptoms seen in boys the X-ALD. X-ALD should not be confused with neonatal adrenoleukodsystrophy, which is a disease of newborns and young infants and belongs to the group of peroxisomal biogenesis disorders."}
{"_id":"7901eff6-5ccc-4b58-a62b-1bf4a2610e8d","text":"Adrenal function must be tested periodically in all patients with ALD. Treatment with adrenal hormones can be lifesaving. Symptomatic and supportive treatments for ALD include physical therapy, psychological support, and special education. Recent evidence suggests that a mixture of oleic acid and erucic acid, known as \"Lorenzo's Oil,\" administered to boys with X-ALD prior to symptom onset can prevent or delay the appearance of the childhood cerebral form It is not known whether Lorenzo's Oil will have any beneficial effects in AMN. Furthermore, Lorenzo's Oil has no beneficial effect in symptomatic boys with X-ALD. Bone marrow transplantations can provide long-term benefit to boys who have early evidence of the childhood cerebral form of X-ALD, but the procedure carries risk of mortality and morbidity and is not recommended for those whose symptoms are already severe or who have the adult-onset or neonatal forms."}
{"_id":"10223181-ddb4-4254-840e-4b6492faf81a","text":"Prognosis for patients with childhood cerebral X-ALD is generally poor due to progressive neurological deterioration unless bone marrow transplantation is performed early. Death usually occurs within 1 to 10 years after the onset of symptoms. Adult-onset AMN will progress over decades."}
{"_id":"4d6270ca-7587-429f-a0c1-e1799ccb3154","text":"The NINDS supports research on genetic disorders such as ALD. The aim of this research is to find ways to prevent, treat, and cure these disorders. Studies are currently underway to identify new biomarkers of disease progression and to determine which patients will develop the childhood cerebral form of X-ALD. A recent case study in Europe demonstrated that the combination of gene therapy with bone marrow transplantation, using the patient's own bone marrow cells, may arrest disease progression in childhood cerebral X-ALD. A therapeutic trail in the United States is currently being discussed with the U.S. Food and Drug Administration."}
{"_id":"5bbd8d97-11d4-4789-b11c-7523ea29a61f","text":"Hydromyelia refers to an abnormal widening of the central canal of the spinal cord that creates a cavity in which cerebrospinal fluid (commonly known as spinal fluid) can accumulate. As spinal fluid builds up, it may put abnormal pressure on the spinal cord and damage nerve cells and their connections. Hydromyelia is sometimes used interchangeably with syringomyelia, the name for a condition that also involves cavitation in the spinal cord. In hydromyelia, the cavity that forms is connected to the fourth ventricle in the brain, and is almost always associated in infants and children with hydrocephalus or birth defects such as Chiari Malformation II and Dandy-Walker syndrome. Syringomyelia, however, features a closed cavity and occurs primarily in adults, the majority of whom have Chiari Malformation type 1 or have experienced spinal cord trauma. Symptoms, which may occur over time, include weakness of the hands and arms, stiffness in the legs; and sensory loss in the neck and arms. Some individuals have severe pain in the neck and arms. Diagnosis is made by magnetic resonance imaging (MRI), which reveals abnormalities in the anatomy of the spinal cord.."}
{"_id":"0634f0e2-27c0-4676-bc27-06abfb7c1375","text":"Generally, physicians recommend surgery for children with hydromyelia if they have moderate or severe neurological deficits. Surgical treatment re-establishes the normal flow of spinal fluid."}
{"_id":"8a19cb2d-308d-424e-a463-1fdc70fd8fac","text":"Surgery may permanently or temporarily relieve symptoms, but it can also cause a number of severe complications. In rare cases, hydromyelia may resolve on its own without any medical intervention."}
{"_id":"82fe5a9c-6ce7-4b0f-a30e-6e2bd24ce265","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to hydromyelia in its clinics and laboratories at The National Institutes of Health (NIH) and supports additional research through grants to major research institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure abnormalities of the spinal cord such as hydromyelia."}
{"_id":"a5d697ef-1f3e-4198-a69d-a0ae2abe63f0","text":"Joubert syndrome is a rare brain malformation characterized by the absence or underdevelopment of the cerebellar vermis- an area of the brain that controls balance and coordination -- as well as a malformed brain stem (molar tooth sign). The most common features of Joubert syndrome in infants include abnormally rapid breathing (hyperpnea), decreased muscle tone (hypotonia), abnormal eye movements, impaired intellectual development, and the inability to coordinate voluntary muscle movements (ataxia). Physical deformities may be present, such as extra fingers and toes (polydactyly), cleft lip or palate, and tongue abnormalities. Kidney and liver abnormalities can develop, and seizures may also occur. Many cases of Joubert syndrome appear to be sporadic (not inherited). In most other cases, Joubert syndrome is inherited in an autosomal recessive manner (meaning both parents must have a copy of the mutation) via mutation in at least 10 different genes, including NPHP1, AHI1, and CEP290."}
{"_id":"a620834c-64f5-4777-8b98-7afdd404525f","text":"Treatment for Joubert syndrome is symptomatic and supportive. Infant stimulation and physical, occupational, and speech therapy may benefit some children. Infants with abnormal breathing patterns should be monitored. Screening for progressive eye, liver, and kidney complications associated with Joubert-related disorders should be performed on a regular basis."}
{"_id":"3ab5fa84-bcc9-4891-9a10-67855cd17a12","text":"The prognosis for infants with Joubert syndrome depends on whether or not the cerebellar vermis is partially developed or entirely absent, as well as on the extent and severity of other organ involvement, such as the kidneys and liver. Some children have a mild form of the disorder, with minimal motor disability and good mental development, while others may have severe motor disability, moderate impaired mental development, and multi-organ impairments."}
{"_id":"caf1d08f-9d79-44a5-b659-ace1e593aa38","text":"The NINDS supports research on the development of the nervous system and the cerebellum. This research is critical for increasing our understanding of Joubert syndrome, and for developing methods of treatment and prevention. NINDS, in conjunction with the NIH Office of Rare Disorders, sponsored a symposium on Joubert syndrome in 2002. Research priorities for the disorder were outlined at this meeting."}
{"_id":"2a4436fd-b73f-4871-80a7-7f3ed9ffefc7","text":"An infantile spasm (IS) is a specific type of seizure seen in an epilepsy syndrome of infancy and childhood known as West Syndrome. West Syndrome is characterized by infantile spasms, developmental regression, and a specific pattern on electroencephalography (EEG) testing called hypsarrhythmia (chaotic brain waves). The onset of infantile spasms is usually in the first year of life, typically between 4-8 months. The seizures primarily consist of a sudden bending forward of the body with stiffening of the arms and legs; some children arch their backs as they extend their arms and legs. Spasms tend to occur upon awakening or after feeding, and often occur in clusters of up to 100 spasms at a time. Infants may have dozens of clusters and several hundred spasms per day. Infantile spasms usually stop by age five, but may be replaced by other seizure types. Many underlying disorders, such as birth injury, metabolic disorders, and genetic disorders can give rise to spasms, making it important to identify the underlying cause. In some children, no cause can be found."}
{"_id":"1d89207b-df4d-4ea4-a4dc-42bbee7450a6","text":"Treatment with corticosteroids such as prednisone is standard, although serious side effects can occur. Several newer antiepileptic medications, such as topiramate may ease some symptoms. Vigabatrin (Sabril) has been approved by the U.S. Food and Drug Administration to treat infantile spasms in children ages one month to two years. Some children have spasms as the result of brain lesions, and surgical removal of these lesions may result in improvement."}
{"_id":"556b9a4f-60f9-43eb-95ce-e1ce101fe6da","text":"The prognosis for children with IS is dependent on the underlying causes of the seizures. The intellectual prognosis for children with IS is generally poor because many babies with IS have neurological impairment prior to the onset of spasms. Epileptic spasms usually reduce in number by mid-childhood, but more than half of the children with IS will develop other types of seizures. There appears to be a close relationship between IS and Lennox-Gastaut Syndrome, an epileptic disorder of later childhood."}
{"_id":"ccc36563-de30-4764-a761-863fe0a15b0f","text":"The NINDS supports broad and varied programs of research on epilepsy and other seizure disorders. This research is aimed at discovering new ways to prevent, diagnose, and treat these disorders and, ultimately, to find cures for them. Hopefully, more effective and safer treatments, such as neuroprotective agents, will be developed to treat IS and West Syndrome."}
{"_id":"6f653bf8-5565-4614-ba02-6d3af31a5a4f","text":"Arachnoid cysts are cerebrospinal fluid-filled sacs that are located between the brain or spinal cord and the arachnoid membrane, one of the three membranes that cover the brain and spinal cord. Primary arachnoid cysts are present at birth and are the result of developmental abnormalities in the brain and spinal cord that arise during the early weeks of gestation. Secondary arachnoid cysts are not as common as primary cysts and develop as a result of head injury, meningitis, or tumors, or as a complication of brain surgery. The majority of arachnoid cysts form outside the temporal lobe of the brain in an area of the skull known as the middle cranial fossa. Arachnoid cysts involving the spinal cord are rarer. The location and size of the cyst determine the symptoms and when those symptoms begin. Most individuals with arachnoid cysts develop symptoms before the age of 20, and especially during the first year of life, but some people with arachnoid cysts never have symptoms. Males are four times more likely to have arachnoid cysts than females.\n                \nTypical symptoms of an arachnoid cyst around the brain include headache, nausea and vomiting, seizures, hearing and visual disturbances, vertigo, and difficulties with balance and walking. Arachnoid cysts around the spinal cord compress the spinal cord or nerve roots and cause symptoms such as progressive back and leg pain and tingling or numbness in the legs or arms. Diagnosis usually involves a brain scan or spine scan using diffusion-weighted MRI (magnetic resonance imaging) which helps distinguish fluid-filled arachnoid cysts from other types of cysts."}
{"_id":"9345b992-dff8-45e6-9176-c30479f21b31","text":"There has been active debate about how to treat arachnoid cysts. The need for treatment depends mostly upon the location and size of the cyst. If the cyst is small, not disturbing surrounding tissue, and not causing symptoms, some doctors will refrain from treatment. In the past, doctors placed shunts in the cyst to drain its fluid. Now with microneurosurgical techniques and endoscopic tools that allow for minimally invasive surgery, more doctors are opting to surgically remove the membranes of the cyst or open the cyst so its fluid can drain into the cerebrospinal fluid and be absorbed."}
{"_id":"e1d3bb1f-9771-484b-b74b-4ba82338af2f","text":"Untreated, arachnoid cysts may cause permanent severe neurological damage when progressive expansion of the cyst(s) or bleeding into the cyst injures the brain or spinal cord. Symptoms usually resolve or improve with treatment."}
{"_id":"b19519fd-6256-4461-8b15-d998095a45cc","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to brain abnormalities and disorders of the nervous system such as arachnoid cysts in laboratories at the National Institutes of Health (NIH), and supports additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure neurological disorders such as arachnoid cysts."}
{"_id":"c5ecfe01-f01e-451b-a615-cddac90264c4","text":"Behcet's disease is a rare, chronic inflammatory disorder. The cause of Behcet's disease is unknown, but current research suggests that both genetic and environmental factors play a role. Behcet's disease generally begins when individuals are in their 20s or 30s, although it can happen at any age. It tends to occur more often in men than in women. Symptoms of Behcet's disease include recurrent ulcers in the mouth (resembling canker sores) and on the genitals, and eye inflammation. The disorder may also cause various types of skin lesions, arthritis, bowel inflammation, meningitis (inflammation of the membranes of the brain and spinal cord), and cranial nerve palsies. Behcet's is a multi-system disease; it may involve all organs and affect the central nervous system, causing memory loss and impaired speech, balance, and movement.\n                \nThe effects of the disease may include blindness, stroke, swelling of the spinal cord, and intestinal complications. The disease is common in the Middle East, particularly in Turkey, and in Far Eastern nations such as Japan and Korean, but is less common in the United States."}
{"_id":"5f13c6f0-4fa4-4697-996a-91528742041a","text":"Treatment for Behcet's disease is symptomatic and supportive. Medication may be prescribed to reduce inflammation and\/or regulate the immune system. Immunosuppressive therapy may be considered."}
{"_id":"c0fe0d67-6cc6-4865-b18b-875beea62b2d","text":"Behcet's disease is a lifelong disorder that comes and goes. Permanent remission of symptoms has not been reported."}
{"_id":"8c678034-71d3-489a-b7a1-82e660b189ed","text":"The NINDS supports research on painful neurological disorders such as Behcet's disease. The National Human Genome Research Institute, another Institute of the National Institutes of Health, conducts research into the genomic basis of Behcet's disease. This research is aimed at discovering the causes of these disorders and finding ways to treat, prevent, and, ultimately, cure them."}
{"_id":"e01bb883-ab73-480d-852f-a99866f87c2c","text":"Pelizaeus-Merzbacher disease (PMD) is a rare, progressive, degenerative central nervous system disorder in which coordination, motor abilities, and intellectual function deteriorate. The disease is one of a group of gene-linked disorders known as the leukodystrophies, which affect growth of the myelin sheath -- the fatty covering that wraps around and protects nerve fibers in the brain. The disease is caused by a mutation in the gene that controls the production of a myelin protein called proteolipid protein-1 (PLP1). PMD is inherited as an X-linked recessive trait; the affected individuals are male and the mothers are carriers of the PLP1 mutation. Severity and onset of the disease ranges widely, depending on the type of PLP1 mutation. PMD is one of a spectrum of diseases associated with PLP1, which also includes Spastic Paraplegia Type 2 (SPG2). The PLP1-related disorders span a continuum of neurologic symptoms that range from severe central nervous system involvement (PMD) to progressive weakness and stiffness of the legs (SPG2). There are four general classifications within this spectrum of diseases. In order of severity, they are:\n                \n- Connatal PMD, which is the most severe type and involves delayed mental and physical development and severe neurological symptoms; - Classic PMD, in which the early symptoms include muscle weakness, involuntary movements of the eyes (nystagmus), and delays in motor development within the first year of life; - Complicated SPG2, which features motor development issues and brain involvement, and, - Pure SPG2, which includes cases of PMD that do not have neurologic complications.\n                \nNoticeable changes in the extent of myelination can be detected by MRI analyses of the brain. Additional symptoms of PMD may include slow growth, tremor, failure to develop normal control of head movement, and deteriorating speech and cognitive function."}
{"_id":"e96da383-a3a2-459e-81f7-af76f7f7a43e","text":"There is no cure for Pelizaeus-Merzbacher disease, nor is there a standard course of treatment. Treatment is symptomatic and supportive and may include medication for movement disorders."}
{"_id":"d32cc8db-cd47-4c47-8dff-918c768e6cda","text":"The prognosis for those with the severe forms of Pelizaeus-Merzbacher disease is poor, with progressive deterioration until death. On the other end of the disease spectrum, individuals with the mild form, in which spastic paraplegia is the chief symptom, may have nearly normal activity and life span."}
{"_id":"f3a8f3fe-ef80-466b-a199-fe29ebd62a24","text":"NINDS supports research on gene-linked disorders, including the leukodystrophies. The goals of this research are to increase scientific understanding of these disorders and to find ways to prevent, treat, and ultimately cure them."}
{"_id":"61d8fa20-85b4-4fd6-9b38-e194aef29984","text":"Barth syndrome (BTHS) is a rare, genetic disorder of lipid metabolism that primarily affects males. It is caused by a mutation in the tafazzin gene (TAZ, also called G4.5) which leads to decreased production of an enzyme required to produce cardiolipin. Cardiolipin is an essential lipid that is important in energy metabolism. BTHS, which affects multiple body systems, is considered serious. Its main characteristics often include combinations in varying degrees of heart muscle weakness (cardiomyopathy), neutropenia (low white blood cell cunt, which may lead to an increased risk for bacterial infections), reduced muscle tone (hypotonia), muscle weakness, undeveloped skeletal muscles, delayed growth, fatigue, varying degrees of physical disability, and methylglutaconic aciduria (an increase in an organic acid that results in abnormal mitochondria function). Although some with BTHS may have all of these characteristics, others may have only one or two and are often misdiagnosed. BTHS is an X-linked genetic condition passed from mother to son through the X chromosome. A mother who is a carrier of BTHS typically shows no signs or symptoms of the disorder herself. On average, 50 percent of children born to a carrier mother will inherit the defective gene, but only boys will develop symptoms. All daughters born to an affected male will be carriers but typically will not have symptoms."}
{"_id":"122d153a-fb6c-4ee8-99ab-fd9c3e4d1a59","text":"There is no specific treatment for Barth syndrome. Bacterial infections caused by neutropenia can be effectively treated with antibiotics. The drug granulocyte colony stimulating factor, or GCSF, can stimulate white cell production by the bone marrow and help combat infection. Medicines may be prescribed to control heart problems. The dietary supplement carnitine has aided some children with Barth syndrome but in others it has caused increasing muscle weakness and even precipitated heart failure. Only careful dietary monitoring directed by a physician or nutritionist familiar with the disorder can ensure proper caloric and nutritional intake."}
{"_id":"3a7079e6-0067-4b54-b997-983b785ac86e","text":"Early and accurate diagnosis is key to prolonged survival for boys born with Barth syndrome. The disorder was once considered uniformly fatal in infancy, but some individuals are now living much longer. Severe infections and cardiac failure are common causes of death in affected children."}
{"_id":"5d5edc7b-e6d4-4749-be00-dc2867da6b0e","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS supports research on genetic disorders such as Barth syndrome, including basic research on mitochondrial dysfunction and investigations of other inborn errors of metabolism. Scientists have identified many of the genetic mutations that cause mitochondrial diseases and have created animal models which can be used to investigate potential treatments. Scientists hope to develop unique approaches to treating mitochondrial diseases through a better understanding of mitochondrial biology. Because people affected by mitochondrial disease often have a mixture of healthy and mutant mitochondria in their cells, effective therapy could involve getting the healthy mitochondria to take over for the diseased ones."}
{"_id":"628ddd28-cc0c-4e5b-9608-b1777aef0b92","text":"The diagnostic category of pervasive developmental disorders (PDD) refers to a group of disorders characterized by delays in the development of socialization and communication skills. Parents may note symptoms as early as infancy, although the typical age of onset is before 3 years of age. Symptoms may include problems with using and understanding language; difficulty relating to people, objects, and events; unusual play with toys and other objects; difficulty with changes in routine or familiar surroundings, and repetitive body movements or behavior patterns. Autism (a developmental brain disorder characterized by impaired social interaction and communication skills, and a limited range of activities and interests) is the most characteristic and best studied PDD. Other types of PDD include Asperger's Syndrome, Childhood Disintegrative Disorder, and Rett's Syndrome. Children with PDD vary widely in abilities, intelligence, and behaviors. Some children do not speak at all, others speak in limited phrases or conversations, and some have relatively normal language development. Repetitive play skills and limited social skills are generally evident. Unusual responses to sensory information, such as loud noises and lights, are also common."}
{"_id":"39ad7aa1-1770-4e01-a3dc-99413168d490","text":"There is no known cure for PDD. Medications are used to address specific behavioral problems; therapy for children with PDD should be specialized according to need. Some children with PDD benefit from specialized classrooms in which the class size is small and instruction is given on a one-to-one basis. Others function well in standard special education classes or regular classes with additional support."}
{"_id":"7a38dcf3-9c29-4860-a288-bdc3dc5d3084","text":"Early intervention including appropriate and specialized educational programs and support services plays a critical role in improving the outcome of individuals with PDD. PDD is not fatal and does not affect normal life expectancy."}
{"_id":"3dc3bb4f-3204-4a12-aa5d-e8cf1abe3ccd","text":"The NINDS conducts and supports research on developmental disabilities, including PDD. Much of this research focuses on understanding the neurological basis of PDD and on developing techniques to diagnose, treat, prevent, and ultimately cure this and similar disorders."}
{"_id":"47800993-ad63-4958-9047-d8b5a314cd5d","text":"Krabbe disease is a rare, inherited metabolic disorder in which harmful amounts of lipids (fatty materials such as oils and waxes) build up in various cells and tissues in the body and destroys brain cells. Krabbe disease, also known as globoid cell leukodystrophy, ischaracterized by the presence of globoid cells (cells that have more than one nucleus) that break down the nerves protective myelin coating. Krabbe disease is caused by a deficiency of galactocerebrosidase, an essential enzyme for myelin metabolism. The disease most often affects infants, with onset before age 6 months, but can occur in adolescence or adulthood. Symptoms include severe deterioration of mental and motor skills, muscle weakness, hypertonia (inability of a muscle to stretch), myoclonic seizures (sudden, shock-like contractions of the limbs), and spasticity (involuntary and awkward movement). Other symptoms may include irritability, unexplained fever, blindness, difficulty with swallowing, and deafness."}
{"_id":"0c280eae-a34f-4962-be5c-d89511e2355f","text":"There is no cure for Krabbe disease. Results of a very small clinical trial of children with infantile Krabbe disease found that children who received umbilical cord blood stem cells from unrelated donors prior to symptom onset developed with little neurological impairment. Bone marrow transplantation may help some people. Generally, treatment for the disorder is symptomatic and supportive. Physical therapy may help maintain or increase muscle tone and circulation."}
{"_id":"204cee6b-cd1e-4e1c-97c6-00fa6ff37868","text":"Krabbe disease in infants is generally fatal before age 2. Individuals with a later onset form of the disease generally have a milder course of the disease and live significantly longer."}
{"_id":"2239636f-3339-4085-bdab-d632c0dd865e","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS is a component of the National Institutes of Health, the largest supporter of biomedical research in the world. Hamatopoietic stem cell transplantation -- using stem cells from umbilical cord blood or bone marrow -- has been shown to benefit some individuals when given early in the course of the disease. Scientists plan to test hematopoietic stem cell transplantation plus gene therapy to see if it dramatically increases life expectancy in a mouse model of the disease. Also in a mouse mode, NINDS-funded scientists are testing a combined treatment approach that uses a harmless virus to increase protein production, along with blood stem cell transplantation and small-molecule-based drugs, to reduce neuroinflammation, cell death, and nerve cell degeneration seen in Krabbe disease."}
{"_id":"e2c0060c-6f1e-49d2-8f38-e19dd21453df","text":"Chronic inflammatory demyelinating polyneuropathy (CIDP) is a neurological disorder characterized by progressive weakness and impaired sensory function in the legs and arms. The disorder, which is sometimes called chronic relapsing polyneuropathy, is caused by damage to the myelin sheath (the fatty covering that wraps around and protects nerve fibers) of the peripheral nerves. Although it can occur at any age and in both genders, CIDP is more common in young adults, and in men more so than women. It often presents with symptoms that include tingling or numbness (beginning in the toes and fingers), weakness of the arms and legs, loss of deep tendon reflexes (areflexia), fatigue, and abnormal sensations. CIDP is closely related to Guillain-Barre syndrome and it is considered the chronic counterpart of that acute disease."}
{"_id":"c6097302-2353-4a4d-9083-f6c7539122aa","text":"Treatment for CIDP includes corticosteroids such as prednisone, which may be prescribed alone or in combination with immunosuppressant drugs. Plasmapheresis (plasma exchange) and intravenous immunoglobulin (IVIg) therapy are effective. IVIg may be used even as a first-line therapy. Physiotherapy may improve muscle strength, function and mobility, and minimize the shrinkage of muscles and tendons and distortions of the joints."}
{"_id":"7a057a0a-dfe1-47a0-b116-9aeaac2e2ab9","text":"The course of CIDP varies widely among individuals. Some may have a bout of CIDP followed by spontaneous recovery, while others may have many bouts with partial recovery in between relapses. The disease is a treatable cause of acquired neuropathy and initiation of early treatment to prevent loss of nerve axons is recommended. However, some individuals are left with some residual numbness or weakness."}
{"_id":"23914c63-7d91-42dc-a4e9-9e620aa52f93","text":"The NINDS supports a broad program of research on disorders of the nervous system, including CIDP. Much of this research is aimed at increasing the understanding of these disorders and finding ways to prevent, treat, and cure them."}
{"_id":"e1ee4969-eeb0-4b14-9a0a-a503059888f4","text":"Asperger syndrome (AS) is a developmental disorder. It is an autism spectrum disorder (ASD), one of a distinct group of neurological conditions characterized by a greater or lesser degree of impairment in language and communication skills, as well as repetitive or restrictive patterns of thought and behavior. Other ASDs include: classic autism, Rett syndrome, childhood disintegrative disorder, and pervasive developmental disorder not otherwise specified (usually referred to as PDD-NOS). Unlike children with autism, children with AS retain their early language skills.\n                \nThe most distinguishing symptom of AS is a childs obsessive interest in a single object or topic to the exclusion of any other. Children with AS want to know everything about their topic of interest and their conversations with others will be about little else. Their expertise, high level of vocabulary, and formal speech patterns make them seem like little professors. Other characteristics of AS include repetitive routines or rituals; peculiarities in speech and language; socially and emotionally inappropriate behavior and the inability to interact successfully with peers; problems with non-verbal communication; and clumsy and uncoordinated motor movements.\n                \nChildren with AS are isolated because of their poor social skills and narrow interests. They may approach other people, but make normal conversation impossible by inappropriate or eccentric behavior, or by wanting only to talk about their singular interest.Children with AS usually have a history of developmental delays in motor skills such as pedaling a bike, catching a ball, or climbing outdoor play equipment. They are often awkward and poorly coordinated with a walk that can appear either stilted or bouncy."}
{"_id":"fc4d533c-d79d-4cf9-8405-1f2be7d629d1","text":"The ideal treatment for AS coordinates therapies that address the three core symptoms of the disorder: poor communication skills, obsessive or repetitive routines, and physical clumsiness. There is no single best treatment package for all children with AS, but most professionals agree that the earlier the intervention, the better.\n                \nAn effective treatment program builds on the childs interests, offers a predictable schedule, teaches tasks as a series of simple steps, actively engages the childs attention in highly structured activities, and provides regular reinforcement of behavior. It may include social skills training, cognitive behavioral therapy, medication for co-existing conditions, and other measures."}
{"_id":"f7785444-472d-4bc7-8e63-67543eb13bbc","text":"With effective treatment, children with AS can learn to cope with their disabilities, but they may still find social situations and personal relationships challenging. Many adults with AS are able to work successfully in mainstream jobs, although they may continue to need encouragement and moral support to maintain an independent life."}
{"_id":"570e1ca7-dce5-4f36-a519-f76a9b17071f","text":"Many of the Institutes at the NIH, including the NINDS, are sponsoring research to understand what causes AS and how it can be effectively treated. One study is using functional magnetic resonance imaging (fMRI) to show how abnormalities in particular areas of the brain cause changes in brain function that result in the symptoms of AS and other ASDs.Other studies include aclinical trial testing the effectiveness of an anti-depressant in individuals with AS and HFA who exhibit high levels of obsessive\/ritualistic behavior and a long-range study to collect and analyze DNA samples from a large group of children with AS and HFA and their families to identify genes and genetic interactions that are linked to AS and HFA."}
{"_id":"aee3c1d8-9a0a-4621-a62c-10cb78a06dd8","text":"Corticobasal degeneration is a progressive neurological disorder characterized by nerve cell loss and atrophy (shrinkage) of multiple areas of the brain including the cerebral cortex and the basal ganglia. Corticobasal degeneration progresses gradually. Initial symptoms, which typically begin at or around age 60, may first appear on one side of the body (unilateral), but eventually affect both sides as the disease progresses. Symptoms are similar to those found in Parkinson disease, such as poor coordination, akinesia (an absence of movements), rigidity (a resistance to imposed movement), disequilibrium (impaired balance); and limb dystonia (abnormal muscle postures). Other symptoms such as cognitive and visual-spatial impairments, apraxia (loss of the ability to make familiar, purposeful movements), hesitant and halting speech, myoclonus (muscular jerks), and dysphagia (difficulty swallowing) may also occur. An individual with corticobasal degeneration eventually becomes unable to walk."}
{"_id":"2e423899-1168-4a28-97b9-8916ef322478","text":"There is no treatment available to slow the course of corticobasal degeneration, and the symptoms of the disease are generally resistant to therapy. Drugs used to treat Parkinson disease-type symptoms do not produce any significant or sustained improvement. Clonazepam may help the myoclonus. Occupational, physical, and speech therapy can help in managing disability."}
{"_id":"8842e966-3c40-4af8-b3dd-40ab983f4df1","text":"Corticobasal degeneration usually progresses slowly over the course of 6 to 8 years. Death is generally caused by pneumonia or other complications of severe debility such as sepsis or pulmonary embolism."}
{"_id":"6e33d4ba-523f-4a08-8092-3e479db5525a","text":"The NINDS supports and conducts research studies on degenerative disorders such as corticobasal degeneration. The goals of these studies are to increase scientific understanding of these disorders and to find ways to prevent, treat, and cure them."}
{"_id":"6ab6ec12-7e4c-492d-abd2-c7c36687cbf2","text":"The mucopolysaccharidoses are a group of inherited metabolic diseases in which a defective or missing enzyme causes large amounts of complex sugar molecules to accumulate in harmful amounts in the body's cells and tissues. This accumulation causes permanent, progressive cellular damage that affects appearance, physical abilities, organ and system functioning, and, in most cases, mental development.Depending on the type of mucopolysaccharidosis, affected individuals may have normal intellect or may be profoundly impaired, may experience developmental delay, or have severe behavioral problems. Physical symptoms generally include coarse or rough facial features, thick lips, an enlarged mouth and tongue, short stature with a disproportionately short trunk (dwarfism), abnormal bone size or shape (and other skeletal irregularities), thickened skin, enlarged organs such as the liver or spleen, hernias, and excessive body hair growth."}
{"_id":"4f30a519-8d73-4bb1-8aa2-c0bcb2cf9c56","text":"Currently there is no cure for these disease syndromes.Medical care is directed at treating systemic conditions and improving the person's quality of life. Physical therapy and daily exercise may delay joint problems and improve the ability to move.Surgery to remove tonsils and adenoids may improve breathing among affected individuals with obstructive airway disorders and sleep apnea. Surgery can also correct hernias, help drain excessive cerebrospinal fluid from the brain, and free nerves and nerve roots compressed by skeletal and other abnormalities. Corneal transplants may improve vision among individuals with significant corneal clouding.Enzyme replacement therapies are currently in use for several MPS disorders and are beig tested in the other MPS disorders. Enzyme replacement therapy has proven useful in reducing non-neurological symptoms and pain."}
{"_id":"13d4d605-31c4-4632-9e96-1f8db6fbbd48","text":"The mucopolysaccharidoses syndromes share many clinical features but have varying degrees of severity. Most individuals with a mucopolysaccharidosis syndrome generally experience a period of normal development followed by a decline in physical and mental function. Longevity is dependent upon the particular syndrome. For example, children with a form of mucopolysaccharidosis called Hurler syndrome often die before age 10 from obstructive airway disease, respiratory infections, or cardiac complications. A child with the type known as Scheie syndrome can live into adulthood, while one with a mild case of the type known as Hunter syndrome may live into his or her 50s or beyond."}
{"_id":"c2d51607-38f5-4647-ba00-7752b87b8b89","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease.The NINDS, along with other Institutes at the National Institutes of Health, supports the Lysosomal Disease network, a network of centers that address some of the major challenges in the diagnosis, management, and therapy of diseases, including the mucopolysaccharidoses. Centers are conducting longitudinal studies of the natural history and\/or treatment of these disorders. Scientists are working to identify the genes associated with the mucopolysaccharidoses syndromes and plan to test new therapies in animal models and in humans. Other research funded by the NINDS has shown that viral-delivered gene therapy in animal models of the mucopolysaccharidoses can stop the buildup of storage materials in brain cells and improve learning and memory. Researchers are planning additional studies to understand how gene therapy prompts recovery of mental function in these animal models, but it may be years before such treatment is available to humans."}
{"_id":"51ba274d-35ef-489e-a8cb-45461c997465","text":"Klippel-Trenaunay syndrome (KTS) is a rare congenital malformation involving blood and lymph vessels and abnormal growth of soft and bone tissue. Typical symptoms include hemangiomas (abnormal benign growths on the skin consisting of masses of blood vessels) and varicose veins. Fused toes or fingers, or extra toes or fingers, may be present. In some cases, internal bleeding may occur as a result of blood vessel malformations involving organs such as the stomach, rectum, vagina, liver, spleen, bladder, kidneys, lungs, or heart. Individuals are also at risk for blood clots. The cause of the disorder is unknown. A similar port-wine stain disorder in which individuals have vascular anomalies on the face as well as in the brain is Sturge-Weber syndrome. These individuals may experience seizures and mental deficiency. In some cases, features of the Klippel-Trenaunay syndrome and Sturge-Weber syndrome coincide. Another overlapping condition is the Parkes-Weber syndrome, which is characterized by abnormal connectivity between the arterial and venous system (arteriovenous fistulas)."}
{"_id":"b776e1fe-7feb-4494-b341-2374ee9582ad","text":"There is no cure for KTS. Treatment is symptomatic. Laser surgery can diminish or erase some skin lesions. Surgery may correct discrepancies in limb size, but orthopedic devices may be more appropriate."}
{"_id":"e316632e-b257-45be-9a33-5f606012369e","text":"KTS is often a progressive disorder, and complications may be life-threatening. However, many individuals can live well while managing their symptoms."}
{"_id":"d6fa2965-d9e6-418c-9401-11843dd4eb0f","text":"The NINDS supports research on congenital disorders such as KTS with the goal of finding new means to treat and prevent them."}
{"_id":"d9e9c129-55f2-46fe-beaa-710f1517656d","text":"Periventricular leukomalacia (PVL) is characterized by the death of the white matter of the brain due to softening of the brain tissue. It can affect fetuses or newborns; premature babies are at the greatest risk of the disorder. PVL is caused by a lack of oxygen or blood flow to the periventricular area of the brain, which results in the death or loss of brain tissue. The periventricular area-the area around the spaces in the brain called ventricles-contains nerve fibers that carry messages from the brain to the body's muscles. Although babies with PVL generally have no outward signs or symptoms of the disorder, they are at risk for motor disorders, delayed mental development, coordination problems, and vision and hearing impairments. PVL may be accompanied by a hemorrhage or bleeding in the periventricular-intraventricular area (the area around and inside the ventricles), and can lead to cerebral palsy. The disorder is diagnosed by ultrasound of the head."}
{"_id":"508cfd9a-35ad-4395-94f0-447768d5b691","text":"There is no specific treatment for PVL. Treatment is symptomatic and supportive. Children with PVL should receive regular medical screenings to determine appropriate interventions."}
{"_id":"d680dbb2-1a66-4fa7-8b2f-591cb3c21605","text":"The prognosis for individuals with PVL depends upon the severity of the brain damage. Some children exhibit fairly mild symptoms, while others have significant deficits and disabilities."}
{"_id":"b22813fd-df18-4926-a02d-9090b9cf0be2","text":"The NINDS supports and conducts research on brain injuries such as PVL. Much of this research is aimed at finding ways to prevent and treat these disorders."}
{"_id":"52dcd303-f049-4c81-a6de-ea079d75faea","text":"Brown-Sequard syndrome (BSS) is a rare neurological condition characterized by a lesion in the spinal cord which results in weakness or paralysis (hemiparaplegia) on one side of the body and a loss of sensation (hemianesthesia) on the opposite side. BSS may be caused by a spinal cord tumor, trauma (such as a puncture wound to the neck or back), ischemia (obstruction of a blood vessel), or infectious or inflammatory diseases such as tuberculosis, or multiple sclerosis."}
{"_id":"f9f7b036-5e9d-48db-baf6-6bc858d077ff","text":"Generally treatment for individuals with BSS focuses on the underlying cause of the disorder. Early treatment with high-dose steroids may be beneficial in many cases. Other treatment is symptomatic and supportive."}
{"_id":"7788a6c4-8f0d-47e6-a410-76fa616fb502","text":"The prognosis for individuals with BSS varies depending on the cause of the disorder."}
{"_id":"4e768e0d-90ea-47f2-b4a0-10ab0b4190f7","text":"The NINDS supports and conducts a wide range of research on spinal cord disorders such as BSS. The goal of this research is to find ways to prevent, treat, and, ultimately, cure these disorders."}
{"_id":"aba0b199-32db-456c-8ff7-99358af3ce8d","text":"Lupus (also called systemic lupus erythematosus) is a disorder of the immune system. Normally, the immune system protects the body against invading infections and cancers. In lupus, the immune system is over-active and produces increased amounts of abnormal antibodies that attack the body's tissues and organs. Lupus can affect many parts of the body, including the joints, skin, kidneys, lungs, heart, nervous system, and blood vessels. The signs and symptoms of lupus differ from person to person; the disease can range from mild to life threatening.\n                \nInitial symptoms of lupus may begin with a fever, vascular headaches, epilepsy, or psychoses. A striking feature of lupus is a butterfly shaped rash over the cheeks. In addition to headache, lupus can cause other neurological disorders, such as mild cognitive dysfunction, organic brain syndrome, peripheral neuropathies, sensory neuropathy, psychological problems (including personality changes, paranoia, mania, and schizophrenia), seizures, transverse myelitis, and paralysis and stroke."}
{"_id":"316e58b1-0ce5-4722-85b5-b07b845125dd","text":"There is no cure for lupus. Treatment is symptomatic. With a combination of medication, rest, exercise, proper nutrition, and stress management, most individuals with lupus can often achieve remission or reduce their symptom levels. Medications used in the treatment of lupus may include aspirin and other nonsteroidal anti-inflammatory medications, antimalarials, corticosteroids, and immunosuppressive drugs."}
{"_id":"4b21f82b-ecf9-4fb0-8ec2-6a04003d96d0","text":"The prognosis for lupus varies widely depending on the organs involved and the intensity of the inflammatory reaction. The course of lupus is commonly chronic and relapsing, often with long periods of remission. Most individuals with lupus do not develop serious health problems and have a normal lifespan with periodic doctor visits and treatments with various drugs."}
{"_id":"66150141-e0e9-402f-b3ec-4eeebcaef1be","text":"Investigators researching lupus seek to increase scientific understanding of the disorder and to find ways to treat, prevent, and ultimately, cure it. Several components of the National Institutes of Health support research on lupus."}
{"_id":"b986894a-2cca-4fcc-a522-a387810dde8a","text":"The gangliosidoses are a group of inherited metabolic diseases caused by a deficiency of the different proteins needed to break down fatty substances called lipids. Excess buildup of these fatty materials (oils, waxes, steroids, and other compounds) can cause permanent damage in the cells and tissues in the brain and nervous systems, particularly in nerve cells. There are two distinct groups of the gangliosidoses, which affect males and females equally.\n                \nThe GM1 gangliosidoses are caused by a deficiency of the enzyme beta-galactosidase. Signs of early infantile GM1 gangliodisosis (the most severe subtype, with onset shortly after birth) may include neurodegeneration, seizures, liver and spleen enlargement, coarsening of facial features, skeletal irregularities, joint stiffness, distended abdomen, muscle weakness, exaggerated startle response, and problems with gait. About half of affected persons develop cherry-red spots in the eye. Children may be deaf and blind by age 1.Onset of late infantile GM1 gangliosidosisis typically between ages 1 and 3 years. Signs include an inability to control movement, seizures, dementia, and difficulties with speech. Adult GM1 gangliosidosis strikes between ages 3 and 30, with symptoms that include the wasting away of muscles, cloudiness in the corneas, and dystonia (sustained moscle contractions that case twisting and repetitive movements or abnormal postures). Non-cancerous skin blemishes may develop on the lower part of the trunk of the body. Adult GM1 is usually less severe and progresses more slowly than other forms of the disorder.\n                \nThe GM2 gangliosidoses include Tay-Sachs disease and its more severe form, called Sandhoff disease, both of whichresult from a deficiency of the enzyme beta-hexosaminidase. Symptoms begin by age 6 months and include progressive mental deterioration, cherry-red spots in the retina, marked startle reflex, and seizures. Children with Tay-Sachs may also have dementia, progressive loss of hearing, some paralysis, and difficulty in swallowing that may require a feeding tube. A rarer form of the disorder, which occurs in individuals in their twenties and early thirties, is characterized by an unsteady gait and progressive neurological deterioration. Additional signs of Sandhoff disease include weakness in nerve signaling that causes muscles to contract, early blindness, spasticity, muscle contractions, an abnormally enlarged head, and an enlarged liver and spleen."}
{"_id":"fe30bcf7-2738-4517-940a-6618968910db","text":"No specific treatment exists for the gangliosidoses. Anticonvulsants may initially control seizures. Other supportive treatment includes proper nutrition and hydration and keeping the airway open."}
{"_id":"acd52ead-d57b-48dc-87df-b2e724e6fd1f","text":"Children with early infantile GM1 often die by age 3 from cardiac complications or pneumonia. Children with the early-onset form of Tay-Sachs disease may eventually need a feeding tube and often die by age 4 from recurring infection. Children with Sandhoff disease generally die by age 3 from respiratory infections."}
{"_id":"d7285652-1ab8-475d-88a4-964e03b6eb95","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS is a part of the National Institutes of Health (NIH), the largest supporter of biomedical research in the world. Scientists are studying the mechanisms by which the lipids accumulating in these disorders cause harm to the body. NINDS-funded research on the gangliosidoses also includes using variations of magnetic resonance imaging to develop a biomarker (a sign that may indicate risk of a disease and improve diagnosis) to effectively evaluate brain chemistry and disease progression, and expanding the use of virus-delivered gene therapy seen in an animal model of Tay-Sachs and Sandhoff diseases for use in humans."}
{"_id":"c12f8c40-bff4-44ac-81c3-aa244fe10614","text":"Paroxysmal hemicrania is a rare form of headache that usually begins in adulthood. Patients experience severe throbbing, claw-like, or boring pain usually on one side of the face; in, around, or behind the eye; and occasionally reaching to the back of the neck. This pain may be accompanied by red and tearing eyes, a drooping or swollen eyelid on the affected side of the face, and nasal congestion. Patients may also feel dull pain, soreness, or tenderness between attacks. Attacks of paroxysmal hemicrania typically occur from 5 to 40 times per day and last 2 to 30 minutes. The disorder has two forms: chronic, in which patients experience attacks on a daily basis for a year or more, and episodic, in which the headaches may remit for months or years. Certain movements of the head or neck or external pressure to the neck may trigger these headaches in some patients. The disorder is more common in women than in men."}
{"_id":"d90135af-9256-4305-a2d4-2219c7693334","text":"The nonsteroidal anti-inflammatory drug (NSAID) indomethacin often provides complete relief from symptoms. Other less effective NSAIDs, calcium-channel blocking drugs (such as verapamil), and corticosteroids may be used to treat the disorder. Patients with both paroxysmal hemicrania and trigeminal neuralgia (a condition of the 5th cranial nerve that causes sudden, severe pain typically felt on one side of the jaw or cheek) should receive treatment for each disorder."}
{"_id":"4849a7a2-dd1b-4e9a-bf53-6c31e2f13365","text":"Many patients experience complete to near-complete relief of symptoms following physician-supervised medical treatment. Paroxysmal hemicrania may last indefinitely but has been known to go into remission or stop spontaneously."}
{"_id":"fda12d26-f44e-401c-81b4-871d428eaa03","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) support research related to paroxysmal hemicrania through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure headache disorders such as paroxysmal hemicrania."}
{"_id":"f18716d9-2ae0-485e-9b6f-8ff348efbdb9","text":"The myopathies are neuromuscular disorders in which the primary symptom is muscle weakness due to dysfunction of muscle fiber. Other symptoms of myopathy can include include muscle cramps, stiffness, and spasm. Myopathies can be inherited (such as the muscular dystrophies) or acquired (such as common muscle cramps). Myopathies are grouped as follows: congenital myopathies: characterized by developmental delays in motor skills; skeletal and facial abnormalities are occasionally evident at birth muscular dystrophies: characterized by progressive weakness in voluntary muscles; sometimes evident at birth mitochondrial myopathies: caused by genetic abnormalities in mitochondria, cellular structures that control energy; include Kearns-Sayre syndrome, MELAS and MERRF glycogen storage diseases of muscle: caused by mutations in genes controlling enzymes that metabolize glycogen and glucose (blood sugar); include Pompe's, Andersen's and Cori's diseases myoglobinurias: caused by disorders in the metabolism of a fuel (myoglobin) necessary for muscle work; include McArdle, Tarui, and DiMauro diseases dermatomyositis: an inflammatory myopathy of skin and muscle myositis ossificans: characterized by bone growing in muscle tissue familial periodic paralysis: characterized by episodes of weakness in the arms and legs polymyositis, inclusion body myositis, and related myopathies: inflammatory myopathies of skeletal muscle neuromyotonia: characterized by alternating episodes of twitching and stiffness; and stiff-man syndrome: characterized by episodes of rigidity and reflex spasms common muscle cramps and stiffness, and tetany: characterized by prolonged spasms of the arms and legs"}
{"_id":"7b245325-3d15-4d88-85ce-ab1522758c6b","text":"Treatments for the myopathies depend on the disease or condition and specific causes. Supportive and symptomatic treatment may be the only treatment available or necessary for some disorders. Treatment for other disorders may include drug therapy, such as immunosuppressives, physical therapy, bracing to support weakened muscles, and surgery."}
{"_id":"598543eb-74c7-463e-882f-373bd3c59a26","text":"The prognosis for individuals with a myopathy varies. Some individuals have a normal life span and little or no disability. For others, however, the disorder may be progressive, severely disabling, life-threatening, or fatal."}
{"_id":"96e1fed6-5b3c-439c-96a9-d58e6462d3ea","text":"The NINDS supports and conducts an extensive research program on neuromuscular disorders such as the myopathies. Much of this research is aimed at increasing scientific understanding of these disorders, and finding ways to prevent, treat, and cure them."}
{"_id":"a9d0912c-d9d9-4d1f-9231-2089cf7881d9","text":"Troyer syndrome is one of more than 40 genetically-distinct neurological disorders known collectively as the hereditary spastic paraplegias. These disorders are characterized by their paramount feature of progressive muscle weakness and spasticity in the legs. Additional symptoms of Troyer syndrome (also called SPG20) include leg contractures, difficulty walking, speech disorders, drooling, atrophy of the hand muscles, developmental delays, fluctuating emotions, and short stature. Onset is typically in early childhood, and symptoms gradually worsen over time. Troyer syndrome is an autosomal recessive disorder (meaning that both parents must carry and pass on the defective gene that produces the illness) that results from a mutation in the spastic paraplegia gene (SPGP20) located in chromosome 13 that results in loss of the spartin proteins. The disease was first observed in Amish families in Ohio. Diagnosis is made by specialized genetic testing."}
{"_id":"40e7685c-6540-476b-be3a-f99899cf1c70","text":"There are no specific treatments to prevent or slow the progressive degeneration seen in Troyer syndrome. Symptomatic therapy includes antispasmodic drugs and physical therapy to improve muscle strength and maintain range of motion in the legs. Assistive devices may be needed to help with walking."}
{"_id":"30a48511-da6b-434a-aff3-f6861680ed2d","text":"Prognosis varies, although the disease is progressive. Some patients may have a mild form of the disease while others eventually lose the ability to walk normally. Troyer syndrome does not shorten the normal life span."}
{"_id":"78933318-c83c-4c17-bccd-7bed265863ed","text":"The NINDS supports research on genetic disorders such as the hereditary spastic paraplegias. A gene for Troyer syndrome has been identified and others may be identified in the future. Understanding how these genes cause Troyer syndrome and the hereditary spastic paraplegias in general will lead to ways to prevent, treat, and cure these disorders."}
{"_id":"494725f6-930f-42aa-9727-f145e0f9e64e","text":"A stroke occurs when the blood supply to part of the brain is suddenly interrupted or when a blood vessel in the brain bursts, spilling blood into the spaces surrounding brain cells. Brain cells die when they no longer receive oxygen and nutrients from the blood or there is sudden bleeding into or around the brain. The symptoms of a stroke include sudden numbness or weakness, especially on one side of the body; sudden confusion or trouble speaking or understanding speech; sudden trouble seeing in one or both eyes; sudden trouble with walking, dizziness, or loss of balance or coordination; or sudden severe headache with no known cause. There are two forms of stroke: ischemic - blockage of a blood vessel supplying the brain, and hemorrhagic - bleeding into or around the brain."}
{"_id":"d2d2e3ed-81d1-4c6e-90bb-0e53a6bafe33","text":"Generally there are three treatment stages for stroke: prevention, therapy immediately after the stroke, and post-stroke rehabilitation. Therapies to prevent a first or recurrent stroke are based on treating an individual's underlying risk factors for stroke, such as hypertension, atrial fibrillation, and diabetes. Acute stroke therapies try to stop a stroke while it is happening by quickly dissolving the blood clot causing an ischemic stroke or by stopping the bleeding of a hemorrhagic stroke. Post-stroke rehabilitation helps individuals overcome disabilities that result from stroke damage. Medication or drug therapy is the most common treatment for stroke. The most popular classes of drugs used to prevent or treat stroke are antithrombotics (antiplatelet agents and anticoagulants) and thrombolytics."}
{"_id":"d9025695-4cbe-48a4-a65a-25b12fd4c202","text":"Although stroke is a disease of the brain, it can affect the entire body. A common disability that results from stroke is complete paralysis on one side of the body, called hemiplegia. A related disability that is not as debilitating as paralysis is one-sided weakness or hemiparesis. Stroke may cause problems with thinking, awareness, attention, learning, judgment, and memory. Stroke survivors often have problems understanding or forming speech. A stroke can lead to emotional problems. Stroke patients may have difficulty controlling their emotions or may express inappropriate emotions. Many stroke patients experience depression. Stroke survivors may also have numbness or strange sensations. The pain is often worse in the hands and feet and is made worse by movement and temperature changes, especially cold temperatures.\n                \nRecurrent stroke is frequent; about 25 percent of people who recover from their first stroke will have another stroke within 5 years."}
{"_id":"11af0529-a654-4a4c-b353-7df31ab73c9e","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts stroke research and clinical trials at its laboratories and clinics at the National Institutes of Health (NIH), and through grants to major medical institutions across the country. Currently, NINDS researchers are studying the mechanisms of stroke risk factors and the process of brain damage that results from stroke. Basic research has also focused on the genetics of stroke and stroke risk factors. Scientists are working to develop new and better ways to help the brain repair itself to restore important functions. New advances in imaging and rehabilitation have shown that the brain can compensate for function lost as a result of stroke."}
{"_id":"39110407-7552-4870-b4f9-aaf34c28b7a6","text":"Parkinson's disease (PD) belongs to a group of conditions called motor system disorders, which are the result of the loss of dopamine-producing brain cells. The four primary symptoms of PD are tremor, or trembling in hands, arms, legs, jaw, and face; rigidity, or stiffness of the limbs and trunk; bradykinesia, or slowness of movement; and postural instability, or impaired balance and coordination. As these symptoms become more pronounced, patients may have difficulty walking, talking, or completing other simple tasks. PD usually affects people over the age of 60. Early symptoms of PD are subtle and occur gradually. In some people the disease progresses more quickly than in others. As the disease progresses, the shaking, or tremor, which affects the majority of people with PD may begin to interfere with daily activities. Other symptoms may include depression and other emotional changes; difficulty in swallowing, chewing, and speaking; urinary problems or constipation; skin problems; and sleep disruptions. There are currently no blood or laboratory tests that have been proven to help in diagnosing sporadic PD. Therefore the diagnosis is based on medical history and a neurological examination. The disease can be difficult to diagnose accurately. Doctors may sometimes request brain scans or laboratory tests in order to rule out other diseases."}
{"_id":"099f1155-8fd4-4ff7-9c32-3b4c158ca942","text":"At present, there is no cure for PD, but a variety of medications provide dramatic relief from the symptoms. Usually, affected individuals are given levodopa combined with carbidopa. Carbidopa delays the conversion of levodopa into dopamine until it reaches the brain. Nerve cells can use levodopa to make dopamine and replenish the brain's dwindling supply. Although levodopa helps at least three-quarters of parkinsonian cases, not all symptoms respond equally to the drug. Bradykinesia and rigidity respond best, while tremor may be only marginally reduced. Problems with balance and other symptoms may not be alleviated at all. Anticholinergics may help control tremor and rigidity. Other drugs, such as bromocriptine, pramipexole, and ropinirole, mimic the role of dopamine in the brain, causing the neurons to react as they would to dopamine. An antiviral drug, amantadine, also appears to reduce symptoms. In May 2006, the FDA approved rasagiline to be used along with levodopa for patients with advanced PD or as a single-drug treatment for early PD.\n                \nIn some cases, surgery may be appropriate if the disease doesn't respond to drugs. A therapy called deep brain stimulation (DBS) has now been approved by the U.S. Food and Drug Administration. In DBS, electrodes are implanted into the brain and connected to a small electrical device called a pulse generator that can be externally programmed. DBS can reduce the need for levodopa and related drugs, which in turn decreases the involuntary movements called dyskinesias that are a common side effect of levodopa. It also helps to alleviate fluctuations of symptoms and to reduce tremors, slowness of movements, and gait problems. DBS requires careful programming of the stimulator device in order to work correctly."}
{"_id":"814b7648-2feb-44c3-88d9-66fae40bb660","text":"PD is both chronic, meaning it persists over a long period of time, and progressive, meaning its symptoms grow worse over time. Although some people become severely disabled, others experience only minor motor disruptions. Tremor is the major symptom for some individuals, while for others tremor is only a minor complaint and other symptoms are more troublesome. It is currently not possible to predict which symptoms will affect an individual, and the intensity of the symptoms also varies from person to person."}
{"_id":"d12b4813-b8b6-4b22-9233-5e0568091c97","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts PD research in laboratories at the National Institutes of Health (NIH) and also supports additional research through grants to major medical institutions across the country. Current research programs funded by the NINDS are using animal models to study how the disease progresses and to develop new drug therapies. Scientists looking for the cause of PD continue to search for possible environmental factors, such as toxins, that may trigger the disorder, and study genetic factors to determine how defective genes play a role. Other scientists are working to develop new protective drugs that can delay, prevent, or reverse the disease.\n                \nhttp:\/\/www.ninds.nih.gov\/research\/parkinsonsweb\/index.htm"}
{"_id":"93601edb-94ca-42b0-9a02-5bc04173c386","text":"Melkersson-Rosenthal syndrome is a rare neurological disorder characterized by recurring facial paralysis, swelling of the face and lips (usually the upper lip), and the development of folds and furrows in the tongue. Onset is in childhood or early adolescence. After recurrent attacks (ranging from days to years in between), swelling may persist and increase, eventually becoming permanent. The lip may become hard, cracked, and fissured with a reddish-brown discoloration. The cause of Melkersson-Rosenthal syndrome is unknown, but there may be a genetic predisposition. It can be symptomatic of Crohn's disease or sarcoidosis."}
{"_id":"03dbbbf9-eaeb-4ed1-876b-172cebf9d95b","text":"Treatment is symptomatic and may include medication therapies with nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids to reduce swelling, as well as antibiotics and immunosuppressants. Surgery may be recommended to relieve pressure on the facial nerves and to reduce swollen tissue, but its effectiveness has not been established. Massage and electrical stimulation may also be prescribed."}
{"_id":"757ca7ed-7a77-4558-bc81-08999d53e9fb","text":"Melkersson-Rosenthal syndrome may recur intermittently after its first appearance. It can become a chronic disorder. Follow-up care should exclude the development of Crohn's disease or sarcoidosis."}
{"_id":"951d75fe-59f6-42b4-8bce-701096752bb6","text":"The NINDS supports research on neurological disorders such as Melkersson-Rosenthal syndrome. Much of this research is aimed at increasing knowledge of these disorders and finding ways to treat, prevent, and ultimately cure them."}
{"_id":"228127d3-7894-4997-990d-74efb6ee05cc","text":"Sjgren's syndrome is an autoimmune disorder in which immune cells attack and destroy the glands that produce tears and saliva. Sjgren's syndrome is also associated with rheumatic disorders such as rheumatoid arthritis. The hallmark symptoms of the disorder are dry mouth and dry eyes. In addition, Sjogren's syndrome may cause skin, nose, and vaginal dryness, and may affect other organs of the body including the kidneys, blood vessels, lungs, liver, pancreas, and brain.  Sjgren's syndrome affects 1-4 million people in the United States. Most people are more than 40 years old at the time of diagnosis. Women are 9 times more likely to have Sjgren's syndrome than men."}
{"_id":"6dd3fee2-472e-4885-8033-edf1a419730f","text":"There is no known cure for Sjgren's syndrome nor is there a specific treatment to restore gland secretion. Treatment is generally symptomatic and supportive. Moisture replacement therapies may ease the symptoms of dryness. Nonsteroidal anti-inflammatory drugs may be used to treat musculoskeletal symptoms. For individuals with severe complications, corticosteroids or immunosuppressive drugs may be prescribed."}
{"_id":"276beb22-f2b5-4c08-b7ca-492a8bf99025","text":"Sjgren's syndrome can damage vital organs of the body with symptoms that may remain stable, worsen, or go into remission. Some people may experience only the mild symptoms of dry eyes and mouth, while others go through cycles of good health followed by severe disease. Many patients are able to treat problems symptomatically. Others are forced to cope with blurred vision, constant eye discomfort, recurrent mouth infections, swollen parotid glands, hoarseness, and difficulty in swallowing and eating. Debilitating fatigue and joint pain can seriously impair quality of life."}
{"_id":"d2de176a-0808-48e2-aef8-9be8ab847eca","text":"The goals of research on disorders such as Sjgren's syndrome focus on increasing knowledge and understanding of the disorder, improving diagnostic techniques, testing interventions, and finding ways to treat, prevent, and cure the disease."}
{"_id":"f57e5fc7-ac5b-4d26-b67c-6b0eb1c36cac","text":"Hydranencephaly is a rare condition in which the brain's cerebral hemispheres are absent and replaced by sacs filled with cerebrospinal fluid. An infant with hydranencephaly may appear normal at birth. The infant's head size and spontaneous reflexes such as sucking, swallowing, crying, and moving the arms and legs may all seem normal. However, after a few weeks the infant usually becomes irritable and has increased muscle tone. After a few months of life, seizures and hydrocephalus (excessive accumulation of cerebrospinal fluid in the brain) may develop. Other symptoms may include visual impairment, lack of growth, deafness, blindness, spastic quadriparesis (paralysis), and intellectual deficits. Hydranencephaly is considered to be an extreme form of porencephaly (a rare disorder characterized by a cyst or cavity in the cerebral hemispheres) and may be caused by vascular infections or traumatic disorders after the 12th week of pregnancy. Diagnosis may be delayed for several months because early behavior appears to be relatively normal. Some infants may have additional abnormalities at birth including seizures, myoclonus (spasm or twitching of a muscle or group of muscles), and respiratory problems."}
{"_id":"70153be9-781a-4268-8371-5594e30ae73f","text":"There is no definitive treatment for hydranencephaly. Treatment is symptomatic and supportive. Hydrocephalus may be treated with a shunt (a surgically implanted tube that diverts fluid from one pathway to another)."}
{"_id":"99dddab1-3fd4-42c5-a0ef-dfb75cd7cbae","text":"The outlook for children with hydranencephaly is generally poor, and many children with this disorder die before age 1. However, in rare cases, children with hydranencephaly may survive for several years or more."}
{"_id":"2f2f0cad-f286-4dda-8d0b-6d508069d92f","text":"The NINDS conducts and supports a wide range of studies that explore the complex mechanisms of normal brain development. The knowledge gained from these fundamental studies provides the foundation for understanding how this process can go awry and, thus, offers hope for new means to treat and prevent developmental brain disorders, including hydranencephaly."}
{"_id":"3fec7802-3b5d-42c2-bcc8-27fb03979007","text":"Progressive multifocal leukoencephalopathy (PML) is a disease of the white matter of the brain, caused by a virus infection that targets cells that make myelin--the material that insulates nerve cells (neurons). Polyomavirus JC (often called JC virus) is carried by a majority of people and is harmless except among those with lowered immune defenses. The disease is rare and occurs in patients undergoing chronic corticosteroid or immunosuppressive therapy for organ transplant, or individuals with cancer (such as Hodgkins disease or lymphoma). Individuals with autoimmune conditions such as multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosis -- some of whom are treated with biological therapies that allow JC virus reactivation -- are at risk for PML as well. PML is most common among individuals with HIV-1 infection \/ acquired immune deficiency syndrome (AIDS). Studies estimate that prior to effective antiretroviral therapy, as many as 5 percent of persons infected with HIV-1 eventually develop PML that is an AIDS-defining illness. However, current HIV therapy using antiretroviral drugs (ART), which effectively restores immune system function, allows as many as half of all HIV-PML patients to survive, although they may sometimes have an inflammatory reaction in the regions of the brain affected by PML. The symptoms of PML are diverse, since they are related to the location and amount of damage in the brain, and may evolve over the course of several weeks to months The most prominent symptoms are clumsiness; progressive weakness; and visual, speech, and sometimes personality changes. The progression of deficits leads to life-threatening disability and (frequently) death. A diagnosis of PML can be made following brain biopsy or by combining observations of a progressive course of the disease, consistent white matter lesions visible on a magnetic resonance imaging (MRI) scan, and the detection of the JC virus in spinal fluid."}
{"_id":"224dd976-8c0b-4170-bef4-018e9a62cfab","text":"Currently, the best available therapy is reversal of the immune-deficient state, since there are no effective drugs that block virus infection without toxicity. Reversal may be achieved by using plasma exchange to accelerate the removal of the therapeutic agents that put patients at risk for PML. In the case of HIV-associated PML, immediately beginning anti-retroviral therapy will benefit most individuals. Several new drugs that laboratory tests found effective against infection are being used in PML patients with special permission of the U.S. Food and Drug Administration. Hexadecyloxypropyl-Cidofovir (CMX001) is currently being studied as a treatment option for JVC because of its ability to suppress JVC by inhibiting viral DNA replication."}
{"_id":"3f925e8d-7fa2-4862-80aa-e1aeaea8305e","text":"In general, PML has a mortality rate of 30-50 percent in the first few months following diagnosis but depends on the severity of the underlying disease and treatment received. Those who survive PML can be left with severe neurological disabilities."}
{"_id":"0568817a-7595-45e4-bf77-8e7ae1417f08","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to PML in laboratories at the NIH, and support additional research through grants to majorresearch institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders such as PML."}
{"_id":"6837d232-01b4-4731-a8f4-ed990dbdccb9","text":"Williams Syndrome (WS) is a rare genetic disorder characterized by mild to moderate delays in cognitive development or learning difficulties, a distinctive facial appearance, and a unique personality that combines over-friendliness and high levels of empathy with anxiety. The most significant medical problem associated with WS is cardiovascular disease caused by narrowed arteries. WS is also associated with elevated blood calcium levels in infancy. A random genetic mutation (deletion of a small piece of chromosome 7), rather than inheritance, most often causes the disorder. However, individuals who have WS have a 50 percent chance of passing it on if they decide to have children. The characteristic facial features of WS include puffiness around the eyes, a short nose with a broad nasal tip, wide mouth, full cheeks, full lips, and a small chin. People with WS are also likely to have a long neck, sloping shoulders, short stature, limited mobility in their joints, and curvature of the spine. Some individuals with WS have a star-like pattern in the iris of their eyes. Infants with WS are often irritable and colicky, with feeding problems that keep them from gaining weight. Chronic abdominal pain is common in adolescents and adults. By age 30, the majority of individuals with WS have diabetes or pre-diabetes and mild to moderate sensorineural hearing loss (a form of deafness due to disturbed function of the auditory nerve). For some people, hearing loss may begin as early as late childhood. WS also is associated with a characteristic cognitive profile of mental strengths and weaknesses composed of strengths in verbal short-term memory and language, combined with severe weakness in visuospatial construction (the skills used to copy patterns, draw, or write). Within language, the strongest skills are typically in concrete, practical vocabulary, which in many cases is in the low average to average range for the general population. Abstract or conceptual-relational vocabulary is much more limited. Most older children and adults with WS speak fluently and use good grammar. More than 50% of children with WS have attention deficit disorders (ADD or ADHD), and about 50% have specific phobias, such as a fear of loud noises. The majority of individuals with WS worry excessively."}
{"_id":"69a2b9b7-7ecd-4232-aeed-5151e2257cf0","text":"There is no cure for Williams syndrome, nor is there a standard course of treatment. Because WS is an uncommon and complex disorder, multidisciplinary clinics have been established at several centers in the       United States   . Treatments are based on an individuals particular symptoms. People with WS require regular cardiovascular monitoring for potential medical problems, such as symptomatic narrowing of the blood vessels, high blood pressure, and heart failure"}
{"_id":"200eebcb-a244-4321-9e74-7a15f91e99aa","text":"The prognosis for individuals with WS varies. Some degree of impaired intellect is found in most people with the disorder. Some adults are able to function independently, complete academic or vocational school, and live in supervised homes or on their own; most live with a caregiver. Parents can increase the likelihood that their child will be able to live semi-independently by teaching self-help skills early. Early intervention and individualized educational programs designed with the distinct cognitive and personality profiles of WS in mind also help individuals maximize their potential. Medical complications associated with the disorder may shorten the lifespans of some individuals with WS."}
{"_id":"ba9e3c0e-bc37-401b-acda-8221a0e284c4","text":"The National Institutes of Health (NIH), and the National Institute of Neurological Disorders and Stroke (NINDS), have funded many of the research studies exploring the genetic and neurobiological origins of WS. In the early 1990s, researchers located and identified the genetic mutation responsible for the disorder: the deletion of a small section of chromosome 7 that contains approximately 25 genes. NINDS continues to support WS researchers including, for example, groups that are attempting to link specific genes with the corresponding facial, cognitive, personality, and neurological characteristics of WS."}
{"_id":"d5a65177-9001-4690-a3d9-8f46a69ed441","text":"Hypotonia is a medical term used to describe decreased muscle tone. Normally, even when relaxed, muscles have a very small amount of contraction that gives them a springy feel and provides some resistance to passive movement. It is not the same as muscle weakness, although the two conditions can co-exist. Muscle tone is regulated by signals that travel from the brain to the nerves and tell the muscles to contract. Hypotonia can happen from damage to the brain, spinal cord, nerves, or muscles. The damage can be the result of trauma, environmental factors, or genetic, muscle, or central nervous system disorders. For example, it can be seen in Down syndrome, muscular dystrophy, cerebral palsy, Prader-Willi syndrome, myotonic dystrophy, and Tay-Sachs disease. Sometimes it may not be possible to find what causes the hypotonia. Infants with hypotonia have a floppy quality or rag doll appearance because their arms and legs hang by their sides and they have little or no head control. Other symptoms of hypotonia include problems with mobility and posture, breathing and speech difficulties, ligament and joint laxity, and poor reflexes. Hypotonia does not affect intellect. The opposite of hypotonia is hypertonia."}
{"_id":"4bfcb386-3675-479c-bc29-88ee4d6730c1","text":"Treatment begins with a thorough diagnostic evaluation, usually performed by a neurologist, including an assessment of motor and sensory skills, balance and coordination, mental status, reflexes, and functioning of the nerves. Diagnostic tests that may be helpful include a CT or MRI scan of the brain, an EMG to evaluate nerve and muscle function, or an EEG to measure electrical activity in the brain. Once a diagnosis has been made, the underlying condition is treated first, followed by symptomatic and supportive therapy for the hypotonia. Physical therapy can improve motor control and overall body strength. Occupational therapy can help relearn ways to address activities of daily living. Speech-language therapy can help breathing, speech, and swallowing difficulties. Therapy for infants and young children may also include sensory stimulation programs."}
{"_id":"5a16926d-647a-4d92-a0f0-3d13e13e6f34","text":"Hypotonia can be a life-long condition. In some cases, however, muscle tone improves over time."}
{"_id":"787e2a19-04fd-40d0-9c2c-5cc216d30bb2","text":"The NINDS supports research on conditions that can result from neurological disorders, such as hypotonia. Much of this research is aimed at learning more about these conditions and finding ways to prevent and treat them."}
{"_id":"7ff0f04a-59b1-4796-bc6a-38a07b9bd037","text":"Cushing's syndrome, also called hypercortisolism, is a rare endocrine disorder caused by chronic exposure of the body's tissues to excess levels of cortisol - a hormone naturally produced by the adrenal gland. Exposure to too much cortisol can occur from long-term use of synthetic glucocorticoid hormones to treat inflammatory illnesses. Pituitary adenomas (benign tumors of the pituitary gland) that secrete increased amounts of ACTH (adrenocorticotropic hormone, a substance that controls the release of cortisol) can also spur overproduction of cortisol. Tumors of the adrenal gland and ectopic ACTH syndrome (a condition in which ACTH is produced by various types of potentially malignant tumors that occur in different parts of the body) can cause similar problems with cortisol balance. Common symptoms of Cushing's syndrome include upper body obesity, severe fatigue and muscle weakness, high blood pressure, backache, elevated blood sugar, easy bruising, and bluish-red stretch marks on the skin. In women, there may be increased growth of facial and body hair, and menstrual periods may become irregular or stop completely. Neurological symptoms include difficulties with memory and neuromuscular disorders."}
{"_id":"30dd0dc1-152c-4116-847b-fffbfd8312ea","text":"Treatment of Cushing's syndrome depends on the cause of excess cortisol. If the cause is long-term use of a medication being used to treat another disorder, the physician may reduce the dosage until symptoms are under control. Surgery or radiotherapy may be used to treat pituitary adenomas. Surgery, radiotherapy, chemotherapy, immunotherapy, or a combination of these may be used to treat ectopic ACTH syndrome. The aim of surgical treatment is to cure hypercortisolism by removing the tumor while minimizing the chance of endocrine deficiency or long-term dependence on medications. The U.S. Food and Drug Administration has approved pasireotide diasparate, taken by injection, for individuals who cannot be helped through surgery."}
{"_id":"6ad41b39-cfb1-45bf-a14a-b2e359266859","text":"The prognosis for those with Cushing's syndrome varies depending on the cause of the disease. Most cases of Cushing's syndrome can be cured. Many individuals with Cushing's syndrome show significant improvement with treatment, although some may find recovery complicated by various aspects of the causative illness. Some kinds of tumors may recur."}
{"_id":"4cda742a-1cf0-45cf-854e-1ad398d724dc","text":"NINDS supports research on Cushing's syndrome aimed at finding new ways to diagnose, treat, and cure the disorder."}
{"_id":"7cdee4a4-e876-42fe-93e6-ec22c57b7e3d","text":"Moyamoya disease is a rare, progressive cerebrovascular disorder caused by blocked arteries at the base of the brain in an area called the basal ganglia. The name moyamoya means puff of smoke in Japanese and describes the look of the tangle of tiny vessels formed to compensate for the blockage. Moyamoya disease was first described in Japan in the 1960s and it has since been found in individuals in the other countries around the world; its incidence is higher in Asian countries than in Europe or North America. The disease primarily affects children, but it can also occur in adults. In children, the first symptom of Moyamoya disease is often stroke, or recurrent transient ischemic attacks (TIA, commonly referred to as mini-strokes), frequently accompanied by muscular weakness or paralysis affecting one side of the body, or seizures. Adults may also experience these symptoms that arise from blocked arteries, but more often experience a hemorrhagic stroke due to bleeding into the brain from the abnormal brain vessels. Individuals with this disorder may have disturbed consciousness, problems with speaking and understanding speech, sensory and cognitive impairments, involuntary movements, and vision problems.About one in 10 individuals with Moyamoya disease has a close relative who is also affected; in these cases researchers think that Moyamoya disease is the result of inherited genetic abnormalities.Studies that look for the abnormal gene(s) may help reveal the biomechanisms that cause the disorder."}
{"_id":"ee41db31-fc43-47c5-879f-be9c73d33a18","text":"There are several types of surgery that can restore blood flow (revascularization) to the brain by opening narrowed blood vessels or by bypassing blocked arteries. Children usually respond better to revascularization surgery than adults, but the majority of individuals have no further strokes or related problems after surgery."}
{"_id":"30345a5c-e292-4d73-93cf-838a8f7c409b","text":"Without surgery, the majority of individuals with Moyamoya disease will experience mental decline and multiple strokes because of the progressive narrowing of arteries.Without treatment,Moyamoya diseasecan be fatal as the result ofintracerebral hemorrhage (bleeding within the brain)."}
{"_id":"39c35033-a82d-4cb2-812f-665df0b3e524","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS conducts and supports neurological research aimed at understanding why diseases develop in the brain, and that focus on finding ways to prevent, treat, or cure them.Anti-angiogenic therapy uses drugs that either activate and promote cell growth or directly block the growing blood vessel cells. NINDS-funded researchers are testing the anti-angiogenic drug Apo-Timop, part of a class of drugs called beta-blockers, which may lead to the development of new anti-angiogenics for people with vascular malformations. In other research, Other NINDS-funded research hopes to improve the understanding of this disease by determining whether infections injure blood vessels and thereby predispose children to stroke. It will also determine causes of recurrence, a crucial step toward developing ways to prevent repeated strokes in children."}
{"_id":"86df4f52-ff47-400b-bc1f-36bfe3f83cf9","text":"The pituitary is a small, bean-sized gland that is below the hypothalamus, a structure at the base of the brain, by a thread-like stalk that contains both blood vessels and nerves. It controls a system of hormones in the body that regulate growth, metabolism, the stress response, and functions of the sex organs via the thyroid gland, adrenal gland, ovaries, and testes. A pituitary tumor is an abnormal growth of cells within the pituitary gland. Most pituitary tumors are benign, which means they are non-cancerous, grow slowly and do not spread to other parts of the body; however they can make the pituitary gland produce either too many or too few hormones, which can cause problems in the body. Tumors that make hormones are called functioning tumors, and they can cause a wide array of symptoms depending upon the hormone affected. Tumors that dont make hormones are called non-functioning tumors. Their symptoms are directly related to their growth in size and include headaches, vision problems, nausea, and vomiting. Diseases related to hormone abnormalities include Cushings disease, in which fat builds up in the face, back and chest, and the arms and legs become very thin; and acromegaly, a condition in which the hands, feet, and face are larger than normal. Pituitary hormones that impact the sex hormones, such as estrogen and testosterone, can make a woman produce breast milk even though she is not pregnant or nursing, or cause a man to lose his sex drive or lower his sperm count. Pituitary tumors often go undiagnosed because their symptoms resemble those of so many other more common diseases."}
{"_id":"676f4b97-1209-4f7f-b778-1891edc311af","text":"Generally, treatment depends on the type of tumor, the size of the tumor, whether the tumor has invaded or pressed on surrounding structures, such as the brain and visual pathways, and the individuals age and overall health. Three types of treatment are used: surgical removal of the tumor; radiation therapy, in which high-dose x-rays are used to kill the tumor cells; and drug therapy to shrink or destroy the tumor. Medications are also sometimes used to block the tumor from overproducing hormones. For some people, removing the tumor will also stop the pituitarys ability to produce a specific hormone. These individuals will have to take synthetic hormones to replace the ones their pituitary gland no longer produces."}
{"_id":"89bea879-fc97-4c1a-a878-d83c859264f1","text":"If diagnosed early enough, the prognosis is usually excellent. If diagnosis is delayed, even a non-functioning tumor can cause problems if it grows large enough to press on the optic nerves, the brain, or the carotid arteries (the vessels that bring blood to the brain). Early diagnosis and treatment is the key to a good prognosis."}
{"_id":"0dd881ef-843d-4573-a0e8-449929c7974f","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to brain tumors, including pituitary tumors, in their laboratories at the NIH and also support research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure pituitary tumors."}
{"_id":"5a47d935-28e0-4ace-80a4-81614c72f466","text":"Foot drop describes the inability to raise the front part of the foot due to weakness or paralysis of the muscles that lift the foot. As a result, individuals with foot drop scuff their toes along the ground or bend their knees to lift their foot higher than usual to avoid the scuffing, which causes what is called a steppage gait. Foot drop can be unilateral (affecting one foot) or bilateral (affecting both feet). Foot drop is a symptom of an underlying problem and is either temporary or permanent, depending on the cause. Causes include: neurodegenerative disorders of the brain that cause muscular problems, such as multiple sclerosis, stroke, and cerebral palsy; motor neuron disorders such as polio, some forms of spinal muscular atrophy and amyotrophic lateral sclerosis (commonly known as Lou Gehrigs disease); injury to the nerve roots, such as in spinal stenosis; peripheral nerve disorders such as Charcot-Marie-Tooth disease or acquired peripheral neuropathy; local compression or damage to the peroneal nerve as it passes across the fibular bone below the knee; and muscle disorders, such as muscular dystrophy or myositis."}
{"_id":"d4367636-670d-419f-bf63-44f6dbc6de76","text":"Treatment depends on the specific cause of foot drop. The most common treatment is to support the foot with light-weight leg braces and shoe inserts, called ankle-foot orthotics. Exercise therapy to strengthen the muscles and maintain joint motion also helps to improve gait. Devices that electrically stimulate the peroneal nerve during footfall are appropriate for a small number of individuals with foot drop. In cases with permanent loss of movement, surgery that fuses the foot and ankle joint or that transfers tendons from stronger leg muscles is occasionally performed."}
{"_id":"20494cfd-dc87-47f4-beeb-6a5889133c34","text":"The prognosis for foot drop depends on the cause. Foot drop caused by trauma or nerve damage usually shows partial or even complete recovery. For progressive neurological disorders, foot drop will be a symptom that is likely to continue as a lifelong disability, but it will not shorten life expectancy."}
{"_id":"e0027f71-a79b-4e97-b312-ca29acb70a08","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to the neurological conditions that cause foot drop in its laboratories at the National Institutes of Health (NIH), and also supports additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure the kinds of neurological disorders that cause foot drop."}
{"_id":"5bcefbf9-0ec1-4387-a46c-f8d662ea333e","text":"Central cord syndrome is the most common form of incomplete spinal cord injury characterized by impairment in the arms and hands and to a lesser extent in the legs. The brain's ability to send and receive signals to and from parts of the body below the site of injury is reduced but not entirely blocked. This syndrome is associated with damage to the large nerve fibers that carry information directly from the cerebral cortex to the spinal cord. These nerves are particularly important for hand and arm function. Symptoms may include paralysis or loss of fine control of movements in the arms and hands, with relatively less impairment of leg movements. Sensory loss below the site of the injury and loss of bladder control may also occur, as well as painful sensations such as tinging, burning, or dull ache. The overall amount and type of functional loss is dependent upon the severity of nerve damage. Central cord syndrome is usually the result of trauma that causes damage to the vertebrae in the neck or herniation of the vertebral discs. It also may develop in persons over the age of 50 due to gradual weakening of the vertebrae and discs, which narrows the spinal column and may contribute to compression of the spinal cord when the neck is hyper-extended."}
{"_id":"974a1d69-b452-4c1a-9ca1-fe63dd7c485e","text":"There is no cure for central cord syndrome although some people recover near-normal function. There is no standard course of treatment, although drug therapy, surgery, and rest are often part of the program. Magnetic resonance imaging (MRI) is used to indicate the degree of spinal cord compression and vertebral instability. Vertebral instability due to acute traumatic injury or cervical disc herniation is often treated by surgery to prevent further damage to the spinal cord. Recent reports indicate that earlier surgery may improve chances for recovery. Numerous recent studies suggest that surgery also can be beneficial in individuals with persistent compression of the spinal cord and ongoing neurological deterioration."}
{"_id":"cb357957-bd6c-4829-b55a-d6ade8fb4e59","text":"The prognosis for central cord syndrome varies, but most people whose syndrome is caused by trauma have some recovery of neurological function. Evaluation of abnormal signals on MRI images can help predict he likelihood that neurological recovery may occur naturally. Those who receive medical intervention soon after their injury often have good outcomes. Many people with the disorder recover substantial function after their initial injury, and the ability to walk is recovered in most cases, although some impairment may remain. Improvement occurs first in the legs, then the bladder, and may be seen in the arms. Hand function recovers last, if at all. Recovery is generally better in younger patients, compared to those over the age of 50."}
{"_id":"70150daf-ed69-4612-bb98-474e4cf8b281","text":"Our understanding of central cord syndrome has increased greatly in recent decades as a result of research funded conducted by the National Institute of Neurological Disorders and Stroke (NINDS). Much of this research focuses on finding better ways to prevent, treat, and ultimately cure neurological disorders such as central cord syndrome."}
{"_id":"0f6a57ec-9dda-4ef8-8b36-4b3a48770f51","text":"Anencephaly is a defect in the closure of the neural tube during fetal development. The neural tube is a narrow channel that folds and closes between the 3rd and 4th weeks of pregnancy to form the brain and spinal cord of the embryo. Anencephaly occurs when the \"cephalic\" or head end of the neural tube fails to close, resulting in the absence of a major portion of the brain, skull, and scalp. Infants with this disorder are born without a forebrain (the front part of the brain) and a cerebrum (the thinking and coordinating part of the brain). The remaining brain tissue is often exposed--not covered by bone or skin. A baby born with anencephaly is usually blind, deaf, unconscious, and unable to feel pain. Although some individuals with anencephaly may be born with a rudimentary brain stem, the lack of a functioning cerebrum permanently rules out the possibility of ever gaining consciousness. Reflex actions such as breathing and responses to sound or touch may occur.\n                \nThe cause of anencephaly is unknown. Although it is thought that a mother's diet and vitamin intake may play a role, scientists believe that many other factors are also involved.\n                \nRecent studies have shown that the addition of folic acid (vitamin B9) to the diet of women of childbearing age may significantly reduce the incidence of neural tube defects. Therefore it is recommended that all women of childbearing age consume 0.4 mg of folic acid daily."}
{"_id":"c26231c6-2356-4d63-8592-8c1cfb3b7e4b","text":"There is no cure or standard treatment for anencephaly. Treatment is supportive."}
{"_id":"2b6b0125-ead3-4c27-8bc3-d6f735e85f08","text":"The prognosis for babies born with anencephaly is extremely poor. If the infant is not stillborn, then he or she will usually die within a few hours or days after birth."}
{"_id":"a77550c0-513b-4b94-aec2-6820f53fb1c1","text":"Research supported by the NINDS includes studies to understand how the brain and nervous system normally develop. These studies contribute to a greater understanding of neural tube disorders, such as anencephaly, and open promising new avenues to treat and prevent neurological birth defects."}
{"_id":"45554c8f-484c-48c6-bf6c-aa6309754795","text":"Cytomegalovirus (CMV) is a virus found throughout the world that infects between 50 to 80 percent of all adults in the United States by the age of 40. CMV is in the same family of viruses that causes cold sores (herpes simplex virus), infectious mononucleosis (Epstein-Barr virus), and chickenpox\/shingles (varicella zoster virus).  Most people who acquire CVM as children or adults display no signs of illness or have mild symptoms such as fever, fatigue, or tender lymph nodes. People with a compromised immune system may have more severe forms of infection involving the nervous system.\n                \nA hallmark of CMV infection is that the virus cycles through periods of dormancy and active infection during the life of the individual Infected persons of any age periodically shed the virus in their body fluids, such as saliva, urine, blood, tears, semen, or breast milk. CMV is most commonly transmitted when infected body fluids come in contact with the mucous membranes of an uninfected person, but the virus can also pass from mother to fetus during pregnancy."}
{"_id":"61c450df-7dde-47bd-b34f-b5d7d7fcbf0f","text":"Since the virus remains in the person for life, there is no treatment to eliminate CMV infection. However, minimizing contact with infected body fluids can decrease the risk of viral transmission between individuals or from mother to fetus. Contact can be minimized by using gloves or other protective barriers when handling body fluids or contaminated materials (such as diapers or tissues), avoiding shared dishes, utensils, and other personal items, and consistent and thorough hand-washing. \n                \nAntiviral drugs (ganciclovir and others)can be used to prevent or control the symptoms of CMV infection in immunocompromised individuals or some infants with congenital infection. CMV immunoglobulin may also be used in some patients. Vaccines are in the development and human clinical trial stages, which shows that vaccines may help prevent initial CMV infection or decrease the severity of symptoms."}
{"_id":"e7da1a38-a451-4787-9a5e-01a5f239ac23","text":"For most people CMV infection is not a problem. However, two groups of people are at high risk of neurological or other severe symptoms that may lead to long-term effects:\n                \n- Unborn infants whose mothers have CMV infection. CMVis the most common congenital infection in the U.S. Most infants will have no permanent health consequences, but a small number will have at birth or will develop long-term neurological conditions, such as hearing loss, visual impairment, seizures, or disabilities f mental or physical function. The highest risk of these severe effects on the fetus is for women who acquire CMV infection for the first time during pregnancy. The risk is much lower for women who have had CMV infection in the past before pregnancy. - Immunocompromised individuals. CMV infection may be severe in solid organ or blood cell transplant recipients, people with untreated or end-stage HIV-AIDS, or others with altered immune function. Infection may affect the brain (encephalitis), spinal cord (myelitis), eye (retinitis), or other organs such as the lungs (pneumonia) or intestinal gract (gastritis, enteritis, or colitis). In addition, transplant recipients may develop organ rejection or graft-versus-host disease associated with CMV infection."}
{"_id":"0bf033e3-05d6-48e3-8108-ff3ae5f39b18","text":"The National Institute of Neurological Disorders and Stroke (NINDS), and other institutes of the National Institutes of Health (NIH), conduct research related to CMV infection in laboratories at the NIH, and support additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent and treat CMV infection in people at risk of severe neurological consequences, especially a safe and effective CMV vaccine."}
{"_id":"bd9d07ed-ba20-4c14-9d55-e917b16a4fd7","text":"The muscular dystrophies (MD) are a group of more than 30 genetic diseases characterized by progressive weakness and degeneration of the skeletal muscles that control movement. Some forms of MD are seen in infancy or childhood, while others may not appear until middle age or later. The disorders differ in terms of the distribution and extent of muscle weakness (some forms of MD also affect cardiac muscle), age of onset, rate of progression, and pattern of inheritance. Duchenne MD is the most common form of MD and primarily affects boys. It is caused by the absence of dystrophin, a protein involved in maintaining the integrity of muscle. Onset is between 3 and 5 years and the disorder progresses rapidly. Most boys are unable to walk by age 12, and later need a respirator to breathe. Girls in these families have a 50 percent chance of inheriting and passing the defective gene to their children. Boys with Becker MD (very similar to but less severe than Duchenne MD) have faulty or not enough dystrophin. Facioscapulohumeral MD usually begins in the teenage years. It causes progressive weakness in muscles of the face, arms, legs, and around the shoulders and chest. It progresses slowly and can vary in symptoms from mild to disabling. Myotonic MD is the disorder's most common adult form and is typified by prolonged muscle spasms, cataracts, cardiac abnormalities, and endocrine disturbances. Individuals with myotonic MD have long, thin faces, drooping eyelids, and a swan-like neck."}
{"_id":"b1038fc7-b4dd-49a8-8389-cd037d860417","text":"There is no specific treatment to stop or reverse any form of MD. Treatment may include physical therapy, respiratory therapy, speech therapy, orthopedic appliances used for support, and corrective orthopedic surgery. Drug therapy includes corticosteroids to slow muscle degeneration, anticonvulsants to control seizures and some muscle activity, immunosuppressants to delay some damage to dying muscle cells, and antibiotics to fight respiratory infections. Some individuals may benefit from occupational therapy and assistive technology. Some patients may need assisted ventilation to treat respiratory muscle weakness and a pacemaker for cardiac abnormalities."}
{"_id":"4acf16e5-14fd-44b1-bb42-936e59e94ced","text":"The prognosis for people with MD varies according to the type and progression of the disorder. Some cases may be mild and progress very slowly over a normal lifespan, while others produce severe muscle weakness, functional disability, and loss of the ability to walk. Some children with MD die in infancy while others live into adulthood with only moderate disability."}
{"_id":"22ec17c5-5300-41e9-a410-9237e8a81ac5","text":"The NINDS supports a broad program of research studies on MD. The goals of these studies are to understand MD and to develop techniques to diagnose, treat, prevent, and ultimately cure the disorder.\n                \nThe NINDS is a member of the Muscular Dystrophy Coordinating Committee (MDCC). For additional information, please visit: http:\/\/www.ninds.nih.gov\/about_ninds\/groups\/mdcc\/"}
{"_id":"e7a73b67-b1eb-4a16-92ef-cd9e397ff193","text":"Tourette syndrome (TS) is a neurological disorder characterized by repetitive, stereotyped, involuntary movements and vocalizations called tics. The first symptoms of TS are almost always noticed in childhood. Some of the more common tics include eye blinking and other vision irregularities, facial grimacing, shoulder shrugging, and head or shoulder jerking. Perhaps the most dramatic and disabling tics are those that result in self-harm such as punching oneself in the face, or vocal tics including coprolalia (uttering swear words) or echolalia (repeating the words or phrases of others). Many with TS experience additional neurobehavioral problems including inattention, hyperactivity and impulsivity, and obsessive-compulsive symptoms such as intrusive thoughts\/worries and repetitive behaviors."}
{"_id":"64b79424-78a6-429f-9139-21dcdfd5601d","text":"Because tic symptoms do not often cause impairment, the majority of people with TS require no medication for tic suppression. However, effective medications are available for those whose symptoms interfere with functioning. There is no one medication that is helpful to all people with TS, nor does any medication completely eliminate symptoms. Effective medications are also available to treat some of the associated neurobehavioral disorders that can occur in patients with TS."}
{"_id":"41b055cd-0f65-4fac-abe8-3c04129130cc","text":"Although TS can be a chronic condition with symptoms lasting a lifetime, most people with the condition experience their worst symptoms in their early teens, with improvement occurring in the late teens and continuing into adulthood. As a result, some individuals may actually become symptom free or no longer need medication for tic suppression."}
{"_id":"26871d3d-497a-4baf-9e99-d2ba5c1c7d97","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research in laboratories at the NIH and support additional research through grants to major medical institutions across the country. Knowledge about TS comes from studies across a number of medical and scientific disciplines, including genetics, neuroimaging, neuropathology, clinical trials, epidemiology, neurophysiology, neuroimmunology, and descriptive\/diagnostic clinical science. Findings from these studies will provide clues for more effective therapies."}
{"_id":"56b6fec6-8a68-4829-8bed-59a4ba344bfa","text":"Hypertonia is a condition in which there is too much muscle tone so that arms or legs, for example, are stiff and difficult to move. Muscle tone is regulated by signals that travel from the brain to the nerves and tell the muscle to contract. Hypertonia happens when the regions of the brain or spinal cord that control these signals are damaged. This can occur for many reasons, such as a blow to the head, stroke, brain tumors, toxins that affect the brain, neurodegenerative processes such as in multiple sclerosis or Parkinson's disease, or neurodevelopmental abnormalities such as in cerebral palsy.\n                \nHypertonia often limits how easily the joints can move. If it affects the legs, walking can become stiff and people may fall because it is difficult for the body to react quickly enough to regain balance. If hypertonia is severe, it can cause a joint to become \"frozen,\" which doctors call a joint contracture.\n                \nSpasticity is a term that is often used interchangeably with hypertonia. Spasticity, however, is a particular type of hypertonia in which the muscles' spasms are increased by movement. In this type, patients usually have exaggerated reflex responses.\n                \nRigidity is another type of hypertonia in which the muscles have the same amount of stiffness independent of the degree of movement. Rigidity usually occurs in diseases such as Parkinson's disease, that involve the basal ganglia (a deep region of the brain). To distinguish these types of hypertonia, a doctor will as the patient to relax and then will move the arm or leg at different speeds and in a variety of directions."}
{"_id":"f48fa954-873f-4008-bdf0-3d3d088fa487","text":"Muscle relaxing drugs such as baclofen, diazepam, and dantrolene may be prescribed to reduce spasticity. All of these drugs can be taken by mouth, but baclofen may also be injected directly into the cerebrospinal fluid through an implanted pump. Botulinum toxin is often used to relieve hypertonia in a specific area of the body because its effects are local, not body-wide. People with hypertonia should try to preserve as much movement as possibly by exercising within their limits and using physical therapy.\n                \nDrugs that affect the dopamine system (dopamine is a chemical in the brain) such as levodopa\/carbidopa, or entacapone, are often used to treat the rigidity associated with Parkinson's disease."}
{"_id":"c718e8d3-d6ba-446a-940f-1504f6ebea83","text":"The prognosis depends upon the severity of the hypertonia and its cause. In some cases, such as cerebral palsy, the hypertonia may not change over the course of a lifetime. in other cases, the hypertonia may worsen along with the underlying disease If the hypertonia is mild, it has little or no effect on a person's health. If there is moderate hypertonia, falls or joint contractures may have an impact on a person's health and safety. If the hypertonia is so severe that is caused immobility, potential consequences include increased bone fragility and fracture, infection, bed sores, and pneumonia."}
{"_id":"a6c2e796-7058-416d-a1cf-4e27e5c3d38c","text":"NINDS supports research on brain and spinal cord disorders that can cause hypertonia. The goals of this research are to learn more about how the nervous system adapts after injury or disease and to find ways to prevent and treat these disorders."}
{"_id":"1ec16ad5-9a73-478f-8ff8-0e25cf53b795","text":"Friedreich's ataxia is a rare inherited disease that causes progressive damage to the nervous system and movement problems. Neurological symptoms include awkward, unsteady movements, impaired sensory function, speech problems, and vision and hearing loss. Thinking and reasoning abilities are not affected.Impaired muscle coordination (ataxia) results from the degeneration of nerve tissue in the spinal cord and of nerves that control muscle movement in the arms and legs. Symptoms usually begin between the ages of 5 and 15 but can appear in adulthood or later. The first symptom is usually difficulty in walking. The ataxia gradually worsens and slowly spreads to the arms and then the trunk. People lave loss of sensation in the arms and legs, which may spread to other parts of the body. Many people with Friedreich's ataxia develop scoliosis (a curving of the spine to one side), which, if severe, may impair breathing. Other symptoms include chest pain, shortness of breath, and heart problems. Some individuals may develop diabetes. Doctors diagnose Friedreich's ataxia by performing a careful clinical examination, which includes a medical history and a thorough physical examination. Several tests may be performed, including electromyogram (EMG, which measures the electrical activity of cells) and genetic testing."}
{"_id":"c9a95dac-0902-4d1b-a918-89af5544355c","text":"There is currently no effective cure or treatment for Friedreich's ataxia. However, many of the symptoms and accompanying complications can be treated to help individuals maintain optimal functioning as long as possible. Diabetes and heart problems can be treated with medications. Orthopedic problems such as foot deformities and scoliosis can be treated with braces or surgery. Physical therapy may prolong use of the arms and legs."}
{"_id":"ef227c37-ce77-4cd8-bf29-035c2e9087d3","text":"Generally, within 15 to 20 years after the appearance of the first symptoms, the person is confined to a wheelchair, and in later stages of the disease, individuals may become completely incapacitated. Friedreich's ataxia can shorten life expectancy; heart disease is the most common cause of death. Many individuals with Friedreich's ataxia die in early adulthood, but some people with less severe symptoms live into their 60s, 70s, or longer."}
{"_id":"e70da14e-5a19-4f13-ab5e-3528eed35a33","text":"Friedreich's ataxia is caused by a mutation in the protein frataxin, which is involved in the function of mitochondriathe energy producing power plants of the cell. Frataxin controls important steps in mitochondrial iron metabolism and overall cell iron stability.NINDS-funded researchers are studying the metabolic functions of mitochondria in individuals with Friedreichs ataxia. Ongoing research is aimed at understanding the molecular basis for and mechanisms involved in the inactivation of the gene that provides instructions for frataxin, which could lead to potential ways to reverse the silencing and restore normal gene function.And researchers are using next-generation sequencing (which can quickly identify the structure of millions of small fragments of DNA at the same time) to identify novel genes in Friedreich's ataxia."}
{"_id":"0cae6303-99a1-4577-93db-9be6d73e6477","text":"Wilson disease (WD) is a rare inherited disorder of copper metabolism in which excessive amounts of copper accumulate in the body. The buildup of copper leads to damage in the liver, brain, and eyes. Although copper accumulation begins at birth, symptoms of the disorder only appear later in life. The most characteristic sign of WD is the Kayser-Fleisher ring  a rusty brown ring around the cornea of the eye that can best be viewed using an ophthalmologists slit lamp. The primary consequence for most individuals with WD is liver disease, appearing in late childhood or early adolescence as acute hepatitis, liver failure, or progressive chronic liver disease in the form of chronic active hepatitis or cirrhosis of the liver. In others, the first symptoms are neurological, occur later in adulthood, and commonly include slurred speech (dysarthria), difficulty swallowing (dysphagia), and drooling. Other symptoms may include tremor of the head, arms, or legs; impaired muscle tone, and sustained muscle contractions that produce abnormal postures, twisting, and repetitive movements (dystonia); and slowness of movements (bradykinesia). Individuals may also experience clumsiness (ataxia) and loss of fine motor skills. One-third of individuals with WD will also experience psychiatric symptoms such as an abrupt personality change, bizarre and inappropriate behavior, depression accompanied by suicidal thoughts, neurosis, or psychosis. WD is diagnosed with tests that measure the amount of copper in the blood, urine, and liver."}
{"_id":"421a3c23-06b9-4d0a-a873-0dad69129ecf","text":"WD requires lifelong treatment, generally using drugs that remove excess copper from the body and prevent it from re-accumulating. Zinc, which blocks the absorption of copper in the stomach and causes no serious side effects, is often considered the treatment of choice. Penicillamine and trientine are copper chelators that increase urinary excretion of copper; however, both drugs have some side effects. Tetrathiomolybdate is an investigational copper chelating drug with a lower toxicity profile, but it has not been approved by the Food and Drug Administration for the treatment of WD and its long-term safety and effectiveness arent known. A low-copper diet is also recommended, which involves avoiding mushrooms, nuts, chocolate, dried fruit, liver, and shellfish. In rare cases where there is severe liver disease, a liver transplant may be needed. Symptomatic treatment for symptoms of muscle spasm, stiffness, and tremor may include anticholinergics, tizanidine, baclofen, levodopa, or clonazepam."}
{"_id":"293d5df3-eb24-4c1b-89fe-f425e06b570f","text":"Early onset of the disease may foretell a worse prognosis than later onset. If the disorder is detected early and treated appropriately, an individual with WD can usually enjoy normal health and a normal lifespan. If not treated, however, WD can cause brain damage, liver failure, and death. The disease requires lifelong treatment."}
{"_id":"87f52037-ca82-4d09-b0ac-bfbfea42291f","text":"The National Institute of Neurological Disorders and Stroke, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and other institutes of the National Institutes of Health (NIH) conduct and\/or support research related to Wilson disease. Growing knowledge of the copper transporting gene ATP7B, which in its mutated form causes WD, should lead to the design of better therapies for this disorder."}
{"_id":"5c70c58e-7085-4dcd-9a76-91d5878d289b","text":"A cerebral aneurysm is a weak or thin spot on a blood vessel in the brain that balloons out and fills with blood. An aneurysm can press on a nerve or surrounding tissue, and also leak or burst, which lets blood spill into surrounding tissues (called a hemorrhage). Cerebral aneurysms can occur at any age, although they are more common in adults than in children and are slightly more common in women than in men. The signs and symptoms of an unruptured cerebral aneurysm will partly depend on its size and rate of growth. For example, a small, unchanging aneurysm will generally produce no symptoms, whereas a larger aneurysm that is steadily growing may produce symptoms such as headache, numbness, loss of feeling in the face or problems with the eyes. Immediately after an aneurysm ruptures, an individual may experience such symptoms as a sudden and unusually severe headache, nausea, vision impairment, vomiting, and loss of consciousness."}
{"_id":"fec3501f-b1c8-4cbe-8fec-d9fded45c9eb","text":"For unruptured aneurysms, treatment may be recommended for large or irregularly-shaped aneurysms or for those causing symptoms. Emergency treatment for individuals with a ruptured cerebral aneurysm may be required to restore deteriorating respiration and reduce abnormally high pressure within the brain. Treatment is necessary to prevent the aneurysm from rupturing again. Surgical treatment prevents repeat aneurysm rupture by placing a metal clip at the base of the aneurysm. Individuals for whom surgery is considered too risky may be treated by inserting the tip of a catheter into an artery in the groin and advancing it through the blood stream to the site of the aneurysm, where it is used to insert metal coils that induce clot formation within the aneurysm."}
{"_id":"c80b3968-2f7f-4247-8e03-f54701d5a9af","text":"The prognosis for a individual with a ruptured cerebral aneurysm depends on the location of the aneurysm, extent of bleeding or rebleeding, the person's age, general health, pre-existing neurological conditions, adn time between rupture and medical attention. Early diagnosis and treatment are important. A burst cerebral aneurysm may be fatal or could lead to hemorrhagic stroke, vasospasm (in which other blood vessels in the brain contract and limit blood flow), hydrocephalus, coma, or short-term and\/or permanent brain damage. Recovery from treatment or rupture may take weeks to months."}
{"_id":"2a7300ad-b0aa-4dc8-a9ca-66df3738800f","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research in its laboratories at the National Institutes of Health (NIH) and also supports additional research through grants to major medical institutions. The NINDS supports a broad range of basic and clinical research on intracranial aneurysms and other vascular lesions of the nervous system. The Familial Intracranial Aneurysm study seeks to identify possible genes that may increase the risk of development of aneurysms in blood vessels in the brain. Other research projects include genome-wide studies to identify genes or DNA sequences that may indicate families harboring one type of aneurysm may be at increased risk of another type; studies of chromosomes to identify aneurysm-related genes; and additional research on microsurgical clipping and endovascular surgery to treat various types of ruptured and unruptured aneurysms."}
{"_id":"4e0c4e1d-a256-417b-9ff6-fac264461b0a","text":"Charcot-Marie-Tooth disease (CMT) is one of the most common inherited neurological disorders, affecting approximately 1 in 2,500 people in theUnited States. CMT, also known as hereditary motor and sensory neuropathy (HMSN) or peroneal muscular atrophy, comprises a group of disorders caused by mutations in genes that affect the normal function of the peripheral nerves. The peripheral nerves lie outside the brain and spinal cord and supply the muscles and sensory organs in the limbs. A typical feature includes weakness of the foot and lower leg muscles, which may result in foot drop and a high-stepped gait with frequent tripping or falling. Foot deformities, such as high arches and hammertoes (a condition in which the middle joint of a toe bends upwards), are also characteristic due to weakness of the small muscles in the feet. In addition, the lower legs may take on an \"inverted champagne bottle\" appearance due to the loss of muscle bulk. Later in the disease, weakness and muscle atrophy may occur in the hands, resulting in difficulty with fine motor skills. Some individuals experience pain, which can range from mild to severe."}
{"_id":"34593392-bef3-4b27-bc0f-b592ca130502","text":"There is no cure for CMT, but physical therapy, occupational therapy, braces and other orthopedic devices, and orthopedic surgery can help people cope with the disabling symptoms of the disease. In addition, pain-killing drugs can be prescribed for patients who have severe pain."}
{"_id":"89e1c630-bdcc-49bc-92a6-d9f730593bab","text":"Onset of symptoms of CMT is most often in adolescence or early adulthood, however presentation may be delayed until mid-adulthood. Progression of symptoms is very gradual. The degeneration of motor nerves results in muscle weakness and atrophy in the extremities (arms, legs, hands, or feet), and the degeneration of sensory nerves results in a reduced ability to feel heat, cold, and pain. There are many forms of CMT disease. The severity of symptoms may vary greatly among individuals and some people may never realize they have the disorder. CMT is not fatal and people with most forms of CMT have a normal life expectancy."}
{"_id":"8bf51c0b-8793-4040-96c1-078c01b8eea5","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts CMT research in its laboratories at the National Institutes of Health (NIH) and also supports CMT research through grants to major medical institutions across the country. Ongoing research includes efforts to identify more of the mutant genes and proteins that cause the various disease subtypes. This research includes studies in the laboratory to discover the mechanisms of nerve degeneration and muscle atrophy, and clinical studies to find therapies to slow down or even reverse nerve degeneration and muscle atrophy."}
{"_id":"18803016-cfe5-4653-92cc-1f363968fa0b","text":"Alternating hemiplegia is a rare neurological disorder that develops in childhood, most often before the child is 18 months old. The disorder is characterized by recurrent episodes of paralysis that involve one or both sides of the body, multiple limbs, or a single limb. The paralysis may affect different parts of the body at different times and may be brief or last for several days. Oftentimes these episodes will resolve after sleep. Affected children may also have abnormal movements involving stiffening or \"dance-like\" movements of a limb, as well as walking and balance problems. Some children have seizures. Children may have normal or delayed development. There are both benign and more serious forms of the disorder. Most children do not have a family history of the disorder; however, recent studies have show that some children with a family history have mutations in the genes CACNA1A, SCN1A, and ATP1A2. Mutations in the ATP1A2 gene have previously been associated with families affect by familial hemiplegic migraine."}
{"_id":"529b848b-f8fe-4721-b320-00d789715b23","text":"Drug therapy including verapamil may help to reduce the severity and duration of attacks of paralysis associated with the more serious form of alternating hemiplegia"}
{"_id":"dc4bdcf0-a0f3-4c38-9739-9bcd42ed11b8","text":"Children with the benign form of alternating hemiplegia have a good prognosis. Those who experience the more severe form have a poor prognosis because intellectual and mental capacities do not respond to drug therapy, and balance and gait problems continue. Over time, walking unassisted becomes difficult or impossible."}
{"_id":"63c33f68-8a63-4cc6-a54a-7d2d991a667e","text":"The NINDS supports research on paralytic disorders such as alternating hemiplegia, with the goals of learning more about these disorders and finding ways to prevent, treat and, ultimately cure them."}
{"_id":"7f300cc6-3c8a-4ef0-98a0-06594591bab3","text":"Meralgia paresthetica is a disorder characterized by tingling, numbness, and burning pain in the outer side of the thigh. The disorder is caused by compression of the lateral femoral cutaneous nerve, a sensory nerve to the skin, as it exits the pelvis. People with the disorder often notice a patch of skin that is sensitive to touch and sometimes painful. Meralgia paresthetica should not be associated with weakness or radiating pain from the back."}
{"_id":"837baa68-dbb8-45da-865e-2899b38b8cc0","text":"Treatment for meralgia paresthetica is symptomatic and supportive. The majority of cases improve with conservative treatment by wearing looser clothing and losing weight. Medications used to treat neurogenic pain, such as anti-seizure or anti-depressant medications, may alleviate symptoms of pain. In a few cases, in which pain is persistent or severe, surgical intervention may be indicated."}
{"_id":"940c8863-935d-4551-8251-ed9bb147aa62","text":"Meralgia paresthetica usually has a good prognosis. In most cases, meralgia paresthetica will improve with conservative treatment or may even spontaneously resolve. Surgical intervention is not always fully successful."}
{"_id":"84a2ec59-58c9-449f-8069-fe843e76aa51","text":"Within the NINDS research programs, meralgia paresthetica is addressed primarily through studies associated with pain research. NINDS vigorously pursues a research program seeking new treatments for pain and nerve damage with the ultimate goal of reversing these debilitating conditions."}
{"_id":"f42a2f0e-b59d-4ec0-a6e5-8824721d388a","text":"Neurosyphilis is a disease of the coverings of the brain, the brain itself, or the spinal cord. It can occur in people with syphilis, especially if they are left untreated. Neurosyphilis is different from syphilis because it affects the nervous system, while syphilis is a sexually transmitted disease with different signs and symptoms. There are five types of neurosyphilis:\n                \n- asymptomatic neurosyphilis - meningeal neurosyphilis - meningovascular neurosyphilis - general paresis, and - tabes dorsalis.\n                \nAsymptomatic neurosyphilis means that neurosyphilis is present, but the individual reports no symptoms and does not feel sick. Meningeal syphilis can occur between the first few weeks to the first few years of getting syphilis. Individuals with meningeal syphilis can have headache, stiff neck, nausea, and vomiting. Sometimes there can also be loss of vision or hearing. Meningovascular syphilis causes the same symptoms as meningeal syphilis but affected individuals also have strokes. This form of neurosyphilis can occur within the first few months to several years after infection. General paresis can occur between 3  30 years after getting syphilis. People with general paresis can have personality or mood changes. Tabes dorsalis is characterized by pains in the limbs or abdomen, failure of muscle coordination, and bladder disturbances. Other signs include vision loss, loss of reflexes and loss of sense of vibration, poor gait, and impaired balance. Tabes dorsalis can occur anywhere from 5  50 years after initial syphilis infection. General paresis and tabes dorsalis are now less common than the other forms of neurosyphilis because of advances made in prevention, screening, and treatment. People with HIV\/AIDS are at higher risk of having neurosyphilis."}
{"_id":"dd163bd1-5d77-4385-943d-6151e1997b3d","text":"Penicillin, an antibiotic, is used to treat syphilis. Individuals with neurosyphilis can be treated with penicillin given by vein, or by daily intramuscular injections for 10  14 days. If they are treated with daily penicillin injections, individuals must also take probenecid by mouth four times a day. Some medical professionals recommend another antibiotic called ceftriaxone for neurosyphilis treatment. This drug is usually given daily by vein, but it can also be given by intramuscular injection. Individuals who receive ceftriaxone are also treated for 10 - 14 days. People with HIV\/AIDS who get treated for neurosyphilis may have different outcomes than individuals without HIV\/AIDS."}
{"_id":"b6cef991-2d72-425e-bc10-f5617ebd2706","text":"Prognosis can change based on the type of neurosyphilis and how early in the course of the disease people with neurosyphilis get diagnosed and treated. Individuals with asymptomatic neurosyphilis or meningeal neurosyphilis usually return to normal health. People with meningovascular syphilis, general paresis, or tabes dorsalis usually do not return to normal health, although they may get much better. Individuals who receive treatment many years after they have been infected have a worse prognosis. Treatment outcome is different for every person."}
{"_id":"5c5c1e1a-3d29-49f2-bf20-872c0c204526","text":"The National Institute of Neurological Disorders and Stroke supports and conducts research on neurodegenerative disorders, such as neurosyphilis, in an effort to find ways to prevent, treat, and ultimately cure these disorders."}
{"_id":"7601c69b-6496-4a0e-9e69-b92ece15a18b","text":"Neuromyelitis optica (NMO) is an autoimmune disease of the central nervous system (CNS) that predominantly affects the optic nerves and spinal cord. It is sometimes also referred to as NMO spectrum disorder.In NMO, the body's immune system mistakenly attacks healthy cells and proteins in the body, must often those in the spinal cord and eyes. Individuals with NMO develop optic neuritis, which caused pain in the eye and vision loss. Individuals also develop transverse myelitis, which causes weakness or paralysis of arms and legs,and numbness, along with loss of bladder and bowel control Magnetic resonance imaging of the spine often shows an abnormality that extends over long segments of the spinal cord. Individuals may also develop episodes of severe nausea and vomiting, with hiccups from involvement of a part of the brain that ocntrols vomiting The disease is caused by abnormal autoantibodies that bind to a protein called aquaporin-4. Binding of the aquaporin-4 antibody activates other components of the immune system, causing inflammation and damage to these cells. This also results in the brain and spinal cord the loss of myelin, the fatty substance that acts as insulation around nerve fibers and helps nerve signals move from cell to cell.\n                \nNMO is different from multiple sclerosis (MS). Attacks are usually more severe in NMO than in MS, and NMO is treated differently than MS. Most individuals with NMO experience clusters of attacks days to months or years apart, followed by partial recovery during periods of remission. Women are more often affected by NMO than men. African Americans are at greater risk of the disease than are Caucasians. The onset of NMO varies from childhood to adulthood, with two peaks, one in childhood and the other in adults in their 40s."}
{"_id":"bd80f6a0-d637-46f8-bd65-e4359199a782","text":"There is no cure for NMO and no FDA-approved therapies, but there are therapies to treat an attack while it is happening, to reduce symptoms, and to prevent relapses.NMO relapses and attacks are often treated with corticosteroid drugs and plasma exchange (also called plasmapheresis, a process used to remove harmful antibodies from the bloodstream). Immunosuppressvie drugs used to prevent attacks include mycophenolate mofetil, rituximab, and azathioprine. Pain, stiffness, muscle spasms, and bladder and bowel control problems can be managed with medicaitons and therapies. Individuals with major disability will require the combined efforts to physical and occupational therapists, along with social services professionals to address complex rehabilitation needs."}
{"_id":"356acbb9-45c6-4d07-9d9f-2912ec31d5fa","text":"Most individuals with NMO have an unpredictable, relapsing course of disease with attacks occurring months or years apart. Disability is cumulative, the result of each attack damaging new areas of the central nervous system. Some individuals are severely affected by NMO and can lose vision in both eyes and the use of their arms and legs. Most individuals experience some degree of permanent limb weakness or vision loss from NMO. However, reducing the number of attacks with immunosuppressive medications may help prevent with accumulation of disability. Rarely, muscle weakness can be severe enough to cause breathing difficulties and may require the use of artificial ventilation."}
{"_id":"cc7f6158-063d-4ef6-916b-ba962252a993","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS is a component of the National Institutes of Health, the leading supporter of biomedical research in the world. NINDS researchers are working to better understand the process by which the immune system destroys or attacks the nerve insulating substance called myelin in autoijmune diseases or disorders. Other work focuses on strategies to repair demyelinated spinal cords, including approaches using cell transplantation. this research may lead to a grater understanding of the mechanisms responsible for damaging myelin and may ultimately provide a means to prevent and treat transverse myelitis An NINDS-funded study comparing clinical MRI and lumbar puncture of healthy individuals to those with symptoms of immune-related central nervous system damage hopes to identify processes or mechanisms to inhibit or minimize spinal tissue damage and enhance recovery mechanisms. Multiple studies are looking at ways to target different components of the immune system known to be involved in NMO spectrum disorders to allow more directly targeted treatment of this disease."}
{"_id":"cedf6907-22c4-4058-a47e-fa6697bd80a0","text":"Tay-Sachs disease is a inherited metabolic disease caused by the harmful buildup of lipids (fatty materials such as oils and acids) in various cells and tissues in the body. It is part of a group of genetic disorders called the GM2 gangliosidoses. Tay-Sachs and its variant form are caused by a deficiency in the enzyme hexosaminidase A. Affected children appear to develop normally until about age 6 months. Then, symptoms begin and include progressive loss of mental ability, dementia, blindness, increased startle reflex to noise, progressive loss of hearing leading to deafness, and difficulty with swallowing. Seizures may begin in the child's second year. Persons with Tay-Sachs also have \"cherry-red\" spots in their eyes.A much rarer form of the disorder, called late-onset Tay-Sachs disease, occurs in individuals in their twenties and early thirties and is characterized by an unsteady gait and progressive neurological deterioration. The incidence of Tay-Sachs has been particularly high among people of Eastern European and Askhenazi Jewish descent., as well as in certain French Canadians and Louisiana Cajuns. Affected individuals and carriers of Tay-Sachs disease can be identified by a blood test that measures hexosaminidase A activity. Both parents must carry the mutated gene in order to have an affected child. In these instances, there is a 25 percent chance with each pregnancy that the child will be affected with Tay-Sachs disease. Prenatal diagnosis is available if desired. A very severe form of Tay-Sachs disease is know as Sandhoff disease, which is not limited to any ethnic group."}
{"_id":"68463f4d-a276-4862-9208-13eb31c2a470","text":"Presently there is no specific treatment for Tay-Sachs disease. Anticonvulsant medicine may initially control seizures. Other supportive treatment includes proper nutrition and hydration and techniques to keep the airway open. Children may eventually need a feeding tube."}
{"_id":"c69744c2-1044-4945-a473-885ed127f7b1","text":"Even with the best of care, children with Tay-Sachs disease usually die by age 4, from recurring infection."}
{"_id":"bb2467a9-c3b5-4842-a0f6-ce05121e84fc","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS is a part of the National Institutes of Health (NIH), the leading supporter of biomedical research in the world. the NINDS and other NIH Institutes supports the Lysosomal Diseases Netowrk, which addresses some of the major challenges in the diagnosis, management, and therapy of rare diseases, including the lipid storage diseases. Additional research funded by the NINDS focuses on better understanding how neurological defects arise in lipid storage disorders and on the development of new treatments targeting disease mechanisms, including gene therapies, cell-based therapies, and pharmacological approaches. NINDS-funded research on the gangliosidoses includes using variations of magnetic resonance imaging to develop a biomarker (a sign that may indicate risk of a disease and improve diagnosis) to effectively evaluate brain biochemistry and disease progression. Other research is expanding the use of virus-delivered gene therapy seen in an animall model of Tay-Sachs disease for use in humans."}
{"_id":"13e02c11-8e2c-4cc9-8fe1-621bc9277eca","text":"Dyssynergia Cerebellaris Myoclonica refers to a collection of rare, degenerative, neurological disorders characterized by epilepsy, cognitive impairment, myoclonus, and progressive ataxia. Symptoms include seizures, tremor, and reduced muscle coordination. Onset of the disorder generally occurs in early adulthood. Tremor may begin in one extremity and later spread to involve the entire voluntary muscular system. Arms are usually more affected than legs. Some of the cases are due to mitochondrial abnormalities."}
{"_id":"9b409a41-1d6f-4877-8eee-37306a73839e","text":"Treatment of Dyssynergia Cerebellaris Myoclonica is symptomatic. Myoclonus and seizures may be treated with drugs like valproate."}
{"_id":"dbf1d325-c00e-48b7-92d8-680a76949290","text":"The progression of the disorder is usually 10 years or longer."}
{"_id":"237107b3-7635-4e4f-9cde-5500fe8c07d9","text":"The NINDS supports a broad range of research on neurodegenerative disorders such as Dyssynergia Cerebellaris Myoclonica. The goals of this research are to find ways to prevent, treat, and cure these kinds of disorders."}
{"_id":"08e4c475-a931-4071-aae9-703bc239b0f6","text":"Encephalopathy is a term for any diffuse disease of the brain that alters brain function or structure. Encephalopathy may be caused by infectious agent (bacteria, virus, or prion), metabolic or mitochondrial dysfunction, brain tumor or increased pressure in the skull, prolonged exposure to toxic elements (including solvents, drugs, radiation, paints, industrial chemicals, and certain metals), chronic progressive trauma, poor nutrition, or lack of oxygen or blood flow to the brain. The hallmark of encephalopathy is an altered mental state. Depending on the type and severity of encephalopathy, common neurological symptoms are progressive loss of memory and cognitive ability, subtle personality changes, inability to concentrate, lethargy, and progressive loss of consciousness. Other neurological symptoms may include myoclonus (involuntary twitching of a muscle or group of muscles), nystagmus (rapid, involuntary eye movement), tremor, muscle atrophy and weakness, dementia, seizures, and loss of ability to swallow or speak. Blood tests, spinal fluid examination, imaging studies, electroencephalograms, and similar diagnostic studies may be used to differentiate the various causes of encephalopathy."}
{"_id":"771f1a0e-14ff-41d4-a1d1-ec4ee18d7cd6","text":"Treatment is symptomatic and varies, according to the type and severity of the encephalopathy. Your physician can provide specific instructions for proper care and treatment. Anticonvulsants may be prescribed to reduce or halt any seizures. Changes to diet and nutritional supplements may help some patients. In severe cases, dialysis or organ replacement surgery may be needed."}
{"_id":"bb1b5a55-8940-4b3a-8c04-0a67a6a2e010","text":"Treating the underlying cause of the disorder may improve symptoms. However, the encephalopathy may cause permanent structural changes and irreversible damage to the brain. Some encephalopathies can be fatal."}
{"_id":"3265e38d-0643-4859-83cd-a28988d67331","text":"The NINDS supports and conducts research on brain diseases. Much of this research is aimed at characterizing the agents that cause these disorders, clarifying the mechanisms underlying them, and, ultimately, finding ways to prevent, treat, and cure them."}
{"_id":"47c9c5dc-b9fc-4f55-8367-8ff20e85fffd","text":"Sturge-Weber syndrome is a neurological disorder indicated at birth by a port-wine stain birthmark on the forehead and upper eyelid of one side of the face. The birthmark can vary in color from light pink to deep purple and is caused by an overabundance of capillaries around the trigeminal nerve just beneath the surface of the face. Sturge-Weber syndrome is also accompanied by abnormal blood vessels on the brain surface and the loss of nerve cells and calcification of underlying tissue in the cerebral cortex of the brain on the same side of the brain as the birthmark. Neurological symptoms include seizures that begin in infancy and may worsen with age. Convulsions usually happen on the side of the body opposite the birthmark and vary in severity. There may be intermittent or permanent muscle weakness on the same side. Some children will have developmental delays and cognitive impairment; most will have glaucoma (increased pressure within the eye) at birth or developing later. The increased pressure within the eye can cause the eyeball to enlarge and bulge out of its socket (buphthalmos). There is an increased risk for migraine headaches. Sturge-Weber syndrome rarely affects other body organs."}
{"_id":"d382f5ff-4694-4aca-9a05-f6a635e6a5a1","text":"Treatment for Sturge-Weber syndrome is symptomatic. Laser treatment may be used to lighten or remove the birthmark.  Anticonvulsant medications may be used to control seizures. Persons with drug-resistant seizures may be treated by surgical removal of epileptic brain tissue. Surgery may be performed on more serious cases of glaucoma. Physical therapy should be considered for infants and children with muscle weakness. Educational therapy is often prescribed for those with impaired cognition or developmental delays. Doctors recommend yearly monitoring for glaucoma."}
{"_id":"e26e2d12-c8d5-41ac-a7a8-5aedc0a77adb","text":"Although it is possible for the birthmark and atrophy in the cerebral cortex to be present without symptoms, most infants will develop convulsive seizures during their first year of life. There is a greater likelihood of intellectual impairment when seizures start before the age of 2 and are resistant to treatment. Prognosis is worst in the minority of children who have both sides of the brain affected by the blood vessel abnormalities."}
{"_id":"87dc86d5-7256-438c-aac7-95ad4e41317c","text":"The NINDS supports a broad program of research to better understand congenital seizure disorders. This research is aimed at developing techniques to diagnose, treat, prevent, and ultimately cure disorders such as Sturge-Weber syndrome."}
{"_id":"2ea5b85b-328e-42c9-826f-9de62f7140ee","text":"Kennedy's disease is an inherited motor neuron disease that affects males. It is one of a group of disorders called lower motor neuron disorders (which involve disruptions in the transmission of nerve cell signals in the brain to nerve cells in the brain stem and spinal cord). Onset of the disease is usually between the ages of 20 and 40, although it has been diagnosed in men from their teens to their 70s. Early symptoms include tremor of the outstretched hands, muscle cramps with exertion, and fasciculations (fleeting muscle twitches visible under the skin). Eventually, individuals develop limb weakness which usually begins in the pelvic or shoulder regions. Weakness of the facial and tongue muscles may occur later in the course of the disease and often leads to dysphagia (difficulty in swallowing), dysarthria (slurring of speech), and recurrent aspiration pneumonia. Some individuals develop gynecomastia (excessive enlargement of male breasts) and low sperm count or infertility. Still others develop non-insulin-dependent diabetes mellitus.\n                \nKennedy's disease is an x-linked recessive disease, which means the patient's mother carries the defective gene on one of her X chromosomes. Daughters of patients with Kennedy's disease are also carriers and have a 1 in 2 chance of having a son affected with the disease. Parents with concerns about their children may wish to talk to a genetic counselor."}
{"_id":"f07dcb4e-bc82-44f3-bb3b-4a0aefec548a","text":"Currently there is no known cure for Kennedy's disease. Treatment is symptomatic and supportive. Physical therapy and rehabilitation to slow muscle weakness and atrophy may prove helpful."}
{"_id":"59573cac-7eab-4dca-8a81-986b9d7366a9","text":"Kennedy's disease is slowly progressive. Individuals tend to remain ambulatory until late in the disease, although some may be wheelchair-bound during later stages. The life span of individuals with Kennedy's disease is usually normal."}
{"_id":"c3590ca0-a8e2-423f-8a46-7e502a8f0aec","text":"The NINDS supports a broad spectrum of research on motor neuron diseases, such as Kennedy's disease. Much of this research is aimed at increasing scientific understanding of these diseases and, ultimately, finding ways to prevent, treat, and cure them."}
{"_id":"4bb26331-969c-464d-9b83-888d756d573d","text":"The neurofibromatoses are genetic disorders that cause tumors to grow in the nervous system. The tumors begin in the supporting cells that make up the nerves and the myelin sheath--the thin membrane that envelops and protects the nerves. These disorders cause tumors to grow on nerves and, less frequently, in the brain and spinal cord, and produce other abnormalities such as skin changes and bone deformities. Although many affected persons inherit the disorder, between 30 and 50 percent of new cases arise spontaneously through mutation (change) in an individual's genes. Once this change has taken place, the mutant gene can be passed on to succeeding generations. There are three forms of neurofibromatosis (NF):\n                \n- NF1 is the more common type of the disorder. Symptoms of NF1, which may be evident at birth and nearly always by the time the child is 10 years old, may include light brown spots on the skin (\"cafe-au-lait\" spots), two or more growths on the iris of the eye, a tumor on the optic nerve, a larger than normal head circumference, and abnormal development of the spine, a skull bone, or the tibia.   - NF2 is less common and is characterized by slow-growing tumors on the vestibular branch of the right and left eighth cranial nerves, which are called vestibular schwannomas or acoustic neuromas.. The tumors press on and damage neighboring nerves and reduce hearing.  - The distinctive feature of schwannomatosis is the development of multiple schwannomas (tumors made up of certain cells) everywhere in the body except on the vestibular branch of the 8th cranial nerve. The dominant symptom is pain, which develops as a schwannoma enlarges or compresses nerves or adjacent tissue. Some people may develop numbness, tingling, or weakness in the fingers and toes."}
{"_id":"deecc7b6-a8b6-424b-904e-860aeb61ab04","text":"Treatment may include surgery, focused radiation, or chemotherapy. Surgery to remove NF2 tumors completely is one option. Surgery for vestibular schwannomas does not restore hearing and usually reduces hearing. Sometimes surgery is not performed until functional hearing is lost completely. Surgery may result in damage to the facial nerve and some degree of facial paralysis. Focused radiation of vestibular schwannoma carries of a lower risk of facial paralysis than open surgery, but is more effective o shrinking small to moderate tumors than larger tumors. Chemotherapy with a drug that targets the blood vessels of vestibular schwannoma can reduce the size of the tumor and improves hearing, but some tumors do not respond at all and sometimes respond only temporarily. Bone malformations can often be corrected surgically, and surgery can also correct cataracts and retinal abnormalities. Pain usually subsides when tumors are removed completely."}
{"_id":"c345aecc-fb49-4a05-9e35-75668f7627b1","text":"In most cases, symptoms of NF1 are mild, and individuals live normal and productive lives. In some cases, however, NF1 can be severely debilitating and may cause cosmetic and psychological issues. The course of NF2 varies greatly among individuals. Loss of hearing in both ears develops in most individuals with NF2. In some cases of NF2, the damage to nearby vital structures, such as other cranial nerves and the brain stem, can be life-threatening. Most individuals with schwannomatosis have significant pain. In some extreme cases the pain will be severe and disabling."}
{"_id":"250d3d26-2979-4f40-a407-587516a43e0d","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. NINDS researchers are working to identify signaling pathways in the nervous system, with the hope of eventually developing drugs and techniques to help diagnose and treat NF. Understanding the natural history of tumors in NF and determining possible factors that may regulate their growth patterns is another aim of NIH researchers Ongoing research continues to discover additional genes that appear to play a role in NF-related tumor suppression or growth Continuing research on these genes and their proteins is beginning to reveal how this novel family of growth regulators controls how and where tumors form and grow Researchers also hope to develop new and more effective treatments for neurofibromatosis. Several agents have been tested or are under investigation for NF2, including the monoclonal antibody, bevacizumab, which improves hearing in some individuals with NF2.Because schwannomas are particularly hard to treat tumors, NINDS researchers are developing a new treatment option, which uses a virus to kill tumor cells. Additional NINDS-funded researchers are testing novel radiation and chemotherapy regimens for NF1-related malignant tumors of the peripheral nerves."}
{"_id":"31dacded-6bbe-4073-9276-47f466e8bc67","text":"Aicardi-Goutieres syndrome (AGS) is an inherited encephalopathy that affects newborn infants and usually results in severe mental and physical handicap. There are two forms of the syndrome: an early-onset form that is severe, and a late-onset form that has less impact upon neurological function. The early-onset form affects about 20 percent of all babies who have AGS. These infants are born with neurological and liver abnormalities, such as enlargement of the liver and spleen and elevated liver enzymes. Their jittery behavior and poor feeding ability mimic congenital viral infection.\n                \nBabies with later-onset AGS begin having symptoms after the first weeks or months of normal development, which appear as a progressive decline in head growth, weak or stiffened muscles (spasticity), and cognitive and developmental delays that range from moderate to severe. Symptoms last for several months, and include irritability, inconsolable crying, intermittent fever, seizures, and loss of developmental skills. Children may also have puffy swelling on the fingers, toes, and ears that resemble chilblains. A number of children have a noticeable startle reaction to sudden noise. For babies with the later-onset form, as symptoms lessen, there is no further worsening of the disease.\n                \nAGS is difficult to diagnose since many of the symptoms are similar to those of other disorders. Diagnosis is made based on the clinical symptoms of the disease, as well as characteristic brain abnormalities that can be seen in an MRI brain scan. Cerebrospinal fluid (CSF), taken using a \"spinal tap,\" can also be tested for increased levels of a specific immune system cell (a lymphocyte), which indicates a condition known as chronic lymphocytosis. These cells are normally only elevated during infection, so that lymphocytosis without evidence of infection can be used as an indicator of AGS. CSF may also be tested for elevated levels of a substance known as interferon-gamma, which can also support a diagnosis of AGS.\n                \nThe mutations of four different genes are associated with AGS:\n                \n- Aicardi-Goutieres syndrome-1 (AGS1) and AGS5 (an autosomal dominant form) are caused by a mutation in the TREX1 gene, - AGS2 is caused by a mutation in the RNASEH2B gene, - AGS3 is caused by a mutation in the RNASEH2C gene, - AGS4 is caused by a mutation in the RNASEH2A gene.\n                \nMost cases of AGS are inherited in an autosomal recessive manner, which means that both parents of a child with AGS must carry a single copy of the defective gene responsible for the disease. Parents do not have any symptoms of disease, but with every child they have together, there is a one in four chance that the baby will receive two copies of the defective gene and inherit AGS.\n                \nNOTE: AGS is distinct from the similarly named Aicardi syndrome (characterized by absence of a brain structure (corpus callosum), and spinal, skeletal, and eye abnormalities)."}
{"_id":"bcc9c71a-5ddc-4695-a1d2-27f840bc4395","text":"Depending upon the severity of symptoms, children may require chest physiotherapy and treatment for respiratory complications. To ensure adequate nutrition and caloric intake, some infants may require special accommodations for diet and feeding. Seizures may be managed with standard anticonvulsant medications. Children should be monitored for evidence of glaucoma in the first few months of life, and later for evidence of scoliosis, diabetes, and underactive thyroid.The prognosis depends upon the severity of symptoms."}
{"_id":"ff3c1ee7-640a-43ef-a11a-298925a456f9","text":"The prognosis depends upon the severity of symptoms. Children with early-onset AGS have the highest risk of death. Children with the later-onset form may be left with weakness or stiffness in the peripheral muscles and arms, weak muscles in the trunk of the body, and poor head control. Almost all children with AGS have mild to severe intellectual and physical impairment."}
{"_id":"86a9b10b-a4c5-4043-9875-36361b121e6b","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) support research related to AGS through grants to major medical institutions across the country. Current research is aimed at finding new methods for treating and ultimately preventing or curing AGS."}
{"_id":"3fda06fe-cf77-4670-8b02-2d0634d7aea0","text":"Pseudotumor cerebri literally means \"false brain tumor.\" It is likely due to high pressure within the skull caused by the buildup or poor absorption of cerebrospinal fluid (CSF). The disorder is most common in women between the ages of 20 and 50. Symptoms of pseudotumor cerebri, which include headache, nausea, vomiting, and pulsating sounds within the head, closely mimic symptoms of large brain tumors."}
{"_id":"8198f698-3619-49f7-bee1-e8383f68d65e","text":"Obesity, other treatable diseases, and some medications can cause raised intracranial pressure and symptoms of pseudotumor cerebri. A thorough medical history and physical examination is needed to evaluate these factors. If a diagnosis of pseudotumor cerebri is confirmed, close, repeated ophthalmologic exams are required to monitor any changes in vision. Drugs may be used to reduce fluid buildup and to relieve pressure. Weight loss through dieting or weight loss surgery and cessation of certain drugs (including oral contraceptives, tetracycline, and a variety of steroids) may lead to improvement. Surgery may be needed to remove pressure on the optic nerve. Therapeutic shunting, which involves surgically inserting a tube to drain CSF from the lower spine into the abdominal cavity, may be needed to remove excess CSF and relieve CSF pressure."}
{"_id":"9d73af9c-003b-48bc-9f7d-a19f274d2f39","text":"The disorder may cause progressive, permanent visual loss in some patients. In some cases, pseudotumor cerebri recurs."}
{"_id":"b543719b-f5e3-4a86-a22f-d8dc435149f4","text":"The NINDS conducts and supports research on disorders of the brain and nervous system, including pseudotumor cerebri. This research focuses primarily on increasing scientific understanding of these disorders and finding ways to prevent, treat, and cure them."}
{"_id":"748766ad-72f7-414c-8614-a0272f8a0621","text":"Schilder's disease is a rare progressive demyelinating disorder which usually begins in childhood. Schilder's disease is not the same as Addison-Schilder disease (adrenoleukodystrophy). Symptoms may include dementia, aphasia, seizures, personality changes, poor attention, tremors, balance instability, incontinence, muscle weakness, headache, vomiting, and vision and speech impairment. The disorder is a variant of multiple sclerosis."}
{"_id":"29d7ddc3-34c8-4537-92e6-f372e47d8c4b","text":"Treatment for the disorder follows the established standards in multiple sclerosis and includes corticosteroids, beta-interferon or immunosuppressive therapy, and symptomatic treatment."}
{"_id":"ba5daa3b-0e3c-4dcf-8374-8a6c3da7f2ff","text":"As with multiple sclerosis, the course and prognosis of Schilder's disease are unpredictable. For some individuals the disorder is progressive with a steady, unremitting course. Others may experience significant improvement and even remission. In some cases, Schilder's disease is fatal."}
{"_id":"e83b985f-bae6-4d47-b605-4712b81cc1c5","text":"The NINDS supports and conducts an extensive research program on demyelinating disorders such as Schilder's disease. Much of this research focuses on learning more about these disorders and finding ways to prevent, treat, and cure them."}
{"_id":"5ea4ceee-ed82-410b-bc3b-48309c40f943","text":"Tarlov cysts are sacs filled with cerebrospinal fluid that most often affect nerve roots in the sacrum, the group of bones at the base of the spine. These cysts (also known as meningeal or perineural cysts) can compress nerve roots, causing lower back pain, sciatica (shock-like or burning pain in the lower back, buttocks, and down one leg to below the knee), urinary incontinence, headaches (due to changes in cerebrospinal fluid pressure), constipation, sexual dysfunction, and some loss of feeling or control of movement in the leg and\/or foot. Pressure on the nerves next to the cysts can also cause pain and deterioration of surrounding bone. Tarlov cysts can be diagnosed using magnetic resonance imaging (MRI); however, it is estimated that the majority of the cysts observed by MRI cause no symptoms. Tarlov cysts may become symptomatic following shock, trauma, or exertion that causes the buildup of cerebrospinal fluid. Women are at much higher risk of developing these cysts than are men."}
{"_id":"d70849f3-0a15-4cf3-9b8b-f987ec526498","text":"Tarlov cysts may be drained and shunted to relieve pressure and pain, but relief is often only temporary and fluid build-up in the cysts will recur. Corticosteroid injections may also temporarily relieve pain. Other drugs may be prescribed to treat chronic pain and depression. Injecting the cysts with fibrin glue (a combination of naturally occurring substances based on the clotting factor in blood) may provide temporary relief of pain. Some scientists believe the herpes simplex virus, which thrives in an alkaline environment, can cause Tarlov cysts to become symptomatic. Making the body less alkaline, through diet or supplements, may lessen symptoms. Microsurgical removal of the cyst may be an option in select individuals who do not respond to conservative treatments and who continue to experience pain or progressive neurological damage."}
{"_id":"4b8242ac-cb04-4ead-b217-6c83b378e99c","text":"In some instances Tarlov cysts can cause nerve pain and other pain, weakness, or nerve root compression. Acute and chronic pain may require changes in lifestyle. If left untreated, nerve root compression can cause permanent neurological damage."}
{"_id":"538bfb3e-3a3a-4ff8-929c-d46944cac19d","text":"The NINDS, a component of the National Institutes of Health within the U.S. Department of Health and Human Services, vigorously pursues a research program seeking new treatments to reduce and prevent pain and nerve damage."}
{"_id":"3ca46052-0456-4de0-9c1f-7b89e87f8767","text":"An unpredictable disease of the central nervous system, multiple sclerosis (MS) can range from relatively benign to somewhat disabling to devastating, as communication between the brain and other parts of the body is disrupted. Many investigators believe MS to be an autoimmune disease -- one in which the body, through its immune system, launches a defensive attack against its own tissues. In the case of MS, it is the nerve-insulating myelin that comes under assault. Such assaults may be linked to an unknown environmental trigger, perhaps a virus.\n                \nMost people experience their first symptoms of MS between the ages of 20 and 40; the initial symptom of MS is often blurred or double vision, red-green color distortion, or even blindness in one eye. Most MS patients experience muscle weakness in their extremities and difficulty with coordination and balance. These symptoms may be severe enough to impair walking or even standing. In the worst cases, MS can produce partial or complete paralysis. Most people with MS also exhibit paresthesias, transitory abnormal sensory feelings such as numbness, prickling, or \"pins and needles\" sensations. Some may also experience pain. Speech impediments, tremors, and dizziness are other frequent complaints. Occasionally, people with MS have hearing loss. Approximately half of all people with MS experience cognitive impairments such as difficulties with concentration, attention, memory, and poor judgment, but such symptoms are usually mild and are frequently overlooked. Depression is another common feature of MS."}
{"_id":"6dc70691-fabf-4c43-bb44-0f483ab39fec","text":"There is as yet no cure for MS. Many patients do well with no therapy at all, especially since many medications have serious side effects and some carry significant risks. However, three forms of beta interferon (Avonex, Betaseron, and Rebif) have now been approved by the Food and Drug Administration for treatment of relapsing-remitting MS. Beta interferon has been shown to reduce the number of exacerbations and may slow the progression of physical disability. When attacks do occur, they tend to be shorter and less severe. The FDA also has approved a synthetic form of myelin basic protein, called copolymer I (Copaxone), for the treatment of relapsing-remitting MS. Copolymer I has few side effects, and studies indicate that the agent can reduce the relapse rate by almost one third. Other FDA approved drugs to treat relapsing forms of MS in adults include teriflunomide and dimethyl fumarate. An immunosuppressant treatment, Novantrone (mitoxantrone), isapproved by the FDA for the treatment of advanced or chronic MS. The FDA has also approved dalfampridine (Ampyra) to improve walking in individuals with MS.\n                \nOne monoclonal antibody, natalizumab (Tysabri), was shown in clinical trials to significantly reduce the frequency of attacks in people with relapsing forms of MS and was approved for marketing by the U.S. Food and Drug Administration (FDA) in 2004. However, in 2005 the drugs manufacturer voluntarily suspended marketing of the drug after several reports of significant adverse events. In 2006, the FDA again approved sale of the drug for MS but under strict treatment guidelines involving infusion centers where patients can be monitored by specially trained physicians.\n                \nWhile steroids do not affect the course of MS over time, they can reduce the duration and severity of attacks in some patients. Spasticity, which can occur either as a sustained stiffness caused by increased muscle tone or as spasms that come and go, is usually treated with muscle relaxants and tranquilizers such as baclofen, tizanidine, diazepam, clonazepam, and dantrolene. Physical therapy and exercise can help preserve remaining function, and patients may find that various aids -- such as foot braces, canes, and walkers -- can help them remain independent and mobile. Avoiding excessive activity and avoiding heat are probably the most important measures patients can take to counter physiological fatigue. If psychological symptoms of fatigue such as depression or apathy are evident, antidepressant medications may help. Other drugs that may reduce fatigue in some, but not all, patients include amantadine (Symmetrel), pemoline (Cylert), and the still-experimental drug aminopyridine. Although improvement of optic symptoms usually occurs even without treatment, a short course of treatment with intravenous methylprednisolone (Solu-Medrol) followed by treatment with oral steroids is sometimes used."}
{"_id":"6e252257-82de-4159-8e25-8fdf1eea6eec","text":"A physician may diagnose MS in some patients soon after the onset of the illness. In others, however, doctors may not be able to readily identify the cause of the symptoms, leading to years of uncertainty and multiple diagnoses punctuated by baffling symptoms that mysteriously wax and wane. The vast majority of patients are mildly affected, but in the worst cases, MS can render a person unable to write, speak, or walk. MS is a disease with a natural tendency to remit spontaneously, for which there is no universally effective treatment."}
{"_id":"0350ff6d-bff0-4c06-906b-4b0b0affad1c","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research in laboratories at the NIH and also support additional research through grants to major medical institutions across the country. Scientists continue their extensive efforts to create new and better therapies for MS. One of the most promising MS research areas involves naturally occurring antiviral proteins known as interferons. Beta interferon has been shown to reduce the number of exacerbations and may slow the progression of physical disability. When attacks do occur, they tend to be shorter and less severe. In addition, there are a number of treatments under investigation that may curtail attacks or improve function. Over a dozen clinical trials testing potential therapies are underway, and additional new treatments are being devised and tested in animal models.\n                \nIn 2001, the National Academies\/Institute of Medicine, a Federal technical and scientific advisory agency, prepared a strategic review of MS research. To read or download the National Academies\/Institute of Medicine report, go to: \"Multiple Sclerosis: Current Status and Strategies for the Future.\""}
{"_id":"f1e18ca5-ca1f-4267-aab5-0027ad4a7919","text":"Moebius syndrome is a rare birth defect caused by the absence or underdevelopment of the 6th and 7th cranial nerves, which control eye movements and facial expression. Many of the other cranial nerves may also be affected, including the 3rd, 5th, 8th, 9th, 11th and 12th. The first symptom, present at birth, is an inability to suck. Other symptoms can include: feeding, swallowing, and choking problems; excessive drooling; crossed eyes; lack of facial expression; inability to smile; eye sensitivity; motor delays; high or cleft palate; hearing problems and speech difficulties. Children with Moebius syndrome are unable to move their eyes back and forth. Decreased numbers of muscle fibers have been reported. Deformities of the tongue, jaw, and limbs, such as clubfoot and missing or webbed fingers, may also occur. As children get older, lack of facial expression and inability to smile become the dominant visible symptoms. Approximately 30 to 40 percent of children with Moebius syndrome have some degree of autism.\n                \nThere are four recognized categories of Moebius syndrome:\n                \n- Group I, characterized by small or absent brain stem nuclei that control the cranial nerves; - Group II, characterized by loss and degeneration of neurons in the facial peripheral nerve; - Group III, characterized by loss and degeneration of neurons and other brain cells, microscopic areas of damage, and hardened tissue in the brainstem nuclei, and, - Group IV, characterized by muscular symptoms in spite of a lack of lesions in the cranial nerve."}
{"_id":"81c5b8f1-454c-4c50-8e8a-7a0dac199c84","text":"There is no specific course of treatment for Moebius syndrome. Treatment is supportive and in accordance with symptoms. Infants may require feeding tubes or special bottles to maintain sufficient nutrition. Surgery may correct crossed eyes and improve limb and jaw deformities. Physical and speech therapy often improves motor skills and coordination, and leads to better control of speaking and eating abilities. Plastic reconstructive surgery may be beneficial in some individuals. Nerve and muscle transfers to the corners of the mouth have been performed to provide limited ability to smile."}
{"_id":"ec14e44a-0335-4e54-b50f-dc972717d9e5","text":"There is no cure for Moebius syndrome. In spite of the impairments that characterize the disorder, proper care and treatment give many individuals a normal life expectancy."}
{"_id":"e102e91f-75a4-4949-b0dc-ab2f99d0af89","text":"The NINDS conducts and supports a broad range of research on neurogenetic disorders, including Moebius syndrome. The goals of these studies are to develop improved techniques to diagnose, treat, and eventually cure these disorders."}
{"_id":"f9d13565-6463-44ba-bb2f-04c718307710","text":"Thyrotoxic myopathy is a neuromuscular disorder that may accompany hyperthyroidism (Graves' disease, caused by overproduction of the thyroid hormone thyroxine). Symptoms may include muscle weakness, myalgias (muscle tenderness), wasting of the pelvic girdle and shoulder muscles, fatigue, and\/or heat intolerance. Thyroid myopathy may be associated with rhabdomyolysis (acute muscle breakdown), damage to the muscles that control eye movement, and temporary, but severe, attacks of muscle weakness that are associated with low blood potassium levels (known as periodic paralysis)."}
{"_id":"fc86bc81-d186-404c-9031-82c61524d53c","text":"Treatment involves restoring normal levels of thyroid hormone and may include thyroid drugs, radioactive iodine, and sometimes partial or complete surgical removal of the thyroid."}
{"_id":"a5b12c95-aaf8-43ba-b8f7-d43b5e09f5d0","text":"With treatment, muscle weakness may improve or be reversed."}
{"_id":"84ee5f89-5e5f-448b-b33f-c47b942c5bfc","text":"The NINDS supports a broad range of research on neuromuscular disorders such as thyrotoxic myopathy. Much of this research is aimed at learning more about these disorders and finding ways to prevent and treat them."}
{"_id":"0b559a1e-15f9-414e-9dfd-55a08973cb76","text":"Neuroacanthocytosis refers to a group of genetic conditions that are characterized by movement disorders and acanthocytosis (abnormal, spiculated red blood cells). Four syndromes are classified as neuroacanthocytosis: Chorea-acanthocytosis, McLeod syndrome, Huntington's disease-like 2 (HDL2), and panthothenate kinase-associated neurodegeneration (PKAN). Acanthocytosis may not always be observed in HDL2 and PKAN. These disorders are caused by different genetic mutations, and the signs and symptoms vary, but usually include chorea (involuntary, dance-like movements), parkinsonism (slowness of movement), dystonia (abnormal body postures), and problems walking. There may also be muscle weakness, involuntary movements of the face and tongue, tongue\/lip biting (which is mostly characteristic of Chorea-acanthocytosis), as well as difficulty with speech and eating, cognitive impairment, psychiatric symptoms, and seizures. Individuals with McLeod syndrome often have cardiac problems. Many features of these disorders are due to degeneration of the basal ganglia, a part of the brain that controls movement. Additional disorders that are also known have neurologic symptoms, acanthocytosis, and either lipoprotein disorders or systemic findings. The diagnosis of neuroacanthocytosis is typically based on the symptoms and clinical observation, a review of family history, and the evaluation of specific laboratory and imaging studies."}
{"_id":"f0a053ae-3dd0-43a3-aa6f-d96d2ad001a5","text":"There are currently no treatments to prevent or slow the progression of neuroacanthocytosis and treatment is symptomatic and supportive. Medications that block dopamine, such as some of the antipsychotics, may decrease the involuntary movements. Botulinum toxin injections usually improve symptoms of dystonia. A feeding tube may be needed for individuals with feeding difficulties to maintain proper nutrition. Seizures may be treated with a variety of anticonvulsants, and antidepressants may also be appropriate for some individuals. Speech, occupational, and physical therapy may also be beneficial."}
{"_id":"fafbdd09-15fc-43f6-8436-77b1c7f019e3","text":"Neuroacanthocytosis is a progressive disease, and in some cases may be complicated by poor nutritional status, cardiac abnormalities, and pneumonia."}
{"_id":"1cda2bde-8b49-4999-8ff5-bdca9985d230","text":"The NINDS supports research on disorders such as neuroacanthocytosis, aimed at increasing scientific understanding of the disorders and finding ways to prevent and treat them. The genetic mutations responsible for some types of neuroacanthocytosis have recently been identified. Researchers are examining the role of the basal ganglia in neuroacanthocytosis and hope to correlate the specific genetic abnormalities with the clinical features of the disease. Other research is aimed at identifying possible causes of sudden death related to heart muscle abnormalities, which are observed in some individuals with neuroacanthocytosis."}
{"_id":"4d547f0f-ea60-4d84-ad97-33e8e8628d44","text":"Sotos syndrome (cerebral gigantism) is a rare genetic disorder caused by mutation in the NSD1 gene on chromosome 5. It is characterized by excessive physical growth during the first few years of life. Children with Sotos syndrome tend to be large at birth and are often taller, heavier, and have larger heads (macrocrania) than is normal for their age. Symptoms of the disorder, which vary among individuals, include a disproportionately large and long head with a slightly protrusive forehead and pointed chin, large hands and feet, hypertelorism (an abnormally increased distance between the eyes), and down-slanting eyes. The disorder is often accompanied by mild cognitive impairment; delayed motor, cognitive, and social development; hypotonia (low muscle tone), and speech impairments. Clumsiness, an awkward gait, and unusual aggressiveness or irritability may also occur. Although most cases of Sotos syndrome occur sporadically (meaning they are not known to be inherited), familial cases have also been reported."}
{"_id":"c8ee87f3-d3f6-4f1f-be4e-bea94b490f7b","text":"There is no standard course of treatment for Sotos syndrome. Treatment is symptomatic."}
{"_id":"5748bde3-b88e-45fd-af74-d7da86170275","text":"Sotos syndrome is not a life-threatening disorder and patients may have a normal life expectancy. The initial abnormalities of Sotos syndrome usually resolve as the growth rate becomes normal after the first few years of life. Developmental delays may improve in the school-age years, and adults with Sotos syndrome are likely to be within the normal range for intellect and height. However, coordination problems may persist into adulthood."}
{"_id":"92d5a22c-73bb-4bd1-a542-a1891984e336","text":"The NINDS supports and conducts a wide range of studies which focus on identifying and learning more about the genes involved in normal brain development. The knowledge gained from these fundamental studies provides the foundation for understanding how this process can go awry and, thus, may eventually give clues to understanding disorders such as Sotos syndrome."}
{"_id":"f48c3039-fefa-4981-97cb-6accd594bf7a","text":"Cerebro-oculo-facio-skeletal syndrome (COFS) is a pediatric, genetic, degenerative disorder that involves the brain and the spinal cord. It is characterized by craniofacial and skeletal abnormalities, severely reduced muscle tone, and impairment of reflexes. Symptoms may include large, low-set ears, small eyes, microcephaly (abnormal smallness of the head), micrognathia (abnormal smallness of the jaws), clenched fists, wide-set nipples, vision impairments, involuntary eye movements, and impaired cognitive development, which can be moderate or severe. Respiratory infections are frequent. COFS is diagnosed at birth. Ultrasound technology can detect fetuses with COFS at an early stage of pregnancy, as the fetus moves very little, and some of the abnormalities result, in part, from lack of movement.\n                \nA small number of individuals with COFS have a mutation in the \"ERCC6\" gene and are more appropriately diagnosed as having Cockayne Syndrome Type II. Other individuals with COFS may have defects in the xeroderma pigmentosum genes \"XPG\" or \"XPD.\" Still others who are diagnosed with COFS have no identifiable genetic defect and are presumably affected because of mutations in a distinct, as-yet-unknown gene.\n                \nNOTE: This disorder is not the same as Cohen's syndrome (cerebral obesity ocular skeletal syndrome)."}
{"_id":"7bc2b37a-cf5c-4c5d-8732-bf560f5d1944","text":"Treatment is supportive and symptomatic. Individuals with the disorder often require tube feeding. Because COFS is genetic, genetic counseling is available."}
{"_id":"c4150549-f5d2-43f3-b0b1-0e0344a595da","text":"COFS is a fatal disease. Most children do not live beyond five years."}
{"_id":"c0cbb04e-8d3d-4d88-a815-9f3b9e05e8ed","text":"The NINDS supports research on genetic disorders such as COFS. The goals of this research include finding ways to prevent, treat, and cure these disorders."}
{"_id":"df8850d8-3081-4be5-bc4e-e8ade7f5d8af","text":"Piriformis syndrome is a rare neuromuscular disorder that occurs when the piriformis muscle compresses or irritates the sciatic nerve-the largest nerve in the body. The piriformis muscle is a narrow muscle located in the buttocks. Compression of the sciatic nerve causes pain-frequently described as tingling or numbness-in the buttocks and along the nerve, often down to the leg. The pain may worsen as a result of sitting for a long period of time, climbing stairs, walking, or running."}
{"_id":"0b43125c-bd46-4600-9095-50d4c8c5cc8b","text":"Generally, treatment for the disorder begins with stretching exercises and massage. Anti-inflammatory drugs may be prescribed. Cessation of running, bicycling, or similar activities may be advised. A corticosteroid injection near where the piriformis muscle and the sciatic nerve meet may provide temporary relief. In some cases, surgery is recommended."}
{"_id":"23200ce1-87ba-4640-a39a-669c3157784d","text":"The prognosis for most individuals with piriformis syndrome is good. Once symptoms of the disorder are addressed, individuals can usually resume their normal activities. In some cases, exercise regimens may need to be modified in order to reduce the likelihood of recurrence or worsening."}
{"_id":"5b5dd8cd-6a53-49fa-a896-beb2fc5e880e","text":"Within the NINDS research programs, piriformis syndrome is addressed primarily through studies associated with pain research. NINDS vigorously pursues a research program seeking new treatments for pain and nerve damage with the ultimate goal of reversing debilitating conditions such as piriformis syndrome."}
{"_id":"ad94ede7-eece-440a-b4c9-2b5368551443","text":"Spinal cord infarction is a stroke either within the spinal cord or the arteries that supply it. It is caused by arteriosclerosis or a thickening or closing of the major arteries to the spinal cord. Frequently spinal cord infarction is caused by a specific form of arteriosclerosis called atheromatosis, in which a deposit or accumulation of lipid-containing matter forms within the arteries. Symptoms, which generally appear within minutes or a few hours of the infarction, may include intermittent sharp or burning back pain, aching pain down through the legs, weakness in the legs, paralysis, loss of deep tendon reflexes, loss of pain and temperature sensation, and incontinence."}
{"_id":"56f14cbd-bc21-42b1-8706-bcbaecdb838f","text":"Treatment is symptomatic. Physical and occupational therapy may help individuals recover from weakness or paralysis. A catheter may be necessary for patients with urinary incontinence."}
{"_id":"3e6a2cc3-2de8-4eca-8334-d51f66b4ead8","text":"Recovery depends upon how quickly treatment is received and how severely the body is compromised. Paralysis may persist for many weeks or be permanent. Most individuals have a good chance of recovery."}
{"_id":"a846925f-09f2-47e1-a546-eea14fae2a8f","text":"NINDS conducts and supports research on disorders of the spinal cord such as spinal cord infarction, aimed at learning more about these disorders and finding ways to prevent and treat them."}
{"_id":"caa23abc-1267-41ed-a0c2-2f9f3117cd9e","text":"Repetitive motion disorders (RMDs) are a family of muscular conditions that result from repeated motions performed in the course of normal work or daily activities. RMDs include carpal tunnel syndrome, bursitis, tendonitis, epicondylitis, ganglion cyst, tenosynovitis, and trigger finger. RMDs are caused by too many uninterrupted repetitions of an activity or motion, unnatural or awkward motions such as twisting the arm or wrist, overexertion, incorrect posture, or muscle fatigue. RMDs occur most commonly in the hands, wrists, elbows, and shoulders, but can also happen in the neck, back, hips, knees, feet, legs, and ankles. The disorders are characterized by pain, tingling, numbness, visible swelling or redness of the affected area, and the loss of flexibility and strength. For some individuals, there may be no visible sign of injury, although they may find it hard to perform easy tasks Over time, RMDs can cause temporary or permanent damage to the soft tissues in the body -- such as the muscles, nerves, tendons, and ligaments - and compression of nerves or tissue. Generally, RMDs affect individuals who perform repetitive tasks such as assembly line work, meatpacking, sewing, playing musical instruments, and computer work. The disorders may also affect individuals who engage in activities such as carpentry, gardening, and tennis."}
{"_id":"ef2b6396-ee37-4138-8229-07fc64ede9b3","text":"Treatment for RMDs usually includes reducing or stopping the motions that cause symptoms. Options include taking breaks to give the affected area time to rest, and adopting stretching and relaxation exercises. Applying ice to the affected area and using medications such as pain relievers, cortisone, and anti-inflammatory drugs can reduce pain and swelling. Splints may be able to relieve pressure on the muscles and nerves. Physical therapy may relieve the soreness and pain in the muscles and joints. In rare cases, surgery may be required to relieve symptoms and prevent permanent damage. Some employers have developed ergonomic programs to help workers adjust their pace of work and arrange office equipment to minimize problems."}
{"_id":"373582ab-6034-4afa-a7e4-785c8e3d1d76","text":"Most individuals with RMDs recover completely and can avoid re-injury by changing the way they perform repetitive movements, the frequency with which they perform them, and the amount of time they rest between movements. Without treatment, RMDs may result in permanent injury and complete loss of function in the affected area."}
{"_id":"7d8ba638-1612-4a12-b181-2f0c35ba141f","text":"Much of the on-going research on RMDs is aimed at prevention and rehabilitation. The National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) funds research on RMDs."}
{"_id":"5dc5e147-e310-4da1-b7e6-bc390722e214","text":"Klippel-Feil Syndrome is a rare disorder characterized by the congenital fusion of two or more cervical (neck) vertebrae. It is caused by a failure in the normal segmentation or division of the cervical vertebrae during the early weeks of fetal development. The most common signs of the disorder are short neck, low hairline at the back of the head, and restricted mobility of the upper spine. The fused vertebrae can cause nerve damage and pain in the head, neck, or back. Associated abnormalities may include scoliosis (curvature of the spine), spina bifida (a birth defect of the spine), cleft palate, respiratory problems, and heart malformations. Other features may include joint pain; anomalies of the head and face, skeleton, sex organs, muscles, brain and spinal cord, arms, legs, and fingers; and difficulties hearing. Most cases are sporadic (happen on their own) but mutations in the GDF6 (growth differentiation factor 6) or GDF3 (growth differentiation factor 3) genes can cause the disorder. These genes make proteins that are involved in bone development and segmentation of the vertebrae."}
{"_id":"78156fcc-c066-4353-854d-8c41f53ac972","text":"Treatment for Klippel-Feil Syndrome is symptomatic and may include surgery to relieve cervical or craniocervical instability and constriction of the spinal cord, and to correct scoliosis. Physical therapy may also be useful."}
{"_id":"f9a9ed1e-d795-49a6-9fa1-b3737b4f98a7","text":"The prognosis for most individuals with Klippel-Feil Syndrome is good if the disorder is treated early and appropriately. Activities that can injure the neck should be avoided."}
{"_id":"4f53a73f-37ad-4a3c-8ca0-c55eb1587b5d","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge abuot the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. Research supported by the NINDS includes studies to understand how the brain and nervous system normally develop and function and how they are affected by disease and trauma. These studies contribute to a greater understanding of birth defects such as Klippel-Feil Syndrome and open promising new avenues for treatment."}
{"_id":"3faca60c-0259-4735-bd71-faf32cc0a140","text":"Carpal tunnel syndrome (CTS) occurs when the median nerve, which runs from the forearm into the palm of the hand, becomes pressed or squeezed at the wrist. The carpal tunnel is a narrow, rigid passageway of ligament and bones at the base of the hand that houses the median nerve and the tendons that bend the fingers. The median nerve provides feeling to the palm side of the thumb and to most of the fingers. Symptoms usually start gradually, with numbness, tingling, weakness, and sometimes pain in the hand and wrist. People might have difficulty with tasks such as driving or reading a book. Decreased hand strength may make it difficult to grasp small objects or perform other manual tasks. In some cases no direct cause of the syndrome can be identified. Contributing factors include trauma or injury to the wrist that causes swelling, thyroid disease, rheumatoid arthritis, and fluid retention during pregnancy. Women are three times more likely than men to develop carpal tunnel syndrome. The disorder usually occurs only in adults."}
{"_id":"cae333db-7ba9-48a0-a1a7-94224fd5071f","text":"Initial treatment generally involves immobilizing the wrist in a splint, nonsteroidal anti-inflammatory drugs to temporarily reduce swelling, and injections of corticosteroid drugs (such as prednisone). For more severe cases, surgery may be recommended."}
{"_id":"93640f00-a33a-47c0-9428-e7f9b78f6a5d","text":"In general, carpal tunnel syndrome responds well to treatment, but less than half of individuals report their hand(s) feeling completely normal following surgery. Some residual numbness or weakness is common. At work, people can perform stretching exercises, take frequent rest breaks, wear splints to keep wrists straight, and use correct posture and wrist position to help prevent or worsen symptoms. Wearing fingerless gloves can help keep hands warm and flexible."}
{"_id":"d620f808-a3db-473b-89d3-49992472e362","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to conduct fundamental research on the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. NINDS-funded scientists are studying the factors that lead to long-lasting nerve pain disorders, and how the affected nerves are related to symptoms of numbness, loss of function, and pain. Researchers also are examining biomechanical stresses that contribute to the nerve damage responsible for symptoms of carpal tunnel syndrome in order to better understand, treat, and prevent it."}
{"_id":"d8f9e1bc-564b-4837-a65a-03ae9a2c0131","text":"Opsoclonus myoclonus is a rare neurological disorder characterized by an unsteady, trembling gait, myoclonus (brief, shock-like muscle spasms), and opsoclonus (irregular, rapid eye movements). Other symptoms may include difficulty speaking, poorly articulated speech, or an inability to speak. A decrease in muscle tone, lethargy, irritability, and malaise (a vague feeling of bodily discomfort) may also be present. Opsoclonus myoclonus may occur in association with tumors or viral infections. It is often seen in children with tumors."}
{"_id":"617e6f91-3508-4140-9f7b-4a8b8e60ea55","text":"Treatment for opsoclonus myoclonus may include corticosteroids or ACTH (adrenocorticotropic hormone). In cases where there is a tumor present, treatment such as chemotherapy, surgery, or radiation may be required."}
{"_id":"1f14682b-bb3e-46c9-aedd-859b48356326","text":"The prognosis for opsoclonus myoclonus varies depending on the symptoms and the presence and treatment of tumors. With treatment of the underlying cause of the disorder, there may be an improvement of symptoms. The symptoms sometimes recur without warning. Generally the disorder is not fatal."}
{"_id":"256d93dc-0a0d-4a29-87b7-fb250451ccdd","text":"The NINDS supports and conducts research on movement disorders such as opsoclonus myoclonus. These studies are aimed at increasing knowledge about these disorders and finding ways to prevent, treat, and cure them."}
{"_id":"12e50dd9-7ce2-42b0-adb3-54b769583fa8","text":"Dysautonomia refers to a disorder of autonomic nervous system (ANS) function that generally involves failure of the sympathetic or parasympathetic components of the ANS, but dysautonomia involving excessive or overactive ANS actions also can occur. Dysautonomia can be local, as in reflex sympathetic dystrophy, or generalized, as in pure autonomic failure. It can be acute and reversible, as in Guillain-Barre syndrome, or chronic and progressive. Several common conditions such as diabetes and alcoholism can include dysautonomia. Dysautonomia also can occur as a primary condition or in association with degenerative neurological diseases such as Parkinson's disease. Other diseases with generalized, primary dysautonomia include multiple system atrophy and familial dysautonomia. Hallmarks of generalized dysautonomia due to sympathetic failure are impotence (in men) and a fall in blood pressure during standing (orthostatic hypotension). Excessive sympathetic activity can present as hypertension or a rapid pulse rate."}
{"_id":"f9c8b920-fb8d-4064-afc6-0eb80151f9f4","text":"There is usually no cure for dysautonomia. Secondary forms may improve with treatment of the underlying disease. In many cases treatment of primary dysautonomia is symptomatic and supportive. Measures to combat orthostatic hypotension include elevation of the head of the bed, water bolus (rapid infusion of water given intravenously), a high-salt diet, and drugs such as fludrocortisone and midodrine."}
{"_id":"330ca0a8-ebcf-43dd-b698-e3b3b7a4920f","text":"The outlook for individuals with dysautonomia depends on the particular diagnostic category. People with chronic, progressive, generalized dysautonomia in the setting of central nervous system degeneration have a generally poor long-term prognosis. Death can occur from pneumonia, acute respiratory failure, or sudden cardiopulmonary arrest."}
{"_id":"b8b809ba-0709-42e7-9236-1c4cf108256c","text":"The NINDS supports and conducts research on dysautonomia. This research aims to discover ways to diagnose, treat, and, ultimately, prevent these disorders."}
{"_id":"77d82001-cffa-4a26-ab59-de780dfa13f6","text":"Metachromatic leukodystrophy (MLD) is one of a group of genetic disorders called the leukodystrophies, which are characterized by the toxic buildup of lipids (fatty materials such as oils and waxes) and other storage materials in cells in the white matter of the central nervous system and peripheral nerves. The buildup of storage materials impairs the growth or development of the myelin sheath, the fatty covering that acts as an insulator around nerve fibers. (Myelin, which lends its color to the white matter of the brain, is a complex substance made up of a mixture of fats and proteins.) MLD is one of several lipid storage diseases, which result in the harmful buildup of lipids in brain cells and other cells and tissues in the body. People with lipid storage diseases either do not produce enough of one of the enzymes needed to break down (metabolize) lipids or they produce enzymes that do not work properly. Some leukodystrophies are caused by genetic defects of enzymes that regulate the metabolism of fats needed in myelin synthesis. MLD, which affects males and females, is cause by a deficiency of the enzyme arylsulfatase A. MLD has three characteristic forms: late infantile, juvenile, and adult. Late infantile MLD typically begins between 12 and 20 months following birth. Infants appear normal at first but develop difficulty walking after the first year of life and eventually lose the ability to walk. Other symptoms include muscle wasting and weakness,developmental delays, progressive loss of vision leading to blindness, impaired swallowing, and dementia before age 2. Most children with this form of MLD die by age 5. Symptoms of the juvenile form of MLD (which begins between 3-10 years of age) include impaired school performance, mental deterioration, an inability to control movements, seizures, and dementia. Symptoms continue to get worse, and death eventually occurs 10 to 20 years following disease onset.. The adult form commonly begins after age 16, with symptoms that include psychiatric disturbances, seizures, tremor, impaired concentration, depression, and dementia. Death generally occurs within 6 to 14 years after onset of symptoms."}
{"_id":"ea9555fb-0922-4afa-9d15-0eb18fc3d028","text":"There is no cure for MLD. Bone marrow transplantation may delay progression of the disease in some infantile-onset cases. Other treatment is symptomatic and supportive. Considerable progress has been made with regard to gene therapy in an animal model of MLD and in clinical trials."}
{"_id":"c25b548a-a013-410c-bf64-55aa5ac8434c","text":"The prognosis for MLD is poor. Most children within the infantile form die by age 5. Symptoms of the juvenile form progress with death occurring 10 to 20 years following onset. Those persons affected by the adult form typically die withing 6 to 14 years following onset of symptoms."}
{"_id":"b4413cdb-c17b-448c-ad48-3ac9428b51ba","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS is a part of the National Institutes of Health (NIH), the leading supporter of biomedical research in the world. Research funded by the NINDS focuses on better understanding how neurological defects arise in lipid storage disorders and on the development of new treatments targeting disease mechanisms, including gene therapies, cell-based therapies, and pharmacological approaches. NINDS-funded preclinical research aims to study the effectiveness and safety of virus-based delivery of the normal ARSA gene to promote gene expression throughout the central nervous system and overcome the mutation-caused deficiency. If successful, the project could lead to trials in humans. Other research hopes to study the use of patient-specific induced pluripotent stem cells (cells that are capable of becoming other types of cells) in correcting the gene deficiency in metachromatic leukodystrophy."}
{"_id":"e43f6b02-c9d2-46ca-b2d7-75fa84966cc5","text":"Atrial fibrillation (AF) describes the rapid, irregular beating of the left atrium (upper chamber) of the heart. These rapid contractions of the heart are weaker than normal contractions, resulting in slow flow of blood in the atrium. The blood pools and becomes sluggish and can result in the formation of blood clots. If a clot leaves the heart and travels to the brain, it can cause a stroke by blocking the flow of blood through cerebral arteries. Some people with AF have no symptoms, but others may experience a fluttering feeling in the area of the chest above the heart, chest pain, lightheadness or fainting, shortness of breath, and fatigue. AF is diagnosed by an electrocardiogram (ECG), a device that records the hearts electrical activity. Other tests are often performed to rule out contributing causes, such as high blood pressure, an overactive thyroid gland, heart failure, faulty heart valves, lung disease, and stimulant or alcohol abuse. Some people will have no identifiable cause for their AF."}
{"_id":"56ba3b41-32f7-4703-bd7e-76caeb39b3eb","text":"Within a few hours after onset of a stroke, treatment with drugs or devices that dissolve or break up the clot can restore blood flow to the brain and lead to a better recovery. To prevent strokes related to AF, doctors often prescribe medications to prevent formation of clots in the heart, which can travel to the brain and cause stroke. Immediately after a stroke, doctors may temporarily administer heparin by injection, while starting an oral medication for long-term protection from clots. The most commonly used drug has been warfarin. People taking warfarin must be closely monitored to make sure their blood is thin enough to prevent clots, but not so thin as to promote bleeding. Since some foods, vitamin supplements, and medications can affect warfarin action, keeping the blood just thin enough can be tricky. More recently, a number of new blood thinners, including dabigatran, rivaroxaban, and apixaban, have been shown to be as effective as warfarin in stroke prevention. These newer medications do not require regular blood test monitoring and may have less tendency to cause bleeding due to making the blood too thin. Some individuals with AF may have a lower risk of stroke and may be treated with aspirin, either alone or with another antiplatelet agency like clopidogrel. Other treatments for AF include medications such as beta blockers or calcium channel blockers to slow the heartbeat, and anti-arrhythmic drugs or electrical cardioversion (which delivers an electrical shock to the heart) to normalize the heartbeat."}
{"_id":"c18e3c69-d6d4-45bc-a05e-83cd3f1e76d2","text":"AF, which affects as many as 2.2 million Americans, increases an individuals risk of stroke by 4 to 6 times on average. The risk increases with age. In people over 80 years old, AF is the direct cause of 1 in 4 strokes. Treating individuals with warfarin or new blood thinners reduces the rate of stroke for those who have AF by approximately one-half to two- thirds. People with AF can have multiple strokes, including silent strokes (strokes that don't show physical symptoms but show up on a brain scan) that, over time, can cause dementia, so prevention is important."}
{"_id":"241b051a-d2ab-418e-bf75-4d035ece883a","text":"The National Institute of Neurological Disorders and Stroke (NINDS) is the leading Federal agency directing and funding research relevant to AF and stroke prevention. The NINDS conducts basic and clinical research in its laboratories and clinics at the National Institutes of Health (NIH), and also supports additional research through grants to major research institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders such as AF that can increase the risk of stroke."}
{"_id":"bd992348-8ac5-4e14-b1ee-62da5e7718f9","text":"The pain of a migraine headache is often described as an intense pulsing or throbbing pain in one area of the head. However, it is much more; the International Headache Society diagnoses a migraine by its pain and number of attacks (at least 5, lasting 4-72 hours if untreated), and additional symptoms including nausea and\/or vomiting, or sensitivity to both light and sound. Migraine is three times more common in women than in men and affects more than 10 percent of people worldwide. Roughly one-third of affected individuals can predict the onset of a migraine because it is preceded by an \"aura,\" visual disturbances that appear as flashing lights, zig-zag lines or a temporary loss of vision. People with migraine tend to have recurring attacks triggered by a number of different factors, including stress, anxiety, hormonal changes, bright or flashing lights, lack of food or sleep, and dietary substances. Migraine in some women may relate to changes in hormones and hormonal levels during their menstrual cycle. For many years, scientists believed that migraines were linked to the dilation and constriction of blood vessels in the head. Investigators now believe that migraine has a genetic cause."}
{"_id":"aee1527f-8684-4fda-bc2e-da784ee74b9b","text":"There is no absolute cure for migraine since its pathophysiology has yet to be fully understood. There are two ways to approach the treatment of migraine headache with drugs: prevent the attacks, or relieve the symptoms during the attacks. Prevention involves the use of medications and behavioral changes. Drugs originally developed for epilepsy, depression, or high blood pressure to prevent future attacks have been shown to be extremely effective in treating migraine. Botulinum toxin A has been shown to be effective in prevention of chronic migraine. Behaviorally, stress management strategies, such as exercise, relaxation techniques, biofeedback mechanisms, and other therapies designed to limit daily discomfort, may reduce the number and severity of migraine attacks. Making a log of personal triggers of migraine can also provide useful information for trigger-avoiding lifestyle changes, including dietary considerations, eating regularly scheduled meals with adequate hydration, stopping certain medications, and establishing a consistent sleep schedule. Hormone therapy may help some women whose migraines seem to be linked to their menstrual cycle. A weight loss program is recommended for obese individuals with migraine.\n                \nRelief of symptoms, or acute treatments, during attacks consists of sumatriptan, ergotamine drugs, and analgesics such as ibuprofen and aspirin. The sooner these treatments are administered, the more effective they are."}
{"_id":"34b90598-f8a9-4735-95a8-9af16a6cdbc2","text":"Responsive prevention and treatment of migraine is incredibly important. Evidence shows an increased sensitivity after each successive attack, eventually leading to chronic daily migraine in some individuals With proper combination of drugs for prevention and treatment of migraine attacks most individuals can overcome much of the discomfort from this debilitating disorder. Women whose migraine attacks occur in association with their menstrual cycle are likely to have fewer attacks and milder symptoms after menopause."}
{"_id":"70d9edc0-ba14-4e7e-bf78-a63a883f1a21","text":"Researchers believe that migraine is the result of fundamental neurological abnormalities caused by genetic mutations at work in the brain. New models are aiding scientists in studying the basic science involved in the biological cascade, genetic components and mechanisms of migraine. Understanding the causes of migraine as well as the events that effect them will give researchers the opportunity to develop and test drugs that could be more targeted to preventing or interrupting attacks entirely. Therapies currently being tested for their effectiveness in treating migraine include magnesium, coenzyme Q10, vitamin B12, riboflavin, fever-few, and butterbur. \n                \nIn 2010, a team of researchers found a common mutation in the gene TRESK which contains instructions for a certain potassium ion channel. Potassium channels are important for keeping a nerve cell at rest and mutations in them can lead to overactive cells that respond to much lower levels of pain. Large genetic analyses similar to the one used to identify TRESK will most likely lead to the identification of a number of other genes linked to migraine."}
{"_id":"845e2e2b-f00b-4027-aa43-1174346d747d","text":"Aicardi syndrome is a rare genetic disorder that primarily affects newborn girls. The condition is sporadic, meaning it is not known to pass from parent to child. (An exception is a report of two sisters and a pair of identical twins, all of whom were affected.) The mutation that causes Aicardi syndrome has not been identified, but it is thought to be caused by a dominant mutation that appears for the first time in a family in an x-linked gene that may be lethal in certain males.. Aicardi syndrome can be seen in boys born with an extra \"X\" chromosome. (Females have two X chromosomes, while males normally have an X and a Y chromosome.) The precise gene or genetic mechanism causing Aicardi syndrome is not yet known.\n                \nOriginally, Aicardi syndrome was characterized by three main features: 1) partial or complete absence of the structure (corpus callosum) that links the two halves of the brain (2) infantile spasms (a type of seizure disorder), and 3) chorioretinal lacunae, lesions on the retina that look like yellowish spots. However, Aicardi syndrome is now known to have a much broader spectrum of abnormalities than was initially described. Not all girls with the condition have the three features described above and many girls have additional feature such as lower tone around the head and trunk, microcephaly (small head circumference), and spasticity in the limbs.\n                \nTypical findings in the brain of girls with Aicardi syndrome include heterotopias, which are groups of brain cells that, during development, migrated to the wrong area of brain; polymicrogyria or pachygyria, which are numerous small, or too few, brain folds; and cysts, (fluid filled cavities) in the brain. Girls with Aicardi syndrome have varying degrees of intellectual disability and developmental delay. Many girls also have developmental abnormalities of their optic nerves and some have microphthalmia (small eyes). Skeletal problems such as absent or abnormal ribs and abnormalities of vertebrae in the spinal column (including hemivertebrae and butterfly vertebrae) have also been reported. Some girls also have skin problems, facial asymmetry, small hands, and an increased incidence of tumors.\n                \n(Aicardi syndrome is distinct from Aicardi-Goutieres syndrome, which is an inherited encephalopathy that affects newborn infants.)"}
{"_id":"a526f1c7-bbea-46dd-9775-35257b028c3e","text":"There is no cure for Aicardi syndrome nor is there a standard course of treatment. Treatment generally involves medical management of seizures and programs to help parents and children cope with developmental delays. Long-term management by a pediatric neurologist with expertise in the management of infantile spasms is recommended."}
{"_id":"298e9dbf-e556-4524-b7d6-be76496dd784","text":"The prognosis for girls with Aicardi syndrome varies according to the severity of their symptoms. There is an increased risk for death in childhood and adolescence, but survivors into adulthood have been described."}
{"_id":"14989849-46ee-4b3a-b009-ce2854543e3b","text":"The NINDS supports and conducts research on neurogenetic disorders such as Aicardi syndrome. The goals of this research are to locate and understand the genes involved and to develop techniques to diagnose, treat, prevent, and ultimately cure disorders such as Aicardi syndrome."}
{"_id":"b5e156ed-15ed-4d37-bf2e-3c47ce5fcbdc","text":"Adult Refsum disease (ARD) is a rare genetic disease that causes weakness or numbness of the hands and feet (peripheral neuropathy). Due to a genetic abnormality, people with ARD disease lack the enzyme in peroxisomes that break down phytanic acid, a type of fat found in certain foods. As a result, toxic levels of phytanic acid build up in the brain, blood, and other tissues. The disease usually begins in late childhood or early adulthood with increasing night blindness due to degeneration of the retina (retinitis pigmentosa). If the disease progresses, other symptoms may include deafness, loss of the sense of smell (anosmia), problems with balance and coordination (ataxia), dry and scaly skin (ichthyosis), and heartbeat abnormalities (cardiac arrhythmias). Some individuals will have shortened bones in their fingers or toes, or a visibly shortened fourth toe. Although the disease usually appears in early childhood, some people will not develop symptoms until their 40s or 50s."}
{"_id":"c79dc7ba-fc91-4321-a8a2-cf895948f36d","text":"The primary treatment for ARD is to restrict or avoid foods that contain phytanic acid, including dairy products; beef and lamb; and fatty fish such as tuna, cod, and haddock. Some individuals may also require plasma exchange (plasmapheresis) in which blood is drawn, filtered, and reinfused back into the body, to control the buildup of phytanic acid."}
{"_id":"fc161435-6e8d-4bf2-9768-b1bc4f44c064","text":"ARD is treatable because phytanic acid is not produced by the body, but is only found in foods. With treatment, muscle weakness, numbness, and dry and scaly skin generally disappear. However, vision and hearing problems may persist and the sense of smell may not return. Untreated, ARD can lead to sudden death caused by heartbeat abnormalities."}
{"_id":"c27349cf-d0d6-42d4-87ee-2f14a498bcdd","text":"The National Institute of Neurological Disorders and Stroke (NINDS) supports research related to Adult Refsum Disease through grants to major research institutions across the country. Research is focused on finding better ways to prevent, treat, and ultimately cure ARD and other peroxisomal disorders."}
{"_id":"e3741fe1-8378-4009-9d5f-95c88fb00b4a","text":"Frontotemporal dementia (FTD) describes a clinical syndrome associated with shrinking of the frontal and temporal anterior lobes of the brain. Originally known as Picks disease, the name and classification of FTD has been a topic of discussion for over a century. The current designation of the syndrome groups together Picks disease, primary progressive aphasia, and semantic dementia as FTD. Some doctors propose adding corticobasal degeneration and progressive supranuclear palsy to FTD and calling the group Pick Complex. These designations will continue to be debated. As it is defined today, the symptoms of FTD fall into two clinical patterns that involve either (1) changes in behavior, or (2) problems with language. The first type features behavior that can be either impulsive (disinhibited) or bored and listless (apathetic) and includes inappropriate social behavior; lack of social tact; lack of empathy; distractability; loss of insight into the behaviors of oneself and others; an increased interest in sex; changes in food preferences; agitation or, conversely, blunted emotions; neglect of personal hygiene; repetitive or compulsive behavior, and decreased energy and motivation. The second type primarily features symptoms of language disturbance, including difficulty making or understanding speech, often in conjunction with the behavioral types symptoms. Spatial skills and memory remain intact. There is a strong genetic component to the disease; FTD often runs in families."}
{"_id":"fededdfc-5b40-4dd8-9104-e221feca9dff","text":"No treatment has been shown to slow the progression of FTD. Behavior modification may help control unacceptable or dangerous behaviors. Aggressive, agitated, or dangerous behaviors could require medication. Anti-depressants have been shown to improve some symptoms."}
{"_id":"1a8da875-6f13-4f1a-b6ac-cfd564ebf79d","text":"The outcome for people with FTD is poor. The disease progresses steadily and often rapidly, ranging from less than 2 years in some individuals to more than 10 years in others. Eventually some individuals with FTD will need 24-hour care and monitoring at home or in an institutionalized care setting."}
{"_id":"614bfab7-ea75-48d8-9732-8a80dd9725ab","text":"The National Institute of Neurological Disorders and Stroke (NINDS), and other institutes of the National Institutes of Health (NIH), conduct research related to FTD in laboratories at the NIH, and also support additional research through grants to major medical institutions across the country."}
{"_id":"788f4a88-9d5d-4561-b4cb-e52d3994cf4e","text":"Shaken baby syndrome is a type of inflicted traumatic brain injury that happens when a baby is violently shaken. A baby has weak neck muscles and a large, heavy head. Shaking makes the fragile brain bounce back and forth inside the skull and causes bruising, swelling, and bleeding, which can lead to permanent, severe brain damage or death. The characteristic injuries of shaken baby syndrome are subdural hemorrhages (bleeding in the brain), retinal hemorrhages (bleeding in the retina), damage to the spinal cord and neck, and fractures of the ribs and bones. These injuries may not be immediately noticeable. Symptoms of shaken baby syndrome include extreme irritability, lethargy, poor feeding, breathing problems, convulsions, vomiting, and pale or bluish skin. Shaken baby injuries usually occur in children younger than 2 years old, but may be seen in children up to the age of 5."}
{"_id":"15823f0d-46c8-4e33-94d2-3d385217fac5","text":"Emergency treatment for a baby who has been shaken usually includes life-sustaining measures such as respiratory support and surgery to stop internal bleeding and bleeding in the brain. Doctors may use brain scans, such as MRI and CT, to make a more definite diagnosis."}
{"_id":"d1eba09e-4562-433a-a055-97e167899b28","text":"In comparison with accidental traumatic brain injury in infants, shaken baby injuries have a much worse prognosis. Damage to the retina of the eye can cause blindness. The majority of infants who survive severe shaking will have some form of neurological or mental disability, such as cerebral palsy or cognitive impairment, which may not be fully apparent before 6 years of age. Children with shaken baby syndrome may require lifelong medical care."}
{"_id":"103ff060-e802-4d94-8645-c1d2db7425a1","text":"The National Institute of Neurological Disorders and Stroke (NINDS), and other institutes of the National Institutes of Health (NIH), conduct research related to shaken baby syndrome in laboratories at the NIH and also support additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to treat and heal medical conditions such as shaken baby syndrome."}
{"_id":"f0b526a2-33a0-4fa8-bfec-bd988a48f4f9","text":"Gerstmann-Straussler-Scheinker disease (GSS) is an extremely rare, neurodegenerative brain disorder. It is almost always inherited and is found in only a few families around the world. Onset of the disease usually occurs between the ages of 35 and 55. In the early stages, patients may experience varying levels of ataxia (lack of muscle coordination), including clumsiness, unsteadiness, and difficulty walking. As the disease progresses, the ataxia becomes more pronounced and most patients develop dementia. Other symptoms may include dysarthria (slurring of speech), nystagmus (involuntary movements of the eyes), spasticity (rigid muscle tone), and visual disturbances, sometimes leading to blindness. Deafness also can occur. In some families, parkinsonian features are present. GSS belongs to a family of human and animal diseases known as the transmissible spongiform encephalopathies (TSEs). Other TSEs include Creutzfeldt-Jakob disease, kuru, and fatal familial insomnia."}
{"_id":"8625912e-a7e9-4864-aff0-48449a8f3d96","text":"There is no cure for GSS, nor are there any known treatments to slow progression of the disease. Current therapies are aimed at alleviating symptoms and making the patient as comfortable as possible."}
{"_id":"6d465160-fd39-4644-83c6-27a4f60e62f9","text":"GSS is a slowly progressive condition usually lasting from 2 to 10 years. The disease ultimately causes severe disability and finally death, often after the patient goes into a coma or has a secondary infection such as aspiration pneumonia due to an impaired ability to swallow."}
{"_id":"52d989d8-6755-49bd-acb8-8095eba0cbfd","text":"The NINDS supports and conducts research on TSEs, including GSS. Much of this research is aimed at characterizing the agents that cause these disorders, clarifying the mechanisms underlying them, and, ultimately, finding ways to prevent, treat, and cure them."}
{"_id":"cb9a1643-8c60-4e89-9aaa-c12a38af965c","text":"Syringomyelia (sear-IN-go-my-EEL-ya) is a disorder in which a fluid-filled cyst forms within the spinal cord. This cyst, called a syrinx, expands and elongates over time, destroying the center of the spinal cord. Since the spinal cord connects the brain to nerves in the extremities, this damage results in pain, weakness, and stiffness in the back, shoulders, arms, or legs. Symptoms vary among individuals. Other symptoms may include headaches and a loss of the ability to feel extremes of hot or cold, especially in the hands.Signs of the disorder tend to develop slowly, although sudden onset may occur with coughing or straining. If not treated surgically, syringomyelia often leads to progressive weakness in the arms and legs, loss of hand sensation, and chronic, severe pain. In most cases, the disorder is related to a congenital abnormality of the brain called a Chiari I malformation. This malformation causes the lower part of the cerebellum to protrude from its normal location in the back of the head, through the hole connecting the skull and spine, and into the cervical or neck portion of the spinal canal. Syringomyelia may also occur as a complication of trauma, meningitis, hemorrhage, a tumor, or other condition. Symptoms may appear months or even years after the initial injury, starting with pain, weakness, and sensory impairment originating at the site of trauma. Some cases of syringomyelia are familial, although this is rare."}
{"_id":"9721e794-f9af-4224-b38d-9b0ffa37cb37","text":"Surgery is usually recommended for individuals with syringomyelia, with the type of surgery and its location dependent on the type of syrinx. In persons with syringomyelia that is associated with the Chiara I malformation, a procedure that removes skulll bone and expands the space around the malformation usually prevents new symptoms from developing and results in the syrinx becoming smaller. In some individuals it may be necessary to drain the syrinx, which can be accomplished using a catheter, drainage tubes, and valves. Recurrence of syringomyelia after surgery may make additional operations necessary; these may not be completely successful over the long term.\n                \nIn the absence of symptoms, syringomyelia is usually not treated. In addition, a physician may recommend not treating the condition in individuals of advanced age or in cases where there is no progression of symptoms. Whether treated or not, many individuals are told to avoid activities that involve straining."}
{"_id":"2dcfd5d6-4e4a-4eac-8c18-82751819dfe6","text":"Symptoms usually begin in young adulthood, with symptoms of one form usually beginning between the ages of 25 and 40. If not treated surgically (when needed), syringomyelia often leads to progressive weakness in the arms and legs, loss of hand sensation, and chronic, severe pain. Symptoms may worsen with straining or any activity that causes cerebrospinal fluid pressure to fluctuate. Some individuals may have long periods of stability. Surgery results in stabilization or modest improvement in symptoms for most individuals. Delay in treatment may result in irreversible spinal cord injury."}
{"_id":"6b7d4959-ab1f-4bb7-8a4e-ace26a02da17","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. NINDS investigators are studying how syrinxes first form, as well as the mechanisms of the disorders. NINDS investigators have found that the normal flow of cerebrospinal fluid that occurs with each heartbeat is obstructed in people with syringomyelia. Surgical procedures that relieve this obstruction usually result in the syrinx becoming much smaller in size. Studies are also underway to identify and better understand genetic factors that influence the development of Chiari I malformations and syringomyelia. Researchers hope to better understand the role of birth defects of the skull and brain in the development of hindbrain malformations that can lead to syringomyelia. Diagnostic technology is another area for continued research. \n                \nNINDS scientists are examining individuals who either have syringomyelia or are at risk of developing the disorder. They are investigating the factors that influence its development, progression, and treatment by recording more than 5 years of symptoms, muscle strength, overall function, and magnetic resonance imaging (MRI) scan findings from individuals who receive standard treatment for syringomyelia. Study results may allow scientists to provide more accurate recommendations to future individuals with syringomyelia regarding optimal surgical or non-surgical treatments."}
{"_id":"f1736d72-d415-4a4e-b9ca-062f5eab4456","text":"Dandy-Walker Syndrome is a congenital brain malformation involving the cerebellum (an area of the back of the brain that coordinates movement) and the fluid-filled spaces around it. The key features of this syndrome are an enlargement of the fourth ventricle (a small channel that allows fluid to flow freely between the upper and lower areas of the brain and spinal cord), a partial or complete absence of the area of the brain between the two cerebellar hemispheres (cerebellar vermis), and cyst formation near the lowest part of the skull. An increase in the size and pressure of the fluid spaces surrounding the brain (hydrocephalus) may also be present. The syndrome can appear dramatically or develop unnoticed. Symptoms, which often occur in early infancy, include slow motor development and progressive enlargement of the skull. In older children, symptoms of increased intracranial pressure (pressure within the skull) such as irritability and vomiting, and signs of cerebellar dysfunction such as unsteadiness, lack of muscle coordination, or jerky movements of the eyes may occur. Other symptoms include increased head circumference, bulging at the back of the skull, abnormal breathing problems, and problems with the nerves that control the eyes, face and neck. Dandy-Walker Syndrome is sometimes associated with disorders of other areas of the central nervous system, including absence of the area made up of nerve fibers connecting the two cerebral hemispheres (corpus callosum) and malformations of the heart, face, limbs, fingers and toes."}
{"_id":"668647c5-493c-4910-b200-d2b89cbe4ca7","text":"Treatment for individuals with Dandy-Walker Syndrome generally consists of treating the associated problems, if needed. A surgical procedure called a shunt may be required to drain off excess fluid within the brain, which will reduce pressure inside the skull and improve symptoms. Treatment may also include various forms of therapy (physicial, occupational) and specialized education."}
{"_id":"8f399838-9715-4143-a233-98fa0a339a11","text":"The effect of Dandy-Walker Syndrome on intellectual development is variable, with some children having normal cognition and others never achieving normal intellectual development even when the excess fluid buildup is treated early and correctly. Longevity depends on the severity of the syndrome and associated malformations. The presence of multiple congenital defects may shorten life span."}
{"_id":"588b2c3a-5c17-4b89-b934-04e2a991f152","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. The NINDS conducts and supports a wide range of studies that explore the complex mechanisms of normal brain development. Researchers are studying DNA samples from individuals with Dandy-Walker syndrome to identify genes involved with the syndrome, as well as to better understand its causes and improve diagnosis and treatment options. Other research indicates that mothers with diabetes and those with rubella (German measles) during pregnancy are more likely to have a child with Dandy-Walker syndrome."}
{"_id":"4434f83a-e28b-4965-880c-6c6dd593b47d","text":"Spina bifida (SB) is a neural tube defect (a disorder involving incomplete development of the brain, spinal cord, and\/or their protective coverings) caused by the failure of the fetus's spine to close properly during the first month of pregnancy. Infants born with SB sometimes have an open lesion on their spine where significant damage to the nerves and spinal cord has occurred. Although the spinal opening can be surgically repaired shortly after birth, the nerve damage is permanent, resulting in varying degrees of paralysis of the lower limbs. Even when there is no lesion present there may be improperly formed or missing vertebrae and accompanying nerve damage. In addition to physical and mobility difficulties, most individuals have some form of learning disability. The types of SB are: myelomeningocele, the severest form, in which the spinal cord and its protective covering (the meninges) protrude from an opening in the spine; meningocele in which the spinal cord develops normally but the meninges and spinal fluid) protrude from a spinal opening; closed neural tube defects, which consist of a group of defects in which development of the spinal cord is affected by malformations of the fat, bone, or meninges; and and occulta, the mildest form, in which one or more vertebrae are malformed and covered by a layer of skin. SB may also cause bowel and bladder complications, and many children with SB have hydrocephalus (excessive accumulation of cerebrospinal fluid in the brain)."}
{"_id":"4a6c33e3-72db-41c9-8470-ee056cb30f0e","text":"There is no cure for SB because the nerve tissue cannot be replaced or repaired. Treatment for the variety of effects of SB may include surgery, medication, and physiotherapy. Many individuals with SB will need assistive devices such as braces, crutches, or wheelchairs. Ongoing therapy, medical care, and\/or surgical treatments may be necessary to prevent and manage complications throughout the individual's life. Surgery to close the newborn's spinal opening is generally performed within 24 hours after birth to minimize the risk of infection and to preserve existing function in the spinal cord."}
{"_id":"e6704ac8-a4ce-41d1-8900-bc788f2b0cfd","text":"The prognosis for individuals with SB depends on the number and severity of abnormalities. Prognosis is poorest for those with complete paralysis, hydrocephalus, and other congenital defects. With proper care, most children with SB live well into adulthood."}
{"_id":"3ace30bb-4dbb-416c-bb4c-252a61033702","text":"The NINDS supports a broad range of research on neural tube defects such as SB aimed at finding ways to treat, prevent, and, ultimately, cure these disorders. Recent studies have shown that the addition of folic acid to the diet of women of child-bearing age may significantly reduce the incidence of neural tube defects. Therefore it is recommended that all women of child-bearing age consume 400 micrograms of folic acid daily."}
{"_id":"71a3069d-84cc-4c4e-a532-a23d7e4d3df3","text":"Acute or short-term low back pain generally lasts from a few days to a few weeks. Most acute back pain is the result of trauma to the lower back or a disorder such as arthritis. Pain from trauma may be caused by a sports injury, work around the house or in the garden, or a sudden jolt such as a car accident or other stress on spinal bones and tissues. Symptoms may range from muscle ache to shooting or stabbing pain, limited flexibility and range of motion, or an inability to stand straight. Chronic back pain is pain that persists for more than 3 months. It is often progressive and the cause can be difficult to determine."}
{"_id":"b7e7cf11-8ef2-41bb-b2a9-8f9ef05c6092","text":"Most low back pain can be treated without surgery. Treatment involves using over-the-counter pain relievers to reduce discomfort and anti-inflammatory drugs to reduce inflammation. The goal of treatment is to restore proper function and strength to the back, and prevent recurrence of the injury. Medications are often used to treat acute and chronic low back pain. Effective pain relief may involve a combination of prescription drugs and over-the-counter remedies. Although the use of cold and hot compresses has never been scientifically proven to quickly resolve low back injury, compresses may help reduce pain and inflammation and allow greater mobility for some individuals. Bed rest is recommended for only 12 days at most. Individuals should resume activities as soon as possible. Exercise may be the most effective way to speed recovery from low back pain and help strengthen back and abdominal muscles. In the most serious cases, when the condition does not respond to other therapies, surgery may relieve pain caused by back problems or serious musculoskeletal injuries."}
{"_id":"f69068ee-c0f9-46d8-8273-50da38723343","text":"Most patients with back pain recover without residual functional loss, but individuals should contact a doctor if there is not a noticeable reduction in pain and inflammation after 72 hours of self-care. Recurring back pain resulting from improper body mechanics or other nontraumatic causes is often preventable. Engaging in exercises that don't jolt or strain the back, maintaining correct posture, and lifting objects properly can help prevent injuries. Many work-related injuries are caused or aggravated by stressors such as heavy lifting, vibration, repetitive motion, and awkward posture. Applying ergonomic principles  designing furniture and tools to protect the body from injury  at home and in the workplace can greatly reduce the risk of back injury and help maintain a healthy back."}
{"_id":"132eff55-ac24-454a-ae1f-85700d0a34b5","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct pain research in laboratories at the NIH and also support pain research through grants to major medical institutions across the country. Currently, researchers are examining the use of different drugs to effectively treat back pain, in particular, chronic pain that has lasted at least 6 months. Other studies are comparing different health care approaches to the management of acute low back pain (standard care versus chiropractic, acupuncture, or massage therapy). These studies are measuring symptom relief, restoration of function, and patient satisfaction. Other research is comparing standard surgical treatments to the most commonly used standard nonsurgical treatments to measure changes in health-related quality of life among patients suffering from spinal stenosis."}
{"_id":"e2352609-7f72-4d41-b3b0-5ced37995d99","text":"Neuroleptic malignant syndrome is a life-threatening, neurological disorder most often caused by an adverse reaction to neuroleptic or antipsychotic drugs. Symptoms include high fever, sweating, unstable blood pressure, stupor, muscular rigidity, and autonomic dysfunction. In most cases, the disorder develops within the first 2 weeks of treatment with the drug; however, the disorder may develop any time during the therapy period. The syndrome can also occur in people taking anti-Parkinsonism drugs known as dopaminergics if those drugs are discontinued abruptly."}
{"_id":"53ffeb4e-d820-4a55-bf3d-6a223334dfcc","text":"Generally, intensive care is needed. The neuroleptic or antipsychotic drug is discontinued, and the fever is treated aggressively. A muscle relaxant may be prescribed. Dopaminergic drugs, such as a dopamine agonist, have been reported to be useful."}
{"_id":"b7c678f8-d466-4c2d-8448-f6bacc5ef7fb","text":"Early identification of and treatment for individuals with neuroleptic malignant syndrome improves outcome. If clinically indicated, a low potency neuroleptic can be reintroduced very slowly when the individual recovers, although there is a risk that the syndrome might recur. Another alternative is to substitute another class of drugs for the neuroleptic. Anesthesia may be a risk to individuals who have experienced neuroleptic malignant syndrome."}
{"_id":"25212d35-0d9b-4b41-bd57-d1974351e3d5","text":"The NINDS supports research on neurological disorders such as neuroleptic malignant syndrome. Much of this research focuses on finding ways to prevent and treat the disorder."}
{"_id":"7f08515c-2ec7-476f-9c2e-83cbae55f164","text":"Antiphospholipid syndrome (APS) is an autoimmune disorder caused when antibodies -- immune system cells that fight off bacteria and viruses -- mistakenly attack healthy body tissues and organs. In APS, specific antibodies activate the inner lining of blood vessels, which leads to the formation of blood clots in arteries or veins. APS is sometimes called sticky blood syndrome, because of the increased tendency to form blood clots in the veins and arteries. The symptoms of APS are due to the abnormal blood clotting. Clots can develop in the veins of the legs and lungs, or in the placenta of pregnant women. One of the most serious complications of APS occurs when a clot forms in the brain and causes a stroke. Other neurological symptoms include chronic headaches, dementia (similar to the dementia of Alzheimers disease), and seizures. Infrequently, individuals will develop chorea (a movement disorder in which the body and limbs writhe uncontrollably), cognitive dysfunction (such as poor memory), transverse myelitis, depression or psychosis, optic neuropathy, or sudden hearing loss. In pregnant women, clots in the placenta can cause miscarriages. APS is diagnosed by the presence of a positive antiphospholipid antibody and either a history of blood clots in an artery or vein or a history of multiple miscarriages or other pregnancy problems. Some individuals will have a characteristic lacy, net-like red rash called livedo reticularis over their wrists and knees."}
{"_id":"b806cbac-352d-480d-81e4-e863d5cb5a1c","text":"The main goal of treatment is to thin the blood to reduce clotting. At present, the recommended treatment is low-dose aspirin. For individuals who have already had a stroke or experience recurrent clots, doctors recommend treatment with the anticoagulant warfarin. Pregnant women are treated with either aspirin or another anticoagulant -- heparin -- since warfarin can cause birth defects."}
{"_id":"ca105510-56ed-46b4-9200-5be43090e0d6","text":"APS improves significantly with anticoagulation therapy, which reduces the risk of further clots in veins and arteries. Treatment should be lifelong, since there is a high risk of further clots in individuals who stop warfarin treatment. Doctors often recommend that individuals stop smoking, exercise regularly, and eat a healthy diet to prevent high blood pressure and diabetes, which are diseases that increase the risk for stroke. Treating pregnant women with aspirin or heparin usually prevents miscarriages related to APS."}
{"_id":"50eefdf1-6505-4683-bb03-04c81192d64f","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) support research on APS through grants to major medical institutions across the country.NINDS-funded research is looking at ways to reduce clotting and prevent stroke. Among other NIH-funded research efforts, scientists are examining the role of antiphospholipid antibodies in clotting and pregnancy loss, which is commonly seen in individuals with lupus. Another project hopes to identify potential inherited risk factors for the development of APS."}
{"_id":"969ab92e-6ac3-4089-baaa-e7c4bd8a0b4b","text":"Kearns-Sayre syndrome (KSS) is a rare neuromuscular disorder with onset usually before the age of 20 years. It is the result of abnormalities in the DNA of mitochondria - small rod-like structures found in every cell of the body that produce the energy that drives cellular functions. The mitochondrial diseases correlate with specific DNA mutations that cause problems with many of the organs and tissues in the body. KSS is characterized by progressive limitation of eye movements until there is complete immobility, accompanied by eyelid droop. It is also associated with abnormal accumulation of pigmented material on the membrane lining the eyes. Additional symptoms may include mild skeletal muscle weakness, heart block (a cardiac conduction defect), short stature, hearing loss, an inability to coordinate voluntary movements (ataxia), impaired cognitive function, and diabetes. Seizures are infrequent. Several endocrine disorders can be associated with KSS."}
{"_id":"3528fc42-15bc-45b8-a6c7-67f6df2a1109","text":"There is currently no effective way to treat mitochondria abnormalities in KSS. Treatment is generally symptomatic and supportive. Management of KSS involves multiple specialties depending on the organs involved. The most essential is a regular and long-term follow-up with cardiologists. Conduction problems of heart impulse like heart block may be treated with a pacemaker. Other consultations may include audiology, ophthalmology, endocrinology, neurology, and neuropsychiatry. Hearing aids may be required. There is typically no treatment for limitation in eye movement. Endocrinology abnormalities can be treated with drugs."}
{"_id":"8971b3c2-5bfb-4d50-aef9-f37e65cb3f92","text":"KSS is a slowly progressive disorder. The prognosis for individuals with KSS varies depending on the severity and the number of organs involved. Early diagnosis and periodic electrocardiogram (ECG) are important since heart block can cause death in 20 percent of patients. Early pacemaker implantation can be of great benefit and offer a longer life expectancy in many patients."}
{"_id":"89ef867f-d2f4-49a0-b731-693622e54a62","text":"The NINDS supports research on neuromuscular disorders such as KSS. The goals of this research are to increase understanding of these disorders, and to find ways to prevent, treat, and, ultimately, cure them. The most promising approach for treatment in the future will be to alter replication or destroy abnormal mitochondria."}
{"_id":"f7f4f2ba-46b5-4d8d-8f03-7aa460457b62","text":"Restless legs syndrome (RLS) is a neurological disorder characterized by unpleasant sensations in the legs and an uncontrollable, and sometimes overwhelming, urge to move them for relief. Individuals affected with the disorder often describe the sensations as throbbing, polling, or creeping. The sensations range in severity from uncomfortable to irritating to painful."}
{"_id":"6f81bf50-80e1-48b8-b449-557a634a1510","text":"For those with mild to moderate symptoms, many physicians suggest certain lifestyle changes and activities to reduce or eliminate symptoms. Decreased use of caffeine, alcohol, and tobacco may provide some relief. Physicians may suggest that certain individuals take supplements to correct deficiencies in iron, folate, and magnesium. Taking a hot bath, massaging the legs, or using a heating pad or ice pack can help relieve symptoms in some patients.\n                \nPhysicians also may suggest a variety of medications to treat RLS, including dopaminergics, benzodiazepines (central nervous system depressants), opioids, and anticonvulsants. The drugs ropinirole, pramipexole, gabapentin enacarbil, and rotigotine have been approved by the U.S. Food and Drug Administration for treating moderate to severe RLS. The Relaxis pad, which the person can place at the site of discomfort when in bed and provides 30 minutes of vibrations (counterstimulation) that ramp off after 30 minutes, also has been approved by the FDA."}
{"_id":"161914c2-1caf-4cd7-ad95-56780571117d","text":"RLS is generally a life-long condition for which there is no cure. Symptoms may gradually worsen with age. Nevertheless, current therapies can control the disorder, minimizing symptoms and increasing periods of restful sleep. In addition, some individuals have remissions, periods in which symptoms decrease or disappear for days, weeks, or months, although symptoms usually eventually reappear."}
{"_id":"618e44cc-7aed-4cfe-bc91-73e51d272562","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct and support RLS research in laboratories at the NIH and at major medical institutions across the country. The goal of this research is to increase scientific understanding of RLS, find improved methods of diagnosing and treating the syndrome, and discover ways to prevent it."}
{"_id":"5f3d1d50-054f-45f1-aba4-81a8b7659d1b","text":"Infantile Refsum disease (IRD) is a medical condition within the Zellweger spectrum of perixisome biogenesis disorders (PBDs), inherited genetic disorders that damage the white matter of the brain and affect motor movements. PBDs are part of a larger group of disorders called the leukodystrophies. The Zellweger spectrum of PBDs include related, but not more severe, disorders referred to as Zellweger syndrome (ZS) and neonatal adrenoleukodystrophy. Collectively, these disorders are caused by inherited defects in any one of 12 genes, called PEX genes, which are required for the normal formation and function of peroxisomes. Peroxisomes are cell structures required for the normal formation and function of the brain, eyes, liver, kidneys, and bone. They contain enzymes that break down toxic substances in the cells, including very long chain fatty acids and phytanic acid (a type of fat found in certain foods), and synthesize certain fatty materials (lipids) that are required for cell function. When peroxisomes are not functioning, there is over-accumulation of very long chain fatty acids and phytanic acid, and a lack of bile acids and plasmalogens--specialized lipids found in cell membranes and the myelin sheaths and encase and protect nerve fibers.. IRD has some residual perixisome function, resulting in less severe disease than in Zellweger syndrome. Symptoms of IRD begin in infancy with retinitis pigmentosa, a visual impairment that often leads to blindness, and hearing problems that usually progress to deafness by early childhood. Other symptoms may include rapid, jerky eye movements (nystagmus); floppy muscle tone (hypotonia) and lack of muscle coordination (ataxia); mental and growth disabilities; abnormal facial features; enlarged liver; and white matter abnormalities of brain myelin. At the mildest extreme of the disorder, intellect may be preserved. Although Adult Refsum disease and IRD have similar names, they are separate disorders caused by different gene defects."}
{"_id":"8505efbd-7e49-4948-9b1e-bf91ade0e91b","text":"The primary treatment for IRD is to avoid foods that contain phytanic acid, including dairy products; beef and lamb; and fatty fish such as tuna, cod, and haddock. Although this prevents the accumulation of phytanic acid, it does not address the accumulation of very long chain fatty acids, and the deficiency of bile acids and plasmalogens."}
{"_id":"8436ede3-5666-4d38-9df9-4f22708da316","text":"IRD is a fatal disease, but some children will survive into their teens and twenties, and possibly even beyond."}
{"_id":"730f1217-a44c-499f-b996-ec5cdc520841","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to IRDin its laboratories at the National Institutes of Health (NIH), and also supports additional research through grants to major medical institutions across the country. Research is focused on finding better ways to prevent, treat, and ultimately cure disorders such as the PBDs."}
{"_id":"6d575377-3276-49d9-97c4-c29c69c91694","text":"Reye's syndrome (RS) is primarily a children's disease, although it can occur at any age. It affects all organs of the body but is most harmful to the brain and the liver--causing an acute increase of pressure within the brain and, often, massive accumulations of fat in the liver and other organs. RS is defined as a two-phase illness because it generally occurs in conjunction with a previous viral infection, such as the flu or chicken pox. The disorder commonly occurs during recovery from a viral infection, although it can also develop 3 to 5 days after the onset of the viral illness. RS is often misdiagnosed as encephalitis, meningitis, diabetes, drug overdose, poisoning, sudden infant death syndrome, or psychiatric illness. Symptoms of RS include persistent or recurrent vomiting, listlessness, personality changes such as irritability or combativeness, disorientation or confusion, delirium, convulsions, and loss of consciousness. If these symptoms are present during or soon after a viral illness, medical attention should be sought immediately. The symptoms of RS in infants do not follow a typical pattern; for example, vomiting does not always occur. Epidemiologic evidence indicates that aspirin (salicylate) is the major preventable risk factor for Reye's syndrome. The mechanism by which aspirin and other salicylates trigger Reye's syndrome is not completely understood. A \"Reye's-like\" illness may occur in children with genetic metabolic disorders and other toxic disorders. A physician should be consulted before giving a child any aspirin or anti-nausea medicines during a viral illness, which can mask the symptoms of RS."}
{"_id":"56e0dd11-c055-42a1-ac3b-8103d14a4b4e","text":"There is no cure for RS. Successful management, which depends on early diagnosis, is primarily aimed at protecting the brain against irreversible damage by reducing brain swelling, reversing the metabolic injury, preventing complications in the lungs, and anticipating cardiac arrest. It has been learned that several inborn errors of metabolism mimic RS in that the first manifestation of these errors may be an encephalopathy with liver dysfunction. These disorders must be considered in all suspected cases of RS. Some evidence suggests that treatment in the end stages of RS with hypertonic IV glucose solutions may prevent progression of the syndrome."}
{"_id":"0eeb0375-ff3b-47fb-ae91-2150463bec2b","text":"Recovery from RS is directly related to the severity of the swelling of the brain. Some people recover completely, while others may sustain varying degrees of brain damage. Those cases in which the disorder progresses rapidly and the patient lapses into a coma have a poorer prognosis than those with a less severe course. Statistics indicate that when RS is diagnosed and treated in its early stages, chances of recovery are excellent. When diagnosis and treatment are delayed, the chances for successful recovery and survival are severely reduced. Unless RS is diagnosed and treated successfully, death is common, often within a few days."}
{"_id":"7233c873-3a76-4435-a41f-55217e2406e6","text":"Much of the research on RS focuses on answering fundamental questions about the disorder such as how problems in the body's metabolism may trigger the nervous system damage characteristic of RS and what role aspirin plays in this life-threatening disorder. The ultimate goal of this research is to improve scientific understanding, diagnosis and medical treatment of RS."}
{"_id":"adcf827d-04b0-4ab6-bdce-80d6349b7c80","text":"Cerebral arteriosclerosis is the result of thickening and hardening of the walls of the arteries in the brain. Symptoms of cerebral arteriosclerosis include headache, facial pain, and impaired vision.\n                \nCerebral arteriosclerosis can cause serious health problems. If the walls of an artery are too thick, or a blood clot becomes caught in the narrow passage, blood flow to the brain can become blocked and cause an ischemic stroke. When the thickening and hardening is uneven, arterial walls can develop bulges (called aneurysms). If a bulge ruptures, bleeding in the brain can cause a hemorrhagic stroke. Both types of stroke can be fatal.\n                \nCerebral arteriosclerosis is also related to a condition known as vascular dementia, in which small, symptom-free strokes cause cumulative damage and death to neurons (nerve cells) in the brain. Personality changes in the elderly, such as apathy, weeping, transient befuddlement, or irritability, might indicate that cerebral arteriosclerosis is present in the brain. Computer tomography (CT) and magnetic resonance imaging (MRI) of the brain can help reveal the presence of cerebral arteriosclerosis before ischemic strokes, hemorrhagic strokes, or vascular dementia develop."}
{"_id":"277c1991-7ffb-46ee-b5c3-5506dff41b16","text":"Treatment for cerebral arteriosclerosis can include medications or surgery. Physicians also may recommend treatments to help people control high blood pressure, quit cigarette smoking, and reduce cholesterol levels, all of which are risk factors for cerebral arteriosclerosis."}
{"_id":"f144fb15-ae5b-439d-ad3b-b20f51938316","text":"Cerebral arteriosclerosis can lead to life threatening health events such as ischemic or hemorrhagic strokes. People who survive stroke may have long-term neurological and motor impairments."}
{"_id":"e23b0be3-c1f7-497b-8065-caa68595a596","text":"The NINDS supports an extensive research program on stroke and conditions that can lead to stroke. Much of this research is aimed at finding ways to prevent and treat conditions such as cerebral arteriosclerosis."}
{"_id":"e7191480-887f-4a18-ab66-fba9e9cddae1","text":"Schizencephaly is an extremely rare developmental birth defect characterized by abnormal slits, or clefts, in the cerebral hemispheres of the brain. Babies with clefts in both hemispheres (called bilateral clefts) commonly have developmental delays, delays in speech and language skills, and problems with brain-spinal cord communication. Individuals with clefts in only one hemisphere (called unilateral clefts) are often paralyzed on one side of the body, but may have average to near-average intelligence. Individuals with schizencephaly may also have an abnormally small head, cognitive delay and impairment, partial or complete paralysis, or poor muscle tone. Most will experience seizures. Some individuals may have an excessive accumulation of fluid in the brain called hydrocephalus."}
{"_id":"9d1afdea-d617-4711-bd84-2b1618b80d80","text":"Treatment generally consists of physical therapy and drugs to prevent seizures. In cases that are complicated by hydrocephalus, a surgically implanted tube, called a shunt, is often used to divert fluid to another area of the body where it can be absorbed."}
{"_id":"b6c19858-9feb-4d49-ab8a-fbc5c2b2201a","text":"The prognosis for individuals with schizencephaly varies depending on the size of the clefts and the extent of neurological disabilities."}
{"_id":"0bb011aa-761a-4427-b67d-d2ccbad09ec8","text":"The NINDS conducts and supports a wide range of studies that explore the mechanisms of normal brain development. The knowledge gained from these fundamental studies provides the foundation for understanding how to prevent or treat developmental brain defects such as schizencephaly."}
{"_id":"fc78f2be-1f8c-4461-96a5-10748948b221","text":"The inflammatory myopathies are a group of diseases, with no known cause, that involve chronic muscle inflammation accompanied by muscle weakness. The three main types of chronic, or persistent, inflammatory myopathy are polymyositis, dermatomyositis, and inclusion body myositis (IBM). These rare disorders may affect both adults and children, although dermatomyositis is more common in children. Polymyositis and dermatomyositis are more common in women than in men. General symptoms of chronic inflammatory myopathy include slow but progressive muscle weakness that starts in the proximal musclesthose muscles closest to the trunk of the body. Other symptoms include fatigue after walking or standing, tripping or falling, and difficulty swallowing or breathing. Some patients may have slight muscle pain or muscles that are tender to the touch. Polymyositis affects skeletal muscles (involved with making movement) on both sides of the body. Dermatomyositis is characterized by a skin rash that precedes or accompanies progressive muscle weakness. IBM is characterized by progressive muscle weakness and wasting. Juvenile myositis has some similarities to adult dermatomyositis and polymyositis."}
{"_id":"cf76fe45-50fc-4366-9ccc-20b64ea76e77","text":"The chronic inflammatory myopathies cant be cured in most adults but many of the symptoms can be treated. Options include medication, physical therapy, exercise, heat therapy (including microwave and ultrasound), orthotics and assistive devices, and rest. Polymyositis and dermatomyositis are first treated with high doses of prednisone or another corticosteroid drug. This is most often given as an oral medication but can be delivered intravenously. Immunosuppressant drugs, such as azathioprine and methotrexate, may reduce inflammation in people who do not respond well to prednisone. IBM has no standard course of treatment. The disease is generally unresponsive to corticosteroids and immunosuppressive drugs."}
{"_id":"38f8301e-f309-4c0e-b1bc-ea08e7cdd3e7","text":"Most cases of dermatomyositis respond to therapy. The prognosis for polymyositis varies. Most individuals respond fairly well to therapy, but some people have a more severe disease that does not respond adequately to therapies and are left with significant disability. IBM is generally resistant to all therapies and its rate of progression appears to be unaffected by currently available treatments."}
{"_id":"badd1999-0764-4662-ae4e-b1bd650a6c93","text":"The National Institutes of Health (NIH), through the collaborative efforts of its National Institute of Neurological Disorders and Stroke (NINDS), National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), and National Institute of Environmental Health Sciences (NIEHS), conducts and supports a wide range of research on neuromuscular disorders, including the inflammatory myopathies. The NINDS and NIAMS are funding DNA analyses using microarrays to characterize patterns of muscle gene expression among adult and juvenile individuals with distinct subtypes of inflammatory myopathies. Findings will be used to refine disease classification and provide clues to the pathology of these disorders. Other NIH-funded research is studying prior viral infection as a precursor to inflammatory myopathy. Other research hopes to determine whether the drug infliximab, which blocks a protein that is associated with harmful inflammation, is safe and effective in treating dermatomyositis and polymyositis."}
{"_id":"543a92b7-cd0c-41fd-9d9c-353169caa166","text":"Stiff-person syndrome (SPS) is a rare neurological disorder with features of an autoimmune disease. SPS is characterized by fluctuating muscle rigidity in the trunk and limbs and a heightened sensitivity to stimuli such as noise, touch, and emotional distress, which can set off muscle spasms. Abnormal postures, often hunched over and stiffened, are characteristic of the disorder. People with SPS can be too disabled to walk or move, or they are afraid to leave the house because street noises, such as the sound of a horn, can trigger spasms and falls. SPS affects twice as many women as men.  It is frequently associated with other autoimmune diseases such as diabetes, thyroiditis, vitiligo, and pernicious anemia. Scientists dont yet understand what causes SPS, but research indicates that it is the result of an autoimmune response gone awry in the brain and spinal cord. The disorder is often misdiagnosed as Parkinsons disease, multiple sclerosis, fibromyalgia, psychosomatic illness, or anxiety and phobia. A definitive diagnosis can be made with a blood test that measures the level of glutamic acid decarboxylase (GAD) antibodies in the blood. People with SPS have elevated levels of GAD, an antibody that works against an enzyme involved in the synthesis of an important neurotransmitter in the brain."}
{"_id":"a2efa940-97fd-446a-af52-b105dd5a99fc","text":"People with SPS respond to high doses of diazepam and several anti-convulsants, gabapentin and tiagabine. A recent study funded by the NINDS demonstrated the effectiveness of intravenous immunoglobulin (IVIg) treatment in reducing stiffness and lowering sensitivity to noise, touch, and stress in people with SPS."}
{"_id":"8931bc4d-0b4d-4a19-bec2-fa1cde35d013","text":"Treatment with IVIg, anti-anxiety drugs, muscle relaxants, anti-convulsants, and pain relievers will improve the symptoms of SPS, but will not cure the disorder. Most individuals with SPS have frequent falls and because they lack the normal defensive reflexes; injuries can be severe. With appropriate treatment, the symptoms are usually well controlled."}
{"_id":"f64a176b-ed46-4a67-82f6-b0fb22d16ee1","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to SPS in its laboratories at the National Institutes of Health (NIH), and also supports additional research through grants to major medical institutions across the country. A study using the drug rituximab proved ineffective in treating individuals with the disorder. Current research is focused on understanding the cause of the disease and the role of the anti-GAD antibodies."}
{"_id":"af84e62c-988b-444a-9481-70ebcdc8a0cc","text":"Hereditary spastic paraplegia (HSP), also called familial spastic paraparesis (FSP), refers to a group of inherited disorders that are characterized by progressive weakness and spasticity (stiffness) of the legs. Early in the disease course, there may be mild gait difficulties and stiffness. These symptoms typically slowly progress so that eventually individuals with HSP may require the assistance of a cane, walker, or wheelchair. Though the primary features of \"pure\" HSP are progressive lower limb spasticity and weakness, complicated forms may be accompanied by other symptoms. These additional symptoms include impaired vision due to cataracts and problems with the optic nerve and retina of the eye, ataxia (lack of muscle coordination), epilepsy, cognitive impairment, peripheral neuropathy, and deafness. The diagnosis of HSP is primarily by neurological examination and testing to rule out other disorders. Brain MRI abnormalities, such as a thin corpus callosum, may be seen in some of the complicated forms of HSP. Several genetic mutations have been identified which underlie various forms of HSP, and specialized genetic testing and diagnosis are available at some medical centers. HSP has several forms of inheritance. Not all children in a family will necessarily develop symptoms, although they may be carriers of the abnormal gene. Symptoms may begin in childhood or adulthood, depending on the particular HSP gene involved."}
{"_id":"3ba718e5-7a2d-47f6-9adc-ef9d1ead66bf","text":"There are no specific treatments to prevent, slow, or reverse HSP. Symptomatic treatments used for spasticity, such as muscle relaxants, are sometimes helpful. Regular physical therapy is important for muscle strength and to preserve range of motion."}
{"_id":"404edf59-bf33-48e2-99c3-bc75b67149e6","text":"The prognosis for individuals with HSP varies Some individuals are very disabled and others have only mild disability. The majority of individuals with uncomplicated HSP have a normal life expectancy."}
{"_id":"4ead129a-5e05-4745-b24e-3e944c608a90","text":"The NINDS supports research on genetic disorders such as HSP. More than 30 genes that are responsible for several forms of HSP have been identified, and many more will likely be identified in the future. These genes generally encode proteins that normally help maintain the function of axons in the spinal cord. Understanding how mutations of these genes cause HSP should lead to ways to prevent, treat, and cure HSP."}
{"_id":"69ceaff9-6a2a-46e7-b56f-407b6be943ee","text":"Leukodystrophy refers to progressive degeneration of the white matter of the brain due to imperfect growth or development of the myelin sheath, the fatty covering that acts as an insulator around nerve fiber. Myelin, which lends its color to the white matter of the brain, is a complex substance made up of at least ten different chemicals. The leukodystrophies are a group of disorders that are caused by genetic defects in how myelin produces or metabolizes these chemicals. Each of the leukodystrophies is the result of a defect in the gene that controls one (and only one) of the chemicals. Specific leukodystrophies include metachromatic leukodystrophy, Krabb disease, adrenoleukodystrophy, Pelizaeus-Merzbacher disease, Canavan disease, Childhood Ataxia with Central Nervous System Hypomyelination or CACH (also known as Vanishing White Matter Disease), Alexander disease, Refsum disease, and cerebrotendinous xanthomatosis. The most common symptom of a leukodystrophy disease is a gradual decline in an infant or child who previously appeared well. Progressive loss may appear in body tone, movements, gait, speech, ability to eat, vision, hearing, and behavior. There is often a slowdown in mental and physical development. Symptoms vary according to the specific type of leukodystrophy, and may be difficult to recognize in the early stages of the disease."}
{"_id":"a446d8e8-b9eb-434d-af23-b8511e484ff1","text":"Treatment for most of the leukodystrophies is symptomatic and supportive, and may include medications, physical, occupational, and speech therapies; and nutritional, educational, and recreational programs. Bone marrow transplantation is showing promise for a few of the leukodystrophies."}
{"_id":"8a9168ad-3c40-45c2-9a24-8f4cb8aaf227","text":"The prognosis for the leukodystrophies varies according to the specific type of leukodystrophy."}
{"_id":"fc934f37-6bee-4462-b4e0-556b8a56c838","text":"The NINDS supports research on genetic disorders, including the leukodystrophies. The goals of this research are to increase scientific understanding of these disorders, and to find ways to prevent, treat, and, ultimately, cure them."}
{"_id":"06e316b7-4a04-4812-87fc-ab6dfa0e4a33","text":"Canavan disease is a gene-linked neurological disorder in which the brain degenerates into spongy tissue riddled with microscopic fluid-filled spaces. Canavan disease has been classified as one of a group of genetic disorders known as the leukodystrophies. Recent research has indicated that the cells in the brain responsible for making myelin sheaths, known as oligodendrocytes, cannot properly complete this critical developmental task. Myelin sheaths are the fatty covering that act as insulators around nerve fibers in the brain, as well as providing nutritional support for nerve cells. In Canavan disease, many oligodendrocytes do not mature and instead die, leaving nerve cell projections known as axons vulnerable and unable to properly function. Canavan disease is caused by mutation in the gene for an enzyme called aspartoacylase, which acts to break down the concentrated brain chemical known as N-acetyl-aspartate.\n                \nSymptoms of Canavan disease usually appear in the first 3 to 6 months of life and progress rapidly. Symptoms include lack of motor development, feeding difficulties, abnormal muscle tone (weakness or stiffness), and an abnormally large, poorly controlled head. Paralysis, blindness, or hearing loss may also occur. Children are characteristically quiet and apathetic. Although Canavan disease may occur in any ethnic group, it is more frequent among Ashkenazi Jews from eastern Poland, Lithuania, and western Russia, and among Saudi Arabians. Canavan disease can be identified by a simple prenatal blood test that screens for the missing enzyme or for mutations in the gene that controls aspartoacylase. Both parents must be carriers of the defective gene in order to have an affected child. When both parents are found to carry the Canavan gene mutation, there is a one in four (25 percent) chance with each pregnancy that the child will be affected with Canavan disease."}
{"_id":"073a99e2-6877-48a5-b34d-1cf67b63bfeb","text":"Canavan disease causes progressive brain atrophy. There is no cure, nor is there a standard course of treatment. Treatment is symptomatic and supportive."}
{"_id":"295f8817-d776-42bd-ba13-c25583d7a7f2","text":"The prognosis for Canavan disease is poor. Death usually occurs before age 10, although some children may survive into their teens and twenties."}
{"_id":"f903f3ff-6e85-48ed-933d-88ce711a29be","text":"The gene for Canavan disease has been located. Many laboratories offer prenatal screening for this disorder to populations at risk. Scientists have developed animal models for this disease and are using the models to test potential therapeutic strategies. Three strategies are currently under investigation: gene transfer to the brain in order to replace the mutated gene for the enzyme; metabolic therapy to provide a crucial missing metabolite (acetate); and enzyme therapy where the enzyme aspartoacylase is engineered to be able to enter the brain and is injected in the the blood stream. Encouraging results have been obtained using these strategies."}
{"_id":"c398def6-0d6e-4418-94e9-d6a70d5cb0fb","text":"Alexander disease is one of a group of neurological conditions known as the leukodystrophies, disorders that are the result of abnormalities in myelin, the white matter that protects nerve fibers in the brain. Alexander disease is a progressive and often fatal disease. The destruction of white matter is accompanied by the formation of Rosenthal fibers, which are abnormal clumps of protein that accumulate in non-neuronal cells of the brain called astrocytes. Rosenthal fibers are sometimes found in other disorders, but not in the same amount or area of the brain that are featured in Alexander disease. The infantile form is the most common type of Alexander disease. It has an onset during the first two years of life. Usually there are both mental and physical developmental delays, followed by the loss of developmental milestones, an abnormal increase in head size, and seizures. The juvenile form of Alexander disease is less common and has an onset between the ages of two and thirteen. These children may have excessive vomiting, difficulty swallowing and speaking, poor coordination, and loss of motor control. Adult-onset forms of Alexander disease are less common. The symptoms sometimes mimic those of Parkinsons disease or multiple sclerosis, or may present primarily as a psychiatric disorder. The disease occurs in both males and females, and there are no ethnic, racial, geographic, or cultural\/economic differences in its distribution."}
{"_id":"d5718f1a-1162-456d-a750-803133b79d5d","text":"There is no cure for Alexander disease, nor is there a standard course of treatment. Treatment of Alexander disease is symptomatic and supportive."}
{"_id":"2ecd752c-b9f3-4d2a-a878-5c700d685b30","text":"The prognosis for individuals with Alexander disease is generally poor. Most children with the infantile form do not survive past the age of 6. Juvenile and adult onset forms of the disorder have a slower, more lengthy course."}
{"_id":"bcf92775-9676-434e-97a5-9456dfa01e2f","text":"Recent discoveries show that most individuals (approximately 90 percent) with Alexander disease have a mutation in the gene that makes glial fibrillary acidic protein (GFAP). GFAP is a normal component of the brain, but it is unclear how the mutations in this genecauses the disease. In most cases mutations occur spontaneously are not inherited from parents.A small number of people thought to have Alexander disease do not have identifiable mutations in GFAP, which leads researchers to believe that there may be other genetic or perhaps even non-genetic causes of Alexander disease. Current research is aimed at understanding the mechanisms by which the mutations cause disease, developing better animal models for the disorder, and exploring potential strategies for treatment. At present, there is no exact animal model for the disease; however, mice have been engineered to produce the same mutant forms of GFAP found in individuals with Alexander disease. These mice form Rosenthal fibers and have a predisposition for seizures, but do not yet mimic all features of human disease (such as the leukodystrophies). One clinical study is underway to identify biomarkers of disease severity or progression in samples of blood or cerebrospinal fluid. Such biomarkers, if found, would be a major advantage for evaluating the response to any treatments that are developed in the future."}
{"_id":"ccf4013a-f24d-4ed7-99a2-45186392fac8","text":"Narcolepsy is a chronic neurological disorder caused by the brain's inability to regulate sleep-wake cycles normally. At various times throughout the day, people with narcolepsy experience irresistable bouts ofsleep. If the urge becomes overwhelming, individuals will fall asleep for periods lasting from a few seconds to several minutes. In rare cases, some people may remain asleep for an hour or longer. In addition to excessive daytime sleepiness (EDS), three other major symptoms frequently characterize narcolepsy: cataplexy, or the sudden loss of voluntary muscle tone; vivid hallucinations during sleep onset or upon awakening; and brief episodes of total paralysis at the beginning or end of sleep. Narcolepsy is not definitively diagnosed in most patients until 10 to 15 years after the first symptoms appear. The cause of narcolepsy remains unknown. It is likely that narcolepsy involves multiple factors interacting to cause neurological dysfunction and sleep disturbances."}
{"_id":"d87676ea-d5e7-4285-a594-3a747cf3f31b","text":"There is no cure for narcolepsy. In 1999, after successful clinical trial results, the U.S. Food and Drug Administration (FDA) approved a drug called modafinil for the treatment of EDS. Two classes of antidepressant drugs have proved effective in controlling cataplexy in many patients: tricyclics (including imipramine, desipramine, clomipramine, and protriptyline) and selective serotonin reuptake inhibitors (including fluoxetine and sertraline). Drug therapy should be supplemented by behavioral strategies. For example, many people with narcolepsy take short, regularly scheduled naps at times when they tend to feel sleepiest. Improving the quality of nighttime sleep can combat EDS and help relieve persistent feelings of fatigue. Among the most important common-sense measures people with narcolepsy can take to enhance sleep quality are actions such as maintaining a regular sleep schedule, and avoiding alcohol and caffeine-containing beverages before bedtime. The drug Xyrem (sodium oxybate or gamma hydroxybutyrate, also known as GHB) was approved in July 2002 for treating cataplexy and in November 2005 for EDS in people who have narcolepsy. Due to safety concerns associated with the use of this drug, the distribution of Xyrem is tightly restricted."}
{"_id":"7d53978c-18c9-4536-ba0f-ddb96821c506","text":"None of the currently available medications enables people with narcolepsy to consistently maintain a fully normal state of alertness. But EDS and cataplexy, the most disabling symptoms of the disorder, can be controlled in most patients with drug treatment. Often the treatment regimen is modified as symptoms change. Whatever the age of onset, patients find that the symptoms tend to get worse over the two to three decades after the first symptoms appear. Many older patients find that some daytime symptoms decrease in severity after age 60."}
{"_id":"8ae0b22b-dfa9-4cb3-b260-8251b0f62005","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research into narcolepsy and other sleep disorders in laboratories at the NIH and also support additional research through grants to major medical institutions across the country. The NINDS continues to support investigations into the basic biology of sleep, including the brain mechanisms involved in generating and regulating sleep. Within the National Heart, Lung, and Blood Institute, also a component of the NIH, the       National        Center   on Sleep Disorders Research (NCSDR) coordinates Federal government sleep research activities and shares information with private and nonprofit groups."}
{"_id":"177e70e2-ccab-469c-9035-31051f780634","text":"AIDS is primarily an immune system disorder caused by the human immunodeficiency virus (HIV), but it can also affect the nervous system. HIV does not appear to directly invade nerve cells but it jeopardizes their health and function, causing symptoms such as confusion, forgetfulness, behavioral changes, headaches, progressive weakness and loss of sensation in the arms and legs, cognitive motor impairment, or damage to the peripheral nerves. Other complications that can occur as a result of HIV infection or the drugs used to treat it include pain, seizures, shingles, spinal cord problems, lack of coordination, difficult or painful swallowing, anxiety disorder, depression, fever, vision loss, gait disorders, destruction of brain tissue, and coma. Other AIDS-related nervous system disorders may be caused by certain cancers or by illnesses that would not otherwise affect people with healthy immune systems.\n                \nAmong the most common neurological complications are: AIDS dementia complex, causing symptoms such as encephalitis (inflammation of the brain), behavioral changes, and a gradual decline in cognitive function; central nervous system lymphomas, cancerous tumors that either begin in the brain or result from a cancer that has spread from another site in the body; cryptococcal meningitis; cytomegalovirus infections; herpes virus infections; neuropathy; neurosyphilis; progressive multifocal leukoencephalopathy (PML); and psychological and neuropsychiatric disorders."}
{"_id":"8bf79448-a952-4983-bd0b-9fe541ed60f0","text":"No single treatment can cure the neurological complications of AIDS. Some disorders require aggressive therapy while others are treated symptomatically.\n                \nMedicines range from analgesics sold over the counter to antiepileptic drugs, opiates, corticosteroids, and some classes of antidepressants. Other treatments include radiation therapy or chemotherapy to kill or shrink cancerous brain tumors that may be caused by HIV, antifungal or antimalarial drugs to combat certain bacterial infections, and penicillin to treat neurosyphilis. Aggressive antiretroviral therapy is used to treat AIDS dementia complex, PML, and cytomegalovirus encephalitis. HAART, or highly active antiretroviral therapy, combines at least three drugs to reduce the amount of virus circulating in the blood and may also delay the start of some infections."}
{"_id":"605d257d-fb1c-4bb4-86ba-0b9bab2dbb8f","text":"The overall prognosis for individuals with AIDS in recent years has improved significantly because of new drugs and treatments. AIDS clinicians often fail to recognize neurological complications of AIDS. Those who suspect they are having neurological complications should be sure to discuss these with their doctor."}
{"_id":"eedb7667-bcb1-4b74-968d-94e1f6d697f8","text":"Within the Federal government, the National Institute of Neurological Disorders and Stroke (NINDS), one part of the National Institutes of Health (NIH), supports research on the neurological consequences of AIDS. The NINDS works closely with its sister agency, the National Institute of Allergy and Infectious Diseases (NIAID), which has primary responsibility for research related to HIV and AIDS."}
{"_id":"e7a96431-ae8a-42e6-b371-a46a1fe7314c","text":"Tabes dorsalis is a slow degeneration of the nerve cells and nerve fibers that carry sensory information to the brain. The degenerating nerves are in the dorsal columns of the spinal cord (the portion closest to the back of the body) and carry information that help maintain a person's sense of position. Tabes dorsalis is the result of an untreated syphilis infection. Symptoms may not appear for some decades after the initial infection and include weakness, diminished reflexes, unsteady gait, progressive degeneration of the joints, loss of coordination, episodes of intense pain and disturbed sensation, personality changes, dementia, deafness, visual impairment, and impaired response to light. The disease is more frequent in males than in females. Onset is commonly during mid-life. The incidence of tabes dorsalis is rising, in part due to co-associated HIV infection."}
{"_id":"c0a8a00c-05a7-4b7c-b54b-ebf218cb46bd","text":"Penicillin, administered intravenously, is the treatment of choice. Associated pain can be treated with opiates, valproate, or carbamazepine. Patients may also require physical or rehabilitative therapy to deal with muscle wasting and weakness. Preventive treatment for those who come into sexual contact with an individual with tabes dorsalis is important."}
{"_id":"168db876-e5e2-45be-81b3-beee84896370","text":"If left untreated, tabes dorsalis can lead to paralysis, dementia, and blindness. Existing nerve damage cannot be reversed."}
{"_id":"e6006ec9-12b8-453b-a8a5-d59eb16934a2","text":"The NINDS supports and conducts research on neurodegenerative disorders, such as tabes dorsalis, in an effort to find ways to prevent, treat, and, ultimately, cure these disorders."}
{"_id":"5ef79093-cc56-43ea-b283-3e8705400790","text":"Herpes zoster oticus, also called Ramsay Hunt Syndrome or Ramsay Hunt Syndrome type II, is a common complication of shingles. Shingles is an infection caused by the varicella-zoster virus, which is the virus that causes chickenpox. Shingles occurs in people who have had chickenpox and represents a reactivation of the dormant varicella-zoster virus. Herpes zoster oticus, which is caused by the spread of the varicella-zoster virus to facial nerves, is characterized by intense ear pain, a rash around the ear, mouth, face, neck, and scalp, and paralysis of facial nerves. Other symptoms may include hearing loss, vertigo (abnormal sensation of movement), and tinnitus (abnormal sounds). Taste loss in the tongue and dry mouth and eyes may also occur."}
{"_id":"2f2b8f94-564d-4c94-98d4-f36e8ed30fdb","text":"Some cases of herpes zoster oticus do not require treatment. When treatment is needed, medications such as antiviral drugs or corticosteroids may be prescribed. Vertigo may be treated with the drug diazepam"}
{"_id":"68f4d3a6-a1c1-4408-a8c0-1b0db3e40ea4","text":"Generally, the prognosis of herpes zoster oticus is good. However, in some cases, hearing loss may be permanent. Vertigo may last for days or weeks. Facial paralysis may be temporary or permanent."}
{"_id":"313d97b4-495e-4bcb-a4fb-705e432624ee","text":"The NINDS supports research on shingles and shingles-related conditions. Current studies focus on the relationship between the persistence of neurotropic viruses and development of neurological diseases including herpes simplex and varicella-zoster viruses."}
{"_id":"a3b2811c-d937-4265-92f7-383d3e7a6816","text":"Hemicrania continua is a chronic and persistent form of headache marked by continuous pain that varies in severity, always occurs on the same side of the face and head, and is superimposed with additional debilitating symptoms. on the continuous but fluctuating pain are occasional attacks of more severe pain. A small percentage of individuals with hemicrania continua have bilateral pain, or pain on both sides of the head. A headache is considered hemicrania continua if the person has had a one-sided daily or continuous headache of moderate intensity with occasional short, piercing head pain for more than 3 months without shifting sides or pain-free periods. The headache must also be completely responsive to treatment with the non-steroidal anti-inflammatory drug drug indomethacin. It must have at least one of the following symptoms: eye redness and\/or tearing, nasal congestion and\/or runny nose, ptosis (drooping eyelid) and miosis (contracture of the iris). Occasionally, individuals will also have forehead sweating and migraine symptoms, such as throbbing pain, nausea and\/or vomiting, or sensitivity to light and sound. The disorder has two forms: chronic, with daily headaches, and remitting, in which headaches may occur for a period as long as 6 months and are followed by a pain-free period of weeks to months until the pain returns. Most patients experience attacks of increased pain three to five times per 24-hour cycle. This disorder is more common in women than in men. Physical exertion and alcohol use may increase the severity of headache pain in some patients. The cause of this disorder is unknown."}
{"_id":"68efbc26-3c46-4730-909f-e5c2eef70064","text":"Indomethacin provides rapid relief from symptoms. Patients must take between 25 and 300 milligrams of indomethacin daily and indefinitely to decrease symptoms. Some individuals may need to take acid-suppression medicine due to a gastrointestinal side effect. For those who cannot tolerate the side effects, another NSAID, celecoxib, has been shown to have less complications and can be prescribed. Amitriptyline and other tricyclic antidepressants are also effective in some individuals with hemicrania continua as a preventative treatment."}
{"_id":"e51fb10a-6d72-423e-a36c-e8c7cd4ae9a0","text":"Individuals may obtain complete to near-complete relief of symptoms with proper medical attention and daily medication. Some people may not be able to tolerate long-term use of indomethacin and may have to rely on less effective NSAIDs."}
{"_id":"296d651e-e80b-43c4-9cc1-e4ccf67a8474","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) support research related to hemicrania continua through grants to medical research institutions across the country. Much of this research focuses on understanding hemicrania continua in order to finding better ways to prevent, treat, and ultimately cure the disorder."}
{"_id":"f69ad58f-1393-4960-8ae8-53073a435293","text":"Paroxysmal choreoathetosis is a movement disorder characterized by episodes or attacks of involuntary movements of the limbs, trunk, and facial muscles. The disorder may occur in several members of a family, or in only a single family member. Prior to an attack some individuals experience tightening of muscles or other physical symptoms. Involuntary movements precipitate some attacks, and other attacks occur when the individual has consumed alcohol or caffeine, or is tired or stressed. Attacks can last from 10 seconds to over an hour. Some individuals have lingering muscle tightness after an attack. Paroxysmal choreoathetosis frequently begins in early adolescence. A gene associated with the disorder has been discovered. The same gene is also associated with epilepsy."}
{"_id":"caaf69db-f0c7-4739-aa27-eedd9447c646","text":"Drug therapy, particularly carbamazepine, has been very successful in reducing or eliminating attacks of paroxysmal choreoathetosis. While carbamazepine is not effective in every case, other drugs have been substituted with good effect."}
{"_id":"493386da-d07a-4714-b38b-c0ae2db5891f","text":"Generally, paroxysmal choreoathetosis lessens with age, and many adults have a complete remission. Because drug therapy is so effective, the prognosis for the disorder is good."}
{"_id":"8f337fe7-2f41-4288-a1e9-273c7509e0cf","text":"NINDS supports and conducts research on movement disorders such as paroxysmal choreoathetosis. Much of this research is aimed at finding ways to prevent and treat these disorders."}
{"_id":"4e07912d-e8c6-47d6-a28b-de89cf5c5453","text":"For several decades the term tropical spastic paraparesis (TSP) has been used to describe a chronic and progressive disease of the nervous system that affects adults living in equatorial areas of the world and causes progressive weakness, stiff muscles, muscle spasms, sensory disturbance, and sphincter dysfunction. The cause of TSP was obscure until the mid-1980s, when an important association was established between the human retrovirus  human T-cell lymphotrophic virus type 1 (also known as HTLV-1)  and TSP. TSP is now called HTLV-1 associated myelopathy\/ tropical spastic paraparesis or HAM\/TSP. The HTLV-1 retrovirus is thought to cause at least 80 percent of the cases of HAM\/TSP by impairing the immune system. In addition to neurological symptoms of weakness and muscle stiffness or spasms, in rare cases individuals with HAM\/TSP also exhibit uveitis (inflammation of the uveal tract of the eye), arthritis (inflammation of one or more joints), pulmonary lymphocytic alveolitis (inflammation of the lung), polymyositis (an inflammatory muscle disease), keratoconjunctivitis sicca (persistent dryness of the cornea and conjunctiva), and infectious dermatitis (inflammation of the skin). The other serious complication of HTLV-1 infection is the development of adult T-cell leukemia or lymphoma. Nervous system and blood-related complications occur only in a very small proportion of infected individuals, while most remain largely without symptoms throughout their lives.\n                \nThe HTLV-1 virus is transmitted person-to-person via infected cells: breast-feeding by mothers who are seropositive (in other words, have high levels of virus antibodies in their blood), sharing infected needles during intravenous drug use, or having sexual relations with a seropositive partner. Less than 2 percent of HTLV-1 seropositive carriers will become HAM\/TSP patients."}
{"_id":"a72c287d-f397-4d47-992a-cb9205ee5326","text":"There is no established treatment program for HAM\/TSP. Corticosteroids may relieve some symptoms, but arent likely to change the course of the disorder. Clinical studies suggest that interferon alpha provides benefits over short periods and some aspects of disease activity may be improved favorably using interferon beta. Stiff and spastic muscles may be treated with lioresal or tizanidine. Urinary dysfunction may be treated with oxybutynin."}
{"_id":"c005acd9-7f1b-41ef-8a6e-41305c19c11e","text":"HAM\/TSP is a progressive disease, but it is rarely fatal. Most individuals live for several decades after the diagnosis. Their prognosis improves if they take steps to prevent urinary tract infection and skin sores, and if they participate in physical and occupational therapy programs."}
{"_id":"5571c0dd-ff35-4dd2-8a9e-62f26dd6ecc6","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to HAM\/TSP in laboratories at the NIH, and support additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders such as HAM\/TSP."}
{"_id":"8fa54ae8-f566-46b6-96cf-d16b51a05481","text":"Alpers' disease is a progressive, neurodevelopmental, mitochondrial DNA depletion syndrome characterized by three co-occurring clinical symptoms: psychomotor regression (dementia); seizures; and liver disease. It is an autosomal recessive disease caused by mutation in the gene for the mitochondrial DNA polymerase POLG. The disease occurs in about one in 100,000 persons. Most individuals with Alpers' disease do not show symptoms at birth and develop normally for weeks to years before the onset of symptoms. Diagnosis is established by testing for the POLG gene. Symptoms typically occur months before tissue samples show the mitochondrial DNA depletion, so that these depletion studies cannot be used for early diagnosis. About 80 percent of individuals with Alpers' disease develop symptoms in the first two years of life, and 20 percent develop symptoms between ages 2 and 25. The first symptoms of the disorder are usually nonspecific and may include hypoglycemia secondary to underlying liver disease, failure to thrive, infection-associated encephalopathy, spasticity, myoclonus (involuntary jerking of a muscle or group of muscles), seizures, or liver failure. An increased protein level is seen in cerebrospinal fluid analysis. Cortical blindness (loss of vision due to damage to the area of the cortex that controls vision) develops in about 25 percent of cases. Gastrointestinal dysfunction and cardiomyopathy may occur. Dementia is typically episodic and often associated with an infection that occurs while another disease is in process. Seizures may be difficult to control and unrelenting seizures can cause developmental regression as well. \"Alpers-like\" disorders without liver disease are genetically different and have a different clinical course. Fewer than one-third of individuals with the \"Alpers-like\" phenotype without liver disease have POLG mutations."}
{"_id":"88894b52-59ce-49c1-8b71-6185b5289d2b","text":"There is no cure for Alpers' disease and no way to slow its progression. Treatment is symptomatic and supportive. Anticonvulsants may be used to treat the seizures, but at times the seizures do not respond well to therapy, even at high doses. Therefore, the benefit of seizure control should be weights against what could be excessive sedation from the anticonvulsant.. Valproate should not be used since it can increase the risk of liver failure. Physical therapy may help to relieve spasticity and maintain or increase muscle tone."}
{"_id":"da939b82-66b3-408d-a0be-0cc3b29f3090","text":"The prognosis for individuals with Alpers' disease is poor. Those with the disease usually die within their first decade of life. Continuous, unrelenting seizures often lead to death. Liver failure and cardiorespiratory failure due to brain, spinal cord, and nerve involvement may also occur."}
{"_id":"7767942c-51ba-46ba-8168-69b61627b6d4","text":"The NINDS supports research on gene-linked neurodegenerative disorders such as Alpers' disease. The goals of this research are to increase scientific understanding of these disorders, and to find ways to prevent, treat, and cure them."}
{"_id":"07a377c3-b801-411f-80b1-6c70726d3a47","text":"Myasthenia gravis is a chronic autoimmune neuromuscular disease characterized by varying degrees of weakness of the skeletal (voluntary) muscles of the body. Symptoms vary in type and intensity. The hallmark of myasthenia gravis is muscle weakness that increases during periods of activity and improves after periods of rest. Muscles that control eye and eyelid movements, facial expression, chewing, talking, and swallowing are often, but not always, involved. The muscles that control breathing and neck and limb movements may also be affected. Myasthenia gravis is caused by a defect in the transmission of nerve impulses to muscles. Normally when impulses travel down the nerve, the nerve endings release a neurotransmitter substance called acetylcholine. In myasthenia gravis, antibodies produced by the body's own immune system block, alter, or destroy the receptors for acetylcholine. The first noticeable symptoms of myasthenia gravis may be weakness of the eye muscles, difficulty in swallowing, or slurred speech. Myasthenia gravis is an autoimmune disease because the immune system--which normally protects the body from foreign organisms--mistakenly attacks itself.. It is not directly inherited nor is it contagious."}
{"_id":"2b72ae85-4e21-485f-bbe7-341e0b85b8a3","text":"Myasthenia gravis can be controlled. Some medications improve neuromuscular transmission and increase muscle strength, and some suppress the production of abnormal antibodies. These medications must be used with careful medical follow up because they may cause major side effects. Thymectomy, the surgical removal of the thymus gland (which often is abnormal in those with myasthenia gravis), improves symptoms in certain individuals Other therapies include plasmapheresis, a procedure in which abnormal antibodies are removed from the blood, and high-dose intravenous immune globulin, which temporarily modifies the immune system and provides the body with normal antibodies from donated blood."}
{"_id":"77942522-7c24-459b-82ce-40c6939b7747","text":"With treatment, most individuals with myasthenia can significantly improve their muscle weakness. Some case of myasthenia gravis may go into remission temporarily, and muscle weakness may disappear so that medications can be discontinued. In a few cases, the severe weakness of myasthenia gravis may cause respiratory failure, which requires immediate emergency medical care."}
{"_id":"680cb5d8-f617-44e8-925d-8e3361e9a0d1","text":"Scientists are evaluating new and improving current treatments for myasthenia gravis. Different drugs are being tested, either alone or in combination with existing drug therapies, to see if they are effective in treating the disorder. One study seeks to understand the molecular basis of synaptic transmission in the nervous system. Thymectomy is being studied in individuals who do not have thymoma, to assess long-term benefit the surgery may have over medical therapy alone. And investigators are examining the safety and efficacy of autologous hematopoietic stem cell transplantation to treat refractory and severe myasthenia gravis."}
{"_id":"5ae9b79c-4281-47f3-a199-ed1dad57347c","text":"Spinal Muscular Atrophy (SMA) Types I, II, and III belong to a group of hereditary diseases that cause weakness and wasting of the voluntary muscles in the arms and legs of infants and children. The disorders are caused by an abnormal or missing gene known as the survival motor neuron gene 1 (SMN1), which is responsible for the production of a protein essential to motor neurons. Without this protein, lower motor neurons in the spinal cord degenerate and die. The type of SMA (I, II, or III) is determined by the age of onset and the severity of symptoms. Type I (also known as Werdnig-Hoffman disease, or infantile-onset SMA) is evident at birth or within the first few months. Symptoms include floppy limbs and trunk, feeble movements of the arms and legs, swallowing and feeding difficulties, and impaired breathing. Type II (the intermediate form) usually begins 6 and 18 months of age. Legs tend to be more impaired than arms. Children with Type II may able to sit and some may be able to stand or walk with help. Symptoms of Type III (also called Kugelberg-Welander disease) appear between 2 and 17 years of age and include difficulty running, climbing steps, or rising from a chair. The lower extremities are most often affected. Complications include scoliosis and chronic shortening of muscles or tendons around joints."}
{"_id":"7e123f1a-80a9-447c-b820-2f670bc81484","text":"There is no cure for SMA. Treatment consists of managing the symptoms and preventing complications."}
{"_id":"294c8629-f266-46cf-8ecd-51be98ba9733","text":"The prognosis is poor for babies with SMA Type I. Most die within the first two years. For children with SMA Type II, the prognosis for life expectancy or for independent standing or walking roughly correlates with how old they are when they first begin to experience symptoms - older children tend to have less severe symptoms Life expectancy is reduced but some individuals live into adolescence or young adulthood. Individuals with SMA type III may be prone to respiratory infections but with care may have a normal lifespan."}
{"_id":"41152335-bb47-4cff-ba07-fdd92cf08b96","text":"Between 2003 and 2012, the NINDS piloted the Spinal Muscular Atrophy Project to expedite therapeutics development for this hereditary neurodegenerative disease. The Project was designed to accelerate the research process by identifying drugs that increase the level of SMN protein in cultured cells, so that they could be used as potential leads for further drug discovery and clinical testing. Read more about the history of this pioneering effort and how it led to collaboration with several pharmaceutical and biotechnology companies."}
{"_id":"dfb87e72-a32e-45e2-a362-2d6a2bcbd8b3","text":"Alzheimer's disease (AD) is an age-related, non-reversible brain disorder that develops over a period of years. Initially, people experience memory loss and confusion, which may be mistaken for the kinds of memory changes that are sometimes associated with normal aging. However, the symptoms of AD gradually lead to behavior and personality changes, a decline in cognitive abilities such as decision-making and language skills, and problems recognizing family and friends. AD ultimately leads to a severe loss of mental function. These losses are related to the worsening breakdown of the connections between certain neurons in the brain and their eventual death. AD is one of a group of disorders called dementias that are characterized by cognitive and behavioral problems. It is the most common cause of dementia among people age 65 and older.\n                \nThere are three major hallmarks in the brain that are associated with the disease processes of AD.\n                \n- Amyloid plaques, which are made up of fragments of a protein called beta-amyloid peptide mixed with a collection of additional proteins, remnants of neurons, and bits and pieces of other nerve cells. - Neurofibrillary tangles (NFTs), found inside neurons, are abnormal collections of a protein called tau. Normal tau is required for healthy neurons. However, in AD, tau clumps together. As a result, neurons fail to function normally and eventually die. - Loss of connections between neurons responsible for memory and learning. Neurons can't survive when they lose their connections to other neurons. As neurons die throughout the brain, the affected regions begin to atrophy, or shrink. By the final stage of AD, damage is widespread and brain tissue has shrunk significantly."}
{"_id":"81c2e8a9-0130-43b8-8ac9-0cf82db8c509","text":"Currently there are no medicines that can slow the progression of AD. However, four FDA-approved medications are used to treat AD symptoms. These drugs help individuals carry out the activities of daily living by maintaining thinking, memory, or speaking skills. They can also help with some of the behavioral and personality changes associated with AD. However, they will not stop or reverse AD and appear to help individuals for only a few months to a few years. Donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne) are prescribed to treat mild to moderate AD symptoms. Donepezil was recently approved to treat severe AD as well. The newest AD medication is memantine (Namenda), which is prescribed to treat moderate to severe AD symptoms."}
{"_id":"505d0d9e-9872-4ce2-a944-2a962a81839f","text":"In very few families, people develop AD in their 30s, 40s, and 50s. This is known as \"early onset\" AD. These individuals have a mutation in one of three different inherited genes that causes the disease to begin at an earlier age. More than 90 percent of AD develops in people older than 65. This form of AD is called \"late-onset\" AD, and its development and pattern of damage in the brain is similar to that of early-onset AD. The course of this disease varies from person to person, as does the rate of decline. In most people with AD, symptoms first appear after age 65.\n                \nWe don't yet completely understand the causes of late-onset AD, but they probably include genetic, environmental, and lifestyle factors. Although the risk of developing AD increases with age, AD and dementia symptoms are not a part of normal aging. There are also some forms of dementia that aren't related to brain diseases such as AD, but are caused by systemic abnormalities such as metabolic syndrome, in which the combination of high blood pressure, high cholesterol, and diabetes causes confusion and memory loss."}
{"_id":"363f2314-d86f-4131-bf05-12fa358a82c0","text":"The National Institute of Neurological Disorders and Stroke (NINDS) supports basic and translational research related to AD through grants to major medical institutions across the country. Current studies are investigating how the development of beta amyloid plaques damages neurons, and how abnormalities in tau proteins create the characteristic neurofibrillary tangles of AD. Other research is exploring the impact of risk factors associated with the development of AD, such as pre-existing problems with blood flow in the blood vessels of the brain. Most importantly, the NINDS supports a number of studies that are developing and testing new and novel therapies that can relieve the symptoms of AD and potentially lead to a cure.\n                \nOn May 15, 2012 the Obama Administration announced the release of the National Alzheimers Plan. U.S. Secretary of Health and Human Services Kathleen Sebelius reaffirmed our nations commitment to conquering Alzheimers disease and related dementias, with a specific goal of finding effective ways to prevent and treat the disease by 2025."}
{"_id":"19468818-c78c-42c1-9bec-3a77ef1ad91e","text":"Incontinentia pigmenti (IP) is an inherited disorder of skin pigmentation that is also associated with abnormalities of the teeth, skeletal system, eyes, and central nervous system. It is one of a group of gene-linked diseases known as neurocutaneous disorders. In most cases, IP is caused by mutations in a gene called NEMO (NF-kappaB essential modulator). Males are more severely affected than females. Discolored skin is caused by excessive deposits of melanin (normal skin pigment). Most newborns with IP will develop discolored skin within the first two weeks. The pigmentation involves the trunk and extremities, is slate-grey, blue or brown, and is distributed in irregular marbled or wavy lines. The discoloration fades with age. Neurological problems include loss of brain tissue (known as cerebral atrophy), the formation of small cavities in the central white matter of the brain, and the loss of neurons in the cerebellar cortex. About 20% of children with IP will have slow motor development, muscle weakness in one or both sides of the body, impaired cognitive development, and seizures. They are also likely to have visual problems, including crossed eyes, cataracts, and severe visual loss. Dental problems are also common, including missing or peg-shaped teeth. A related disorder, incontinentia pigmenti achromians, features skin patterns of light, unpigmented swirls and streaks that are the reverse of IP. Associated neurological problems are similar."}
{"_id":"e86a781d-9502-4def-bf00-aac28a9344be","text":"The skin abnormalities of IP usually disappear by adolescence or adulthood without treatment. Diminished vision may be treated with corrective lenses, medication, or, in severe cases, surgery. A specialist may treat dental problems. Neurological symptoms such as seizures, muscle spasms, or mild paralysis may be controlled with medication and\/or medical devices and with the advice of a neurologist."}
{"_id":"4bbb5d68-5606-4970-9626-11d4f77814b2","text":"Although the skin abnormalities usually regress, and sometimes disappear completely, there may be residual neurological difficulties."}
{"_id":"00d6ad90-9141-4d64-bd56-6bd52df2434b","text":"Researchers have begun to use genetic linkage studies to map the location of genes associated with the neurocutaneous disorders. Research supported by the NINDS includes studies to understand how the brain and nervous system normally develop and function and how they are affected by genetic mutations. These studies contribute to a greater understanding of gene-linked disorders such as IP, and have the potential to open promising new avenues of treatment."}
{"_id":"c37c0966-92d9-461a-bd1b-e6836e8e65ec","text":"Whipple's disease is a multi-system infectious bacterial disease that interferes with the body's ability to metabolize fats. Caused by the bacterium Tropheryma whipplei, the disorder can affect any system in the body, including the brain, eyes, heart, joints, and lungs, but usually occurs in the gastrointestinal system. Neurological symptoms occur in up to 40 percent of individuals and may include dementia, abnormalities of eye and facial muscle movements, headaches, seizures, loss of muscle control, memory loss, weakness, and vision problems. Gastrointestinal symptoms may include diarrhea, weight loss, fatigue, weakness, and abdominal bleeding and pain. Fever, cough, anemia, heart and lung damage, darkening of the skin, and joint soreness may also be present. The disease is more common in men and neurological symptoms are more common in individuals who have severe abdominal disease, Rarely, neurological symptoms may appear without gastrointestinal symptoms and can mimic symptoms of almost any neurologic disease.."}
{"_id":"5eb9ba86-cf91-40c1-aeeb-7e256196d0d3","text":"The standard treatment for Whipple's disease is a prolonged course of antibiotics (up to two years), including penicillin and cefriaxone or doxycycline with hydroxychloroquine. Sulfa drugs (sulfonamides) such as sulfadizine or solfamethoxazole can treat neurological symptoms. Relapsing neurologic Whipple's disease. (marked by bouts of worsening of symptoms) is sometimes treated with a combination of antibiotics and weekly injections of interfron gamma, a substance made by the body that activates the immune system."}
{"_id":"3cc6a2cc-2b13-41a7-b554-ecf1f6249349","text":"Generally, long-term antibiotic treatment to destroy the bacteria can relieve symptoms and cure the disease. If left untreated, the disease is progressive and fatal. Individuals with involvement of the central nervous system generally have a worse prognosis and may be left with permanent neurologic disability. Deficits may persist and relapses may still occur in individuals who receive appropriate treatment in a timely fashion. Prognosis may improve with earlier recognition, diagnosis, and treatment of the disorder."}
{"_id":"b9f2ccb9-c851-4161-8388-45605d662932","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS supportsa broad range of research on disorders that affect the central nervous system. The National Institute of Diabetes and Digestive and Kidney Diseases also supports research on disorders such as Whipple's disease. Much of this research is aimed at learning more about these disorders and finding ways to prevent, treat, and, ultimately, cure them."}
{"_id":"e3094c7c-44f1-4c28-b7c1-ac1afc002594","text":"Landau-Kleffner syndrome (LKS) is a rare, childhood neurological disorder characterized by the sudden or gradual development of aphasia (the inability to understand or express language) and an abnormal electro-encephalogram (EEG). LKS affects the parts of the brain that control comprehension and speech. The disorder usually occurs in children between the ages of 5 and 7 years. Typically, children with LKS develop normally but then lose their language skills for no apparent reason. While many of the affected individuals have seizures, some do not. The disorder is difficult to diagnose and may be misdiagnosed as autism, pervasive developmental disorder, hearing impairment, learning disability, auditory\/verbal processing disorder, attention deficit disorder, childhood schizophrenia, or emotional\/behavioral problems."}
{"_id":"9b3a59ad-80b4-4f65-a849-e2af70270d47","text":"Treatment for LKS usually consists of medications, such as anticonvulsants and corticosteroids, and speech therapy, which should be started early. A controversial treatment option involves a surgical technique called multiple subpial transection in which the pathways of abnormal electrical brain activity are severed"}
{"_id":"efb386c4-a941-4a6c-8d56-19f9b936e1c6","text":"The prognosis for children with LKS varies. Some affected children may have a permanent severe language disorder, while others may regain much of their language abilities (although it may take months or years). In some cases, remission and relapse may occur. The prognosis is improved when the onset of the disorder is after age 6 and when speech therapy is started early. Seizures generally disappear by adulthood."}
{"_id":"adcb6b3c-b354-4483-be94-70ee64de57bd","text":"The NINDS supports broad and varied programs of research on epilepsy and developmental disorders. This research is aimed at discovering new ways to prevent, diagnose, and treat epilepsy and developmental disorders and, ultimately, to find cures for them."}
{"_id":"68b7e92b-c196-4164-802a-248381967a29","text":"Central pain syndrome is a neurological condition caused by damage to or dysfunction of the central nervous system (CNS), which includes the brain, brainstem, and spinal cord. This syndrome can be caused by stroke, multiple sclerosis, tumors, epilepsy, brain or spinal cord trauma, or Parkinson's disease. The character of the pain associated with this syndrome differs widely among individuals partly because of the variety of potential causes. Central pain syndrome may affect a large portion of the body or may be more restricted to specific areas, such as hands or feet. The extent of pain is usually related to the cause of the CNS injury or damage. Pain is typically constant, may be moderate to severe in intensity, and is often made worse by touch, movement, emotions, and temperature changes, usually cold temperatures. Individuals experience one or more types of pain sensations, the most prominent being burning. Mingled with the burning may be sensations of \"pins and needles;\" pressing, lacerating, or aching pain; and brief, intolerable bursts of sharp pain similar to the pain caused by a dental probe on an exposed nerve. Individuals may have numbness in the areas affected by the pain. The burning and loss of touch sensations are usually most severe on the distant parts of the body, such as the feet or hands. Central pain syndrome often begins shortly after the causative injury or damage, but may be delayed by months or even years, especially if it is related to post-stroke pain."}
{"_id":"67ffd843-c2b4-4b3f-89d3-a4f5c643ae9b","text":"Pain medications often provide some reduction of pain, but not complete relief of pain, for those affected by central pain syndrome. Tricyclic antidepressants such as nortriptyline or anticonvulsants such as neurontin (gabapentin) can be useful. Lowering stress levels appears to reduce pain."}
{"_id":"984a8e45-e20f-47fa-b801-ab867b85f145","text":"Central pain syndrome is not a fatal disorder, but the syndrome causes disabling chronic pain and suffering among the majority of individuals who have it."}
{"_id":"91ded947-b0e5-4a85-a2b9-3af4fa16a4e4","text":"The NINDS vigorously pursues a research program seeking new treatments for chronic pain and nervous system damage. The goals of this research are to develop ways to more effectively treat and potentially reverse debilitating conditions such as central pain syndrome."}
{"_id":"07f26677-7478-47e4-a051-3b64e48e0d1f","text":"Complex regional pain syndrome (CRPS) is a chronic pain condition. The key symptom of CRPS is continuous, intense pain out of proportion to the severity of the injury, which gets worse rather than better over time. CRPS most often affects one of the arms, legs, hands, or feet. Often the pain spreads to include the entire arm or leg. Typical features include dramatic changes in the color and temperature of the skin over the affected limb or body part, accompanied by intense burning pain, skin sensitivity, sweating, and swelling. Doctors arent sure what causes CRPS. In some cases the sympathetic nervous system plays an important role in sustaining the pain. Another theory is that CRPS is caused by a triggering of the immune response, which leads to the characteristic inflammatory symptoms of redness, warmth, and swelling in the affected area."}
{"_id":"13a7bcbe-7c1b-4be5-8847-ee67bb3639c1","text":"Because there is no cure for CRPS, treatment is aimed at relieving painful symptoms. Doctors may prescribe topical analgesics, antidepressants, corticosteroids, and opioids to relieve pain. However, no single drug or combination of drugs has produced consistent long-lasting improvement in symptoms. Other treatments may include physical therapy, sympathetic nerve block, spinal cord stimulation, and intrathecal drug pumps to deliver opioids and local anesthetic agents via the spinal cord."}
{"_id":"942dd715-2d58-4acf-abd3-8f941294322b","text":"The prognosis for CRPS varies from person to person. Spontaneous remission from symptoms occurs in certain individuals. Others can have unremitting pain and crippling, irreversible changes in spite of treatment."}
{"_id":"11420a3a-8ce4-4e6f-adf1-65d2c04222f8","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research relating to CRPS and also support additional research through grants to major medical institutions across the country. NINDS-supported scientists are studying new approaches to treat CRPS and intervene more aggressively after traumatic injury to lower the chances of developing the disorder. Researchers hope to identify specific cellular and molecular changes in sensory neurons following peripheral nerve injury to better understand the processes that underlie neuroplasticity (the brains ability to reorganize or form new nerve connections and pathways following injury or death of nerve cells). Identifying these mechanisms could provide targets for new drug therapies that could improve recovery following regeneration. Other researchers hope to better understand how CRPS develops by studying immune system activation and peripheral nerve signaling using an animal model of the disorder."}
{"_id":"5481ab30-2f8a-4906-bf9f-1d4e27210775","text":"Arteriovenous malformations (AVMs) are abnormal, snarled tangles of blood vessels that cause multiple irregular connections between the arteries and veins. These malformations most often occur in the spinal cord and in any part of the brain or on its surface, but can develop elsewhere in the body. AVMs can damage the brain and spinal cord by reducing the amount of oxygen reaching neurological tissues, bleeding into surrounding tissue (hemorrhage) that can cause stroke or brain damage, and by compressing or displacing parts of the brain or spinal cord. Many people with an AVM experience few, if any, significant symptoms, which can include headache, weakness, seizures, pain, and problems with speech, vision, or movement. Most often AVMs are congenital, but they can appear sporadically. In some cases the AVM may be inherited, but it is more likely that other inherited conditions increase the risk of having an AVM. The malformations tend to be discovered only incidentally, usually during treatment for an unrelated disorder or at autopsy."}
{"_id":"aa5ac9d4-fafa-4541-ab09-dea811a9ed29","text":"Treatment options depend on the type of AVM, its location, noticeable symptoms, and the general health condition of the individual. Medication can often alleviate general symptoms such as headache, back pain, and seizures caused by AVMs and other vascular lesions. The definitive treatment for AVMs is either surgery to either remove the AVM or to create an artificial blood clot to close the lesion or focused irradiation treatment that is designed to damage the blood vessel walls and close the lesion. The decision to treat an AVM requires a careful consideration of possible benefits versus risks."}
{"_id":"4df26715-3c65-4bdd-ae06-8617e8e8e4d4","text":"The greatest potential danger posed by AVMs is hemorrhage. Most episodes of bleeding remain undetected at the time they occur because they are not severe enough to cause significant neurological damage. But massive, even fatal, bleeding episodes do occur. Whenever an AVM is detected, the individual should be carefully and consistently monitored for any signs of instability that may indicate an increased risk of hemorrhage. Individuals who are treated require brain imaging afterwards to evaluate if the AVM has been completely removed or destroyed. The risk of hemorrhage remains if some of the AVM persists despite treatment."}
{"_id":"b56839f5-d8c1-427c-9ed1-c712dcdcf2c0","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. The NINDS has established an Arteriovenous Study Group to learn more about the natural causes of AVMs and to improve surgical treatment of these lesions. An NINDS study at Columbia University, A Randomized Trial of Unruptured Brain AVMs (ARUBA), showed that medical management alone is superior to medical management and interventional therapy (conventional surgery, endovascular procedures, and radiosurgery) for improving the long-term outcome of individuals with unruptured brain arteriovenous malformations. Data from a recently closed observational phase will show if the disparities continued over the additional five years of follow-up.\n                \nAmong other NINDS-funded research, scientists are testing a class of drugs called beta-blockers to see if they may lead to the development of new treatments for people with vascular malformations. Other NINDS-funded investigators hope to develop biomarkers (signs that may indicate risk of a disease) for AVM that may improve risk assessment and aid in the choice of therapy that may provide maximize benefit with minimal risk to the individual. Additional NINDS-funded research hopes to determine molecular pathways fundamental to the formation of brain AVMs."}
{"_id":"233e44e4-7b18-4662-93ed-7d7df30b1e0d","text":"Ataxia-telangiectasia is a rare, childhood neurological disorder that causes degeneration in the part of the brain that controls motor movements and speech. The first signs of the disease are unsteady walking and slurred speech, usually occurring during the first five years of life. Telangiectasias (tiny, red \"spider\" veins), which appear in the corners of the eyes or on the surface of the ears and cheeks, are characteristic of the disease, but are not always present and generally do not appear in the first years of life. About 35 percent of those with A-T develop cancer, most frequently acute lymphocytic leukemia or lymphoma. The most unusual symptom is an acute sensitivity to ionizing radiation, such as X-rays or gamma rays. Many individuals with A-T have a weakened immune system, making them susceptible to recurrent respiratory infections. Other features of the disease may include mild diabetes mellitus, premature graying of the hair, difficulty swallowing, and delayed physical and sexual development. Children with A-T usually have normal or above normal intelligence."}
{"_id":"eb99cc04-d62e-499d-8a2d-82dec4f144fc","text":"There is no cure for A-T and, currently, no way to slow the progression of the disease. Treatment is symptomatic and supportive. Physical and occupational therapy help to maintain flexibility. Speech therapy is important, teaching children to control air flow to the vocal cords. Gamma-globulin injections may be useful if immunoglobulin levels are sufficiently reduced to weaken the immune system. High-dose vitamin regimens and antioxidants such as alpha lipoic acid also may also be used."}
{"_id":"6f8b3ce1-d10e-40df-90d2-aa1c091f43c8","text":"Average lifespan has been improving for years, for unknown reasons, and varies with the severity of the underlying mutations, ATM (ataxia-telangiectasia mutated) protein levels, and residual ATM kinase activity. Some individuals with later onset of disease and slower progression survive into their 50s."}
{"_id":"914bc41c-86c6-45c5-8aca-35b623f77ed2","text":"NINDS-supported researchers discovered the gene responsible for A-T, known as ATM (ataxia-telangiectasia mutated) in 1995. This gene makes a protein that activates many (probably more than 700) other proteins that control cell cycle, DNA repair, and cell death. Without it, cells are unable to activate the cellular checkpoints that protect against the damage of ionizing radiation and other agents that can harm DNA. In addition to supporting basic research on A-T, NINDS also funds research aimed at A-T drug development, including development of animal models, gene and stem-cell based therapies, and high-throughput drug screens. The NINDS also leads a trans-NIH A-T Working Group whose members include NINDS, NHLBI, NIEHS, NCI, NEI, NIGMS, NHGRI, NIA, NIAID, NICHD, and ORD."}
{"_id":"bbbf7d99-9564-451e-85d5-f36b3e002f83","text":"Klver-Bucy syndrome is a rare behavioral impairment that is associated with damage to both of the anterior temporal lobes of the brain. It causes individuals to put objects in their mouths and engage in inappropriate sexual behavior. Other symptoms may include visual agnosia (inability to visually recognize objects), loss of normal fear and anger responses, memory loss, distractibility, seizures, and dementia. The disorder may be associated with herpes encephalitis and trauma, which can result in brain damage."}
{"_id":"20ccbb29-cd91-4410-83d1-c6a9eddcb6eb","text":"Treatment is symptomatic and supportive, and may include drug therapy."}
{"_id":"148d28be-883b-4982-84a7-d017d49befc7","text":"There is no cure for Klver-Bucy syndrome. The disorder is not life-threatening, but the patient can be difficult to manage. With treatment, symptoms may slowly decline."}
{"_id":"11078e1e-1d7d-4e91-8118-372a10aa3dfa","text":"NINDS supports and conducts research on neurobehavioral disorders such as Klver-Bucy syndrome. Much of the research focuses on learning more about these disorders and finding ways to prevent and treat them."}
{"_id":"7191128b-8df7-4c8d-8729-f16d80b8bc7e","text":"Niemann-Pick disease (NP) refers to a group of inherited metabolic disorders known as lipid storage diseases. Lipids (fatty materials such as waxes, fatty acids, oils, and cholesterol) and proteins are usually broken down into smaller components to provide energy for the body. In Niemann-Pick disease, harmful quantities of lipids accumulate in the brain, spleen, liver, lungs, and bone marrow. Neurological symptoms may include ataxia (lack of muscle control during voluntary movements such as walking), loss of muscle tone, brain degeneration, increased sensitivity to touch, spasticity (stiff muscles and awkward movement), and slurred speech. Other symptoms may include feeding and swallowing difficulties, eye paralysis, learning problems, and an enlarged liver and spleen. There may be clouding of the cornea and a characteristic cherry-red halo develops around the center of the retina. The disease has three categories. Type A, the most severe form, occurs in early infancy and is seen primarily in Jewish families. It is characterized by progressive weakness, an enlarged liver and spleen, swollen lymph nodes, and profound brain damage by six months of age. Children with this type rarely live beyond 18 months. Type B usually occurs in the pre-teen years, with symptoms that include ataxia and peripheral neuropathy. The brain is generally not affected. Other symptoms include enlarged liver and spleen, and pulmonary difficulties. In types A and B, insufficient activity of an enzyme called sphingomyelinase causes the build up of toxic amounts of sphingomyelin, a fatty substance present in every cell of the body. Type C may appear early in life or develop in the teen or adult years. It is caused by a lack of the NPC1 or NPC2 proteins. Affected individuals may have extensive brain damage that can cause an inability to look up and down, difficulty in walking and swallowing, and progressive loss of vision and hearing. There may be moderate enlargement of the spleen and liver. Individuals wit Type C who share a common ancestral background in Nova Scotia were previously referred to as Type D."}
{"_id":"5253b0e4-f457-4aae-bf63-9440619b40b7","text":"There is currently no cure for Niemann-Pick disease. Treatment is supportive. Children usually die from infection or progressive neurological loss. There is currently no effective treatment for persons with type A. Bone marrow transplantation has been attempted in a few individuals with type B. The development of enzyme replacement and gene therapies might also be helpful for those with type B. restricting one's diet does not prevent the buildup of lipids in cells and tissues."}
{"_id":"d323143b-3120-4c56-8f0e-063dd376c900","text":"Infants with type A die in infancy. Children with Type B may live a comparatively long time, but may require supplemental oxygen because of lung impairment. The life expectancy of persons with type C varies: some individuals die in childhood while others who appear to be less severely affected can live into adulthood."}
{"_id":"420506a5-81c3-460e-ac4f-a1562692f4fc","text":"The National Institute of Neurological Disorders and Stroke (NINDS), a part of the National Institutes of Health (NIH), conducts and supports research about Niemann-Pick disease through research grants to research institutions across the country. Investigators at the NINDS have identified two different genes that, when defective, contribute to Niemann-Pick disease type C. NINDS scientists are studying the mechanisms by which lipids accumulating in these storage diseases causes harm to the body. Additional research studies hope to identify biomarkers (signs that may indicate risk of a disease and improve diagnosis) for the lipid storage disorders."}
{"_id":"a09e153d-928e-402e-94dc-5e55917ee53d","text":"Lennox-Gastaut syndrome is a severe form of epilepsy. Seizures usually begin before 4 years of age. Seizure types, which vary among patients, include tonic (stiffening of the body, upward deviation of the eyes, dilation of the pupils, and altered respiratory patterns), atonic (brief loss of muscle tone and consciousness, causing abrupt falls), atypical absence (staring spells), and myoclonic (sudden muscle jerks). There may be periods of frequent seizures mixed with brief, relatively seizure-free periods. Most children with Lennox-Gastaut syndrome experience some degree of impaired intellectual functioning or information processing, along with developmental delays, and behavioral disturbances. Lennox-Gastaut syndrome can be caused by brain malformations, perinatal asphyxia, severe head injury, central nervous system infection and inherited degenerative or metabolic conditions. In 30-35 percent of cases, no cause can be found."}
{"_id":"051ea076-58a3-4abd-95ac-ff3502fa53de","text":"Treatment for Lennox-Gastaut syndrome includes clobazam and anti-epileptic medications such as valproate, lamotrigine, felbamate, or topiramate. There is usually no single antiepileptic medication that will control seizures. Children who improve initially may later show tolerance to a drug or have uncontrollable seizures."}
{"_id":"cc5e4802-9097-427d-a07a-9b56170d7596","text":"The prognosis for individuals with Lennox-Gastaut syndrome varies. There is no cure for the disorder. Complete recovery, including freedom from seizures and normal development, is very unusual."}
{"_id":"9955e257-3c58-4d81-8b62-b4f5470d18b5","text":"The NINDS conducts and supports a broad program of basic and clinical research on epilepsy including Lennox-Gastaut syndrome. These studies are aimed at finding the causes of these disorders, improving the diagnosis, and developing new medications and other therapies."}
{"_id":"2a76b158-b1ee-479c-b3f6-6bb9269ece08","text":"Paresthesia refers to a burning or prickling sensation that is usually felt in the hands, arms, legs, or feet, but can also occur in other parts of the body. The sensation, which happens without warning, is usually painless and described as tingling or numbness, skin crawling, or itching.  Most people have experienced temporary paresthesia -- a feeling of \"pins and needles\" -- at some time in their lives when they have sat with legs crossed for too long, or fallen asleep with an arm crooked under their head. It happens when sustained pressure is placed on a nerve. The feeling quickly goes away once the pressure is relieved.  Chronic paresthesia is often a symptom of an underlying neurological disease or traumatic nerve damage. Paresthesia can be caused by disorders affecting the central nervous system, such as stroke and transient ischemic attacks (mini-strokes), multiple sclerosis, transverse myelitis, and encephalitis. A tumor or vascular lesion pressed up against the brain or spinal cord can also cause paresthesia. Nerve entrapment syndromes, such as carpal tunnel syndrome, can damage peripheral nerves and cause paresthesia accompanied by pain. Diagnostic evaluation is based on determining the underlying condition causing the paresthetic sensations. An individual's medical history, physical examination, and laboratory tests are essential for the diagnosis. Physicians may order additional tests depending on the suspected cause of the paresthesia."}
{"_id":"9b9b128d-3562-4ba6-9d43-dfa11b76a19f","text":"The appropriate treatment for paresthesia depends on accurate diagnosis of the underlying cause."}
{"_id":"adaf0644-7d59-4d0b-9dfd-3d827795f825","text":"The prognosis for those with paresthesia depends on the severity of the sensations and the associated disorders."}
{"_id":"ead8d58c-a1cd-4e98-a1e4-4252b662c752","text":"The NINDS supports research on disorders of the brain, spinal cord, and peripheral nerves that can cause paresthesia. The goals of this research are to increase scientific understanding of these disorders and to find ways to prevent, treat, and cure them."}
{"_id":"72e60ebb-8c49-4701-9b7a-fcc80e4c9d4a","text":"Myoclonus refers to a sudden, involuntary jerking of a muscle or group of muscles. In its simplest form, myoclonus consists of a muscle twitch followed by relaxation. A hiccup is an example of this type of myoclonus. Other familiar examples of myoclonus are the jerks or \"sleep starts\" that some people experience while drifting off to sleep. These simple forms of myoclonus occur in normal, healthy persons and cause no difficulties. When more widespread, myoclonus may involve persistent, shock-like contractions in a group of muscles. Myoclonic jerking may develop in people with multiple sclerosis, Parkinson's disease, Alzheimer's disease, or Creutzfeldt-Jakob disease. Myoclonic jerks commonly occur in persons with epilepsy, a disorder in which the electrical activity in the brain becomes disordered and leads to seizures. Myoclonus may develop in response to infection, head or spinal cord injury, stroke, brain tumors, kidney or liver failure, lipid storage disease, chemical or drug poisoning, or other disorders. It can occur by itself, but most often it is one of several symptoms associated with a wide variety of nervous system disorders."}
{"_id":"705fc397-5702-47d0-badf-60e3dd3b6452","text":"Treatment of myoclonus focuses on medications that may help reduce symptoms. The drug of first choice is clonazepam, a type of tranquilizer. Many of the drugs used for myoclonus, such as barbiturates, phenytoin, and primidone, are also used to treat epilepsy. Sodium valproate is an alternative therapy for myoclonus and can be used either alone or in combination with clonazepam. Myoclonus may require the use of multiple drugs for effective treatment."}
{"_id":"2b2f766a-143a-4efc-891b-7f33696e15e0","text":"Simple forms of myoclonus occur in normal, healthy persons and cause no difficulties. In some cases, myoclonus begins in one region of the body and spreads to muscles in other areas. More severe cases of myoclonus can distort movement and severely limit a person's ability to eat, talk, or walk. These types of myoclonus may indicate an underlying disorder in the brain or nerves. Although clonazepam and sodium valproate are effective in the majority of people with myoclonus, some people have adverse reactions to these drugs. The beneficial effects of clonazepam may diminish over time if the individual develops a tolerance for the drug."}
{"_id":"68226052-f27a-4dcd-843e-7c7c66e9b687","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research relating to myoclonus in its laboratories at the National Institutes of Health (NIH) and also supports additional research through grants to major medical institutions across the country. Scientists are seeking to understand the underlying biochemical basis of involuntary movements and to find the most effective treatment for myoclonus and other movement disorders. Researchers may be able to develop drug treatments that target specific biochemical changes involved in myoclonus. By combining several of these drugs, scientists hope to achieve greater control of myoclonic symptoms."}
{"_id":"7ba800f8-d414-437d-855a-44fcbfcf803b","text":"Dermatomyositis is one of a group of muscle diseases known as the inflammatory myopathies, which are characterized by chronic muscle inflammation accompanied by muscle weakness. Dermatomyositis cardinal symptom is a skin rash that precedes, accompanies, or follows progressive muscle weakness. The rash looks patchy, with purple or red discolorations, and characteristically develops on the eyelids and on muscles used to extend or straighten joints, including knuckles, elbows, knees, and toes. Red rashes may also occur on the face, neck, shoulders, upper chest, back, and other locations, and there may be swelling in the affected areas. The rash sometimes occurs without obvious muscle involvement. Adults with dermatomyositis may experience weight loss, a low-grade fever, inflamed lungs, and be sensitive to light such that the rash or muscle disease gets worse. Children and adults with dermatomyositis may develop calcium deposits, which appear as hard bumps under the skin or in the muscle (called calcinosis). Calcinosis most often occurs 1-3 years after the disease begins. These deposits are seen more often in children with dermatomyositis than in adults. In some cases of dermatomyositis, distal muscles (muscles located away from the trunk of the body, such as those in the forearms and around the ankles and wrists) may be affected as the disease progresses. Dermatomyositis may be associated with collagen-vascular or autoimmune diseases, such as lupus."}
{"_id":"4433602e-d98b-4c69-9203-8a94efaa402e","text":"There is no cure for dermatomyositis, but the symptoms can be treated. Options include medication, physical therapy, exercise, heat therapy (including microwave and ultrasound), orthotics and assistive devices, and rest. The standard treatment for dermatomyositis is a corticosteroid drug, given either in pill form or intravenously. Immunosuppressant drugs, such as azathioprine and methotrexate, may reduce inflammation in people who do not respond well to prednisone. Periodic treatment using intravenous immunoglobulin can also improve recovery. Other immunosuppressive agents used to treat the inflammation associated with dermatomyositis include cyclosporine A, cyclophosphamide, and tacrolimus. Physical therapy is usually recommended to prevent muscle atrophy and to regain muscle strength and range of motion. Many individuals with dermatomyositis may need a topical ointment, such as topical corticosteroids, for their skin disorder. They should wear a high-protection sunscreen and protective clothing. Surgery may be required to remove calcium deposits that cause nerve pain and recurrent infections."}
{"_id":"a1e92e4d-b7f0-49db-ab39-b1d0eed63196","text":"Most cases of dermatomyositis respond to therapy. The disease is usually more severe and resistant to therapy in individuals with cardiac or pulmonary problems."}
{"_id":"25919bb0-97fe-4203-a22e-cc190fb06d07","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research relating to dermatomyositis in laboratories at the NIH and support additional research through grants to major medical institutions across the country. Currently funded research is exploring patterns of gene expression among the inflammatory myopathies, the role of viral infection as a precursor to the disorders, and the safety and efficacy of various treatment regimens."}
{"_id":"6024a743-c473-462d-baa3-3b3596e4865c","text":"Agnosia is a rare disorder characterized by an inability to recognize and identify objects or persons. People with agnosia may have difficulty recognizing the geometric features of an object or face or may be able to perceive the geometric features but not know what the object is used for or whether a face is familiar or not. Agnosia can be limited to one sensory modality such as vision or hearing. For example, a person may have difficulty in recognizing an object as a cup or identifying a sound as a cough. Agnosia can result from strokes, dementia, developmental disorders, or other neurological conditions. It typically results from damage to specific brain areas in the occipital or parietal lobes of the brain. People with agnosia may retain their cognitive abilities in other areas."}
{"_id":"c9dd694e-3fc1-4e37-8840-85590d160040","text":"Treatment is generally symptomatic and supportive. The primary cause of the disorder should be determined in order to treat other problems that may contribute to or result in agnosia."}
{"_id":"0df24929-523e-4866-a05f-ce9d76488019","text":"Agnosia can compromise quality of life."}
{"_id":"6648026e-62c3-403d-bf90-e4f88b4fcee3","text":"The NINDS supports research on disorders of the brain such as agnosia with the goal of finding ways to prevent or cure them."}
{"_id":"c3d0c196-a223-4f21-b269-21fa6ca12b04","text":"Rett syndrome is a childhood neurodevelopmental disorder that affects females almost exclusively. The child generally appears to grow and develop normally, before symptoms begin. Loss of muscle tone is usually the first symptom. Other early symptoms may include a slowing of development, problems crawling or walking, and diminished eye contact. As the syndrome progresses, a child will lose purposeful use of her hands and the ability to speak. Compulsive hand movements such as wringing and washing follow the loss of functional use of the hands. The inability to perform motor functions is perhaps the most severely disabling feature of Rett syndrome, interfering with every body movement, including eye gaze and speech."}
{"_id":"c4056bb4-0271-465e-b762-89170ee2d887","text":"There is no cure for Rett syndrome. Treatment for the disorder is symptomatic, focusing on the management of symptoms, and supportive. Medication may be needed for breathing irregularities and motor difficulties, and antiepileptic drugs may be used to control seizures. Occupational therapy, physiotherapy, and hydrotherapy may prolong mobility. Some children may require special equipment and aids such as braces to arrest scoliosis, splints to modify hand movements, and nutritional programs to help them maintain adequate weight. Special academic, social, vocational, and support services may be required in some cases."}
{"_id":"6c85ff30-75be-482f-8289-6b75824fbc47","text":"The course of Rett syndrome, including the age of onset and the severity of symptoms, varies from child to child. Despite the difficulties with symptoms, most individuals with Rett syndrome continue to live well into middle age and beyond. Because the disorder is rare, very little is known about long-term prognosis and life expectancy."}
{"_id":"2620b156-0893-439a-b38c-11484f39ab72","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to Rett syndrome in laboratories at the NIH, and also support additional Rett syndrome research through grants to major medical institutions across the country. The discovery of the Rett syndrome gene in 1999 provides a basis for further genetic studies. Understanding the cause of this disorder is necessary for developing new therapies to manage specific symptoms, as well as for providing better methods of diagnosis."}
{"_id":"ceea6591-0f05-4732-9ba3-0969eff1d6b8","text":"The brachial plexus is a network of nerves that conducts signals from the spine to the shoulder, arm, and hand. Brachial plexus injuries are caused by damage to those nerves. Symptoms may include a limp or paralyzed arm; lack of muscle control in the arm, hand, or wrist; and a lack of feeling or sensation in the arm or hand. Brachial plexus injuries can occur as a result of shoulder trauma, tumors, or inflammation. There is a rare syndrome called Parsonage-Turner Syndrome, or brachial plexitis, which causes inflammation of the brachial plexus without any obvious shoulder injury. This syndrome can begin with severe shoulder or arm pain followed by weakness and numbness. In infants, brachial plexus injuries may happen during birth if the babys shoulder is stretched during passage in the birth canal (see Brachial Plexus Birth Injuries). \n                \nThe severity of a brachial plexus injury is determined by the type of damage done to the nerves. The most severe type, avulsion, is caused when the nerve root is severed or cut from the spinal cord. There is also an incomplete form of avulsion in which part of the nerve is damaged and which leaves some opportunity for the nerve to slowly recover function. Neuropraxia, or stretch injury, is the mildest type of injury Neuropraxia damages the protective covering of the nerve, which causes problems with nerve signal conduction, but does not always damage the nerve underneath."}
{"_id":"2dd241e5-3d75-4ae1-a9bf-2588bf275f89","text":"Some brachial plexus injuries may heal without treatment. Many children who are injured during birth improve or recover by 3 to 4 months of age. Treatment for brachial plexus injuries includes physical therapy and, in some cases, surgery."}
{"_id":"39a25b0c-7dd6-4cea-84e8-d092cd32d557","text":"The site and type of brachial plexus injury determines the prognosis. For avulsion and rupture injuries, there is no potential for recovery unless surgical reconnection is made in a timely manner. The potential for recovery varies for neuroma and neuropraxia injuries. Most individuals with neuropraxia injuries recover spontaneously with a 90-100% return of function."}
{"_id":"62b87309-5d23-4ff8-a60a-ac28a375d2f8","text":"The NINDS conducts and supports research on injuries to the nervous system such as brachial plexus injuries. Much of this research is aimed at finding ways to prevent and treat these disorders."}
{"_id":"27cdd54d-4f18-402c-b57b-1179dd6c2c1b","text":"Dementia is not a specific disease. It is a descriptive term for a collection of symptoms that can be caused by a number of disorders that affect the brain. People with dementia have significantly impaired intellectual functioning that interferes with normal activities and relationships. They also lose their ability to solve problems and maintain emotional control, and they may experience personality changes and behavioral problems, such as agitation, delusions, and hallucinations. While memory loss is a common symptom of dementia, memory loss by itself does not mean that a person has dementia. Doctors diagnose dementia only if two or more brain functions - such as memory and language skills -- are significantly impaired without loss of consciousness. Some of the diseases that can cause symptoms of dementia are Alzheimers disease, vascular dementia, Lewy body dementia, frontotemporal dementia, Huntingtons disease, and Creutzfeldt-Jakob disease. Doctors have identified other conditions that can cause dementia or dementia-like symptoms including reactions to medications, metabolic problems and endocrine abnormalities, nutritional deficiencies, infections, poisoning, brain tumors, anoxia or hypoxia (conditions in which the brains oxygen supply is either reduced or cut off entirely), and heart and lung problems. Although it is common in very elderly individuals, dementia is not a normal part of the aging process."}
{"_id":"c640f4b6-3f26-4a56-9c86-80acf65e4c9e","text":"Drugs to specifically treat Alzheimers disease and some other progressive dementias are now available. Although these drugs do not halt the disease or reverse existing brain damage, they can improve symptoms and slow the progression of the disease. This may improve an individuals quality of life, ease the burden on caregivers, or delay admission to a nursing home. Many researchers are also examining whether these drugs may be useful for treating other types of dementia. Many people with dementia, particularly those in the early stages, may benefit from practicing tasks designed to improve performance in specific aspects of cognitive functioning. For example, people can sometimes be taught to use memory aids, such as mnemonics, computerized recall devices, or note taking."}
{"_id":"174d1929-e030-4d56-a166-a6dab0030df3","text":"There are many disorders that can cause dementia. Some, such as Alzheimers disease or Huntingtons disease, lead to a progressive loss of mental functions. But other types of dementia can be halted or reversed with appropriate treatment. People with moderate or advanced dementia typically need round-the-clock care and supervision to prevent them from harming themselves or others. They also may need assistance with daily activities such as eating, bathing, and dressing."}
{"_id":"71aca478-cd45-4dc0-9eea-79cc6e0eb1f1","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to dementia in laboratories at the NIH and also support additional dementia research through grants to major medical institutions across the country. Current research focuses on many different aspects of dementia. This research promises to improve the lives of people affected by the dementias and may eventually lead to ways of preventing or curing these disorders."}
{"_id":"abc0b2c4-6ead-4530-b0ed-5714803cb466","text":"The motor neuron diseases (MNDs) are a group of progressive neurological disorders that destroy cells that control essential muscle activity such as speaking, walking, breathing, and swallowing. Normally, messages from nerve cells in the brain (called upper motor neurons) are transmitted to nerve cells in the brain stem and spinal cord (called lower motor neurons) and from them to particular muscles. When there are disruptions in these signals, the result can be gradual muscle weakening, wasting away, and uncontrollable twitching (called fasciculations). Eventually, the ability to control voluntary movement can be lost. MNDs may be inherited or acquired, and they occur in all age groups. MNDs occur more commonly in men than in women, and symptoms may appear after age 40. In children, particularly in inherited or familial forms of the disease, symptoms can be present at birth or appear before the child learns to walk.\n                \nThe causes of sporadic (noninherited) MNDs are not known, but environmental, toxic, viral, or genetic factors may be implicated. Common MNDs include amyotrophic lateral sclerosis (ALS), progressive bulbar palsy, primary lateral sclerosis, and progressive muscular atrophy. Other MNDs include the many inherited forms of spinal muscular atrophy and post-polio syndrome, a condition that can strike polio survivors decades after their recovery from poliomyelitis."}
{"_id":"50ba4cac-7aab-4257-a62b-516132e7cab9","text":"There is no cure or standard treatment for the MNDs. Symptomatic and supportive treatment can help patients be more comfortable while maintaining their quality of life. The drug riluzole (Rilutek), which as of this date is the only drug approved by the U.S. Food and Drug Administration to treat ALS, prolongs life by 2-3 months but does not relieve symptoms. Other medicines that may help reduce symptoms include muscle relaxants such as baclofen, tizanidine, and the benzodiazepines for spasticity; glycopyrrolate and atropine to treat excessive saliva; and anticonvulsants and nonsteroidal anti-inflammatory drugs to relieve pain. Panic attacks can be treated with benzodiazepines. Some patients may require stronger medicines such as morphine to cope with musculoskeletal abnormalities or pain in later stages of the disorders, and opiates are used to provide comfort care in terminal stages of the disease.\n                \nPhysical and speech therapy, occupational therapy, and rehabilitation may help to improve posture, prevent joint immobility, slow muscle weakness and atrophy, and cope with swallowing difficulties. Applying heat may relieve muscle pain. Assistive devices such as supports or braces, orthotics, speech synthesizers, and wheelchairs help some patients retain independence. Proper nutrition and a balanced diet are essential to maintaining weight and strength."}
{"_id":"60153e46-6a31-4756-af22-420a1aa81a38","text":"Prognosis varies depending on the type of MND and the age of onset. Some MNDs, such as primary lateral sclerosis and Kennedy disease, are not fatal and progress slowly. Patients with spinal muscular atrophy may appear to be stable for long periods, but improvement should not be expected. Some MNDs, such as ALS and some forms of spinal muscular atrophy, are fatal."}
{"_id":"a6f8a64c-a62b-405c-88ab-8dc182c237eb","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS is a component of the National Institutes of Health (NIH), the leading supporter of biomedical research in the world. Researchers are testing whether different drugs, agents, or interventions are safe and effective in slowing the progression of motor neuron diseasess. NIH is also conducting clinical trials to study drugs to stimulate muscle growth in Kennedys disease and to suppress endogenous retroviruses in individuals with ALS. A large NIH-led collaborative study is investigating the genes and gene activity, proteins, and modifications of adult stem cell models from both healthy people and those with ALS,spinal muscular atrophy, and other neurodegenerative diseases to better understand the function of neurons and other support cells and identify candidate therapeutic compounds.\n                \n\n                \nconducts research related to the MNDs in its laboratories at the National Institutes of Health (NIH), and also supports additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders such as the MNDs."}
{"_id":"7b250fc3-d7e4-4b7d-add9-d54741239497","text":"Hydrocephalus is a condition in which the primary characteristic is excessive accumulation of cerebrospinal fluid (CSF) -- the clear fluid that surrounds the brain and spinal cord. This excessive accumulation results in an abnormal dilation of the spaces in the brain called ventricles. This dilation causes potentially harmful pressure on the tissues of the brain. Hydrocephalus may be congenital or acquired. Congenital hydrocephalus is present at birth and may be caused by genetic abnormalities or developmental disorders such as spina bifida and encephalocele. Acquired hydrocephalus develops at the time of birth or at some point afterward and can affect individuals of all ages. For example, hydrocephalus ex-vacuo occurs when there is damage to the brain caused by stroke or traumatic injury. Normal pressure hydrocephalus occurs most often among the elderly. It may result from a subarachnoid hemorrhage, head trauma, infection, tumor, or complications of surgery, although many people develop normal pressure hydrocephalus without an obvious cause. Symptoms of hydrocephalus vary with age, disease progression, and individual differences in tolerance to CSF. In infancy, the most obvious indication of hydrocephalus is often the rapid increase in head circumference or an unusually large head size. In older children and adults, symptoms may include headache followed by vomiting, nausea, papilledema (swelling of the optic disk, which is part of the optic nerve), downward deviation of the eyes (called \"sunsetting\"), problems with balance, poor coordination, gait disturbance, urinary incontinence, slowing or loss of development (in children), lethargy, drowsiness, irritability, or other changes in personality or cognition, including memory loss. Hydrocephalus is diagnosed through clinical neurological evaluation and by using cranial imaging techniques such as ultrasonography, computer tomography (CT), magnetic resonance imaging (MRI), or pressure-monitoring techniques."}
{"_id":"e7548788-699a-4a31-ae3b-3b95b1197191","text":"Hydrocephalus is most often treated with the surgical placement of a shunt system. This system diverts the flow of CSF from a site within the central nervous system to another area of the body where it can be absorbed as part of the circulatory process. A limited number of individuals can be treated with an alternative procedure called third ventriculostomy. In this procedure, a small hole is made in the floor of the third ventricle, allowing the CSF to bypass the obstruction and flow toward the site of resorption around the surface of the brain."}
{"_id":"58569262-d198-4377-9a6f-9958a262fadd","text":"The prognosis for individuals diagnosed with hydrocephalus is difficult to predict, although there is some correlation between the specific cause of hydrocephalus and the patient's outcome. Prognosis is further complicated by the presence of associated disorders, the timeliness of diagnosis, and the success of treatment. The symptoms of normal pressure hydrocephalus usually get worse over time if the condition is not treated, although some people may experience temporary improvements. If left untreated, progressive hydrocephalus is fatal, with rare exceptions. The parents of children with hydrocephalus should be aware that hydrocephalus poses risks to both cognitive and physical development. Treatment by an interdisciplinary team of medical professionals, rehabilitation specialists, and educational experts is critical to a positive outcome. Many children diagnosed with the disorder benefit from rehabilitation therapies and educational interventions, and go on to lead normal lives with few limitations."}
{"_id":"a78dfe9c-c7b2-4d87-8291-d6adc1050338","text":"The NINDS conducts and supports a wide range of fundamental studies that explore the complex mechanisms of normal brain development. Much of this research focuses on finding better ways to protect, treat, and ultimately cure disorders such as hydrocephalus."}
{"_id":"0d5f8b83-8ed0-464c-9093-ef85d1184afc","text":"Encephaloceles are rare neural tube defects characterized by sac-like protrusions of the brain and the membranes that cover it through openings in the skull. These defects are caused by failure of the neural tube to close completely during fetal development. The result is a groove down the midline of the upper part of the skull, or the area between the forehead and nose, or the back of the skull. When located in the back of the skull, encephaloceles are often associated with neurological problems. Usually encephaloceles are dramatic deformities diagnosed immediately after birth, but occasionally a small encephalocele in the nasal and forehead region can go undetected. Encephaloceles are often accompanied by craniofacial abnormalities or other brain malformations. Symptoms and associated abnormalities of encephaloceles may include hydrocephalus (excessive accumulation of cerebrospinal fluid in the brain), spastic quadriplegia (paralysis of the arms and legs), microcephaly (abnormally small head), ataxia (uncoordinated movement of the voluntary muscles, such as those involved in walking and reaching), developmental delay, vision problems, mental and growth retardation, and seizures. Some affected children may have normal intelligence. There is a genetic component to the condition; it often occurs in families with a history of spina bifida and anencephaly in family members."}
{"_id":"e038fe8e-0cf5-4bd3-9d25-45e2e67311a7","text":"Generally, surgery is performed during infancy to place the protruding tissues back into the skull, remove the sac, and correct the associated craniofacial abnormalities. Even large protrusions can often be removed without causing major functional disability. Hydrocephalus associated with encephaloceles may require surgical treatment with a shunt. Other treatment is symptomatic and supportive."}
{"_id":"98d88992-eb35-4cfa-8205-a0de2a17edf6","text":"The prognosis for individuals with encephaloceles varies depending on the type of brain tissue involved, the location of the sacs, and the accompanying brain malformations."}
{"_id":"506c9fe5-abe2-40da-8df9-ab33d09c3552","text":"The NINDS conducts and supports a wide range of studies that explore the complex mechanisms of normal brain development. The knowledge gained from these fundamental studies provides the foundation for understanding how this process can go awry and offers hope for new means to treat and prevent congenital brain disorders including neural tube defects such as encephaloceles."}
{"_id":"14aefdc1-833f-4328-a243-1684daf538d4","text":"Apraxia (called \"dyspraxia\" if mild) is a neurological disorder characterized by loss of the ability to execute or carry out skilled movements and gestures, despite having the desire and the physical ability to perform them. Apraxia results from dysfunction of the cerebral hemispheres of the brain, especially the parietal lobe, and can arise from many diseases or damage to the brain.  There are several kinds of apraxia, which may occur alone or together. The most common is buccofacial or orofacial apraxia, which causes the inability to carry out facial movements on command such as licking lips, whistling, coughing, or winking. Other types of apraxia include limb-kinetic apraxia (the inability to make fine, precise movements with an arm or leg), ideomotor apraxia (the inability to make the proper movement in response to a verbal command), ideational apraxia (the inability to coordinate activities with multiple, sequential movements, such as dressing, eating, and bathing), verbal apraxia (difficulty coordinating mouth and speech movements), constructional apraxia (the inability to copy, draw, or construct simple figures), and oculomotor apraxia (difficulty moving the eyes on command). Apraxia may be accompanied by a language disorder called aphasia. Corticobasal ganglionic degeneration is a disease that causes a variety of types of apraxia, especially in elderly adults."}
{"_id":"5ef77357-7d4f-4436-92fa-8cb7caf70d2f","text":"Generally, treatment for individuals with apraxia includes physical, speech,or occupational therapy. If apraxia is a symptom of another disorder, the underlying disorder should be treated."}
{"_id":"c28a5537-febc-468b-93b3-dcb7b46cba43","text":"The prognosis for individuals with apraxia varies and depends partly on the underlying cause. Some individuals improve significantly while others may show very little improvement."}
{"_id":"37de29b7-b5cf-4786-8b05-dc4e191c91d2","text":"The NINDS supports research on movement disorders and conditions such as apraxia. The goals of this research are to increase scientific understanding of these disorders, and to find ways to prevent, treat, and cure them."}
{"_id":"040a2030-abf9-4ded-8f79-cf67ac17ddf4","text":"Paraneoplastic syndromes are a group of rare disorders that are triggered by an abnormal immune system response to a cancerous tumor known as a \"neoplasm.\" Paraneoplastic syndromes are thought to happen when cancer-fighting antibodies or white blood cells (known as T cells) mistakenly attack normal cells in the nervous system. These disorders typically affect middle-aged to older people and are most common in individuals with lung, ovarian, lymphatic, or breast cancer. Neurologic symptoms generally develop over a period of days to weeks and usually occur prior to the tumor being discovered. These symptoms may include difficulty in walking or swallowing, loss of muscle tone, loss of fine motor coordination, slurred speech, memory loss, vision problems, sleep disturbances, dementia, seizures, sensory loss in the limbs, and vertigo or dizziness. Paraneoplastic syndromes include Lambert-Eaton myasthenic syndrome, stiff-person syndrome, encephalomyelitis, myasthenia gravis, cerebellar degeneration, limbic or brainstem encephalitis, neuromyotonia, opsoclonus, and sensory neuropathy."}
{"_id":"d3dd8993-636f-444c-b6ae-61fdc6d4c53d","text":"When present, the tumor and cancer are treated first, followed by efforts to decrease the autoimmune response -- either through steroids such as cortisone or prednisone, high-dose intravenous immunoglobulin, or irradiation. Plasmapheresis, a process that cleanses antibodies from the blood, may ease symptoms in people with paraneoplastic disorders that affect the peripheral nervous system. Speech and physical therapy may help individuals regain some functions."}
{"_id":"4003136a-3375-441b-bdab-16bb8f20d9a3","text":"There are no cures for paraneoplastic syndromes. There are no available treatments to stop progressive neurological damage. Generally, the stage of cancer at diagnosis determines the outcome."}
{"_id":"a471efe5-f999-462d-82fd-8a3e8e443b22","text":"Research on paraneoplastic syndromes is aimed at enhancing scientific understanding and evaluating new therapeutic interventions. Researchers seek to learn what causes the autoimmune response in these disorders. Studies are directed at developing tests that detect the presence of antibodies. Scientists also hope to develop animal models for these diseases, which may be used to determine effective treatment strategies."}
{"_id":"944ecee2-cfc7-4574-8e3a-1ba94b094b38","text":"Megalencephaly, also called macrencephaly, is a condition in which an infant or child has an abnormally large, heavy, and usually malfunctioning brain. By definition, the brain weight is greater than average for the age and gender of the child. Head enlargement may be evident at birth or the head may become abnormally large in the early years of life. Megalencephaly is thought to be related to a disturbance in the regulation of cell production in the brain. In normal development, neuron proliferation - the process in which nerve cells divide to form new generations of cells - is regulated so that the correct number of cells is produced in the proper place at the appropriate time. In a megalencephalic brain, too many cells are produced either during development or progressively as part of another disorder, such as one of the neurofibromatoses or leukodystrophies. Symptoms of megalencephaly include delayed development, seizures, and corticospinal (brain cortex and spinal cord) dysfunction. Megalencephaly affects males more often than females. Unilateral megalencephaly or hemimegalencephaly is a rare condition that is characterized by the enlargement of one side of the brain. Children with this disorder may have a large, asymmetrical head accompanied by seizures, partial paralysis, and impaired cognitive development. Megalencephaly is different from macrocephaly (also called megacephaly or megalocephaly), which describes a big head, and which doesnt necessarily indicate abnormality. Large head size is passed down through the generations in some families."}
{"_id":"1809e5a6-eba0-4ac3-a193-6222d26239ca","text":"There is no standard treatment for megalencephaly. Treatment will depend upon the disorder with which the megalencephaly is associated and will address individual symptoms and disabilities."}
{"_id":"4986df61-0477-4015-9b67-d2e68b6406ef","text":"The prognosis for infants and children with megalencephaly depends upon the underlying cause and the associated neurological disorders. The prognosis for children with hemimegalencephaly is poor."}
{"_id":"84a24ff9-e19b-4c93-8ed8-6ae1364948f2","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to megalencephaly in laboratories at the NIH and also support additional research through grants to major medical institutions across the country. Much of this research explores the complex mechanisms of normal brain development. The knowledge gained from these fundamental studies will provide a foundation for developing ways to prevent megalencephaly and the other cephalic disorders."}
{"_id":"95807051-843c-4f3a-a5cc-0685e653c1fa","text":"Diabetic neuropathy is a peripheral nerve disorder caused by diabetes or poor blood sugar control. The most common types of diabetic neuropathy result in problems with sensation in the feet. It can develop slowly after many years of diabetes or may occur early in the disease. The symptoms are numbness, pain, or tingling in the feet or lower legs. The pain can be intense and require treatment to relieve the discomfort. The loss of sensation in the feet may also increase the possibility that foot injuries will go unnoticed and develop into ulcers or lesions that become infected. In some cases, diabetic neuropathy can be associated with difficulty walking and some weakness in the foot muscles. There are other types of diabetic-related neuropathies that affect specific parts of the body. For example, diabetic amyotrophy causes pain, weakness and wasting of the thigh muscles, or cranial nerve infarcts that may result in double vision, a drooping eyelid, or dizziness. Diabetes can also affect the autonomic nerves that control blood pressure, the digestive tract, bladder function, and sexual organs. Problems with the autonomic nerves may cause lightheadedness, indigestion, diarrhea or constipation, difficulty with bladder control, and impotence."}
{"_id":"78476f25-47ef-4127-8240-9020e5b735c0","text":"The goal of treating diabetic neuropathy is to prevent further tissue damage and relieve discomfort. The first step is to bring blood sugar levels under control by diet and medication. Another important part of treatment involves taking special care of the feet by wearing proper fitting shoes and routinely checking the feet for cuts and infections. Analgesics, low doses of antidepressants, and some anticonvulsant medications may be prescribed for relief of pain, burning, or tingling. Some individuals find that walking regularly, taking warm baths, or using elastic stockings may help relieve leg pain."}
{"_id":"1b66cf24-fb48-4220-9d2d-f517dde8804d","text":"The prognosis for diabetic neuropathy depends largely on how well the underlying condition of diabetes is handled. Treating diabetes may halt progression and improve symptoms of the neuropathy, but recovery is slow. The painful sensations of diabetic neuropathy may become severe enough to cause depression in some patients."}
{"_id":"39466533-f566-40b3-b1be-0ed17ff7a4b0","text":"The NINDS conducts and supports research on diabetic neuropathy to increase understanding of the disorder and find ways to prevent and cure it. New medications are currently being examined to assess improvement or stabilization of neuropathic symptoms."}
{"_id":"510b9613-8b2b-4c49-8e9d-d0455a961c3a","text":"Wernicke's encephalopathy is a degenerative brain disorder caused by the lack of thiamine (vitamin B1). It may result from alcohol abuse, dietary deficiencies, prolonged vomiting, eating disorders, or the effects of chemotherapy. B1 deficiency causes damage to the brain's thalamus and hypothalamus. Symptoms include mental confusion, vision problems, coma, hypothermia, low blood pressure, and lack of muscle coordination (ataxia). Korsakoff syndrome (also called Korsakoff's amnesic syndrome) is a memory disorder that results from vitamin B1 deficiency and is associated with alcoholism. Korsakoff's syndrome damages nerve cells and supporting cells in the brain and spinal cord, as well as the part of the brain involved with memory. Symptoms include amnesia, tremor, coma, disorientation, and vision problems, The disorder's main features are problems in acquiring new information or establishing new memories, and in retrieving previous memories. Although Wernicke's and Korsakoff's are related disorders, some scientists believe them to be different stages of the same disorder, which is called Wernicke-Korsakoff syndrome. Wernicke's encephalopathy represents the \"acute\" phase of the disorder and Korsakoff's amnesic syndrome represents the disorder progressing to a \"chronic\" or long-lasting stage."}
{"_id":"700bc9d8-aa9c-40d7-924b-d0d0d992b114","text":"Treatment involves replacement of thiamine and providing proper nutrition and hydration. In some cases, drug therapy is also recommended.Stopping alcohol use may prevent further nerve and brain damage. In individuals with Wernicke's encephalopathy, it is very important to start thiamine replacement before beginning nutritional replenishment."}
{"_id":"68e6a3a1-ef71-4475-ab73-287344d9a7f6","text":"Most symptoms of Wernicke's encephalopathy can be reversed if detected and treated promptly and completely. Stopping alcohol use may prevent further nerve and brain damage. However, improvement in memory function is slow and, usually, incomplete. Without treatment, these disorders can be disabling and life-threatening."}
{"_id":"7d27d5a9-7c30-4dc9-9054-49375f23cd44","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS supports research on neurological disorders such as Wernicke's encephalopathy, Korsakoff's amnesic syndrome, and Wernicke-Korsakoff syndrome, to expand our understanding of the functional changes of the diseases and ways to treat them..One areas of research is studying how exercise can improve cognitive functioning based on modulation of certain nerve cells in a rodent model of amnesia produced by by thiamine deficiency. The National Institute of Alcohol Abuse and Alcoholism also supports research on these disorders."}
{"_id":"7984aaa7-2c25-4c05-81b3-1ac51c75b015","text":"Cerebellar degeneration is a process in which neurons in the cerebellum - the area of the brain that controls coordination and balance - deteriorate and die. Diseases that cause cerebellar degeneration can also involve other areas of the central nervous system,including the spinal cord, medulla oblongata, cerebral cortex, and brain stem. Cerebellar degeneration may be the result of inherited genetic mutations that alter the normal production of specific proteins that are necessary for the survival of neurons.\n                \nAssociated diseases: Diseases that are specific to the brain, as well as diseases that occur in other parts of the body, can cause neurons to die in the cerebellum. Neurological diseases that feature cerebellar degeneration include:\n                \n- ischemic or hemorrhagic stroke, when there is lack of blood flow or oxygen to the cerebellum - cerebellar cortical atrophy, multisystem atrophy, and olivopontocerebellar degeneration, progressive degenerative disorders in which cerebellar degeneration is a key feature - Friedreichs ataxia, and other spinocerebellar ataxias, which are caused by inherited genetic mutations that result in ongoing loss of neurons in the cerebellum, brain stem, and spinal cord - transmissible spongiform encephalopathies (such as Creutzfeldt-Jakob disease) in which abnormal proteins cause inflammation in the brain, including the cerebellum - multiple sclerosis, in which damage to the insulating membrane (myelin) that wraps around and protects nerve cells can involve the cerebellum  Other diseases that can cause cerebellar degeneration include: - chronic alcohol abuse that leads to temporary or permanent cerebellar damage - paraneoplastic disorders, in which a malignancy (cancer) in other parts of the body produces substances that cause immune system cells to attack neurons in the cerebellum  Symptoms of cerebellar degeneration: The most characteristic symptom of cerebellar degeneration is a wide-based, unsteady, lurching walk, often accompanied by a back and forth tremor in the trunk of the body. Other symptoms may include slow, unsteady and jerky movement of the arms or legs, slowed and slurred speech, and nystagmus -- rapid, small movements of the eyes."}
{"_id":"67dcdd28-f872-4db5-99d5-e5ba228f048b","text":"The NINDS funds research to find the genes involved in diseases that cause cerebellar degeneration. Discovering these genes, identifying their mutations, and understanding how the abnormal proteins they produce cause cerebellar degeneration may eventually help scientists find ways to prevent, treat, and even cure the diseases that involve cerebellar degeneration."}
{"_id":"472537bb-10ef-43e8-8a96-e494202aec49","text":"Parry-Romberg syndrome is a rare disorder characterized by slowly progressive deterioration (atrophy) of the skin and soft tissues of half of the face (hemifacial atrophy), usually the left side. It is more common in females than in males. Initial facial changes usually involve the tissues above the upper jaw (maxilla) or between the nose and the upper corner of the lip (nasolabial fold) and subsequently progress to the angle of the mouth, areas around the eye, the brow, the ear, and the neck. The deterioration may also affect the tongue, the soft and fleshy part of the roof of the mouth, and the gums. The eye and cheek of the affected side may become sunken and facial hair may turn white and fall out (alopecia). In addition, the skin overlying affected areas may become darkly pigmented (hyperpigmentation) with, in some cases, areas of hyperpigmentation and patches of unpigmented skin (vitiligo). Parry-Romberg syndrome is also accompanied by neurological abnormalities including seizures and episodes of severe facial pain (trigeminal neuralgia). The onset of the disease usually begins between the ages of 5 and 15 years. The progression of the atrophy often lasts from 2 to 10 years, and then the process seems to enter a stable phase. Muscles in the face may atrophy and there may be bone loss in the facial bones. Problems with the retina and optic nerve may occur when the disease surrounds the eye."}
{"_id":"b92482d7-d570-4ba8-b8be-112425048831","text":"There is no cure and there are no treatments that can stop the progression of Parry-Romberg syndrome. Reconstructive or microvascular surgery may be needed to repair wasted tissue. The timing of surgical intervention is generally agreed to be the best following exhaustion of the disease course and completion of facial growth. Most surgeons will recommend a waiting period of one or two years before proceeding with reconstruction. Muscle or bone grafts may also be helpful. Other treatment is symptomatic and supportive."}
{"_id":"ad215f9f-50be-47dd-804c-690e31bc8901","text":"The prognosis for individuals with Parry-Romberg syndrome varies. In some cases, the atrophy ends before the entire face is affected. In mild cases, the disorder usually causes no disability other than cosmetic effects."}
{"_id":"11747b7e-5402-475f-ab3b-4fffe224209a","text":"The NINDS supports research on neurological disorders such as Parry-Romberg syndrome with the goal of finding ways to prevent, treat, and cure them."}
{"_id":"42e3196f-8b40-48c1-8c73-144d5c7aa316","text":"Myotonia congenita is an inherited neuromuscular disorder characterized by the inability of muscles to quickly relax after a voluntary contraction. The condition is present from early childhood, but symptoms can be mild. Most children will be 2 or 3 years old when parents first notice their muscle stiffness, particularly in the legs, often provoked by sudden activity after rest. The disease doesnt cause muscle wasting; in fact, it may cause muscle enlargement. Muscle strength is increased. There are two forms of the disorder: Becker-type, which is the most common form; and Thomsens disease, which is a rare and milder form. The disorder is cause by mutations in a gene responsible for shutting off electrical excitation in the muscles."}
{"_id":"41be0886-5516-4945-9b14-03272c912908","text":"Most people with myotonia congenita dont require special treatments. Stiff muscles usually resolve with exercise, or light movement, especially after resting. For individuals whose symptoms are more limiting, doctors have had some success with medications such as quinine, or anticonvulsant drugs such as phenytoin. Physical therapy and other rehabilitative therapies are also sometimes used to improve muscle function."}
{"_id":"745e9418-3e8a-43d8-8eec-ae26bdf8c29a","text":"Most individuals with myotonia congenita lead long, productive lives. Although muscle stiffness may interfere with walking, grasping, chewing, and swallowing, it is usually relieved with exercise."}
{"_id":"05dfb30b-0535-404a-a767-cadee03f1ad2","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to myotonia congenita and also supports additional research through grants to major research institutions across the country. Current research is exploring how, at the molecular level, the defective gene in myotonia congenita causes the specific symptoms of the disorder. Additional research is focused on developing animal models of the disorder to test potential treatments and therapies."}
{"_id":"c2ee5f80-800d-437c-aa1f-8bd33fc2c5b2","text":"A myopathy is a disorder of the muscles that usually results in weakness. Congenital myopathy refers to a group of muscle disorders that appear at birth or in infancy. Typically, an infant with a congenital myopathy will be \"floppy,\" have difficulty breathing or feeding, and will lag behind other babies in meeting normal developmental milestones such as turning over or sitting up.\n                \nMuscle weakness can occur for many reasons, including a problem with the muscle, a problem with the nerve that stimulates the muscle, or a problem with the brain. Therefore, to diagnose a congenital myopathy, a neurologist will perform a detailed physical exam as well as tests to determine the cause of weakness. If a myopathy is suspected, possible tests include a blood test for a muscle enzyme called creatine kinase, an electromyogram (EMG) to evaluate the electrical activity of the muscle, a muscle biopsy, and genetic testing.\n                \nThere are currently seven distinct types of congenital myopathy, with some variation in symptoms, complications, treatment options, and outlook.\n                \nNemaline myopathy is the most common congenital myopathy. Infants usually have problems with breathing and feeding. Later, some skeletal problems may arise, such as scoliosis (curvature of the spine). In general, the weakness does not worsen during life.\n                \nMyotubular myopathy is rare and only affects boys. Weakness and floppiness are so severe that a mother may notice reduced movements of the baby in her womb during pregnancy. There are usually significant breathing and swallowing difficulties; many children do not survive infancy. Osteopenia (weakening of the bones) is also associated with this disorder.\n                \nCentronuclear myopathy is rare and begins in infancy or early childhood with weakness of the arms and legs, droopy eyelids, and problems with eye movements. Weakness often gets worse with time.\n                \nCentral core disease varies among children with regard to the severity of problems and the degree of worsening over time. Usually, there is mild floppiness in infancy, delayed milestones, and moderate limb weakness, which do not worsen much over time. Children with central core disease may have life-threatening reactions to general anesthesia. Treatment with the drug salbutamol has been shown to reduce weakness significantly, although it does not cure the disorder.\n                \nMulti-minicore disease has several different subtypes. Common to most is severe weakness of the limbs and scoliosis. Often breathing difficulties occur as well. Some children have weakened eye movements.\n                \nCongenital fiber-type disproportion myopathy is a rare disorder that begins with floppiness, limb and facial weakness, and breathing problems.\n                \nHyaline body myopathy is a disorder characterized by the specific appearance under the microscope of a sample of muscle tissue. It probably includes several different causes. Because of this, the symptoms are quite variable."}
{"_id":"3d5460cc-53e1-47ff-ae33-6167a8d517d5","text":"Currently, only central core disease has an effective treatment (see above). There are no known cures for any of these disorders. Supportive treatment may involve orthopedic treatments, as well as physical, occupational or speech therapy."}
{"_id":"37b96c52-cd05-437e-b33b-163a700f9d65","text":"When breathing difficulties are severe, and particularly if there is also a problem with feeding and swallowing, infants may die of respiratory failure or complications such as pneumonia. Sometimes muscle weakness can lead to skeletal problems, such as scoliosis, reduced mobility of joints, or hip problems. The heart muscle is rarely involved."}
{"_id":"169aec97-cd50-4e79-8e35-27c4dfd69723","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to congenital myopathies in their laboratories at the NIH and also support additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure the disorders that make up the congenital myopathies."}
{"_id":"a09fd6d5-2189-43c4-871a-3f8ce2cd22c4","text":"Ataxia often occurs when parts of the nervous system that control movement are damaged. People with ataxia experience a failure of muscle control in their arms and legs, resulting in a lack of balance and coordination or a disturbance of gait. While the term ataxia is primarily used to describe this set of symptoms, it is sometimes also used to refer to a family of disorders. It is not, however, a specific diagnosis.\n                \nMost disorders that result in ataxia cause cells in the part of the brain called the cerebellum to degenerate, or atrophy. Sometimes the spine is also affected. The phrases cerebellar degeneration and spinocerebellar degeneration are used to describe changes that have taken place in a persons nervous system; neither term constitutes a specific diagnosis. Cerebellar and spinocerebellar degeneration have many different causes. The age of onset of the resulting ataxia varies depending on the underlying cause of the degeneration.\n                \nMany ataxias are hereditary and are classified by chromosomal location and pattern of inheritance: autosomal dominant, in which the affected person inherits a normal gene from one parent and a faulty gene from the other parent; and autosomal recessive, in which both parents pass on a copy of the faulty gene. Among the more common inherited ataxias are Friedreichs ataxia and Machado-Joseph disease. Sporadic ataxias can also occur in families with no prior history.\n                \nAtaxia can also be acquired. Conditions that can cause acquired ataxia include stroke, multiple sclerosis, tumors, alcoholism, peripheral neuropathy, metabolic disorders, and vitamin deficiencies."}
{"_id":"94ad12d1-e497-404b-afdb-1bf745779915","text":"There is no cure for the hereditary ataxias. If the ataxia is caused by another condition, that underlying condition is treated first. For example, ataxia caused by a metabolic disorder may be treated with medications and a controlled diet. Vitamin deficiency is treated with vitamin therapy. A variety of drugs may be used to either effectively prevent symptoms or reduce the frequency with which they occur. Physical therapy can strengthen muscles, while special devices or appliances can assist in walking and other activities of daily life."}
{"_id":"c70b6fa0-cb28-44be-8e53-6682e38ce1b5","text":"The prognosis for individuals with ataxia and cerebellar\/spinocerebellar degeneration varies depending on its underlying cause."}
{"_id":"c9bb207c-6337-417a-ae14-be4919b70f1e","text":"The NINDS supports and conducts a broad range of basic and clinical research on cerebellar and spinocerebellar degeneration, including work aimed at finding the cause(s) of ataxias and ways to treat, cure, and, ultimately, prevent them. Scientists are optimistic that understanding the genetics of these disorders may lead to breakthroughs in treatment."}
{"_id":"3a872b2a-79e5-4e4a-b3ea-5e07c733c372","text":"Septo-optic dysplasia (SOD) is a rare disorder characterized by abnormal development of the optic disk, pituitary deficiencies, and often agenesis (absence) of the septum pellucidum (the part of the brain that separates the anterior horns or the lateral ventricles of the brain). Symptoms may include blindness in one or both eyes, pupil dilation in response to light, nystagmus (a rapid, involuntary to-and-fro movement of the eyes), inward and outward deviation of the eyes, hypotonia (low muscle tone), and hormonal problems. Seizures may also occur. In a few cases, jaundice (prolonged yellow skin discoloration) may occur at birth. Intellectual problems vary in severity among individuals. While some children with SOD have normal intelligence, others have learning disabilities. Most, however, are developmentally delayed due to vision impairment or neurological problems."}
{"_id":"baccb9d4-560d-4db1-a61c-886a1bbdbd21","text":"Treatment for SOD is symptomatic. Hormone deficiencies may be treated with hormone replacement therapy. The optical problems associated with SOD are generally not treatable. Vision, physical, and occupational therapies may be required."}
{"_id":"7c0a259f-6b69-4940-ad48-d410c6145348","text":"The prognosis for individuals with SOD varies according to the presence and severity of symptoms."}
{"_id":"1ccf10c2-12c3-47b8-8cf4-f871ec32eae8","text":"The NINDS supports and conducts neurogenetic research which focuses on identifying and studying the genes involved in normal brain development. The knowledge gained from these fundamental studies provides the foundation for understanding how this process can go awry and, thus, may eventually give clues to understanding disorders such as SOD."}
{"_id":"f19dbc25-def3-475c-8bee-388f1f641277","text":"Coffin-Lowry syndrome is a rare genetic disorder characterized by craniofacial (head and facial) and skeletal abnormalities, delayed intellectual development, short stature, and hypotonia. Characteristic facial features may include an underdeveloped upper jaw bone (maxillary hypoplasia), a broad nose, protruding nostrils (nares), an abnormally prominent brow, down-slanting eyelid folds (palpebral fissures), widely spaced eyes (hypertelorism), large low-set ears, and unusually thick eyebrows. Skeletal abnormalities may include abnormal front-to-back and side-to-side curvature of the spine (kyphoscoliosis), unusual prominence of the breastbone (pigeon chest, or pectus carinatum), dental abnormalities, and short, hyperextensible, tapered fingers. Other features may include feeding and respiratory problems, developmental delay, hearing impairment, awkward gait, stimulus-induced drop episodes, and heart and kidney involvement. The disorder affects males and females in equal numbers, but symptoms are usually more severe in males. The disorder is caused by a defective gene, RSK2, which is found in 1996 on the X chromosome (Xp22.2-p22.1). Thus, the syndrome is typically more severe in males because males have only one X chromosome, while females have two. It is unclear how changes (mutations) in the DNA structure of the gene lead to the clinical findings."}
{"_id":"ea333796-2eda-4fce-9ca2-92e99f2bfc3c","text":"There is no cure and no standard course of treatment for Coffin-Lowry syndrome. Treatment is symptomatic and supportive, and may include physical and speech therapy and educational services."}
{"_id":"52c598cc-1bac-4236-83a9-a38ca30596a7","text":"The prognosis for individuals with Coffin-Lowry syndrome varies depending on the severity of symptoms. Early intervention may improve the outlook for patients. Life span is reduced in some individuals with Coffin-Lowry syndrome."}
{"_id":"7c07199f-da08-4b19-9a31-1eb6ac0485cd","text":"The NINDS supports and conducts research on genetic disorders, such as Coffin-Lowry syndrome, in an effort to find ways to prevent, treat, and ultimately cure these disorders."}
{"_id":"82fa7940-d83e-44e5-8070-67aa3e8dad0b","text":"Lipoid proteinosis (LP) is a rare disease that affects the skin and the brain. Three distinctive features characterize the disease: a hoarse voice, unusual growths on the skin and mucus membranes, and damage to the temporal lobes or hippocampus of the brain. The symptoms of LP may begin as early as infancy with hoarseness or a weak cry, due to growths on the vocal cords. Skin lesions appear sometime in the next 3 years, leaving acne- or pox-like scars on the face, hands, and mucous membranes. The most characteristic symptom of LP is waxy, yellow, bead-like bumps along the upper and lower edges of the eyelids. Brain damage develops over time and is associated with the development of cognitive abilities and epileptic seizures. Damage to the amygdala, a part of the brain that regulates emotions and perceptions, leads to difficulties in discriminating facial expressions and in making realistic judgments about the trustworthiness of other people. LP is a hereditary disease that equally affects males and females. Nearly a quarter of all reported cases have been in the Afrikaner population of South Africa, but the disease is increasingly being reported from other parts of the world including India. The gene responsible for LP has recently been identified. It performs an unknown function in the skin related to the production of collagen."}
{"_id":"353589b1-201f-415e-87e8-1e6cf6d2b6b0","text":"There is no cure for LP. Some doctors have had success treating the skin eruptions with oral steroid drugs and oral dimethyl sulphoxide (DMSO). Carbon dioxide laser surgery of thickened vocal cords and eyelid bumps has proved helpful in some studies. Dermabrasion may improve the appearance of the skin lesions. Seizures, if present, may be treated with anticonvulsants."}
{"_id":"3d2640d6-fde7-42bb-8b77-e20f29be2177","text":"Lipoid proteinosis has a stable or slowly progressive course. Children with LP may have behavioral or learning difficulties, along with seizures. Obstruction in the throat may require a tracheostomy. Mortality rates in infants and adults are slightly increased because of problems with throat obstructions and upper respiratory tract infections."}
{"_id":"f5e506d8-3e7a-4a92-b6c7-10d423713c43","text":"The National Institute of Neurological Disorders and Stroke (NINDS), and other institutes of the National Institutes of Health (NIH), conduct research related to neurological diseases such as lipoid proteinosis in laboratories at the NIH, and also support additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders, such as lipoid proteinosis."}
{"_id":"eaec477a-13ed-4cbd-a2ce-a81ab2413a2e","text":"Kleine-Levin syndrome is a rare disorder that primarily affects adolescent males (approximately 70 percent of those with Kleine-Levin syndrome are male). It is characterized by recurring but reversible periods of excessive sleep (up to 20 hours per day). Symptoms occur as \"episodes,\" typically lasting a few days to a few weeks. Episode onset is often abrupt, and may be associated with flu-like symptoms. Excessive food intake, irritability, childishness, disorientation, hallucinations, and an abnormally uninhibited sex drive may be observed during episodes. Mood can be depressed as a consequence, but not a cause, of the disorder. Affected individuals are completely normal between episodes, although they may not be able to remember afterwards everything that happened during the episode. It may be weeks or more before symptoms reappear. Symptoms may be related to malfunction of the hypothalamus and thalamus, parts of the brain that govern appetite and sleep."}
{"_id":"9acfe3f0-18d2-4b4a-abed-7818e8efd788","text":"There is no definitive treatment for Kleine-Levin syndrome and watchful waiting at home, rather than pharmacotherapy, is most often advised. Stimulant pills, including amphetamines, methylphenidate, and modafinil, are used to treat sleepiness but may increase irritability and will not improve cognitive abnormalities. Because of similarities between Kleine-Levin syndrome and certain mood disorders, lithium and carbamazepine may be prescribed and, in some cases, have been shown to prevent further episodes. This disorder should be differentiated from cyclic re-occurrence of sleepiness during the premenstrual period in teen-aged girls, which may be controlled with birth control pills. It also should be differentiated from encephalopathy, recurrent depression, or psychosis."}
{"_id":"14379db4-d8c6-4981-a436-fb58d8baa331","text":"Episodes eventually decrease in frequency and intensity over the course of eight to 12 years."}
{"_id":"67292944-2af6-44c3-b084-7fa707412276","text":"NINDS supports a broad range of clinical and basic research on diseases causing sleep disorders in an effort to clarify the mechanisms of these conditions and to develop better treatments for them."}
{"_id":"eec3d8ef-e2fe-4563-b691-98535a8fd52e","text":"Vasculitis is an inflammation of blood vessels, which includes the veins, arteries, and capillaries. Inflammation occurs with infection or is thought to be due to a faulty immune system response. It also can be caused by other immune system disease, an allergic reaction to medicines or toxins, and by certain blood cancers. Vasculitic disorders can cause problems in any organ system, including the central (CNS) and peripheral (PNS) nervous systems. Vasculitis disorders, or syndromes, of the CNS and PNS are characterized by the presence of inflammatory cells in and around blood vessels, and secondary narrowing or blockage of the blood vessels that nourish the brain, spinal cord, or peripheral nerves.\n                \nA vasculitic syndrome may begin suddenly or develop over time. Symptoms include headaches, especially a headache that doesnt go away; fever, rapid weight loss; confusion or forgetfulness leading to dementia; swelling of the brain, pain while chewing or swallowing; paralysis or numbness, usually in the arms or legs; and visual disturbances, such as double vision, blurred vision, or blindness\n                \nSome of the better understood vasculitis syndromes are temporal arteritis (also called giant cell arteritis or cranial arteritis--a chronic inflammatory disorder of large blood vessels) and Takayasus disease, which affects larger aortas and may cause stoke."}
{"_id":"f74d7c9c-4e07-4ac1-a6f4-3e1d490d21e6","text":"Treatment for a vasculitis syndrome depends upon the specific diagnosis, which can be difficult, as some diseases have similar symptoms of vasculitis. Most of the syndromes respond well to steroid drugs, such as prednisolone. Some may also require treatment with an immunosuppressive drug, such as cyclophosphamide. Aneurysms involved with vasculitis can be treated surgfically."}
{"_id":"332e13ab-8249-42fa-822d-39b4b441d965","text":"The prognosis is dependent upon the specific syndrome, however, some of the syndromes are fatal if left untreated."}
{"_id":"973e8236-8707-44af-a267-92daa1716610","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. Several NINDS-funded investigators are studying blood vessel damage and cerebral blood flow as it relates to stroke. The NINDS also funds research on vascular cognitive impairment, which is an important contributor to aging-related cognitive decline and is the result of impaired performance of the brain's small blood vessels. Additionally, the NINDS and other institutes of the National Institutes of Health (NIH) conduct research relating to vasculitis syndromes in laboratories at the NIH and also support vasculitis research through grants to major medical institutions across the country. The NINDS supports The Vasculitis Clinical Research Consortium (VCRC), a network of academic medical centers, patient support organizations, and clinical research resources dedicated to conducting clinical research and improving the care of individuals with various vasculitis disorders."}
{"_id":"da23b3e7-97bd-4cb5-b7a6-355239afccb7","text":"Menkes disease is caused by a defective gene named ATPTA1 that regulates the metabolism of copper in the body. The disease primarily affects male infants. Copper accumulates at abnormally low levels in the liver and brain, but at higher than normal levels in the kidney and intestinal lining. Affected infants may be born prematurely, but appear healthy at birth and develop normally for 6 to 8 weeks. Then symptoms begin, including floppy muscle tone, seizures, and failure to thrive. Menkes disease is also characterized by subnormal body temperature and strikingly peculiar hair, which is kinky, colorless or steel-colored, and breaks easily. There is often extensive neurodegeneration in the gray matter of the brain. Arteries in the brain may be twisted with frayed and split inner walls. This can lead to rupture or blockage of the arteries. Weakened bones (osteoporosis) may result in fractures."}
{"_id":"5145a205-dbe4-4eae-acf6-36aed3173b76","text":"Treatment with daily copper injections may improve the outcome in Menkes disease if it begins within days after birth. Other treatment is symptomatic and supportive."}
{"_id":"1e38f4c5-8bb9-4ebb-90b8-52ecc96e7a84","text":"Since newborn screening for this disorder is not available, and early detection is infrequent because the clinical signs of Menkes disease are subtle in the beginning, the disease is rarely treated early enough to make a significant difference. The prognosis for babies with Menkes disease is poor. Most children with Menkes disease die within the first decade of life."}
{"_id":"2d801128-6d76-4a33-9d63-6e505f1d2929","text":"Recent research sponsored by the NINDS developed a blood test that could be given to newborns at risk for Menkes disease based on a positive family history for the disorder or other indications. The test measures 4 different chemicals in the blood and, depending upon their levels, can accurately diagnose the presence of Menkes disease before symptoms appear. Study results showed higher survival rates for children given the earliest copper injection treatment and improved, if not normal, 2. Additional research is being performed by the Eunice Kennedy Shriver National Institute of Child Health and Human Development, in collaboration with the NINDS, that applies gene therapy approaches to Menkes disease.3\n                \n\n                \n1. Kaler, SG. The neurology of STPAT copper transporter disease: emerging concepts and future trends. Nature Reviews Neurology, 2001:7:15-19..\n                \n2. Kaler SG, et al.Neonatal Diagnosis and Treatment of Menkes Disease. N Engl J Med 2008;358:605-14.\n                \n3. Donsante, A. et. al. ATPTA gene addition to the choroid plexus results in long-term rescue of the lethal copper transport defect in a Menkes disease mouse model. Molecular Therapy (in press as of August 2011)."}
{"_id":"72075f1a-cabc-4847-a729-b7babce1760e","text":"Tumors of the brain and spinal cord are abnormal growths of tissue found inside the skull or the bony spinal column. The brain and spinal cord are the primary components of the central nervous system (CNS). Benign tumors are noncancerous, and malignant tumors are cancerous. The CNS is housed within rigid, bony quarters (i.e., the skull and spinal column), so any abnormal growth, whether benign or malignant, can place pressure on sensitive tissues and impair function. Tumors that originate in the brain or spinal cord are called primary tumors. Most primary tumors are caused by out-of-control growth among cells that surround and support neuron, specific genetic disease (such as neurofibromatosis type 1 and tuberous sclerosis), or from exposure to radiation or cancer-causing chemicals. Metastatic, or secondary, tumors in the CNS are caused by cancer cells that break away from a primary tumor located in another region of the body. Tumors can place pressure on sensitive tissues and impair function..Symptoms of brain tumors include headaches, seizures, nausea and vomiting, poor vision or hearing, changes in behavior, unclear thinking, and unsteadiness. Spinal cord tumor symptoms include pain, numbness, and paralysis. Diagnosis is made after a neurological examination, special imaging techniques (computed tomography, and magnetic resonance imaging, positron emission tomography), laboratory tests, and a biopsy (in which a sample of tissue is taken from a suspected tumor and examined)."}
{"_id":"3b702dc9-5947-4ee2-8e7d-81032b4a0a0d","text":"The three most commonly used treatments are surgery, radiation, and chemotherapy. Doctors also may prescribe steroids to reduce the tumor-related swelling inside the CNS."}
{"_id":"f809efd5-ef11-4c8e-9c61-19c7688b1158","text":"Symptoms of brain and spinal cord tumors generally develop slowly and worsen over time unless they are treated. The tumor may be classified as benign or malignant and given a numbered score that reflects its rate of malignancy. This score can help doctors determine how to treat the tumor and predict the likely outcome, or prognosis, for the individual."}
{"_id":"8f399924-19d4-499e-b718-ebdff531e719","text":"Scientists continue to investigate ways to better understand, diagnose, and treat CNS tumors. Experimental treatment options may include new drugs, gene therapy, surgery , radiation, biologic modulators that enhance the body's overall immune system to recognize and fight cancer cells, and a combination of therapies. Of particular interest to scientists is the development of tailored therapeutics--involving a combination of targeted agents that use different molecules to reduce tumor gene activity and suppress uncontrolled growth by killing or reducing the production of tumor cells--to treat tumors based on their genetic makeup. Researchers continue to search for additional clinical biomarkers (molecules or other substances in the blood or tissue that can be used to diagnose or monitor a particular disorder) of CNS tumors. Other researchers are testing different drugs and molecules to see if they can modulate the normal activity of the blood-brain barrier and better target tumor cells and associated blood vessels. Also under investigation are ways to improve drug delivery to the tumor and to prevent the side-effects of cancer treatments."}
{"_id":"ae61906e-5780-4e11-bf84-bdca5b962be7","text":"Hypersomnia is characterized by recurrent episodes of excessive daytime sleepiness or prolonged nighttime sleep. Different from feeling tired due to lack of or interrupted sleep at night, persons with hypersomnia are compelled to nap repeatedly during the day, often at inappropriate times such as at work, during a meal, or in conversation. These daytime naps usually provide no relief from symptoms. Patients often have difficulty waking from a long sleep, and may feel disoriented. Other symptoms may include anxiety, increased irritation, decreased energy, restlessness, slow thinking, slow speech, loss of appetite, hallucinations, and memory difficulty. Some patients lose the ability to function in family, social, occupational, or other settings. Hypersomnia may be caused by another sleep disorder (such as narcolepsy or sleep apnea), dysfunction of the autonomic nervous system, or drug or alcohol abuse. In some cases it results from a physical problem, such as a tumor, head trauma, or injury to the central nervous system. Certain medications, or medicine withdrawal, may also cause hypersomnia. Medical conditions including multiple sclerosis, depression, encephalitis, epilepsy, or obesity may contribute to the disorder. Some people appear to have a genetic predisposition to hypersomnia; in others, there is no known cause. Typically, hypersomnia is first recognized in adolescence or young adulthood."}
{"_id":"dd810525-6a25-4966-8456-7251f73a0114","text":"Treatment is symptomatic in nature. Stimulants, such as amphetamine, methylphenidate, and modafinil, may be prescribed. Other drugs used to treat hypersomnia include clonidine, levodopa, bromocriptine, antidepressants, and monoamine oxidase inhibitors. Changes in behavior (for example avoiding night work and social activities that delay bed time) and diet may offer some relief. Patients should avoid alcohol and caffeine."}
{"_id":"31a83b0b-9d50-4718-9ae0-e1bcb8494ab3","text":"The prognosis for persons with hypersomnia depends on the cause of the disorder. While the disorder itself is not life threatening, it can have serious consequences, such as automobile accidents caused by falling asleep while driving. The attacks usually continue indefinitely."}
{"_id":"d2fafedd-392e-460e-8f5b-bb5a2fc26547","text":"The NINDS supports and conducts research on sleep disorders such as hypersomnia. The goal of this research is to increase scientific understanding of the condition, find improved methods of diagnosing and treating it, and discover ways to prevent it."}
{"_id":"6e0141b2-51ec-4ab8-b7a8-ed4623b8cd72","text":"Guillain-Barr syndrome is a disorder in which the body's immune system attacks part of the peripheral nervous system. The first symptoms of this disorder include varying degrees of weakness or tingling sensations in the legs. In many instances, the weakness and abnormal sensations spread to the arms and upper body. These symptoms can increase in intensity until the muscles cannot be used at all and the person is almost totally paralyzed. In these cases, the disorder is life-threatening and is considered a medical emergency. The individual is often put on a ventilator to assist with breathing. Most individuals, however, have good recovery from even the most severe cases of Guillain-Barr syndrome (GBS), although some continue to have some degree of weakness. Guillain-Barr syndrome is rare. Usually Guillain-Barr occurs a few days or weeks after the person has had symptoms of a respiratory or gastrointestinal viral infection. Occasionally, surgery will trigger the syndrome. In rare instances, vaccinations may increase the risk of GBS. The disorder can develop over the course of hours or days, or it may take up to 3 to 4 weeks. No one yet knows why Guillain-Barr strikes some people and not others or what sets the disease in motion. What scientists do know is that the body's immune system begins to attack the body itself, causing what is known as an autoimmune disease. Guillain-Barr is called a syndrome rather than a disease because it is not clear that a specific disease-causing agent is involved. Reflexes such as knee jerks are usually lost. Because the signals traveling along the nerve are slower, a nerve conduction velocity (NCV) test can give a doctor clues to aid the diagnosis. The cerebrospinal fluid that bathes the spinal cord and brain contains more protein than usual, so a physician may decide to perform a spinal tap."}
{"_id":"d73202f3-e1f1-4dca-bffe-1c32ef41bfc3","text":"There is no known cure for Guillain-Barr syndrome, but therapies can lessen the severity of the illness and accelerate the recovery in most patients. There are also a number of ways to treat the complications of the disease. Currently, plasmapheresis (also known as plasma exchange) and high-dose immunoglobulin therapy are used. Plasmapheresis seems to reduce the severity and duration of the Guillain-Barr episode. In high-dose immunoglobulin therapy, doctors give intravenous injections of the proteins that in small quantities, the immune system uses naturally to attack invading organism. Investigators have found that giving high doses of these immunoglobulins, derived from a pool of thousands of normal donors, to Guillain-Barr patients can lessen the immune attack on the nervous system. The most critical part of the treatment for this syndrome consists of keeping the patient's body functioning during recovery of the nervous system. This can sometimes require placing the patient on a ventilator, a heart monitor, or other machines that assist body function."}
{"_id":"cbf98e5b-ab45-4583-bdda-c15dffd3d405","text":"Guillain-Barr syndrome can be a devastating disorder because of its sudden and unexpected onset. Most people reach the stage of greatest weakness within the first 2 weeks after symptoms appear, and by the third week of the illness 90 percent of all patients are at their weakest. The recovery period may be as little as a few weeks or as long as a few years. About 30 percent of those with Guillain-Barr still have a residual weakness after 3 years. About 3 percent may suffer a relapse of muscle weakness and tingling sensations many years after the initial attack."}
{"_id":"e26916a4-ea5e-4552-8377-c9e30cfd3dbf","text":"Scientists are concentrating on finding new treatments and refining existing ones. Scientists are also looking at the workings of the immune system to find which cells are responsible for beginning and carrying out the attack on the nervous system. The fact that so many cases of Guillain-Barr begin after a viral or bacterial infection suggests that certain characteristics of some viruses and bacteria may activate the immune system inappropriately. Investigators are searching for those characteristics. Neurological scientists, immunologists, virologists, and pharmacologists are all working collaboratively to learn how to prevent this disorder and to make better therapies available when it strikes."}
{"_id":"38c83296-6d0d-4a53-96f7-1d94246434ff","text":"CADASIL (Cerebral Autosomal Dominant Arteriopathy with Sub-cortical Infarcts and Leukoencephalopathy) is an inherited form of cerebrovascular disease that occurs when the thickening of blood vessel walls blocks the flow of blood to the brain. The disease primarily affects small blood vessels in the white matter of the brain. A mutation in the Notch3 gene alters the muscular walls in these small arteries. CADASIL is characterized by migraine headaches and multiple strokes progressing to dementia. Other symptoms include cognitive deterioration, seizures, vision problems, and psychiatric problems such as severe depression and changes in behavior and personality. Individuals may also be at higher risk of heart attack. Symptoms and disease onset vary widely, with signs typically appearing in the mid-30s. Some individuals may not show signs of the disease until later in life. CADASIL  formerly known by several names, including hereditary multi-infarct dementia  is one cause of vascular cognitive impairment (dementia caused by lack of blood to several areas of the brain). It is an autosomal dominant inheritance disorder, meaning that one parent carries and passes on the defective gene. Most individuals with CADASIL have a family history of the disorder. However, because the genetic test for CADASIL was not available before 2000, many cases were misdiagnosed as multiple sclerosis, Alzheimer's disease, or other neurodegenerative diseases."}
{"_id":"8d396752-eb49-4d06-aec4-0cbf002577b4","text":"There is no treatment to halt this genetic disorder. Individuals are given supportive care. Migraine headaches may be treated by different drugs and a daily aspirin may reduce stroke and heart attack risk. Drug therapy for depression may be given. Affected individuals who smoke should quit as it can increase the risk of stroke in CADASIL. Other stroke risk factors such as hypertension, hyperlipidemia, diabetes, blood clotting disorders and obstructive sleep apnea also should be aggressively treated.."}
{"_id":"8d6536f1-ccb3-4952-b5de-6b2843d7553f","text":"Symptoms usually progress slowly. By age 65, the majority of persons with CADASIL have cognitive problems and dementia. Some will become dependent due to multiple strokes."}
{"_id":"409c83c4-d569-4266-b12b-c5b3a1661a97","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts stroke research and clinical trials at its laboratories and clinics at the National Institutes of Health (NIH) and through grants to major medical institutions across the country. Scientists are currently studying different drugs to reduce cognitive problems seen in patients with CADASIL. Researchers are also looking at ways to overcome an over-reaction to hormones that lead to high blood pressure and poor blood supply in patients with CADASIL."}
{"_id":"8d963307-63ca-49ba-8b2e-e15d9cb1dc68","text":"Cerebral hypoxia refers to a condition in which there is a decrease of oxygen supply to the brain even though there is adequate blood flow. Drowning, strangling, choking, suffocation, cardiac arrest, head trauma, carbon monoxide poisoning, and complications of general anesthesia can create conditions that can lead to cerebral hypoxia. Symptoms of mild cerebral hypoxia include inattentiveness, poor judgment, memory loss, and a decrease in motor coordination. Brain cells are extremely sensitive to oxygen deprivation and can begin to die within five minutes after oxygen supply has been cut off. When hypoxia lasts for longer periods of time, it can cause coma, seizures, and even brain death. In brain death, there is no measurable activity in the brain, although cardiovascular function is preserved. Life support is required for respiration."}
{"_id":"bb28a885-242b-4d20-b605-a286efa61d26","text":"Treatment depends on the underlying cause of the hypoxia, but basic life-support systems have to be put in place: mechanical ventilation to secure the airway; fluids, blood products, or medications to support blood pressure and heart rate; and medications to suppress seizures."}
{"_id":"b4877669-645c-4284-9f12-0bf6c96149d2","text":"Recovery depends on how long the brain has been deprived of oxygen and how much brain damage has occurred, although carbon monoxide poisoning can cause brain damage days to weeks after the event. Most people who make a full recovery have only been briefly unconscious. The longer someone is unconscious, the higher the chances of death or brain death and the lower the chances of a meaningful recovery. During recovery, psychological and neurological abnormalities such as amnesia, personality regression, hallucinations, memory loss, and muscle spasms and twitches may appear, persist, and then resolve."}
{"_id":"43734c97-f82e-495e-b2cf-843d732e31e6","text":"The NINDS supports and conducts studies aimed at understanding neurological conditions that can damage the brain, such as cerebral hypoxia. The goals of these studies are to find ways to prevent and treat these conditions."}
{"_id":"c146dc5f-46de-4b0e-8f55-54c435296ecc","text":"Cerebral atrophy is a common feature of many of the diseases that affect the brain. Atrophy of any tissue means loss of cells. In brain tissue, atrophy describes a loss of neurons and the connections between them. Atrophy can be generalized, which means that all of the brain has shrunk; or it can be focal, affecting only a limited area of the brain and resulting in a decrease of the functions that area of the brain controls. If the cerebral hemispheres (the two lobes of the brain that form the cerebrum) are affected, conscious thought and voluntary processes may be impaired.\n                \nAssociated Diseases\/Disorders: The pattern and rate of progression of cerebral atrophy depends on the disease involved. Diseases that cause cerebral atrophy include:\n                \n- stroke and traumatic brain injury - Alzheimers disease, Picks disease, and fronto-temporal dementia - cerebral palsy, in which lesions (damaged areas) may impair motor coordination - Huntingtons disease, and other hereditary diseases that are associated with genetic mutations - leukodystrophies, such as Krabbe disease, which destroy the myelin sheath that protects axons - mitochondrial encephalomyopathies, such as Kearns-Sayre syndrome, which interfere with the basic functions of neurons - multiple sclerosis, which causes inflammation, myelin damage, and lesions in cerebral tissue - infectious diseases, such as encephalitis, neurosyphilis, and AIDS, in which an infectious agent or the inflammatory reaction to it destroys neurons and their axons\n                \nSymptoms of cerebral atrophy: Many diseases that cause cerebral atrophy are associated with dementia, seizures, and a group of language disorders called the aphasias.\n                \n- Dementia is characterized by a progressive impairment of memory and intellectual function that is severe enough to interfere with social and work skills. Memory, orientation, abstraction, ability to learn, visual-spatial perception, and higher executive functions such as planning, organizing, and sequencing may also be impaired. - Seizures can take different forms, appearing as disorientation, repetitive movements, loss of consciousness, or convulsions. - Aphasias are a group of disorders characterized by disturbances in speaking and understanding language. Receptive aphasia causes impaired comprehension. Expressive aphasia is reflected in odd choices of words, the use of partial phrases, disjointed clauses, and incomplete sentences."}
{"_id":"f7b524df-9266-4647-b6a5-d2a4aa6d97ef","text":"The NINDS funds research looking at many of the diseases and disorders that cause cerebral atrophy. Understanding the biological mechanisms that cause neurons to die in the brain will help researchers find ways to prevent, treat, and even cure the diseases that lead to cerebral atrophy."}
{"_id":"271f06f9-71c2-4e9a-992e-3a966db395a9","text":"The term \"pinched nerve\" is a colloquial term and not a true medical term. It is used to describe one type of damage or injury to a nerve or set of nerves. The injury may result from compression, constriction, or stretching. Symptoms include numbness, \"pins and needles\" or burning sensations, and pain radiating outward from the injured area. One of the most common examples of a single compressed nerve is the feeling of having a foot or hand \"fall asleep.\" A \"pinched nerve\" frequently is associated with pain in the neck or lower back. This type of pain can be caused by inflammation or pressure on the nerve root as it exits the spine. If the pain is severe or lasts a long time, you may need to have further evaluation from your physician. Several problems can lead to similar symptoms of numbness, pain, and tingling in the hands or feet but without pain in the neck or back. These can include peripheral neuropathy, carpal tunnel syndrome, and tennis elbow. The extent of such injuries may vary from minor, temporary damage to a more permanent condition. Early diagnosis is important to prevent further damage or complications. Pinched nerve is a common cause of on-the-job injury."}
{"_id":"44c6c14a-7baf-4b22-bc95-f1f22861b844","text":"The most frequently recommended treatment for pinched nerve is rest for the affected area. Nonsteroidal anti-inflammatory drugs (NSAIDs) or corticosteroids may be recommended to help alleviate pain. Physical therapy is often useful, and splints or collars may be used to relieve symptoms. Depending on the cause and severity of the pinched nerve, surgery may be needed."}
{"_id":"72bc9d48-6a5d-4079-b340-d6802f38a603","text":"With treatment, most people recover from pinched nerve. However, in some cases, the damage is irreversible."}
{"_id":"9a4dc283-9145-4a2e-9314-3a7a7a3d5205","text":"Within the NINDS research programs, pinched nerves are addressed primarily through studies associated with pain research. NINDS vigorously pursues a research program seeking new treatments for pain and nerve damage with the ultimate goal of reversing debilitating conditions such as pinched nerves."}
{"_id":"3fb5f461-f1d7-43c4-ba20-aea91684a9f7","text":"Fabry disease is caused by the lack of or faulty enzyme needed to metabolize lipids, fat-like substances that include oils, waxes, and fatty acids. The disease is also called alpha-galactosidase-A deficiency. A mutation in the gene that controls this enzyme causes insufficient breakdown of lipids, which build up to harmful levels in the autonomic nervous system (which controls involuntary functions such as breathing and digestion), cardiovascular system, eyes, and kidneys. Symptoms usually begin during childhood or adolescence and include burning sensations in the arms and legs that gets worse with exercise and hot weather and small, non-cancerous, raised reddish-purple blemishes on the skin. Excess material buildup can lead to clouding in the corneas. Lipid storage may lead to impaired blood circulation and increased risk of heart attack or stroke. The heart may also become enlarged and the kidneys may become progressively impaired, leading to renal failure. Other signs include decreased sweating, fever, and gastrointestinal difficulties.Fabry disease is the only X-linked lipid storage disease (where the mother carries the affected gene on the X chromosome that determines the child's gender and passes it to her son). Boys have a 50 percent chance of inheriting the disorder and her daughters have a 50 percent chance of being a carrier. A milder form is common in females, and occasionally some affected females may have severe symptoms similar to males with the disorder."}
{"_id":"88a04965-c7df-45f5-bf5b-affb891043e1","text":"Enzyme replacement therapy has been approved by the U.S. Food and Drug Administration for the treatment of Fabry disease. Enzyme replacement therapy can reduce lipid storage, ease pain, and preserve organ function in some individuals with the disorder. The pain that accompanies the disease may be treated with anticonvulsants. Gastrointestinal hyperactivity may be treated with metoclopramide. Some individuals may require dialysis or kidney transplantation. Restricting one's diet does not prevent lipid buildup in cells and tissues."}
{"_id":"c2240ea2-9826-4c01-a169-e1fb229ec4fc","text":"Individuals with Fabry disease often die prematurely of complications from strokes, heart disease, or kidney failure."}
{"_id":"7b5e1262-2b3e-428c-8df1-10700ab20921","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease.The NINDS supports research to find ways to treat and prevent lipid storage diseases such as Fabry disease. Researchers hope to identify biomarkers -- signs that may indicate risk of a disease and improve diagnosis -- for Fabry disease and other lipid storage diseases that will speed the development of novel therapeutics for these disorders. One NINDS-funded project is evaluating a rat model of Fabry disease, through which researchers hope to develop new proteins to increase the potency of enzyme replacement therapy."}
{"_id":"43318089-eb32-44a1-a1ee-8262e68e3621","text":"Iniencephaly is a rare birth defect caused by improper closure of the neural tube (the part of a human embryo that becomes the brain and spinal cord) during fetal development.  Iniencephaly is in the same family of neural tube defects as spina bifida, but it is more severe. In iniencephaly, the defect results in extreme retroflexion (backward bending) of the head combined with severe distortion of the spine. Diagnosis is made immediately after birth because an infants head is so severely bent backward that the face looks upward. In most infants the neck is absent and the skin of the face is connected directly to the skin of the chest, while the scalp is directly connected to the skin of the back. Most infants with iniencephaly have additional birth defects, such as anencephaly (in which major sections of the brain fail to form), cephalocele (in which part of the cranial contents protrudes from the skull), and cyclopia (in which the two cavities of the eyes fuse into one). Additional birth defects include the lack of a lower jaw bone or a cleft lip and palate. Other parts of the body may be affected, and infants can have cardiovascular disorders, diaphragmatic hernias, and gastrointestinal malformations. For reasons that are still unknown, the disorder is more common among females. No single gene has been identified as the cause for iniencephaly, or any of the neural tube defects. Scientists think these defects have complex causes, mostly likely a mix of genetic and environmental factors."}
{"_id":"79455fe1-7974-4f2f-a67c-32323cab26c1","text":"There is no standard treatment for iniencephaly since most infants rarely live longer than a few hours. Medicine is based more on prevention using supplementation with folic acid. Numerous studies have demonstrated that mothers can reduce the risk of neural tube birth defects such as iniencephaly by up to 70 percent with daily supplements of at least 4 mg of folic acid. Pregnant women should avoid taking antiepileptic drugs, diuretics, antihistamines, and sulfa drugs, which have been shown to be associated with an increased risk of neural tube defects. Maternal obesity and diabetes are also known to increase the risk for these disorders."}
{"_id":"a6c442e8-21b5-4364-8ccc-d75505e2f045","text":"The prognosis for infants with iniencephaly is extremely poor. Newborns seldom survive much past childbirth. The distortions of the babys body also pose a danger to the mother's life during delivery."}
{"_id":"ced07a7e-e09b-4bf0-98e4-b0f49a629ffc","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to iniencephaly in laboratories at the NIH and also support additional research through grants to major medical institutions across the country. Much of this research explores the complex mechanisms of neural tube development. The knowledge gained from these fundamental studies will provide a foundation for developing ways to prevent iniencephaly and the other neural tube defects."}
{"_id":"bc8793db-11b0-4886-80a2-929db688a4ee","text":"Developmental dyspraxia is a disorder characterized by an impairment in the ability to plan and carry out sensory and motor tasks. Generally, individuals with the disorder appear \"out of sync\" with their environment. Symptoms vary and may include poor balance and coordination, clumsiness, vision problems, perception difficulties, emotional and behavioral problems, difficulty with reading, writing, and speaking, poor social skills, poor posture, and poor short-term memory. Although individuals with the disorder may be of average or above average intelligence, they may behave immaturely."}
{"_id":"3814ae6e-224b-4c77-9356-8ceaeacef499","text":"Treatment is symptomatic and supportive and may include occupational and speech therapy, and \"cueing\" or other forms of communication such as using pictures and hand gestures. Many children with the disorder require special education."}
{"_id":"c2e1263c-a1a8-48f2-b54d-fd70eba38a81","text":"Developmental dyspraxia is a lifelong disorder. Many individuals are able to compensate for their disabilities through occupational and speech therapy."}
{"_id":"abd92adf-1005-4a43-aec4-9d1a7842569a","text":"The NINDS supports research on developmental disorders, such as developmental dyspraxia, aimed at learning more about these disorders, and finding ways to prevent and treat them."}
{"_id":"62af0365-629c-4881-9eff-2c53f7ab4e5e","text":"Fibromuscular dysplasia (FMD) is the abnormal development or growth of cells in the walls of arteries that can cause the vessels to narrow or bulge. The carotid arteries, which pass through the neck and supply blood to the brain, are commonly affected. Arteries within the brain and kidneys can also be affected. A characteristic string of beads pattern caused by the alternating narrowing and enlarging of the artery can block or reduce blood flow to the brain, causing a stroke or mini-stroke. Some patients experience no symptoms of the disease while others may have high blood pressure, dizziness or vertigo, chronic headache, intracranial aneurysm, ringing in the ears, weakness or numbness in the face, neck pain, or changes in vision. FMD is most often seen in persons age 25 to 50 years and affects women more often than men. More than one family member may be affected by the disease. The cause of FMD is unknown. An angiogram can detect the degree of narrowing or obstruction of the artery and identify changes such as a tear (dissection) or weak area (aneurysm) in the vessel wall. FMD can also be diagnosed using computed tomography, magnetic resonance imaging, or ultrasound."}
{"_id":"e975f4ae-8018-40b9-9eb7-13723cdd2695","text":"There is no standard protocol to treat FMD. Any treatment to improve blood flow is based on the arteries affected and the progression and severity of the disease. The carotid arteries should be tested if FMD is found elsewhere in the body since carotid involvement is linked to an increased risk of stroke. Patients with minimal narrowing may take a daily antiplatelet such as an aspirin or an anticoagulant to thin the blood and reduce the chances that a clot might form. Medications such as aspirin can also be taken for headache and neck pain, symptoms that can come from FMD. Patients with arterial disease who smoke should be encouraged to quit as smoking worsens the disease. Further treatment may include angioplasty, in which a small balloon is inserted through a catheter and inflated to open the artery. Small tubes called stents may be inserted to keep arteries open. Surgery may be needed to treat aneurysms that have the potential to rupture and cause bleeding within the brain."}
{"_id":"70da1183-2f2f-44a6-9123-2268bb5c4e15","text":"Currently there is no cure for FMD. Medicines and angioplasty can reduce the risk of initial or recurrent stroke. In rare cases, FMD-related aneurysms can burst and bleed into the brain, causing stroke, permanent nerve damage, or death."}
{"_id":"8d9a68c1-d9bd-4d9d-bbfd-6bdc349b4953","text":"The National Institute of Neurological Disorders and Stroke (NINDS), a component of the National Institutes of Health (NIH) within the U.S. Department of Health and Human Services, is the nations primary funding source for research on the brain and nervous system. The NINDS conducts research on stroke and vascular lesions of the nervous system and supports studies through grants to medical institutions across the country."}
{"_id":"9ba3f214-f25e-4c40-91dd-072c863239a6","text":"There are four types of headache: vascular, muscle contraction (tension), traction, and inflammatory. Vascular headaches include \"cluster headaches, which cause repeated episodes of intense pain, and headaches resulting from high blood pressure,and toxic headache produced by fever. Muscle contraction headaches appear to involve the tightening or tensing of facial and neck muscles. Traction and inflammatory headaches are symptoms of other disorders, ranging from stroke to sinus infection. Like other types of pain, headaches can serve as warning signals of more serious disorders. This is particularly true for headaches caused by inflammation, including those related to meningitis as well as those resulting from diseases of the sinuses, spine, neck, ears, and teeth. The most common type of primary headache (not caused by another medical condition) is migraine. Migraine headaches are usually characterized by severe pain on one or both sides of the head, an upset stomach, and, at times, disturbed vision.  Women are more likely than men to have migraine headaches."}
{"_id":"3fa155ee-0af2-4ab9-a551-5d2f1d33b670","text":"When headaches occur three or more times a month, preventive treatment is usually recommended. Drug therapy, biofeedback training, stress reduction, and elimination of certain foods from the diet are the most common methods of preventing and controlling migraine and other vascular headaches. Regular exercise, such as swimming or vigorous walking, can also reduce the frequency and severity of migraine headaches. Drug therapy for migraine is often combined with biofeedback and relaxation training. One of the most commonly used drugs for the relief of migraine symptoms is sumatriptan. Drugs used to prevent migraine also include methysergide maleate, which counteracts blood vessel constriction; propranolol hydrochloride, which also reduces the frequency and severity of migraine headaches; ergotamine tartrate, a vasoconstrictor that helps counteract the painful dilation stage of the headache; amitriptyline, an antidepressant; valproic acid, an anticonvulsant; and verapamil, a calcium channel blocker."}
{"_id":"9e28a192-49cc-42ce-a21f-53b6b16a8291","text":"Not all headaches require medical attention. But some types of headache are signals of more serious disorders and call for prompt medical care. These include: sudden, severe headache or sudden headache associated with a stiff neck; headaches associated with fever, convulsions, or accompanied by confusion or loss of consciousness; headaches following a blow to the head, or associated with pain in the eye or ear; persistent headache in a person who was previously headache free; and recurring headache in children. Migraine headaches may last a day or more and can strike as often as several times a week or as rarely as once every few years."}
{"_id":"28483e2d-078f-4ba0-a79b-3cef72fcd57b","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research relating to headaches at its laboratories at the National Institutes of Health (NIH), and supports additional research through grants to major medical institutions across the country. NINDS also supports and conducts studies to improve the diagnosis of headaches and to find ways to prevent them."}
{"_id":"ddf2aa3a-1a0b-467b-ba15-baec782125e6","text":"Cerebellar hypoplasia is a neurological condition in which the cerebellum is smaller than usual or not completely developed. Cerebellar hypoplasia is a feature of a number of congenital (present at birth) malformation syndromes, such as Walker-Warburg syndrome (a form of muscular dystrophy. It is also associated with several inherited metabolic disorders, such as Williams syndrome, and some of the neurodegenerative disorders that begin in early childhood, such as ataxia telangiectasia. In an infant or young child, symptoms of a disorder that features cerebellar hypoplasia might include floppy muscle tone, developmental or speech delay, problems with walking and balance, seizures, intellectual disability, and involuntary side to side movements of the eyes. In an older child, symptoms might include headache, dizzy spells, clumsiness, and hearing impairment."}
{"_id":"e913e7c2-ee0e-43ab-a81b-c590227ca291","text":"There is no standard course of treatment for cerebellar hypoplasia. Treatment depends upon the underlying disorder and the severity of symptoms. Generally, treatment is symptomatic and supportive."}
{"_id":"766a22a9-fd96-491c-ad68-8fbbbf68f6f6","text":"The prognosis is dependent upon the underlying disorder. Some of the disorders that are associated with cerebellar hypoplasia are progressive, which means the condition will worsen over time, and will most likely have a poor prognosis. Other disorders that feature cerebellar hypoplasia are not progressive, such as those that are the result of abnormal brain formation during fetal development, and might have a better outcome."}
{"_id":"505c255a-5017-4d71-a5ea-eb34d726d739","text":"The National Institute of Neurological Disorders and Stroke (NINDS) supports research related to cerebellar hypoplasia and its associated disorders through grants to major research institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders that feature cerebellar hypoplasia."}
{"_id":"9eb6f57e-6b61-43bb-9473-e2488f0fed6f","text":"Transverse myelitis is a neurological disorder caused by inflammation across both sides of one level, or segment, of the spinal cord. The segment of the spinal cord at which the damage occurs determines which parts of the body are affected. Damage at one segment will affect function at that segment and segments below it. In people with transverse myelitis, inflammation usually occurs at the thoracic (upper back) level, causing problems with leg movement and bowel and bladder control, which require signals from the lower segments of the spinal cord. What usually begins as a sudden onset of lower back pain, muscle weakness, or abnormal sensations in the toes and feet can rapidly progress to more severe symptoms, including paralysis, urinary retention, and loss of bowel control."}
{"_id":"7049e86a-9d33-4407-8c08-9db83987bac8","text":"No effective cure currently exists for people with transverse myelitis. Physicians often prescribe corticosteroid therapy during the first few weeks of illness to decrease inflammation. Following initial therapy, the most critical part of the treatment for this disorder consists of keeping the patients body functioning while hoping for either complete or partial spontaneous recovery of the nervous system. If an individual begins to recover limb control, physical therapy begins to help improve muscle strength, coordination, and range of motion."}
{"_id":"c47a0442-b4c7-4227-9ab8-f2016539dccd","text":"Most individuals will have only one episode of transverse myelitis. Recovery usually begins within 2 to 12 weeks of the onset of symptoms and may continue for up to 2 years and in some cases longer--requiring aggressive physical therapy and rehabilitation. However, if there is no improvement within the first 3 to 6 months, complete recovery is unlikely (although some recovery can occur). Historic data, shows that about one-third of people affected with transverse myelitis experience good or full recovery from their symptoms. Another one-third show only fair recovery and are left with significant deficits. The remaining one-third show no recovery at all, with marked dependence on others for basic functions of daily living. New, more aggressive treatment protocols may result in greater recovery statistics."}
{"_id":"3d6b7f44-faae-4623-a8bc-00b0d9bb0620","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to transverse myelitis in its laboratories at the National Institutes of Health (NIH), and also supports additional transverse myelitis research through grants to major medical institutions across the country. Some studies focus on strategies to repair the spinal cord, including approaches using cell transplantation. The NINDS also funds researchers who are using animal models of spinal cord injury to study strategies for replacement or regeneration of spinal cord nerve cells. The knowledge gained from such research should lead to a greater knowledge of the mechanisms responsible for transverse myelitis and may ultimately provide a means to prevent and treat this disorder."}
{"_id":"599b26d6-cf31-41fb-bc58-e6d612dfb4e3","text":"Tremor is an unintentional, rhythmic, muscle movement involving to-and-fro movements of one or more parts of the body. Most tremors occur in the hands, although they can also affect the arms, head, face, voice, trunk, and legs. Sometimes tremor is a symptom of another neurological disorder or a side effect of certain drugs, but the most common form occurs in otherwise healthy people. Some forms of tremor are inherited and run in families, while others have no known cause. Excessive alcohol consumption or alcohol withdrawal can kill certain nerve cells, resulting in tremor, especially in the hand. Other causes include an overactive thyroid and the use of certain drugs. Tremor may occur at any age but is most common in middle-aged and older persons.\n                \nThere are several forms of tremor, including:\n                \nEssential tremor (sometimes called benign essential tremor) is the most common form of abnormal tremor.The hands are most often affected but the head, voice, tongue, legs, and trunk may also be involved. Head tremor may be seen as a \"yes-yes\" or \"no-no\" motion. Onset is most common after age 40, although symptoms can appear at any age. Parkinsonian tremor is caused by damage to structures within the brain that control movement. The tremor is classically seen as a \"pill-rolling\" action of the hands but may also affect the chin, lips, legs, and trunk. Dystonic tremor occurs in individuals of all ages who are affected by dystonia, a movement disorder in which sustained involuntary muscle contractions cause twisting motions or painful postures or positions."}
{"_id":"580c0c9b-bdbd-44f3-bc47-6ba7fd0aad39","text":"There is no cure for most tremors. The appropriate treatment depends on accurate diagnosis of the cause. Drug treatment for parkinsonian tremor involves levodopa or dopamine-like drugs such as pramipexole and ropinirole. Essential tremor may be treated with propranolol or other beta blockers (such as nadolol) and primidone, an anticonvulsant drug. Dystonic tremor may respond to clonazepam, anticholinergic drugs, and intramuscular injections of botulinum toxin. Eliminating tremor \"triggers\" such as caffeine and other stimulants from the diet is often recommended. Physical therapy may help to reduce tremor and improve coordination and muscle control for some individuals. Surgical intervention, such as thalamotomy and deep brain stimulation, are usually performed only when the tremor is severe and does not respond to drugs."}
{"_id":"de7384ca-e965-4142-9274-764ad80c8b83","text":"Although tremor is not life-threatening, it can be embarrassing to some people and make it harder to perform daily tasks."}
{"_id":"a5d09eeb-fdf9-4ef1-ab1f-56763211575b","text":"The National Institute of Neurological Disorders and Stroke, a unit of the National Institutes of Health (NIH) within the U.S. Department of Health and Human Services, is the nations leading federal funder of research on disorders of the brain and nervous system. The NINDS sponsors research on tremor both at its facilities at the NIH and through grants to medical centers. Scientists are evaluating the effectiveness of certain drugs and searching for genes that can cause certain forms of tremor."}
{"_id":"927f1c21-18f5-4d2e-b8c2-df0a3ce06bba","text":"Sandhoff disease is a rare, inherited lipid storage disorder that progressively destroys nerve cells in the brain and spinal cord. It is caused by a deficiency of the enzyme beta-hexosaminidase, which results in the harmful accumulation of certain fats (lipids) in the brain and other organs of the body. Sandhoff disease is a severe form of Tay-Sachs disease, the incidence of which had been particularly high in people of Eastern European and Ashkenazi Jewish descent, but Sandhoff disease is not limited to any ethnic group. Onset of the disorder usually occurs at 6 months of age. Neurological symptoms may include progressive nervous system deterioration, problems initiating and controlling muscles and movement, increased startle reaction to sound, early blindness, seizures, spasticity (non-voluntary and awkward movement), and myoclonus (shock-like contractions of a muscle. Other symptoms may include macrocephaly (an abnormally enlarged head), cherry-red spots in the eyes, frequent respiratory infections, doll-like facial appearance, and an enlarged liver and spleen. Each parent must carry the defective gene and pass it on to the child. Individuals who carry only one copy of the mutated gene typically do not show signs and symptoms of the disorder."}
{"_id":"8e72bc75-9336-41e6-b729-d08f4df0adef","text":"There is no specific treatment for Sandhoff disease. Supportive treatment includes proper nutrition and hydration and keeping the airway open. Anticonvulsants may initially control seizures."}
{"_id":"32e9081c-f995-45b2-a2b9-95c17104919a","text":"The prognosis for individuals with Sandhoff disease is poor. Death usually occurs by age 3 and is generally caused by respiratory infections."}
{"_id":"b2fb3e96-048e-4187-9552-a0bafc993978","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS is a part of the National Institutes of Health, the largest supporter of biomedical research in the world. The NINDS, along with other NIH Institutes, supports the Lysosomal Disease Network, a network of centers that addresses some of the major challenges in the diagnosis, management, and therapy of rare diseases, including the lipid storage diseases. Research funded by the NINDS focuses on better understanding of how neurological deficits rise in lipid storage diseases and on the development of new treatments targeting disease mechanisms, including gene therapies, cell-based therapies, and pharmacological approaches. NINDS funded research on the gangliosidoses includes variations of magnetic resonance imaging to develop a biomarker (a sign that may indicate risk of a disease and improve diagnosis) to effectively evaluate brain biochemistry and disease progression, and expanding the use of virus-delivered gene therapy seen in an animal model of Tay-Sachs and Sandhoff diseases for use in humans."}
{"_id":"2dbd3932-8d88-4112-acfb-0d7012e39e2e","text":"Tethered spinal cord syndrome is a neurological disorder caused by tissue attachments that limit the movement of the spinal cord within the spinal column. Attachments may occur congenitally at the base of the spinal cord (conus medullaris) or they may develop near the site of an injury to the spinal cord. These attachments cause an abnormal stretching of the spinal cord. The course of the disorder is progressive. In children, symptoms may include lesions, hairy patches, dimples, or fatty tumors on the lower back; foot and spinal deformities; weakness in the legs; low back pain; scoliosis; and incontinence. This type of tethered spinal cord syndrome appears to be the result of improper growth of the neural tube during fetal development, and is closely linked to spina bifida. Tethered spinal cord syndrome may go undiagnosed until adulthood, when pain, sensory and motor problems, and loss of bowel and bladder control emerge. This delayed presentation of symptoms is related to the degree of strain placed on the spinal cord over time and may be exacerbated during sports or pregnancy, or may be due to narrowing of the spinal column (stenosis) with age. Tethering may also develop after spinal cord injury and scar tissue can block the flow of fluids around the spinal cord. Fluid pressure may cause cysts to form in the spinal cord, a condition called syringomyelia. This can lead to additional loss of movement, feeling or the onset of pain or autonomic symptoms."}
{"_id":"f52528d8-d258-4d20-8176-501908376078","text":"MRI imaging is often used to evaluate individuals with these symptoms, and can be used to diagnose the location of the tethering, lower than normal position of the conus medullaris, or presence of a tumor or fatty mass (lipoma). In children, early surgery is recommended to prevent further neurological deterioration. Regular follow-up is important: retethering may occur in some individuals during periods of rapid growth and may be seen between five to nine years of age. If surgery is not advisable, spinal cord nerve roots may be cut to relieve pain. In adults, surgery to free (detether) the spinal cord can reduce the size and further development of cysts in the cord and may restore some function or alleviate other symptoms. Other treatment is symptomatic and supportive."}
{"_id":"d13c9757-0ba5-49ae-8404-a12f96342811","text":"With treatment, individuals with tethered spinal cord syndrome have a normal life expectancy. However, some neurological and motor impairments may not be fully correctable. Surgery soon after symptoms emerge appears to improve chances for recovery and can prevent further functional decline."}
{"_id":"eaf87315-6e59-4ec2-b4ca-e489cee0a795","text":"The NINDS conducts and supports research on disorders of the spinal cord. The goals of this research are to find ways to prevent, treat, and cure these disorders."}
{"_id":"d6332996-0dd6-4041-ae86-081bc45520f9","text":"Progressive supranuclear palsy (PSP) is a rare brain disorder that causes serious and progressive problems with control of gait and balance, along with complex eye movement and thinking problems. One of the classic signs of the disease is an inability to aim the eyes properly, which occurs because of lesions in the area of the brain that coordinates eye movements. Some individuals describe this effect as a blurring. Affected individualsoften show alterations of mood and behavior, including depression and apathy as well as progressive mild dementia.\n                \nThe disorder's long name indicates that the disease begins slowly and continues to get worse (progressive), and causes weakness (palsy) by damaging certain parts of the brain above pea-sized structures called nuclei that control eye movements (supranuclear).\n                \nPSP was first described as a distinct disorder in 1964, when three scientists published a paper that distinguished the condition from Parkinson's disease. It is sometimes referred to as Steele-Richardson-Olszewski syndrome, reflecting the combined names of the scientists who defined the disorder. Although PSP gets progressively worse, no one dies from PSP itself."}
{"_id":"426642de-56a0-42e8-a3f2-9c47030b28d7","text":"There is currently no effective treatment for PSP, although scientists are searching for better ways to manage the disease. In some patients the slowness, stiffness, and balance problems of PSP may respond to antiparkinsonian agents such as levodopa, or levodopa combined with anticholinergic agents, but the effect is usually temporary. The speech, vision, and swallowing difficulties usually do not respond to any drug treatment.. Another group of drugs that has been of some modest success in PSP are antidepressant medications. The most commonly used of these drugs are Prozac, Elavil, and Tofranil. The anti-PSP benefit of these drugs seems not to be related to their ability to relieve depression. Non-drug treatment for PSP can take many forms. Patients frequently use weighted walking aids because of their tendency to fall backward. Bifocals or special glasses called prisms are sometimes prescribed for PSP patients to remedy the difficulty of looking down. Formal physical therapy is of no proven benefit in PSP, but certain exercises can be done to keep the joints limber. A surgical procedure, a gastrostomy, may be necessary when there are swallowing disturbances. This surgery involves the placement of a tube through the skin of the abdomen into the stomach (intestine) for feeding purposes."}
{"_id":"999d867f-ef9e-4c9c-8463-eb375062e327","text":"PSP gets progressively worse but is not itself directly life-threatening. It does, however, predispose patients to serious complications such as pneumonia secondary to difficulty in swallowing (dysphagia). The most common complications are choking and pneumonia, head injury, and fractures caused by falls. The most common cause of death is pneumonia. With good attention to medical and nutritional needs, however, most PSP patients live well into their 70s and beyond."}
{"_id":"d482d4df-9817-4a1d-bd23-e7a3fc470541","text":"Research is ongoing on Parkinson's and Alzheimer's diseases. Better understanding of those common, related disorders will go a long way toward solving the problem of PSP, just as studying PSP may help shed light on Parkinson's and Alzheimer's diseases."}
{"_id":"8ec96c52-05e3-4d2a-9c70-0b407ad5e53d","text":"Binswanger's disease (BD), also called subcortical vascular dementia, is a type of dementia caused by widespread, microscopic areas of damage to the deep layers of white matter in the brain. The damage is the result of the thickening and narrowing (atherosclerosis) of arteries that feed the subcortical areas of the brain. Atherosclerosis (commonly known as \"hardening of the arteries\") is a systemic process that affects blood vessels throughout the body. It begins late in the fourth decade of life and increases in severity with age. As the arteries become more and more narrowed, the blood supplied by those arteries decreases and brain tissue dies. A characteristic pattern of BD-damaged brain tissue can be seen with modern brain imaging techniques such as CT scans or magnetic resonance imaging (MRI). The symptoms associated with BD are related to the disruption of subcortical neural circuits that control what neuroscientists call executive cognitive functioning: short-term memory, organization, mood, the regulation of attention, the ability to act or make decisions, and appropriate behavior. The most characteristic feature of BD is psychomotor slowness - an increase in the length of time it takes, for example, for the fingers to turn the thought of a letter into the shape of a letter on a piece of paper. Other symptoms include forgetfulness (but not as severe as the forgetfulness of Alzheimer's disease), changes in speech, an unsteady gait, clumsiness or frequent falls, changes in personality or mood (most likely in the form of apathy, irritability, and depression), and urinary symptoms that aren't caused by urological disease. Brain imaging, which reveals the characteristic brain lesions of BD, is essential for a positive diagnosis."}
{"_id":"08055832-7438-4df6-ac38-668efba4ed79","text":"There is no specific course of treatment for BD. Treatment is symptomatic. People with depression or anxiety may require antidepressant medications such as the serotonin-specific reuptake inhibitors (SSRI) sertraline or citalopram. Atypical antipsychotic drugs, such as risperidone and olanzapine, can be useful in individuals with agitation and disruptive behavior. Recent drug trials with the drug memantine have shown improved cognition and stabilization of global functioning and behavior. The successful management of hypertension and diabetes can slow the progression of atherosclerosis, and subsequently slow the progress of BD. Because there is no cure, the best treatment is preventive, early in the adult years, by controlling risk factors such as hypertension, diabetes, and smoking."}
{"_id":"8e4a6a0f-1e3f-45c4-8c7d-d82104db4228","text":"BD is a progressive disease; there is no cure. Changes may be sudden or gradual and then progress in a stepwise manner. BD can often coexist with Alzheimer's disease. Behaviors that slow the progression of high blood pressure, diabetes, and atherosclerosis -- such as eating a healthy diet and keeping healthy wake\/sleep schedules, exercising, and not smoking or drinking too much alcohol -- can also slow the progression of BD."}
{"_id":"2526ecad-5d53-4028-8f8e-09b269a3bd32","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to BD in its laboratories at the National Institutes of Health (NIH), and also supports additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure neurological disorders, such as BD."}
{"_id":"7fd67c34-88ec-494f-a701-627ec01588eb","text":"Dravet syndrome, also called severe myoclonic epilepsy of infancy (SMEI), is a severe form of epilepsy. It appears during the first year of life with frequent febrile seizures  fever-related seizures that, by definition, are rare beyond age 5. Later, other types of seizures typically arise, including myoclonus (involuntary muscle spasms). Status epilepticus  a state of continuous seizure requiring emergency medical care  also may occur. Children with Dravet syndrome typically experience poor development of language and motor skills, hyperactivity, and difficulty relating to others.\n                \nIn 30 to 80 percent of cases, Dravet syndrome is caused by defects in a gene required for the proper function of brain cells. Borderline SMEI (SMEB) and another type of infant-onset epilepsy called generalized epilepsy with febrile seizures plus (GEFS+) are caused by defects in the same gene. In GEFS+, febrile seizures may persist beyond age 5."}
{"_id":"5ce39b22-1741-496e-8a6e-792491be15a9","text":"Seizures in Dravet syndrome are difficult to control, but can be reduced by anticonvulsant drugs. A ketogenic diet, high in fats and low in carbohydrates, also may be beneficial."}
{"_id":"406170b9-cbec-4922-81c9-7cd1c9f6054f","text":"As children with Dravet syndrome get older, their decline in cognitive function stabilizes, and in many, it improves slightly. However, most teenagers with Dravet syndrome are dependent on caregivers. The degree of cognitive impairment appears to correlate with the frequency of seizures."}
{"_id":"2028fb29-db2c-421d-978f-2bf9feb00edf","text":"The NINDS conducts and supports a broad program of basic and clinical research on all types of epilepsy, including Dravet syndrome. Study of the genetic defects responsible for Dravet syndrome and related disorders is expected to lead to the development of effective drug therapies."}
{"_id":"aa19761e-3b85-4026-9487-87f5407e6042","text":"The mucolipidoses (ML) are a group of inherited metabolic diseases that affect the bodys ability to carry out the normal turnover of various materials within cells. In ML, abnormal amounts of carbohydrates and fatty materials (lipids) accumulate in cells. Because our cells are not able to handle such large amounts of these substances, damage to the cells occurs, causing symptoms that range from mild learning disabilities to severe intellectual impairment and skeletal deformities.\n                \nThe group includes four diseases:\n                \n- Mucolipidosis I (sialidosis)  - Mucolipidosis II (inclusion-cell, or I-cell, disease)  - Mucolipidosis III (pseudo-Hurler polydystrophy)  - Mucolipidosis IV\n                \nThe MLs are classified as lysosomal storage diseases because they involve increased storage of substances in the lysosomes, which are specialized sac-like components within most cells. Individuals with ML are born with a genetic defect in which their bodies either do not produce enough enzymes or, in some instances, produce ineffective forms of enzymes. Without functioning enzymes, lysosomes cannot break down carbohydrates and lipids and transport them to their normal destination. The molecules then accumulate in the cells of various tissues in the body, leading to swelling and damage of organs.\n                \nThe mucolipidoses occur only when a child inherits two copies of the defective gene, one from each parent. When both parents carry a defective gene, each of their children faces a one in four chance of developing one of the MLs."}
{"_id":"e48aad32-7217-4e90-9ab4-076182cbbeb7","text":"No cures or specific therapies for ML currently exists. Therapies are generally geared toward treating symptoms and providing supportive care to the child. For individuals with corneal clouding, surgery to remove the thin layer over the eye has been shown to reduce the cloudiness in the eye. However, this improvement may be only temporary. Physical and occupational therapy may help children with motor delays. Children with language delays may benefit from speech therapy. Children at risk for failure to thrive (growth failure) may need nutritional supplements, especially iron and vitamin B12 for persons with ML IV. Respiratory infections should be treated immediately and fully with antibiotics."}
{"_id":"6a2b3906-91ca-4d6e-ab88-1a16f2f5eba2","text":"Symptoms of ML can be congenital (present at birth) or begin in early childhood or adolescence. Early symptoms can include skeletal abnormalities, vision problems and developmental delays. Over time, many children with ML develop poor mental capacities, have difficulty reaching normal developmental milestones, and, in many cases, eventually die of the disease."}
{"_id":"2fb40ca8-659c-4fe5-9ad5-2b4f59dd2e6f","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. Investigators are conducting studies to determine the effects of ML genetic mutations in various animal models of the disease. Studying the disease mechanisms in these models may allow scientists to develop treatments for people with an ML disorder.Clinical trials include a natural history of individuals with ML IV, to better understand the disease and identify potential outcomes, and longitudinal studies to better understand disease progression, assess current therapies, and identify potential treatments."}
{"_id":"cfde7c33-e52d-45d5-a9c1-b3d294eca225","text":"Hereditary neuropathies are a group of inherited disorders affecting the peripheral nervous system. The hereditary neuropathies are divided into four major subcategories: hereditary motor and sensory neuropathy, hereditary sensory neuropathy, hereditary motor neuropathy, and hereditary sensory and autonomic neuropathy. The most common type is Charcot-Marie-Tooth disease, one of the hereditary motor and sensory neuropathies. Symptoms of the hereditary neuropathies vary according to the type and may include sensory symptoms such as numbness, tingling, and pain in the feet and hands; or motor symptoms such as weakness and loss of muscle bulk, particularly in the lower leg and feet muscles. Certain types of hereditary neuropathies can affect the autonomic nerves, resulting in impaired sweating, postural hypotension, or insensitivity to pain. Some people may have foot deformities such as high arches and hammer toes, thin calf muscles (having the appearance of an inverted champagne glass) or scoliosis (curvature of the spine). The symptoms of hereditary neuropathies may be apparent at birth or appear in middle or late life. They can vary among different family members, with some family members being more severely affected than others. The hereditary neuropathies can be diagnosed by blood tests for genetic testing, nerve conduction studies, and nerve biopsies."}
{"_id":"e7be47e3-868f-45a6-aa56-332fbb0bb8c6","text":"There are no standard treatments for hereditary neuropathies. Treatment is mainly symptomatic and supportive. Medical treatment includes physical therapy and if needed, pain medication. Orthopedic surgery may be needed to correct severe foot or other skeletal deformities. Bracing may also be used to improve mobility."}
{"_id":"8881678e-4dcd-4417-b475-d27f92659d62","text":"The prognosis for individuals with hereditary neuropathies depends upon the type of neuropathy. Some hereditary neuropathies have very mild symptoms and may go undiagnosed for many years. Other types are more severe and are associated with more disabilities. Genetic counseling is important to understand further details about the disease and prognosis."}
{"_id":"11ba9e28-8cf5-442f-b77f-6ab95b4dd187","text":"The NINDS supports research on neuromuscular disorders, such as hereditary neuropathies, aimed at learning more about these disorders and finding ways to prevent and treat them."}
{"_id":"faabc5a8-2318-40c3-9a8e-a15ea3759160","text":"Glossopharyngeal neuralgia (GN) is a rare pain syndrome that affects the glossopharyngeal nerve (the ninth cranial nerve that lies deep within the neck) and causes sharp, stabbing pulses of pain in the back of the throat and tongue, the tonsils, and the middle ear. The excruciating pain of GN can last for a few seconds to a few minutes, and may return multiple times in a day or once every few weeks. Many individuals with GN relate the attacks of pain to specific trigger factors such as swallowing, drinking cold liquids, sneezing, coughing, talking, clearing the throat, and touching the gums or inside the mouth. GN can be caused by compression of the glossopharyngeal nerve, but in some cases, no cause is evident. Like trigeminal neuralgia, it is associated with multiple sclerosis. GN primarily affects the elderly."}
{"_id":"fc4b9c4f-3639-4f00-98cf-fba97e605070","text":"Most doctors will attempt to treat the pain first with drugs. Some individuals respond well to anticonvulsant drugs, such as carbamazepine and gabapentin. Surgical options, including nerve resection, tractotomy, or microvascular decompression, should be considered when individuals either dont respond to, or stop responding to, drug therapy. Surgery is usually successful at ending the cycles of pain, although there may be some sensory loss in the mouth, throat, or tongue."}
{"_id":"ac8431f6-40af-4a95-965b-c8fe6915c726","text":"Some individuals recover from an initial attack and never have another. Others will experience clusters of attacks followed by periods of short or long remission. Individuals may lose weight if they fear that chewing, drinking, or eating will cause an attack."}
{"_id":"d65a498a-3882-444e-a127-103a63b9e7fd","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes at the National Institutes of Health conduct research related to GN and support additional research through grants to major research institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders such as GN."}
{"_id":"9b1d2e94-1f0b-4deb-ab6b-7334d580633b","text":"Gaucher disease is one of the inherited metabolic disorders known as lipid storage diseases. Lipids are fatty materials that include oils, fatty acids, waxes, and steroids (such as cholesterol and estrogen). Gaucher disease is caused by a deficiency of the enzyme glucocerebrosidase. Fatty materials can accumulate in the brain, spleen, liver, lungs, bone marrow, and kidneys. Symptoms may begin in early life or adulthood and include skeletal disorders and bone lesions that may cause pain and fractures, enlarged spleen and liver, liver malfunction, anemia, and yellow spots in the eyes. There are three common clinical subtypes of Gaucher disease. The first category, called type 1 (or nonneuropathic), typically does not affect the brain. Symptoms may begin early in life or in adulthood. People in this group usually bruise easily due to low blood platelets and experience fatigue due to anemia They also may have an enlarged liver and spleen. Many individuals with a mild form of the disorder may not show any symptoms. In type 2 Gaucher disease (acute infantile neuropathic Gaucher disease), symptoms usually begin by 3 months of age and include extensive brain damage, seizures, spasticity, poor ability to suck and swallow, and enlarged liver and spleen. Affecetd children usually die before 2 years of age. In the third category, called type 3 (or chronic neuropathic Gaucher disease), signs of brain involvement such as seizures gradually become apparent. Major symptoms also include skeletal irregularities, eye movement disorders, cognitive deficit, poor coordination, enlarged liver and spleen, respiratory problems, and blood disorders."}
{"_id":"9567b369-1341-4f45-80aa-a85dc94a623b","text":"Enzyme replacement therapy is available for most people with types 1 and 3 Gaucher disease. Given intravenously every two weeks, this therapy decreases liver and spleen size, reduces skeletal abnormalities, and reverses other symptoms of the disorder. The U.S. Food and Drug Administration has approved eligustat tartrate for Gaucher treatment, which works by administering small molecules that reduce the action of the enzyme that catalyzes glucose to ceramide. Surgery to remove the whole or part of the spleen may be required on rare occasions, and blood transfusions may benefit some anemic individuals. Other individuals may require joint replacement surgery to improve mobility and quality of life. There is no effective treatment for severe brain damage that may occur in persons with types 2 and 3 Gaucher disease."}
{"_id":"8e7ad196-4ba1-46e4-9b61-87e4299743e2","text":"Enzyme replacement therapy is very beneficial for type 1 and most type 3 individuals with this condition. Successful bone marrow transplantation can reverse the non-neurological effects of the disease, but the procedure carries a high risk and is rarely performed in individuals with Gaucher disease."}
{"_id":"e0deaab2-0f79-4966-85ee-f01eea5a82a8","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS), a part of the National Institutes of Health), is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS supports research to find ways to treat and prevent lipid storage disorders such as Gaucher disease. For example, researchers hope to identify biomarkers (signs that may indicate risk of a disease and improve diagnosis) for Gaucher disease and other lipid storage diseases; and identify genetic, biochemical, and clinical factors that are associated with disease severity in individuals with Gaucher disease.Additional research is looking at the increased buildup of the protein alpha-synuclein, which is seen in Gaucher disease, Parkinson's disease, and Lewy Body Dementia. Using different models of glucoserebrosidase deficiency, scientists hope to learn how this deficiency impairs the breakdown of lysosomal proteins, including the breakdown of alpha-synuclein."}
{"_id":"894b7393-51ea-43ac-8604-055e4a44167d","text":"Shingles (herpes zoster) is an outbreak of rash or blisters on the skin that is caused by the same virus that causes chickenpox  the varicella-zoster virus. The first sign of shingles is often burning or tingling pain (which can be severe), or sometimes numbness or itch,generally on one side of the body. After several days or a week, a rash of fluid-filled blisters, similar to chickenpox, appears in one area on one side of the body. Shingles pain can be mild or intense. Some people have mostly itching; some feel pain from the gentlest touch or breeze. The most common location for shingles is a band, called a dermatome, spanning one side of the trunk around the waistline. Anyone who has had chickenpox is at risk for shingles. Scientists think that some of the virus particles from the original exposure to the varicella-zoster virus,leave the skin blisters and move into the nervous system. When the varicella-zoster virus reactivates, the virus moves back down the long nerve fibers that extend from the sensory cell bodies to the skin. The viruses multiply, the tell-tale rash erupts, and the person now has shingles."}
{"_id":"ad1a4011-e8cc-43c0-abbf-5ee90d3b9b88","text":"The severity and duration of an attack of shingles can be significantly reduced by immediate treatment with antiviral drugs, which include acyclovir, valcyclovir, or famcyclovir. Antiviral drugs may also help stave off the painful after-effects of shingles known as postherpetic neuralgia. Other treatments for postherpetic neuralgia include steroids, antidepressants, anticonvulsants (including pregabalin and gabapentin enacarbil), and topical agents. The varicella zoster virus vaccine (Zostavax) has been approved by teh food and Drug Administration for adults age 50 and older. Researchers found that giving older adults the vaccine reduced the expected number of later cases of shingles by half. And in people who still got the disease despite immunization, the severity and complications of shingles were dramatically reduced. The shingles vaccine is a preventive therapy and not a treatment for those who already have shingles or long-lasting nerve pain (postherpetic neuralgia)."}
{"_id":"2ba1d8c6-18ae-4da0-9fc7-42ee9f8c293e","text":"For most healthy people who receive treatment soon after the outbreak of blisters, the lesions heal, the pain subsides within 3 to 5 weeks, and the blisters often leave no scars. However, shingles is a serious threat in immunosuppressed individuals  for example, those with HIV infection or who are receiving cancer treatments that can weaken their immune systems. People who receive organ transplants are also vulnerable to shingles because they are given drugs that suppress the immune system. \n                \nA person with a shingles rash can pass the virus to someone, usually a child, who has never had chickenpox, but the child will develop chickenpox, not shingles. A person with chickenpox cannot give shingles to someone else. Shingles comes from the virus hiding inside the person's body, not from an outside source."}
{"_id":"87f7339f-2dd5-4dd4-9271-ab1928c5f0b7","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS supports research on viral proteins and virus defense mechanisms in neurons to understand why the varicella-zoster virus establishes latency uniquely in neurons and not in other cell types. Other studies focus on how VZV travels along sensory nerve fibers, or axons, and its role in latency and viral reactivation. Scientists also hope to identify molecular mechanisms that regulate the expression of latent viral genes, which may lead to targeted therapy to prevent reactivation. Other studies hope to better understand cellular changes that lead to persistent pain."}
{"_id":"2be3c5b5-14bd-4dda-8860-8c3918e8fa0d","text":"Leigh's disease is a rare inherited neurometabolic disorder that affects the central nervous system. This progressive disorder begins in infants between the ages of three months and two years.Rarely, it occurs in teenagers and adults.Leigh's disease can be caused by mutations in mitochondrial DNA or by deficiencies of an enzyme called pyruvate dehydrogenase. Symptoms of Leigh's disease usually progress rapidly. The earliest signs may be poor sucking ability,and the loss of head control and motor skills.These symptoms may be accompanied by loss of appetite, vomiting, irritability, continuous crying, and seizures. As the disorder progresses, symptoms may also include generalized weakness, lack of muscle tone, and episodes of lactic acidosis, which can lead to impairment of respiratory and kidney function.\n                \nIn Leighs disease, genetic mutations in mitochondrial DNA interfere with the energy sources that run cells in an area of the brain that plays a role in motor movements.The primary function of mitochondria is to convert the energy in glucose and fatty acids into a substance called adenosine triphosphate ( ATP). The energy in ATP drives virtually all of a cell's metabolic functions. Genetic mutations in mitochondrial DNA, therefore, result in a chronic lack of energy in these cells, which in turn affects the central nervous system and causes progressive degeneration of motor functions.\n                \nThere is also a form of Leighs disease (called X-linked Leigh's disease) which is the result of mutations in a gene that produces another group of substances that are important for cell metabolism. This gene is only found on the X chromosome."}
{"_id":"b9afb261-b2c9-43da-ab16-bdb73662ecee","text":"The most common treatment for Leigh's disease is thiamine or Vitamin B1. Oral sodium bicarbonate or sodium citrate may also be prescribed to manage lactic acidosis. Researchers are currently testing dichloroacetate to establish its effectiveness in treating lactic acidosis. In individuals who have the X-linked form of Leighs disease, a high-fat, low-carbohydrate diet may be recommended."}
{"_id":"91fe93de-d9de-4283-8abb-5468188e0031","text":"The prognosis for individuals with Leigh's disease is poor. Individuals who lack mitochondrial complex IV activity and those with pyruvate dehydrogenase deficiency tend to have the worst prognosis and die within a few years. Those with partial deficiencies have a better prognosis, and may live to be 6 or 7 years of age. Some have survived to their mid-teenage years."}
{"_id":"19d2a3f4-437e-481b-8e39-e365b67f0488","text":"The NINDS supports and encourages a broad range of basic and clinical research on neurogenetic disorders such as Leigh's disease. The goal of this research is to understand what causes these disorders and then to apply these findings to new ways to diagnose, treat, and prevent them."}
{"_id":"0b90357a-6a85-4539-9c7a-6bf516738255","text":"Kuru is a rare and fatal brain disorder that occurred at epidemic levels during the 1950s-60s among the Fore people in the highlands of New Guinea. The disease was the result of the practice of ritualistic cannibalism among the Fore, in which relatives prepared and consumed the tissues (including brain) of deceased family members. Brain tissue from individuals with kuru was highly infectious, and the disease was transmitted either through eating or by contact with open sores or wounds. Government discouragement of the practice of cannibalism led to a continuing decline in the disease, which has now mostly disappeared.\n                \nKuru belongs to a class of infectious diseases called transmissible spongiform encephalopathies (TSEs), also known as prion diseases. The hallmark of a TSE disease is misshapen protein molecules that clump together and accumulate in brain tissue. Scientists believe that misshapen prion proteins have the ability to change their shape and cause other proteins of the same type to also change shape. Other TSEs include Creutzfeldt-Jakob disease and fatal familial insomnia in humans, bovine spongiform encephalopathy in cattle (also known as mad cow disease), scrapie in sheep and goats, and chronic wasting disease in deer and elk."}
{"_id":"4ab70f1e-053e-4308-8909-5abeb03130ca","text":"There were no treatments that could control or cure kuru, other than discouraging the practice of cannibalism. Currently, there are no cures or treatments for any of the other TSE diseases."}
{"_id":"6c4d493b-37b2-40d0-b761-f0a59f136403","text":"Similar to other the TSEs, kuru had a long incubation period; it was years or even decades before an infected person showed symptoms. Because kuru mainly affected the cerebellum, which is responsible for coordination, the usual first symptoms were an unsteady gait, tremors, and slurred speech. (Kuru is the Fore word for shiver.) Unlike most of the other TSEs, dementia was either minimal or absent. Mood changes were often present. Eventually, individuals became unable to stand or eat, and they died in a comatose state from 6 to 12 months after the first appearance of symptoms."}
{"_id":"631ca4a5-c3e3-4e89-a2aa-b665a5e5d171","text":"The NINDS funds research to better understand the genetic, molecular, and cellular mechanisms that underlie the TSE diseases. Findings from this research will lead to ways to diagnose, treat, prevent, and ultimately cure these diseases."}
{"_id":"c3316e42-7a63-494e-a1d8-cf1a41903f9b","text":"Neurodegeneration with brain iron accumulation (NBIA) is a rare, inherited, neurological movement disorder characterized by an abnormal accumulation of iron in the brain and progressive degeneration of the nervous system. Symptoms, which vary greatly among patients and usually develop during childhood, may include dystonia (slow writhing, distorting muscle contractions of the limbs, face, or trunk), dysarthria (slurred or slow speech) choreoathetosis (involuntary, purposeless jerky muscle movements), muscle rigidity (uncontrolled tightness of the muscles), spasticity (sudden, involuntary muscle spasms), and\/or ataxia (inability to coordinate movements), confusion, disorientation, seizures, stupor, and dementia. Visual changes are also common, most often due to atrophy of the optic nerve (optic atrophy) or degeneration of the retinal layer in the back of the eye (retinal degeneration Cognitive decline occurs in some forms of NBIA; the majority of individuals with NBIA do not have cognitive impairment. Several genes have been found that cause NBIA."}
{"_id":"b86d5ab1-f754-419c-a6c1-3b8095697871","text":"There is no cure for NBIA, nor is there a standard course of treatment. Treatment is symptomatic and supportive, and may include physical or occupational therapy, exercise physiology, and\/or speech pathology. Many medications are available to treat the primary symptoms of dystonia and spasticity, including oral medications, intrathecal baclofen pump (in which a small pump is implanted under the skin and is programmed to deliver a specific amount of medication on a regular basis), deep brain stimulation, and botulinum toxin injection."}
{"_id":"88a9e6f7-a48d-4b09-be6a-d90963eab836","text":"NBIA is a progressive condition. Most individuals experience periods of rapid decline lasting weeks to months, with relatively stable periods in between. The rate of progression correlates with the age at onset, meaning that children with early symptoms tend to fare more poorly. For those with early onset, dystonia and spasticity can eventually limit the ability to walk, usually leading to use of a wheelchair by the midteens. Life expectancy is variable, although premature death does occur in NBIA. Premature death usually occurs due to secondary complications such as impaired swallowing or confinement to a bed or wheelchair, which can lead to poor nutrition or aspiration pneumonia. With improved medical care, however, a greater number of affected individuals reach adulthood. For those with atypical, late-onset NBIA, many are diagnosed as adults and live well into adulthood."}
{"_id":"70deac22-da54-4b24-80b5-209d18ccb042","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. NINDS-funded researchers are developing a mouse model of an NBIA disorder to gain insight into the causes of the disease and accelerate ongoing efforts to identify therapeutics to treat it.."}
{"_id":"0f6d56c2-f401-4954-b77b-d3bc2c252e6f","text":"Pompe disease is a rare (estimated at 1 in every 40,000 births), inherited and often fatal disorder that disables the heart and skeletal muscles. It is caused by mutations in a gene that makes an enzyme called acid alpha-glucosidase (GAA). Normally, the body uses GAA to break down glycogen, a stored form of sugar used for energy. The enzyme performs its function in intracellular compartments called lysosomes. Lysosomes are known to function as cellular clearinghouses; they ingest multiple substances including glycogen, which is converted by the GAA into glucose, a sugar that fuels muscles. In Pompe disease, mutations in the GAA gene reduce or completely eliminate this essential enzyme. Excessive amounts of lysosomal glycogen accumulate everywhere in the body, but the cells of the heart and skeletal muscles are the most seriously affected. Researchers have identified up to 300 different mutations in the GAA gene that cause the symptoms of Pompe disease, which can vary widely in terms of age of onset and severity. The severity of the disease and the age of onset are related to the degree of enzyme deficiency.\n                \nEarly onset (or the infantile form) is the result of complete or near complete deficiency of GAA. Symptoms begin in the first months of life, with feeding problems, poor weight gain, muscle weakness, floppiness, and head lag. Respiratory difficulties are often complicated by lung infections. The heart is grossly enlarged. Many infants with Pompe disease also have enlarged tongues. Most babies die from cardiac or respiratory complications before their first birthday.\n                \nLate onset (or juvenile\/adult) Pompe disease is the result of a partial deficiency of GAA. The onset can be as early as the first decade of childhood or as late as the sixth decade of adulthood. The primary symptom is muscle weakness progressing to respiratory weakness and death from respiratory failure after a course lasting several years. The heart is usually not involved. A diagnosis of Pompe disease can be confirmed by screening for the common genetic mutations or measuring the level of GAA enzyme activity in a blood sample. Once Pompe disease is diagnosed, testing of all family members and a consultation with a professional geneticist are recommended. Carriers are most reliably identified via genetic mutation analysis."}
{"_id":"c0523b0b-97b3-4385-933f-7b47db066f5a","text":"Individuals with Pompe disease are best treated by a team of specialists (such as cardiologist, neurologist, and respiratory therapist) knowledgeable about the disease, who can offer supportive and symptomatic care. The discovery of the GAA gene has led to rapid progress in understanding the biological mechanisms and properties of the GAA enzyme. As a result, an enzyme replacement therapy has been developed that has shown, in clinical trials with infantile-onset patients, to decrease heart size, maintain normal heart function, improve muscle function, tone, and strength, and reduce glycogen accumulation. A drug called alglucosidase alfa (Myozyme), has received FDA approval for the treatment of infants and children with Pompe disease. Another algluosidase alfa drug, Lumizyme, has been approved for late-onset (non-infantile) Pompe disease."}
{"_id":"4ff9d197-7eaf-46aa-8c85-8b475c0cbf2f","text":"Without enzyme replacement therapy, the hearts of babies with infantile onset Pompe disease progressively thicken and enlarge. These babies die before the age of one year from either cardiorespiratory failure or respiratory infection. For individuals with late onset Pompe disease, the prognosis is dependent upon the age of onset. In general, the later the age of onset, the slower the progression of the disease. Ultimately, the prognosis is dependent upon the extent of respiratory muscle involvement."}
{"_id":"347a652f-19bd-4659-ae13-171536c8259d","text":"The National Institute of Neurological Disorders and Stroke (NINDS) supports Pompe research through grants to major research institutions across the country. Research related to Pompe disease is conducted in one of the laboratories of the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) at the National Institutes of Health. Much of Pompe-related research focuses on finding better ways to prevent, treat, and ultimately cure this disorder."}
{"_id":"da7b56a0-9a28-4d3b-b657-590a643b11af","text":"Dysgraphia is a neurological disorder characterized by writing disabilities. Specifically, the disorder causes a person's writing to be distorted or incorrect. In children, the disorder generally emerges when they are first introduced to writing. They make inappropriately sized and spaced letters, or write wrong or misspelled words, despite thorough instruction. Children with the disorder may have other learning disabilities; however, they usually have no social or other academic problems. Cases of dysgraphia in adults generally occur after some trauma. In addition to poor handwriting, dysgraphia is characterized by wrong or odd spelling, and production of words that are not correct (i.e., using \"boy\" for \"child\"). The cause of the disorder is unknown, but in adults, it is usually associated with damage to the parietal lobe of the brain."}
{"_id":"df760967-b210-4bac-9ac2-323a12c2372f","text":"Treatment for dysgraphia varies and may include treatment for motor disorders to help control writing movements. Other treatments may address impaired memory or other neurological problems. Some physicians recommend that individuals with dysgraphia use computers to avoid the problems of handwriting."}
{"_id":"81c9d7d5-6ad3-49de-95ff-8b35987b7fc4","text":"Some individuals with dysgraphia improve their writing ability, but for others, the disorder persists."}
{"_id":"10814798-2bf7-4f11-8184-287128784aa8","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) support dysgraphia research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to treat, and ultimately, prevent dysgraphia."}
{"_id":"052ad0bc-d8f8-4f47-b470-e15dffc5e426","text":"Orthostatic hypotension is a sudden fall in blood pressure that occurs when a person assumes a standing position. It is due to a lesion of the baroreflex loop, which senses a change in blood pressure and adjusts heart rate and activates sympathetic nerve system fibers to cause the blood vessels to narrow and correct blood pressure. It may also be caused by hypovolemia (a decreased amount of blood in the body), resulting from the excessive use of diuretics, vasodilators, or other types of drugs, dehydration, or prolonged bed rest. The disorder may be associated with Addison's disease, diabetes, and certain neurological disorders including Multiple System Atrophy with Orthostatic Hypotension (formerly known as Shy-Drager syndrome), autonomic system neuropathies, and other dysautonomias. Symptoms, which generally occur after sudden standing, include dizziness, lightheadedness, blurred vision, and syncope (temporary loss of consciousness)."}
{"_id":"22c91cea-7fa4-4c29-9de9-24b022d8b783","text":"When orthostatic hypotension is caused by hypovolemia due to medications, the disorder may be reversed by adjusting the dosage or by discontinuing the medication. When the condition is caused by prolonged bed rest, improvement may occur by sitting up with increasing frequency each day. In some cases, physical counterpressure such as elastic hose or whole-body inflatable suits may be required. Dehydration is treated with salt and fluids. More severe cases can be treated with drugs, such as midodrine, to raise blood pressure."}
{"_id":"9bce8c8b-c4c3-4541-a0ff-b220471d446d","text":"The prognosis for individuals with orthostatic hypotension depends on the underlying cause of the condition."}
{"_id":"cf5d6dd2-c773-4589-ae60-9a2a522259c5","text":"The NINDS supports research on conditions such as neurogenic orthostatic hypotension aimed at increasing scientific understanding of the condition and finding ways to treat and prevent it."}
{"_id":"ac51eae8-464d-48c2-afa3-aa787eb8d487","text":"Huntington's disease (HD) is an inherited disorder that causes degeneration of brain cells, called neurons, in motor control regions of the brain, as well as other areas. Symptoms of the disease, which gets progressively worse, include uncontrolled movements (called chorea), abnormal body postures, and changes in behavior, emotion, judgment, and cognition. People with HD also develop impaired coordination, slurred speech, and difficulty feeding and swallowing. HD typically begins between ages 30 and 50. An earlier onset form called juvenile HD, occurs under age 20. Symptoms of juvenile HD differ somewhat from adult onset HD and include unsteadiness, rigidity, difficulty at school, and seizures. More than 30,000 Americans have HD.  Huntingtons disease is caused by a mutation in the gene for a protein called huntingtin. The defect causes the cytosine, adenine, and guanine (CAG) building blocks of DNA to repeat many more times than is normal. Each child of a parent with HD has a 50-50 chance of inheriting the HD gene. If a child does not inherit the HD gene, he or she will not develop the disease and generally cannot pass it to subsequent generations. There is a small risk that someone who has a parent with the mutated gene but who did not inherit the HD gene may pass a possibly harmful genetic sequence to her\/his children. A person who inherits the HD gene will eventually develop the disease. A genetic test, coupled with a complete medical history and neurological and laboratory tests, helps physicians diagnose HD."}
{"_id":"7ab0136e-b5dd-4dae-a4d3-afa7e2467fb7","text":"There is no treatment that can stop or reverse the course of HD. Tetrabenazine is prescribed for treating Huntingtons-associated chorea. It is the only drug approved by the U.S. Food and Drug Administration specifically for use against HD. Antipsychotic drugs may help to alleviate chorea and may also be used to help control hallucinations, delusions, and violent outbursts. Drugs may be prescribed to treat depression and anxiety. Drugs used to treat the symptoms of HD may have side effects such as fatigue, sedation, decreased concentration, restlessness, or hyperexcitability, and should be only used when symptoms create problems for the individual."}
{"_id":"57e624e1-d493-49b3-8470-b017685a4249","text":"Huntingtons disease causes disability that gets worse over time. People with this disease usually die within 15 to 20 years following diagnosis. At this time, no treatment is available to slow, stop or reverse the course of HD."}
{"_id":"4fca6b11-e012-4d82-bdf4-1ef243a83b7e","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. A major focus of research on HD is to understand the toxicity of mutant huntingin protein to brain cells and to develop potential drugs for counteracting it. Animal models of the disorder allow scientists to study mechanisms of the disease and to move forward with strategies most likely to work and least likely to cause harm for individuals. The HD gene discovery is allowing scientists to recruit individuals who carry the HD gene into clinical studies early  before they become ill. Researchers hope to understand how the defective gene affects various structures in the brain and the body's chemistry and metabolism. Since some of the clinical symptoms in neurodegenerative diseases may be caused by the ultimate malfunctioning of neuronal circuits rather than by the loss of individual cells, scientists are using cutting-edge methods such as optogenetics (where neurons are activated or silenced in the brains of living animals using light beams) to probe the cause and progression of such circuit defects in HD. Scientists are also using stem cells to study disease mechanisms and test potential therapeutic drugs.\n                \nThe NINDS-funded PREDICT-HD study seeks to identify biomarkers (biological changes that can be used to predict, diagnose, or monitor a disease) for HD. One goal of PREDICT-HD is to determine if the progression of the disease correlates with changes in brain scans images, or with chemical changes in blood, urine, or cerebrospinal fluid. A large and related NINDS-supported study aims to identify additional genetic factors in people that influence the course of the disease. Since individuals with the same CAG expansions can differ widely in the age of disease onset and severity of symptoms, researchers are trying to identify variations in the genomes of individuals with HD that account for those differences in the hopes that they will point to new targets for disease intervention and therapy."}
{"_id":"33b3ca50-64f1-4639-9d53-248bec769ad7","text":"Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, are a group of rare degenerative brain disorders characterized by tiny holes that give the brain a \"spongy\" appearance. These holes can be seen when brain tissue is viewed under a microscope.\n                \nCreutzfeldt-Jakob disease (CJD) is the most well-known of the human TSEs. It is a rare type of dementia that affects about one in every one million people each year. Other human TSEs include kuru, fatal familial insomnia (FFI), and Gerstmann-Straussler-Scheinker disease (GSS). Kuru was identified in people of an isolated tribe in Papua New Guinea and has now almost disappeared. FFI and GSS are extremely rare hereditary diseases, found in just a few families around the world. A new type of CJD, called variant CJD (vCJD), was first described in 1996 and has been found in Great Britain and several other European countries. The initial symptoms of vCJD are different from those of classic CJD and the disorder typically occurs in younger patients. Research suggests that vCJD may have resulted from human consumption of beef from cattle with a TSE disease called bovine spongiform encephalopathy (BSE), also known as \"mad cow disease.\" Other TSEs found in animals include scrapie, which affects sheep and goats; chronic wasting disease, which affects elk and deer; and transmissible mink encephalopathy. In a few rare cases, TSEs have occurred in other mammals such as zoo animals. These cases are probably caused by contaminated feed. CJD and other TSEs also can be transmitted experimentally to mice and other animals in the laboratory.\n                \nResearch suggests that TSEs are caused by an abnormal version of a protein called a prion (prion is short for proteinaceous infectious particle). Prion proteins occur in both a normal form, which is a harmless protein found in the body's cells, and in an infectious form, which causes disease. The harmless and infectious forms of the prion protein are nearly identical, but the infectious form takes on a different folded shape from the normal protein.\n                \nHuman TSEs can occur three ways: sporadically; as hereditary diseases; or through transmission from infected individuals. Sporadic TSEs may develop because some of a person's normal prions spontaneously change into the infectious form of the protein and then alter the prions in other cells in a chain reaction. Inherited cases arise from a change, or mutation, in the prion protein gene that causes the prions to be shaped in an abnormal way. This genetic change may be transmitted to an individual's offspring. Transmission of TSEs from infected individuals is relatively rare. TSEs cannot be transmitted through the air or through touching or most other forms of casual contact. However, they may be transmitted through contact with infected tissue, body fluids, or contaminated medical instruments. Normal sterilization procedures such as boiling or irradiating materials do not prevent transmission of TSEs.\n                \nSymptoms of TSEs vary, but they commonly include personality changes, psychiatric problems such as depression, lack of coordination, and\/or an unsteady gait. Patients also may experience involuntary jerking movements called myoclonus, unusual sensations, insomnia, confusion, or memory problems. In the later stages of the disease, patients have severe mental impairment and lose the ability to move or speak."}
{"_id":"858c73d3-c3b5-4774-a09d-fd2478ec330d","text":"TSEs tend to progress rapidly and usually culminate in death over the course of a few months to a few years."}
{"_id":"d83c08ed-fa5d-4223-b66b-e6c27eccdcdf","text":"There is currently no treatment that can halt progression of any of the TSEs. Treatment is aimed at alleviating symptoms and making the patient as comfortable as possible. A clinical trial of a potential therapy for CJD is expected to begin soon at the University of California at San Francisco."}
{"_id":"6b08b50b-68ef-4317-bfc1-a96f63fdd502","text":"The NINDS conducts and supports research on TSEs. This research is aimed at determining how abnormal prion proteins lead to disease, at finding better tests for diagnosing CJD and other disorders, and ultimately at finding ways to treat TSEs."}
{"_id":"d395b662-d8f0-4809-a7fb-9511e0d35178","text":"Neurosarcoidosis is a manifestation of sarcoidosis in the nervous system. Sarcoidosis is a chronic inflammatory disorder that typically occurs in adults between 20 and 40 years of age and primarily affects the lungs, but can also impact almost every other organ and system in the body. Neurosarcoidosis is characterized by inflammation and abnormal cell deposits in any part of the nervous system  the brain, spinal cord, or peripheral nerves. It most commonly occurs in the cranial and facial nerves, the hypothalamus (a specific area of the brain), and the pituitary gland. It is estimated to develop in 5 to 15 percent of those individuals who have sarcoidosis. Weakness of the facial muscles on one side of the face (Bells palsy) is a common symptom of neurosarcoidosis. The optic and auditory nerves can also become involved, causing vision and hearing impairments. It can cause headache, seizures, memory loss, hallucinations, irritability, agitation, and changes in mood and behavior. Neurosarcoidosis can appear in an acute, explosive fashion or start as a slow chronic illness. Because neurosarcoidosis manifests in many different ways, a diagnosis may be difficult and delayed."}
{"_id":"aef73b95-d36a-4a28-ac59-a0a619dc88f5","text":"There is no agreed upon standard of treatment for neurosarcoidosis. Doctors generally recommend corticosteroid therapy as first-line therapy for individuals with the condition. Additional treatment with immunomodulatory drugs such as hydroxychloroquine, pentoxyfilline, thalidomide, and infliximab, and immunosuppressive drugs such as methotrexate, azathioprine, cyclosporin, and cyclophosphamide, have benefited some individuals. While the use of corticosteroids and other immunosuppressive drugs is effective, these medications also have undesirable side effects. Side effects and experience with certain drugs may play a role in medication choices."}
{"_id":"488aba99-2cbb-4dd2-9e67-9e4d48a6beb7","text":"The prognosis for patients with neurosarcoidosis varies. Approximately two-thirds of those with the condition will recover completely; the remainder will have a chronically progressing or on-and-off course of illness. Complications resulting from immunosuppressive treatments, such as cryptococcal and tuberculous meningitis, progressive multifocal leukoencephalopathy, and inclusion body myositis, may be fatal for a small percentage of individuals."}
{"_id":"d28fec61-fec6-471a-b4ed-b443d3038c49","text":"The National Institute of Neurological Disorders and Stroke (NINDS) has joined with other institutes of the National Institutes of Health (NIH) to form a trans-NIH working group to coordinate and fund research into the disease mechanisms of sarcoidosis, predisposing factors, genetic underpinnings, and the potential for clinical therapies. Grants are supporting research at major medical institutions across the country. The outcomes of this research will be better ways to diagnose, treat, and ultimately cure sarcoidosis and neurosarcardoisis."}
{"_id":"102c862a-95e4-45d9-a3e4-c5ac15df5aad","text":"Mitochondrial myopathies are a group of neuromuscular diseases caused by damage to the mitochondriasmall, energy-producing structures that serve as the cells' \"power plants.\" Nerve cells in the brain and muscles require a great deal of energy, and thus appear to be particularly damaged when mitochondrial dysfunction occurs. Some of the more common mitochondrial myopathies include Kearns-Sayre syndrome, myoclonus epilepsy with ragged-red fibers, and mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes. The symptoms of mitochondrial myopathies include muscle weakness or exercise intolerance, heart failure or rhythm disturbances, dementia, movement disorders, stroke-like episodes, deafness, blindness, droopy eyelids, limited mobility of the eyes, vomiting, and seizures. The prognosis for these disorders ranges in severity from progressive weakness to death. Most mitochondrial myopathies occur before the age of 20, and often begin with exercise intolerance or muscle weakness. During physical activity, muscles may become easily fatigued or weak. Muscle cramping is rare, but may occur. Nausea, headache, and breathlessness are also associated with these disorders."}
{"_id":"c5c2e1e8-4b69-4fa9-ba75-a0d8451e8e9d","text":"Although there is no specific treatment for any of the mitochondrial myopathies, physical therapy may extend the range of movement of muscles and improve dexterity. Vitamin therapies such as riboflavin, coenzyme Q, and carnitine (a specialized amino acid) may provide subjective improvement in fatigue and energy levels in some patients."}
{"_id":"f7782864-0125-4ec9-873d-adb07c3e091c","text":"The prognosis for patients with mitochondrial myopathies varies greatly, depending largely on the type of disease and the degree of involvement of various organs. These disorders cause progressive weakness and can lead to death."}
{"_id":"4a16711c-a342-44e8-a384-e106ff33fb52","text":"The NINDS conducts and supports research on mitochondrial myopathies. The goals of this research are to increase scientific understanding of these disorders and to find ways to effectively treat, prevent, or potentially cure them."}
{"_id":"2377ce8c-b99f-49cd-8460-66747325f76a","text":"Lissencephaly, which literally means \"smooth brain,\" is a rare, gene-linked brain malformation characterized by the absence of normal convolutions (folds) in the cerebral cortex and an abnormally small head (microcephaly). In the usual condition of lissencephaly, children usually have a normal sized head at birth. In children with reduced head size at birth, the condition microlissencephaly is typically diagnosed. Lissencephaly is caused by defective neuronal migration during embryonic development, the process in which nerve cells move from their place of origin to their permanent location within the cerebral cortex gray matter. Symptoms of the disorder may include unusual facial appearance, difficulty swallowing, failure to thrive, muscle spasms, seizures, and severe psychomotor retardation. Hands, fingers, or toes may be deformed. Lissencephaly may be associated with other diseases including isolated lissencephaly sequence, Miller-Dieker syndrome, and Walker-Warburg syndrome. Sometimes it can be difficult to distinguish between these conditions clinically so consultation with national experts is recommended to help ensure correct diagnosis and possible molecular testing."}
{"_id":"e907d840-1e56-4153-bc5c-b7eb712f788b","text":"There is no cure for lissencephaly, but children can show progress in their development over time. Supportive care may be needed to help with comfort, feeding, and nursing needs. Seizures may be particularly problematic but anticonvulsant medications can help. Progressive hydrocephalus (an excessive accumulation of cerebrospinal fluid in the brain) is very rare, seen only in the subtype of Walker-Warburg syndrome, but may require shunting. If feeding becomes difficult, a gastrostomy tube may be considered."}
{"_id":"d4e51101-b102-4769-8665-7bffd16d6db2","text":"The prognosis for children with lissencephaly depends on the degree of brain malformation. Many will die before the age of 10 years. The cause of death is usually aspiration of food or fluids, respiratory disease, or severe seizures. Some will survive, but show no significant development -- usually not beyond a 3- to 5-month-old level. Others may have near-normal development and intelligence. Because of this range, it is important to seek the opinion of specialists in lissencephaly and support from family groups with connection to these specialists."}
{"_id":"043209f9-4495-4858-9234-234c3891d59f","text":"The NINDS conducts and supports a wide range of studies that explore the complex systems of normal brain development, including neuronal migration. Recent studies have identified genes that are responsible for lissencephaly. The knowledge gained from these studies provides the foundation for developing treatments and preventive measures for neuronal migration disorders."}
{"_id":"638390c3-d69f-4890-8172-6309680dc841","text":"Multiple system atrophy with orthostatic hypotension is the current classification for a neurological disorder that was once called Shy-Drager syndrome. A progressive disorder of the central and autonomic nervous systems, it is characterized by orthostatic hypotension (an excessive drop in blood pressure when standing up) which causes dizziness or fainting. Multiple system atrophy can occur without orthostatic hypotension, but instead have urinary involvement (urgency\/incontinence). Doctors classify the disorder into 3 types: the Parkinsonian-type includes symptoms of Parkinson's disease such as slow movement, stiff muscles, and tremor; the cerebellar-type, which causes problems with coordination and speech; and the combined-type, which includes symptoms of both parkinsonism and cerebellar failure. Problems with urinary incontinence, constipation, and sexual impotence in men happen early in the course of the disease. Other symptoms include generalized weakness, double vision or other vision disturbances, difficulty breathing and swallowing, sleep disturbances, and decreased sweating. Because the disease resembles others, a correct diagnosis may take years."}
{"_id":"631b2ee2-14a5-4436-8bba-a848002864b9","text":"There is no cure for multiple system atrophy with orthostatic hypotension. Treatment is aimed at controlling symptoms. Anti-Parkinson medication such as Sinemet may improve the general sense of well-being. Medications to elevate blood pressure while standing are often used, but may cause high blood pressure when lying down. Individuals should sleep with the head of the bed elevated. An artificial feeding tube or breathing tube may be required for problems with swallowing and breathing."}
{"_id":"ec4c3910-3ab8-4a47-a34f-7c071d6810eb","text":"Most individuals with multiple system atrophy with orthostatic hypotension die within 7 to 10 years after the onset of symptoms. A problem with the respiratory system is the most common cause of death."}
{"_id":"e2df631f-8ac8-45ff-a017-54293396a596","text":"The NINDS supports research on disorders of the autonomic nervous system, including multiple system atrophy with orthostatic hypotension. This research is aimed at developing techniques to diagnose, treat, and prevent these disorders. Currently there are ongoing treatment trials of drugs to treat MSA."}
{"_id":"1aa1aa7c-3aea-4376-8d50-4bd865019f34","text":"A transient ischemic attack (TIA) is a transient stroke that lasts only a few minutes. It occurs when the blood supply to part of the brain is briefly interrupted. TIA symptoms, which usually occur suddenly, are similar to those of stroke but do not last as long. Most symptoms of a TIA disappear within an hour, although they may persist for up to 24 hours. Symptoms can include: numbness or weakness in the face, arm, or leg, especially on one side of the body; confusion or difficulty in talking or understanding speech; trouble seeing in one or both eyes; and difficulty with walking, dizziness, or loss of balance and coordination."}
{"_id":"50867e5f-48d3-45e0-8e39-9f22c5e06b81","text":"Because there is no way to tell whether symptoms are from a TIA or an acute stroke, patients should assume that all stroke-like symptoms signal an emergency and should not wait to see if they go away. A prompt evaluation (within 60 minutes) is necessary to identify the cause of the TIA and determine appropriate therapy. Depending on a patient's medical history and the results of a medical examination, the doctor may recommend drug therapy or surgery to reduce the risk of stroke in people who have had a TIA. The use of antiplatelet agents, particularly aspirin, is a standard treatment for patients at risk for stroke. People with atrial fibrillation (irregular beating of the heart) may be prescribed anticoagulants."}
{"_id":"7696d766-c06e-464f-b1b5-478b64a3e946","text":"TIAs are often warning signs that a person is at risk for a more serious and debilitating stroke. About one-third of those who have a TIA will have an acute stroke some time in the future. Many strokes can be prevented by heeding the warning signs of TIAs and treating underlying risk factors. The most important treatable factors linked to TIAs and stroke are high blood pressure, cigarette smoking, heart disease, carotid artery disease, diabetes, and heavy use of alcohol. Medical help is available to reduce and eliminate these factors. Lifestyle changes such as eating a balanced diet, maintaining healthy weight, exercising, and enrolling in smoking and alcohol cessation programs can also reduce these factors."}
{"_id":"287179c3-0e5d-4ae0-956e-b6bc3a3cfed8","text":"NINDS is the leading supporter of research on stroke and TIA in the U.S. and sponsors studies ranging from clinical trials to investigations of basic biological mechanisms as well as studies with animals."}
{"_id":"dd63ad54-a393-4f1a-966f-7f3aa48b698a","text":"Porencephaly is an extremely rare disorder of the central nervous system in which a cyst or cavity filled with cerebrospinal fluid develops in the brain. It is usually the result of damage from stroke or infection after birth (the more common type), but it can also be caused by abnormal development before birth (which is inherited and less common). Diagnosis is usually made before an infant reaches his or her first birthday. Symptoms of porencephaly include delayed growth and development, spastic hemiplegia (slight or incomplete paralysis), hypotonia (low muscle tone), seizures (often infantile spasms), and macrocephaly (large head) or microcephaly (small head). Children with porencephaly may have poor or absent speech development, epilepsy, hydrocephalus (accumulation of fluid in the brain), spastic contractures (shrinkage or shortening of the muscles), and cognitive impairment."}
{"_id":"391d25e2-6c1e-4939-84ba-ab86b78b3c86","text":"Treatment may include physical therapy, medication for seizures, and the placement of a shunt in the brain to remove excess fluid in the brain."}
{"_id":"1287bcfb-a071-4aa6-8abd-9d59e0135a53","text":"The prognosis for children with porencephaly varies according to the location and extent of the cysts or cavities. Some children with this disorder develop only minor neurological problems and have normal intelligence, while others may be severely disabled and die before their second decade of life."}
{"_id":"21068461-754c-4486-b3ee-543f9ba3e9de","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to porencephaly in laboratories at the NIH and also support additional research through grants to major medical institutions across the country. Much of this research explores the complex mechanisms of normal brain development. The knowledge gained from these fundamental studies will provide a foundation for developing ways to prevent porecephaly and the other cephalic disorders."}
{"_id":"758ccdc6-79b2-491f-9001-b9d75fd9d0a5","text":"Machado-Joseph disease (MJD), which is also called spinocerebellar ataxia type 3, is a rare hereditary ataxia (ataxia is a medical term meaning lack of muscle control). The disease is characterized by slowly progressive clumsiness and weakness in the arms and legs, spasticity, a staggering lurching gait easily mistaken for drunkenness, difficulty with speech and swallowing, involuntary eye movements, double vision, and frequent urination. Some individuals also have dystonia (sustained muscle contractions that cause twisting of the body and limbs, repetitive movements, abnormal postures, and rigidity) or symptoms similar to those of Parkinson's disease. Others have twitching of the face or tongue, or peculiar bulging eyes. Almost all individuals with MJD experience vision problems, including double vision or blurred vision, loss of the ability to distinguish color and\/or contrast, and inability to control eye movements."}
{"_id":"670d6688-9113-4f18-960c-26db544888d8","text":"MJD is incurable, but some symptoms of the disease can be treated. For those individuals who show parkinsonian features, levodopa therapy can help for many years. Treatment with antispasmodic drugs, such as baclofen, can help reduce spasticity. Botulinum toxin can also treat severe spasticity as well as some symptoms of dystonia. Speech problems and trouble swallowing can be treated with medication and speech therapy. Physiotherapy can help patients cope with disability associated with gait problems. Physical aids, such as walkers and wheelchairs, can assist with everyday activities."}
{"_id":"9a6a8583-35de-4255-9633-170c85ca5d9a","text":"The severity of the disease is related to the age of onset, with earlier onset associated with more severe forms of the disease. Symptoms can begin any time between early adolescence and about 70 years of age. MJD is a progressive disease, meaning that symptoms get worse with time. Life expectancy ranges from the mid-thirties for those with severe forms of MJD to a normal life expectancy for those with mild forms. The cause of death for those who die early is often aspiration pneumonia."}
{"_id":"ed650eab-d865-4595-aaaf-81b98ba11c7c","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts MJD research in its laboratories at the National Institutes of Health (NIH) and also supports MJD research through grants to major medical institutions across the country. Ongoing research includes studies to better understand the genetic, molecular, and cellular mechanisms that underlie inherited neurodegenerative diseases such as MJD. Other research areas include the development of novel therapies to treat the symptoms of MJD, efforts to identify diagnostic markers and to improve current diagnostic procedures for the disease, and population studies to identify affected families."}
{"_id":"c2249f5c-0de8-478e-b06a-2c7b9aeefb16","text":"Sleep apnea is a common sleep disorder characterized by brief interruptions of breathing during sleep. These episodes usually last 10 seconds or more and occur repeatedly throughout the night. People with sleep apnea will partially awaken as they struggle to breathe, but in the morning they will not be aware of the disturbances in their sleep. The most common type of sleep apnea is obstructive sleep apnea (OSA), caused by relaxation of soft tissue in the back of the throat that blocks the passage of air. Central sleep apnea (CSA) is caused by irregularities in the brains normal signals to breathe. Most people with sleep apnea will have a combination of both types. The hallmark symptom of the disorder is excessive daytime sleepiness. Additional symptoms of sleep apnea include restless sleep, loud snoring (with periods of silence followed by gasps), falling asleep during the day, morning headaches, trouble concentrating, irritability, forgetfulness, mood or behavior changes, anxiety, and depression. Not everyone who has these symptoms will have sleep apnea, but it is recommended that people who are experiencing even a few of these symptoms visit their doctor for evaluation. Sleep apnea is more likely to occur in men than women, and in people who are overweight or obese."}
{"_id":"6187fbf7-99bc-4ba9-8279-dbeeef21c2f3","text":"There are a variety of treatments for sleep apnea, depending on an individuals medical history and the severity of the disorder. Most treatment regimens begin with lifestyle changes, such as avoiding alcohol and medications that relax the central nervous system (for example, sedatives and muscle relaxants), losing weight, and quitting smoking. Some people are helped by special pillows or devices that keep them from sleeping on their backs, or oral appliances to keep the airway open during sleep. If these conservative methods are inadequate, doctors often recommend continuous positive airway pressure (CPAP), in which a face mask is attached to a tube and a machine that blows pressurized air into the mask and through the airway to keep it open. Also available are machines that offer variable positive airway pressure (VPAP) and automatic positive airway pressure (APAP). There are also surgical procedures that can be used to remove tissue and widen the airway. Some individuals may need a combination of therapies to successfully treat their sleep apnea."}
{"_id":"859b0927-7c83-4feb-9fd5-7b05341d71fb","text":"Untreated, sleep apnea can be life threatening. Excessive daytime sleepiness can cause people to fall asleep at inappropriate times, such as while driving. Sleep apnea also appears to put individuals at risk for stroke and transient ischemic attacks (TIAs, also known as mini-strokes), and is associated with coronary heart disease, heart failure, irregular heartbeat, heart attack, and high blood pressure. Although there is no cure for sleep apnea, recent studies show that successful treatment can reduce the risk of heart and blood pressure problems."}
{"_id":"62a6fd68-06da-4395-9444-72f9fe98e7e9","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to sleep apnea in laboratories at the NIH, and also support additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure sleep disorders, such as sleep apnea."}
{"_id":"1d7379bd-6628-4699-8aa8-2f96e58f053f","text":"Central pontine myelinolysis (CPM) is a neurological disorder that most frequently occurs after too rapid medical correction of sodium deficiency (hyponatremia). The rapid rise in sodium concentration is accompanied by the movement of small molecules and pulls water from brain cells. Through a mechanism that is only partly understood, the shift in water and brain molecules leads to the destruction of myelin, a substance that surrounds and protects nerve fibers. Nerve cells (neurons) can also be damaged. Certain areas of the brain are particularly susceptible to myelinolysis, especially the part of the brain stem called the pons. Some individuals will also have damage in other areas of the brain, which is called extrapontine myelinolysis (EPM). Experts estimate that 10 percent of those with CPM will also have areas of EPM.\n                \nThe initial symptoms of myelinolysis, which begin to appear 2 to 3 days after hyponatremia is corrected, include a depressed level of awareness, difficulty speaking (dysarthria or mutism), and difficulty swallowing (dysphagia). Additional symptoms often arise over the next 1-2 weeks, including impaired thinking, weakness or paralysis in the arms and legs, stiffness, impaired sensation, and difficulty with coordination. At its most severe, myelinolysis can lead to coma, locked-in syndrome (which is the complete paralysis of all of the voluntary muscles in the body except for those that control the eyes), and death.\n                \nAlthough many affected people improve over weeks to months, some have permanent disability. Some also develop new symptoms later, including behavioral or intellectual impairment or movement disorders like parkinsonism or tremor.\n                \nAnyone, including adults and children, who undergoes a rapid rise in serum sodium is at risk for myelinolysis. Some individuals who are particularly vulnerable are those with chronic alcoholism and those who have had a liver transplant. Myelinolysis has occurred in individuals undergoing renal dialysis, burn victims, people with HIV-AIDS, people over-using water loss pills (diuretics), and women with eating disorders such as anorexia or bulimia. The risk for CPM is greater if the serum (blood) sodium was low for at least 2 days before correction."}
{"_id":"e9c3d246-9f3b-46e6-aeed-29f515729a2a","text":"The ideal treatment for myelinolysis is to prevent the disorder by identifying individuals at risk and following careful guidelines for evaluation and correction of hyponatremia. These guidelines aim to safely restore the serum sodium level, while protecting the brain. For those who have hyponatremia for at least 2 days, or for whom the duration is not known, the rate of rise in the serum sodium concentration should be kept below 10 mmol\/L during any 24-hour period, if possible.\n                \nFor those who develop myelinolysis, treatment is supportive. Some physicians have tried to treat myelinolysis with steroid medication or other experimental therapies, but none has been proven effective. Individuals are likely to require extensive and prolonged physical therapy and rehabilitation. Those individuals who develop parkinsonian symptoms may respond to the dopaminergic drugs that work for individuals with Parkinsons disease."}
{"_id":"e4a81a41-8971-4aa6-b766-77de9a9308c1","text":"The prognosis for myelinolysis varies. Some individuals die and others recover completely. Although the disorder was originally considered to have a mortality rate of 50 percent or more, improved imaging techniques and early diagnosis have led to a better prognosis for many people. Most individuals improve gradually, but still continue to have challenges with speech, walking, emotional ups and downs, and forgetfulness."}
{"_id":"3a8193e2-d4d0-4006-b524-934242ed891c","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS is a component of the National Institutes of Health, the leading supporter of biomedical research in the world.\n                \nThe NINDS conducts and supports research to better understand conditions that affect the protective myelin coating around nerve fibers and ways to prevent and treat the destruction of myelin. Scientists hope to develop drugs that can prevent brain cells from dying or help them produce new myelin. Research funded by the NIH's National Institute of Diabetes and Digestive and Kidney Diseases aims to understand the biological mechanisms involved in water balance in the body."}
{"_id":"9c066803-18dc-487d-8293-70225df58742","text":"von Hippel-Lindau disease (VHL) is a rare, genetic multi-system disorder in which non-cancerous tumors grow in certain parts of the body. Slow-growing hemgioblastomas -- benign tumors with many blood vessels -- may develop in the brain, spinal cord, the retinas of the eyes, and near the inner ear. Cysts (fluid-filled sacs) may develop around the hemangioblastomas. Other types of tumors develop in the adrenal glands, the kidneys, or the pancreas. Symptoms of VHL vary among individuals and depend on the size and location of the tumors. Symptoms may include headaches, problems with balance and walking, dizziness, weakness of the limbs, vision problems, deafness in one ear, and high blood pressure. Individuals with VHL are also at a higher risk than normal for certain types of cancer, especially kidney cancer."}
{"_id":"6e810317-cc7b-4520-9e56-7037b22771f7","text":"Treatment for VHL varies according to the location and size of the tumor. In general, the objective of treatment is to treat the tumors before they grow to a size large enough to cause permanent problems by putting pressure on the brain or spinal cord. this pressure can block the flow of cerebrospinal fluid in the nervous system, impair vision, or create deafness. Treatment of most cases of VHL usually involves surgery to remove the tumors before they become harmful. Certain tumors can be treated with focused high-dose irradiation. Individuals with VHL need careful monitoring by a physician and\/or medical team familiar with the disorder."}
{"_id":"431e3098-7d24-4c83-b0c3-8f1a2576efc8","text":"The prognosis for individuals with VHL depends on then number, location, and complications of the tumors. Untreated, VHL may result in blindness and\/or permanent brain damage. With early detection and treatment the prognosis is significantly improved. Death is usually caused by complications of brain tumors or kidney cancer."}
{"_id":"c45652b4-88d6-4875-a92f-d92ebfec4bc4","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. The NINDS pursues a vigorous program of research aimed at preventing and treating disorders that cause tumors in the brain and spinal cord such as VHL. A natural history study hopes to learn more about the growth of brain and spinal cord tumors, as well as cysts that develop in association with them in individuals with VHL. Researchers will examine how fast the tumors grow and try to determine which factors (such as puberty, pregnancy, menopause, or blood proteins) affect tumor growth. Based on laboratory findings, NINDS researchers are planning drug trials for individuals with VHL. For example, NNDS scientists hope to learn if a drug that fights other cancers might slow the growth of hemangioblastomas in some people with VHL. The NIH's National Cancer Institute conducts research aimed at treating kidney tumors in individuals with VHL, as well as studies to identify gene mutations in people who are at risk of developing the disease.."}
{"_id":"107d115e-f281-48b3-859f-4efd320adbf7","text":"Infantile neuroaxonal dystrophy (INAD) is a rare inherited neurological disorder. It affects axons, the part of a nerve cell that carries messages from the brain to other parts of the body, and causes progressive loss of vision, muscular control, and mental skills. While the basic genetic and metabolic causes are unknown, INAD is the result of an abnormal build-up of toxic substances in nerves that communicate with muscles, skin, and the conjunctive tissue around the eyes. Symptoms usually begin within the first 2 years of life, with the loss of head control and the ability to sit, crawl, or walk, accompanied by deterioration in vision and speech. Some children may have seizures. Distinctive facial deformities may be present at birth, including a prominent forehead, crossed eyes, an unusually small nose or jaw, and large, low-set ears. INAD is an autosomal recessive disorder, which means that both parents must be carriers of the defective gene that causes INAD to pass it on to their child. Electrophysiology (nerve conduction velocities) may be helpful for diagnosis, although diagnosis is usually confirmed by tissue biopsy of skin, rectum, nerve or conjunctive tissue to confirm the presence of characteristic swellings (spheroid bodies) in the nerve axons."}
{"_id":"d4762d8e-fa17-462e-8aec-5cb78a657d25","text":"There is no cure for INAD and no treatment that can stop the progress of the disease. Treatment is symptomatic and supportive. Doctors can prescribe medications for pain relief and sedation. Physiotherapists and other physical therapists can teach parents and caregivers how to position and seat their child, and to exercise arms and legs to maintain comfort."}
{"_id":"3c42c4c7-9b1c-46d2-8a30-17af0e9cec40","text":"INAD is a progressive disease. Once symptoms begin, they will worsen over time. Generally, a babys development starts to slow down between the ages of 6 months to 3 years. The first symptoms may be slowing of motor and mental development, followed by loss or regression of previously acquired skills. Rapid, wobbly eye movements and squints may be the first symptoms, followed by floppiness in the body and legs (more than in the arms). For the first few years, a baby with INAD will be alert and responsive, despite being increasingly physically impaired. Eventually, because of deterioration in vision, speech, and mental skills, the child will lose touch with its surroundings. Death usually occurs between the ages of 5 to 10 years."}
{"_id":"b4a84e33-d07c-468b-8aa9-a4acc72e3c7d","text":"Researchers continue to search for the defective gene that causes INAD in hopes of developing drugs that can stop the disease. The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to INAD in its laboratories at the National Institutes of Health (NIH), and also supports additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders such as INAD."}
{"_id":"dc82d9dc-eeed-4928-80ca-474d075ef0e8","text":"Chiari malformations (CMs) are structural defects in the cerebellum, the part of the brain that controls balance. When the indented bony space at the lower rear of the skull is smaller than normal, the cerebellum and brain stem can be pushed downward. The resulting pressure on the cerebellum can block the flow of cerebrospinal fluid (the liquid that surrounds and protects the brain and spinal cord) and can cause a range of symptoms including dizziness, muscle weakness, numbness, vision problems, headache, and problems with balance and coordination. Symptoms may change for some individuals depending on buildup of CNS and any resulting pressure on tissue and nerves. CMs are classified by the severity of the disorder and the parts of the brain that protrude into the spinal canal. The most common is Type I, which may not cause symptoms and is often found by accident during an examination for another condition. Type II (also called Arnold-Chiari malformation) is usually accompanied by a myelomeningocele-a form of spina bifida that occurs when the spinal canal and backbone do not close before birth, causing the spinal cord to protrude through an opening in the back. This can cause partial or complete paralysis below the spinal opening. Type III is the most serious form of CM, and causes severe neurological defects. Other conditions sometimes associated with CM include hydrocephalus, syringomyelia (a fluid-filled cyst in the spinal cord), and spinal curvature."}
{"_id":"f62c778a-e075-4052-8d2d-2e2ecd1a1af7","text":"Medications may ease certain symptoms, such as pain. Surgery is the only treatment available to correct functional disturbances or halt the progression of damage to the central nervous system. More than one surgery may be needed to treat the condition. Some CMs have no noticeable symptoms and do not interfere with the person's activities of daily living."}
{"_id":"fed1edd4-b2e8-4bda-86cc-ddaf59bfbe55","text":"Many people with Type I CM are asymptomatic and do not know they have the condition. Many individuals with the more severe types of CM and have surgery see a reduction in their symptoms and\/or prolonged periods of relative stability, although paralysis is generally permanent."}
{"_id":"951677bd-17e7-4152-8a96-b9ca61606c28","text":"The NINDS supports research on disorders of the brain and nervous system such as Chiari malformations. The goals of this research are to increase scientific understanding of these disorders and to find ways to prevent, treat, and, ultimately, cure them. Current NINDS-funded research includes studies to better understand the genetic factors responsible for the malformation, and factors that influence the development, progression, and relief of symptoms among people with syringomyelia, including those with Chiari I malformations."}
{"_id":"263e6daa-5c5f-4a45-9caa-2e1557187565","text":"Neurotoxicity occurs when the exposure to natural or manmade toxic substances (neurotoxicants) alters the normal activity of the nervous system. This can eventually disrupt or even kill neurons, key cells that transmit and process signals in the brain and other parts of the nervous system. Neurotoxicity can result from exposure to substances used in chemotherapy, radiation treatment, drug therapies, and organ transplants, as well as exposure to heavy metals such as lead and mercury, certain foods and food additives, pesticides, industrial and\/or cleaning solvents, cosmetics, and some naturally occurring substances. Symptoms may appear immediately after exposure or be delayed. They may include limb weakness or numbness; loss of memory, vision, and\/or intellect; headache; cognitive and behavioral problems; and sexual dysfunction. Individuals with certain disorders may be especially vulnerable to neurotoxicants."}
{"_id":"455fa458-34e0-4c3a-8678-84d700dc1ab2","text":"Treatment involves eliminating or reducing exposure to the toxic substance, followed by symptomatic and supportive therapy."}
{"_id":"d574fad2-df1d-4885-b8af-b5864b5b0742","text":"The prognosis depends upon the length and degree of exposure and the severity of neurological injury. In some instances, exposure to neurotoxicants can be fatal. In others, patients may survive but not fully recover. In other situations, many individuals recover completely after treatment."}
{"_id":"3a7be5fd-bd1c-446c-9384-a0970154e155","text":"The NINDS supports research on disorders of the brain and nervous system such as neurotoxicity, aimed at learning more about these disorders and finding ways to prevent and treat them. Scientists are investigating the role occupational or environmental toxicants have on progressive neurodegenerative disorders such as Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis, and dementia. Also being studied are the mechanisms that trigger neuroimmune responses in the central nervous system and the possibility that some brain disorders in children may occur when environmental triggers interact with genes."}
{"_id":"9a6aab4c-fc52-4b1b-a9a3-c96e13d3c888","text":"All forms of myasthenia are due to problems in the communication between nerve cells and muscles. Most involve the activities of neurotransmitters. Neurotransmitters are chemicals that allow neurons to relay information from one cell to the next. For neurotransmitters to be effective, the nerve cell must release the neurotransmitter properly, and the muscle cell must be able to detect the neurotransmitter and respond to its signal properly.\n                \nThe most common type of myasthenia, myasthenia gravis, is caused by an abnormal immune response in which antibodies block the ability of the muscle to detect the neurotransmitter. Congenital myasthenia, however, differs from myasthenia gravis because the disrupted communication isn't caused by antibodies, but by genetic defects.\n                \nThere are several different subtypes of congenital myasthenia, each the result of a specific genetic mutation. Since all types of myasthenia are due to the inability of nerves to trigger muscle activity, they all involve weakness, although there is some variability in the specific muscles affected.\n                \nSymptoms of congenital myasthenia usually appear in the first few years of childhood, but may not be noticeable until much later, occasionally remaining unrecognized until adulthood. If the symptoms begin in infancy, they usually appear as \"floppiness\" and a failure to meet developmental milestones, such as rolling over or sitting up. Some infants may also have episodes of choking or pauses in breathing. If the symptoms begin in toddlers or preschool children, they appear as weakness during physical activities or an inability to perform age-appropriate actions, such as running or climbing. In addition, if eye muscles are involved, children may have droopy eyelids, \"lazy eye,\" or double vision. If mouth or throat muscles are involved, children may have difficulty speaking or swallowing. An important characteristic of myasthenia is that the weakness worsens during continuous activity, with strength returning, at least partially, after resting.\n                \nCongenital myasthenia is an inherited (genetic) disorder. All but one known subtype are recessive disorders, which means that a child will have to have two copies of the abnormal gene (one from each parent) in order to develop the disease. To diagnose congenital myasthenia, a neurologist will test various muscles to determine if they grow weaker with repeated activity. The doctor will also test the electrical activity of nerves and muscles using electromyography (EMG) and nerve conduction tests (NCS). Blood tests are often used to determine if antibodies could be causing the symptoms. Genetic tests may be ordered."}
{"_id":"9b33ab41-c574-469a-afa1-5b5fa9e84825","text":"The possibilities for treatment depend on the specific subtype of congenital myasthenia. Most treatments attempt to improve the signaling between nerve cell and muscle. These drugs include pyridostigmine, fluoxetine, ephedrine, and 3,4-diaminopyridine. Treatments to alter the immune system are not used for this form of myasthenia. There are no treatments to cure the underlying genetic abnormality."}
{"_id":"bcaff35a-fbbf-445c-9fbd-32189e4f2355","text":"The prognosis depends on the specific subtype of congenital myasthenia, the muscles involved, and the age at onset of symptoms. If a child has difficulty breathing, feeding, or swallowing, they may be vulnerable to pneumonia or respiratory failure. In other cases, weakness is stable and does not worsen over time. In one subtype, weakness improves with time. Life-span is normal in most cases in which respiratory function is not compromised."}
{"_id":"9d2300d5-1d48-4467-a704-7847c0b13422","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) support research related to congenital myasthenia through grants to major research institutions across the country. Much of this research focuses on finding better ways to prevent, treat and ultimately cure disorders such as congenital myasthenia."}
{"_id":"1cb25732-b256-4ab8-af66-973a8a9e12b3","text":"Attention deficit-hyperactivity disorder (ADHD) is a neurobehavioral disorder that affects 3-5 percent of all American children. It interferes with a person's ability to stay on a task and to exercise age-appropriate inhibition (cognitive alone or both cognitive and behavioral). Some of the warning signs of ADHD include failure to listen to instructions, inability to organize oneself and school work, fidgeting with hands and feet, talking too much, leaving projects, chores and homework unfinished, and having trouble paying attention to and responding to details. There are several types of ADHD: a predominantly inattentive subtype, a predominantly hyperactive-impulsive subtype, and a combined subtype. ADHD is usually diagnosed in childhood, although the condition can continue into the adult years."}
{"_id":"69bc520c-0d9b-4ecf-84fa-dbdf0b983e18","text":"The usual course of treatment may include medications such as methylphenidate (Ritalin) or dextroamphetamine (Dexedrine), which are stimulants that decrease impulsivity and hyperactivity and increase attention. Most experts agree that treatment for ADHD should address multiple aspects of the individual's functioning and should not be limited to the use of medications alone. Treatment should include structured classroom management, parent education (to address discipline and limit-setting), and tutoring and\/or behavioral therapy for the child."}
{"_id":"c75c0326-e0ef-4039-9536-24c1394cd0eb","text":"There is no \"cure\" for ADHD. Children with the disorder seldom outgrow it; however, some may find adaptive ways to accommodate the ADHD as they mature."}
{"_id":"f6b8f925-5ad0-4e1a-a23f-0b68abe0378c","text":"Several components of the NIH support research on developmental disorders such as ADHD. Research programs of the NINDS, the National Institute of Mental Health (NIMH), and the National Institute of Child Health and Human Development (NICHD) seek to address unanswered questions about the causes of ADHD, as well as to improve diagnosis and treatment."}
{"_id":"5907f3f0-6fa7-4252-8bb9-504af6bcda6b","text":"Tremor is an unintentional, somewhat rhythmic, muscle movement involving to-and-fro movements (oscillations) of one or more parts of the body. Essential tremor (previously called benign essential tremor) is the most common form of abnormal tremor. (In some people, tremor is a symptom of a neurological disorder or appears as a side effect of certain drugs.) Although it may be mild and nonprogressive in some people, in others the tremor is slowly progressive, starting on one side of the body but eventually affecting both sides. Hand tremor is most common but the head, arms, voice, tongue, legs, and trunk may also be involved. Hand tremor may cause problems with purposeful movements such as eating, writing, sewing, or shaving. Head tremor may be seen as a \"yes-yes\" or \"no-no\" motion. Essential tremor may be accompanied by mild gait disturbance. Heightened emotion, stress, fever, physical exhaustion, or low blood sugar may trigger tremors or increase their severity. There may be mild degeneration in the certain parts of the cerebellum in persons with essential tremor. Onset is most common after age 40, although symptoms can appear at any age. Children of a parent who has essential tremor have up to a 50 percent chance of inheriting the condition. Essential tremor is not associated with any known pathology."}
{"_id":"aa7999ea-bc84-490f-aa45-8d9a7414ddc1","text":"There is no definitive cure for essential tremor. Symptomatic drug therapy may include propranolol or other beta blockers and primidone, an anticonvulsant drug. Eliminating tremor \"triggers\" such as caffeine and other stimulants from the diet is often recommended. Physical and occupational therapy may help to reduce tremor and improve coordination and muscle control for some individuals. Deep brain stimulation uses a surgically implanted, battery-operated medical device called a neurostimulator to delivery electrical stimulation to targeted areas of the brain that control movement, temporarily blocking the nerve signals that cause tremor. Other surgical intervention is effective but may have side effects."}
{"_id":"2be03475-01bb-46ba-a536-6d2016dddba9","text":"Although essential tremor is not life-threatening, it can make it harder to perform daily tasks and is embarrassing to some people. Tremor frequency may decrease as the person ages, but the severity may increase, affecting the person's ability to perform certain tasks or activities of daily living. In many people the tremor may be mild throughout life."}
{"_id":"9e117491-a2f6-4fd9-87c0-2976689ca719","text":"The National Institute of Neurological Disorders and Stroke, a unit of the National Institutes of Health (NIH) within the U.S. Department of Health and Human Services, is the nation's leading federal funder of research on disorders of the brain and nervous system. The NINDS sponsors research on tremor both at its facilities at the NIH and through grants to medical centers.\n                \nScientists at the NINDS are evaluating the effectiveness of 1-octanol, a substance similar to alcohol but less intoxicating, for treating essential tremor. Results of two previous NIH studies have shown this agent to be promising as a potential new treatment.\n                \nScientists are also studying the effectiveness of botulinum toxin as a treatment for a variety of involuntary movement disorders, including essential tremor of the hand."}
{"_id":"177381d4-b2be-47e0-ad15-579a21709127","text":"The epilepsies are a spectrum of brain disorders ranging from severe, life-threatening and disabling, to ones that are much more benign. In epilepsy, the normal pattern of neuronal activity becomes disturbed, causing strange sensations, emotions, and behavior or sometimes convulsions, muscle spasms, and loss of consciousness. The epilepsies have many possible causes and there are several types of seizures. Anything that disturbs the normal pattern of neuron activityfrom illness to brain damage to abnormal brain developmentcan lead to seizures. Epilepsy may develop because of an abnormality in brain wiring, an imbalance of nerve signaling chemicals called neurotransmitters, changes in important features of brain cells called channels, or some combination of these and other factors. Having a single seizure as the result of a high fever (called febrile seizure) or head injury does not necessarily mean that a person has epilepsy. Only when a person has had two or more seizures is he or she considered to have epilepsy. A measurement of electrical activity in the brain and brain scans such as magnetic resonance imaging or computed tomography are common diagnostic tests for epilepsy."}
{"_id":"e8677fa6-88d9-4b2f-8974-63f5d33d05bc","text":"Once epilepsy is diagnosed, it is important to begin treatment as soon as possible. For about 70 percent of those diagnosed with epilepsy, seizures can be controlled with modern medicines and surgical techniques. Some drugs are more effective for specific types of seizures. An individual with seizures, particularly those that are not easily controlled, may want to see a neurologist specifically trained to treat epilepsy. In some children, special diets may help to control seizures when medications are either not effective or cause serious side effects."}
{"_id":"d39f2bb6-8481-4761-8049-d3cd21334f4a","text":"While epilepsy cannot be cured, for some people the seizures can be controlled with medication, diet, devices, and\/or surgery. Most seizures do not cause brain damage, but ongoing uncontrolled seizures may cause brain damage. It is not uncommon for people with epilepsy, especially children, to develop behavioral and emotional problems in conjunction with seizures. Issues may also arise as a result of the stigma attached to having epilepsy, which can led to embarrassment and frustration or bullying, teasing, or avoidance in school and other social settings. For many people with epilepsy, the risk of seizures restricts their independence (some states refuse drivers licenses to people with epilepsy) and recreational activities.\n                \nEpilepsy can be a life-threatening condition. Some people with epilepsy are at special risk for abnormally prolonged seizures or sudden unexplained death in epilepsy."}
{"_id":"10dfd92d-0b95-4b61-81ca-71f4589e9a96","text":"Scientists are studying the underlying causes of the epilepsies in children, adults, and the elderly, as well as seizures that occur following brain trauma, stroke, and brain tumors. Ongoing research is focused on developing new model systems that can be used to more quickly screen potential new treatments for the epilepsies. The identification of genes or other genetic information that may influence or cause the epilepsies may allow doctors to prevent the disorders or to predict which treatments will be most beneficial to individuals with specific types of epilepsy. Scientists also continue to study how neurotransmitters interact with brain cells to control nerve firing and how non-neuronal cells in the brain contribute to seizures. Researchers funded by the National Institutes of Health have developed a flexible brain implant that could one day be used to treat seizures. Scientists are continually improving MRI and other brain scans that may assist in diagnosing the epilepsies and identify the source, or focus, of the seizures in the brain. Other areas of study include prevention of seizures and the role of inflammation in epilepsy. Patients may enter trials of experimental drugs and surgical interventions.\n                \nMore about epilepsy research"}
{"_id":"b4681e94-c58b-4710-98c4-1c0c6c94b4ee","text":"Zellweger syndrome is one of a group of four related diseases called peroxisome biogenesis disorders (PBD). The diseases are caused by defects in any one of 13 genes, termed PEX genes, required for the normal formation and function of peroxisomes. The PBDs are divided into two groups: Zellweger spectrum disorders and Rhizomelic Chondrodysplasia Punctua spectrum. The Zellweger spectrum is comprised of three disorders that have considerable overlap of features. These include Zellweger syndrome (ZS, the most severe form), neonatal adrenoleukodystrophy (NALD), and Infantile Refsum disease (IRD, the least severe form).\n                \nPeroxisomes are cell structures that break down toxic substances and synthesize lipids (fatty acids. oils, and waxes) that are necessary for cell function. Peroxisomes are required for normal brain development and function and the formation of myelin, the whitish substance that coats nerve fibers. They are also required for normal eye, liver, kidney, and bone functions. Zellweger spectrum disorders result from dysfunctional lipid metabolism, including the over-accumulation of very long-chain fatty acids and phytanic acid, and defects of bile acids and plasmalogens--specialized lipids found in cell membranes and myelin sheaths of nerve fibers. Symptoms of these disorders include an enlarged liver; characteristic facial features such as a high forehead, underdeveloped eyebrow ridges, and wide-set eyes; and neurological abnormalities such as cognitive impairment and seizures. Infants will Zellweger syndrome also lack muscle tone, sometimes to the point of being unable to move, and may not be able to suck or swallow. Some babies will be born with glaucoma, retinal degeneration, and impaired hearing. Jaundice and gastrointestinal bleeding also may occur."}
{"_id":"0391dd71-d69e-4d60-8a04-1ea764ef0d33","text":"There is no cure for Zellweger syndrome, nor is there a standard course of treatment. Since the metabolic and neurological abnormalities that cause the symptoms of Zellweger syndrome are caused during fetal development, treatments to correct these abnormalities after birth are limited. Most treatments are symptomatic and supportive."}
{"_id":"d2f9578c-3cca-4873-b961-8daaf917bcaf","text":"The prognosis for infants with Zellweger syndrome is poor. Most infants do not survive past the first 6 months, and usually succumb to respiratory distress, gastrointestinal bleeding, or liver failure."}
{"_id":"eb4cf2ae-0747-443d-bfa0-0f55bb3470f6","text":"The National Institute of Neurological Disorders and Stroke (NINDS), and other institutes of the National Institutes of Health (NIH), conduct research exploring the molecular and genetic basis of Zellweger syndrome and the other PBDs, and also support additional research through grants to major research institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders such as Zellweger syndrome."}
{"_id":"a46c9f3c-746f-48bd-8fdb-aed5126e1660","text":"A coma, sometimes also called persistent vegetative state, is a profound or deep state of unconsciousness. Persistent vegetative state is not brain-death. An individual in a state of coma is alive but unable to move or respond to his or her environment. Coma may occur as a complication of an underlying illness, or as a result of injuries, such as head trauma. . Individuals in such a state have lost their thinking abilities and awareness of their surroundings, but retain non-cognitive function and normal sleep patterns. Even though those in a persistent vegetative state lose their higher brain functions, other key functions such as breathing and circulation remain relatively intact. Spontaneous movements may occur, and the eyes may open in response to external stimuli. Individuals may even occasionally grimace, cry, or laugh. Although individuals in a persistent vegetative state may appear somewhat normal, they do not speak and they are unable to respond to commands."}
{"_id":"863da6de-1ec5-4874-a4f4-c048cbd199d1","text":"Once an individual is out of immediate danger, the medical care team focuses on preventing infections and maintaining a healthy physical state. This will often include preventing pneumonia and bedsores and providing balanced nutrition. Physical therapy may also be used to prevent contractures (permanent muscular contractions) and deformities of the bones, joints, and muscles that would limit recovery for those who emerge from coma."}
{"_id":"4e6b2386-fef8-4164-ba2f-b944823c4cf3","text":"The outcome for coma and persistent vegetative state depends on the cause, severity, and site of neurological damage. Individuals may emerge from coma with a combination of physical, intellectual, and psychological difficulties that need special attention. Recovery usually occurs gradually, with some acquiring more and more ability to respond. Some individuals never progress beyond very basic responses, but many recover full awareness. Individuals recovering from coma require close medical supervision. A coma rarely lasts more than 2 to 4 weeks. Some patients may regain a degree of awareness after persistent vegetative state. Others may remain in that state for years or even decades. The most common cause of death for someone in a persistent vegetative state is infection, such as pneumonia."}
{"_id":"528cacb1-d77a-4893-9f39-a254883fa8b0","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to coma in their laboratories at the NIH and also support additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent and treat coma."}
{"_id":"14a67c4d-6fab-40b4-b713-b0f1265c2f85","text":"Acute disseminated encephalomyelitis (ADEM) is characterized by a brief but widespread attack of inflammation in the brain and spinal cord that damages myelin  the protective covering of nerve fibers. ADEM often follows viral or bacterial infections, or less often, vaccination for measles, mumps, or rubella. The symptoms of ADEM appear rapidly, beginning with encephalitis-like symptoms such as fever, fatigue, headache, nausea and vomiting, and in the most severe cases, seizures and coma. ADEM typically damages white matter (brain tissue that takes its name from the white color of myelin), leading to neurological symptoms such as visual loss (due to inflammation of the optic nerve)in one or both eyes, weakness even to the point of paralysis, and difficulty coordinating voluntary muscle movements (such as those used in walking). ADEM is sometimes misdiagnosed as a severe first attack of multiple sclerosis (MS), since the symptoms and the appearance of the white matter injury on brain imaging may be similar. However, ADEM has several features which differentiate it from MS. First, unlike MS patients, persons with ADEM will have rapid onset of fever, a history of recent infection or immunization, and some degree of impairment of consciousness, perhaps even coma; these features are not typically seen in MS. Children are more likely than adults to have ADEM, whereas MS is a rare diagnosis in children. In addition, ADEM usually consists of a single episode or attack of widespread myelin damage, while MS features many attacks over the course of time. Doctors will often use imaging techniques, such as MRI (magnetic resonance imaging), to search for old and new lesions (areas of damage) on the brain. The presence of older brain lesions on MRI suggest that the condition may be MS rather than ADEM, since MS can cause brain lesions before symptoms become obvious. In rare situations, a brain biopsy may be necessary to differentiate between ADEM and some other diseases that involve inflammation and damage to myelin.."}
{"_id":"5082422e-54c3-4999-a46e-640b1a62f18e","text":"Treatment for ADEM is targeted at suppressing inflammation in the brain using anti-inflammatory drugs. Most individuals respond to several days of intravenous corticosteroids such as methylprednisolone, followed by oral corticosteroid treatment. When corticosteroids fail to work, plasmapheresis or intravenous immunoglobulin therapy are possible secondary treatment options that are reported to help in some severe cases. Additional treatment is symptomatic and supportive."}
{"_id":"10f59e78-950d-406c-81f5-20d951c0653b","text":"Corticosteroid therapy typically helps hasten recovery from most ADEM symptoms. The long-term prognosis for individuals with ADEM is generally favorable. For most individuals, recovery begins within days, and within six months the majority of ADEM patients will have total or near total recoveries. Others may have mild to moderate lifelong impairment ranging from cognitive difficulties, weakness, loss of vision, or numbness. Severe cases of ADEM can be fatal but this is a very rare occurrence. ADEM can recur, usually within months of the initial diagnosis, and is treated by restarting corticosteroids. A small fraction of individuals who are initially diagnosed as having ADEM can go on to develop MS, but there is currently no method or known risk factors to predict whom those individuals will be."}
{"_id":"c09707ea-230b-40b0-aa10-2689795615a3","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to ADEM in laboratories at the NIH, and also support additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure demyelinating disorders such as ADEM."}
{"_id":"b0d6c4d4-201b-4275-aabc-7cc329d2c029","text":"Myotonia is a medical term that refers to a neuromuscular condition in which the relaxation of a muscle is impaired. It can affect any muscle group. Repeated effort will be needed to relax the muscle, although the condition usually improves after the muscles have warmed-up. Individuals with myotonia may have trouble releasing their grip on objects or may have difficulty rising from a seated position. They may walk with a stiff, awkward gait. Myotonia is caused by an abnormality in the muscle membrane, and is often associated with inherited neurological disorders. Myotonia is commonly seen in individuals with myotonic muscular dystrophy, myotonia congenita, and in people who have one of a group of neurological disorders called the channelopathies, which are inherited diseases that are caused by mutations in the chloride sodium or potassium channels that regulate the muscle membrane. Myotonia may also be triggered by exposure to cold."}
{"_id":"cffef837-2c75-4bba-a950-cde12fb568d7","text":"Treatment for myotonia may include mexiletine, quinine, phenytoin, and other anticonvulsant drugs. Physical therapy and other rehabilitative measures may help muscle function."}
{"_id":"deee68c8-6a07-4939-b338-593be39e9950","text":"Myotonia is a chronic disorder. Symptoms may improve later in life."}
{"_id":"525d5a7e-ed68-4dae-9a3e-7fdc020c82a5","text":"The National Institute of Neurological Disorders and Stroke supports and conducts an extensive research program on neuromuscular disorders. The goals of this research are to learn more about these disorders and to find ways to treat, prevent, and cure them."}
{"_id":"595fae49-743f-4335-b022-4dea8df25678","text":"Creutzfeldt-Jakob disease (CJD) is a rare, degenerative,fatal brain disorder. Typically, onset of symptoms occurs at about age 60. There are three major categories of CJD: sporadic (the most common form, in which people do not have any risk factors for the disease); hereditary (in which the person has a family member with the disease and tests positive for a genetic mutation), and acquired (in which the disease is transmitted by exposure to brain and nervous system tissue, usually through certain medical procedures. A form called variant CJD can be acquired by eating meat from cattle affected by a disease similar to CJD, called bovine spongiform encephalopathy (commonly called mad cow disease). Symptoms of CJD include problems with muscular coordination, personality changes including progressive and severe mental impairment, impaired vision that may lead to blindness, and involuntary muscle jerks called myoclonus. People eventually lose the ability to move and speak and enter a coma. Tests that help in the diagnosis of CJD include electroencephalography (which measures brain waves), detection of certain proteins in the fluid that surrounds the brain and spinal cord, and magnetic resonance imaging.. The first concern is to rule out treatable forms of dementia such as encephalitis or chronic meningitis. The only way to confirm a diagnosis of CJD is by brain biopsy or autopsy. In a brain biopsy, a neurosurgeon removes a small piece of tissue from the person's brain so that it can be examined by a neurologist. Because a correct diagnosis of CJD does not help the individual, a brain biopsy is discouraged unless it is need to rule out a treatable disorder. ."}
{"_id":"09b0fcb9-bc33-4f40-9259-371050d93585","text":"There is no treatment that can cure or control CJD, although studies of a variety of drugs are now in progress. Current treatment is aimed at alleviating symptoms and making the person as comfortable as possible. Opiate drugs can help relieve pain, and the drugs clonazepam and sodium valproate may help relieve involuntary muscle jerks.Intravenous fluids and artificial feeding may be needed in later stages of the disease."}
{"_id":"577ed16b-7eea-4cca-b586-8bf6ac502746","text":"About 70 percent of individuals die within one year. In the early stages of disease, people may have failing memory, behavioral changes, lack of coordination and visual disturbances. As the illness progresses, mental deterioration becomes pronounced and involuntary movements, blindness, weakness of extremities, and coma may occur."}
{"_id":"43561589-c8ec-41d2-9fe5-62924f4dce70","text":"The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. The leading scientific theory at this time maintains that CJD is caused by a type of protein called a prion. The harmless and the infectious forms of the prion protein are nearly identical, but the infectious form takes a different folded shape than the normal protein. Researchers are trying to discover factors that influence prion infectivity and how the disorder damages the brain. Using rodent models of the disease and brain tissue from autopsies, researchers are also trying to develop improved diagnostic tests for CJD and to learn what changes ultimately kill the neurons so that effective treatments can be developed."}
{"_id":"c7657e87-909e-409e-bb3f-5c503bd2431a","text":"Chorea is an abnormal involuntary movement disorder, one of a group of neurological disorders called dyskinesias, which are caused by overactivity of the neurotransmitter dopamine in the areas of the brain that control movement. Chorea is characterized by brief, irregular contractions that are not repetitive or rhythmic, but appear to flow from one muscle to the next. Chorea often occurs with athetosis, which adds twisting and writhing movements. Chorea is a primary feature of Huntington's disease, a progressive, hereditary movement disorder that appears in adults, but it may also occur in a variety of other conditions. Syndenham's chorea occurs in a small percentage (20 percent) of children and adolescents as a complication of rheumatic fever. Chorea can also be induced by drugs (levodopa, anti-convulsants, and anti-psychotics) metabolic and endocrine disorders, and vascular incidents."}
{"_id":"e2e57366-4388-4082-8198-c0523bbcc580","text":"There is no standard course of treatment for chorea. Treatment depends on the type of chorea and the associated disease. Treatment for Huntington's disease is supportive, while treatment for Syndenham's chorea usually involves antibiotic drugs to treat the infection, followed by drug therapy to prevent recurrence. Adjusting medication dosages can treat drug-induced chorea. Metabolic and endocrine-related choreas are treated according to the cause(s) of symptoms."}
{"_id":"263bc272-fa27-49ea-8fa4-ecc933e90881","text":"The prognosis for individuals with chorea varies depending on the type of chorea and the associated disease. Huntington's disease is a progressive, and ultimately, fatal disease. Syndenham's chorea is treatable and curable."}
{"_id":"dd57bfbf-dd73-448b-9562-fbef4b7cc669","text":"The NINDS supports research on movement disorders such as chorea. The goals of this research are to increase understanding of these disorders and to find ways to prevent and treat them."}
{"_id":"8a15309f-5a13-4623-ab5e-3de9c1f1d1ea","text":"Ohtahara syndrome is a neurological disorder characterized by seizures. The disorder affects newborns, usually within the first three months of life (most often within the first 10 days) in the form of epileptic seizures. Infants have primarily tonic seizures, but may also experience partial seizures, and rarely, myoclonic seizures. Ohtahara syndrome is most commonly caused by metabolic disorders or structural damage in the brain, although the cause or causes for many cases cant be determined. Most infants with the disorder show significant underdevelopment of part or all of the cerebral hemispheres. The EEGs of infants with Ohtahara syndrome reveal a characteristic pattern of high voltage spike wave discharge followed by little activity. This pattern is known as burst suppression. Doctors have observed that boys are more often affected than girls."}
{"_id":"bc56809d-6aa0-4da6-b74e-683517eea1ce","text":"Antiepileptic drugs are used to control seizures, but are unfortunately not usually very effective for this disorder. Corticosteroids are occasionally helpful. In cases where there is a focal brain lesion (damage contained to one area of the brain) surgery may be beneficial. Other therapies are symptomatic and supportive."}
{"_id":"1a71c38a-c98b-4b47-ab31-385be4890e3d","text":"The course of Ohtahara syndrome is severely progressive. Seizures become more frequent, accompanied by delays in physical and cognitive development.Some children will die in infancy; others will survive but be profoundly handicapped. As they grow, some children will progress into other epileptic disorders such as West syndrome and Lennox-Gestaut syndrome."}
{"_id":"1c803017-4c33-41b7-b17f-8f7f781772e5","text":"The NINDS conducts and supports an extensive research program on seizures and seizure-related disorders. Much of this research is aimed at increasing scientific understanding of these disorders and finding ways to prevent, treat, and potentially cure them."}
{"_id":"4b42d34f-6ccb-485c-9ab5-ef9dd1416554","text":"Postural orthostatic tachycardia syndrome (POTS) is one of a group of disorders that have orthostatic intolerance (OI) as their primary symptom. OI describes a condition in which an excessively reduced volume of blood returns to the heart after an individual stands up from a lying down position. The primary symptom of OI is lightheadedness or fainting. In POTS, the lightheadedness or fainting is also accompanied by a rapid increase in heartbeat of more than 30 beats per minute, or a heart rate that exceeds 120 beats per minute, within 10 minutes of rising. The faintness or lightheadedness of POTS are relieved by lying down again. Anyone at any age can develop POTS, but the majority of individuals affected (between 75 and 80 percent) are women between the ages of 15 to 50 years of age. Some women report an increase in episodes of POTS right before their menstrual periods. POTS often begins after a pregnancy, major surgery, trauma, or a viral illness. It may make individuals unable to exercise because the activity brings on fainting spells or dizziness.\n                \nDoctors aren't sure yet what causes the reduced return of blood to the heart that occurs in OI, or why the heart begins to beat so rapidly in POTS. Current thinking is that there are a number of mechanisms. Some individuals have peripheral denervation (neuropathic POTS); some have symptoms that are due to sustained or parosyxmal overactivity of the sympathetic nervous system (hyperadrenergic POTS); and many individuals with POTS have significant deconditioning."}
{"_id":"ae4f3af0-e663-4660-9fe0-5601d98b06b9","text":"Therapies for POTS are targeted at relieving low blood volume or regulating circulatory problems that could be causing the disorder. No single treatment has been found to be effect for all. A number of drugs seem to be effective in the short term. Whether they help in long term is uncertain. Simple interventions such as adding extra salt to the diet and attention to adequate fluid intake are often effective. The drugs fludrocortisone (for those on a high salt diet) and midodrine in low doses are often used to increase blood volume and narrow blood vessels. Drinking 16 ounces of water (2 glassfuls) before getting up can also help raise blood pressure. Some individuals are helped by beta receptor blocking agents. There is some evidence that an exercise program can gradually improve orthostatic tolerance."}
{"_id":"4fd4356b-794f-479e-a8e0-75f7d1eb0c2d","text":"POTS may follow a relapsing-remitting course, in which symptoms come and go, for years. In most cases (approximately 80 percent), an individual with POTS improves to some degree and becomes functional, although some residual symptoms are common."}
{"_id":"db87ec0e-621c-49d6-8d64-8908191f65b9","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other Institutes of the National Institutes of Health (NIH) conduct research related to POTS and support additional research through grants to major research institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders such as POTS. NINDS-funded researchers are investigating if low levels of the hormone aldosterone contribute to low blood volume in individuals with POTS, and if high levels of angiotensin II, a peptide that helps regulate blood volume, leads to decreased adrenal sensitivity. Other NINDS-funded research is investigating the hypothesis that POTS is a syndrome of different subtypes, with different underlying mechanisms. Additionally, the NINDS funds the Autonomic Rare Diseases Consortium to further understand disorders such as orthostatic hypotension and hopefully alter the course of disease."}
{"_id":"6454d9ff-eb40-4361-9422-1f1d5328ad4f","text":"Rasmussens encephalitis is a rare, chronic inflammatory neurological disease that usually affects only one hemisphere of the brain. It usually occurs in children under the age of 10 (more rarely in adolescents and adults), and is characterized by frequent and severe seizures, loss of motor skills and speech, paralysis on one side of the body (hemiparesis), inflammation of the brain (encephalitis), and mental deterioration. Most individuals with Rasmussens encephalitis will experience frequent seizures and progressive brain damage in the affected hemisphere of the brain over the course of the first 8 to 12 months, and then enter a phase of permanent, but stable, neurological deficits. Rasmussens encephalitis has features of an autoimmune disease in which immune system cells enter the brain and cause inflammation and damage.Research is ongoing into the causes of this rare disease."}
{"_id":"da00cc5c-6af5-4807-8bfe-1efe475b8739","text":"Anti-epileptic drugs are usually not effective in controlling seizures. Recent studies have shown some success with treatments that suppress or modulate the immune system, in particular those that use corticosteroids, intravenous immunoglobulin, or tacrolimus. Surgery to control seizures may be performed in later stages of the disease when neurological deficits stabilize. Surgical procedures, such as functional hemispherectomy and hemispherotomy, may reduce the frequency of seizures and also improve behavior and cognitive abilities."}
{"_id":"197a51b2-7344-4fb7-b9c1-2540d4259f21","text":"The prognosis for individuals with Rasmussens encephalitis varies. Despite the advances in medical treatment, none has yet been shown to halt the progress of the disease in the long term. The disorder may lead to severe neurological deficits or it may cause only milder impairments. For some children, surgery decreases seizures. However, most individuals with Rasmussens encephalitis are left with some paralysis, cognitive deficits, and problems with speech. In some cases, the disease can progress to involve the opposite brain hemisphere."}
{"_id":"cdd4e6a9-63d1-4c6a-9c82-a7f9f523bd5b","text":"The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to Rasmussens encephalitis in its laboratories at the National Institutes of Health (NIH), and also supports additional research through grants to major research institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure progressive neurological disorders, such as Rasmussens encephalitis."}
{"_id":"84810905-c9bd-477f-ad74-f5c5048382bf","text":"Sydenham chorea (SD) is a neurological disorder of childhood resulting from infection via Group A beta-hemolytic streptococcus (GABHS), the bacterium that causes rheumatic fever. SD is characterized by rapid, irregular, and aimless involuntary movements of the arms and legs, trunk, and facial muscles. It affects girls more often than boys and typically occurs between 5 and 15 years of age. Some children will have a sore throat several weeks before the symptoms begin, but the disorder can also strike up to 6 months after the fever or infection has cleared. Symptoms can appear gradually or all at once, and also may include uncoordinated movements, muscular weakness, stumbling and falling, slurred speech, difficulty concentrating and writing, and emotional instability. The symptoms of SD can vary from a halting gait and slight grimacing to involuntary movements that are frequent and severe enough to be incapacitating. The random, writhing movements of chorea are caused by an auto-immune reaction to the bacterium that interferes with the normal function of a part of the brain (the basal ganglia) that controls motor movements. Due to better sanitary conditions and the use of antibiotics to treat streptococcal infections, rheumatic fever, and consequently SD, are rare in North America and Europe. The disease can still be found in developing nations."}
{"_id":"a5c11e09-4d2c-4dda-9d68-6cddcbd7a21b","text":"There is no specific treatment for SD. For people with the mildest form, bed rest during the period of active movements is sufficient. When the severity of movements interferes with rest, sedative drugs, such as barbiturates or benzodiazepines, may be needed. Antiepileptic medications, such as valproic acid, are often prescribed. Doctors also recommend that children who have had SD take penicillin over the course of the next 10 years to prevent additional manifestations of rheumatic fever."}
{"_id":"02d3dbca-707c-4b61-b98c-2dd49c1dcbcb","text":"Most children recover completely from SD, although a small number will continue to have disabling, persistent chorea despite treatment. The duration of symptoms varies, generally from 3 to 6 weeks, but some children will have symptoms for several months. Cardiac complications may occur in a small minority of children, usually in the form of endocarditis. In a third of the children with the disease, SD will recur, typically 1  to 2  years after the initial attack. Researchers have noted an association between recurrent SD and the later development of the abrupt onset forms of obsessive-compulsive disorder, attention deficit\/hyperactivity disorder, tic disorders, and autism, which they call PANDAS, for Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus infection. Further studies are needed to determine the nature of the association and the biological pathways that connect streptococcal infection, autoimmune response, and the later development of these specific behavioral disorders."}
{"_id":"2dfa4865-4b4f-4d43-a7b6-3cac85c8db3f","text":"The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to SD in laboratories at the NIH, and support additional research through grants to major medical institutions across the country. Currently, researchers are studying how the interplay of genetic, developmental, and environmental factors could determine a childs vulnerability to SD after a GABHS infection. Other researchers are exploring whether children whose symptoms either begin or get worse following a GABHS infection share a common set of abnormal biomolecular pathways responsible for their similar clinical symptoms."}
{"_id":"426ef0bb-5d34-4e07-ae12-5bf46de39fee","text":"Fahr's Syndrome is a rare, genetically dominant, inherited neurological disorder characterized by abnormal deposits of calcium in areas of the brain that control movement, including the basal ganglia and the cerebral cortex. Symptoms of the disorder may include deterioration of motor function, dementia, seizures, headache, dysarthria (poorly articulated speech), spasticity (stiffness of the limbs) and spastic paralysis, eye impairments, and athetosis (involuntary, writhing movements). Fahr's Syndrome can also include symptoms characteristic of Parkinson's disease such as tremors, muscle rigidity, a mask-like facial appearance, shuffling gait, and a \"pill-rolling\" motion of the fingers. These symptoms generally occur later in the development of the disease. More common symptoms include dystonia (disordered muscle tone) and chorea (involuntary, rapid, jerky movements). Age of onset is typically in the 40s or 50s, although it can occur at any time in childhood or adolescence."}
{"_id":"f135ce52-810b-4689-97ea-ef85527b931d","text":"There is no cure for Fahr's Syndrome, nor is there a standard course of treatment. Treatment addresses symptoms on an individual basis."}
{"_id":"f16944a2-aa99-405e-a7ed-296d32f67aac","text":"The prognosis for any individual with Fahr's Syndrome is variable and hard to predict. There is no reliable correlation between age, extent of calcium deposits in the brain, and neurological deficit. Since the appearance of calcification is age-dependent, a CT scan could be negative in a gene carrier who is younger than the age of 55."}
{"_id":"8905482c-60a7-490e-86c2-1a09861f9d7c","text":"The NINDS supports and conducts research on neurogenetic disorders such as Fahr's Syndrome. The goals of this research are to locate and understand the actions of the genes involved in this disorder. Finding these genes could lead to effective ways to treat and prevent Fahr's Syndrome."}
{"_id":"b3d39715-c512-4a0e-a4d1-9a3169aeee72","text":"Lactose is a sugar found in milk and milk products. The small intestinethe organ where most food digestion and nutrient absorption take placeproduces an enzyme called lactase. Lactase breaks down lactose into two simpler forms of sugar: glucose and galactose. The body then absorbs these simpler sugars into the bloodstream."}
{"_id":"5e65d2e3-adc0-4e68-9194-cbf30421d158","text":"Lactose intolerance is a condition in which people have digestive symptomssuch as bloating, diarrhea, and gasafter eating or drinking milk or milk products.\n                \nLactase deficiency and lactose malabsorption may lead to lactose intolerance:\n                \n- Lactase deficiency. In people who have a lactase deficiency, the small intestine produces low levels of lactase and cannot digest much lactose.  - Lactose malabsorption. Lactase deficiency may cause lactose malabsorption. In lactose malabsorption, undigested lactose passes to the colon. The colon, part of the large intestine, absorbs water from stool and changes it from a liquid to a solid form. In the colon, bacteria break down undigested lactose and create fluid and gas. Not all people with lactase deficiency and lactose malabsorption have digestive symptoms.\n                \nPeople have lactose intolerance when lactase deficiency and lactose malabsorption cause digestive symptoms. Most people with lactose intolerance can eat or drink some amount of lactose without having digestive symptoms. Individuals vary in the amount of lactose they can tolerate.\n                \nPeople sometimes confuse lactose intolerance with a milk allergy. While lactose intolerance is a digestive system disorder, a milk allergy is a reaction by the bodys immune system to one or more milk proteins. An allergic reaction to milk can be life threatening even if the person eats or drinks only a small amount of milk or milk product. A milk allergy most commonly occurs in the first year of life, while lactose intolerance occurs more often during adolescence or adulthood.1,2\n                \n\n                \nFour Types of Lactase Deficiency   Four types of lactase deficiency may lead to lactose intolerance:   - Primary lactase deficiency, also called lactase nonpersistence, is the most common type of lactase deficiency. In people with this condition, lactase production declines over time. This decline often begins at about age 2; however, the decline may begin later. Children who have lactase deficiency may not experience symptoms of lactose intolerance until late adolescence or adulthood. Researchers have discovered that some people inherit genes from their parents that may cause a primary lactase deficiency.   - Secondary lactase deficiency results from injury to the small intestine. Infection, diseases, or other problems may injure the small intestine. Treating the underlying cause usually improves the lactose tolerance.   - Developmental lactase deficiency may occur in infants born prematurely. This condition usually lasts for only a short time after they are born.   - Congenital lactase deficiency is an extremely rare disorder in which the small intestine produces little or no lactase enzyme from birth. Genes inherited from parents cause this disorder."}
{"_id":"98853848-3b92-4f0d-b696-fe060417354a","text":"Four types of lactase deficiency may lead to lactose intolerance:\n                \n- Primary lactase deficiency, also called lactase nonpersistence, is the most common type of lactase deficiency. In people with this condition, lactase production declines over time. This decline often begins at about age 2; however, the decline may begin later. Children who have lactase deficiency may not experience symptoms of lactose intolerance until late adolescence or adulthood. Researchers have discovered that some people inherit genes from their parents that may cause a primary lactase deficiency.  - Secondary lactase deficiency results from injury to the small intestine. Infection, diseases, or other problems may injure the small intestine. Treating the underlying cause usually improves the lactose tolerance.  - Developmental lactase deficiency may occur in infants born prematurely. This condition usually lasts for only a short time after they are born.  - Congenital lactase deficiency is an extremely rare disorder in which the small intestine produces little or no lactase enzyme from birth. Genes inherited from parents cause this disorder."}
{"_id":"0c7954bc-8ca1-4859-88cd-bd7359584870","text":"Common symptoms of lactose intolerance include\n                \n- abdominal bloating, a feeling of fullness or swelling in the abdomen  - abdominal pain  - diarrhea  - gas  - nausea\n                \nSymptoms occur 30 minutes to 2 hours after consuming milk or milk products. Symptoms range from mild to severe based on the amount of lactose the person ate or drank and the amount a person can tolerate."}
{"_id":"1284f6e8-b32d-4296-8949-7a4d8b6cd820","text":"A health care provider makes a diagnosis of lactose intolerance based on\n                \n- medical, family, and diet history, including a review of symptoms  - a physical exam  - medical tests\n                \nMedical, family, and diet history. A health care provider will take a medical, family, and diet history to help diagnose lactose intolerance. During this discussion, the health care provider will review a patients symptoms. However, basing a diagnosis on symptoms alone may be misleading because digestive symptoms can occur for many reasons other than lactose intolerance. For example, other conditions such as irritable bowel syndrome, celiac disease, inflammatory bowel disease, or small bowel bacterial overgrowth can cause digestive symptoms.\n                \nPhysical exam. A physical exam may help diagnose lactose intolerance or rule out other conditions that cause digestive symptoms. During a physical exam, a health care provider usually\n                \n- checks for abdominal bloating  - uses a stethoscope to listen to sounds within the abdomen  - taps on the abdomen to check for tenderness or pain\n                \nA health care provider may recommend eliminating all milk and milk products from a persons diet for a short time to see if the symptoms resolve. Symptoms that go away when a person eliminates lactose from his or her diet may confirm the diagnosis of lactose intolerance.\n                \nMedical tests. A health care provider may order special tests to provide more information. Health care providers commonly use two tests to measure how well a person digests lactose:\n                \n- Hydrogen breath test. This test measures the amount of hydrogen in a persons breath. Normally, only a small amount of hydrogen is detectable in the breath when a person eats or drinks and digests lactose. However, undigested lactose produces high levels of hydrogen. For this test, the patient drinks a beverage that contains a known amount of lactose. A health care provider asks the patient to breathe into a balloon-type container that measures breath hydrogen level. In most cases, a health care provider performs this test at a hospital, on an outpatient basis. Smoking and some foods and medications may affect the accuracy of the results. A health care provider will tell the patient what foods or medications to avoid before the test.  - Stool acidity test. Undigested lactose creates lactic acid and other fatty acids that a stool acidity test can detect in a stool sample. Health care providers sometimes use this test to check acidity in the stools of infants and young children. A child may also have glucose in his or her stool as a result of undigested lactose. The health care provider will give the childs parent or caretaker a container for collecting the stool specimen. The parent or caretaker returns the sample to the health care provider, who sends it to a lab for analysis."}
{"_id":"e94ce3e7-3c29-48dc-b3d8-3c88f09e73f5","text":"Many people can manage the symptoms of lactose intolerance by changing their diet. Some people may only need to limit the amount of lactose they eat or drink. Others may need to avoid lactose altogether. Using lactase products can help some people manage their symptoms.\n                \nFor people with secondary lactase deficiency, treating the underlying cause improves lactose tolerance. In infants with developmental lactase deficiency, the ability to digest lactose improves as the infants mature. People with primary and congenital lactase deficiency cannot change their bodys ability to produce lactase."}
{"_id":"c89db1b1-01d4-4d1d-9280-66e59ad902a3","text":"People may find it helpful to talk with a health care provider or a registered dietitian about a dietary plan. A dietary plan can help people manage the symptoms of lactose intolerance and make sure they get enough nutrients. Parents, caretakers, childcare providers, and others who serve food to children with lactose intolerance should follow the dietary plan recommended by the childs health care provider or registered dietitian.\n                \nMilk and milk products. Gradually introducing small amounts of milk or milk products may help some people adapt to them with fewer symptoms. Often, people can better tolerate milk or milk products by having them with meals, such as having milk with cereal or having cheese with crackers. People with lactose intolerance are generally more likely to tolerate hard cheeses, such as cheddar or Swiss, than a glass of milk. A 1.5ounce serving of low-fat hard cheese has less than 1 gram of lactose, while a 1-cup serving of low-fat milk has about 11 to 13 grams of lactose.2\n                \nHowever, people with lactose intolerance are also more likely to tolerate yogurt than milk, even though yogurt and milk have similar amounts of lactose.2\n                \nLactose-free and lactose-reduced milk and milk products. Lactose-free and lactose-reduced milk and milk products are available at most supermarkets and are identical nutritionally to regular milk and milk products. Manufacturers treat lactose-free milk with the lactase enzyme. This enzyme breaks down the lactose in the milk. Lactose-free milk remains fresh for about the same length of time or, if it is ultra-pasteurized, longer than regular milk. Lactose-free milk may have a slightly sweeter taste than regular milk.\n                \nLactase products. People can use lactase tablets and drops when they eat or drink milk products. The lactase enzyme digests the lactose in the food and therefore reduces the chances of developing digestive symptoms. People should check with a health care provider before using these products because some groups, such as young children and pregnant and breastfeeding women, may not be able to use them."}
{"_id":"e4380939-79e4-4a3e-ad02-f5c80c2d67eb","text":"- Lactose is a sugar found in milk and milk products.  - Lactose intolerance is a condition in which people have digestive symptomssuch as bloating, diarrhea, and gasafter eating or drinking milk or milk products.  - A health care provider makes a diagnosis of lactose intolerance based on medical, family, and diet history, including a review of symptoms; a physical exam; and medical tests.  - Basing a diagnosis on symptoms alone may be misleading because digestive symptoms can occur for many reasons other than lactose intolerance.  - Most people with lactose intolerance can tolerate some amount of lactose in their diet and do not need to avoid milk or milk products completely. However, individuals vary in the amount of lactose they can tolerate.  - Research suggests that adults and adolescents with lactose malabsorption could eat or drink at least 12 grams of lactose in one sitting without symptoms or with only minor symptoms. This amount is the amount of lactose in 1 cup of milk.  - Many people can manage the symptoms of lactose intolerance by changing their diet. Some people may only need to limit the amount of lactose they eat or drink. Others may need to avoid lactose altogether.  - People may find it helpful to talk with a health care provider or a registered dietitian to determine if their diet provides adequate nutrients including calcium and vitamin D. To help ensure coordinated and safe care, people should discuss their use of complementary and alternative medical practices, including their use of dietary supplements, with their health care provider.  - Lactose is in all milk and milk products. Manufacturers also often add milk and milk products to boxed, canned, frozen, packaged, and prepared foods. People can check the ingredients on food labels to find possible sources of lactose in food products."}
{"_id":"e1d8440d-41fd-426b-ac0b-51ec1127a8c2","text":"Crohn's disease is a disease that causes inflammation,* or swelling, and irritation of any part of the digestive tractalso called the gastrointestinal (GI) tract. The part most commonly affected is the end part of the small intestine, called the ileum.\n                \n*See the Pronunciation Guide for tips on how to say the words in bold type.\n                \nCrohns disease is one of two main forms of diseases of the GI tract named inflammatory bowel disease (IBD). The other form, called ulcerative colitis, affects the large intestine, which includes the colon and the rectumthe lower end of the large intestine, leading to the anus.\n                \nWith Crohns disease, chronicor long lastinginflammation may cause scar tissue to form in the lining of the intestine. When scar tissue builds up, the passage can become narrow, causing food and stool to move through the GI tract more slowlywhich can lead to pain, cramps, and diarrhea."}
{"_id":"4921ea87-ef2e-415c-bc58-880adb106a3d","text":"Both men and women can get Crohn's disease, and it can run in families. People with Crohns disease may have a blood relative with the disease or another type of IBD. Crohns disease most commonly starts between the ages of 13 and 30."}
{"_id":"5346eeb3-c342-427b-af2a-754b96faad58","text":"Researchers are studying the possible causes of Crohns disease. Your bodys natural defense system, called the immune system, protects you from infection by fighting against bacteria, viruses, and other things that can make you sick. Researchers believe that with Crohns disease, the immune system attacks harmless bacteria and viruses. During the attack, white blood cells gather in the intestinal lining. The white blood cells cause chronic inflammation, which leads to ulcers, or sores, and damage to the intestines.\n                \nOther factors associated with Crohns disease are\n                \n- genesthe traits passed down from your parents  - unknown triggers caused by the environment"}
{"_id":"6b0816cc-9193-45ab-be00-db03e48c1642","text":"Crohn's disease symptoms can be different for each person. The most common symptoms of Crohns disease are\n                \n- abdominal painoften in the lower right area of the abdomen  - diarrhea  - bleeding in the rectum, which can be seen in a persons underwear, in the toilet, or in a bowel movement; rectal bleeding can be serious and may not stop without medical help  - weight loss  - fever"}
{"_id":"d5728ac1-3af2-4cfd-880a-381b480102fc","text":"A doctor will perform a physical exam and tests to diagnose Crohns disease. During your visit, the doctor will ask about your symptoms and medical history.\n                \nThe doctor may order blood tests, which involve drawing blood at a health care providers office or commercial facility and sending the sample to a lab for analysis. Blood tests can show anemia caused by bleeding. Anemia is a condition in which red blood cells are fewer or smaller than normal, which means less oxygen is carried to the bodys cells. Blood tests can also show a high white blood cell count, a sign of chronic inflammation.\n                \n\n                \nYou may also be asked for a stool sample. A stool test is commonly used to rule out other causes of GI diseases, such as infections. The doctor will give you a container for catching and storing the stool. The sample is returned to the doctor or a commercial facility and sent to a lab for analysis. A stool sample can also be used to check if you have bleeding or inflammation.\n                \nOther tests may be needed to diagnose Crohn's disease. The following tests are all performed at a hospital or outpatient center.\n                \n- Colonoscopy. Colonoscopy is the most commonly used test to specifically diagnose Crohns disease. This test is used to look inside your rectum, entire colon, and ileum. The health care provider will give you written bowel prep instructions to follow at home before the test. You may need to follow a clear liquid diet for 1 to 3 days before the test. You will need to take laxatives and enemas the evening before the test, and you will likely have one or more enemas about 2 hours before the test. A laxative is medicine that loosens stool and increases bowel movements. An enema involves flushing water, laxative, or sometimes a mild soap solution into the anus using a special squirt bottle.  For the test, you will lie on a table while the doctor inserts a flexible tube into your anus. A small camera on the tube sends a video image of the intestinal lining to a computer screen. The doctor can see inflammation, ulcers, or bleeding. The doctor may also perform a biopsy. The doctor will look at the tissue with a microscope to confirm the diagnosis of Crohns disease. In most cases, youll be given a light sedative, and possibly pain medicine, to help you relax. You will not feel the biopsy.  Cramping or bloating may occur during the first hour after the test. Driving is not permitted for 24 hours after the test to allow the sedative time to wear off. Before the appointment, you should make plans for a ride home. By the next day, you should fully recover and go back to your normal diet.    - Flexible sigmoidoscopy. This test is used to look inside the rectum and lower colon. The health care provider will give you written bowel prep instructions to follow at home before the test. You may need to follow a clear liquid diet for 1 to 3 days before the test. You may also need a laxative or enema the night before the test. And youll have one or more enemas about 2 hours before the procedure.  For the test, you will lie on a table while the doctor inserts a flexible tube into your anus. You will not need a sedative for the test. A small camera on the tube sends a video image of the intestinal lining to a computer screen. The doctor can see inflammation, ulcers, or bleeding. The doctor may also perform a biopsy by snipping a bit of tissue from the intestinal lining. The doctor will look at the tissue with a microscope to confirm the diagnosis of Crohns disease. You will not feel the biopsy.  You can usually go back to your normal diet after the test, though you may have cramping or bloating during the first hour after the test.    - Computerized tomography (CT) scan. A CT scan uses x rays and computers to create images of the inside of the body. For the test, you will lie on a table that slides into a tunnel-shaped device where the x rays are taken. The technician may give you a solution to drink and an injection of a special dye through a needle inserted into an arm vein. You will not need a sedative for the test. CT scans can be used to help diagnose Crohn's disease.    - Upper GI series (x rays). An upper GI series may be done to look at the small intestine. No eating or drinking is allowed for 8 hours before the procedure. You will not need a sedative for the test. During the procedure, you will stand or sit in front of an x-ray machine and drink barium, a chalky liquid. The barium coats the small intestine, making signs of the disease show up more clearly on x rays.  After the test, you may go back to your normal diet, though you may have nausea or bloating for a short time. Traces of barium in the GI tract cause stools to be white or light colored for a few days after the test.    - Lower GI series (x rays). A lower GI series may be done to look at the large intestine. The health care provider will give you written bowel prep instructions to follow at home before the test. You will be asked to follow a clear liquid diet for 1 to 3 days before the test. A laxative or enema is usually used the evening before a lower GI series. Enemas are sometimes repeated the morning of the test.  For the test, you will lie on a table while the doctor inserts a flexible tube into your anus. You will not need a sedative for the test. The large intestine is filled with barium, making signs of the disease show up more clearly on x rays. After the test, you may go back to your normal diet, though you may have bloating. You also may have some soreness of the anus. Traces of barium in the GI tract cause stools to be white or light colored for a few days after the test."}
{"_id":"65ad2766-a7e2-4323-842e-7268f7c7bb49","text":"Intestinal blockage can occur in people with Crohns disease when scar tissue blocks the intestinal passage. A narrow intestinal passage is called a stricture. When the passage blocks completely, food and stool stop moving, causing abdominal cramps and vomiting. If you have these symptoms, you should see a health care provider right away.\n                \nUlcers from Crohns disease can cause tunnels to form through the inflamed areas, or even the healthy parts, of the intestine. These tunnels are called fistulas. Fistulas are seen most often in the areas around the rectum and anus. Sometimes a pocket of infection, called an abscess, can form in and around the fistulas. Most fistulas can be treated with medicines, but sometimes surgery is needed.\n                \nPeople with Crohns disease often have anemia, which can be caused by the disease itself or by iron deficiency. Anemia may make a person feel tired.\n                \nPeople with Crohns disease, particularly if they have been treated with steroid medicines, may have weakness of their bonescalled osteoporosis or osteomalacia.\n                \nPeople with Crohns disease may also have arthritis, skin problems, swelling in the eyes or mouth, kidney stones, gallstones, and liver problems. Some people with Crohns disease may have restless legs syndromeextreme leg discomfort the person feels while sitting or lying down. These problems may go away during treatment, but some must be treated with medicines.\n                \nPeople who have Crohns disease may not get enough nutrition, such as protein, vitamins, or calories, because they\n                \n- have an upset stomach that keeps them from eating enough calories  - may not be able to absorb nutrients in the intestine\n                \nChildren with Crohns disease may fail to grow normally and may have low height for their age."}
{"_id":"2bf39c9a-37c0-42d1-ada5-fe6f0b5d33fc","text":"Treatment for Crohns disease depends on\n                \n- where the disease is located in the GI tract  - what problems you already have from the disease  - what past treatments you have had for the disease\n                \nThe goals of treatment are to\n                \n- decrease the inflammation  - relieve symptoms such as abdominal pain, diarrhea, and rectal bleeding  - correct nutritional problems\n                \nTreatment may include\n                \n- medicines  - surgery  - eating, diet, and nutrition\n                \n\n                \nMedicines\n                \nOne or more of the following medicines may be used to treat Crohns disease:\n                \n- Anti-inflammation medicines may be used first to treat your Crohn's disease. These medicines help lower inflammation in the intestine and relieve the pain and diarrhea. Sometimes anti-inflammation medicines cause side effects, so you should talk with your health care provider about what to expect.  - Steroids also help lower inflammation. Steroids are similar to natural chemicals in the body. However, steroids are used only for a short time because long-term use can lead to serious side effects.  - Immune system suppressors. Azathioprine and 6-mercaptopurine work by keeping your immune system from attacking harmless foreign substances. Immune system suppressors also cause side effects, so you should talk with your health care provider about what to expect.  - Biological therapies. Biological therapies are medicines that are given by an injection in the vein, infliximab (Remicade), or an injection in the skin, adalimumab (HUMIRA). Your health care provider may treat you with these medicines if others are not helping to decrease inflammation, or if you have fistulas with abscesses. The goals for using these medicines are to get you better, keep you better, and avoid long-term steroid use.  - Antibiotics. Antibiotics are used to treat bacterial overgrowth in the small intestine caused by stricture, fistulas, or surgery. For this common problem, the doctor may prescribe one or more of the following antibiotics: ampicillin, sulfonamide, cephalosporin, tetracycline, or metronidazole.\n                \n\n                \n- Anti-diarrheal medicines and fluid replacements. Diarrhea and abdominal cramps are often relieved when the inflammation improves, but more medicine may be needed. Anti-diarrheal medicines include diphenoxylate, loperamide, and codeine. People with diarrhea should drink plenty of fluids to prevent dehydrationloss of fluids from the body. If diarrhea does not improve, the person should see the doctor promptly for possible treatment with fluids given through a small tube inserted into an arm vein.\n                \nSurgery\n                \nSome people with Crohns disease need surgery if medicines are no longer working to control blockage, fistulas, abscesses, and bleeding. A surgeon performs the procedure in a hospital, where you will receive medicine to make you sleep during the surgery.\n                \nOne or more of the following surgeries may be needed:\n                \n- Intestinal resection. The surgeon removes the diseased section of intestine and puts the ends of the intestine back together.  - Proctocolectomy. Proctocolectomy is surgery to remove the rectum and part or all of the colon. An ileostomy is performed with a proctocolectomy.  - Ileostomy. Ileostomy is an operation to create an openingcalled a stomafor the stool to exit the body when the ends of the intestine cannot be put back together. To create a stoma, an end of the intestine is brought out through a small opening made on the lower right part of the abdomen near the beltline. The stoma is about the size of a quarter. An ostomy pouch is worn outside the body over the stoma to collect waste, and it is emptied several times a day. Your health care provider may refer you to an ostomy nursea specialist who cares for people with an ostomy pouch.\n                \nSurgery usually does not cure Crohn's disease forever. Sometimes you need to have more than one surgery because the disease returns next to where the intestine was removed. Because Crohns disease can return after surgery, you can talk with your health care provider and other patients to get as much information as possible before having surgery."}
{"_id":"bb64542c-c6f0-4b27-aaba-2fdb54b47996","text":"Your health care provider may start you on a special diet, so you get extra nutrition and calories. High-calorie liquid supplements are often used to give you the extra calories and right amount of vitamins and minerals to keep you healthy. During acute phases of the disease, you may need to receive intravenous nutrition to give the intestine a rest.\n                \nNo foods are known to cause injury or inflammation to the intestine. But foods such as hot spices, alcohol, greasy foods, and milk products may make diarrhea and cramping worse. You should eat a healthy diet and avoid foods that make symptoms worse. Your health care provider may refer you to a dietitian to help you with meal planning."}
{"_id":"2a324ad5-4fde-4778-9fec-9e79608fb1d0","text":"- Crohn's disease is a disease that causes inflammation, or swelling, and irritation of any part of the digestive tractalso called the gastrointestinal (GI) tract.  - People with Crohns disease may have a blood relative with the disease or another type of inflammatory bowel disease (IBD).  - Symptoms of Crohns disease include abdominal pain, diarrhea, bleeding, weight loss, and fever.  - A physical exam, blood tests, stool tests, and other tests are needed to diagnose Crohns disease.  - Problems of Crohns disease include intestinal blockage, fistulas, abscesses, anemia, and slower growth in children.  - Doctors treat Crohns disease with medicines, surgery, diet, and nutrition.  - People with Crohns disease should eat a healthy diet and avoid foods that make symptoms worse.  - Quitting smoking can help make Crohns disease less severe. Ask your health care provider if you need help quitting smoking.  - Support groups may help lower stress for people with Crohns disease.  - Most people with Crohns disease are able to work, raise families, and live full lives.  - Many women with Crohns disease can become pregnant and have a baby. You should talk with your health care provider before getting pregnant."}
{"_id":"5548e454-1103-422a-ba14-c8dd7cd4ccdc","text":"The digestive system is made up of the gastrointestinal (GI) tractalso called the digestive tractand the liver, pancreas, and gallbladder. The GI tract is a series of hollow organs joined in a long, twisting tube from the mouth to the anus. The hollow organs that make up the GI tract are the mouth, esophagus, stomach, small intestine, large intestinewhich includes the colon and rectumand anus. Food enters the mouth and passes to the anus through the hollow organs of the GI tract. The liver, pancreas, and gallbladder are the solid organs of the digestive system. The digestive system helps the body digest food, which includes breaking food down into nutrients the body needs. Nutrients are substances the body uses for energy, growth, and cell repair."}
{"_id":"ef086c73-49b8-4e98-8375-40b35741d02c","text":"Smoking has been found to increase the risk of cancers of the3\n                \n- mouth  - esophagus  - stomach  - pancreas\n                \n3\n                \n,\n                \n4\n                \n,\n                \n5\n                \n- liver  - colon  - rectum\n                \nMore information about the link between smoking and cancers of the digestive system can be found on the National Cancer Institute website at www.cancer.gov\/cancertopics\/tobacco\/smoking."}
{"_id":"6b008b39-1790-44bd-be0c-731000461693","text":"Smoking contributes to many common disorders of the digestive system, such as heartburn and gastroesophageal reflux disease (GERD), peptic ulcers, and some liver diseases. Smoking increases the risk of Crohns disease, colon polyps, and pancreatitis, and it may increase the risk of gallstones."}
{"_id":"d9a5b374-7554-40e9-80c4-2a4a13baa91c","text":"Eating, diet, and nutrition can play a role in causing, preventing, and treating some of the diseases and disorders of the digestive system that are affected by smoking, including heartburn and GERD, liver diseases, Crohns disease, colon polyps, pancreatitis, and gallstones. More information about eating, diet, and nutrition and these conditions can be found on the Digestive Diseases A-Z list."}
{"_id":"14b8a29f-e812-4176-bc20-5afe3868910d","text":"- Smoking has been found to increase the risk of cancers of the mouth, esophagus, stomach, and pancreas. Research suggests that smoking may also increase the risk of cancers of the liver, colon, and rectum.  - Smoking increases the risk of heartburn and gastroesophageal reflux disease (GERD).  - Smoking increases the risk of peptic ulcers.  - Smoking may worsen some liver diseases, including primary biliary cirrhosis and nonalcoholic fatty liver disease (NAFLD).  - Current and former smokers have a higher risk of developing Crohns disease than people who have never smoked.  - People who smoke are more likely to develop colon polyps.  - Smoking increases the risk of developing pancreatitis.  - Some studies have shown that smoking may increase the risk of developing gallstones. However, research results are not consistent and more study is needed.  - Quitting smoking can reverse some of the effects of smoking on the digestive system."}
{"_id":"85c25aa2-fff6-4197-98f0-6892f71319ed","text":"Blood pressure is the force of blood pushing against blood vessel walls as the heart pumps out blood, and high blood pressure, also called hypertension, is an increase in the amount of force that blood places on blood vessels as it moves through the body. Factors that can increase this force include higher blood volume due to extra fluid in the blood and blood vessels that are narrow, stiff, or clogged.\n                \nBlood pressure test results are written with two numbers separated by a slash. For example, a health care provider will write a blood pressure result as 120\/80. A health care provider will say this blood pressure result as 120 over 80. The top number is called the systolic pressure and represents the pressure as the heart beats and pushes blood through the blood vessels. The bottom number is called the diastolic pressure and represents the pressure as blood vessels relax between heartbeats.\n                \nMost people without chronic health conditions have a normal blood pressure if it stays below 120\/80. Prehypertension is a systolic pressure of 120 to 139 or a diastolic pressure of 80 to 89. High blood pressure is a systolic pressure of 140 or above or a diastolic pressure of 90 or above.1\n                \nPeople should talk with their health care provider about their individual blood pressure goals and how often they should have their blood pressure checked."}
{"_id":"b5d36319-0d09-4991-878c-9bbeda101615","text":"The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the two kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra fluid. The urine flows from the kidneys to the bladder through tubes called ureters. The bladder stores urine. When the bladder empties, urine flows out of the body through a tube called the urethra, located at the bottom of the bladder. In men the urethra is long, while in women it is short.\n                \nKidneys work at the microscopic level. The kidney is not one large filter. Each kidney is made up of about a million filtering units called nephrons. Each nephron filters a small amount of blood. The nephron includes a filter, called the glomerulus, and a tubule. The nephrons work through a two-step process. The glomerulus lets fluid and waste products pass through it; however, it prevents blood cells and large molecules, mostly proteins, from passing. The filtered fluid then passes through the tubule, which sends needed minerals back to the bloodstream and removes wastes. The final product becomes urine."}
{"_id":"53fddb90-36e5-4c96-973c-96be6fcd0df1","text":"Most people with high blood pressure do not have symptoms. In rare cases, high blood pressure can cause headaches.\n                \nKidney disease also does not have symptoms in the early stages. A person may have swelling called edema, which happens when the kidneys cannot get rid of extra fluid and salt. Edema can occur in the legs, feet, or ankles and less often in the hands or face. Once kidney function decreases further, symptoms can include\n                \n- appetite loss  - nausea  - vomiting  - drowsiness or feeling tired  - trouble concentrating  - sleep problems  - increased or decreased urination  - generalized itching or numbness  - dry skin  - headaches  - weight loss  - darkened skin  - muscle cramps  - shortness of breath  - chest pain"}
{"_id":"82e9c86c-72a8-436d-85bd-3e0cc3ea5624","text":"A health care provider diagnoses high blood pressure when multiple blood pressure testsoften repeated over several visits to a health care providers officeshow that a systolic blood pressure is consistently above 140 or a diastolic blood pressure is consistently above 90. Health care providers measure blood pressure with a blood pressure cuff. People can also buy blood pressure cuffs at discount chain stores and drugstores to monitor their blood pressure at home.\n                \nKidney disease is diagnosed with urine and blood tests.\n                \nUrine Tests\n                \nDipstick test for albumin. A dipstick test performed on a urine sample can detect the presence of albumin in the urine. Albumin is a protein in the blood that can pass into the urine when the kidneys are damaged. A patient collects the urine sample in a special container in a health care providers office or a commercial facility. The office or facility tests the sample onsite or sends it to a lab for analysis. For the test, a nurse or technician places a strip of chemically treated paper, called a dipstick, into the urine. Patches on the dipstick change color when blood or protein is present in urine.\n                \nUrine albumin-to-creatinine ratio. A health care provider uses the albumin and creatinine measurement to determine the ratio between the albumin and creatinine in the urine. Creatinine is a waste product in the blood that is filtered in the kidneys and excreted in the urine. A urine albumin-to-creatinine ratio above 30 mg\/g may be a sign of kidney disease.\n                \nBlood Test\n                \nA blood test involves having blood drawn at a health care providers office or a commercial facility and sending the sample to a lab for analysis. A health care provider may order a blood test to estimate how much blood the kidneys filter each minute, called the estimated glomerular filtration rate (eGFR). The results of the test indicate the following:\n                \n- eGFR of 60 or above is in the normal range  - eGFR below 60 may indicate kidney damage  - eGFR of 15 or below may indicate kidney failure\n                \n\n                \nGet Screened for Kidney Disease   Kidney disease, when found early, can be treated to prevent more serious disease and other complications. The National Kidney Foundation recommends people with high blood pressure receive the following regular screenings:   - blood pressure tests   - urine albumin   - eGFR    Health care providers will help determine how often people with high blood pressure should be screened."}
{"_id":"2b51f2d2-eeb2-452d-be9c-28b1f3b17125","text":"The best way to slow or prevent kidney disease from high blood pressure is to take steps to lower blood pressure. These steps include a combination of medication and lifestyle changes, such as\n                \n- healthy eating  - physical activity  - maintaining a healthy weight  - quitting smoking  - managing stress\n                \nNo matter what the cause of the kidney disease, high blood pressure can increase damage to the kidneys. People with kidney disease should keep their blood pressure below 140\/90.4\n                \nMedication\n                \nMedications that lower blood pressure can also significantly slow the progression of kidney disease. Two types of blood pressure-lowering medications, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), have been shown effective in slowing the progression of kidney disease. Many people require two or more medications to control their blood pressure. In addition to an ACE inhibitor or an ARB, a health care provider may prescribe a diuretica medication that helps the kidneys remove fluid from the blood. A person may also need beta blockers, calcium channel blockers, and other blood pressure medications."}
{"_id":"a28a2513-5439-4fbc-8fb5-17e82672dcf0","text":"Following a healthy eating plan can help lower blood pressure. A health care provider may recommend the Dietary Approaches to Stop Hypertension (DASH) eating plan. DASH focuses on fruits, vegetables, whole grains, and other foods that are heart healthy and lower in sodium, which often comes from salt. The DASH eating plan\n                \n- is low in fat and cholesterol  - features fat-free or low-fat milk and dairy products, fish, poultry, and nuts  - suggests less red meat, sweets, added sugars, and sugar-containing beverages  - is rich in nutrients, protein, and fiber\n                \nRead more about DASH at www.nhlbi.nih.gov\/health\/resources\/heart\/hbp-dash-index.htm.\n                \nA dietitian may also recommend this type of diet for people who have already developed kidney disease. A diet low in sodium and liquid intake can help reduce edema and lower blood pressure. Reducing saturated fat and cholesterol can help control high levels of lipids, or fats, in the blood.\n                \nHealth care providers may recommend that people with kidney disease eat moderate or reduced amounts of protein, though the benefits of reducing protein in a persons diet is still being researched. Proteins break down into waste products that the kidneys filter from the blood. Eating more protein than the body needs may burden the kidneys and cause kidney function to decline faster. However, protein intake that is too low may lead to malnutrition, a condition that occurs when the body does not get enough nutrients. People with kidney disease who are on a restricted protein diet should be monitored with blood tests that can show low nutrient levels.\n                \nIn addition, consuming too much alcohol raises blood pressure, so people should limit alcoholic drinkstwo per day for men and one per day for women.\n                \nA health care provider can help people change their diet to meet their individual needs.\n                \nPhysical Activity\n                \nRegular physical activity can lower blood pressure and reduce the chances of other health problems. A health care provider can provide information about how much and what kinds of activity are safe. Most people should try to get at least 30 to 60 minutes of activity most or all days of the week. A person can do all physical activity at once or break up activities into shorter periods of at least 10 minutes each. Moderate activities include brisk walking, dancing, bowling, riding a bike, working in a garden, and cleaning the house.\n                \nBody Weight\n                \nPeople who are overweight or obese should aim to reduce their weight by 7 to 10 percent during the first year of treatment for high blood pressure. This amount of weight loss can lower the chance of health problems related to high blood pressure. Overweight is defined as a body mass index (BMI)a measurement of weight in relation to heightof 25 to 29. A BMI of 30 or higher is considered obese. A BMI lower than 25 is the goal for keeping blood pressure under control.5\n                \nSmoking\n                \nPeople who smoke should quit. Smoking can damage blood vessels, raise the chance of high blood pressure, and worsen health problems related to high blood pressure. People with high blood pressure should talk with their health care provider about programs and products they can use to quit smoking.\n                \nStress\n                \nLearning how to manage stress, relax, and cope with problems can improve emotional and physical health. Some activities that may help reduce stress include\n                \n- exercising  - practicing yoga or tai chi  - listening to music  - focusing on something calm or peaceful  - meditating"}
{"_id":"4197c6f7-b548-45c3-9930-dac878f94e6b","text":"- Blood pressure is the force of blood pushing against blood vessel walls as the heart pumps out blood, and high blood pressure, also called hypertension, is an increase in the amount of force that blood places on blood vessels as it moves through the body.  - High blood pressure can damage blood vessels in the kidneys, reducing their ability to work properly. When the force of blood flow is high, blood vessels stretch so blood flows more easily. Eventually, this stretching scars and weakens blood vessels throughout the body, including those in the kidneys.  - High blood pressure is the second leading cause of kidney failure in the United States after diabetes.  - A health care provider diagnoses high blood pressure when multiple blood pressure testsoften repeated over several visits to a health care providers officeshow that a systolic blood pressure is consistently above 140 or a diastolic blood pressure is consistently above 90.  - Kidney disease is diagnosed with urine and blood tests.  - The best way to slow or prevent kidney damage from high blood pressure is to take steps to lower blood pressure. These steps include a combination of medication and lifestyle changes, such as      - healthy eating    - physical activity    - maintaining a healthy weight    - quitting smoking    - managing stress    - No matter what the cause of the kidney disease, high blood pressure can increase damage to the kidneys. People with kidney disease should keep their blood pressure below 140\/90."}
{"_id":"8f575c6b-d3cd-47f8-aac3-10e6c095a999","text":"Hypoglycemia, also called low blood glucose or low blood sugar, occurs when blood glucose drops below normal levels. Glucose, an important source of energy for the body, comes from food. Carbohydrates are the main dietary source of glucose. Rice, potatoes, bread, tortillas, cereal, milk, fruit, and sweets are all carbohydrate-rich foods.\n                \nAfter a meal, glucose is absorbed into the bloodstream and carried to the body's cells. Insulin, a hormone made by the pancreas, helps the cells use glucose for energy. If a person takes in more glucose than the body needs at the time, the body stores the extra glucose in the liver and muscles in a form called glycogen. The body can use glycogen for energy between meals. Extra glucose can also be changed to fat and stored in fat cells. Fat can also be used for energy.\n                \nWhen blood glucose begins to fall, glucagonanother hormone made by the pancreassignals the liver to break down glycogen and release glucose into the bloodstream. Blood glucose will then rise toward a normal level. In some people with diabetes, this glucagon response to hypoglycemia is impaired and other hormones such as epinephrine, also called adrenaline, may raise the blood glucose level. But with diabetes treated with insulin or pills that increase insulin production, glucose levels can't easily return to the normal range.\n                \nHypoglycemia can happen suddenly. It is usually mild and can be treated quickly and easily by eating or drinking a small amount of glucose-rich food. If left untreated, hypoglycemia can get worse and cause confusion, clumsiness, or fainting. Severe hypoglycemia can lead to seizures, coma, and even death.\n                \nIn adults and children older than 10 years, hypoglycemia is uncommon except as a side effect of diabetes treatment. Hypoglycemia can also result, however, from other medications or diseases, hormone or enzyme deficiencies, or tumors."}
{"_id":"07502915-a899-450e-ab19-1f38da32a090","text":"Hypoglycemia, also called low blood glucose or low blood sugar, occurs when blood glucose drops below normal levels. Glucose, an important source of energy for the body, comes from food. Carbohydrates are the main dietary source of glucose. Rice, potatoes, bread, tortillas, cereal, milk, fruit, and sweets are all carbohydrate-rich foods.\n                \nAfter a meal, glucose is absorbed into the bloodstream and carried to the body's cells. Insulin, a hormone made by the pancreas, helps the cells use glucose for energy. If a person takes in more glucose than the body needs at the time, the body stores the extra glucose in the liver and muscles in a form called glycogen. The body can use glycogen for energy between meals. Extra glucose can also be changed to fat and stored in fat cells. Fat can also be used for energy.\n                \nWhen blood glucose begins to fall, glucagonanother hormone made by the pancreassignals the liver to break down glycogen and release glucose into the bloodstream. Blood glucose will then rise toward a normal level. In some people with diabetes, this glucagon response to hypoglycemia is impaired and other hormones such as epinephrine, also called adrenaline, may raise the blood glucose level. But with diabetes treated with insulin or pills that increase insulin production, glucose levels can't easily return to the normal range.\n                \nHypoglycemia can happen suddenly. It is usually mild and can be treated quickly and easily by eating or drinking a small amount of glucose-rich food. If left untreated, hypoglycemia can get worse and cause confusion, clumsiness, or fainting. Severe hypoglycemia can lead to seizures, coma, and even death.\n                \nIn adults and children older than 10 years, hypoglycemia is uncommon except as a side effect of diabetes treatment. Hypoglycemia can also result, however, from other medications or diseases, hormone or enzyme deficiencies, or tumors."}
{"_id":"648dc8c0-e64c-4ab7-94d7-6146d3c79794","text":"Hypoglycemia causes symptoms such as\n                \n- hunger  - shakiness  - nervousness  - sweating  - dizziness or light-headedness  - sleepiness  - confusion  - difficulty speaking  - anxiety  - weakness\n                \nHypoglycemia can also happen during sleep. Some signs of hypoglycemia during sleep include\n                \n- crying out or having nightmares  - finding pajamas or sheets damp from perspiration  - feeling tired, irritable, or confused after waking up"}
{"_id":"fb57c504-8318-437a-86b6-e4e9180796f9","text":"Hypoglycemia causes symptoms such as\n                \n- hunger  - shakiness  - nervousness  - sweating  - dizziness or light-headedness  - sleepiness  - confusion  - difficulty speaking  - anxiety  - weakness\n                \nHypoglycemia can also happen during sleep. Some signs of hypoglycemia during sleep include\n                \n- crying out or having nightmares  - finding pajamas or sheets damp from perspiration  - feeling tired, irritable, or confused after waking up"}
{"_id":"1c1f89fe-9148-402f-a546-6ff5e104bdef","text":"Diabetes Medications\n                \nHypoglycemia can occur as a side effect of some diabetes medications, including insulin and oral diabetes medicationspillsthat increase insulin production, such as\n                \n- chlorpropamide (Diabinese)  - glimepiride (Amaryl)  - glipizide (Glucotrol, Glucotrol XL)  - glyburide (DiaBeta, Glynase, Micronase)  - nateglinide (Starlix)  - repaglinide (Prandin)  - sitagliptin (Januvia)  - tolazamide  - tolbutamide\n                \nCertain combination pills can also cause hypoglycemia, including\n                \n- glipizide + metformin (Metaglip)  - glyburide + metformin (Glucovance)  - pioglitazone + glimepiride (Duetact)  - rosiglitazone + glimepiride (Avandaryl)  - sitagliptin + metformin (Janumet)\n                \nOther types of diabetes pills, when taken alone, do not cause hypoglycemia. Examples of these medications are\n                \n- acarbose (Precose)  - metformin (Glucophage)  - miglitol (Glyset)  - pioglitazone (Actos)  - rosiglitazone (Avandia)\n                \nHowever, taking these pills along with other diabetes medicationsinsulin, pills that increase insulin production, or bothincreases the risk of hypoglycemia.\n                \nIn addition, use of the following injectable medications can cause hypoglycemia:\n                \n- Pramlintide (Symlin), which is used along with insulin  - Exenatide (Byetta), which can cause hypoglycemia when used in combination with chlorpropamide, glimepiride, glipizide, glyburide, tolazamide, and tolbutamide\n                \nMore information about diabetes medications is provided in the NIDDK health topic, What I need to know about Diabetes Medicines, or by calling 18008608747.\n                \nOther Causes of Hypoglycemia\n                \nIn people on insulin or pills that increase insulin production, low blood glucose can be due to\n                \n- meals or snacks that are too small, delayed, or skipped  - increased physical activity  - alcoholic beverages"}
{"_id":"c86d423f-6572-4622-aad2-168d5d621a86","text":"Diabetes Medications\n                \nHypoglycemia can occur as a side effect of some diabetes medications, including insulin and oral diabetes medicationspillsthat increase insulin production, such as\n                \n- chlorpropamide (Diabinese)  - glimepiride (Amaryl)  - glipizide (Glucotrol, Glucotrol XL)  - glyburide (DiaBeta, Glynase, Micronase)  - nateglinide (Starlix)  - repaglinide (Prandin)  - sitagliptin (Januvia)  - tolazamide  - tolbutamide\n                \nCertain combination pills can also cause hypoglycemia, including\n                \n- glipizide + metformin (Metaglip)  - glyburide + metformin (Glucovance)  - pioglitazone + glimepiride (Duetact)  - rosiglitazone + glimepiride (Avandaryl)  - sitagliptin + metformin (Janumet)\n                \nOther types of diabetes pills, when taken alone, do not cause hypoglycemia. Examples of these medications are\n                \n- acarbose (Precose)  - metformin (Glucophage)  - miglitol (Glyset)  - pioglitazone (Actos)  - rosiglitazone (Avandia)\n                \nHowever, taking these pills along with other diabetes medicationsinsulin, pills that increase insulin production, or bothincreases the risk of hypoglycemia.\n                \nIn addition, use of the following injectable medications can cause hypoglycemia:\n                \n- Pramlintide (Symlin), which is used along with insulin  - Exenatide (Byetta), which can cause hypoglycemia when used in combination with chlorpropamide, glimepiride, glipizide, glyburide, tolazamide, and tolbutamide\n                \nMore information about diabetes medications is provided in the NIDDK health topic, What I need to know about Diabetes Medicines, or by calling 18008608747.\n                \nOther Causes of Hypoglycemia\n                \nIn people on insulin or pills that increase insulin production, low blood glucose can be due to\n                \n- meals or snacks that are too small, delayed, or skipped  - increased physical activity  - alcoholic beverages"}
{"_id":"ac185c07-39cf-4fad-a9c7-fc41a70df56a","text":"Diabetes treatment plans are designed to match the dose and timing of medication to a person's usual schedule of meals and activities. Mismatches could result in hypoglycemia. For example, taking a dose of insulinor other medication that increases insulin levelsbut then skipping a meal could result in hypoglycemia.\n                \nTo help prevent hypoglycemia, people with diabetes should always consider the following:\n                \n- Their diabetes medications. A health care provider can explain which diabetes medications can cause hypoglycemia and explain how and when to take medications. For good diabetes management, people with diabetes should take diabetes medications in the recommended doses at the recommended times. In some cases, health care providers may suggest that patients learn how to adjust medications to match changes in their schedule or routine.  - Their meal plan. A registered dietitian can help design a meal plan that fits one's personal preferences and lifestyle. Following one's meal plan is important for managing diabetes. People with diabetes should eat regular meals, have enough food at each meal, and try not to skip meals or snacks. Snacks are particularly important for some people before going to sleep or exercising. Some snacks may be more effective than others in preventing hypoglycemia overnight. The dietitian can make recommendations for snacks.  - Their daily activity. To help prevent hypoglycemia caused by physical activity, health care providers may advise      - checking blood glucose before sports, exercise, or other physical activity and having a snack if the level is below 100 milligrams per deciliter (mg\/dL)    - adjusting medication before physical activity    - checking blood glucose at regular intervals during extended periods of physical activity and having snacks as needed    - checking blood glucose periodically after physical activity    - Their use of alcoholic beverages. Drinking alcoholic beverages, especially on an empty stomach, can cause hypoglycemia, even a day or two later. Heavy drinking can be particularly dangerous for people taking insulin or medications that increase insulin production. Alcoholic beverages should always be consumed with a snack or meal at the same time. A health care provider can suggest how to safely include alcohol in a meal plan.  - Their diabetes management plan. Intensive diabetes managementkeeping blood glucose as close to the normal range as possible to prevent long-term complicationscan increase the risk of hypoglycemia. Those whose goal is tight control should talk with a health care provider about ways to prevent hypoglycemia and how best to treat it if it occurs.\n                \nWhat to Ask the Doctor about Diabetes Medications\n                \nPeople who take diabetes medications should ask their doctor or health care provider\n                \n- whether their diabetes medications could cause hypoglycemia  - when they should take their diabetes medications  - how much medication they should take  - whether they should keep taking their diabetes medications when they are sick  - whether they should adjust their medications before physical activity  - whether they should adjust their medications if they skip a meal"}
{"_id":"0187bfc7-b5ec-4b85-8dc2-da9625d5e264","text":"Signs and symptoms of hypoglycemia vary from person to person. People with diabetes should get to know their signs and symptoms and describe them to their friends and family so they can help if needed. School staff should be told how to recognize a child's signs and symptoms of hypoglycemia and how to treat it.\n                \nPeople who experience hypoglycemia several times in a week should call their health care provider. They may need a change in their treatment plan: less medication or a different medication, a new schedule for insulin or medication, a different meal plan, or a new physical activity plan.\n                \nPrompt Treatment for Hypoglycemia\n                \nWhen people think their blood glucose is too low, they should check the blood glucose level of a blood sample using a meter. If the level is below 70 mg\/dL, one of these quick-fix foods should be consumed right away to raise blood glucose:\n                \n- 3 or 4 glucose tablets  - 1 serving of glucose gelthe amount equal to 15 grams of carbohydrate  - 1\/2 cup, or 4 ounces, of any fruit juice  - 1\/2 cup, or 4 ounces, of a regularnot dietsoft drink  - 1 cup, or 8 ounces, of milk  - 5 or 6 pieces of hard candy  - 1 tablespoon of sugar or honey\n                \nRecommended amounts may be less for small children. The child's doctor can advise about the right amount to give a child.\n                \nThe next step is to recheck blood glucose in 15 minutes to make sure it is 70 mg\/dL or above. If it's still too low, another serving of a quick-fix food should be eaten. These steps should be repeated until the blood glucose level is 70 mg\/dL or above. If the next meal is an hour or more away, a snack should be eaten once the quick-fix foods have raised the blood glucose level to 70 mg\/dL or above.\n                \nFor People Who Take Acarbose (Precose) or Miglitol (Glyset)\n                \nPeople who take either of these diabetes medications should know that only pure glucose, also called dextroseavailable in tablet or gel formwill raise their blood glucose level during a low blood glucose episode. Other quick-fix foods and drinks won't raise the level quickly enough because acarbose and miglitol slow the digestion of other forms of carbohydrate.\n                \nHelp from Others for Severe Hypoglycemia\n                \nSevere hypoglycemiavery low blood glucosecan cause a person to pass out and can even be life threatening. Severe hypoglycemia is more likely to occur in people with type 1 diabetes. People should ask a health care provider what to do about severe hypoglycemia. Another person can help someone who has passed out by giving an injection of glucagon. Glucagon will rapidly bring the blood glucose level back to normal and help the person regain consciousness. A health care provider can prescribe a glucagon emergency kit. Family, friends, or coworkersthe people who will be around the person at risk of hypoglycemiacan learn how to give a glucagon injection and when to call 911 or get medical help.\n                \nPhysical Activity and Blood Glucose Levels\n                \nPhysical activity has many benefits for people with diabetes, including lowering blood glucose levels. However, physical activity can make levels too low and can cause hypoglycemia up to 24 hours afterward. A health care provider can advise about checking the blood glucose level before exercise. For those who take insulin or one of the oral medications that increase insulin production, the health care provider may suggest having a snack if the glucose level is below 100 mg\/dL or adjusting medication doses before physical activity to help avoid hypoglycemia. A snack can prevent hypoglycemia. The health care provider may suggest extra blood glucose checks, especially after strenuous exercise.\n                \nHypoglycemia When Driving\n                \nHypoglycemia is particularly dangerous if it happens to someone who is driving. People with hypoglycemia may have trouble concentrating or seeing clearly behind the wheel and may not be able to react quickly to road hazards or to the actions of other drivers. To prevent problems, people at risk for hypoglycemia should check their blood glucose level before driving. During longer trips, they should check their blood glucose level frequently and eat snacks as needed to keep the level at 70 mg\/dL or above. If necessary, they should stop for treatment and then make sure their blood glucose level is 70 mg\/dL or above before starting to drive again.\n                \nHypoglycemia Unawareness\n                \nSome people with diabetes do not have early warning signs of low blood glucose, a condition called hypoglycemia unawareness. This condition occurs most often in people with type 1 diabetes, but it can also occur in people with type 2 diabetes. People with hypoglycemia unawareness may need to check their blood glucose level more often so they know when hypoglycemia is about to occur. They also may need a change in their medications, meal plan, or physical activity routine.\n                \nHypoglycemia unawareness develops when frequent episodes of hypoglycemia lead to changes in how the body reacts to low blood glucose levels. The body stops releasing the hormone epinephrine and other stress hormones when blood glucose drops too low. The loss of the body's ability to release stress hormones after repeated episodes of hypoglycemia is called hypoglycemia-associated autonomic failure, or HAAF.\n                \nEpinephrine causes early warning symptoms of hypoglycemia such as shakiness, sweating, anxiety, and hunger. Without the release of epinephrine and the symptoms it causes, a person may not realize that hypoglycemia is occurring and may not take action to treat it. A vicious cycle can occur in which frequent hypoglycemia leads to hypoglycemia unawareness and HAAF, which in turn leads to even more severe and dangerous hypoglycemia. Studies have shown that preventing hypoglycemia for a period as short as several weeks can sometimes break this cycle and restore awareness of symptoms. Health care providers may therefore advise people who have had severe hypoglycemia to aim for higher-than-usual blood glucose targets for short-term periods.\n                \nBeing Prepared for Hypoglycemia\n                \nPeople who use insulin or take an oral diabetes medication that can cause low blood glucose should always be prepared to prevent and treat low blood glucose by\n                \n- learning what can trigger low blood glucose levels  - having their blood glucose meter available to test glucose levels; frequent testing may be critical for those with hypoglycemia unawareness, particularly before driving a car or engaging in any hazardous activity  - always having several servings of quick-fix foods or drinks handy  - wearing a medical identification bracelet or necklace  - planning what to do if they develop severe hypoglycemia  - telling their family, friends, and coworkers about the symptoms of hypoglycemia and how they can help if needed\n                \nNormal and Target Blood Glucose Ranges          Normal Blood Glucose Levels in People Who Do Not Have Diabetes          Upon wakingfasting    70 to 99 mg\/dL        After meals    70 to 140 mg\/dL          Target Blood Glucose Levels in People Who Have Diabetes          Before meals    70 to 130 mg\/dL        1 to 2 hours after the start of a meal    below 180 mg\/dL\n                \nFor people with diabetes, a blood glucose level below 70 mg\/dL is considered hypoglycemia."}
{"_id":"b8d64f64-ccc7-4382-b0f2-4fcbee86ba92","text":"Signs and symptoms of hypoglycemia vary from person to person. People with diabetes should get to know their signs and symptoms and describe them to their friends and family so they can help if needed. School staff should be told how to recognize a child's signs and symptoms of hypoglycemia and how to treat it.\n                \nPeople who experience hypoglycemia several times in a week should call their health care provider. They may need a change in their treatment plan: less medication or a different medication, a new schedule for insulin or medication, a different meal plan, or a new physical activity plan.\n                \nPrompt Treatment for Hypoglycemia\n                \nWhen people think their blood glucose is too low, they should check the blood glucose level of a blood sample using a meter. If the level is below 70 mg\/dL, one of these quick-fix foods should be consumed right away to raise blood glucose:\n                \n- 3 or 4 glucose tablets  - 1 serving of glucose gelthe amount equal to 15 grams of carbohydrate  - 1\/2 cup, or 4 ounces, of any fruit juice  - 1\/2 cup, or 4 ounces, of a regularnot dietsoft drink  - 1 cup, or 8 ounces, of milk  - 5 or 6 pieces of hard candy  - 1 tablespoon of sugar or honey\n                \nRecommended amounts may be less for small children. The child's doctor can advise about the right amount to give a child.\n                \nThe next step is to recheck blood glucose in 15 minutes to make sure it is 70 mg\/dL or above. If it's still too low, another serving of a quick-fix food should be eaten. These steps should be repeated until the blood glucose level is 70 mg\/dL or above. If the next meal is an hour or more away, a snack should be eaten once the quick-fix foods have raised the blood glucose level to 70 mg\/dL or above.\n                \nFor People Who Take Acarbose (Precose) or Miglitol (Glyset)\n                \nPeople who take either of these diabetes medications should know that only pure glucose, also called dextroseavailable in tablet or gel formwill raise their blood glucose level during a low blood glucose episode. Other quick-fix foods and drinks won't raise the level quickly enough because acarbose and miglitol slow the digestion of other forms of carbohydrate.\n                \nHelp from Others for Severe Hypoglycemia\n                \nSevere hypoglycemiavery low blood glucosecan cause a person to pass out and can even be life threatening. Severe hypoglycemia is more likely to occur in people with type 1 diabetes. People should ask a health care provider what to do about severe hypoglycemia. Another person can help someone who has passed out by giving an injection of glucagon. Glucagon will rapidly bring the blood glucose level back to normal and help the person regain consciousness. A health care provider can prescribe a glucagon emergency kit. Family, friends, or coworkersthe people who will be around the person at risk of hypoglycemiacan learn how to give a glucagon injection and when to call 911 or get medical help.\n                \nPhysical Activity and Blood Glucose Levels\n                \nPhysical activity has many benefits for people with diabetes, including lowering blood glucose levels. However, physical activity can make levels too low and can cause hypoglycemia up to 24 hours afterward. A health care provider can advise about checking the blood glucose level before exercise. For those who take insulin or one of the oral medications that increase insulin production, the health care provider may suggest having a snack if the glucose level is below 100 mg\/dL or adjusting medication doses before physical activity to help avoid hypoglycemia. A snack can prevent hypoglycemia. The health care provider may suggest extra blood glucose checks, especially after strenuous exercise.\n                \nHypoglycemia When Driving\n                \nHypoglycemia is particularly dangerous if it happens to someone who is driving. People with hypoglycemia may have trouble concentrating or seeing clearly behind the wheel and may not be able to react quickly to road hazards or to the actions of other drivers. To prevent problems, people at risk for hypoglycemia should check their blood glucose level before driving. During longer trips, they should check their blood glucose level frequently and eat snacks as needed to keep the level at 70 mg\/dL or above. If necessary, they should stop for treatment and then make sure their blood glucose level is 70 mg\/dL or above before starting to drive again.\n                \nHypoglycemia Unawareness\n                \nSome people with diabetes do not have early warning signs of low blood glucose, a condition called hypoglycemia unawareness. This condition occurs most often in people with type 1 diabetes, but it can also occur in people with type 2 diabetes. People with hypoglycemia unawareness may need to check their blood glucose level more often so they know when hypoglycemia is about to occur. They also may need a change in their medications, meal plan, or physical activity routine.\n                \nHypoglycemia unawareness develops when frequent episodes of hypoglycemia lead to changes in how the body reacts to low blood glucose levels. The body stops releasing the hormone epinephrine and other stress hormones when blood glucose drops too low. The loss of the body's ability to release stress hormones after repeated episodes of hypoglycemia is called hypoglycemia-associated autonomic failure, or HAAF.\n                \nEpinephrine causes early warning symptoms of hypoglycemia such as shakiness, sweating, anxiety, and hunger. Without the release of epinephrine and the symptoms it causes, a person may not realize that hypoglycemia is occurring and may not take action to treat it. A vicious cycle can occur in which frequent hypoglycemia leads to hypoglycemia unawareness and HAAF, which in turn leads to even more severe and dangerous hypoglycemia. Studies have shown that preventing hypoglycemia for a period as short as several weeks can sometimes break this cycle and restore awareness of symptoms. Health care providers may therefore advise people who have had severe hypoglycemia to aim for higher-than-usual blood glucose targets for short-term periods.\n                \nBeing Prepared for Hypoglycemia\n                \nPeople who use insulin or take an oral diabetes medication that can cause low blood glucose should always be prepared to prevent and treat low blood glucose by\n                \n- learning what can trigger low blood glucose levels  - having their blood glucose meter available to test glucose levels; frequent testing may be critical for those with hypoglycemia unawareness, particularly before driving a car or engaging in any hazardous activity  - always having several servings of quick-fix foods or drinks handy  - wearing a medical identification bracelet or necklace  - planning what to do if they develop severe hypoglycemia  - telling their family, friends, and coworkers about the symptoms of hypoglycemia and how they can help if needed\n                \nNormal and Target Blood Glucose Ranges          Normal Blood Glucose Levels in People Who Do Not Have Diabetes          Upon wakingfasting    70 to 99 mg\/dL        After meals    70 to 140 mg\/dL          Target Blood Glucose Levels in People Who Have Diabetes          Before meals    70 to 130 mg\/dL        1 to 2 hours after the start of a meal    below 180 mg\/dL\n                \nFor people with diabetes, a blood glucose level below 70 mg\/dL is considered hypoglycemia."}
{"_id":"85759337-4dfc-47aa-b2dc-2ef967d27c04","text":"Two types of hypoglycemia can occur in people who do not have diabetes:\n                \n- Reactive hypoglycemia, also called postprandial hypoglycemia, occurs within 4 hours after meals.  - Fasting hypoglycemia, also called postabsorptive hypoglycemia, is often related to an underlying disease.\n                \nSymptoms of both reactive and fasting hypoglycemia are similar to diabetes-related hypoglycemia. Symptoms may include hunger, sweating, shakiness, dizziness, light-headedness, sleepiness, confusion, difficulty speaking, anxiety, and weakness.\n                \nTo find the cause of a patient's hypoglycemia, the doctor will use laboratory tests to measure blood glucose, insulin, and other chemicals that play a part in the body's use of energy.\n                \nReactive Hypoglycemia\n                \nDiagnosis\n                \nTo diagnose reactive hypoglycemia, the doctor may\n                \n- ask about signs and symptoms  - test blood glucose while the patient is having symptoms by taking a blood sample from the arm and sending it to a laboratory for analysis*  - check to see whether the symptoms ease after the patient's blood glucose returns to 70 mg\/dL or above after eating or drinking\n                \nA blood glucose level below 70 mg\/dL at the time of symptoms and relief after eating will confirm the diagnosis. The oral glucose tolerance test is no longer used to diagnose reactive hypoglycemia because experts now know the test can actually trigger hypoglycemic symptoms.\n                \nCauses and Treatment\n                \nThe causes of most cases of reactive hypoglycemia are still open to debate. Some researchers suggest that certain people may be more sensitive to the body's normal release of the hormone epinephrine, which causes many of the symptoms of hypoglycemia. Others believe deficiencies in glucagon secretion might lead to reactive hypoglycemia.\n                \nA few causes of reactive hypoglycemia are certain, but they are uncommon. Gastricor stomachsurgery can cause reactive hypoglycemia because of the rapid passage of food into the small intestine. Rare enzyme deficiencies diagnosed early in life, such as hereditary fructose intolerance, also may cause reactive hypoglycemia.\n                \nTo relieve reactive hypoglycemia, some health professionals recommend\n                \n- eating small meals and snacks about every 3 hours  - being physically active  - eating a variety of foods, including meat, poultry, fish, or nonmeat sources of protein; starchy foods such as whole-grain bread, rice, and potatoes; fruits; vegetables; and dairy products  - eating foods high in fiber  - avoiding or limiting foods high in sugar, especially on an empty stomach\n                \nThe doctor can refer patients to a registered dietitian for personalized meal planning advice. Although some health professionals recommend a diet high in protein and low in carbohydrates, studies have not proven the effectiveness of this kind of diet to treat reactive hypoglycemia.\n                \nFasting Hypoglycemia\n                \nDiagnosis\n                \nFasting hypoglycemia is diagnosed from a blood sample that shows a blood glucose level below 50 mg\/dL after an overnight fast, between meals, or after physical activity.\n                \nCauses and Treatment\n                \nCauses of fasting hypoglycemia include certain medications, alcoholic beverages, critical illnesses, hormonal deficiencies, some kinds of tumors, and certain conditions occurring in infancy and childhood.\n                \nMedications. Medications, including some used to treat diabetes, are the most common cause of hypoglycemia. Other medications that can cause hypoglycemia include\n                \n- salicylates, including aspirin, when taken in large doses  - sulfa medications, which are used to treat bacterial infections  - pentamidine, which treats a serious kind of pneumonia  - quinine, which is used to treat malaria\n                \nIf using any of these medications causes a person's blood glucose level to fall, the doctor may advise stopping the medication or changing the dose.\n                \nAlcoholic beverages. Drinking alcoholic beverages, especially binge drinking, can cause hypoglycemia. The body's breakdown of alcohol interferes with the liver's efforts to raise blood glucose. Hypoglycemia caused by excessive drinking can be serious and even fatal.\n                \nCritical illnesses. Some illnesses that affect the liver, heart, or kidneys can cause hypoglycemia. Sepsis, which is an overwhelming infection, and starvation are other causes of hypoglycemia. In these cases, treating the illness or other underlying cause will correct the hypoglycemia.\n                \nHormonal deficiencies. Hormonal deficiencies may cause hypoglycemia in very young children, but rarely in adults. Shortages of cortisol, growth hormone, glucagon, or epinephrine can lead to fasting hypoglycemia. Laboratory tests for hormone levels will determine a diagnosis and treatment. Hormone replacement therapy may be advised.\n                \nTumors. Insulinomas are insulin-producing tumors in the pancreas. Insulinomas can cause hypoglycemia by raising insulin levels too high in relation to the blood glucose level. These tumors are rare and do not normally spread to other parts of the body. Laboratory tests can pinpoint the exact cause. Treatment involves both short-term steps to correct the hypoglycemia and medical or surgical measures to remove the tumor.\n                \nConditions occurring in infancy and childhood. Children rarely develop hypoglycemia. If they do, causes may include the following:\n                \n- Brief intolerance to fasting, often during an illness that disturbs regular eating patterns. Children usually outgrow this tendency by age 10.  - Hyperinsulinism, which is the overproduction of insulin. This condition can result in temporary hypoglycemia in newborns, which is common in infants of mothers with diabetes. Persistent hyperinsulinism in infants or children is a complex disorder that requires prompt evaluation and treatment by a specialist.  - Enzyme deficiencies that affect carbohydrate metabolism. These deficiencies can interfere with the body's ability to process natural sugars, such as fructose and galactose, glycogen, or other metabolites.  - Hormonal deficiencies such as lack of pituitary or adrenal hormones.\n                \n\n                \n*A personal blood glucose monitor cannot be used to diagnose reactive hypoglycemia."}
{"_id":"8dfc96d4-ea54-4963-a676-76f094609782","text":"Diabetes-related Hypoglycemia\n                \n- When people with diabetes think their blood glucose level is low, they should check it and treat the problem right away.  - To treat hypoglycemia, people should have a serving of a quick-fix food, wait 15 minutes, and check their blood glucose again. They should repeat the treatment until their blood glucose is 70 mg\/dL or above.  - People at risk for hypoglycemia should keep quick-fix foods in the car, at workanywhere they spend time.  - People at risk for hypoglycemia should be careful when driving. They should check their blood glucose frequently and snack as needed to keep their level 70 mg\/dL or above.\n                \nHypoglycemia Unrelated to Diabetes\n                \n- In reactive hypoglycemia, symptoms occur within 4 hours of eating. People with reactive hypoglycemia are usually advised to follow a healthy eating plan recommended by a registered dietitian.  - Fasting hypoglycemia can be caused by certain medications, critical illnesses, hereditary enzyme or hormonal deficiencies, and some kinds of tumors. Treatment targets the underlying problem."}
{"_id":"93d90c63-1f59-4fb8-98fb-7c844bf2e61b","text":"A kidney stone is a solid piece of material that forms in a kidney when substances that are normally found in the urine become highly concentrated. A stone may stay in the kidney or travel down the urinary tract. Kidney stones vary in size. A small stone may pass on its own, causing little or no pain. A larger stone may get stuck along the urinary tract and can block the flow of urine, causing severe pain or bleeding.\n                \nKidney stones are one of the most common disorders of the urinary tract. Each year in the United States, people make more than a million visits to health care providers and more than 300,000 people go to emergency rooms for kidney stone problems.1\n                \nUrolithiasis is the medical term used to describe stones occurring in the urinary tract. Other frequently used terms are urinary tract stone disease and nephrolithiasis. Terms that describe the location of the stone in the urinary tract are sometimes used. For example, a ureteral stoneor ureterolithiasisis a kidney stone found in the ureter."}
{"_id":"173b83e3-85e5-4d5d-a801-23e83e6d34e7","text":"The urinary tract is the bodys drainage system for removing wastes and extra water. The urinary tract includes two kidneys, two ureters, a bladder, and a urethra. The kidneys are two bean-shaped organs, each about the size of a fist. They are located near the middle of the back, just below the rib cage, one on each side of the spine. Every day, the two kidneys process about 200 quarts of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra water. The urine flows from the kidneys to the bladder through tubes called ureters. The bladder stores urine until releasing it through urination. When the bladder empties, urine flows out of the body through a tube called the urethra at the bottom of the bladder."}
{"_id":"ad40bc5b-5b1c-4a58-8da5-c36ab6ff2045","text":"Anyone can get a kidney stone, but some people are more likely to get one. Men are affected more often than women, and kidney stones are more common in non-Hispanic white people than in non-Hispanic black people and Mexican Americans. Overweight and obese people are more likely to get a kidney stone than people of normal weight. In the United States, 8.8 percent of the population, or one in 11 people, have had a kidney stone.2"}
{"_id":"21d8474d-7643-408e-9d51-59eb1b18d714","text":"Kidney stones can form when substances in the urinesuch as calcium, oxalate, and phosphorusbecome highly concentrated. Certain foods may promote stone formation in people who are susceptible, but scientists do not believe that eating any specific food causes stones to form in people who are not susceptible. People who do not drink enough fluids may also be at higher risk, as their urine is more concentrated.\n                \nPeople who are at increased risk of kidney stones are those with\n                \n- hypercalciuria, a condition that runs in families in which urine contains unusually large amounts of calcium; this is the most common condition found in those who form calcium stones  - a family history of kidney stones  - cystic kidney diseases, which are disorders that cause fluid-filled sacs to form on the kidneys  - hyperparathyroidism, a condition in which the parathyroid glands, which are four pea-sized glands located in the neck, release too much hormone, causing extra calcium in the blood  - renal tubular acidosis, a disease that occurs when the kidneys fail to excrete acids into the urine, which causes a persons blood to remain too acidic  - cystinuria, a condition in which urine contains high levels of the amino acid cystine  - hyperoxaluria, a condition in which urine contains unusually large amounts of oxalate  - hyperuricosuria, a disorder of uric acid metabolism  - gout, a disorder that causes painful swelling of the joints  - blockage of the urinary tract  - chronic inflammation of the bowel  - a history of gastrointestinal (GI) tract surgery\n                \nOthers at increased risk of kidney stones are people taking certain medications including\n                \n- diureticsmedications that help the kidneys remove fluid from the body  - calcium-based antacids  - the protease inhibitor indinavir (Crixivan), a medication used to treat HIV infection  - the anti-seizure medication topiramate (Topamax)"}
{"_id":"c068575e-392e-4924-b700-cf67b31cb082","text":"Four major types of kidney stones can form:\n                \n- Calcium stones are the most common type of kidney stone and occur in two major forms: calcium oxalate and calcium phosphate. Calcium oxalate stones are more common. Calcium oxalate stone formation may be caused by high calcium and high oxalate excretion. Calcium phosphate stones are caused by the combination of high urine calcium and alkaline urine, meaning the urine has a high pH.  - Uric acid stones form when the urine is persistently acidic. A diet rich in purinessubstances found in animal protein such as meats, fish, and shellfishmay increase uric acid in urine. If uric acid becomes concentrated in the urine, it can settle and form a stone by itself or along with calcium.  - Struvite stones result from kidney infections. Eliminating infected stones from the urinary tract and staying infection-free can prevent more struvite stones.  - Cystine stones result from a genetic disorder that causes cystine to leak through the kidneys and into the urine, forming crystals that tend to accumulate into stones."}
{"_id":"41394348-6a76-43f9-8207-f881453faee9","text":"People with kidney stones may have pain while urinating, see blood in the urine, or feel a sharp pain in the back or lower abdomen. The pain may last for a short or long time. People may experience nausea and vomiting with the pain. However, people who have small stones that pass easily through the urinary tract may not have symptoms at all."}
{"_id":"10dd4dd4-4995-420f-af47-7b141cc2fcdf","text":"To diagnose kidney stones, the health care provider will perform a physical exam and take a medical history. The medical history may include questions about family history of kidney stones, diet, GI problems, and other diseases and disorders. The health care provider may perform urine, blood, and imaging tests, such as an x ray or computerized tomography (CT) scan to complete the diagnosis.\n                \n- Urinalysis. Urinalysis is testing of a urine sample. The urine sample is collected in a special container in a health care providers office or commercial facility and can be tested in the same location or sent to a lab for analysis. Urinalysis can show whether the person has an infection or the urine contains substances that form stones.  - Blood test. A blood test involves drawing blood at a health care providers office or commercial facility and sending the sample to a lab for analysis. The blood test can show biochemical problems that can lead to kidney stones.  - Abdominal x ray. An abdominal x ray is a picture created using radiation and recorded on film or on a computer. The amount of radiation used is small. An x ray is performed at a hospital or outpatient center by an x-ray technician, and the images are interpreted by a radiologista doctor who specializes in medical imaging. Anesthesia is not needed. The person will lie on a table or stand during the x ray. The x-ray machine is positioned over the abdominal area. The person will hold his or her breath as the picture is taken so that the picture will not be blurry. The person may be asked to change position for additional pictures. The x rays can show the location of stones in the kidney or urinary tract.  - CT scans. CT scans use a combination of x rays and computer technology to create three-dimensional (3-D) images. A CT scan may include the injection of a special dye, called contrast medium. CT scans require the person to lie on a table that slides into a tunnel-shaped device where the x rays are taken. The procedure is performed in an outpatient center or hospital by an x-ray technician, and the images are interpreted by a radiologist. Anesthesia is not needed. CT scans can show stone locations and conditions that may have caused the stone to form."}
{"_id":"2dd58b28-20f9-4190-bc83-0ae898abc9fe","text":"Treatment for kidney stones usually depends on their size and what they are made of, as well as whether they are causing pain or obstructing the urinary tract. Kidney stones may be treated by a general practitioner or by a urologista doctor who specializes in the urinary tract. Small stones usually pass through the urinary tract without treatment. Still, the person may need pain medication and should drink lots of fluids to help move the stone along. Pain control may consist of oral or intravenous (IV) medication, depending on the duration and severity of the pain. IV fluids may be needed if the person becomes dehydrated from vomiting or an inability to drink. A person with a larger stone, or one that blocks urine flow and causes great pain, may need more urgent treatment, such as\n                \n- Shock wave lithotripsy. A machine called a lithotripter is used to crush the kidney stone. The procedure is performed by a urologist on an outpatient basis and anesthesia is used. In shock wave lithotripsy, the person lies on a table or, less commonly, in a tub of water above the lithotripter. The lithotripter generates shock waves that pass through the persons body to break the kidney stone into smaller pieces to pass more readily through the urinary tract.  - Ureteroscopy. A ureteroscopea long, tubelike instrument with an eyepieceis used to find and retrieve the stone with a small basket or to break the stone up with laser energy. The procedure is performed by a urologist in a hospital with anesthesia. The urologist inserts the ureteroscope into the persons urethra and slides the scope through the bladder and into the ureter. The urologist removes the stone or, if the stone is large, uses a flexible fiber attached to a laser generator to break the stone into smaller pieces that can pass out of the body in the urine. The person usually goes home the same day.\n                \n- Percutaneous nephrolithotomy. In this procedure, a wire-thin viewing instrument called a nephroscope is used to locate and remove the stone. The procedure is performed by a urologist in a hospital with anesthesia. During the procedure, a tube is inserted directly into the kidney through a small incision in the persons back. For large stones, an ultrasonic probe that acts as a lithotripter may be needed to deliver shock waves that break the stone into small pieces that can be removed more easily. The person may have to stay in the hospital for several days after the procedure and may have a small tube called a nephrostomy tube inserted through the skin into the kidney. The nephrostomy tube drains urine and any residual stone fragments from the kidney into a urine collection bag. The tube is usually left in the kidney for 2 or 3 days while the person remains in the hospital."}
{"_id":"b59796d1-d530-491a-99f5-811b48a6c85b","text":"The first step in preventing kidney stones is to understand what is causing the stones to form. The health care provider may ask the person to try to catch the kidney stone as it passes, so it can be sent to a lab for analysis. Stones that are retrieved surgically can also be sent to a lab for analysis.\n                \nThe health care provider may ask the person to collect urine for 24 hours after a stone has passed or been removed to measure daily urine volume and mineral levels. Producing too little urine or having a mineral abnormality can make a person more likely to form stones. Kidney stones may be prevented through changes in eating, diet, and nutrition and medications.\n                \nEating, Diet, and Nutrition\n                \nPeople can help prevent kidney stones by making changes in their fluid intake. Depending on the type of kidney stone a person has, changes in the amounts of sodium, animal protein, calcium, and oxalate consumed can also help.\n                \nDrinking enough fluids each day is the best way to help prevent most types of kidney stones. Health care providers recommend that a person drink 2 to 3 liters of fluid a day. People with cystine stones may need to drink even more. Though water is best, other fluids may also help prevent kidney stones, such as orange juice or lemonade. Talk with your health care provider if you cant drink the recommended amount due to other health problems, such as urinary incontinence, urinary frequency, or kidney failure.\n                \nRecommendations based on the specific type of kidney stone include the following:\n                \nCalcium Oxalate Stones\n                \n- reducing sodium  - reducing animal protein, such as meat, eggs, and fish  - getting enough calcium from food or taking calcium supplements with food  - avoiding foods high in oxalate, such as spinach, rhubarb, nuts, and wheat bran\n                \nCalcium Phosphate Stones\n                \n- reducing sodium  - reducing animal protein  - getting enough calcium from food or taking calcium supplements with food\n                \nUric Acid Stones\n                \n- limiting animal protein\n                \nMore information about how changes in diet affect kidney stone formation is provided in the NIDDK health topic, Diet for Kidney Stone Prevention.\n                \nMedications\n                \nThe health care provider may prescribe certain medications to help prevent kidney stones based on the type of stone formed or conditions that make a person more prone to form stones:\n                \n- hyperuricosuriaallopurinol (Zyloprim), which decreases uric acid in the blood and urine  - hypercalciuriadiuretics, such as hydrochlorothiazide  - hyperoxaluriapotassium citrate to raise the citrate and pH of urine  - uric acid stonesallopurinol and potassium citrate  - cystine stonesmercaptopropionyl glycine, which decreases cystine in the urine, and potassium citrate  - struvite stonesantibiotics, which are bacteria-fighting medications, when needed to treat infections, or acetohydroxamic acid with long-term antibiotic medications to prevent infection\n                \nPeople with hyperparathyroidism sometimes develop calcium stones. Treatment in these cases is usually surgery to remove the parathyroid glands. In most cases, only one of the glands is enlarged. Removing the glands cures hyperparathyroidism and prevents kidney stones."}
{"_id":"a83d61f0-2622-43c4-b333-bd44dafa6cde","text":"- A kidney stone is a solid piece of material that forms in a kidney when substances that are normally found in the urine become highly concentrated.  - Kidney stones are one of the most common disorders of the urinary tract.  - Certain foods may promote stone formation in people who are susceptible, but scientists do not believe that eating any specific food causes stones to form in people who are not susceptible.  - People with kidney stones may have pain while urinating, see blood in the urine, or feel a sharp pain in the back or lower abdomen. However, people who have small stones that pass easily through the urinary tract may not have symptoms at all.  - To diagnose kidney stones, the health care provider will perform a physical exam and take a medical history. The health care provider may perform urine, blood, and imaging tests to complete the diagnosis.  - Treatment for kidney stones usually depends on their size and what they are made of, as well as whether they are causing pain or obstructing the urinary tract. Treatments may include shock wave lithotripsy, ureteroscopy, or percutaneous nephrolithotomy.  - Kidney stones may be prevented through changes in eating, diet, and nutrition and medications."}
{"_id":"f7c975a6-4cf4-4fc5-829c-6de0ccf288d9","text":"Anemia is a condition in which the body has fewer red blood cells than normal. Red blood cells carry oxygen to tissues and organs throughout the body and enable them to use energy from food. With anemia, red blood cells carry less oxygen to tissues and organsparticularly the heart and brainand those tissues and organs may not function as well as they should."}
{"_id":"990c85b5-6e6b-4003-8446-d1eda4c23651","text":"The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine.\n                \nHealthy kidneys produce a hormone called erythropoietin (EPO). A hormone is a chemical produced by the body and released into the blood to help trigger or regulate particular body functions. EPO prompts the bone marrow to make red blood cells, which then carry oxygen throughout the body."}
{"_id":"2bb8418f-3b88-4775-8128-76e130bf5413","text":"When kidneys are diseased or damaged, they do not make enough EPO. As a result, the bone marrow makes fewer red blood cells, causing anemia. When blood has fewer red blood cells, it deprives the body of the oxygen it needs.\n                \nOther common causes of anemia in people with kidney disease include blood loss from hemodialysis and low levels of the following nutrients found in food:\n                \n- iron  - vitamin B12  - folic acid\n                \nThese nutrients are necessary for red blood cells to make hemoglobin, the main oxygen-carrying protein in the red blood cells.\n                \nIf treatments for kidney-related anemia do not help, the health care provider will look for other causes of anemia, including\n                \n- other problems with bone marrow  - inflammatory problemssuch as arthritis, lupus, or inflammatory bowel diseasein which the bodys immune system attacks the bodys own cells and organs  - chronic infections such as diabetic ulcers  - malnutrition"}
{"_id":"ee717fa3-1ec4-4901-aa10-51f831a0aa81","text":"The signs and symptoms of anemia in someone with CKD may include\n                \n- weakness  - fatigue, or feeling tired  - headaches  - problems with concentration  - paleness  - dizziness  - difficulty breathing or shortness of breath  - chest pain\n                \nAnyone having difficulty breathing or with shortness of breath should seek immediate medical care. Anyone who has chest pain should call 911."}
{"_id":"d16568b5-96c3-4398-bf9a-1e0d805756be","text":"Heart problems are a complication of anemia and may include\n                \n- an irregular heartbeat or an unusually fast heartbeat, especially when exercising.  - the harmful enlargement of muscles in the heart.  - heart failure, which does not mean the heart suddenly stops working. Instead, heart failure is a long-lasting condition in which the heart cant pump enough blood to meet the bodys needs."}
{"_id":"44289d8c-5373-4318-9553-571a01ba1dee","text":"A health care provider diagnoses anemia based on\n                \n- a medical history  - a physical exam  - blood tests\n                \nMedical History\n                \nTaking a medical history is one of the first things a health care provider may do to diagnose anemia. He or she will usually ask about the patients symptoms.\n                \nPhysical Exam\n                \nA physical exam may help diagnose anemia. During a physical exam, a health care provider usually examines a patients body, including checking for changes in skin color.\n                \nBlood Tests\n                \nTo diagnose anemia, a health care provider may order a complete blood count, which measures the type and number of blood cells in the body. A blood test involves drawing a patients blood at a health care providers office or a commercial facility. A health care provider will carefully monitor the amount of hemoglobin in the patients blood, one of the measurements in a complete blood count.\n                \nThe Kidney Disease: Improving Global Outcomes Anemia Work Group recommends that health care providers diagnose anemia in males older than age 15 when their hemoglobin falls below 13 grams per deciliter (g\/dL) and in females older than 15 when it falls below 12 g\/dL.2 If someone has lost at least half of normal kidney function and has low hemoglobin, the cause of anemia may be decreased EPO production.\n                \nTwo other blood tests help measure iron levels:\n                \n- The ferritin level helps assess the amount of iron stored in the body. A ferritin score below 200 nanograms (ng) per liter may mean a person has iron deficiency that requires treatment.2  - The transferrin saturation score indicates how much iron is available to make red blood cells. A transferrin saturation score below 30 percent can also mean low iron levels that require treatment.2\n                \nIn addition to blood tests, the health care provider may order other tests, such as tests for blood loss in stool, to look for other causes of anemia."}
{"_id":"d7696899-5f65-477f-8e39-1d61c4d85957","text":"Depending on the cause, a health care provider treats anemia with one or more of the following treatments:\n                \nIron\n                \nThe first step in treating anemia is raising low iron levels. Iron pills may help improve iron and hemoglobin levels. However, for patients on hemodialysis, many studies show pills do not work as well as iron given intravenously.2\n                \nErythropoietin\n                \nIf blood tests indicate kidney disease as the most likely cause of anemia, treatment can include injections of a genetically engineered form of EPO. A health care provider, often a nurse, injects the patient with EPO subcutaneously, or under the skin, as needed. Some patients learn how to inject the EPO themselves. Patients on hemodialysis may receive EPO intravenously during hemodialysis.\n                \nStudies have shown the use of EPO increases the chance of cardiovascular events, such as heart attack and stroke, in people with CKD. The health care provider will carefully review the medical history of the patient and determine if EPO is the best treatment for the patients anemia. Experts recommend using the lowest dose of EPO that will reduce the need for red blood cell transfusions. Additionally, health care providers should consider the use of EPO only when a patients hemoglobin level is below 10 g\/dL. Health care providers should not use EPO to maintain a patients hemoglobin level above 11.5 g\/dL.2 Patients who receive EPO should have regular blood tests to monitor their hemoglobin so the health care provider can adjust the EPO dose when the level is too high or too low.2 Health care providers should discuss the benefits and risks of EPO with their patients.\n                \nMany people with kidney disease need iron supplements and EPO to raise their red blood cell count to a level that will reduce the need for red blood cell transfusions. In some people, iron supplements and EPO will improve the symptoms of anemia.\n                \nRed Blood Cell Transfusions\n                \nIf a patients hemoglobin falls too low, a health care provider may prescribe a red blood cell transfusion. Transfusing red blood cells into the patients vein raises the percentage of the patients blood that consists of red blood cells, increasing the amount of oxygen available to the body.\n                \nVitamin B12 and Folic Acid Supplements\n                \nA health care provider may suggest vitamin B12 and folic acid supplements for some people with CKD and anemia. Using vitamin supplements can treat low levels of vitamin B12 or folic acid and help treat anemia. To help ensure coordinated and safe care, people should discuss their use of complementary and alternative medical practices, including their use of dietary supplements, with their health care provider.\n                \nRead more about vitamin B12 and folic acid on the MedlinePlus website at www.nlm.nih.gov\/medlineplus. Read more about complementary and alternative medicine at www.nccam.nih.gov."}
{"_id":"4b7f9993-0b97-4105-b9e1-62526eb227f7","text":"A health care provider may advise people with kidney disease who have anemia caused by iron, vitamin B12, or folic acid deficiencies to include sources of these nutrients in their diets. Some of these foods are high in sodium or phosphorus, which people with CKD should limit in their diet. Before making any dietary changes, people with CKD should talk with their health care provider or with a dietitian who specializes in helping people with kidney disease. A dietitian can help a person plan healthy meals.\n                \nRead more about nutrition for people with CKD on the National Kidney Disease Education Program website.\n                \nThe following chart illustrates some good dietary sources of iron, vitamin B12, and folic acid.\n                \nFood    Serving Size    Iron    Vitamin B12    Folic Acid          Recommended Daily Value        18 mg    6 mcg    400 mcg        100 percent fortified breakfast cereal     cup (1 oz)    18 mg    6 mcg    394 mcg        beans, baked    1 cup (8 oz)    8 mg    0 mcg    37 mcg        beef, ground    3 oz    2 mg    2 mcg    8 mcg        beef liver    3 oz    5 mg    67 mcg    211 mcg        clams, fried    4 oz    3 mg    1 mcg    66 mcg        spinach, boiled    1 cup (3 oz)    2 mg    0 mcg    115 mcg        spinach, fresh    1 cup (1 oz)    1 mg    0 mcg    58 mcg        trout    3 oz    0 mg    5 mcg    16 mcg        tuna, canned    3 oz    1 mg    1 mcg    2 mcg"}
{"_id":"bd363d2d-1d77-44a3-be9c-307cde99fcb7","text":"- Anemia is a condition in which the body has fewer red blood cells than normal. Red blood cells carry oxygen to tissues and organs throughout the body and enable them to use energy from food.  - Anemia commonly occurs in people with chronic kidney disease (CKD)the permanent, partial loss of kidney function. Most people who have total loss of kidney function, or kidney failure, have anemia.  - When kidneys are diseased or damaged, they do not make enough erythropoietin (EPO). As a result, the bone marrow makes fewer red blood cells, causing anemia.  - Other common causes of anemia in people with kidney disease include blood loss from hemodialysis and low levels of the following nutrients found in food:      - iron    - vitamin B12    - folic acid    - The first step in treating anemia is raising low iron levels.  - If blood tests indicate kidney disease as the most likely cause of anemia, treatment can include injections of a genetically engineered form of EPO.  - Many people with kidney disease need iron supplements and EPO to raise their red blood cell count to a level that will reduce the need for red blood cell transfusions.  - A health care provider may suggest vitamin B12 and folic acid supplements for some people with CKD and anemia.  - A health care provider may advise people with kidney disease who have anemia caused by iron, vitamin B12, or folic acid deficiencies to include sources of these nutrients in their diets."}
{"_id":"e1bb9901-391b-4e89-88b7-ba06ccc3cf25","text":"You and your doctor will work together to choose a treatment that's best for you. The publications of the NIDDK Kidney Failure Series can help you learn about the specific issues you will face.\n                \nBooklets\n                \n- Treatment Methods for Kidney Failure: Hemodialysis  - Treatment Methods for Kidney Failure: Peritoneal Dialysis  - Treatment Methods for Kidney Failure: Kidney Transplantation  - Kidney Failure: Eat Right to Feel Right on Hemodialysis\n                \nFact Sheets\n                \n- Kidney Failure: What to Expect  - Vascular Access for Hemodialysis  - Treatment Methods for Kidney Failure: Hemodialysis  - Hemodialysis Dose and Adequacy  - Peritoneal Dialysis Dose and Adequacy  - Amyloidosis and Kidney Disease  - Anemia in Chronic Kidney Disease  - Chronic Kidney Disease-Mineral and Bone Disorder  - Financial Help for Treatment of Kidney Failure\n                \nLearning as much as you can about your treatment will help make you an important member of your health care team.\n                \n\n                \n\n                \nThis content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. The NIDDK translates and disseminates research findings through its clearinghouses and education programs to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by the NIDDK is carefully reviewed by NIDDK scientists and other experts.\n                \nThe NIDDK would like to thank: John C. Stivelman, M.D., Emory University School of Medicine; Kerri Cavanaugh, M.D., M.H.S., Vanderbilt University\n                \nThis information is not copyrighted. The NIDDK encourages people to share this content freely.\n                \n\n                \n\n                \nJuly 2014"}
{"_id":"585685b6-7bcc-4770-ab67-448b1ed0a5ec","text":"Lupus nephritis is kidney inflammation caused by systemic lupus erythematosus (SLE or lupus). SLE is an autoimmune diseasea disorder in which the bodys immune system attacks the bodys own cells and organs. Up to 60 percent of people with SLE are diagnosed with lupus nephritis, which can lead to significant illness and even death.1"}
{"_id":"79f0055c-9ea9-4693-a533-a2ab726897ee","text":"The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the two kidneys filter about 120 to 150 of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra fluid. The urine flows from the kidneys to the bladder through tubes called ureters. The bladder stores urine until releasing it through urination."}
{"_id":"3b04b831-1a05-488c-ac25-e108791b479a","text":"The symptoms of lupus nephritis may include high blood pressure, foamy urine, and edemaswelling, usually in the legs, feet, or ankles and less often in the hands or face.\n                \nKidney problems often develop at the same time or shortly after lupus symptoms appear and can include\n                \n- joint pain or swelling  - muscle pain  - fever with no known cause  - red rashes, often on the face, which are also called butterfly rashes because of their shape"}
{"_id":"b3063f14-a55d-42e9-858e-c57474a8063c","text":"Lupus nephritis is diagnosed through urine and blood tests and a kidney biopsy:\n                \n- Urinalysis. Urinalysis is testing of a urine sample. The urine sample is collected in a special container in a health care providers office or commercial facility and can be tested in the same location or sent to a lab for analysis. For the test, a nurse or technician places a strip of chemically treated paper, called a dipstick, into the urine. Patches on the dipstick change color when blood or protein is present. A high number of red blood cells or high levels of protein in the urine indicate kidney damage.  - Blood test. A blood test involves drawing blood at a health care providers office or commercial facility and sending the sample to a lab for analysis. The blood test can show high levels of creatinine, a waste product of normal muscle breakdown excreted by the kidneys, which increases when the kidneys are not functioning well.   - Biopsy. A biopsy is a procedure that involves taking a small piece of kidney tissue for examination with a microscope. The biopsy is performed by a health care provider in a hospital with light sedation and local anesthetic. The health care provider uses imaging techniques such as ultrasound or a computerized tomography scan to guide the biopsy needle into the kidney. The kidney tissue is examined in a lab by a pathologista doctor who specializes in diagnosing diseases. The test can confirm a diagnosis of lupus nephritis, determine how far the disease has progressed, and guide treatment. The American College of Rheumatology recommends biopsies for all people with evidence of active lupus nephritis that has not been previously treated."}
{"_id":"91b3630e-896b-443a-ad44-586b019223d0","text":"Lupus nephritis is treated with medications that suppress the immune system, so it stops attacking and damaging the kidneys. Standard treatment includes a corticosteroid, usually prednisone, to reduce inflammation in the kidneys. An immunosuppressive medication, such as cyclophosphamide or mycophenolate mofetil, is typically used with prednisone. These medicationswhen taken as prescribed by a health care providerfurther decrease the activity of the immune system and block the bodys immune cells from attacking the kidneys directly or making antibodies that attack the kidneys. Antibodies are proteins made by the immune system to protect the body from foreign substances such as bacteria or viruses. Hydroxychloroquine, a medication for treating SLE, should also be prescribed or continued for people with lupus nephritis.\n                \nPeople with lupus nephritis that is causing high blood pressure may need to take medications that lower their blood pressure and can also significantly slow the progression of kidney disease. Two types of blood pressure lowering medications, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), have proven effective in slowing the progression of kidney disease. Many people require two or more medications to control their blood pressure. In addition to an ACE inhibitor or an ARB, a diuretica medication that helps the kidneys remove fluid from the bodymay be prescribed. Beta blockers, calcium channel blockers, and other blood pressure medications may also be needed.\n                \nBlood pressure is written with two numbers separated by a slash, 120\/80, and is said as 120 over 80. The top number is called the systolic pressure and represents the pressure as the heart beats and pushes blood through the blood vessels. The bottom number is called the diastolic pressure and represents the pressure as blood vessels relax between heartbeats. High blood pressure is a systolic pressure of 140 or above or a diastolic pressure of 90 or above.2"}
{"_id":"a3d2e17c-72ab-499f-8324-61e7d7f6df77","text":"In many cases, treatment is effective in completely or partially controlling lupus nephritis, resulting in few, if any, further complications. However, even with treatment, 10 to 30 percent of people with lupus nephritis develop kidney failure, described as end-stage renal disease when treated with blood-filtering treatments called dialysis or a kidney transplant.3 Scientists cannot predict who will or will not respond to treatment. The most severe form of lupus nephritis is called diffuse proliferative nephritis. With this type of illness, the kidneys are inflamed, many white blood cells invade the kidneys, and kidney cells increase in number, which can cause such severe damage that scars form in the kidneys. Scars are difficult to treat, and kidney function often declines as more scars form. People with suspected lupus nephritis should get diagnosed and treated as early as possible to prevent such chronic, or long lasting, damage.\n                \nPeople with lupus nephritis are at a high risk for cancer, primarily B-cell lymphomaa type of cancer that begins in the cells of the immune system. They are also at a high risk for heart and blood vessel problems."}
{"_id":"68941a34-1470-4947-b17b-fd9d42f30d38","text":"Eating, diet, and nutrition have not been shown to play a role in causing or preventing lupus nephritis. People with kidney disease that progresses may need to talk with a health care provider about changes they may need to make to their diet. People with lupus nephritis and high blood pressure may benefit from reducing sodium intake, often from salt. More information about nutrition in people with kidney disease is provided in the NIDDK health topics, Nutrition for Early Chronic Kidney Disease in Adults and Nutrition for Advanced Chronic Kidney Disease in Adults."}
{"_id":"e8b6954e-1c77-4b9d-bd40-8d9ffe95982b","text":"- Lupus nephritis is kidney inflammation caused by systemic lupus erythematosus (SLE or lupus).  - The symptoms of lupus nephritis may include high blood pressure, foamy urine, and edema.  - Lupus nephritis is diagnosed through urine and blood tests and a kidney biopsy.  - Lupus nephritis is treated with medications that suppress the immune system, so it stops attacking and damaging the kidneys. Standard treatment includes a corticosteroid, usually prednisone, to reduce inflammation in the kidneys. An immunosuppressive medication, such as cyclophosphamide or mycophenolate mofetil, is typically used with prednisone.  - People with lupus nephritis that is causing high blood pressure may need to take medications that lower their blood pressure, which can also significantly slow the progression of kidney disease.  - In many cases, treatment is effective in completely or partially controlling lupus nephritis, resulting in few, if any, further complications. However, even with treatment, 10 to 30 percent of people with lupus nephritis develop kidney failure."}
{"_id":"805433f7-1733-4737-888c-eca7b7a099e9","text":"Dermatitis herpetiformis is characterized by small, clustered papules and vesicles that erupt symmetrically on the elbows, knees, buttocks, back, or scalp. The face and groin can also be involved. A burning sensation may precede lesion formation. Lesions are usually scratched off by the time a patient comes in for a physical exam, and the rash may appear as erosions and excoriations.\n                \nPatients with DH may also experience dental enamel defects to permanent teeth, which is another manifestation of celiac disease. Less than 20 percent of people with DH have symptoms of celiac disease.3"}
{"_id":"d9c27f7b-83a0-4e88-8db8-2daf5e18e7ba","text":"Dermatitis herpetiformis is caused by the deposit of immunoglobulin A (IgA) in the skin, which triggers further immunologic reactions resulting in lesion formation. DH is an external manifestation of an abnormal immune response to gluten, in which IgA antibodies form against the skin antigen epidermal transglutaminase.\n                \nFamily studies show that 5 percent of first-degree relatives of a person with DH will also have DH. An additional 5 percent of first-degree relatives of a person with DH will have celiac disease.4 Various other autoimmune diseases are associated with DH, the most common being hypothyroidism."}
{"_id":"4a5719af-bab2-4ddb-a07a-f989ae493baa","text":"A skin biopsy is the first step in diagnosing DH. Direct immunofluorescence of clinically normal skin adjacent to a lesion shows granular IgA deposits in the upper dermis. Histology of lesional skin may show microabscesses containing neutrophils and eosinophils. However, histology may reveal only excoriation due to the intense itching that patients experience.\n                \nBlood tests for antiendomysial or anti-tissue transglutaminase antibodies may also suggest celiac disease. Blood tests for epidermal transglutaminase antibodies are positive in more than 90 percent of cases.5 All of these tests will become negative with prolonged adherence to a gluten-free diet.\n                \nA positive biopsy and serology confirm DH and should be taken as indirect evidence of small bowel damage. A biopsy of the small bowel is usually not needed for DH diagnosis. However, if clinical signs of gastrointestinal disease are evident on examination, further workup may be required.2 Whether or not intestinal damage is evident, a gluten-free diet should be implemented because the rash of DH is gluten sensitive.4"}
{"_id":"0bd18654-3af8-4458-96a3-aa7fcda6dc95","text":"The sulfone dapsone can provide immediate relief of symptoms. For patients who cannot tolerate dapsone, sulfapyridine or sulfamethoxypyridazine may be used, although these medications are less effective than dapsone. A strict gluten-free diet is the only treatment for the underlying disease. Even with a gluten-free diet, medication therapy may need to be continued from a few months to 2 years.\n                \nDH can go into remission, which is defined as absence of skin lesions and symptoms of DH for more than 2 years while not taking sulfones or other treatments and not adhering to a gluten-free diet. Cohort studies showing DH remission provide support for reducing sulfone therapy and weaning from a gluten-free diet in patients with well-controlled DH.6"}
{"_id":"484fef5e-3586-4f48-8fd0-0d792730594f","text":"Goodpasture syndrome is a pulmonary-renal syndrome, which is a group of acute illnesses involving the kidneys and lungs. Goodpasture syndrome includes all of the following conditions:\n                \n- glomerulonephritisinflammation of the glomeruli, which are tiny clusters of looping blood vessels in the kidneys that help filter wastes and extra water from the blood  - the presence of anti-glomerular basement membrane (GBM) antibodies; the GBM is part of the glomeruli and is composed of collagen and other proteins  - bleeding in the lungs\n                \nIn Goodpasture syndrome, immune cells produce antibodies against a specific region of collagen. The antibodies attack the collagen in the lungs and kidneys.\n                \nErnest Goodpasture first described the syndrome during the influenza pandemic of 1919 when he reported on a patient who died from bleeding in the lungs and kidney failure. Diagnostic tools to confirm Goodpasture syndrome were not available at that time, so it is not known whether the patient had true Goodpasture syndrome or vasculitis. Vasculitis is an autoimmune conditiona disorder in which the bodys immune system attacks the bodys own cells and organsthat involves inflammation in the blood vessels and can cause similar lung and kidney problems.\n                \nGoodpasture syndrome is sometimes called anti-GBM disease. However, anti-GBM disease is only one cause of pulmonary-renal syndromes, including Goodpasture syndrome.\n                \nGoodpasture syndrome is fatal unless quickly diagnosed and treated."}
{"_id":"8990366d-df6f-4db5-bb31-d8d352da022a","text":"The causes of Goodpasture syndrome are not fully understood. People who smoke or use hair dyes appear to be at increased risk for this condition. Exposure to hydrocarbon fumes, metallic dust, and certain drugs, such as cocaine, may also raise a persons risk. Genetics may also play a part, as a small number of cases have been reported in more than one family member."}
{"_id":"22664500-6b26-403c-80ea-63d7ddf771e1","text":"The symptoms of Goodpasture syndrome may initially include fatigue, nausea, vomiting, and weakness. The lungs are usually affected before or at the same time as the kidneys, and symptoms can include shortness of breath and coughing, sometimes with blood. The progression from initial symptoms to the lungs being affected may be very rapid. Symptoms that occur when the kidneys are affected include blood in the urine or foamy urine, swelling in the legs, and high blood pressure."}
{"_id":"8df8c290-0a8a-4aca-a938-83c0dfb8c572","text":"A health care provider may order the following tests to diagnose Goodpasture syndrome:\n                \n- Urinalysis. Urinalysis is testing of a urine sample. The urine sample is collected in a special container in a health care providers office or commercial facility and can be tested in the same location or sent to a lab for analysis. For the test, a nurse or technician places a strip of chemically treated paper, called a dipstick, into the urine. Patches on the dipstick change color when protein or blood are present in urine. A high number of red blood cells and high levels of protein in the urine indicate kidney damage.  - Blood test. A blood test involves drawing blood at a health care providers office or commercial facility and sending the sample to a lab for analysis. The blood test can show the presence of anti-GBM antibodies.  - Chest x ray. An x ray of the chest is performed in a health care providers office, outpatient center, or hospital by an x-ray technician, and the images are interpreted by a radiologista doctor who specializes in medical imaging. Abnormalities in the lungs, if present, can be seen on the x ray.  - Biopsy. A biopsy is a procedure that involves taking a piece of kidney tissue for examination with a microscope. The biopsy is performed by a health care provider in a hospital with light sedation and local anesthetic. The health care provider uses imaging techniques such as ultrasound or a computerized tomography scan to guide the biopsy needle into the kidney. The tissue is examined in a lab by a pathologista doctor who specializes in diagnosing diseases. The test can show crescent-shaped changes in the glomeruli and lines of antibodies attached to the GBM."}
{"_id":"35ca7c24-8cf5-4086-958f-6bbb6d6cf379","text":"Goodpasture syndrome is usually treated with\n                \n- immunosuppressive medications, such as cyclophosphamide, to keep the immune system from making antibodies  - corticosteroid medications to suppress the bodys autoimmune response  - plasmapheresisa procedure that uses a machine to remove blood from the body, separate certain cells from the plasma, and return just the cells to the persons body; the anti-GBM antibodies remain in the plasma and are not returned to the persons body\n                \nPlasmapheresis is usually continued for several weeks, and immunosuppressive medications may be given for 6 to 12 months, depending on the response to therapy. In most cases, bleeding in the lungs stops and no permanent lung damage occurs. Damage to the kidneys, however, may be long lasting. If the kidneys fail, blood-filtering treatments called dialysis or kidney transplantation may become necessary."}
{"_id":"5bbaf854-7934-4b1c-90db-9f37f3c038ce","text":"Eating, diet, and nutrition have not been shown to play a role in causing or preventing Goodpasture syndrome."}
{"_id":"127846ac-c461-4cad-9903-74ec3dd5eebe","text":"- Goodpasture syndrome is a pulmonary-renal syndrome, which is a group of acute illnesses involving the kidneys and lungs. Goodpasture syndrome includes all of the following conditions:      - glomerulonephritis    - the presence of anti-glomerular basement membrane (GBM) antibodies    - bleeding in the lungs    - Goodpasture syndrome is fatal unless quickly diagnosed and treated.  - People who smoke or use hair dyes appear to be at increased risk for this condition. Exposure to hydrocarbon fumes, metallic dust, and certain drugs may also raise a persons risk.  - The symptoms of Goodpasture syndrome may initially include fatigue, nausea, vomiting, and weakness. The lungs are usually affected before or at the same time as the kidneys, and symptoms can include shortness of breath and coughing, sometimes with blood. Symptoms that occur when the kidneys are affected include blood in the urine or foamy urine, swelling in the legs, and high blood pressure.  - A urinalysis, blood test, chest x ray, and kidney biopsy are used to diagnose Goodpasture syndrome.  - Goodpasture syndrome is usually treated with immunosuppressive medications, corticosteroid medications, and plasmapheresis."}
{"_id":"d6fe0312-e006-4ebc-beb6-e64c2123e83e","text":"Interstitial cystitis*painful bladder syndrome (IC\/PBS) is one of several conditions that causes bladder pain and a need to urinate frequently and urgently. Some doctors have started using the term bladder pain syndrome (BPS) to describe this condition.\n                \nYour bladder is a balloon-shaped organ where your body holds urine. When you have a bladder problem, you may notice certain signs or symptoms.\n                \n*See Pronounciation Guide for tips on how to say the words in bold type."}
{"_id":"8086fde4-7947-4faf-bcaf-e78a04af36d2","text":"Signs of bladder problems include\n                \n-  Urgency. The feeling that you need to go right now! Urgency is normal if you haven't been near a bathroom for a few hours or if you have been drinking a lot of fluids. But you may have a problem if you have strong urges before your bladder has had time to fill. All of a sudden, you feel a strong urge to go. At times, you may even have an accident because the urge strikes so quickly you don't have time to find a bathroom.    - Frequency. The feeling that you need to go much more often than anyone else. Doctors and nurses use the term void, which means to empty the bladder. Most people void between four and seven times a day. Drinking large amounts of fluid can cause more frequent voiding. Taking blood pressure medicines called diuretics, or water pills, can also cause more frequent voiding. If you void more than eight times a day, and you dont take diuretics or drink large amounts of fluid, it may be the sign of a problem.  - Pain. The feeling of more than discomfort when you need to go. Having a full bladder may be uncomfortable, but it should not be painful. You may have a problem if you feel burning or sharp pain in your bladder or urethrathe opening where urine leaves the body.\n                \nSome people may have pain without urgency or frequency. Others have urgency and frequency without pain."}
{"_id":"dbe80760-7944-4115-b08e-2d3426a59912","text":"Many different problems can cause urgency, frequency, and bladder pain. Just a few of them are\n                \n- infections  - bowel disorders  - endometriosistissue that normally lines the womb that appears in other places outside of the womb  - bladder cancer\n                \nYour doctor will ask you questions and run tests to find the cause of your bladder problems. Usually, the doctor will find that you have either an infection or an overactive bladder. But urgency, frequency, and pain are not always caused by infection.\n                \nSometimes the cause is hard to find. If all the test results are normal and all other diseases are ruled out, your doctor may find that you have IC\/PBS."}
{"_id":"304609ed-9eb1-4f06-a64f-f1efb054d7e4","text":"Both men and women can get IC\/PBS, though twice as many women are affected as men. It can occur at any age, but it is most common in middle age.\n                \nPeople with IC\/PBS rarely have bladder pain all the time. The pain usually comes and goes as the bladder fills and then empties. The pain may go away for weeks or months and then return. People with IC\/PBS sometimes refer to an attack of bladder pain as a flare or flare-up. Stress may bring on a flare-up of symptoms in someone who has IC\/PBS. But stress does not cause a person to get IC\/PBS."}
{"_id":"9808cc55-7156-4ed6-babc-fdf26f2bd90c","text":"Finding the cause of bladder pain may require several tests.\n                \nWhile tests may aid your doctor in making a diagnosis of IC\/PBS, a careful review of your symptoms and a physical exam in the office are generally the most important parts of the evaluation."}
{"_id":"77b2e68e-df70-43b8-aae8-ca1d0e4370a5","text":"No one treatment for IC\/PBS has been found that works for everyone. Your doctor or nurse will work with you to find a treatment plan that meets your special needs. The plan may include diet and lifestyle changes, bladder retraining, activity and exercise, physical therapy, and various types of medicines. You should expect some treatment failures along the way, but, with time, you and your doctor or nurse should find a treatment that gives you some relief and helps you cope with your disease.\n                \nDiet and Lifestyle Changes\n                \nSome people with IC\/PBS find that certain foods or drinks bring on their symptoms. Others find no link between symptoms and what they eat.\n                \nLearning what foods cause symptoms for you may require some trial and error. Keep a food diary and note the times you have bladder pain. The diary might reveal that your flare-ups always happen, for example, after you eat tomatoes or oranges.\n                \nSome doctors recommend taking an antacid medicine with meals. The medicine reduces the amount of acid that gets into the urine.\n                \nIf you make changes to your diet, remember to eat a variety of healthy foods.\n                \nBladder Retraining\n                \nBladder retraining is a way to help your bladder hold more urine. People with bladder pain often get in the habit of using the bathroom as soon as they feel pain or urgency. They then feel the need to go before the bladder is really full. The body may get used to frequent voiding. Bladder retraining helps your bladder hold more urine before signaling the urge to urinate.\n                \nKeep a bladder diary to track how you are doing. Start by noting the times when you void. Note how much time goes by between voids. For example, you may find that you return to the bathroom every 40 minutes.\n                \nTry to stretch out the time between voids. If you usually void every 40 minutes, try to wait at least 50 minutes before you go to the bathroom.\n                \nIf your bladder becomes painful, you may use the bathroom. But you may find that your first urge to use the bathroom goes away if you ignore it. Find ways to relax or distract yourself when the first urge strikes.\n                \nAfter a few days, you may be able to stretch the time out to 60 or 70 minutes, and you may find that the urge to urinate does not return as soon.\n                \nActivity\n                \nIf you have IC\/PBS, you may feel the last thing you want to do is exercise. But many people feel that easy activities like walking or gentle stretching exercises help relieve symptoms.\n                \nPhysical Therapy\n                \nYour doctor or nurse may suggest pelvic exercises. The pelvic muscles hold the bladder in place and help control urination. The first step is to find the right muscle to squeeze. A doctor, nurse, or physical therapist can help you. One way to find the muscles is to imagine that you are trying to stop passing gas. Squeeze the muscles you would use. If you sense a \"pulling\" feeling, you have found the right muscles for pelvic exercises.\n                \nYou may need exercises to strengthen those muscles so that it's easier to hold in urine. Or you may need to learn to relax your pelvic muscles if tense muscles are part of your bladder pain.\n                \nSome physical therapists specialize in helping people with pelvic pain. Ask your doctor or nurse to help you find a professional trained in pelvic floor physical therapy.\n                \nReducing Stress\n                \nStress doesn't cause IC\/PBS. But stress can trigger painful flare-ups in someone who has IC\/PBS. Learning to reduce stress in your life by making time for relaxation every day may help control some symptoms of IC\/PBS.\n                \nOral Medicines\n                \nPain pills like aspirin, ibuprofen, or acetominophen can help control mild bladder pain. Advil and Motrin are examples of ibuprofen. Tylenol is an example of acetominophen. Talk with your doctor if you feel you need a stronger pain medicine.\n                \nYour doctor may recommend a medication, pentosan polysulfate sodium, sold as Elmiron, which is approved for treating the pain of IC\/PBS. You may need to take this medicine for up to 6 months before you notice improvement. Elmiron does not work for everyone, but some people with IC\/PBS have found relief taking it. You need a doctor's order for Elmiron. If you don't notice improvement of your symptoms in 6 months, this medicine is not likely to work.\n                \nResearchers are also looking at other kinds of medicines. Medicines that treat heartburn might help bladder symptoms by reducing the amount of acid made in the body. Muscle relaxants can keep the bladder from squeezing at the wrong time. Keeping the bladder muscle relaxed helps ease the symptoms of IC\/PBS.\n                \nBladder Stretching\n                \nThe doctor may stretch the bladder by filling it with liquid. You will be given an anesthetic to prevent pain and help relax your bladder muscles. Some patients have said their symptoms were helped after this treatment.\n                \nBladder Medicines\n                \nMany patients who have IC\/PBS find relief after a treatment in which their bladders are filled with a liquid medicine. The doctor guides a tube into your bladder and slowly fills the bladder with a liquid that eases irritation of the bladder wall. The liquid may be a compound called DMSO or a solution that contains heparin and a pain medicine called lidocaine.\n                \nYou will keep the liquid in your bladder for about 15 minutes and then release it. You can have this treatment once every week or every other week for 1 or 2 months. You may not feel any better until the third or fourth treatment.\n                \nNerve Stimulation\n                \nIf you have tried diet changes, exercise, and medicines and nothing seems to help, you may wish to think about nerve stimulation. This treatment sends mild electrical pulses to the nerves that control the bladder.\n                \nAt first, you may try a system that sends the pulses through electrodes placed on your skin. If this therapy works for you, you may consider having a device put in your body. The device delivers small pulses of electricity to the nerves around the bladder.\n                \nFor some patients, nerve stimulation relieves bladder pain as well as urinary frequency and urgency. For others, the treatment relieves frequency and urgency but not pain. For still other patients, it does not work.\n                \nScientists are not sure why nerve stimulation works. Some believe that the electrical pulses block the pain signals carried in the nerves. If your brain doesn't receive the nerve signal, you don't feel the pain. Others believe that the electricity releases endorphins, which are hormones that block pain naturally.\n                \nSurgery\n                \nAs a last resort, your doctor might suggest surgery to remove part or all of the bladder. Surgery does not cure the pain of IC\/PBS in all cases, but if you have tried every other option and your pain is still unbearable, surgery might be considered.\n                \nTalk with your doctor and family about the possible benefits and side effects."}
{"_id":"77c227cd-1b81-4fb6-bf28-9ad9a7cc49ca","text":"- Bladder problems have many possible causes.  - Your doctor will need to do tests to find the cause of your bladder problems. If all the test results are normal, you may have IC\/PBS.  - No one treatment option for IC\/PBS works for everybody.  - Treatments for IC\/PBS may include changing your diet and exercising.  - Medicines for IC\/PBS may be taken by mouth or put directly into the bladder through a tube by a doctor.  - Nerve stimulation helps some people with IC\/PBS.  - Surgery is a last resort for treating IC\/PBS."}
{"_id":"49dee32c-b2d9-410b-a24b-5a4b1ac5a7e2","text":"Hematuria is blood in the urine. Two types of blood in the urine exist. Blood that can be seen in the urine is called gross hematuria. Blood that cannot be seen in the urine, except when examined with a microscope, is called microscopic hematuria."}
{"_id":"bfe12b2a-97c0-4f83-a7a9-cffdae3a8727","text":"Most people with microscopic hematuria do not have symptoms. People with gross hematuria have urine that is pink, red, or cola-colored due to the presence of red blood cells (RBCs). Even a small amount of blood in the urine can cause urine to change color. In most cases, people with gross hematuria do not have other symptoms. However, people with gross hematuria that includes blood clots in the urine may have pain."}
{"_id":"9f80ed38-9c3e-4379-a3b1-9aae9f37ed4a","text":"The urinary tract is the bodys drainage system for removing wastes and extra water. The urinary tract includes two kidneys, two ureters, a bladder, and a urethra. The kidneys are two bean-shaped organs, each about the size of a fist. They are located near the middle of the back, just below the rib cage, one on each side of the spine. Every day, the two kidneys process about 200 quarts of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra water. The urine flows from the kidneys to the bladder through tubes called ureters. The bladder stores urine until releasing it through urination. When the bladder empties, urine flows out of the body through a tube called the urethra at the bottom of the bladder."}
{"_id":"2ce8f28c-ff94-402a-9ea7-ce1603239966","text":"Hematuria can be caused by menstruation, vigorous exercise, sexual activity, viral illness, trauma, or infection, such as a urinary tract infection (UTI). More serious causes of hematuria include\n                \n- cancer of the kidney or bladder  - inflammation of the kidney, urethra, bladder, or prostatea walnut-shaped gland in men that surrounds the urethra at the neck of the bladder and supplies fluid that goes into semen  - polycystic kidney diseasean inherited disorder characterized by many grape-like clusters of fluid-filled cysts that make both kidneys larger over time, taking over and destroying working kidney tissue  - blood clots  - blood clotting disorders, such as hemophilia  - sickle cell diseasean inherited disorder in which RBCs form an abnormal crescent shape, resulting in less oxygen delivered to the bodys tissues, clogging of small blood vessels, and disruption of healthy blood flow"}
{"_id":"d24a7472-29a9-4f79-8d23-5a48028167ce","text":"Almost anyone, including children and teens, can have hematuria. Factors that increase the chance a person will have hematuria include\n                \n- a family history of kidney disease  - an enlarged prostate, which typically occurs in men age 50 or older  - urinary stone disease  - certain medications including aspirin and other pain relievers, blood thinners, and antibiotics  - strenuous exercise such as long-distance running  - a recent bacterial or viral infection"}
{"_id":"6896b93c-63ed-4115-a524-eefeb65ae90a","text":"Hematuria is diagnosed with urinalysis, which is testing of a urine sample. The urine sample is collected in a special container in a health care providers office or commercial facility and can be tested in the same location or sent to a lab for analysis. For the test, a nurse or technician places a strip of chemically treated paper, called a dipstick, into the urine. Patches on the dipstick change color when RBCs are present in urine. When blood is visible in the urine or a dipstick test of the urine indicates the presence of RBCs, a health care provider examines the urine with a microscope to make an initial diagnosis of hematuria. The next step is to diagnose the cause of the hematuria.\n                \nThe health care provider will take a thorough medical history. If the history suggests a cause that does not require treatment, the urine should be tested again after 48 hours for the presence of RBCs. If two of three urine samples show too many RBCs when viewed with a microscope, more serious causes should be explored. The health care provider may order one or more of the following tests:\n                \n- Urinalysis. Further testing of the urine may be done to check for problems that can cause hematuria, such as infection, kidney disease, and cancer. The presence of white blood cells signals a UTI. RBCs that are misshapen or clumped together to form little tubes, called casts, may indicate kidney disease. Large amounts of protein in the urine, called proteinuria, may also indicate kidney disease. The urine can also be tested for the presence of cancer cells.  - Blood test. A blood test involves drawing blood at a health care providers office or commercial facility and sending the sample to a lab for analysis. A blood test can show the presence of high levels of creatinine, a waste product of normal muscle breakdown, which may indicate kidney disease.  - Biopsy. A biopsy is a procedure that involves taking a piece of kidney tissue for examination with a microscope. The biopsyis performed by a health care provider in a hospital with light sedation and local anesthetic. The health care provider uses imaging techniques such as ultrasound or a computerized tomography (CT) scan to guide the biopsy needle into the kidney. The kidney tissue is examined in a lab by a pathologista doctor who specializes in diagnosing diseases. The test helps diagnose the type of kidney disease causing hematuria.  - Cystoscopy. Cystoscopy is a procedure that uses a tubelike instrument to look inside the urethra and bladder. Cystoscopy is performed by a health care provider in the office, an outpatient facility, or a hospital with local anesthesia. However, in some cases, sedation and regional or general anesthesia are needed. Cystoscopy may be used to look for cancer cells in the bladder, particularly if cancer cells are found with urinalysis. More information is provided in the NIDDK health topic,Cystoscopy and Ureteroscopy.   - Kidney imaging tests. Intravenous pyelogram (IVP) is an x ray of the urinary tract. A special dye, called contrast medium, is injected into a vein in the persons arm, travels through the body to the kidneys, and makes urine visible on the x ray. The contrast medium also shows any blockage in the urinary tract. When a small mass is found with IVP, another imaging test, such as an ultrasound, CT scan, or magnetic resonance imaging (MRI), can be used to further study the mass. Imaging tests are performed in an outpatient center or hospital by a specially trained technician, and the images are interpreted by a radiologista doctor who specializes in medical imaging. Anesthesia is not needed, though light sedation may be used in some cases. Imaging tests may show a tumor, a kidney or bladder stone, an enlarged prostate, or other blockage of the normal flow of urine. More information is provided in the NIDDK health topic, Imaging of the Urinary Tract."}
{"_id":"ba9cc6aa-f178-4b1a-b121-a768bc4cdaaa","text":"Hematuria is treated by treating its underlying cause. If no serious condition is causing hematuria, no treatment is needed. Hematuria caused by a UTI is treated with antibiotics; urinalysis should be repeated 6 weeks after antibiotic treatment ends to be sure the infection has resolved."}
{"_id":"a1435853-ab36-4e55-9599-f0c60ec7117c","text":"Eating, diet, and nutrition have not been shown to play a role in causing or preventing hematuria."}
{"_id":"5510211e-a2d9-4f5a-84ef-69ef7068b383","text":"- Hematuria is blood in the urine.  - Most people with microscopic hematuria do not have symptoms. People with gross hematuria have urine that is pink, red, or cola-colored due to the presence of red blood cells (RBCs).  - Hematuria can be caused by menstruation, vigorous exercise, sexual activity, viral illness, trauma, or infection, such as a urinary tract infection (UTI). More serious causes of hematuria include      - cancer of the kidney or bladder    - inflammation of the kidney, urethra, bladder, or prostate    - polycystic kidney disease    - blood clots    - blood clotting disorders, such as hemophilia    - sickle cell disease    - When blood is visible in the urine or a dipstick test of the urine indicates the presence of RBCs, the urine is examined with a microscope to make an initial diagnosis of hematuria. The next step is to diagnose the cause of the hematuria.  - If a thorough medical history suggests a cause that does not require treatment, the urine should be tested again after 48 hours for the presence of RBCs. If two of three urine samples show too many RBCs when viewed with a microscope, more serious causes should be explored.  - One or more of the following tests may be ordered: urinalysis, blood test, biopsy, cytoscopy, and kidney imaging tests.  - Hematuria is treated by treating its underlying cause."}
{"_id":"3b0523b4-87cf-4bcc-b1a5-7f12e7f217e3","text":"Erectile dysfunction* is when you cannot get or keep an erection firm enough to have sex. You may have ED if you\n                \n- can get an erection sometimes, though not every time  - can get an erection, yet it does not last long enough for sex  - are unable to get an erection at all\n                \nED is sometimes called impotence; however, doctors use this term less often now.\n                \n\n                \n*See the Pronunciation Guide for tips on how to say the words in bold type."}
{"_id":"d9565ea4-a729-452f-9512-6b2d5682fe39","text":"Erectile dysfunction often has more than one cause. Many diseases can damage nerves, arteries, and muscles. Some can lead to ED, such as\n                \n- high blood pressure  - diabetes, when your blood glucose, also called blood sugar, is too high  - clogged arteries  - heart and blood vessel disease  - chronic kidney disease  - multiple sclerosis, a disease that attacks the nerves  - treatments for prostate cancer, including radiation, surgery to remove the prostate, and hormone treatments  - injury to the penis, spinal cord, prostate, bladder, or pelvis  - surgery for bladder cancer  - Peyronies disease, in which scar tissue, called a plaque, forms in the penis\n                \nUnhealthy lifestyle choices, such as smoking, drinking too much alcohol, using illegal drugs, being overweight, and not exercising, can lead to ED.\n                \nMental health problems such as the following can also cause or worsen ED:\n                \n- depression  - fear of sexual failure  - guilt  - low self-esteem  - stress  - worry\n                \nEven when ED has a physical cause, mental health problems can make ED worse. For example, a physical problem may slow your sexual arousal, which may make you more nervous and worsen your ED.\n                \nIn addition, ED can be a side effect of many common medicines. A small number of ED cases result from low testosterone, a male hormone."}
{"_id":"87863478-5c7e-40dc-987a-4b515475767a","text":"Erectile dysfunction affects men of all races and in all parts of the world. Men are more likely to have ED as they get older. For example, ED occurs in\n                \n- about 12 percent of men younger than 60  - 22 percent of men age 60 to 69  - 30 percent of men age 70 or older"}
{"_id":"b42d8331-e5a6-46bc-a443-5d051845a16a","text":"Having ED can cause you to feel depressed or anxious. ED may also cause low self-esteem. When you have ED, you may not have a satisfying sex life. You may not feel as close with your sexual partner, which may strain your relationship.\n                \n\n                \nSee Your Doctor if You Have Erectile Dysfunction, as Erectile Dysfunction Could Mean You Have a More Serious Condition   If you have problems getting or keeping an erection, and the problems last for more than a few weeks, you should talk with your doctor. ED can be a sign of other health problems, such as diabetes or heart disease.   When you meet with your doctor, you might use phrases like, Ive been having problems in the bedroom or Ive been having erection problems. Remember that a healthy sex life is part of a healthy life. Dont be shy about seeking help. Your doctor treats medical problems every day.   If talking with your doctor doesnt put you at ease, ask for a referral to another doctor. Your doctor may send you to a urologista doctor who specializes in sexual and urinary problems."}
{"_id":"0bb1625c-63fe-437e-b65c-0e6fde352f47","text":"To find the cause of your ED, your doctor may\n                \n- take your medical and sexual history  - ask you questions about your mental health  - give you a physical exam  - test your blood  - give you a nighttime erection test  - perform an injection test  - perform a Doppler penile ultrasound\n                \nMedical and Sexual History\n                \nYour doctor will ask general questions about your health, as well as specific questions about your erection problems and your relationship with your sexual partner. Your doctor might ask you questions such as\n                \n- Have you ever had surgery?  - What medicines do you take?  - How sure are you that you can get and keep an erection?  - When you have erections, how often are they hard enough for sex?  - During sex, how often are you able to keep your erection?  - When you try to have sex, how often are you happy with the sex?  - How would you rate your level of sexual desire?  - How often are you able to reach climax and ejaculate?  - Do you have an erection when you wake up in the morning?  - Do you use illegal drugs, drink alcohol, or smoke?\n                \nThe answers to these questions will help your doctor understand the problem.\n                \nBring a list of all the medicines you take, or the actual medicines, to show to your doctor.\n                \nMental Health Questions\n                \nYour doctor may ask you questions about your mental health. For example, the doctor may ask if you feel nervous or depressed. He or she may also ask you to answer questions on paper. The doctor may also ask your sexual partner questions to get more information about the problem.\n                \nPhysical Exam\n                \nA physical exam can help your doctor find the cause of your ED. As part of the exam, the doctor will examine your testes and penis, take your blood pressure, and check for problems with your blood flow.\n                \nBlood Tests\n                \nA blood test involves drawing your blood at a doctors office or a commercial facility and sending the sample to a lab for analysis. Blood tests can show possible causes of ED, such as diabetes, clogged blood vessels, or chronic kidney disease. Low levels of testosterone in your blood can explain why you may have lost interest in sex.\n                \nNighttime Erection Test\n                \nDuring a nighttime erection test, you wear a plastic band around your penis to test whether you have nighttime erections. The band easily breaks if your penis expands. This test shows if you had at least one erection during the night. Another test uses an electronic device that can record the number of erections, how long they last, and how firm they are. A man normally has three to five erections during the night while he sleeps. If you do have an erection, it probably means that your ED is more likely a mental health issue. If you do not have these erections, you probably have nerve damage or poor blood flow to your penis. You may do this test in your home or in a special sleep lab.\n                \nInjection Test\n                \nDuring an injection test, the doctor will inject a medicine into your penis to cause an erection. If the erection is not firm or does not last, it may mean you have a problem with blood flow. This test most often takes place in the doctors office.\n                \nDoppler Penile Ultrasound\n                \nAn x-ray technician most often performs a Doppler penile ultrasound in a doctors office or an outpatient center. During a Doppler penile ultrasound, the x-ray technician or doctor lightly passes a device over your penis to create images of blood vessels in your penis. An injection is used to create an erection. The images can show if you have a blood flow problem. The pictures appear on a computer screen. A radiologista doctor who specializes in medical imaginglooks at the images to find possible problems."}
{"_id":"f82017bb-ebf4-4d3c-b9e6-6c90ff359843","text":"Your doctor can offer you a number of treatments for ED. For many men, the answer is as simple as taking a pill. Other men have to try two or three options before they find a treatment that works for them. Dont give up if the first treatment doesnt work. Finding the right treatment can take time. You may want to talk with your sexual partner about which treatment fits you best as a couple.\n                \nA doctor can treat ED by\n                \n- treating the cause of your ED:      - lifestyle changes    - changing the medicines you take to treat other health problems    - counseling    - prescribing medicines to treat your ED:      - medicine by mouth    - other forms of medicine    - prescribing a vacuum device  - performing surgery:      - implanted devices    - surgery to repair blood vessels\n                \nTreating the Cause of Your Erectile Dysfunction\n                \nThe first step is to treat any health problems that may be causing your ED. Untreated diabetes or high blood pressure may be part of the cause of your ED.\n                \nLifestyle changes. For some men, the following lifestyle changes help:\n                \n- quitting smoking  - drinking less alcohol  - increasing physical activity  - stopping illegal drug use\n                \nChanging medicines you take to treat other health problems. Talk with your doctor about all the medicines you are taking, including over-the-counter medicines. The doctor may find that a medicine you are taking is causing your ED. Your doctor may be able to give you another medicine that works in a different way, or your doctor may tell you to try a lower dose of your medicine.\n                \nCounseling. Counseling can help couples deal with the emotional effects of ED. Some couples find that counseling adds to the medical treatment by making their relationship stronger.\n                \nPrescribing Medicines to Treat Your Erectile Dysfunction\n                \nDepending on which medicine your doctor gives you, you may take it by mouth or by putting it directly into your penis.\n                \nMedicine by mouth. Your doctor may be able to prescribe a pill to treat ED. Common medicines include\n                \n- sildenafil (Viagra)  - vardenafil (Levitra, Staxyn)  - tadalafil (Cialis)  - avanafil (Stendra)\n                \nIf your health is generally good, your doctor may prescribe one of these medicines. You should not take any of these pills to treat ED if you take any nitrates, a type of heart medicine. All ED pills work by increasing blood flow to the penis. They do not cause automatic erections. Talk with your doctor about when to take the pill. You may need to experiment to find out how soon the pill takes effect.\n                \nOther forms of medicine. Taking a pill doesnt work for all men. You may need to use medicine that goes directly into your penis. You may use an injection into the shaft of your penis, or you may use medicine placed in your urethra, at the tip of your penis. The urethra is the tube that carries urine and semen outside of the body. Your doctor will teach you how to use the medicines. They most often cause an erection within minutes. These medicines can be successful, even if other treatments fail.\n                \nPrescribing a Vacuum Device\n                \nAnother way to create an erection is to use a device with a specially designed vacuum tube. You put your penis into the tube, which is connected to a pump. As air is pumped out of the tube, blood flows into your penis and makes it larger and firmer. You then move a specially designed elastic ring from the end of the tube to the base of your penis to keep the blood from flowing back into your body. You may find that using a vacuum device requires some practice.\n                \nPerforming Surgery\n                \nIf the other options fail, you may need surgery to treat ED.\n                \nImplanted devices. A urologist can place a device that fills with fluid or a device with bendable rods inside the penis to create an erection.\n                \nOne kind of implant uses two cylinders that fill with fluid like a balloon. Tubing connects the cylinders to a small ball that holds the fluid. You fill the cylinders by squeezing a small pump that the urologist places under the skin of the scrotum, in front of your testes. The pump causes fluid to flow into the two cylinders in your penis, making it hard. The fluid can make the penis slightly longer and wider. An implant that uses fluids instead of bendable rods leaves the penis in a more natural state when not in use.\n                \nImplants that bend most often have two rods that the urologist places side by side in your penis during surgery. You use your hands to adjust the position of the rods to make your penis straight. Your penis does not get larger. After sex, you bend the rods down.\n                \nImplanted devices do not affect the way sex feels or the ability to have an orgasm.\n                \nOnce you have an implanted device, you must use the device to have an erection every time. Talk with your doctor about the pros and cons of having an implanted device.\n                \nSurgery to repair blood vessels. Doctors treat some cases of ED with surgery to repair the blood vessels that carry blood to the penis. This type of surgery is more likely to work in men younger than 30."}
{"_id":"c8d1367a-0514-4ed4-88cc-5613ba056a7d","text":"You can prevent many of the causes of ED by making healthy lifestyle choices. Following a healthy diet may help prevent ED. Quitting smoking and getting physical activity are also important ways to prevent ED.\n                \nPhysical activity increases blood flow throughout your body, including your penis. Talk with your doctor before starting new activities. If you have not been active, start slow, with easier activities such as walking at a normal pace or gardening. Then you can work up to harder activities such as walking briskly or swimming. Try to aim for at least 30 minutes of activity most days of the week."}
{"_id":"5b0a5bb7-b3e0-49d9-806d-005dce3a6564","text":"To prevent ED, you should eat a healthy diet of whole-grain foods, fruits and vegetables, low-fat dairy foods, and lean meats. A diet that causes you to be overweight and have heart and blood vessel disease can also lead to ED. You should avoid foods high in fat and sodium, the main part of salt. You should also avoid smoking, drinking too much alcohol, or using illegal drugs."}
{"_id":"4f0d04f1-1596-46d0-ad6c-1d44809b2102","text":"- Erectile dysfunction (ED) is when you cannot get or keep an erection firm enough to have sex. You may have ED if you      - can get an erection sometimes, though not every time    - can get an erection, yet it does not last long enough for sex    - are unable to get an erection at all    - An erection occurs when blood flow into the penis increases, making the penis larger and firmer. Hormones, blood vessels, nerves, and muscles all work together to cause an erection.  - ED often has more than one cause. Many diseases can damage nerves, arteries, and muscles.  - To find the cause of your ED, your doctor may      - take your medical and sexual history    - ask you questions about your mental health    - give you a physical exam    - test your blood    - give you a nighttime erection test    - perform an injection test    - perform a Doppler penile ultrasound    - Your doctor can offer you a number of treatments for ED. For many men, the answer is as simple as taking a pill. Other men have to try two or three options before they find a treatment that works for them.  - You can prevent many of the causes of ED by making healthy lifestyle choices. Following a healthy diet may help prevent ED. Quitting smoking and getting physical activity are also important ways to prevent ED."}
{"_id":"0c3669e5-2ae6-4fd8-b129-accc437b92a2","text":"Celiac disease is an immune disorder in which people cannot tolerate gluten because it damages the inner lining of their small intestine and prevents it from absorbing nutrients. The small intestine is the tubeshaped organ between the stomach and large intestine. Gluten is a protein found in wheat, rye, and barley and occasionally in some products such as vitamin and nutrient supplements, lip balms, and certain medications.\n                \nThe immune system is the body's natural defense system and normally protects the body from infection. However, when a person has celiac disease, gluten causes the immune system to react in a way that can cause intestinal inflammationirritation or swellingand long-lasting damage.\n                \nWhen people with celiac disease eat foods or use products containing gluten, their immune system responds by damaging or destroying villithe tiny, fingerlike projections on the inner lining of the small intestine. Villi normally absorb nutrients from food and pass the nutrients through the walls of the small intestine and into the bloodstream. Without healthy villi, people can become malnourished, no matter how much food they eat."}
{"_id":"987ebf8c-c976-4c2b-91b2-597380a294a9","text":"Researchers do not know the exact cause of celiac disease. Celiac disease sometimes runs in families. In 50 percent of people who have celiac disease, a family member, when screened, also has the disease.1\n                \nA person's chances of developing celiac disease increase when his or her genestraits passed from parent to childhave variants, or changes. In celiac disease, certain gene variants and other factors, such as a person's exposure to things in his or her environment, can lead to celiac disease. Read more about genes and genetic conditions at www.ghr.nlm.nih.gov.\n                \nFor most people, eating something with gluten is harmless. For others, an exposure to gluten can cause, or trigger, celiac disease to become active. Sometimes surgery, pregnancy, childbirth, a viral infection, or severe emotional stress can also trigger celiac disease symptoms."}
{"_id":"11be9fc5-e574-4be9-aa62-e20f1d97adf7","text":"As many as one in 141 Americans has celiac disease, although most remain undiagnosed.2 Celiac disease affects children and adults in all parts of the world and is more common in Caucasians and females.\n                \nCeliac disease is also more common among people with certain genetic diseases, including Down syndrome and Turner syndromea condition that affects girls' development."}
{"_id":"ac92a2ed-67d0-4262-9db1-517a5107302d","text":"A person may experience digestive signs and symptoms, or symptoms in other parts of the body. Digestive signs and symptoms are more common in children and can include\n                \n- abdominal bloating  - chronic diarrhea  - constipation  - gas  - pale, foul-smelling, or fatty stool  - stomach pain  - nausea  - vomiting\n                \nBeing unable to absorb nutrients during the years when nutrition is critical to a child's normal growth and development can lead to other health problems, such as\n                \n- failure to thrive in infants  - slowed growth and short stature  - weight loss  - irritability or change in mood  - delayed puberty  - dental enamel defects of permanent teeth\n                \nAdults are less likely to have digestive signs and symptoms and may instead have one or more of the following:\n                \n- anemia  - bone or joint pain  - canker sores inside the mouth  - depression or anxiety  - dermatitis herpetiformis, an itchy, blistering skin rash  - fatigue, or feeling tired  - infertility or recurrent miscarriage  - missed menstrual periods  - seizures  - tingling numbness in the hands and feet  - weak and brittle bones, or osteoporosis  - headaches\n                \nIntestinal inflammation can cause other symptoms, such as\n                \n- feeling tired for long periods of time  - abdominal pain and bloating  - ulcers  - blockages in the intestine\n                \nCeliac disease can produce an autoimmune reaction, or a self-directed immune reaction, in which a person's immune system attacks healthy cells in the body. This reaction can spread outside of the gastrointestinal tract to affect other areas of the body, including the\n                \n- spleen  - skin  - nervous system  - bones  - joints\n                \nRecognizing celiac disease can be difficult because some of its symptoms are similar to those of other diseases and conditions. Celiac disease can be confused with\n                \n- irritable bowel syndrome (IBS)  - iron-deficiency anemia caused by menstrual blood loss  - lactose intolerance  - inflammatory bowel disease  - diverticulitis  - intestinal infections  - chronic fatigue syndrome\n                \nAs a result, celiac disease has long been underdiagnosed or misdiagnosed. As health care providers become more aware of the many varied symptoms of the disease and reliable blood tests become more available, diagnosis rates are increasing, particularly for adults.\n                \n\n                \nDermatitis Herpetiformis   Dermatitis herpetiformis is a chronic, itchy, blistering skin rashusually on the elbows, knees, buttocks, back, or scalpthat affects about 5 to 10 percent of people with celiac disease.3 Men with dermatitis herpetiformis may also have oral or genital lesions. People with dermatitis herpetiformis may have no other signs or symptoms of celiac disease. Skin deposits of antibodiesproteins that react against the body's own cells or tissuescommon in celiac disease cause dermatitis herpetiformis. Ingesting gluten triggers these antibodies.   More information is provided in the NIDDK health topic, Dermatitis Herpetiformis: Skin Manifestation of Celiac Disease."}
{"_id":"850fea7a-d9d7-48b6-b986-80abcf32f325","text":"Signs and symptoms of celiac disease vary from person to person because of numerous factors, including\n                \n- the length of time a person was breastfed as an infant; some studies have shown that the longer an infant was breastfed, the later the symptoms of celiac disease appear  - the age a person started eating gluten  - the amount of gluten a person eats  - agesymptoms can vary between young children and adults  - the degree of damage to the small intestine\n                \nSome people with celiac disease have no signs or symptoms; however, they can still develop complications of the disease over time. Long-term complications include\n                \n- malnutrition  - liver diseases  - intestinal cancer  - lymphoma"}
{"_id":"61facd03-9a76-495f-be7f-a10e4a3c448e","text":"A health care provider diagnoses celiac disease with\n                \n- a medical and family history  - a physical exam  - blood tests  - an intestinal biopsy  - a skin biopsy\n                \nMedical and Family History\n                \nTaking a medical and family history may help a health care provider diagnose celiac disease. He or she will ask the patient or caregiver to provide a medical and family history, specifically if anyone in the patient's family has a history of celiac disease.\n                \nPhysical Exam\n                \nA physical exam may help diagnose celiac disease. During a physical exam, a health care provider usually\n                \n- examines the patient's body for malnutrition or a rash  - uses a stethoscope to listen to sounds within the abdomen  - taps on the patient's abdomen checking for bloating and pain\n                \nBlood Tests\n                \nA blood test involves drawing blood at a health care provider's office or a commercial facility and sending the sample to a lab for analysis. A blood test can show the presence of antibodies that are common in celiac disease.\n                \nIf blood test results are negative and a health care provider still suspects celiac disease, he or she may order additional blood tests, which can affect test results.\n                \nBefore the blood tests, patients should continue to eat a diet that includes foods with gluten, such as breads and pastas. If a patient stops eating foods with gluten before being tested, the results may be negative for celiac disease even if the disease is present.\n                \nIntestinal Biopsy\n                \nIf blood tests suggest that a patient has celiac disease, a health care provider will perform a biopsy of the patient's small intestine to confirm the diagnosis. A biopsy is a procedure that involves taking a piece of tissue for examination with a microscope. A health care provider performs the biopsy in an outpatient center or a hospital. He or she will give the patient light sedation and a local anesthetic. Some patients may receive general anesthesia.\n                \nDuring the biopsy, a health care provider removes tiny pieces of tissue from the patient's small intestine using an endoscopea small, flexible camera with a light. The health care provider carefully feeds the endoscope down the patient's esophagus and into the stomach and small intestine. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining. The health care provider then takes the samples using tiny tools that he or she passes through the endoscope. A pathologista doctor who specializes in examining tissues to diagnose diseasesexamines the tissue in a lab. The test can show damage to the villi in the small intestine.\n                \nSkin Biopsy\n                \nWhen a health care provider suspects that a patient has dermatitis herpetiformis, he or she will perform a skin biopsy. A skin biopsy is a procedure that involves removing tiny pieces of skin tissue for examination with a microscope. A health care provider performs the biopsy in an outpatient center or a hospital. The patient receives a local anesthetic; however, in some cases, the patient will require general anesthesia.\n                \nA pathologist examines the skin tissue in a lab and checks the tissue for antibodies that are common in celiac disease. If the skin tissue tests positive for the antibodies, a health care provider will perform blood tests to confirm celiac disease. If the skin biopsy and blood tests both suggest celiac disease, the patient may not need an intestinal biopsy for diagnosis.\n                \n\n                \nGenetic Tests   In some cases, a health care provider will order genetic blood tests to confirm or rule out a diagnosis of celiac disease. Most people with celiac disease have gene pairs that contain at least one of the human leukocyte antigen (HLA) gene variants.4 However, these variants are also common in people without celiac disease, so their presence alone cannot diagnose celiac disease.   If a biopsy and other blood tests do not give a clear diagnosis of celiac disease, a health care provider may test a patient for HLA gene variants. If the gene variants are not present, celiac disease is unlikely."}
{"_id":"4382e535-df6b-4dfe-84c8-786a6e6abf87","text":"In some cases, a health care provider will order genetic blood tests to confirm or rule out a diagnosis of celiac disease. Most people with celiac disease have gene pairs that contain at least one of the human leukocyte antigen (HLA) gene variants.4 However, these variants are also common in people without celiac disease, so their presence alone cannot diagnose celiac disease.\n                \nIf a biopsy and other blood tests do not give a clear diagnosis of celiac disease, a health care provider may test a patient for HLA gene variants. If the gene variants are not present, celiac disease is unlikely."}
{"_id":"d910d9d2-1609-4a3c-a633-df3c9513fe23","text":"Most people with celiac disease have a significant improvement in symptoms when they follow a gluten-free diet. Health care providers typically refer people to a dietitian who specializes in treating people with the disease. The dietitian will teach the person to avoid gluten while following a healthy and nutritious diet. The dietitian will give the person instructions for how to\n                \n- read food and product labels and identify ingredients that contain gluten  - make healthy choices about the types of foods to eat  - design everyday meal plans\n                \nFor most people, following a gluten-free diet will stop symptoms, heal existing intestinal damage, and prevent further damage. Symptoms may improve within days to weeks of starting the diet. The small intestine usually heals in 3 to 6 months in children. Complete healing can take several years in adults. Once the intestine heals, the villi will absorb nutrients from food into the bloodstream normally.\n                \nSome people with celiac disease show no improvement after starting a gluten-free diet. The most common reason for poor response to dietary changes is that people are still consuming small amounts of gluten, which can damage the small intestineeven in people without symptoms. Most people start responding to the gluten-free diet once they find and eliminate hidden sources of gluten from their diet. Hidden sources of gluten include additives made with wheat, such as\n                \n- modified food starch  - preservatives  - stabilizers\n                \n\n                \nDid you know that medications and nonfood products may contain gluten?   Medications, supplements, and other products may also contain lecithin, a hidden source of gluten. People with celiac disease should ask a pharmacist about the ingredients in   - prescription and over-the-counter medications   - vitamins and mineral supplements   - herbal and nutritional supplements    Other products can be ingested or transferred from a person's hands to his or her mouth. Reading product labels can help people avoid gluten exposure. If a product's label does not list its ingredients, the manufacturer should provide a list upon request.   Products that can contain gluten include   - lipstick, lip gloss, and lip balm   - cosmetics   - skin and hair products   - toothpaste and mouthwash   - glue on stamps and envelopes   - children's modeling dough, such as Play-Doh\n                \nSome people who continue to have symptoms even after changing their diet may have other conditions or disorders that are more common in people with celiac disease. These conditions may include\n                \n- small intestinal bacterial overgrowth, which happens when too many bacteria grow in the small intestine  - pancreatic exocrine insufficiency, in which the pancreas does not produce enough digestive juice  - microscopic colitis, an inflammation of the colon that a health care provider can see only with a microscope  - IBS  - lactose intolerance, a condition in which people have symptoms after consuming milk or milk products  - other food intolerances, which may occur because of continued damage to the intestine\n                \nIn some cases, people continue to have difficulty absorbing nutrients despite following a strict gluten-free diet. People with this condition, known as refractory celiac disease, have severely damaged intestines that cannot heal. Their intestines are not absorbing enough nutrients, so they may need to receive nutrients intravenously. Researchers continue to evaluate medications to treat refractory celiac disease.\n                \nDepending on a person's age at diagnosis, some complications of celiac disease will not improve, such as short stature and dental enamel defects.\n                \nFor people with dermatitis herpetiformis, skin symptoms generally respond to a gluten-free diet and may recur if a person adds gluten back into his or her diet. Medications such as dapsone can control the rash's symptoms. Dapsone does not treat intestinal symptoms or damage, so people with dermatitis herpetiformis should maintain a gluten-free diet, even if they don't have digestive symptoms. Even when a person follows a gluten-free diet, the skin lesions from dermatitis herpetiformis may take months or even years to fully heal and often recur over the years."}
{"_id":"3c8cda90-d3c3-416b-9f38-ca2a04a028b3","text":"Eating, diet, and nutrition play a significant role in treating celiac disease. People with the disease should maintain a gluten-free diet by avoiding products that contain gluten. In other words, a person with celiac disease should not eat most grains, pasta, and cereal, and many processed foods.\n                \nPeople with celiac disease can eat a wellbalanced diet with a variety of foods. They can use potato, rice, soy, amaranth, quinoa, buckwheat, or bean flour instead of wheat flour. They can buy gluten-free bread, pasta, and other products from stores, or order products from special food companies. Meanwhile, \"plain\"meaning no additives or seasoningsmeat, fish, rice, fruits, and vegetables do not contain gluten, so people with celiac disease can eat these foods.\n                \nIn the past, health care providers and dietitians advised people with celiac disease to avoid eating oats. Evidence suggests that most people with the disease can safely eat small amounts of oats, as long as the oats are not contaminated with wheat gluten during processing. People with celiac disease should talk with their health care team when deciding whether to include oats in their diet.\n                \nEating out and shopping can be a challenge. Newly diagnosed people and their families may find support groups helpful as they adjust to a new approach to eating. People with celiac disease should\n                \n- read food labelsespecially canned, frozen, and processed foodsfor ingredients that contain gluten  - avoid ingredients such as hydrolyzed vegetable protein, also called lecithin or soy lecithin  - ask restaurant servers and chefs about ingredients and food preparation inquire whether a gluten-free menu is available  - ask a dinner or party host about glutenfree options before attending a social gathering\n                \nFoods that are packaged as gluten-free tend to cost more than the same foods containing gluten. People following a gluten-free diet may find that naturally gluten-free foods are less expensive. With practice, looking for gluten can become second nature.\n                \nThe Gluten-free Diet: Some Examples\n                \nThe Academy of Nutrition and Dietetics has published recommendations for a glutenfree diet. The following chart illustrates these recommendations. This list is not complete, so people with celiac disease should discuss gluten-free food choices with a dietitian or health care professional who specializes in celiac disease. People with celiac disease should always read food ingredient lists carefully to make sure the food does not contain gluten.\n                \nTable 1. Gluten-free foods and foods that contain gluten\n                \nFoods and Ingredients That Contain Gluten         barley rye triticale (a cross between wheat and rye) wheat, including          - including einkorn, emmer, spelt, kamut      - wheat starch, wheat bran, wheat germ, cracked wheat, hydrolyzed wheat protein        brewer's yeast dextrin malt (unless a gluten-free source is named, such as corn malt) modified food starch oats (not labeled gluten-free) starch         Other Wheat Products That Contain Gluten         bromated flour durum flour enriched flour farina    graham flour phosphated flour plain flour    self-rising flour semolina white flour        Processed Foods That May Contain Wheat, Barley, or Rye*         bouillon cubes brown rice syrup candy chewing gum chips\/potato chips cold cuts, hot dogs, salami, sausage    communion wafers french fries gravies imitation fish matzo and matzo meal rice mixes    sauces seasoned tortilla chips self-basting turkey soups soy sauce vegetables in sauce        *Most of these foods can be found gluten-free. When in doubt, check with the food manufacturer.         Food Products and Ingredients Made from Barley*         ale beer malt malt beverages    malted milk malt extract malt syrup malt vinegar    other fermented beverages porter stout        *People should only consume these foods if they are labeled gluten-freesuch as sorghum-based beeror they list a grain source other than barley, wheat, or ryesuch as corn malt.         Foods That Do Not Contain Gluten         amaranth arrowroot buckwheat cassava corn flax    legumes lentils millet nuts oats (labeled gluten-free) potatoes    quinoa rice sago seeds sorghum soy    tapioca tef (or teff) wild rice yucca\n                \n\n                \nFood Labeling Requirements   On August 2, 2013, the U.S. Food and Drug Administration (FDA) published a new regulation defining the term \"glutenfree\" for voluntary food labeling. This new federal definition standardizes the meaning of \"gluten-free\" foods regulated by the FDA. Foods regulated by the U.S. Department of Agriculture, including meat and egg products, are not subject to this regulation. The regulation requires that any food with the term \"gluten-free\" on the label must meet all of the requirements of the definition, including that the food should contain fewer than 20 parts per million of gluten. The FDA rule also requires foods with the claims \"no gluten,\" \"free of gluten,\" and \"without gluten\" to meet the definition for \"gluten-free.\"   If a food that is labeled \"gluten-free\" includes \"wheat\" on the ingredients list or \"contains wheat\" after the list, the following statement must be included on the label: \"The wheat has been processed to allow this food to meet the Food and Drug Administration requirements for gluten-free food.\" If this statement is included, people with celiac disease may consume foods labeled \"gluten-free.\""}
{"_id":"a4b6ec01-b42d-4c42-aeac-a6becce88532","text":"- Celiac disease is an immune disorder in which people cannot tolerate gluten because it damages the lining of their small intestine and prevents absorption of nutrients.  - When people with celiac disease eat foods or use products containing gluten, their immune system responds by damaging or destroying villithe tiny, fingerlike projections on the inner lining of the small intestine.  - A person may experience digestive signs and symptoms, or symptoms in other parts of the body.  - Recognizing celiac disease can be difficult because some of its symptoms are similar to those of other diseases and conditions.  - Dermatitis herpetiformis is a chronic, itchy, blistering skin rashusually on the elbows, knees, buttocks, back, or scalpthat affects about 5 to 10 percent of people with celiac disease.  - Signs and symptoms of celiac disease vary from person to person because of numerous factors.  - Some people with celiac disease have no signs or symptoms; however, they can still develop complications of the disease over time. Long-term complications include malnutrition, liver diseases, intestinal cancer, and lymphoma.  - A health care provider diagnoses celiac disease with a medical and family history, a physical exam, blood tests, an intestinal biopsy, and a skin biopsy.  - Since celiac disease sometimes runs in families, blood relatives of people with celiac disease should talk with their health care provider about their chances of getting the disease.  - Most people with celiac disease have a significant improvement in symptoms when they follow a gluten-free diet.  - Health care providers typically refer people to a dietitian who specializes in treating people with the disease.  - The dietitian will give the person instructions for how to read food and product labels and identify ingredients that contain gluten.  - Medications, supplements, and other products may also contain a hidden source of gluten.  - People with celiac disease can eat a wellbalanced diet with a variety of foods."}
{"_id":"3c9b1025-a988-49b2-baa9-1bf355f70040","text":"Your nervous system carries signals between your brain and other parts of your body through your spinal cord. Nerves are bundles of special tissues that transmit these signals.\n                \nThe signals share information between your brain and body about how things feel. The signals also send information between your brain and body to control automatic body functions, such as breathing and digestion, and to move your body parts.\n                \nThe nerves in your spinal cord branch out to all of your organs and body parts. All your nerves together make up your nervous system.\n                \nYour nervous system is composed of the\n                \n- central nervous systemyour brain and spinal cord  - cranial* nervesnerves that connect your brain to your head, neck, and face  - peripheral nervous systemnerves that connect your spinal cord to your entire body, including your organs and your arms, hands, legs, and feet\n                \n*See the Pronunciation Guide for tips on how to say the the words in bold type."}
{"_id":"118fd7c4-ed07-443e-8320-ff3dc4cd3c74","text":"Nerve damage symptoms depend on which nerves have damage. Some people have no symptoms or mild symptoms. Other people have painful and long-lasting symptoms. As most nerve damage develops over many years, a person may not notice mild cases for a long time. In some people, the onset of pain may be sudden and severe."}
{"_id":"fef39692-930f-4a35-b3d7-96484b0f7bfa","text":"Peripheral Neuropathy\n                \nPeripheral neuropathy is the most common type of diabetic neuropathy, and it affects the sensory nerves of your feet, legs, hands, and arms. These areas of your body may feel\n                \n- numb  - weak  - cold  - burning or tingling, like pins and needles\n                \nYou may feel extreme pain in these areas of your body, even when they are touched lightly. You also may feel pain in your legs and feet when walking.\n                \nThese feelings are often worse at night and can make it hard to sleep. Most of the time, you will have these feelings on both sides of your body, such as in both feet; however, they can occur just on one side.\n                \n\n                \nYou might have other problems, such as\n                \n- swollen feet  - loss of balance  - loss of muscle tone in your hands and feet  - a deformity or shape change in your toes and feet  - calluses or open sores on your feet\n                \nAutonomic Neuropathy\n                \nAutonomic neuropathy can affect your\n                \n- digestive system  - sex organs  - bladder  - sweat glands  - eyes  - heart rate and blood pressure  - ability to sense low blood glucose\n                \nDigestive system. Damage to nerves in your stomach, intestines, and other parts of your digestive system may\n                \n- make it hard to swallow both solid food and liquids  - cause stomach pain, nausea, vomiting, constipation, or diarrhea  - make it hard to keep your blood glucose under control\n                \nYour doctor or dietitian may advise you to eat smaller, more frequent meals; avoid fatty foods; and eat less fiber.\n                \nSex organs. Damage to nerves in the sex organs may\n                \n- prevent a mans penis from getting firm when he wants to have sex, called erectile dysfunction or impotence. Many men who have had diabetes for several years have impotence.  - prevent a womans vagina from getting wet when she wants to have sex. A woman might also have less feeling around her vagina.\n                \nBladder. Damage to nerves in your bladder may make it hard to know when you need to urinate and when your bladder is empty. This damage can cause you to hold urine for too long, which can lead to bladder infections. You also might leak drops of urine.\n                \n\n                \nSweat glands. Damage to nerves in your sweat glands may prevent them from working properly. Nerve damage can cause you to sweat a lot at night or while eating.\n                \nEyes. Damage to nerves in your pupils, the parts of your eyes that react to changes in light and darkness, may make them slow to respond to these changes. You may have trouble seeing the lights of other cars when driving at night. Your eyes may take longer to adjust when you enter a dark room.\n                \n\n                \nHeart rate and blood pressure. Damage to nerves that control your heart rate and blood pressure may make these nerves respond more slowly to changes in position, stress, physical activity, sleep, and breathing patterns. You might feel dizzy or pass out when you go from lying down to standing up or when you do physical activity. You also might have shortness of breath or swelling in your feet.\n                \n\n                \nAbility to sense low blood glucose. Autonomic nerves also let you know when your blood glucose is low. Damage to these nerves can prevent you from feeling the symptoms of low blood glucose, also called hypoglycemia. This kind of nerve damage is more likely to happen if you have had diabetes for a long time or if your blood glucose has often been too low. Low blood glucose can make you\n                \n- hungry  - dizzy or shaky  - confused  - pale  - sweat more  - weak  - anxious or cranky  - have headaches  - have a fast heartbeat\n                \nSevere hypoglycemia can cause you to pass out. If that happens, youll need help bringing your blood glucose level back to normal. Your health care team can teach your family members and friends how to give you an injection of glucagon, a hormone that raises blood glucose levels quickly. If glucagon is not available, someone should call 911 to get you to the nearest emergency room for treatment.\n                \n\n                \nConsider wearing a diabetes medical alert identification bracelet or necklace. If you have hypoglycemia and are not able to communicate, the emergency team will know you have diabetes and get you the proper treatment. You can find these bracelets or necklaces at your pharmacy or on the Internet. You can also ask your doctor for information on available products.\n                \nOther Neuropathies\n                \nOther types of neuropathies from diabetes can cause\n                \n- damage to the joint and bones of your foot, called Charcots foot, in which you cannot sense pain or the position of your foot  - carpal tunnel syndrome, in which a nerve in your forearm is compressed at your wrist, causing numbness, swelling, and pain in your fingers  - paralysis on one side of your face, called Bells palsy  - double vision or not being able to focus your eyes  - aching behind one eye"}
{"_id":"94abb74f-2778-4aa6-b77c-26ca21153835","text":"The treatment for nerve damage from diabetes is based on your symptoms. No treatment can reverse nerve damage; however, it can help you feel better. Your doctor might suggest taking low doses of medicines that both treat other health problems and help the pain of neuropathy. Some of these medicines include\n                \n- antidepressants  - anticonvulsants, or anti-seizure medicines\n                \nOther treatment options include\n                \n- creams or patches on your skin for burning pain  - over-the-counter pain medicines  - acupuncture, a form of pain treatment that uses needles inserted into your body at certain pressure points  - physical therapy, which helps with muscle weakness and loss of balance  - relaxation exercises, such as yoga  - special shoes to fit softly around sore feet or feet that have changed shape\n                \nYour doctor also can prescribe medicines to help with problems caused by nerve damage in other areas of your body, such as poor digestion, dizziness, sexual problems, and lack of bladder control.\n                \nStopping smoking and drinking alcoholic beverages also may help with symptoms."}
{"_id":"e98ce9cc-3054-4d4a-a2d0-b724b6660ef1","text":"You can keep your nervous system healthy by taking these steps:\n                \n- Eat healthy meals and follow the meal plan that you and your doctor or dietitian have worked out.  - If you drink alcoholic beverages, limit your intake to no more than one drink per day for women and two drinks per day for men. Drinking too many alcoholic beverages can make nerve damage worse.\n                \nMore information is provided in the NIDDK health topic, What I need to know about Eating and Diabetes."}
{"_id":"30fe9f17-ab5b-4c1d-807f-c1e9524e6972","text":"Hemochromatosis is the most common form of iron overload disease. Too much iron in the body causes hemochromatosis. Iron is important because it is part of hemoglobin, a molecule in the blood that transports oxygen from the lungs to all body tissues. However, too much iron in the body leads to iron overloada buildup of extra iron that, without treatment, can damage organs such as the liver, heart, and pancreas; endocrine glands; and joints.\n                \nThe three types of hemochromatosis are primary hemochromatosis, also called hereditary hemochromatosis; secondary hemochromatosis; and neonatal hemochromatosis."}
{"_id":"98ebc868-2202-4b31-97de-0a15718272b1","text":"Primary Hemochromatosis\n                \nInherited genetic defects cause primary hemochromatosis, and mutations in the HFE gene are associated with up to 90 percent of cases.1 The HFE gene helps regulate the amount of iron absorbed from food. The two known mutations of HFE are C282Y and H63D. C282Y defects are the most common cause of primary hemochromatosis.\n                \nPeople inherit two copies of the HFE geneone copy from each parent. Most people who inherit two copies of the HFE gene with the C282Y defect will have higher-than-average iron absorption. However, not all of these people will develop health problems associated with hemochromatosis. One recent study found that 31 percent of people with two copies of the C282Y defect developed health problems by their early fifties.2 Men who develop health problems from HFE defects typically develop them after age 40.1 Women who develop health problems from HFE defects typically develop them after menopause.1\n                \nPeople who inherit two H63D defects or one C282Y and one H63D defect may have higher-than-average iron absorption.3 However, they are unlikely to develop iron overload and organ damage.\n                \nRare defects in other genes may also cause primary hemochromatosis. Mutations in the hemojuvelin or hepcidin genes cause juvenile hemochromatosis, a type of primary hemochromatosis. People with juvenile hemochromatosis typically develop severe iron overload and liver and heart damage between ages 15 and 30.\n                \nSecondary Hemochromatosis\n                \nHemochromatosis that is not inherited is called secondary hemochromatosis. The most common cause of secondary hemochromatosis is frequent blood transfusions in people with severe anemia. Anemia is a condition in which red blood cells are fewer or smaller than normal, which means they carry less oxygen to the bodys cells. Types of anemia that may require frequent blood transfusions include\n                \n- congenital, or inherited, anemias such as sickle cell disease, thalassemia, and Fanconis syndrome  - severe acquired anemias, which are not inherited, such as aplastic anemia and autoimmune hemolytic anemia\n                \nLiver diseasessuch as alcoholic liver disease, nonalcoholic steatohepatitis, and chronic hepatitis C infectionmay cause mild iron overload. However, this iron overload causes much less liver damage than the underlying liver disease causes.\n                \nNeonatal Hemochromatosis\n                \nNeonatal hemochromatosis is a rare disease characterized by liver failure and death in fetuses and newborns. Researchers are studying the causes of neonatal hemochromatosis and believe more than one factor may lead to the disease.\n                \nExperts previously considered neonatal hemochromatosis a type of primary hemochromatosis. However, recent studies suggest genetic defects that increase iron absorption do not cause this disease. Instead, the mothers immune system may produce antibodiesproteins made by the immune system to protect the body from foreign substances such as bacteria or virusesthat damage the liver of the fetus. Women who have had one child with neonatal hemochromatosis are at risk for having more children with the disease.4 Treating these women during pregnancy with intravenous (IV) immunoglobulina solution of antibodies from healthy peoplecan prevent fetal liver damage.4\n                \nResearchers supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) recently found that a combination of exchange transfusionremoving blood and replacing it with donor bloodand IV immunoglobulin is an effective treatment for babies born with neonatal hemochromatosis.5"}
{"_id":"0b24ab26-932e-497e-8fba-f41db6b529e1","text":"A person with hemochromatosis may notice one or more of the following symptoms:\n                \n- joint pain  - fatigue, or feeling tired  - unexplained weight loss  - abnormal bronze or gray skin color  - abdominal pain  - loss of sex drive\n                \nNot everyone with hemochromatosis will develop these symptoms."}
{"_id":"c1766199-7611-4001-81a8-6129c699d9ce","text":"Without treatment, iron may build up in the organs and cause complications, including\n                \n- cirrhosis, or scarring of liver tissue  - diabetes  - irregular heart rhythms or weakening of the heart muscle  - arthritis  - erectile dysfunction\n                \nThe complication most often associated with hemochromatosis is liver damage. Iron buildup in the liver causes cirrhosis, which increases the chance of developing liver cancer.\n                \nFor some people, complications may be the first sign of hemochromatosis. However, not everyone with hemochromatosis will develop complications."}
{"_id":"13a080cb-ab80-4a8c-9107-f25eb2bfb3e2","text":"Health care providers use medical and family history, a physical exam, and routine blood tests to diagnose hemochromatosis or other conditions that could cause the same symptoms or complications.\n                \n- Medical and family history. Taking a medical and family history is one of the first things a health care provider may do to help diagnose hemochromatosis. The health care provider will look for clues that may indicate hemochromatosis, such as a family history of arthritis or unexplained liver disease.    - Physical exam. After taking a medical history, a health care provider will perform a physical exam, which may help diagnose hemochromatosis. During a physical exam, a health care provider usually      - examines a patients body    - uses a stethoscope to listen to bodily sounds    - taps on specific areas of the patients body      - Blood tests. A blood test involves drawing blood at a health care providers office or a commercial facility and sending the sample to a lab for analysis. Blood tests can determine whether the amount of iron stored in the body is higher than normal:1      - The transferrin saturation test shows how much iron is bound to the protein that carries iron in the blood. Transferrin saturation values above or equal to 45 percent are considered abnormal.    - The serum ferritin test detects the amount of ferritina protein that stores ironin the blood. Levels above 300 g\/L in men and 200 g\/L in women are considered abnormal. Levels above 1,000 g\/L in men or women indicate a high chance of iron overload and organ damage.    If either test shows higher-than-average levels of iron in the body, health care providers can order a special blood test that can detect two copies of the C282Y mutation to confirm the diagnosis. If the mutation is not present, health care providers will look for other causes.    - Liver biopsy. Health care providers may perform a liver biopsy, a procedure that involves taking a piece of liver tissue for examination with a microscope for signs of damage or disease. The health care provider may ask the patient to temporarily stop taking certain medications before the liver biopsy. The health care provider may ask the patient to fast for 8 hours before the procedure.  During the procedure, the patient lies on a table, right hand resting above the head. The health care provider applies a local anesthetic to the area where he or she will insert the biopsy needle. If needed, a health care provider will also give sedatives and pain medication. The health care provider uses a needle to take a small piece of liver tissue. He or she may use ultrasound, computerized tomography scans, or other imaging techniques to guide the needle. After the biopsy, the patient must lie on the right side for up to 2 hours and is monitored an additional 2 to 4 hours before being sent home.  A health care provider performs a liver biopsy at a hospital or an outpatient center. The health care provider sends the liver sample to a pathology lab where the pathologista doctor who specializes in diagnosing diseaselooks at the tissue with a microscope and sends a report to the patients health care provider. The biopsy shows how much iron has accumulated in the liver and whether the patient has liver damage.\n                \nHemochromatosis is rare, and health care providers may not think to test for this disease. Thus, the disease is often not diagnosed or treated. The initial symptoms can be diverse, vague, and similar to the symptoms of many other diseases. Health care providers may focus on the symptoms and complications caused by hemochromatosis rather than on the underlying iron overload. However, if a health care provider diagnoses and treats the iron overload caused by hemochromatosis before organ damage has occurred, a person can live a normal, healthy life.\n                \n\n                \nWho should be tested for hemochromatosis?   Experts recommend testing for hemochromatosis in people who have symptoms, complications, or a family history of the disease.   Some researchers have suggested widespread screening for the C282Y mutation in the general population. However, screening is not cost-effective. Although the C282Y mutation occurs quite frequently, the disease caused by the mutation is rare, and many people with two copies of the mutation never develop iron overload or organ damage.   Researchers and public health officials suggest the following:   - Siblings of people who have hemochromatosis should have their blood tested to see if they have the C282Y mutation.   - Parents, children, and other close relatives of people who have hemochromatosis should consider being tested.   - Health care providers should consider testing people who have severe and continuing fatigue, unexplained cirrhosis, joint pain or arthritis, heart problems, erectile dysfunction, or diabetes because these health issues may result from hemochromatosis."}
{"_id":"879c72ef-080e-428d-bb31-53cf17d0f64a","text":"Health care providers treat hemochromatosis by drawing blood. This process is called phlebotomy. Phlebotomy rids the body of extra iron. This treatment is simple, inexpensive, and safe.\n                \nBased on the severity of the iron overload, a patient will have phlebotomy to remove a pint of blood once or twice a week for several months to a year, and occasionally longer. Health care providers will test serum ferritin levels periodically to monitor iron levels. The goal is to bring serum ferritin levels to the low end of the average range and keep them there. Depending on the lab, the level is 25 to 50 g\/L.\n                \nAfter phlebotomy reduces serum ferritin levels to the desired level, patients may need maintenance phlebotomy treatment every few months. Some patients may need phlebotomies more often. Serum ferritin tests every 6 months or once a year will help determine how often a patient should have blood drawn. Many blood donation centers provide free phlebotomy treatment for people with hemochromatosis.\n                \nTreating hemochromatosis before organs are damaged can prevent complications such as cirrhosis, heart problems, arthritis, and diabetes. Treatment cannot cure these conditions in patients who already have them at diagnosis. However, treatment will help most of these conditions improve. The treatments effectiveness depends on the degree of organ damage. For example, treating hemochromatosis can stop the progression of liver damage in its early stages and lead to a normal life expectancy. However, if a patient develops cirrhosis, his or her chance of developing liver cancer increases, even with phlebotomy treatment. Arthritis usually does not improve even after phlebotomy removes extra iron."}
{"_id":"3a14f497-695b-4614-853d-c217d79afc2f","text":"Iron is an essential nutrient found in many foods. Healthy people usually absorb less than 10 percent of iron in the food they eat.6 People with hemochromatosis absorb up to 30 percent of that iron.6 People with hemochromatosis can help prevent iron overload by\n                \n- eating only moderate amounts of iron-rich foods, such as red meat and organ meat  - avoiding supplements that contain iron  - avoiding supplements that contain vitamin C, which increases iron absorption\n                \nPeople with hemochromatosis can take steps to help prevent liver damage, including\n                \n- limiting the amount of alcoholic beverages they drink because alcohol increases their chance of cirrhosis and liver cancer  - avoiding alcoholic beverages entirely if they already have cirrhosis"}
{"_id":"20f9882c-26f0-4b29-87b6-bb2145997ce3","text":"- Hemochromatosis is the most common form of iron overload disease. Too much iron in the body causes hemochromatosis.  - Inherited genetic defects cause primary hemochromatosis.  - Primary hemochromatosis mainly affects Caucasians of Northern European descent.  - A person with hemochromatosis may notice one or more of the following symptoms: joint pain; fatigue, or feeling tired; unexplained weight loss; abnormal bronze or gray skin color; abdominal pain; and loss of sex drive. Not everyone with hemochromatosis will develop these symptoms.  - Without treatment, iron may build up in the organs and cause complications, including cirrhosis, diabetes, irregular heart rhythms or weakening of the heart muscle, arthritis, and erectile dysfunction.  - If a health care provider diagnoses and treats the iron overload caused by hemochromatosis before organ damage has occurred, a person can live a normal, healthy life.  - Experts recommend testing for hemochromatosis in people who have symptoms, complications, or a family history of the disease.  - Health care providers treat hemochromatosis by drawing blood. This process is called phlebotomy."}
{"_id":"a8ad80d4-b4b6-4601-bdb8-1ef573eba32f","text":"Adrenal insufficiency is an endocrine, or hormonal, disorder that occurs when the adrenal glands do not produce enough of certain hormones. The adrenal glands are located just above the kidneys.\n                \nAdrenal insufficiency can be primary or secondary. Addisons disease, the common term for primary adrenal insufficiency, occurs when the adrenal glands are damaged and cannot produce enough of the adrenal hormone cortisol. The adrenal hormone aldosterone may also be lacking. Addisons disease affects 110 to 144 of every 1 million people in developed countries.1\n                \nSecondary adrenal insufficiency occurs when the pituitary glanda pea-sized gland at the base of the brainfails to produce enough adrenocorticotropin (ACTH), a hormone that stimulates the adrenal glands to produce the hormone cortisol. If ACTH output is too low, cortisol production drops. Eventually, the adrenal glands can shrink due to lack of ACTH stimulation. Secondary adrenal insufficiency is much more common than Addisons disease.\n                \n\n                \n1"}
{"_id":"93a5c35b-a781-41a1-b5eb-205adc792304","text":"Adrenal Insufficiency\n                \nThe most common symptoms of adrenal insufficiency are\n                \n- chronic, or long lasting, fatigue   - muscle weakness   - loss of appetite   - weight loss   - abdominal pain\n                \nOther symptoms of adrenal insufficiency can include\n                \n- nausea   - vomiting   - diarrhea   - low blood pressure that drops further when a person stands up, causing dizziness or fainting   - irritability and depression   - craving salty foods   - hypoglycemia, or low blood sugar   - headache   - sweating   - irregular or absent menstrual periods   - in women, loss of interest in sex\n                \nHyperpigmentation, or darkening of the skin, can occur in Addisons disease, although not in secondary adrenal insufficiency. This darkening is most visible on scars; skin folds; pressure points such as the elbows, knees, knuckles, and toes; lips; and mucous membranes such as the lining of the cheek.\n                \nThe slowly progressing symptoms of adrenal insufficiency are often ignored until a stressful event, such as surgery, a severe injury, an illness, or pregnancy, causes them to worsen.\n                \nAdrenal Crisis\n                \nSudden, severe worsening of adrenal insufficiency symptoms is called adrenal crisis. If the person has Addisons disease, this worsening can also be called an Addisonian crisis. In most cases, symptoms of adrenal insufficiency become serious enough that people seek medical treatment before an adrenal crisis occurs. However, sometimes symptoms appear for the first time during an adrenal crisis.\n                \nSymptoms of adrenal crisis include\n                \n- sudden, severe pain in the lower back, abdomen, or legs   - severe vomiting and diarrhea   - dehydration   - low blood pressure   - loss of consciousness\n                \nIf not treated, an adrenal crisis can cause death.\n                \n\n                \nGet Treatment for Adrenal Crisis Right Away   People with adrenal insufficiency who have weakness, nausea, or vomiting need immediate emergency treatment to prevent an adrenal crisis and possible death. An injection with a synthetic glucocorticoid hormone called a corticosteroid can save a persons life. People should make sure to have a corticosteroid injection with them at all times, and make sure their friends and family know how and when to give the injection.   Read more under How is adrenal insufficiency treated?"}
{"_id":"79778bde-cbcc-4b4a-be69-cc527770e9a4","text":"People with adrenal insufficiency who have weakness, nausea, or vomiting need immediate emergency treatment to prevent an adrenal crisis and possible death. An injection with a synthetic glucocorticoid hormone called a corticosteroid can save a persons life. People should make sure to have a corticosteroid injection with them at all times, and make sure their friends and family know how and when to give the injection.\n                \nRead more under How is adrenal insufficiency treated?"}
{"_id":"b6526d6e-57b3-4602-91c4-867e233a3ed9","text":"Autoimmune disorders cause most cases of Addisons disease. Infections and medications may also cause the disease.\n                \nAutoimmune Disorders\n                \nUp to 80 percent of Addisons disease cases are caused by an autoimmune disorder, which is when the bodys immune system attacks the bodys own cells and organs.2 In autoimmune Addisons, which mainly occurs in middle-aged females, the immune system gradually destroys the adrenal cortexthe outer layer of the adrenal glands.2\n                \nPrimary adrenal insufficiency occurs when at least 90 percent of the adrenal cortex has been destroyed.1 As a result, both cortisol and aldosterone are often lacking. Sometimes only the adrenal glands are affected. Sometimes other endocrine glands are affected as well, as in polyendocrine deficiency syndrome.\n                \nPolyendocrine deficiency syndrome is classified into type 1 and type 2. Type 1 is inherited and occurs in children. In addition to adrenal insufficiency, these children may have\n                \n- underactive parathyroid glands, which are four pea-sized glands located on or near the thyroid gland in the neck; they produce a hormone that helps maintain the correct balance of calcium in the body.   - slow sexual development.   - pernicious anemia, a severe type of anemia; anemia is a condition in which red blood cells are fewer than normal, which means less oxygen is carried to the bodys cells. With most types of anemia, red blood cells are smaller than normal; however, in pernicious anemia, the cells are bigger than normal.   - chronic fungal infections.   - chronic hepatitis, a liver disease.\n                \nResearchers think type 2, which is sometimes called Schmidts syndrome, is also inherited. Type 2 usually affects young adults and may include\n                \n- an underactive thyroid gland, which produces hormones that regulate metabolism   - slow sexual development   - diabetes, in which a person has high blood glucose, also called high blood sugar or hyperglycemia   - vitiligo, a loss of pigment on areas of the skin\n                \nInfections\n                \nTuberculosis (TB), an infection that can destroy the adrenal glands, accounts for 10 to 15 percent of Addisons disease cases in developed countries.1 When primary adrenal insufficiency was first identified by Dr. Thomas Addison in 1849, TB was the most common cause of the disease. As TB treatment improved, the incidence of Addisons disease due to TB of the adrenal glands greatly decreased. However, recent reports show an increase in Addisons disease from infections such as TB and cytomegalovirus. Cytomegalovirus is a common virus that does not cause symptoms in healthy people; however, it does affect babies in the womb and people who have a weakened immune systemmostly due to HIV\/AIDS.2 Other bacterial infections, such as Neisseria meningitidis, which is a cause of meningitis, and fungal infections can also lead to Addisons disease.\n                \nOther Causes\n                \nLess common causes of Addisons disease are\n                \n- cancer cells in the adrenal glands   - amyloidosis, a serious, though rare, group of diseases that occurs when abnormal proteins, called amyloids, build up in the blood and are deposited in tissues and organs   - surgical removal of the adrenal glands   - bleeding into the adrenal glands   - genetic defects including abnormal adrenal gland development, an inability of the adrenal glands to respond to ACTH, or a defect in adrenal hormone production   - medication-related causes, such as from anti-fungal medications and the anesthetic etomidate, which may be used when a person undergoes an emergency intubationthe placement of a flexible, plastic tube through the mouth and into the trachea, or windpipe, to assist with breathing\n                \n\n                \n2"}
{"_id":"b43dc821-0213-40dc-9c50-3267db1dd236","text":"A lack of CRH or ACTH causes secondary adrenal insufficiency. The lack of these hormones in the body can be traced to several possible sources.\n                \nStoppage of Corticosteroid Medication\n                \nA temporary form of secondary adrenal insufficiency may occur when a person who has been taking a synthetic glucocorticoid hormone, called a corticosteroid, for a long time stops taking the medication. Corticosteroids are often prescribed to treat inflammatory illnesses such as rheumatoid arthritis, asthma, and ulcerative colitis. In this case, the prescription doses often cause higher levels than those normally achieved by the glucocorticoid hormones created by the body. When a person takes corticosteroids for prolonged periods, the adrenal glands produce less of their natural hormones. Once the prescription doses of corticosteroid are stopped, the adrenal glands may be slow to restart their production of the bodys glucocorticoids. To give the adrenal glands time to regain function and prevent adrenal insufficiency, prescription corticosteroid doses should be reduced gradually over a period of weeks or even months. Even with gradual reduction, the adrenal glands might not begin to function normally for some time, so a person who has recently stopped taking prescription corticosteroids should be watched carefully for symptoms of secondary adrenal insufficiency.\n                \nSurgical Removal of Pituitary Tumors\n                \nAnother cause of secondary adrenal insufficiency is surgical removal of the usually noncancerous, ACTH-producing tumors of the pituitary gland that cause Cushings syndrome. Cushings syndrome is a hormonal disorder caused by prolonged exposure of the bodys tissues to high levels of the hormone cortisol. When the tumors are removed, the source of extra ACTH is suddenly gone and a replacement hormone must be taken until the bodys adrenal glands are able to resume their normal production of cortisol. The adrenal glands might not begin to function normally for some time, so a person who has had an ACTH-producing tumor removed and is going off of his or her prescription corticosteroid replacement hormone should be watched carefully for symptoms of adrenal insufficiency.\n                \nMore information is provided in the NIDDK health topic, Cushings Syndrome.\n                \nChanges in the Pituitary Gland\n                \nLess commonly, secondary adrenal insufficiency occurs when the pituitary gland either decreases in size or stops producing ACTH. These events can result from\n                \n- tumors or an infection in the pituitary   - loss of blood flow to the pituitary   - radiation for the treatment of pituitary or nearby tumors   - surgical removal of parts of the hypothalamus   - surgical removal of the pituitary"}
{"_id":"30b6a404-a651-426e-b173-8553715614ad","text":"In its early stages, adrenal insufficiency can be difficult to diagnose. A health care provider may suspect it after reviewing a persons medical history and symptoms.\n                \nA diagnosis of adrenal insufficiency is confirmed through hormonal blood and urine tests. A health care provider uses these tests first to determine whether cortisol levels are too low and then to establish the cause. Imaging studies of the adrenal and pituitary glands can be useful in helping to establish the cause.\n                \nA lab technician performs the following tests in a health care providers office, a commercial facility, or a hospital.\n                \nHormonal Blood and Urine Tests\n                \n- ACTH stimulation test. The ACTH stimulation test is the most commonly used test for diagnosing adrenal insufficiency. In this test, the patient is given an intravenous (IV) injection of synthetic ACTH, and samples of blood, urine, or both are taken before and after the injection. The cortisol levels in the blood and urine samples are measured in a lab. The normal response after an ACTH injection is a rise in blood and urine cortisol levels. People with Addisons disease or longstanding secondary adrenal insufficiency have little or no increase in cortisol levels.  Both low- and high-dose ACTH stimulation tests may be used depending on the suspected cause of adrenal insufficiency. For example, if secondary adrenal insufficiency is mild or has only recently occurred, the adrenal glands may still respond to ACTH because they have not yet shut down their own production of hormone. Some studies have suggested a low dose1 microgram (mcg)may be more effective in detecting secondary adrenal insufficiency because the low dose is still enough to raise cortisol levels in healthy people, yet not in people with mild or recent secondary adrenal insufficiency. However, recent research has shown that a significant proportion of healthy children and adults can fail the low-dose test, which may lead to unnecessary treatment. Therefore, some health care providers favor using a 250 mcg ACTH test for more accurate results.   - CRH stimulation test. When the response to the ACTH test is abnormal, a CRH stimulation test can help determine the cause of adrenal insufficiency. In this test, the patient is given an IV injection of synthetic CRH, and blood is taken before and 30, 60, 90, and 120 minutes after the injection. The cortisol levels in the blood samples are measured in a lab. People with Addisons disease respond by producing high levels of ACTH, yet no cortisol. People with secondary adrenal insufficiency do not produce ACTH or have a delayed response. CRH will not stimulate ACTH secretion if the pituitary is damaged, so no ACTH response points to the pituitary as the cause. A delayed ACTH response points to the hypothalamus as the cause.\n                \nDiagnosis during Adrenal Crisis\n                \nAlthough a reliable diagnosis is not possible during adrenal crisis, measurement of blood ACTH and cortisol during the crisisbefore treatment with corticosteroids is givenis often enough to make a preliminary diagnosis. Low blood sodium, low blood glucose, and high blood potassium are also sometimes present at the time of adrenal crisis. Once the crisis is controlled, an ACTH stimulation test can be performed to help make a specific diagnosis. More complex lab tests are sometimes used if the diagnosis remains unclear."}
{"_id":"d5f36628-e790-4b84-b359-058c88112531","text":"After Addisons disease is diagnosed, health care providers may use the following tests to look at the adrenal glands, find out whether the disease is related to TB, or identify antibodies associated with autoimmune Addisons disease.\n                \n- Ultrasound of the abdomen. Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. A specially trained technician performs the procedure in a health care providers office, an outpatient center, or a hospital, and a radiologista doctor who specializes in medical imaginginterprets the images; a patient does not need anesthesia. The images can show abnormalities in the adrenal glands, such as enlargement or small size, nodules, or signs of calcium deposits, which may indicate bleeding.   - Tuberculin skin test. A tuberculin skin test measures how a patients immune system reacts to the bacteria that cause TB. A small needle is used to put some testing material, called tuberculin, under the skin. A nurse or lab technician performs the test in a health care providers office; a patient does not need anesthesia. In 2 to 3 days, the patient returns to the health care provider, who will check to see if the patient had a reaction to the test. The test can show if adrenal insufficiency could be related to TB.  To test whether a person has TB infection, which is when TB bacteria live in the body without making the person sick, a special TB blood test is used. To test whether a person has TB disease, which is when TB bacteria are actively attacking a persons lungs and making the person sick, other tests such as a chest x ray and a sample of sputumphlegm that is coughed up from deep in the lungsmay be needed.   - Antibody blood tests. A blood test involves drawing blood at a health care providers office or a commercial facility and sending the sample to a lab for analysis. The blood test can detect antibodiesproteins made by the immune system to protect the body from foreign substancesassociated with autoimmune Addisons disease.\n                \nAfter secondary adrenal insufficiency is diagnosed, health care providers may use the following tests to obtain a detailed view of the pituitary gland and assess how it is functioning:\n                \n- Computerized tomography (CT) scan. CT scans use a combination of x rays and computer technology to create images. For a CT scan, the patient may be given a solution to drink and an injection of a special dye, called contrast medium. CT scans require the patient to lie on a table that slides into a tunnel-shaped device where the x rays are taken. An x-ray technician performs the procedure in an outpatient center or a hospital, and a radiologist interprets the images. The patient does not need anesthesia. A CT scan can show size and shape of the pituitary gland to find out if an abnormality is present.   - Magnetic resonance imaging (MRI). MRI machines use radio waves and magnets to produce detailed pictures of the bodys internal organs and soft tissues without using x rays. An MRI may include the injection of contrast medium. With most MRI machines, the patient lies on a table that slides into a tunnel-shaped device that may be open ended or closed at one end; some machines are designed to allow the patient to lie in a more open space. A specially trained technician performs the procedure in an outpatient center or a hospital, and a radiologist interprets the images. The patient does not need anesthesia, though people with a fear of confined spaces may receive light sedation, taken by mouth. MRIs can be used to produce a three-dimensional (3-D) image of the hypothalamus and the pituitary gland to find out if an abnormality is present.   - Hormonal blood tests. Hormonal blood tests can assess how the pituitary gland is functioning and its ability to produce other hormones."}
{"_id":"b7c75cc9-36b9-4920-b924-8e15a5eb1b5a","text":"Adrenal insufficiency is treated by replacing, or substituting, the hormones that the adrenal glands are not making. The dose of each medication is adjusted to meet the needs of the patient.\n                \nCortisol is replaced with a corticosteroid, such as hydrocortisone, prednisone, or dexamethasone, taken orally one to three times each day, depending on which medication is chosen.\n                \nIf aldosterone is also deficient, it is replaced with oral doses of a mineralocorticoid hormone, called fludrocortisone acetate (Florinef), taken once or twice daily. People with secondary adrenal insufficiency normally maintain aldosterone production, so they do not require aldosterone replacement therapy.\n                \nDuring adrenal crisis, low blood pressure, low blood glucose, low blood sodium, and high blood levels of potassium can be life threatening. Standard therapy involves immediate IV injections of corticosteroids and large volumes of IV saline solution with dextrose, a type of sugar. This treatment usually brings rapid improvement. When the patient can take liquids and medications by mouth, the amount of corticosteroids is decreased until a dose that maintains normal hormone levels is reached. If aldosterone is deficient, the person will need to regularly take oral doses of fludrocortisone acetate.\n                \nResearchers have found that using replacement therapy for DHEA in adolescent girls who have secondary adrenal insufficiency and low levels of DHEA can improve pubic hair development and psychological stress. Further studies are needed before routine supplementation recommendations can be made."}
{"_id":"78872464-09d1-4d40-a0a7-f48bb6c78317","text":"Adrenal crisis is treated with adrenal hormones. People with adrenal crisis need immediate treatment. Any delay can cause death. When people with adrenal crisis are vomiting or unconscious and cannot take their medication, the hormones can be given as an injection.\n                \nA person with adrenal insufficiency should carry a corticosteroid injection at all times and make sure that others know how and when to administer the injection, in case the person becomes unconscious.\n                \nThe dose of corticosteroid needed may vary with a persons age or size. For example, a child younger than 2 years of age can receive 25 milligrams (mg), a child between 2 and 8 years of age can receive 50 mg, and a child older than 8 years should receive the adult dose of 100 mg."}
{"_id":"0adb1973-1757-4bf8-a5f3-b0394d9a2e62","text":"The following steps can help a person prevent adrenal crisis:\n                \n- Ask a health care provider about possibly having a shortage of adrenal hormones, if always feeling tired, weak, or losing weight.   - Learn how to increase the dose of corticosteroid for adrenal insufficiency when ill. Ask a health care provider for written instructions for sick days. First discuss the decision to increase the dose with the health care provider when ill.   - When very ill, especially if vomiting and not able to take pills, seek emergency medical care immediately."}
{"_id":"ac2559ff-3266-4981-844d-54cc84a76b0f","text":"Some people with Addisons disease who are aldosterone deficient can benefit from following a diet rich in sodium. A health care provider or a dietitian can give specific recommendations on appropriate sodium sources and daily sodium guidelines if necessary.\n                \nCorticosteroid treatment is linked to an increased risk of osteoporosisa condition in which the bones become less dense and more likely to fracture. People who take corticosteroids should protect their bone health by consuming enough dietary calcium and vitamin D. A health care provider or a dietitian can give specific recommendations on appropriate daily calcium intake based upon age and suggest the best types of calcium supplements, if necessary."}
{"_id":"8b3b902f-b4f4-468e-a555-ee520d9c7633","text":"- Adrenal insufficiency is an endocrine, or hormonal, disorder that occurs when the adrenal glands do not produce enough of certain hormones.   - Addisons disease, the common term for primary adrenal insufficiency, occurs when the adrenal glands are damaged and cannot produce enough of the adrenal hormone cortisol. The adrenal hormone aldosterone may also be lacking.   - Secondary adrenal insufficiency occurs when the pituitary gland fails to produce enough adrenocorticotropin (ACTH), a hormone that stimulates the adrenal glands to produce cortisol. If ACTH output is too low, cortisol production drops.   - The most common symptoms of adrenal insufficiency are chronic fatigue, muscle weakness, loss of appetite, weight loss, and abdominal pain. The slowly progressing symptoms are often ignored until a stressful event, such as surgery, a severe injury, an illness, or pregnancy, causes them to worsen.   - If not treated, an adrenal crisis can cause death.   - A diagnosis of adrenal insufficiency is confirmed through hormonal blood and urine tests. Imaging studies of the adrenal and pituitary glands can be useful in helping to establish the cause.   - Adrenal insufficiency is treated by replacing, or substituting, the hormones that the adrenal glands are not making.   - Problems can occur in people with adrenal insufficiency who are undergoing surgery, suffer a severe injury, have an illness, or are pregnant. These conditions place additional stress on the body, and people with adrenal insufficiency may need additional treatment to respond and recover.   - People with adrenal insufficiency should always carry identification stating their condition, adrenal insufficiency, in case of an emergency, as well as the supplies necessary to administer an emergency corticosteroid injection."}
{"_id":"39cd1cf6-e13a-48bb-a2f5-e088f42bd88b","text":"Hypothyroidism is a disorder that occurs when the thyroid gland does not make enough thyroid hormone to meet the bodys needs. Thyroid hormone regulates metabolismthe way the body uses energyand affects nearly every organ in the body. Without enough thyroid hormone, many of the bodys functions slow down. About 4.6 percent of the U.S. population age 12 and older has hypothyroidism.1"}
{"_id":"0f045d14-0adc-4ba7-9ea8-cc1fd49c845d","text":"The thyroid is a 2-inch-long, butterfly-shaped gland weighing less than 1 ounce. Located in the front of the neck below the larynx, or voice box, it has two lobes, one on each side of the windpipe. The thyroid is one of the glands that make up the endocrine system. The glands of the endocrine system produce and store hormones and release them into the bloodstream. The hormones then travel through the body and direct the activity of the bodys cells.\n                \nThe thyroid gland makes two thyroid hormones, triiodothyronine (T3) and thyroxine (T4). T3 is made from T4 and is the more active hormone, directly affecting the tissues. Thyroid hormones affect metabolism, brain development, breathing, heart and nervous system functions, body temperature, muscle strength, skin dryness, menstrual cycles, weight, and cholesterol levels."}
{"_id":"3985365a-4aad-4563-a77f-48180708639f","text":"Hypothyroidism has several causes, including\n                \n- Hashimotos disease  - thyroiditis, or inflammation of the thyroid  - congenital hypothyroidism, or hypothyroidism that is present at birth  - surgical removal of part or all of the thyroid  - radiation treatment of the thyroid  - some medications\n                \nLess commonly, hypothyroidism is caused by too much or too little iodine in the diet or by abnormalities of the pituitary gland.\n                \nHashimotos Disease\n                \nHashimotos disease, also called chronic lymphocytic thyroiditis, is the most common cause of hypothyroidism in the United States.1 Hashimotos disease is a form of chronic inflammation of the thyroid gland. Hashimotos disease is also an autoimmune disorder.\n                \nNormally, the immune system protects the body against foreign invaderssuch as viruses and bacteriathat can cause illness. But in autoimmune diseases, the immune system attacks the bodys own cells and organs. With Hashimotos disease, the immune system attacks the thyroid, causing inflammation and interfering with its ability to produce thyroid hormones.\n                \nMore information is provided in the NIDDK health topic, Hashimotos Disease.\n                \nThyroiditis\n                \nThyroiditis causes stored thyroid hormone to leak out of the thyroid gland. At first, the leakage raises hormone levels in the blood, leading to hyperthyroidismwhen thyroid hormone levels are too highthat lasts for 1 or 2 months. Most people then develop hypothyroidism before the thyroid is completely healed.\n                \nSeveral types of thyroiditis can cause hyperthyroidism followed by hypothyroidism:\n                \n- Subacute thyroiditis. This condition involves painful inflammation and enlargement of the thyroid. Experts are not sure what causes subacute thyroiditis, but it may be related to a viral or bacterial infection. The condition usually goes away on its own in a few months.  - Postpartum thyroiditis. This type of thyroiditis develops after a woman gives birth. For more information, see the section titled What happens with pregnancy and thyroid conditions?  - Silent thyroiditis. This type of thyroiditis is called silent because it is painless, as is postpartum thyroiditis, even though the thyroid may be enlarged. Like postpartum thyroiditis, silent thyroiditis is probably an autoimmune condition and sometimes develops into permanent hypothyroidism.\n                \nCongenital Hypothyroidism\n                \nSome babies are born with a thyroid that is not fully developed or does not function properly. If untreated, congenital hypothyroidism can lead to mental retardation and growth failure. Early treatment can prevent these complications, so most newborns in the United States are screened for hypothyroidism.\n                \nSurgical Removal of the Thyroid\n                \nWhen part of the thyroid is removed, the remaining part may produce normal amounts of thyroid hormone, but some people who have this surgery develop hypothyroidism. Removal of the entire thyroid always results in hypothyroidism.\n                \nPart or all of the thyroid may be surgically removed as a treatment for\n                \n- hyperthyroidism  - a large goiter, which is an enlarged thyroid that may cause the neck to appear swollen and can interfere with normal breathing and swallowing  - thyroid nodules, which are noncancerous tumors, called adenomas, or lumps in the thyroid that can produce excess thyroid hormone  - thyroid cancer\n                \nRadiation Treatment of the Thyroid\n                \nRadioactive iodine, a common treatment for hyperthyroidism, gradually destroys the cells of the thyroid. Most people who receive radioactive iodine treatment eventually develop hypothyroidism. People with Hodgkins disease, other lymphomas, and head or neck cancers are treated with radiation, which can also damage the thyroid.\n                \nMedications\n                \nSome drugs can interfere with thyroid hormone production and lead to hypothyroidism, including\n                \n- amiodarone, a heart medication  - interferon alpha, a cancer medication  - lithium, a bipolar disorder medication  - interleukin-2, a kidney cancer medication"}
{"_id":"edb421ac-b700-437a-9b15-1756c326464e","text":"Hypothyroidism has many symptoms that can vary from person to person. Some common symptoms of hypothyroidism are\n                \n- fatigue  - weight gain  - a puffy face  - cold intolerance  - joint and muscle pain  - constipation  - dry skin  - dry, thinning hair  - decreased sweating  - heavy or irregular menstrual periods and impaired fertility  - depression  - slowed heart rate\n                \nHowever, hypothyroidism develops slowly, so many people dont notice symptoms of the disease.\n                \nSymptoms more specific to Hashimotos disease are a goiter and a feeling of fullness in the throat.\n                \nHypothyroidism can contribute to high cholesterol, so people with high cholesterol should be tested for hypothyroidism. Rarely, severe, untreated hypothyroidism may lead to myxedema coma, an extreme form of hypothyroidism in which the bodys functions slow to the point that it becomes life threatening. Myxedema requires immediate medical treatment."}
{"_id":"7f697f1c-d592-49a0-b46c-1e07b0ae6327","text":"Many symptoms of hypothyroidism are the same as those of other diseases, so hypothyroidism usually cannot be diagnosed based on symptoms alone. With suspected hypothyroidism, health care providers take a medical history and perform a thorough physical examination. Health care providers may then use several blood tests to confirm a diagnosis of hypothyroidism and find its cause:\n                \nTSH test. The ultrasensitive TSH test is usually the first test a health care provider performs. This test detects even tiny amounts of TSH in the blood and is the most accurate measure of thyroid activity available. Generally, a TSH reading above normal means a person has hypothyroidism and a reading below normal means a person has hyperthyroidism.\n                \nMildly elevated TSH without symptoms indicates subclinical hypothyroidism. Some health care providers treat subclinical hypothyroidism immediately. Others prefer to leave it untreated but monitor their patients for signs that the condition is worsening.\n                \nHealth care providers may conduct additional tests to help confirm the diagnosis or determine the cause of hypothyroidism.\n                \nT4 test. This test measures the actual amount of circulating thyroid hormone in the blood. In hypothyroidism, the level of T4 in the blood is lower than normal.\n                \nThyroid autoantibody test. This test looks for the presence of thyroid autoantibodies. Most people with Hashimotos disease have these antibodies, but people whose hypothyroidism is caused by other conditions do not.\n                \nMore information about testing for thyroid problems is provided in the NIDDK health topic, Thyroid Tests."}
{"_id":"6767fa49-da24-4925-832a-318542022bcb","text":"Health care providers treat hypothyroidism with synthetic thyroxine, a medication that is identical to the hormone T4. The exact dose will depend on the patients age and weight, the severity of the hypothyroidism, the presence of other health problems, and whether the person is taking other drugs that might interfere with how well the body uses thyroid hormone.\n                \nHealth care providers test TSH levels about 6 to 8 weeks after a patient begins taking thyroid hormone and make any necessary adjustments to the dose. Each time the dose is adjusted, the blood is tested again. Once a stable dose is reached, blood tests are normally repeated in 6 months and then once a year.\n                \nHypothyroidism can almost always be completely controlled with synthetic thyroxine, as long as the recommended dose is taken every day as instructed."}
{"_id":"e2a5db2b-2b18-4792-88df-a41afda0e607","text":"Experts recommend that people eat a balanced diet to obtain most nutrients. More information about diet and nutrition can be found on the National Agricultural Library website at www.nutrition.gov.\n                \nDietary Supplements\n                \nIodine is an essential mineral for the thyroid. However, people with autoimmune thyroid disease may be sensitive to harmful side effects from iodine. Taking iodine drops or eating foods containing large amounts of iodinesuch as seaweed, dulse, or kelpmay cause or worsen hypothyroidism or hyperthyroidism. More information about iodine can be found in the National Library of Medicine fact sheet Iodine in diet, available at www.nlm.nih.gov\/medlineplus\/ency\/article\/002421.htm.\n                \nWomen need more iodine when they are pregnantabout 250 micrograms a day because the baby gets iodine from the mothers diet. In the United States, about 7 percent of pregnant women may not get enough iodine in their diet or through prenatal vitamins.3 Choosing iodized salt salt supplemented with iodineover plain salt and prenatal vitamins containing iodine will ensure this need is met.\n                \nTo help ensure coordinated and safe care, people should discuss their use of dietary supplements, such as iodine, with their health care provider. Tips for talking with health care providers are available through the National Center for Complementary and Integrative Health."}
{"_id":"61d14e6b-8fb9-49f9-b782-1c8e8e9ee2d9","text":"- Hypothyroidism is a disorder that occurs when the thyroid gland does not make enough thyroid hormone to meet the bodys needs. Thyroid hormone regulates metabolism. Without enough thyroid hormone, many of the bodys functions slow down.  - Hypothyroidism has several causes, including      - Hashimotos disease    - thyroiditis    - congenital hypothyroidism    - surgical removal of part or all of the thyroid    - radiation treatment of the thyroid    - some medications    - Hypothyroidism has many symptoms that can vary from person to person. Some common symptoms of hypothyroidism are fatigue, weight gain, cold intolerance, constipation, impaired fertility, and depression.  - Women are much more likely than men to develop hypothyroidism.  - Women with hypothyroidism should discuss their condition with their health care provider before becoming pregnant.  - Hypothyroidism can almost always be completely controlled with synthetic thyroxine, as long as the recommended dose is taken every day as instructed."}
{"_id":"6d783b5d-ee79-42c4-b39c-0a7b2bac1194","text":"A UTI is an infection in the urinary tract. Infections are caused by microbesorganisms too small to be seen without a microscopeincluding fungi, viruses, and bacteria. Bacteria are the most common cause of UTIs. Normally, bacteria that enter the urinary tract are rapidly removed by the body before they cause symptoms. However, sometimes bacteria overcome the bodys natural defenses and cause infection. An infection in the urethra is called urethritis. A bladder infection is called cystitis. Bacteria may travel up the ureters to multiply and infect the kidneys. A kidney infection is called pyelonephritis."}
{"_id":"2faa56e8-aca9-4cc5-bb0e-ec0a3c62b396","text":"The urinary tract is the body's drainage system for removing wastes and extra water. The urinary tract includes two kidneys, two ureters, a bladder, and a urethra. The kidneys are a pair of bean-shaped organs, each about the size of a fist and located below the ribs, one on each side of the spine, toward the middle of the back. Every minute, a persons kidneys filter about 3 ounces of blood, removing wastes and extra water. The wastes and extra water make up the 1 to 2 quarts of urine a person produces each day. The urine travels from the kidneys down two narrow tubes called the ureters. The urine is then stored in a balloonlike organ called the bladder and emptied through the urethra, a tube at the bottom of the bladder.\n                \nWhen the bladder empties, a muscle called the sphincter relaxes and urine flows out of the body through the urethra. The opening of the urethra is at the end of the penis in males and in front of the vagina in females."}
{"_id":"131802a5-e5de-407b-8ab9-d662a533831e","text":"Most UTIs are caused by bacteria that live in the bowel. The bacterium Escherichia coli (E. coli) causes the vast majority of UTIs. Microbes called Chlamydia and Mycoplasma can infect the urethra and reproductive system but not the bladder. Chlamydia and Mycoplasma infections may be sexually transmitted and require treatment of sexual partners.\n                \nThe urinary tract has several systems to prevent infection. The points where the ureters attach to the bladder act like one-way valves to prevent urine from backing up toward the kidneys, and urination washes microbes out of the body. In men, the prostate gland produces secretions that slow bacterial growth. In both sexes, immune defenses also prevent infection. But despite these safeguards, infections still occur. Certain bacteria have a strong ability to attach themselves to the lining of the urinary tract."}
{"_id":"a4d6aac7-4624-46f4-9a8f-3054fc20fab0","text":"Urinary tract infections are the second most common type of infection in the body, accounting for about 8.1 million visits to health care providers each year.1 Women are especially prone to UTIs for anatomical reasons. One factor is that a womans urethra is shorter, allowing bacteria quicker access to the bladder. Also, a womans urethral opening is near sources of bacteria from the anus and vagina. For women, the lifetime risk of having a UTI is greater than 50 percent.2 UTIs in men are not as common as in women but can be serious when they occur."}
{"_id":"b7e5612d-af00-4e2c-a1e1-c3572e94662e","text":"Although everyone has some risk, some people are more prone to getting UTIs than others. People with spinal cord injuries or other nerve damage around the bladder have difficulty emptying their bladder completely, allowing bacteria to grow in the urine that stays in the bladder. Anyone with an abnormality of the urinary tract that obstructs the flow of urinea kidney stone or enlarged prostate, for exampleis at risk for a UTI. People with diabetes or problems with the bodys natural defense system are more likely to get UTIs.\n                \nSexual activity can move microbes from the bowel or vaginal cavity to the urethral opening. If these microbes have special characteristics that allow them to live in the urinary tract, it is harder for the body to remove them quickly enough to prevent infection. Following sexual intercourse, most women have a significant number of bacteria in their urine, but the body normally clears them within 24 hours. However, some forms of birth control increase the risk of UTI. In some women, certain spermicides may irritate the skin, increasing the risk of bacteria invading surrounding tissues. Using a diaphragm may slow urinary flow and allow bacteria to multiply. Condom use is also associated with increased risk of UTIs, possibly because of the increased trauma that occurs to the vagina during sexual activity. Using spermicides with diaphragms and condoms can increase risk even further.\n                \nAnother common source of infection is catheters, or tubes, placed in the urethra and bladder. Catheters interfere with the bodys ability to clear microbes from the urinary tract. Bacteria travel through or around the catheter and establish a place where they can thrive within the bladder. A person who cannot urinate in the normal way or who is unconscious or critically ill often needs a catheter for more than a few days. The Infectious Diseases Society of America recommends using catheters for the shortest time possible to reduce the risk of a UTI.3\n                \nRecurrent Infections\n                \nMany women suffer from frequent UTIs. About 20 percent of young women with a first UTI will have a recurrent infection.4 With each UTI, the risk that a woman will continue having recurrent UTIs increases.5 Some women have three or more UTIs a year. However, very few women will have frequent infections throughout their lives. More typically, a woman will have a period of 1 or 2 years with frequent infections, after which recurring infections cease.\n                \nMen are less likely than women to have a first UTI. But once a man has a UTI, he is likely to have another because bacteria can hide deep inside prostate tissue. Anyone who has diabetes or a problem that makes it hard to urinate may have repeat infections.\n                \nResearch funded by the National Institutes of Health (NIH) suggests that one factor behind recurrent UTIs may be the ability of bacteria to attach to cells lining the urinary tract. One NIH-funded study found that bacteria formed a protective film on the inner lining of the bladder in mice.6 If a similar process can be demonstrated in humans, the discovery may lead to new treatments to prevent recurrent UTIs. Another line of research has indicated that women who are nonsecretors of certain blood group antigens may be more prone to recurrent UTIs because the cells lining the vagina and urethra may allow bacteria to attach more easily. A nonsecretor is a person with an A, B, or AB blood type who does not secrete the normal antigens for that blood type in bodily fluids, such as fluids that line the bladder wall.7\n                \nInfections during Pregnancy\n                \nPregnant women seem no more prone to UTIs than other women. However, when a UTI does occur in a pregnant woman, it is more likely to travel to the kidneys. According to some reports, about 4 to 5 percent of pregnant women develop a UTI.8 Scientists think that hormonal changes and shifts in the position of the urinary tract during pregnancy make it easier for bacteria to travel up the ureters to the kidneys and cause infection. For this reason, health care providers routinely screen pregnant women for bacteria in the urine during the first 3 months of pregnancy."}
{"_id":"fa6ae694-f0e5-4ca4-a210-0d397d51ab14","text":"Symptoms of a UTI vary by age, gender, and whether a catheter is present. Among young women, UTI symptoms typically include a frequent and intense urge to urinate and a painful, burning feeling in the bladder or urethra during urination. The amount of urine may be very small. Older women and men are more likely to be tired, shaky, and weak and have muscle aches and abdominal pain. Urine may look cloudy, dark, or bloody or have a foul smell. In a person with a catheter, the only symptom may be fever that cannot be attributed to any other cause. Normally, UTIs do not cause fever if they are in the bladder. A fever may mean the infection has reached the kidneys or has penetrated the prostate. Other symptoms of a kidney infection include pain in the back or side below the ribs, nausea, and vomiting."}
{"_id":"9893b3a8-2139-4ead-b412-da678b88e02a","text":"To find out whether a person has a UTI, the health care provider will ask about urinary symptoms and then test a sample of urine for the presence of bacteria and white blood cells, which are produced by the body to fight infection. Because bacteria can be found in the urine of healthy individuals, a UTI is diagnosed based both on symptoms and a laboratory test. The person will be asked to give a clean catch urine sample by washing the genital area and collecting a midstream sample of urine in a sterile container. This method of collecting urine helps prevent bacteria around the genital area from getting into the sample and confusing the test results. Usually, the sample is sent to a laboratory, although some health care providers offices are equipped to do the testing. For people with recurring infections and patients in the hospital, the urine may be cultured. The culture is performed by placing part of the urine sample in a tube or dish with a substance that encourages any bacteria present to grow. Once the bacteria have multiplied, which usually takes 1 to 3 days, they can be identified. The health care provider may also order a sensitivity test, which tests the bacteria for sensitivity to different antibiotics to see which medication is best for treating the infection.\n                \nIf a person has recurrent UTIs, the health care provider may order some additional tests to determine if the persons urinary tract is normal.\n                \nKidney and bladder ultrasound. Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. The procedure is performed in a health care providers office, outpatient center, or hospital by a specially trained technician, and the images are interpreted by a radiologista doctor who specializes in medical imaging; anesthesia is not needed. The images can show abnormalities in the kidneys and bladder. However, this test cannot reveal all important urinary abnormalities or measure how well the kidneys work.\n                \nVoiding cystourethrogram. This test is an x-ray image of the bladder and urethra taken while the bladder is full and during urination, also called voiding. As the person lies on the x-ray table, a health care provider inserts the tip of a thin, flexible tube called a catheter through the urethra into the bladder. The bladder and urethra are filled with a special dye called contrast medium, to make the structures clearly visible on the x-ray images. The x rays are taken from various angles while the bladder is full of contrast medium. The catheter is then removed and x-ray images are taken during urination. The procedure is performed in a health care providers office, outpatient center, or hospital by an x-ray technician. The technician is supervised by a radiologist while the images are taken. The radiologist then interprets the images. Anesthesia is not needed, but light sedation may be used for some people. This test can show abnormalities of the inside of the urethra and bladder. The test can also determine whether the flow of urine is normal when the bladder empties.\n                \nComputerized tomography (CT) scan. CT scans use a combination of x rays and computer technology to create three-dimensional (3-D) images. A CT scan may include the injection of contrast medium. CT scans require the person to lie on a table that slides into a tunnel-shaped device where the x rays are taken. The procedure is performed in an outpatient center or hospital by an x-ray technician, and the images are interpreted by a radiologist; anesthesia is not needed. CT scans can provide clearer, more detailed images to help the health care provider understand the problem.\n                \nMagnetic resonance imaging (MRI). MRI machines use radio waves and magnets to produce detailed pictures of the bodys internal organs and soft tissues without using x rays. An MRI may include an injection of contrast medium. With most MRI machines, the person lies on a table that slides into a tunnel-shaped device that may be open ended or closed at one end; some newer machines are designed to allow the person to lie in a more open space. The procedure is performed in an outpatient center or hospital by a specially trained technician, and the images are interpreted by a radiologist; anesthesia is not needed though light sedation may be used for people with a fear of confined spaces. Like CT scans, MRIs can provide clearer, more detailed images.\n                \nRadionuclide scan. A radionuclide scan is an imaging technique that relies on the detection of small amounts of radiation after injection of radioactive chemicals. Because the dose of the radioactive chemicals is small, the risk of causing damage to cells is low. Special cameras and computers are used to create images of the radioactive chemicals as they pass through the kidneys. Radionuclide scans are performed in a health care providers office, outpatient center, or hospital by a specially trained technician, and the images are interpreted by a radiologist; anesthesia is not needed. Radioactive chemicals injected into the blood can provide information about kidney function. Radioactive chemicals can also be put into the fluids used to fill the bladder and urethra for x ray, MRI, and CT imaging.\n                \nUrodynamics. Urodynamic testing is any procedure that looks at how well the bladder, sphincters, and urethra are storing and releasing urine. Most of these tests are performed in the office of a urologista doctor who specializes in urinary problemsby a urologist, physician assistant, or nurse practitioner. Some procedures may require light sedation to keep a person calm. Most urodynamic tests focus on the bladders ability to hold urine and empty steadily and completely. Urodynamic tests can also show whether the bladder is having abnormal contractions that cause leakage. A health care provider may order these tests if there is evidence that the person has some kind of nerve damage.\n                \nCystoscopy. Cystoscopy is a procedure that uses a tubelike instrument to look inside the urethra and bladder. Cystoscopy is performed by a doctor in a health care providers office, outpatient facility, or hospital with local anesthesia. However, in some cases, sedation and regional or general anesthesia are needed. Cystoscopy may be used to look for swelling, redness, and other signs of infection."}
{"_id":"67262264-6ef5-4978-8f40-c09da911170a","text":"Most UTIs are caused by bacteria, which are treated with bacteria-fighting medications called antibiotics or antimicrobials. The choice of medication and length of treatment depend on the patients history and the type of bacteria causing the infection. Some antibiotics may be ruled out if a person has allergies to them. The sensitivity test takes 48 hours to complete and is especially useful in helping the health care provider select the antibiotic most likely to be effective in treating an infection. Longer treatment may be needed if the first antibiotic given is not effective.\n                \nWhen a UTI occurs in a healthy person with a normal, unobstructed urinary tract, the term uncomplicated is used to describe the infection. Most young women who have UTIs have uncomplicated UTIs, which can be cured with 2 or 3 days of treatment. Single-dose treatment is less effective. Longer treatment causes more side effects and is not more effective. A follow-up urinalysis helps to confirm the urinary tract is infection-free. Taking the full course of treatment is important because symptoms may disappear before the infection is fully cleared.\n                \nComplicated UTIs occur when a personfor example, a pregnant woman or a transplant patientis weakened by another condition. A UTI is also complicated when the person has a structural or functional abnormality of the urinary tract, such as an obstructive kidney stone or prostate enlargement that squeezes the urethra. Health care providers should assume that men and boys have a complicated UTI until proven otherwise.\n                \nSeverely ill patients with kidney infections may be hospitalized until they can take fluids and needed medications on their own. Kidney infections may require several weeks of antibiotic treatment. Kidney infections in adults rarely lead to kidney damage or kidney failure unless they go untreated or are associated with urinary tract obstruction.\n                \nBladder infections are generally self-limiting, but antibiotic treatment significantly shortens the duration of symptoms. People usually feel better within a day or two of treatment. Symptoms of kidney and prostate infections last longer. Drinking lots of fluids and urinating frequently will speed healing. If needed, various medications are available to relieve the pain of a UTI. A heating pad on the back or abdomen may also help.\n                \nRecurrent Infections in Women\n                \nHealth care providers may advise women who have recurrent UTIs to try one of the following treatment options:\n                \n- Take low doses of the prescribed antibiotic daily for 6 months or longer. If taken at bedtime, the medication remains in the bladder longer and may be more effective. NIH-supported research has shown this therapy to be effective without causing serious side effects.  - Take a single dose of an antibiotic after sexual intercourse.  - Take a short course2 or 3 daysof an antibiotic when symptoms appear.\n                \nTo try to prevent an infection, health care providers may suggest women\n                \n- drink plenty of water every day  - urinate when the need arises and avoid resisting the urge to urinate  - urinate after sexual intercourse  - switch to a different method of birth control if recurring UTIs are a problem\n                \nInfections during Pregnancy\n                \nDuring pregnancy, bacterial infection of the urineeven in the absence of symptomscan pose risks to both the mother and the baby. Some antibiotics are not safe to take during pregnancy. In selecting the best treatments, health care providers consider various factors such as the medications effectiveness, the stage of pregnancy, the mothers health, and potential effects on the fetus.\n                \nComplicated Infections\n                \nCuring infections that stem from a urinary obstruction or other systemic disorder depends on finding and correcting the underlying problem, sometimes with surgery. If the root cause goes untreated, this group of patients is at risk for kidney damage. Also, such infections tend to arise from a wider range of bacteria and sometimes from more than one type of bacteria at a time.\n                \nInfections in Men\n                \nUrinary tract infections in men are often the result of an obstructionfor example, a urinary stone or enlarged prostateor are from a catheter used during a medical procedure. The first step in treating such an infection is to identify the infecting organism and the medications to which it is sensitive.\n                \nProstate infectionschronic bacterial prostatitisare harder to cure because antibiotics may be unable to penetrate infected prostate tissue effectively. For this reason, men with bacterial prostatitis often need long-term treatment with a carefully selected antibiotic. UTIs in men are frequently associated with acute bacterial prostatitis, which can be life threatening if not treated urgently."}
{"_id":"17c9ce0c-be4e-43b4-bfa7-d89f3680391c","text":"Changing some daily habits may help a person prevent recurrent UTIs.\n                \nEating, Diet, and Nutrition\n                \nDrinking lots of fluid can help flush bacteria from the system. Water is best. Most people should try for six to eight, 8-ounce glasses a day. Talk with your health care provider if you cant drink the recommended amount due to other health problems, such as urinary incontinence, urinary frequency, or kidney failure.\n                \nUrination Habits\n                \nA person should urinate often and when the urge arises. Bacteria can grow when urine stays in the bladder too long. Women and men should urinate shortly after sex to flush away bacteria that might have entered the urethra during sex. Drinking a glass of water will also help flush bacteria away.\n                \nAfter using the toilet, women should wipe from front to back. This step is most important after a bowel movement to keep bacteria from getting into the urethra.\n                \nClothing\n                \nCotton underwear and loose-fitting clothes should be worn, so air can keep the area around the urethra dry. Tight-fitting jeans and nylon underwear should be avoided because they can trap moisture and help bacteria grow.\n                \nBirth Control\n                \nFor women, using a diaphragm or spermicide for birth control can lead to UTIs by increasing bacteria growth. A woman who has trouble with UTIs should try switching to a new form of birth control. Unlubricated condoms or spermicidal condoms increase irritation, which may help bacteria grow. Switching to lubricated condoms without spermicide or using a nonspermicidal lubricant may help prevent UTIs."}
{"_id":"178f8ce9-5d94-4097-bd9e-b70f6f82c968","text":"- Most urinary tract infections (UTIs) arise from one type of bacteria, Escherichia coli (E. coli), which normally lives in the bowel.  - Symptoms of a UTI in adults may include the following:      - a frequent and intense urge to urinate    - a painful, burning feeling in the bladder or urethra during urination    - feeling tired, shaky, and weak    - muscle aches    - abdominal pain    - only small amounts of urine passed, despite a strong urge to urinate    - cloudy, dark, or bloody urine or urine that has a foul smell    - pain in the back or side below the ribs    - nausea and vomiting    - Fever may indicate a kidney or prostate infection.  - Because bacteria can be found in the urine of healthy individuals, a UTI is diagnosed based both on symptoms and a laboratory test.  - UTIs are treated with bacteria-fighting medications called antibiotics or antimicrobials."}
{"_id":"851b6f50-3f96-490e-befe-1e0ef157182c","text":"Diabetes is a complex group of diseases with a variety of causes. People with diabetes have high blood glucose, also called high blood sugar or hyperglycemia.\n                \nDiabetes is a disorder of metabolismthe way the body uses digested food for energy. The digestive tract breaks down carbohydratessugars and starches found in many foodsinto glucose, a form of sugar that enters the bloodstream. With the help of the hormone insulin, cells throughout the body absorb glucose and use it for energy. Insulin is made in the pancreas, an organ located behind the stomach. As the blood glucose level rises after a meal, the pancreas is triggered to release insulin. Within the pancreas, clusters of cells called islets contain beta cells, which make the insulin and release it into the blood.\n                \nDiabetes develops when the body doesnt make enough insulin or is not able to use insulin effectively, or both. As a result, glucose builds up in the blood instead of being absorbed by cells in the body. The bodys cells are then starved of energy despite high blood glucose levels.\n                \nOver time, high blood glucose damages nerves and blood vessels, leading to complications such as heart disease, stroke, kidney disease, blindness, dental disease, and amputations. Other complications of diabetes may include increased susceptibility to other diseases, loss of mobility with aging, depression, and pregnancy problems.\n                \nMain Types of Diabetes\n                \nThe three main types of diabetes are type 1, type 2, and gestational diabetes:\n                \n- Type 1 diabetes, formerly called juvenile diabetes, is usually first diagnosed in children, teenagers, and young adults. In this type of diabetes, the beta cells of the pancreas no longer make insulin because the bodys immune system has attacked and destroyed them.  - Type 2 diabetes, formerly called adult-onset diabetes, is the most common type of diabetes. About 90 to 95 percent of people with diabetes have type 2.1 People can develop type 2 diabetes at any age, even during childhood, but this type of diabetes is most often associated with older age. Type 2 diabetes is also associated with excess weight, physical inactivity, family history of diabetes, previous history of gestational diabetes, and certain ethnicities.   Type 2 diabetes usually begins with insulin resistance, a condition linked to excess weight in which muscle, liver, and fat cells do not use insulin properly. As a result, the body needs more insulin to help glucose enter cells to be used for energy. At first, the pancreas keeps up with the added demand by producing more insulin. But in time, the pancreas loses its ability to produce enough insulin in response to meals, and blood glucose levels rise.  - Gestational diabetes is a type of diabetes that develops only during pregnancy.  The hormones produced during pregnancy increase the amount of insulin needed to control blood glucose levels. If the body cant meet this increased need for insulin, women can develop gestational diabetes during the late stages of pregnancy.  Gestational diabetes usually goes away after the baby is born. Shortly after pregnancy, 5 to 10 percent of women with gestational diabetes continue to have high blood glucose levels and are diagnosed as having diabetes, usually type 2.1 Research has shown that lifestyle changes and the diabetes medication, metformin, can reduce or delay the risk of type 2 diabetes in these women. Babies born to mothers who had gestational diabetes are also more likely to develop obesity and type 2 diabetes as they grow up.  More information about gestational diabetes is provided in the NIDDK health topic, What I need to know about Gestational Diabetes,or by calling 18008608747.\n                \nOther Types of Diabetes\n                \nMany other types of diabetes exist, and a person can exhibit characteristics of more than one type. For example, in latent autoimmune diabetes in adults, people show signs of both type 1 and type 2 diabetes. Other types of diabetes include those caused by genetic defects, diseases of the pancreas, excess amounts of certain hormones resulting from some medical conditions, medications that reduce insulin action, chemicals that destroy beta cells, infections, rare autoimmune disorders, and genetic syndromes associated with diabetes.\n                \nMore information about other types of diabetes is provided in the NIDDK health topic, Causes of Diabetes, or by calling 18008608747."}
{"_id":"32ecfafe-fa1f-4ba4-ad61-b0d4b6c80725","text":"Prediabetes is when blood glucose levels are higher than normal but not high enough for a diagnosis of diabetes. Prediabetes means a person is at increased risk for developing type 2 diabetes, as well as for heart disease and stroke. Many people with prediabetes develop type 2 diabetes within 10 years.\n                \nHowever, modest weight loss and moderate physical activity can help people with prediabetes delay or prevent type 2 diabetes."}
{"_id":"65fe210f-ccfd-4ca1-87fa-7620f328b775","text":"Blood tests are used to diagnosis diabetes and prediabetes because early in the disease type 2 diabetes may have no symptoms. All diabetes blood tests involve drawing blood at a health care providers office or commercial facility and sending the sample to a lab for analysis. Lab analysis of blood is needed to ensure test results are accurate. Glucose measuring devices used in a health care providers office, such as finger-stick devices, are not accurate enough for diagnosis but may be used as a quick indicator of high blood glucose.\n                \nTesting enables health care providers to find and treat diabetes before complications occur and to find and treat prediabetes, which can delay or prevent type 2 diabetes from developing.\n                \nAny one of the following tests can be used for diagnosis:*\n                \n- an A1C test, also called the hemoglobin A1c, HbA1c, or glycohemoglobin test  - a fasting plasma glucose (FPG) test  - an oral glucose tolerance test (OGTT)\n                \n*Not all tests are recommended for diagnosing all types of diabetes. See the individual test descriptions for details.\n                \nAnother blood test, the random plasma glucose (RPG) test, is sometimes used to diagnose diabetes during a regular health checkup. If the RPG measures 200 milligrams per deciliter or above, and the individual also shows symptoms of diabetes, then a health care provider may diagnose diabetes.\n                \nSymptoms of diabetes include\n                \n- increased urination  - increased thirst  - unexplained weight loss\n                \nOther symptoms can include fatigue, blurred vision, increased hunger, and sores that do not heal.\n                \nAny test used to diagnose diabetes requires confirmation with a second measurement unless clear symptoms of diabetes exist.\n                \nThe following table provides the blood test levels for diagnosis of diabetes for nonpregnant adults and diagnosis of prediabetes.\n                \nA1C Test\n                \nThe A1C test is used to detect type 2 diabetes and prediabetes but is not recommended for diagnosis of type 1 diabetes or gestational diabetes. The A1C test is a blood test that reflects the average of a persons blood glucose levels over the past 3 months and does not show daily fluctuations. The A1C test is more convenient for patients than the traditional glucose tests because it does not require fasting and can be performed at any time of the day.\n                \nThe A1C test result is reported as a percentage. The higher the percentage, the higher a persons blood glucose levels have been. A normal A1C level is below 5.7 percent.\n                \nAn A1C of 5.7 to 6.4 percent indicates prediabetes. People diagnosed with prediabetes may be retested in 1 year. People with an A1C below 5.7 percent maystill be at risk for diabetes, depending on the presence of other characteristics that put them at risk, also known as risk factors. People with an A1C above 6.0 percent should be considered at very high risk of developing diabetes. A level of 6.5 percent or above means a person has diabetes.\n                \nLaboratory analysis. When the A1C test is used for diagnosis, the blood sample must be sent to a laboratory using a method that is certified by the NGSP to ensure the results are standardized. Blood samples analyzed in a health care providers office, known as point-of-care tests, are not standardized for diagnosing diabetes.\n                \nAbnormal results. The A1C test can be unreliable for diagnosing or monitoring diabetes in people with certain conditions known to interfere with the results. Interference should be suspected when A1C results seem very different from the results of a blood glucose test. People of African, Mediterranean, or Southeast Asian descent or people with family members with sickle cell anemia or a thalassemia are particularly at risk of interference.\n                \nHowever, not all of the A1C tests are unreliable for people with these diseases. The NGSP provides information about which A1C tests are appropriate to use for specific types of interference and details on any problems with the A1C test at www.ngsp.org.\n                \nFalse A1C test results may also occur in people with other problems that affect their blood or hemoglobin such as chronic kidney disease, liver disease, or anemia.\n                \nMore information about limitations of the A1C test and different forms of sickle cell anemia is provided in the NIDDK health topic, For People of African, Mediterranean, or Southeast Asian Heritage: Important Information about Diabetes Blood Tests, or by calling 18008608747.\n                \nChanges in Diagnostic Testing\n                \nIn the past, the A1C test was used to monitor blood glucose levels but not for diagnosis. The A1C test has now been standardized, and in 2009, an international expert committee recommended it be used for diagnosis of type 2 diabetes and prediabetes.2\n                \nMore information about the A1C test is provided in the NIDDK health topic, The A1C Test and Diabetes, or by calling 18008608747.\n                \nFasting Plasma Glucose Test\n                \nThe FPG test is used to detect diabetes and prediabetes. The FPG test has been the most common test used for diagnosing diabetes because it is more convenient than the OGTT and less expensive. The FPG test measures blood glucose in a person who has fasted for at least 8 hours and is most reliable when given in the morning.\n                \nPeople with a fasting glucose level of 100 to 125 mg\/dL have impaired fasting glucose (IFG), or prediabetes. A level of 126 mg\/dL or above, confirmed by repeating the test on another day, means a person has diabetes.\n                \nOral Glucose Tolerance Test\n                \nThe OGTT can be used to diagnose diabetes, prediabetes, and gestational diabetes. Research has shown that the OGTT is more sensitive than the FPG test, but it is less convenient to administer. When used to test for diabetes or prediabetes, the OGTT measures blood glucose after a person fasts for at least 8 hours and 2 hours after the person drinks a liquid containing 75 grams of glucose dissolved in water.\n                \nIf the 2-hour blood glucose level is between 140 and 199 mg\/dL, the person has a type of prediabetes called impaired glucose tolerance (IGT). If confirmed by a second test, a 2-hour glucose level of 200 mg\/dL or above means a person has diabetes."}
{"_id":"fe5160a6-f10d-418d-9b31-f585fe4f8a6c","text":"Health care providers test for gestational diabetes using the OGTT. Women may be tested during their first visit to the health care provider after becoming pregnant or between 24 to 28 weeks of pregnancy depending on their risk factors and symptoms. Women found to have diabetes at the first visit to the health care provider after becoming pregnant may be diagnosed with type 2 diabetes.\n                \nDefining Safe Blood Glucose Levels for Pregnancy\n                \nMany studies have shown that gestational diabetes can cause complications for the mother and baby. An international, multicenter study, the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study, showed that the higher a pregnant womans blood glucose is, the higher her risk of pregnancy complications. The HAPO researchers found that pregnancy complications can occur at blood glucose levels that were once considered to be normal.\n                \nBased on the results of the HAPO study, new guidelines for diagnosis of gestational diabetes were recommended by the International Association of the Diabetes and Pregnancy Study Groups in 2011. So far, the new guidelines have been adopted by the American Diabetes Association (ADA)3 but not by the American College of Obstetricians and Gynecologists (ACOG)4 or other medical organizations. Researchers estimate these new guidelines, if widely adopted, will increase the proportion of pregnant women diagnosed with gestational diabetes to nearly 18 percent.5\n                \nBoth ADA and ACOG guidelines for using the OGTT in diagnosing gestational diabetes are shown in the following tables.\n                \nRecommendations for Testing Pregnant Women for Diabetes\n                \nTime of testing    ACOG    ADA        At first visit during pregnancy    No recommendation    Test women with risk factors for diabetes using standard testing for diagnosis of type 2 diabetes.  Women found to have diabetes at this time should be diagnosed with type 2 diabetes, not gestational diabetes.        At 24 to 28 weeks of pregnancy    Test women for diabetes based on their history, risk factors, or a 50-gram, 1-hour, nonfasting, glucose challenge testa modified OGTT.  If score is 130140 mg\/dL, test again with fasting, 100-gram, 3-hour OGTT.*    Test all women for diabetes who are not already diagnosed, using a fasting, 75-gram, 2-hour OGTT.*\n                \n\n                \nOGTT Levels for Diagnosis of Gestational Diabetes\n                \nTime of Sample Collection    ACOG Levels**,4 (mg\/dL)    ADA Levels3(mg\/dL)        100-gram Glucose Drink    75-gram Glucose Drink        Fasting, before drinking glucose    95 or above    92 or above        1 hour after drinking glucose    180 or above    180 or above        2 hours after drinking glucose    155 or above    153 or above        3 hours after drinking glucose    140 or above    Not used        Requirements for Diagnosis    TWO or more of the above levels must be met    ONE or more of the above levels must be met\n                \n\n                \n\n                \n\n                \nMore information about treating gestational diabetes is provided in the NIDDK health topic, What I need to know about Gestational Diabetes, or by calling 18008608747."}
{"_id":"8ff9472d-86f5-405d-8882-07f9ab4a070b","text":"A major research study, the Diabetes Prevention Program (DPP), proved that people with prediabetes were able to sharply reduce their risk of developing diabetes during the study by losing 5 to 7 percent of their body weight through dietary changes and increased physical activity.\n                \nStudy participants followed a low-fat, low-calorie diet and engaged in regular physical activity, such as walking briskly five times a week for 30 minutes. These strategies worked well for both men and women in all racial and ethnic groups, but were especially effective for participants age 60 and older. A follow-up study, the Diabetes Prevention Program Outcomes Study (DPPOS), showed losing weight and being physically active provide lasting results. Ten years after the DPP, modest weight loss delayed onset of type 2 diabetes by an average of 4 years.\n                \nThe diabetes medication metformin also lowers the risk of type 2 diabetes in people with prediabetes, especially those who are younger and heavier and women who have had gestational diabetes. The DPPOS showed that metformin delayed type 2 diabetes by 2 years. People at high risk should ask their health care provider if they should take metformin to prevent type 2 diabetes. Metformin is a medication that makes insulin work better and can reduce the risk of type 2 diabetes.\n                \nMore information about insulin resistance, the DPP, or how to lower risk for type 2 diabetes is provided in the NIDDK health topics:\n                \n- Am I at Risk for Type 2 Diabetes?  - Diabetes Prevention Program (DPP)  - Insulin Resistance and Prediabetes\n                \nAdditional information about the DPP, funded under NIH clinical trial number NCT00004992, and the DPPOS, funded under NIH clinical trial number NCT00038727, can be found at www.bsc.gwu.edu\/dpp.\n                \nAs part of its Small Steps, Big Rewards campaign, the National Diabetes Education Program (NDEP) offers several booklets about preventing type 2 diabetes, including information about setting goals, tracking progress, implementing a walking program, and finding additional resources. These materials are available at www.ndep.nih.gov or by calling the NDEP at 1888693NDEP (18886936337)."}
{"_id":"c9015fbc-cb94-414c-870e-efe8fa6a4272","text":"People can manage their diabetes with meal planning, physical activity, and if needed, medications. More information about taking care of type 1 or type 2 diabetes is provided in the NIDDK health topics:\n                \n- What I need to know about Diabetes Medicines  - What I need to know about Eating and Diabetes  - Your Guide to Diabetes: Type 1 and Type 2\n                \nThese NDIC publications are available at http:\/\/www.niddk.nih.gov\/health-information\/health-topics\/Diabetes\/Pages\/default.aspx or by calling 18008608747."}
{"_id":"561bf131-f6c8-4505-8e1a-8c964329a349","text":"- Tests used for diagnosing diabetes and prediabetes include the A1C testfor type 2 diabetes and prediabetesthe fasting plasma glucose (FPG) test, and the oral glucose tolerance test (OGTT). Another blood test, the random plasma glucose (RPG) test, is sometimes used to diagnose diabetes when symptoms are present during a regular health checkup.  - Anyone age 45 or older should consider getting tested for diabetes or prediabetes. People younger than 45 should consider testing if they are overweight or obese and have one or more additional risk factors for diabetes.  - If results of testing are normal, testing should be repeated at least every 3 years. Health care providers may recommend more frequent testing depending on initial results and risk status.  - People whose test results indicate they have prediabetes may be tested again in 1 year and should take steps to prevent or delay type 2 diabetes.  - Many people with prediabetes develop type 2 diabetes within 10 years.  - Modest weight loss and moderate physical activity can help people with prediabetes delay or prevent type 2 diabetes."}
{"_id":"9b97188b-cbf8-405e-813d-876f36e8225d","text":"Mntriers disease causes the ridges along the inside of the stomach wallcalled rugaeto enlarge, forming giant folds in the stomach lining. The rugae enlarge because of an overgrowth of mucous cells in the stomach wall.\n                \nIn a normal stomach, mucous cells in the rugae release protein-containing mucus. The mucous cells in enlarged rugae release too much mucus, causing proteins to leak from the blood into the stomach. This shortage of protein in the blood is known as hypoproteinemia. Mntriers disease also reduces the number of acid-producing cells in the stomach, which decreases stomach acid.\n                \nMntriers disease is also called Mntrier disease or hypoproteinemic hypertrophic gastropathy."}
{"_id":"399b1bb2-fb24-458b-900b-c3ee61573815","text":"Scientists are unsure about what causes Mntriers disease; however, researchers think that most people acquire, rather than inherit, the disease. In extremely rare cases, siblings have developed Mntriers disease as children, suggesting a genetic link.\n                \nStudies suggest that people with Mntriers disease have stomachs that make abnormally high amounts of a protein called transforming growth factor-alpha (TGF-).\n                \nTGF- binds to and activates a receptor called epidermal growth factor receptor. Growth factors are proteins in the body that tell cells what to do, such as grow larger, change shape, or divide to make more cells. Researchers have not yet found a cause for the overproduction of TGF-.\n                \nSome studies have found cases of people with Mntriers disease who also had Helicobacter pylori (H. pylori) infection. H. pylori is a bacterium that is a cause of peptic ulcers, or sores on the lining of the stomach or the duodenum, the first part of the small intestine. In these cases, treatment for H. pylori reversed and improved the symptoms of Mntriers disease.1\n                \nResearchers have linked some cases of Mntriers disease in children to infection with cytomegalovirus (CMV). CMV is one of the herpes viruses. This group of viruses includes the herpes simplex viruses, which cause chickenpox, shingles, and infectious mononucleosis, also known as mono. Most healthy children and adults infected with CMV have no symptoms and may not even know they have an infection. However, in people with a weakened immune system, CMV can cause serious disease, such as retinitis, which can lead to blindness.\n                \nResearchers are not sure how H. pylori and CMV infections contribute to the development of Mntriers disease."}
{"_id":"cb246406-a297-4b6a-a276-0ed3f84d000e","text":"Mntriers disease is rare. The disease is more common in men than in women. The average age at diagnosis is 55.2"}
{"_id":"7a79c2d4-f73b-4953-9590-eafdebc502dd","text":"The most common symptom of Mntriers disease is pain in the upper middle part of the abdomen. The abdomen is the area between the chest and hips.\n                \nOther signs and symptoms of Mntriers disease may include\n                \n- nausea and frequent vomiting  - diarrhea  - loss of appetite  - extreme weight loss  - malnutrition  - low levels of protein in the blood  - swelling of the face, abdomen, limbs, and feet due to low levels of protein in the blood  - anemiatoo few red blood cells in the body, which prevents the body from getting enough oxygendue to bleeding in the stomach\n                \nPeople with Mntriers disease have a higher chance of developing stomach cancer, also called gastric cancer."}
{"_id":"4503a845-8199-414a-8501-0a694e61f2e6","text":"Health care providers base the diagnosis of Mntriers disease on a combination of symptoms, lab findings, findings on upper gastrointestinal (GI) endoscopy, and stomach biopsy results. A health care provider will begin the diagnosis of Mntriers disease by taking a patients medical and family history and performing a physical exam. However, a health care provider will confirm the diagnosis of Mntriers disease through a computerized tomography (CT) scan, an upper GI endoscopy, and a biopsy of stomach tissue. A health care provider also may order blood tests to check for infection with H. pylori or CMV.\n                \nMedical and family history. Taking a medical and family history is one of the first things a health care provider may do to help diagnose Mntriers disease. He or she will ask the patient to provide a medical and family history.\n                \nPhysical exam. A physical exam may help diagnose Mntriers disease. During a physical exam, a health care provider usually\n                \n- examines a patients body  - uses a stethoscope to listen to bodily sounds  - taps on specific areas of the patients body\n                \nCT scan. CT scans use a combination of x rays and computer technology to create images. For a CT scan, a health care provider may give the patient a solution to drink and an injection of a special dye, called contrast medium. CT scans require the patient to lie on a table that slides into a tunnel-shaped device where an x-ray technician takes x rays. An x-ray technician performs the procedure in an outpatient center or a hospital, and a radiologista doctor who specializes in medical imaginginterprets them. The patient does not need anesthesia. CT scans can show enlarged folds in the stomach wall.\n                \nUpper GI endoscopy. This procedure involves using an endoscopea small, flexible tube with a lightto see the upper GI tract, which includes the esophagus, stomach, and duodenum. A gastroenterologista doctor who specializes in digestive diseasesperforms the test at a hospital or an outpatient center. The gastroenterologist carefully feeds the endoscope down the esophagus and into the stomach. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the stomach lining. The gastroenterologist also can take a biopsy of the stomach tissue during the endoscopy. A health care provider may give a patient a liquid anesthetic to gargle or may spray anesthetic on the back of the patients throat. A health care provider will place an intravenous (IV) needle in a vein in the arm to administer sedation. Sedatives help patients stay relaxed and comfortable. The test can show enlarged folds in the stomach wall.\n                \nBiopsy. Biopsy is a procedure that involves taking a piece of stomach tissue for examination with a microscope. A gastroenterologist performs the biopsy at the time of upper GI endoscopy. A pathologista doctor who specializes in diagnosing diseasesexamines the stomach tissue in a lab. The test can diagnose Mntriers disease by showing changes in the stomachs mucous cells and acid-producing cells.\n                \nBlood test. A health care provider will take a blood sample that can show the presence of infection with H. pylori or CMV. A blood test involves drawing blood at a health care providers office or a commercial facility and sending the sample to a lab for analysis."}
{"_id":"0f022b04-2b02-4897-8d72-6632e58e6316","text":"Treatment may include medications, IV protein, blood transfusions, and surgery.\n                \nMedications\n                \nHealth care providers may prescribe the anticancer medication cetuximab (Erbitux) to treat Mntriers disease. Studies have shown that cetuximab blocks the activity of epidermal growth factor receptor and can significantly improve a persons symptoms, as well as decrease the thickness of the stomach wall from the overgrowth of mucous cells. A person receives cetuximab by IV in a health care providers office or an outpatient center. Studies to assess the effectiveness of cetuximab to treat Mntriers disease are ongoing. A health care provider also may prescribe medications to relieve nausea and abdominal pain.\n                \nIn people with Mntriers disease who also have H. pylori or CMV infection, treatment of the infection may improve symptoms. Health care providers prescribe antibiotics to kill H. pylori. Antibiotic regimens may differ throughout the world because some strains of H. pylori have become resistant to certain antibioticsmeaning that an antibiotic that once destroyed the bacterium is no longer effective. Health care providers use antiviral medications to treat CMV infection in a person with a weakened immune system in order to prevent a serious disease from developing as a result of CMV. Antiviral medications cannot kill CMV; however, they can slow down the virus reproduction.\n                \nIntravenous Protein and Blood Transfusions\n                \nA health care provider may recommend an IV treatment of protein and a blood transfusion to a person who is malnourished or anemic because of Mntriers disease. In most cases of children with Mntriers disease who also have had CMV infection, treatment with protein and a blood transfusion led to a full recovery.\n                \nSurgery\n                \nIf a person has severe Mntriers disease with significant protein loss, a surgeon may need to remove part or all of the stomach in a surgery called gastrectomy.\n                \nSurgeons perform gastrectomy in a hospital. The patient will require general anesthesia. Some surgeons perform a gastrectomy through laparoscopic surgery rather than through a wide incision in the abdomen. In laparoscopic surgery, the surgeon uses several smaller incisions and feeds special surgical tools through the incisions to remove the diseased part of the stomach. After gastrectomy, the surgeon may reconstruct the changed portions of the GI tract so that it may continue to function. Usually the surgeon attaches the small intestine to any remaining portion of the stomach or to the esophagus if he or she removed the entire stomach."}
{"_id":"ffbb6136-cebe-4c76-95d7-0f08b33e2edb","text":"Researchers have not found that eating, diet, and nutrition play a role in causing or preventing Mntriers disease. In some cases, a health care provider may prescribe a high-protein diet to offset the loss of protein due to Mntriers disease. Some people with severe malnutrition may require IV nutrition, which is called total parenteral nutrition (TPN). TPN is a method of providing an IV liquid food mixture through a special tube in the chest."}
{"_id":"022547cf-8b5b-44b4-9f1d-a94561bdd1b9","text":"- Mntriers disease causes the ridges along the inside of the stomach wallcalled rugaeto enlarge, forming giant folds in the stomach lining. The rugae enlarge because of an overgrowth of mucous cells in the stomach wall.  - Scientists are unsure about what causes Mntriers disease; however, researchers think that most people acquire, rather than inherit, the disease.  - Mntriers disease is rare. The disease is more common in men than in women.  - The most common symptom of Mntriers disease is pain in the upper middle part of the abdomen.  - Health care providers base the diagnosis of Mntriers disease on a combination of symptoms, lab findings, findings on upper gastrointestinal (GI) endoscopy, and stomach biopsy results.  - Treatment may include medications, intravenous (IV) protein, blood transfusions, and surgery."}
{"_id":"c9ee3334-915d-4b9a-9f3a-5dd416abb55f","text":"An inguinal hernia happens when contents of the abdomenusually fat or part of the small intestinebulge through a weak area in the lower abdominal wall. The abdomen is the area between the chest and the hips. The area of the lower abdominal wall is also called the inguinal or groin region.\n                \nTwo types of inguinal hernias are\n                \n- indirect inguinal hernias, which are caused by a defect in the abdominal wall that is congenital, or present at birth  - direct inguinal hernias, which usually occur only in male adults and are caused by a weakness in the muscles of the abdominal wall that develops over time\n                \nInguinal hernias occur at the inguinal canal in the groin region."}
{"_id":"d4aba2d6-8d9e-4b4c-90e4-00a8561b288b","text":"The inguinal canal is a passage through the lower abdominal wall. People have two inguinal canalsone on each side of the lower abdomen. In males, the spermatic cords pass through the inguinal canals and connect to the testicles in the scrotumthe sac around the testicles. The spermatic cords contain blood vessels, nerves, and a duct, called the spermatic duct, that carries sperm from the testicles to the penis. In females, the round ligaments, which support the uterus, pass through the inguinal canals."}
{"_id":"1f9f4c14-445c-49a3-9655-8843ba842ba4","text":"The cause of inguinal hernias depends on the type of inguinal hernia.\n                \nIndirect inguinal hernias. A defect in the abdominal wall that is present at birth causes an indirect inguinal hernia.\n                \nDuring the development of the fetus in the womb, the lining of the abdominal cavity forms and extends into the inguinal canal. In males, the spermatic cord and testicles descend out from inside the abdomen and through the abdominal lining to the scrotum through the inguinal canal. Next, the abdominal lining usually closes off the entrance to the inguinal canal a few weeks before or after birth. In females, the ovaries do not descend out from inside the abdomen, and the abdominal lining usually closes a couple of months before birth.1\n                \nSometimes the lining of the abdomen does not close as it should, leaving an opening in the abdominal wall at the upper part of the inguinal canal. Fat or part of the small intestine may slide into the inguinal canal through this opening, causing a hernia. In females, the ovaries may also slide into the inguinal canal and cause a hernia.\n                \nIndirect hernias are the most common type of inguinal hernia.2 Indirect inguinal hernias may appear in 2 to 3 percent of male children; however, they are much less common in female children, occurring in less than 1 percent.3\n                \nDirect inguinal hernias. Direct inguinal hernias usually occur only in male adults as aging and stress or strain weaken the abdominal muscles around the inguinal canal. Previous surgery in the lower abdomen can also weaken the abdominal muscles.\n                \nFemales rarely form this type of inguinal hernia. In females, the broad ligament of the uterus acts as an additional barrier behind the muscle layer of the lower abdominal wall. The broad ligament of the uterus is a sheet of tissue that supports the uterus and other reproductive organs."}
{"_id":"5f63feee-2601-444d-82c2-4f8e4bade48b","text":"The first sign of an inguinal hernia is a small bulge on one or, rarely, on both sides of the grointhe area just above the groin crease between the lower abdomen and the thigh. The bulge may increase in size over time and usually disappears when lying down.\n                \nOther signs and symptoms can include\n                \n- discomfort or pain in the groinespecially when straining, lifting, coughing, or exercisingthat improves when resting  - feelings such as weakness, heaviness, burning, or aching in the groin  - a swollen or an enlarged scrotum in men or boys\n                \nIndirect and direct inguinal hernias may slide in and out of the abdomen into the inguinal canal. A health care provider can often move them back into the abdomen with gentle massage."}
{"_id":"bfe333b0-8bc5-4f87-9482-5d26a226e58b","text":"Inguinal hernias can cause the following complications:\n                \n- Incarceration. An incarcerated hernia happens when part of the fat or small intestine from inside the abdomen becomes stuck in the groin or scrotum and cannot go back into the abdomen. A health care provider is unable to massage the hernia back into the abdomen.  - Strangulation. When an incarcerated hernia is not treated, the blood supply to the small intestine may become obstructed, causing strangulation of the small intestine. This lack of blood supply is an emergency situation and can cause the section of the intestine to die.\n                \n\n                \nSeek Immediate Care   People who have symptoms of an incarcerated or a strangulated hernia should seek emergency medical help immediately. A strangulated hernia is a life-threatening condition. Symptoms of an incarcerated or a strangulated hernia include   - extreme tenderness or painful redness in the area of the bulge in the groin   - sudden pain that worsens quickly and does not go away   - the inability to have a bowel movement and pass gas   - nausea and vomiting   - fever"}
{"_id":"333e5610-9081-4fdc-914f-3d60fd3d2a5a","text":"A health care provider diagnoses an inguinal hernia with\n                \n- a medical and family history  - a physical exam  - imaging tests, including x rays\n                \nMedical and family history. Taking a medical and family history may help a health care provider diagnose an inguinal hernia. Often the symptoms that the patient describes will be signs of an inguinal hernia.\n                \nPhysical exam. A physical exam may help diagnose an inguinal hernia. During a physical exam, a health care provider usually examines the patients body. The health care provider may ask the patient to stand and cough or strain so the health care provider can feel for a bulge caused by the hernia as it moves into the groin or scrotum. The health care provider may gently try to massage the hernia back into its proper position in the abdomen.\n                \nImaging tests. A health care provider does not usually use imaging tests, including x rays, to diagnose an inguinal hernia unless he or she\n                \n- is trying to diagnose a strangulation or an incarceration  - cannot feel the inguinal hernia during a physical exam, especially in patients who are overweight  - is uncertain if the hernia or another condition is causing the swelling in the groin or other symptoms\n                \nSpecially trained technicians perform imaging tests at a health care providers office, an outpatient center, or a hospital.\n                \nA radiologista doctor who specializes in medical imaginginterprets the images. A patient does not usually need anesthesia.\n                \nTests may include the following:\n                \n- Abdominal x ray. An x ray is a picture recorded on film or on a computer using a small amount of radiation. The patient will lie on a table or stand during the x ray. The technician positions the x-ray machine over the abdominal area. The patient will hold his or her breath as the technician takes the picture so that the picture will not be blurry. The technician may ask the patient to change position for additional pictures.  - Computerized tomography (CT) scan. CT scans use a combination of x rays and computer technology to create images. For a CT scan, the technician may give the patient a solution to drink and an injection of a special dye, called contrast medium. A health care provider injects the contrast medium into a vein, and the injection will make the patient feel warm all over for a minute or two. The contrast medium allows the health care provider to see the blood vessels and blood flow on the x rays. CT scans require the patient to lie on a table that slides into a tunnel-shaped device where the technician takes the x rays. A health care provider may give children a sedative to help them fall asleep for the test.  - Abdominal ultrasound. Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure."}
{"_id":"8236bdb1-03c2-4466-928d-40e2dd3793a2","text":"Repair of an inguinal hernia via surgery is the only treatment for inguinal hernias and can prevent incarceration and strangulation. Health care providers recommend surgery for most people with inguinal hernias and especially for people with hernias that cause symptoms. Research suggests that men with hernias that cause few or no symptoms may be able to safely delay surgery until their symptoms increase.3,6 Men who delay surgery should watch for symptoms and see a health care provider regularly. Health care providers usually recommend surgery for infants and children to prevent incarceration.1 Emergent, or immediate, surgery is necessary for incarcerated or strangulated hernias.\n                \nA general surgeona doctor who specializes in abdominal surgeryperforms hernia surgery at a hospital or surgery center, usually on an outpatient basis. Recovery time varies depending on the size of the hernia, the technique used, and the age and health of the person.\n                \nHernia surgery is also called herniorrhaphy. The two main types of surgery for hernias are\n                \n- Open hernia repair. During an open hernia repair, a health care provider usually gives a patient local anesthesia in the abdomen with sedation; however, some patients may have      - sedation with a spinal block, in which a health care provider injects anesthetics around the nerves in the spine, making the body numb from the waist down    - general anesthesia\n                \n- The surgeon makes an incision in the groin, moves the hernia back into the abdomen, and reinforces the abdominal wall with stitches. Usually the surgeon also reinforces the weak area with a synthetic mesh or screen to provide additional support.\n                \n- Laparoscopic hernia repair. A surgeon performs laparoscopic hernia repair with the patient under general anesthesia. The surgeon makes several small, half-inch incisions in the lower abdomen and inserts a laparoscopea thin tube with a tiny video camera attached. The camera sends a magnified image from inside the body to a video monitor, giving the surgeon a close-up view of the hernia and surrounding tissue. While watching the monitor, the surgeon repairs the hernia using synthetic mesh or screen.\n                \nPeople who undergo laparoscopic hernia repair generally experience a shorter recovery time than those who have an open hernia repair. However, the surgeon may determine that laparoscopy is not the best option if the hernia is large or if the person has had previous pelvic surgery.\n                \nMost adults experience discomfort and require pain medication after either an open hernia repair or a laparoscopic hernia repair. Intense activity and heavy lifting are restricted for several weeks. The surgeon will discuss when a person may safely return to work. Infants and children also experience some discomfort; however, they usually resume normal activities after several days.\n                \nSurgery to repair an inguinal hernia is quite safe, and complications are uncommon. People should contact their health care provider if any of the following symptoms appear:\n                \n- redness around or drainage from the incision  - fever  - bleeding from the incision  - pain that is not relieved by medication or pain that suddenly worsens\n                \nPossible long-term complications include\n                \n- long-lasting pain in the groin  - recurrence of the hernia, requiring a second surgery  - damage to nerves near the hernia"}
{"_id":"d8428acf-a108-46a0-8032-61e4cd7b8135","text":"People cannot prevent the weakness in the abdominal wall that causes indirect inguinal hernias. However, people may be able to prevent direct inguinal hernias by maintaining a healthy weight and not smoking.\n                \nPeople can keep inguinal hernias from getting worse or keep inguinal hernias from recurring after surgery by\n                \n- avoiding heavy lifting  - using the legs, not the back, when lifting objects  - preventing constipation and straining during bowel movements  - maintaining a healthy weight  - not smoking"}
{"_id":"bff293f4-f34a-4163-942d-14076f13b02c","text":"Researchers have not found that eating, diet, and nutrition play a role in causing inguinal hernias. A person with an inguinal hernia may be able to prevent symptoms by eating high-fiber foods. Fresh fruits, vegetables, and whole grains are high in fiber and may help prevent the constipation and straining that cause some of the painful symptoms of a hernia.\n                \nThe surgeon will provide instructions on eating, diet, and nutrition after inguinal hernia surgery. Most people drink liquids and eat a light diet the day of the operation and then resume their usual diet the next day."}
{"_id":"214c3a4e-5bd8-408f-be07-ea6e56000dc5","text":"- An inguinal hernia happens when contents of the abdomenusually fat or part of the small intestinebulge through a weak area in the lower abdominal wall.  - A defect in the abdominal wall that is present at birth causes an indirect inguinal hernia.  - Direct inguinal hernias usually occur only in male adults as aging and stress or strain weaken the abdominal muscles around the inguinal canal. Females rarely form this type of inguinal hernia.  - The first sign of an inguinal hernia is a small bulge on one or, rarely, on both sides of the grointhe area just above the groin crease between the lower abdomen and the thigh.  - An incarcerated hernia happens when part of the fat or small intestine from inside the abdomen becomes stuck in the groin or scrotum and cannot go back into the abdomen.  - When an incarcerated hernia is not treated, the blood supply to the small intestine may become obstructed, causing strangulation of the small intestine.  - People who have symptoms of an incarcerated or a strangulated hernia should seek emergency medical help immediately. A strangulated hernia is a life-threatening condition.  - Repair of an inguinal hernia via surgery is the only treatment for inguinal hernias and can prevent incarceration and strangulation."}
{"_id":"c598ed49-220c-4cc8-80ea-4f079914c996","text":"Test      Instructions      Results or Dates           A1C test             - Have this blood test at least twice a year. Your result will tell you what your average blood glucose level was for the past 2 to 3 months.         Date: __________  A1C: __________  Next test: __________          Blood lipid (fats) lab tests             - Get a blood test to check your             - total cholesterolaim for below 200        - LDL, or bad, cholesterolaim for below 100        - HDL, or good, cholesterolmen: aim for above 40; women: aim for above 50        - triglyceridesaim for below 150               Date: __________  Total cholesterol: __________  LDL: __________  HDL: __________  Triglycerides: __________  Next test: __________          Kidney function tests             - Once a year, get a urine test to check for protein.      - At least once a year, get a blood test to check for creatinine.         Date: __________  Urine protein: __________  Creatinine: __________  Next test: __________          Dilated eye exam             - See an eye doctor once a year for a complete eye exam that includes using drops in your eyes to dilate your pupils.      - If you are pregnant, have a complete eye exam in your first 3 months of pregnancy. Have another complete eye exam 1 year after your baby is born.         Date: __________  Result: __________  Next test: __________          Dental exam             - See your dentist twice a year for a cleaning and checkup.         Date: __________  Result: __________  Next test: __________           Pneumonia vaccine (recommended by the Centers for Disease Control and Prevention [CDC])              - Get the vaccine if you are younger than 64.      - If youre older than 64 and your shot was more than 5 years ago, get another vaccine.        Date received: __________         Flu vaccine (recommended by the CDC)              - Get a flu shot each year.         Date received: __________         Hepatitis B vaccine (recommended by the CDC)             - Get this vaccine if you are age 19 to 59 and have not had this vaccine.      - Consider getting this vaccine if you are 60 or older and have not had this vaccine.         Date of 1st dose: __________  Date of 2nd dose: __________  Date of 3rd dose: __________\n                \nPDF Version (PDF, 40 KB)"}
{"_id":"8dcd670a-2569-43b3-a16f-0a450bda2783","text":"Diabetes causes blood glucose levels to be above normal. People with diabetes have problems converting food to energy. After food is eaten, it is broken down into a sugar called glucose. Glucose is then carried by the blood to cells throughout the body. The hormone insulin, made in the pancreas, helps the body change blood glucose into energy. People with diabetes, however, either no longer make enough insulin, or their insulin doesn't work properly, or both.\n                \nType 2 diabetes\n                \nType 2 diabetes is the most common type in American Indians. This type of diabetes can occur at any age, even during childhood. People develop type 2 diabetes because the cells in the muscles, liver, and fat do not use insulin properly. Eventually, the body cannot make enough insulin. As a result, the amount of glucose in the blood increases while the cells are starved of energy. Over time, high blood glucose damages nerves and blood vessels, leading to problems such as heart disease, stroke, blindness, kidney failure, and amputation.\n                \nOther kinds of diabetes\n                \nType 1 diabetes\n                \nType 1 diabetes is rare in American Indians. People develop type 1 diabetes when their bodies no longer make any insulin. Type 1 is usually first diagnosed in children or young adults but can develop at any age.\n                \nGestational diabetes\n                \nGestational diabetes is first diagnosed during pregnancy. It occurs when the body doesn't use insulin properly. Having an American Indian family background raises the risk of developing gestational diabetes. Although this form of diabetes usually goes away after the baby is born, a woman who has had it is more likely to develop type 2 diabetes later in life."}
{"_id":"d170b783-65ad-4ee0-b618-63de4a3c23ef","text":"Many people have no visible signs or symptoms of diabetes. Symptoms can also be so mild that you might not notice them. More than 5 million people in the United States have type 2 diabetes and do not know it.\n                \n- increased thirst  - increased hunger   - fatigue   - increased urination, especially at night   - unexplained weight loss   - blurred vision   - sores that do not heal"}
{"_id":"14bde75d-f2fe-4275-bfcd-27689d5c8bbb","text":"- My mother had diabetes when I was born.   - I am overweight.  - I have a parent, brother, or sister with diabetes.  - My family background is American Indian.  - I have had gestational diabetes, or I gave birth to at least one baby weighing more than 9 pounds.  - My blood pressure is 140\/90 mmHg or higher, or I have been told that I have high blood pressure.  - My cholesterol levels are higher than normal. My HDL cholesterol\"good\" cholesterolis below 35 mg\/dL, or my triglyceride level is above 250 mg\/dL.  - I am fairly inactive. I exercise fewer than three times a week."}
{"_id":"faf6fe42-a6b2-4fc9-b66b-e9359f806c7e","text":"- Reach and maintain a reasonable body weight.  - Make wise food choices most of the time.  - Be physically active every day.  - Take your prescribed medicines.\n                \nDoing these things can reduce your risk of developing type 2 diabetes. Keeping your blood pressure and cholesterol on target also helps you stay healthy.\n                \nIf you are pregnant, plan to breastfeed your baby. Ask your health care provider for the names of people to call for help learning to breastfeed. Besides being good for your baby, breastfeeding is good for you. Studies done with the help of Pima Indian volunteers have shown that breastfeeding may lower the baby's risk of becoming overweight and getting diabetes.\n                \nGetting Started.\n                \nMaking changes in your life such as eating less can be hard. You can make the changes easier by taking these steps:\n                \n- Make a plan to change something that you do.  - Decide exactly what you will do and when you will do it.  - Plan what you need to get ready.  - Think about what might prevent you from reaching your goal.  - Find family and friends who will support and encourage you.  - Decide how you will reward yourselfwith a nonfood itemor activitywhen you do what you have planned.\n                \nYour health care provider, a registered dietitian, or a counselor can help you make a plan.\n                \nReach and Maintain a Reasonable Body Weight.\n                \nYour weight affects your health in many ways. Being overweight can keep your body from making and using insulin correctly. The extra weight may also cause high blood pressure. The DPP study showed that losing even a few pounds can help lower your risk of developing type 2 diabetes, because weight loss helps your body use insulin more effectively. Every pound you lose lowers your risk of getting diabetes. In the DPP, people who lost 5 to 7 percent of their body weight lowered their risk of developing type 2 diabetes. They had less than half the risk of developing diabetes as people who didn't make lifestyle changes. A 5- to 7-percent weight loss for a 150-pound person, for example, would be about 7 to 10 pounds. If you're overweight, choose sensible ways to lose weight.\n                \n- Don't use crash diets. Instead, eat smaller servings of the foods you usually have, and limit the amount of fat you eat.  - Increase your physical activity. Aim for at least 30 minutes of exercise most days of the week. Do something you enjoy, like biking or walking with a friend.  - Set a reasonable weight-loss goal, such as losing about a pound a week. Aim for a long-term goal of losing the number of pounds that's right for you.\n                \nChoosing My Weight Loss Goal.\n                \nLosing 5 to 7 percent of your total weight can help lower your risk of getting type 2 diabetes. You are more likely to lose weight if:\n                \n- you're physically active   - you cut down on fat and calories  - Use these steps to choose a goal. Talk with your health care provider and your dietitian about your goal and how to reach it.\n                \nTo find your weight loss goal for losing about 5 to 7 percent of your weight, find the weight closest to yours on the chart below. Follow the row across to see how many pounds you need to lose.\n                \nYour weight in pounds    5 percent loss in pounds*    7 percent loss in pounds**          150    8    11        175    9    12        200    10    14        225    11    16        250    13    18        275    14    19        300    15    21        325    16    23        350    18    25\n                \n*To find your exact weight loss goal in pounds for a 5 percent loss, multiply your weight by .05.\n                \n**To find your exact weight loss goal in pounds for a 7 percent loss, multiply your weight by .07.\n                \nWrite your weight loss goal here:\n                \nTo lower my risk of getting type 2 diabetes, my goal is to lose about ___________ pounds.\n                \nWrite down what you will do to lose weight. I will:\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \n\n                \nChoose a date to start your plan for losing weight and write it here:\n                \nStart date: ___________________\n                \nLook ahead to when you think you can meet your goal. Allow about a week for each pound or half-pound you'd like to lose. Write the date for meeting your goal here:\n                \nEnd date: ___________________\n                \nMake Wise Food Choices Most of The Time\n                \nWhat you eat has a big impact on your health. By making wise food choices, you can help control your body weight, blood glucose, blood pressure, and cholesterol.\n                \n- Keep track of what you eat and drink. People who keep track are more successful in losing weight. You can use the Daily Food and Drink Tracker to write down what you eat and drink.   - Take a look at the serving sizes of the foods you eat. Reduce serving sizes of main courses, meat, desserts, and other foods high in fat. Increase the amount of fruits and vegetables at every meal. Below is a chart for choosing sensible serving sizes using your hand as a measuring guide. Because your hand is proportioned to the rest of your body, it can be used to measure a healthy serving size for your body. Remember, the chart is only a guide. Choose your serving sizes and foods wisely.  - Limit your fat intake to about 25 percent of your total calories. Your health care provider or dietitian can help you figure out how many grams of fat to have every day. You can check food labels for fat content. For example, if your food choices add up to about 2,000 calories a day, try to eat no more than 56 grams of fat. See Ways to Lower The Amount of Fat in Your Meals and Snacks.  - Cut down on calories by eating smaller servings and by cutting back on fat. People in the DPP lifestyle change group lowered their daily calorie total by an average of about 450 calories. Your health care provider or dietitian can work with you to develop a meal plan that helps you lose weight.  - Choose healthy commodity foods (items provided by the government to help people consume a nutritious diet), including those lower in fat.  - When you meet your goal, reward yourself with something special, like a new outfit or a movie.\n                \nChoose Sensible Serving Sizes\n                \nAmount of food    Types of food    Size of one serving (the same size as:)          3 ounces    meat, chicken, turkey, or fish    the palm of a hand or a deck of cards         1 cup    cooked vegetables salads casseroles or stews, such as chili with beans milk     an average-sized fist         1\/2 cup    fruit or fruit juice starchy vegetables, such as potatoes or corn pinto beans and other dried beans rice or noodles cereal     half of an average-sized fist         1 ounce    snack food    one handful         1 Tablespoon    salad dressing    the tip of a thumb         1 teaspoon    margarine    a fingertip\n                \n\n                \nWays to Lower The Amount of Fat in Your Meals and Snacks\n                \n- Choose lower-fat foods. Example: Instead of sunflower seeds (20 grams of fat),  choose pretzels (1 gram).  Savings: 19 grams.    - Use low-fat versions of foods. Example: Instead of regular margarine (5 grams of fat),  use low-fat margarine (2 grams). Savings: 3 grams.    - Use low-fat seasonings. Example: Instead of putting butter and sour cream on your baked potato  (20 grams of fat), have salsa (0 grams). Savings: 20 grams.    - Cook with less fat. Example: Instead of making fried chicken (31 grams of fat),  roast or grill the chicken (9 grams). Savings: 22 grams.\n                \nRemember that low-fat or fat-free products still contain calories. Be careful about how much you eat. In fact, some low-fat or fat-free products are high in calories. Check the food label\n                \nBe Physically Active Every Day\n                \n- Keep track of what you do for exercise and how long you do it. Use the Daily Physical Activity Tracker to keep track of your physical activity.  - Aim for at least 30 minutes of physical activity a day most days of the week.  - Incorporate physical activity into plans with family and friends. Set a good example for your children. Play softball on weekends. Go on a family hike.  - Be active every day. For example, walk to the store, clean the house, or work in the garden, rather than watch TV.\n                \nGetting Started on a Walking Routine\n                \nWalking is a great way to be physically active. Before you get started, talk with your health care provider about whether it's OK for you to walk for exercise. Then get comfortable shoes that provide good support. You can use the Daily Physical Activity Tracker to start your routine gradually. Try to walk at least 5 times a week. Build up little by little to 30 minutes a day of brisk walking.\n                \nMy Walking Program\n                \nWeek number    Warm-up time (minutes) Walk slowly    Fast walk time (minutes) Walk briskly    Cool-down time (minutes) Walk slowly    Total (minutes)          1    5    5    5    15        2    5    8    5    18        3    5    11    5    21        4    5    14    5    24        5    5    17    5    27        6    5    20    5    30        7    5    23    5    33        8    5    26    5    36        9+    5    30    5    40\n                \nTake Your Prescribed Medicines\n                \n\n                \n\n                \nDaily Food and Drink Tracker\n                \nUse the Daily Food and Drink Tracker to keep track of everything you eat and drink. Make a copy of the form for each day. Write down the time, the name of the food or drink, and how much you had. For a free booklet with information on fat grams and calories, call the National Diabetes Education Program at 1888693NDEP (18886936337) and request a copy of the Game Plan Fat and Calorie Counter(PDF, 405.05 KB).\n                \nSample\n                \nDaily Food and Drink TrackerDate: _____________\n                \nTime    Name    Amount    Fat Grams    Calories          8:00 am    oatmeal    1\/2 cup    1    80            fat-free milk    1 cup    0    90\n                \n\n                \nDaily Physical Activity Tracker\n                \nUse the Daily Physical Activity Tracker to keep track of your physical activity. Make a copy of the form for each day. Write down what you do and for how long.\n                \nSample\n                \nDaily Physical Activity TrackerDate: _____________\n                \nType of Activity    Minutes          Walking    20        Gardening    10\n                \n\n                \nDaily Food and Drink TrackerDate: _____________\n                \nTime    Name    Amount    Fat Grams    Calories                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                TOTALS        \n                \nDaily Physical Activity TrackerDate: _____________           Type of Activity     Minutes                                                                                                                                                                                                                                                                                                                                                                                           TOTAL"}
{"_id":"48b26692-1ce3-4300-a560-37712ea9bad9","text":"About once a month, your dialysis care team will test your blood by using one of two formulasURR or Kt\/Vto see whether your treatments are removing enough wastes. Both tests look at one specific waste product, called blood urea nitrogen (BUN), as an indicator for the overall level of waste products in your system. For more information about these measurements, see the NIDDK fact sheet Hemodialysis Dose and Adequacy."}
{"_id":"7ae59db2-6a06-438b-b2fe-864b6c683ad9","text":"Your kidneys do much more than remove wastes and extra fluid. They also make hormones and balance chemicals in your system. When your kidneys stop working, you may have problems with anemia and conditions that affect your bones, nerves, and skin. Some of the more common conditions caused by kidney failure are extreme tiredness, bone problems, joint problems, itching, and \"restless legs.\" Restless legs will keep you awake as you feel them twitching and jumping.\n                \nAnemia and Erythropoietin (EPO)\n                \nAnemia is a condition in which the volume of red blood cells is low. Red blood cells carry oxygen to cells throughout the body. Without oxygen, cells can't use the energy from food, so someone with anemia may tire easily and look pale. Anemia can also contribute to heart problems.\n                \nAnemia is common in people with kidney disease because the kidneys produce the hormone erythropoietin, or EPO, which stimulates the bone marrow to produce red blood cells. Diseased kidneys often don't make enough EPO, and so the bone marrow makes fewer red blood cells. EPO is available commercially and is commonly given to patients on dialysis.\n                \nFor more information about the causes of and treatments for anemia in kidney failure, see the NIDDK fact sheet Anemia in Chronic Kidney Disease.\n                \nRenal Osteodystrophy\n                \nThe term \"renal\" describes things related to the kidneys. Renal osteodystrophy, or bone disease of kidney failure, affects 90 percent of dialysis patients. It causes bones to become thin and weak or formed incorrectly and affects both children and adults. Symptoms can be seen in growing children with kidney disease even before they start dialysis. Older patients and women who have gone through menopause are at greater risk for this disease.\n                \nFor more information about the causes of this bone disease and its treatment in dialysis patients, see the NIDDK fact sheet Chronic Kidney Disease-Mineral and Bone Disorder.\n                \nItching (Pruritus)\n                \nMany people treated with hemodialysis complain of itchy skin, which is often worse during or just after treatment. Itching is common even in people who don't have kidney disease; in kidney failure, however, itching can be made worse by wastes in the bloodstream that current dialyzer membranes can't remove from the blood.\n                \nThe problem can also be related to high levels of parathyroid hormone (PTH). Some people have found dramatic relief after having their parathyroid glands removed. The four parathyroid glands sit on the outer surface of the thyroid gland, which is located on the windpipe in the base of your neck, just above the collarbone. The parathyroid glands help control the levels of calcium and phosphorus in the blood.\n                \nBut a cure for itching that works for everyone has not been found. Phosphate binders seem to help some people; these medications act like sponges to soak up, or bind, phosphorus while it is in the stomach. Others find relief after exposure to ultraviolet light. Still others improve with EPO shots. A few antihistamines (Benadryl, Atarax, Vistaril) have been found to help; also, capsaicin cream applied to the skin may relieve itching by deadening nerve impulses. In any case, taking care of dry skin is important. Applying creams with lanolin or camphor may help.\n                \nSleep Disorders\n                \nPatients on dialysis often have insomnia, and some people have a specific problem called the sleep apnea syndrome, which is often signaled by snoring and breaks in snoring. Episodes of apnea are actually breaks in breathing during sleep. Over time, these sleep disturbances can lead to \"day-night reversal\" (insomnia at night, sleepiness during the day), headache, depression, and decreased alertness. The apnea may be related to the effects of advanced kidney failure on the control of breathing. Treatments that work with people who have sleep apnea, whether they have kidney failure or not, include losing weight, changing sleeping position, and wearing a mask that gently pumps air continuously into the nose (nasal continuous positive airway pressure, or CPAP).\n                \nMany people on dialysis have trouble sleeping at night because of aching, uncomfortable, jittery, or \"restless\" legs. You may feel a strong impulse to kick or thrash your legs. Kicking may occur during sleep and disturb a bed partner throughout the night. The causes of restless legs may include nerve damage or chemical imbalances.\n                \nModerate exercise during the day may help, but exercising a few hours before bedtime can make it worse. People with restless leg syndrome should reduce or avoid caffeine, alcohol, and tobacco; some people also find relief with massages or warm baths. A class of drugs called benzodiazepines, often used to treat insomnia or anxiety, may help as well. These prescription drugs include Klonopin, Librium, Valium, and Halcion. A newer and sometimes more effective therapy is levodopa (Sinemet), a drug used to treat Parkinson's disease.\n                \nSleep disorders may seem unimportant, but they can impair your quality of life. Don't hesitate to raise these problems with your nurse, doctor, or social worker.\n                \nAmyloidosis\n                \nDialysis-related amyloidosis (DRA) is common in people who have been on dialysis for more than 5 years. DRA develops when proteins in the blood deposit on joints and tendons, causing pain, stiffness, and fluid in the joints, as is the case with arthritis. Working kidneys filter out these proteins, but dialysis filters are not as effective. For more information, see the NIDDK fact sheet Amyloidosis and Kidney Disease."}
{"_id":"885a6430-2db9-419c-860b-cc730c5b590a","text":"Insulin is a hormone made in the pancreas, an organ located behind the stomach. The pancreas contains clusters of cells called islets. Beta cells within the islets make insulin and release it into the blood.\n                \nInsulin plays a major role in metabolismthe way the body uses digested food for energy. The digestive tract breaks down carbohydratessugars and starches found in many foodsinto glucose. Glucose is a form of sugar that enters the bloodstream. With the help of insulin, cells throughout the body absorb glucose and use it for energy.\n                \nInsulin's Role in Blood Glucose Control\n                \nWhen blood glucose levels rise after a meal, the pancreas releases insulin into the blood. Insulin and glucose then travel in the blood to cells throughout the body.\n                \n- Insulin helps muscle, fat, and liver cells absorb glucose from the bloodstream, lowering blood glucose levels.  - Insulin stimulates the liver and muscle tissue to store excess glucose. The stored form of glucose is called glycogen.  - Insulin also lowers blood glucose levels by reducing glucose production in the liver.\n                \nIn a healthy person, these functions allow blood glucose and insulin levels to remain in the normal range."}
{"_id":"4b19f115-82da-40af-8fd8-f1ad94bbf9be","text":"Insulin resistance is a condition in which the body produces insulin but does not use it effectively. When people have insulin resistance, glucose builds up in the blood instead of being absorbed by the cells, leading to type 2 diabetes or prediabetes.\n                \nMost people with insulin resistance don't know they have it for many yearsuntil they develop type 2 diabetes, a serious, lifelong disease. The good news is that if people learn they have insulin resistance early on, they can often prevent or delay diabetes by making changes to their lifestyle.\n                \nInsulin resistance can lead to a variety of serious health disorders. The section \"What is metabolic syndrome?\" provides more information about other health disorders linked to insulin resistance."}
{"_id":"c09f1a30-c150-4617-a635-b33e7d2a8794","text":"Although the exact causes of insulin resistance are not completely understood, scientists think the major contributors to insulin resistance are excess weight and physical inactivity.\n                \nExcess Weight\n                \nSome experts believe obesity, especially excess fat around the waist, is a primary cause of insulin resistance. Scientists used to think that fat tissue functioned solely as energy storage. However, studies have shown that belly fat produces hormones and other substances that can cause serious health problems such as insulin resistance, high blood pressure, imbalanced cholesterol, and cardiovascular disease (CVD).\n                \nBelly fat plays a part in developing chronic, or long-lasting, inflammation in the body. Chronic inflammation can damage the body over time, without any signs or symptoms. Scientists have found that complex interactions in fat tissue draw immune cells to the area and trigger low-level chronic inflammation. This inflammation can contribute to the development of insulin resistance, type 2 diabetes, and CVD. Studies show that losing the weight can reduce insulin resistance and prevent or delay type 2 diabetes.\n                \nPhysical Inactivity\n                \nMany studies have shown that physical inactivity is associated with insulin resistance, often leading to type 2 diabetes. In the body, more glucose is used by muscle than other tissues. Normally, active muscles burn their stored glucose for energy and refill their reserves with glucose taken from the bloodstream, keeping blood glucose levels in balance.\n                \nStudies show that after exercising, muscles become more sensitive to insulin, reversing insulin resistance and lowering blood glucose levels. Exercise also helps muscles absorb more glucose without the need for insulin. The more muscle a body has, the more glucose it can burn to control blood glucose levels.\n                \nOther Causes\n                \nOther causes of insulin resistance may include ethnicity; certain diseases; hormones; steroid use; some medications; older age; sleep problems, especially sleep apnea; and cigarette smoking.\n                \n\n                \nDoes sleep matter?   Yes. Studies show that untreated sleep problems, especially sleep apnea, can increase the risk of obesity, insulin resistance, and type 2 diabetes. Night shift workers may also be at increased risk for these problems. Sleep apnea is a common disorder in which a person's breathing is interrupted during sleep. People may often move out of deep sleep and into light sleep when their breathing pauses or becomes shallow. This results in poor sleep quality that causes problem sleepiness, or excessive tiredness, during the day.   Many people aren't aware of their symptoms and aren't diagnosed. People who think they might have sleep problems should talk with their health care provider.   More information about sleep problems is available from the National Heart, Lung, and Blood Institute at http:\/\/www.nhlbi.nih.gov\/health\/resources\/sleep."}
{"_id":"2de13254-dcfd-4402-892b-44b8b4580b59","text":"Prediabetes is a condition in which blood glucose or A1C levelswhich reflect average blood glucose levelsare higher than normal but not high enough for a diagnosis of diabetes. Prediabetes is becoming more common in the United States. The U.S. Department of Health and Human Services estimates that at least 86 million U.S. adults ages 20 or older had prediabetes in 2012.1 People with prediabetes are at increased risk of developing type 2 diabetes and CVD, which can lead to heart attack or stroke."}
{"_id":"f617071b-434e-45d6-8ab4-b040d4386672","text":"Insulin resistance and prediabetes usually have no symptoms. People may have one or both conditions for several years without knowing they have them. Even without symptoms, health care providers can identify people at high risk by their physical characteristics, also known as risk factors. The section \"Who should be tested for prediabetes?\" lists these risk factors.\n                \nPeople with a severe form of insulin resistance may have dark patches of skin, usually on the back of the neck. Sometimes people have a dark ring around their neck. Dark patches may also appear on elbows, knees, knuckles, and armpits. This condition is called acanthosis nigricans."}
{"_id":"55d73d0e-c8d5-4f43-b2f3-d93eacb2c012","text":"Metabolic syndrome, also called insulin resistance syndrome, is a group of traits and medical conditions linked to overweight and obesity that puts people at risk for both CVD and type 2 diabetes. Metabolic syndrome is defined* as the presence of any three of the following2:\n                \n- large waist sizewaist measurement of 40 inches or more for men and 35 inches or more for women  - high triglycerides in the bloodtriglyceride level of 150 milligrams per deciliter (mg\/dL) or above, or taking medication for elevated triglyceride level  - abnormal levels of cholesterol in the bloodHDL, or good, cholesterol level below 40 mg\/dL for men and below 50 mg\/dL for women, or taking medication for low HDL  - high blood pressureblood pressure level of 130\/85 or above, or taking medication for elevated blood pressure  - higher than normal blood glucose levelsfasting blood glucose level of 100 mg\/dL or above, or taking medication for elevated blood glucose\n                \nIn addition to type 2 diabetes, metabolic syndrome has been linked to the following health disorders:\n                \n- obesity  - CVD  - PCOS  - nonalcoholic fatty liver disease  - chronic kidney disease\n                \nHowever, not everyone with these disorders has insulin resistance, and some people may have insulin resistance without getting these disorders.\n                \nPeople who are obese or who have metabolic syndrome, insulin resistance, type 2 diabetes, or prediabetes often also have low-level inflammation throughout the body and blood clotting defects that increase the risk of developing blood clots in the arteries. These conditions contribute to increased risk for CVD.\n                \n*Similar definitions have been developed by the World Health Organization and the American Association of Clinical Endocrinologists."}
{"_id":"88947d7d-6966-456b-9a66-da423a9cc8f4","text":"Health care providers use blood tests to determine whether a person has prediabetes, but they do not usually test specifically for insulin resistance. Insulin resistance can be assessed by measuring the level of insulin in the blood.\n                \nHowever, the test that most accurately measures insulin resistance, called the euglycemic clamp, is too costly and complicated to be used in most health care providers' offices. The clamp is a research tool used by scientists to learn more about glucose metabolism. Research has shown that if blood tests indicate prediabetes, insulin resistance most likely is present.\n                \nBlood Tests for Prediabetes\n                \nAll blood tests involve drawing blood at a health care provider's office or commercial facility and sending the sample to a lab for analysis. Lab analysis of blood is needed to ensure test results are accurate. Glucose measuring devices used in a health care provider's office, such as finger-stick devices, are not accurate enough for diagnosis but may be used as a quick indicator of high blood glucose.\n                \nPrediabetes can be detected with one of the following blood tests:\n                \n- the A1C test  - the fasting plasma glucose (FPG) test  - the oral glucose tolerance test (OGTT)\n                \nA1C test. Sometimes called hemoglobin A1c, HbA1c, or glycohemoglobin test, this test reflects average blood glucose levels over the past 3 months. This test is the most reliable test for prediabetes, but it is not as sensitive as the other tests. In some individuals, it may miss prediabetes that could be caught by glucose tests.\n                \nAlthough some health care providers can quickly measure A1C in their office, that type of measurementcalled a point-of-care testis not considered reliable for diagnosis. For diagnosis of prediabetes, the A1C test should be analyzed in a laboratory using a method that is certified by the NGSP.\n                \nThe A1C test can be unreliable for diagnosing prediabetes in people with certain conditions that are known to interfere with the results. Interference should be suspected when A1C results seem very different from the results of a blood glucose test. People of African, Mediterranean, or Southeast Asian descent, or people with family members with sickle cell anemia or a thalassemia, are particularly at risk of interference. People in these groups may have a less common type of hemoglobin, known as a hemoglobin variant, that can interfere with some A1C tests.\n                \nAn A1C of 5.7 to 6.4 percent indicates prediabetes.\n                \nMore information about the A1C test is provided in the NIDDK health topic, The A1C Test and Diabetes.\n                \nFasting plasma glucose test. This test measures blood glucose in people who have not eaten anything for at least 8 hours. This test is most reliable when done in the morning. Prediabetes found with this test is called IFG.\n                \nFasting glucose levels of 100 to 125 mg\/dL indicate prediabetes.\n                \nOGTT. This test measures blood glucose after people have not eaten for at least 8 hours and 2 hours after they drink a sweet liquid provided by a health care provider or laboratory. Prediabetes found with this test is called IGT.\n                \nA blood glucose level between 140 and 199 mg\/dL indicates prediabetes.\n                \nThe following table lists the blood test levels for a diagnosis of prediabetes."}
{"_id":"26f460c5-62da-4244-b26c-ba3c90be461d","text":"Adopting healthy eating habits can help people lose a modest amount of weight and reverse insulin resistance. Experts encourage people to slowly adopt healthy eating habits that they can maintain, rather than trying extreme weight-loss solutions. People may need to get help from a dietitian or join a weight-loss program for support.\n                \nIn general, people should lose weight by choosing healthy foods, controlling portions, eating less fat, and increasing physical activity. People are better able to lose weight and keep it off when they learn how to adapt their favorite foods to a healthy eating plan.\n                \nThe DASH (Dietary Approaches to Stop Hypertension) eating plan, developed by the NIH, has been shown to be effective in decreasing insulin resistance when combined with weight loss and physical activity. More information on DASH is available at www.nhlbi.nih.gov\/health\/health-topics\/topics\/dash.\n                \nThe U.S. Dietary Guidelines for Americans also offers healthy eating advice and tools for changing eating habits at www.choosemyplate.gov.\n                \nDietary Supplements\n                \nVitamin D studies show a link between people's ability to maintain healthy blood glucose levels and having enough vitamin D in their blood. However, studies to determine the proper vitamin D levels for preventing diabetes are ongoing; no special recommendations have been made about vitamin D levels or supplements for people with prediabetes.\n                \nCurrently, the Institute of Medicine (IOM), the agency that recommends supplementation levels based on current science, provides the following guidelines for daily vitamin D intake:\n                \n- People ages 1 to 70 years may require 600 International Units (IUs).  - People ages 71 and older may require as much as 800 IUs.\n                \nThe IOM also recommended that no more than 4,000 IUs of vitamin D be taken per day.\n                \nTo help ensure coordinated and safe care, people should discuss use of complementary and alternative medicine practices, including the use of dietary supplements, with their health care provider.\n                \nMore information about using dietary supplements to help with diabetes is provided in the NIDDK health topic, Complementary and Alternative Medical Therapies for Diabetes.\n                \n\n                \nPhysical Activity\n                \nRegular physical activity tackles several risk factors at once. Regular physical activity helps the body use insulin properly.\n                \nRegular physical activity also helps a person\n                \n- lose weight  - control blood glucose levels  - control blood pressure  - control cholesterol levels\n                \nPeople in the DPP who were physically active for 30 minutes a day, 5 days a week, reduced their risk of type 2 diabetes. Many chose brisk walking as their physical activity.\n                \nMost people should aim for at least 30 minutes of exercise most days of the week. For best results, people should do both aerobic activities, which use large muscle groups and make the heart beat faster, and muscle strengthening activities.\n                \nAerobic activities include brisk walking, climbing stairs, swimming, dancing, and other activities that increase the heart rate.\n                \nMuscle strengthening activities include lifting weights and doing sit-ups or push-ups.\n                \nPeople who haven't been physically active recently should talk with their health care provider about which activities are best for them and have a checkup before starting an exercise program.\n                \nNot Smoking\n                \nThose who smoke should quit. A health care provider can help people find ways to quit smoking. Studies show that people who get help have a better chance of quitting.\n                \nFor more information about how to reverse insulin resistance and prediabetes with diet and increased physical activity, see the following National Diabetes Education Program publications at www.yourdiabetesinfo.org:    - Get Real! You Don't Have to Knock Yourself Out to Prevent Diabetes!   - More Than 50 Ways to Prevent Diabetes   - Small Steps. Big Rewards. Your Game Plan to Prevent Type 2 Diabetes.\n                \nMedication\n                \nThe medication metformin is recommended for treatment of some individuals at very high risk of developing type 2 diabetes. In the DPP, metformin was shown to be most effective in preventing or delaying the development of type 2 diabetes in younger, heavier people with prediabetes. In general, metformin is recommend for those who are younger than age 60 and have\n                \n- combined IGT and IFG  - A1C above 6 percent  - low HDL cholesterol  - elevated triglycerides  - a parent or sibling with diabetes  - a BMI of at least 35\n                \nMetformin also lowers the risk of diabetes in women who have had gestational diabetes. People at high risk should ask their health care provider if they should take metformin to prevent type 2 diabetes.\n                \nSeveral medications have been shown to reduce type 2 diabetes risk to varying degrees, but the only medication recommended by the ADA for type 2 diabetes prevention is metformin. Other medications that have delayed diabetes have side effects or haven't shown long-lasting benefits. No medication, including metformin, is approved by the U.S. Food and Drug Administration to treat insulin resistance or prediabetes or to prevent type 2 diabetes."}
{"_id":"661d6fea-86fd-4e16-aab3-8688aa66d269","text":"- Insulin is a hormone that helps cells throughout the body absorb glucose and use it for energy. Insulin resistance is a condition in which the body produces insulin but does not use it effectively.  - Insulin resistance increases the risk of developing type 2 diabetes and prediabetes.  - The major contributors to insulin resistance are excess weight, especially around the waist, and physical inactivity.  - Prediabetes is a condition in which blood glucose or A1C levelswhich reflect average blood glucose levelsare higher than normal but not high enough for a diagnosis of diabetes.  - The Diabetes Prevention Program (DPP) study and its follow-up study, the Diabetes Prevention Program Outcomes Study (DPPOS), confirmed that people with prediabetes can often prevent or delay diabetes if they lose a modest amount of weight by cutting fat and calorie intake and increasing physical activity.  - By losing weight and being more physically active, people can reverse insulin resistance and prediabetes, thus preventing or delaying type 2 diabetes.  - People with insulin resistance and prediabetes can decrease their risk for diabetes by eating a healthy diet and reaching and maintaining a healthy weight, increasing physical activity, not smoking, and taking medication.  - The DPP showed the diabetes medication metformin to be most effective in preventing or delaying the development of type 2 diabetes in younger and heavier people with prediabetes and women who have had gestational diabetes."}
{"_id":"f162d939-7865-4ffa-9d63-acdc96cddac0","text":"Amyloidosis is a rare disease that occurs when amyloid proteins are deposited in tissues and organs. Amyloid proteins are abnormal proteins that the body cannot break down and recycle, as it does with normal proteins. When amyloid proteins clump together, they form amyloid deposits. The buildup of these deposits damages a persons organs and tissues. Amyloidosis can affect different organs and tissues in different people and can affect more than one organ at the same time. Amyloidosis most frequently affects the kidneys, heart, nervous system, liver, and digestive tract. The symptoms and severity of amyloidosis depend on the organs and tissues affected."}
{"_id":"5b6c628a-02ac-4116-81b4-c5998d3a94d6","text":"The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the two kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra fluid. The urine flows from the kidneys to the bladder through tubes called ureters. The bladder stores urine. When the bladder empties, urine flows out of the body through a tube called the urethra, located at the bottom of the bladder. In men, the urethra is long, while in women it is short."}
{"_id":"ba54689d-4cdb-41e9-b89f-e3f85c151eed","text":"Primary amyloidosis and dialysis-related amyloidosis are the types of amyloidosis that can affect the kidneys.\n                \nPrimary Amyloidosis of the Kidneys\n                \nThe kidneys are the organs most commonly affected by primary amyloidosis. Amyloid deposits damage the kidneys and make it harder for them to filter wastes and break down proteins. When the kidneys become too damaged, they may no longer be able to function well enough to maintain health, resulting in kidney failure. Kidney failure can lead to problems such as high blood pressure, bone disease, and anemiaa condition in which the body has fewer red blood cells than normal.\n                \nDialysis-related Amyloidosis\n                \nPeople who suffer from kidney failure and have been on long-term dialysis may develop dialysis-related amyloidosis. This type of amyloidosis occurs when a certain protein, called beta-2 microglobulin, builds up in the blood because dialysis does not remove it completely. The two types of dialysis are\n                \n- hemodialysis. Hemodialysis uses a special filter called a dialyzer to remove wastes and extra fluid from the blood.  - peritoneal dialysis. Peritoneal dialysis uses the lining of the abdominal cavitythe space in the body that holds organs such as the stomach, intestines, and liverto filter the blood.\n                \nDialysis-related amyloidosis is a complication of kidney failure because neither hemodialysis nor peritoneal dialysis effectively filters beta-2 microglobulin from the blood. As a result, elevated amounts of beta-2 microglobulin remain in the blood. Dialysis-related amyloidosis is relatively common in people with kidney failure, especially adults older than 60 years of age, who have been on dialysis for more than 5 years.1\n                \nMore information is provided in the NIDDK health topics:\n                \n- Treatment Methods for Kidney Failure: Hemodialysis  - Treatment Methods for Kidney Failure: Peritoneal Dialysis"}
{"_id":"89925672-41b8-466b-bcb3-2ad1415d8e23","text":"The most common sign of primary amyloidosis of the kidneys is nephrotic syndromea collection of signs that indicate kidney damage. The signs of nephrotic syndrome include\n                \n- albuminuriaan increased amount of albumin, a protein, in the urine. A person with nephrotic syndrome excretes more than half a teaspoon of albumin per day.  - hyperlipidemiaa condition in which a persons blood has more-than-normal amounts of fats and cholesterol.  - edemaswelling, typically in a persons legs, feet, or ankles and less often in the hands or face.  - hypoalbuminemiaa condition in which a persons blood has less-than-normal amounts of albumin.\n                \nMore information is provided in the NIDDK health topic, Nephrotic Syndrome in Adults.\n                \nOther signs and symptoms of primary amyloidosis may include\n                \n- fatigue, or feeling tired  - shortness of breath  - low blood pressure  - numbness, tingling, or a burning sensation in the hands or feet  - weight loss"}
{"_id":"a05968c9-6c0c-44f1-a396-9d464e431df9","text":"The symptoms of dialysis-related amyloidosis may include\n                \n- pain, stiffness, and fluid in the joints.  - abnormal, fluid-containing sacs, called cysts, in some bones.  - carpal tunnel syndrome, caused by unusual buildup of amyloid proteins in the wrists. The symptoms of carpal tunnel syndrome include numbness or tingling, sometimes associated with muscle weakness, in the fingers and hands.\n                \nDialysis-related amyloidosis most often affects bones, joints, and the tissues that connect muscle to bone, called tendons. The disease may also affect the digestive tract and organs such as the heart and lungs. Bone cysts caused by dialysis-related amyloidosis can lead to bone fractures. Dialysis-related amyloidosis can also cause tears in tendons and ligaments. Ligaments are tissues that connect bones to other bones."}
{"_id":"49188e40-27d2-4d7c-a342-10c2f56982f2","text":"A health care provider diagnoses primary amyloidosis of the kidneys with\n                \n- a medical and family history  - a physical exam  - urinalysis  - blood tests  - a kidney biopsy\n                \nMedical and Family History\n                \nTaking a medical and family history may help a health care provider diagnose amyloidosis of the kidneys. He or she will ask the patient to provide a medical and family history.\n                \nPhysical Exam\n                \nA physical exam may help diagnose primary amyloidosis of the kidneys. During a physical exam, a health care provider usually\n                \n- examines a patients body to check for swelling  - uses a stethoscope to listen to the lungs  - taps on specific areas of the patients body\n                \nUrinalysis\n                \nA health care provider may use urinalysisthe testing of a urine sampleto check for albumin and amyloid proteins in urine. The patient provides a urine sample in a special container at a health care providers office or a commercial facility. A nurse or technician can test the sample in the same location or send it to a lab for analysis. More-than-normal amounts of albumin in urine may indicate kidney damage due to primary amyloidosis. Amyloid proteins in urine may indicate amyloidosis.\n                \nBlood Tests\n                \nThe health care provider may use blood tests to see how well the kidneys are working and to check for amyloid proteins and hyperlipidemia. A blood test involves drawing a patients blood at a health care providers office or a commercial facility and sending the sample to a lab for analysis. Blood tests for kidney function measure the waste products in the blood that healthy kidneys normally filter out. Hyperlipidemia may indicate nephrotic syndrome. Amyloid proteins in blood may indicate amyloidosis.\n                \nKidney Biopsy\n                \nOnly a biopsy can show the amyloid protein deposits in the kidneys. A health care provider may recommend a kidney biopsy if other tests show kidney damage. A kidney biopsy is a procedure that involves taking a piece of kidney tissue for examination with a microscope. A health care provider performs a kidney biopsy in a hospital with light sedation and local anesthetic. The health care provider uses imaging techniques such as ultrasound or a computerized tomography (CT) scan to guide the biopsy needle into the kidney and take the tissue sample. A pathologista doctor who specializes in diagnosing diseasesexamines the tissue in a lab for amyloid proteins and kidney damage.\n                \nThe biopsy results can help the health care provider determine the best course of treatment. More information is provided in the NIDDK health topic, Kidney Biopsy."}
{"_id":"9714ff8e-0d41-465e-b500-17bd014155d5","text":"A health care provider diagnoses dialysis-related amyloidosis with\n                \n- urinalysis  - blood tests  - imaging tests\n                \nA health care provider can use urinalysis and blood tests to detect the amount of amyloid proteins in urine and blood. Imaging tests, such as x-rays and CT scans, can provide pictures of bone cysts and amyloid deposits in bones, joints, tendons, and ligaments. An x-ray technician performs imaging tests in a health care providers office, an outpatient center, or a hospital. A radiologista doctor who specializes in medical imaginginterprets the images. A patient does not require anesthesia."}
{"_id":"06c9a10d-f65e-413a-97f2-beedddaf23e1","text":"A health care provider treats primary amyloidosis of the kidneys with the following:\n                \n- medication therapy, including chemotherapy  - a stem cell transplant  - treating other conditions\n                \nMedication therapy. The goal of medication therapy, including chemotherapy, is to reduce amyloid protein levels in the blood. Many health care providers recommend combination medication therapy such as\n                \n- melphalan (Alkeran), a type of chemotherapy  - dexamethasone (Decadron), an anti-inflammatory steroid medication\n                \nThese medications can stop the growth of the cells that make amyloid proteins. These medications may cause hair loss and serious side effects, such as nausea, vomiting, and fatigue.\n                \nStem cell transplant. A stem cell transplant is a procedure that replaces a patients damaged stem cells with healthy ones. Stem cells are found in the bone marrow and develop into three types of blood cells the body needs. To prepare for a stem cell transplant, the patient receives high doses of chemotherapy. The actual transplant is like a blood transfusion. The transplanted stem cells travel to the bone marrow to make healthy new blood cells. The chemotherapy a patient receives to prepare for the transplant can have serious side effects, so it is important to talk with the health care provider about the risks of this procedure.\n                \nRead more in What Is a Blood and Marrow Stem Cell Transplant? at www.nhlbi.nih.gov\/health\/health-topics\/topics\/bmsct.\n                \nTreating other conditions. Primary amyloidosis has no cure, so treating some of the side effects and other conditions seen with the disease is essential. Other conditions may include\n                \n- anemiatreatment may include medications  - depressiontreatment may include talking with a mental health counselor and taking medications  - fatiguetreatment may include changes in diet and activity level  - kidney diseasetreatment may include medications to help maintain kidney function or slow the progression of kidney disease\n                \nA patient and his or her family should talk with the health care provider about resources for support and treatment options.\n                \nMore information about kidney disease is provided in the NIDDK health topic, niddk-kidney disease."}
{"_id":"c68547e4-ab40-4f04-9eb8-122cfedee6fd","text":"A health care provider treats dialysis-related amyloidosis with\n                \n- medication therapy  - newer, more effective hemodialysis filters  - surgery  - a kidney transplant\n                \nThe goal of medication therapy and the use of newer, more effective hemodialysis filters is to reduce amyloid protein levels in the blood. Medication therapy can help reduce symptoms such as pain and inflammation. A health care provider may treat a person with dialysis-related amyloidosis who has bone, joint, and tendon problems, such as bone cysts and carpal tunnel syndrome, using surgery.\n                \nDialysis-related amyloidosis has no cure; however, a successful kidney transplant may stop the disease from progressing.\n                \nMore information is provided in the NIDDK health topic, Treatment Methods for Kidney Failure: Transplantation."}
{"_id":"b2946e23-491e-4a04-bb15-b24886e73ce8","text":"Researchers have not found that eating, diet, and nutrition play a role in causing or preventing primary amyloidosis of the kidneys or dialysis-related amyloidosis. People with nephrotic syndrome may make dietary changes such as\n                \n- limiting dietary sodium, often from salt, to help reduce edema and lower blood pressure  - decreasing liquid intake to help reduce edema and lower blood pressure  - eating a diet low in saturated fat and cholesterol to help control more-than-normal amounts of fats and cholesterol in the blood\n                \nHealth care providers may recommend that people with kidney disease eat moderate or reduced amounts of protein. Proteins break down into waste products that the kidneys filter from the blood. Eating more protein than the body needs may burden the kidneys and cause kidney function to decline faster. However, protein intake that is too low may lead to malnutrition, a condition that occurs when the body does not get enough nutrients.\n                \nPeople with kidney disease on a restricted protein diet should receive blood tests that can show low nutrient levels. People with primary amyloidosis of the kidneys or dialysis-related amyloidosis should talk with a health care provider about dietary restrictions to best manage their individual needs."}
{"_id":"727716f9-1308-4f1f-ada6-18e5c5577329","text":"- Amyloidosis is a rare disease that occurs when amyloid proteins are deposited in tissues and organs.  - Primary amyloidosis and dialysis-related amyloidosis are the types of amyloidosis that can affect the kidneys.  - The most common sign of primary amyloidosis of the kidneys is nephrotic syndrome.  - The signs of nephrotic syndrome include      - albuminuriaan elevated amount of albumin in the urine. A person with nephrotic syndrome excretes more than half a teaspoon of albumin per day.    - hyperlipidemiaa condition in which a persons blood has more-than-normal amounts of fats and cholesterol.    - edemaswelling, typically in a persons legs, feet, or ankles and less often in the hands or face.    - hypoalbuminemiaa condition in which a persons blood has less-than-normal amounts of albumin.    - Other signs and symptoms of primary amyloidosis may include      - fatigue, or feeling tired    - shortness of breath    - low blood pressure    - numbness, tingling, or a burning sensation in the hands or feet    - weight loss    - The symptoms of dialysis-related amyloidosis may include      - pain, stiffness, and fluid in the joints.    - abnormal, fluid-containing sacs, called cysts, in some bones.    - carpal tunnel syndrome, caused by unusual buildup of amyloid proteins in the wrists. The symptoms of carpal tunnel syndrome include numbness or tingling, sometimes associated with muscle weakness, in the fingers and hands.    - A health care provider diagnoses primary amyloidosis of the kidneys with      - a medical and family history    - a physical exam    - urinalysis    - blood tests    - a kidney biopsy    - A health care provider diagnoses dialysis-related amyloidosis with      - urinalysis    - blood tests    - imaging tests    - A health care provider treats primary amyloidosis of the kidneys with the following:      - medication therapy, including chemotherapy    - a stem cell transplant    - treating other conditions    - A health care provider treats dialysis-related amyloidosis with      - medication therapy    - newer, more effective hemodialysis filters    - surgery    - a kidney transplant"}
{"_id":"3e6844ef-9869-4a75-a2a9-bb9aebb83fa7","text":"You and your doctor will work together to choose a treatment that's best for you. The publications of the NIDDK Kidney Failure Series can help you learn about the specific issues you will face.\n                \nBooklets\n                \n- What I need to know about Kidney Failure and How its Treated  - Treatment Methods for Kidney Failure: Hemodialysis  - Treatment Methods for Kidney Failure: Peritoneal Dialysis  - Treatment Methods for Kidney Failure: Kidney Transplantation  - Kidney Failure: Eat Right to Feel Right on Hemodialysis\n                \nFact Sheets\n                \n- Kidney Failure: What to Expect  - Vascular Access for Hemodialysis  - Hemodialysis Dose and Adequacy  - Peritoneal Dialysis Dose and Adequacy  - Amyloidosis and Kidney Disease  - Anemia in Chronic Kidney Disease  - Chronic Kidney Disease-Mineral and Bone Disorder  - Financial Help for Treatment of Kidney Failure\n                \nLearning as much as you can about your treatment will help make you an important member of your health care team.\n                \n\n                \n\n                \nThis content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. The NIDDK translates and disseminates research findings through its clearinghouses and education programs to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by the NIDDK is carefully reviewed by NIDDK scientists and other experts.\n                \nThe NIDDK would like to thank: Glenn Chertow, M.D., University of California at San Francisco; William J. Stone, M.D., Vanderbilt University; Morie A. Gertz, M.D., Mayo Clinic\n                \nThis information is not copyrighted. The NIDDK encourages people to share this content freely.\n                \n\n                \n\n                \nSeptember 2014"}
{"_id":"2b3831bc-58c7-4371-9a59-b01911c7938a","text":"Kidney failure means your kidneys no longer work well enough to do their job. You need treatment to replace the work your damaged kidneys have stopped doing. The treatments for kidney failure are\n                \n- hemodialysis  - peritoneal dialysis  - a kidney transplant\n                \nYour kidneys filter wastes and extra fluid from your blood to keep you healthy. The wastes and extra fluid become urine that is stored in your bladder until you urinate. When your kidneys fail, dialysis can take over a small part of the work your damaged kidneys can no longer do. You can make treatments work better by\n                \n- sticking to your treatment schedule  - taking all medicines your doctor prescribes  - following a special diet that keeps wastes from building up in your blood  - being active most days of the week\n                \nHemodialysis\n                \nHemodialysis is a treatment for kidney failure. Hemodialysis uses a machine to filter your blood outside your body. First, a dialysis nurse places two needles into your arm. A pump on the hemodialysis machine draws your blood through one of the needles into a tube. The tube takes the blood to a filter, called a dialyzer. Inside the dialyzer, your blood flows through thin fibers that are like straws. The wastes and extra fluid leave the blood through tiny holes in the fibers. Then, a different tube carries the filtered blood back to your body through the second needle.\n                \nMore information is provided in the NIDDK health topics, Treatment Methods for Kidney Failure: Hemodialysis and Home Hemodialysis.\n                \nPeritoneal Dialysis\n                \ncatheter\n                \nTreatment Methods for Kidney Failure: Peritoneal Dialysis\n                \nKidney Transplant\n                \nA kidney transplant places a healthy kidney from another person into your body. The kidney may come from someone who has just died. Your doctor will place your name on a waiting list for a kidney. A family member or friend might be able to give you a kidney. Then you dont have to wait.\n                \nThe new kidney takes over filtering your blood. The damaged kidneys usually stay where they are. The new kidney is placed in the front lower abdomen, on one side of the bladder. Your body normally attacks anything that shouldnt be there, such as bacteria. Your body will think the new kidney shouldnt be there. You will take medicines called immunosuppressants to keep your body from attacking the new kidney.\n                \nMore information is provided in the NIDDK health topic, Treatment Methods for Kidney Failure: Transplantation.\n                \n*See the Pronunciation Guide for tips on how to say the the words in bold type."}
{"_id":"f77d4850-952f-4833-a600-05b6d47e9d89","text":"Learning about different treatments for kidney failure will help you choose the one that best fits your lifestyle. Talk with your doctor and people on hemodialysis or peritoneal dialysis to learn about the pros and cons of each treatment. Ask your doctor about the transplant waiting list and about medicines required after a transplant. Talk with people who have had kidney transplants and ask how it has changed their lives.\n                \nIf you plan to keep working, think about which treatment can help make that easier. If spending time with family and friends means a lot to you, learn about which treatment may give you the most free time. Find out which treatment will give you the best chance to be healthy and live longer.\n                \nTalking with your doctor ahead of time about your options can help you take control of your care. Understanding the treatment you choose and getting used to the idea that you will be receiving this treatment takes time. If you choose one type of dialysis treatment and find it is not a good fit for your life, talk with your doctor about selecting another type of dialysis treatment that better meets your needs.\n                \nWhile kidney failure can make your life harder, treatments can help improve your life."}
{"_id":"94deef1d-ef5f-4172-8081-ec8ff084ae7f","text":"Eating the right foods can help you feel better when you are on dialysis or have a kidney transplant. Staying healthy with kidney failure requires watching how much of these elements are included in your diet:\n                \n- Protein is in many foods you eat. Protein is in foods from animals and plants. Most diets include both types of protein. Protein provides the building blocks that maintain and repair muscles, organs, and other parts of the body. Too much protein can cause waste to build up in your blood, making your kidneys work harder. However, if you are on hemodialysis or peritoneal dialysis, you need lots of protein to replace the protein that dialysis removes.  - Phosphorus is a mineral that keeps your bones healthy. Phosphorus also keeps blood vessels and muscles working. This mineral is found naturally in foods rich in protein, such as meat, poultry, fish, nuts, beans, and dairy products. Phosphorus is also added to many processed foods. You need phosphorus to turn food into energy; however, too much can cause your bones to weaken.  - Water is in drinks and in foods such as fruits, vegetables, ice cream, gelatin, soup, and popsicles. Your body needs water; however, too much can cause fluid to build up in your body and make your heart work harder.  - Sodium is a part of salt. You can find sodium in many canned, packaged, and fast foods and in seasonings and meats. You need sodium to help control the amount of fluid in your body; however, too much can cause high blood pressure.  - Potassium is a mineral that helps your nerves and muscles work the right way. Potassium is found in fruits and vegetables such as oranges, bananas, tomatoes, and potatoes. You need potassium for healthy nerves and brain cells; however, too much can make your heartbeat irregular.  - Calories are found in all foods and are especially high in oils and sugary foods. You need calories for energy; however, too many can cause weight gain and high blood sugar.\n                \nTalk with your clinics renal dietitian to find a meal plan that works for you. Each treatment requires a different diet. If you are on hemodialysis, you have to stay away from foods such as potatoes and oranges because they have lots of potassium. If you are on peritoneal dialysis, eating potassium is fine. Instead, you may need to watch your calories. Your food needs will also depend on your weight and activity level.\n                \nChanging your diet may be hard at first. Eating the right foods will help you feel better. You will have more strength and energy. Having more energy will help you live a fuller, healthier life. More information is provided in the NIDDK health topic, Eat Right to Feel Right on Hemodialysis."}
{"_id":"8a166f0c-e059-4d0f-a554-152f320359b0","text":"- Kidney failure means your kidneys no longer work well enough to do their job.  - Learning about treatments for kidney failure will help you choose the one that best fits your lifestyle.  - Many people with kidney failure continue to work.  - Physical activity is an important part of staying healthy when you have kidney failure.  - You can help prevent relatives from having kidney failure by talking with them about their risk.  - Eating the right foods can help you feel better when you are on dialysis or have a kidney transplant."}
{"_id":"245ef6a0-791b-4115-91f5-f5f1d3ab496e","text":"Diverticular disease is a condition that occurs when a person has problems from small pouches, or sacs, that have formed and pushed outward through weak spots in the colon wall. Each pouch is called a diverticulum. Multiple pouches are called diverticula.\n                \nThe colon is part of the large intestine. The large intestine absorbs water from stool and changes it from a liquid to a solid form. Diverticula are most common in the lower part of the colon, called the sigmoid colon.\n                \nThe problems that occur with diverticular disease include diverticulitis and diverticular bleeding. Diverticulitis occurs when the diverticula become inflamed, or irritated and swollen, and infected. Diverticular bleeding occurs when a small blood vessel within the wall of a diverticulum bursts."}
{"_id":"6502f408-aec5-4c57-a068-10883ad6ff29","text":"When a person has diverticula that do not cause diverticulitis or diverticular bleeding, the condition is called diverticulosis. Most people with diverticulosis do not have symptoms. Some people with diverticulosis have constipation or diarrhea. People may also have chronic\n                \n- cramping or pain in the lower abdomenthe area between the chest and hips  - bloating\n                \nOther conditions, such as irritable bowel syndrome and stomach ulcers, cause similar problems, so these symptoms do not always mean a person has diverticulosis. People with these symptoms should see their health care provider."}
{"_id":"3a531765-315f-4136-a345-1802f01e43d6","text":"Scientists are not certain what causes diverticulosis and diverticular disease. For more than 50 years, the most widely accepted theory was that a low-fiber diet led to diverticulosis and diverticular disease. Diverticulosis and diverticular disease were first noticed in the United States in the early 1900s, around the time processed foods were introduced into the American diet. Consumption of processed foods greatly reduced Americans fiber intake. Diverticulosis and diverticular disease are common in Western and industrialized countriesparticularly the United States, England, and Australiawhere low-fiber diets are common. The condition is rare in Asia and Africa, where most people eat high-fiber diets.1 Two large studies also indicate that a low-fiber diet may increase the chance of developing diverticular disease.2\n                \nHowever, a recent study found that a low-fiber diet was not associated with diverticulosis and that a high-fiber diet and more frequent bowel movements may be linked to an increased rather than decreased chance of diverticula.3\n                \nOther studies have focused on the role of decreased levels of the neurotransmitter serotonin in causing decreased relaxation and increased spasms of the colon muscle. A neurotransmitter is a chemical that helps brain cells communicate with nerve cells. However, more studies are needed in this area.\n                \nStudies have also found links between diverticular disease and obesity, lack of exercise, smoking, and certain medications including nonsteroidal anti-inflammatory drugs, such as aspirin, and steroids.3\n                \nScientists agree that with diverticulitis, inflammation may begin when bacteria or stool get caught in a diverticulum. In the colon, inflammation also may be caused by a decrease in healthy bacteria and an increase in disease-causing bacteria. This change in the bacteria may permit chronic inflammation to develop in the colon.\n                \n\n                \nWhat is fiber?   Fiber is a substance in foods that comes from plants. Fiber helps soften stool so it moves smoothly through the colon and is easier to pass. Soluble fiber dissolves in water and is found in beans, fruit, and oat products. Insoluble fiber does not dissolve in water and is found in whole-grain products and vegetables. Both kinds of fiber help prevent constipation.   Constipation is a condition in which an adult has fewer than three bowel movements a week or has bowel movements with stools that are hard, dry, and small, making them painful or difficult to pass.   High-fiber foods also have many benefits in preventing and controlling chronic diseases, such as cardiovascular disease, obesity, diabetes, and cancer.2"}
{"_id":"bc9c763e-258b-4eba-98b0-96d2316a7307","text":"Fiber is a substance in foods that comes from plants. Fiber helps soften stool so it moves smoothly through the colon and is easier to pass. Soluble fiber dissolves in water and is found in beans, fruit, and oat products. Insoluble fiber does not dissolve in water and is found in whole-grain products and vegetables. Both kinds of fiber help prevent constipation.\n                \nConstipation is a condition in which an adult has fewer than three bowel movements a week or has bowel movements with stools that are hard, dry, and small, making them painful or difficult to pass.\n                \nHigh-fiber foods also have many benefits in preventing and controlling chronic diseases, such as cardiovascular disease, obesity, diabetes, and cancer.2"}
{"_id":"55d569d3-6123-45f7-9e16-388b6d75114a","text":"Diverticulosis becomes more common as people age, particularly in people older than age 50.3 Some people with diverticulosis develop diverticulitis, and the number of cases is increasing. Although diverticular disease is generally thought to be a condition found in older adults, it is becoming more common in people younger than age 50, most of whom are male.1"}
{"_id":"ac9eb07d-2bad-4e70-bbd0-db6890e44c42","text":"People with diverticulitis may have many symptoms, the most common of which is pain in the lower left side of the abdomen. The pain is usually severe and comes on suddenly, though it can also be mild and then worsen over several days. The intensity of the pain can fluctuate. Diverticulitis may also cause\n                \n- fevers and chills  - nausea or vomiting  - a change in bowel habitsconstipation or diarrhea  - diverticular bleeding\n                \nIn most cases, people with diverticular bleeding suddenly have a large amount of red or maroon-colored blood in their stool. Diverticular bleeding may also cause\n                \n- weakness  - dizziness or light-headedness  - abdominal cramping"}
{"_id":"e371b377-0d92-4b43-b3bf-e5e1b4721dff","text":"Diverticulosis\n                \nHealth care providers often find diverticulosis during a routine x ray or a colonoscopy, a test used to look inside the rectum and entire colon to screen for colon cancer or polyps or to evaluate the source of rectal bleeding.\n                \nDiverticular Disease\n                \nBased on symptoms and severity of illness, a person may be evaluated and diagnosed by a primary care physician, an emergency department physician, a surgeon, or a gastroenterologista doctor who specializes in digestive diseases.\n                \nThe health care provider will ask about the persons health, symptoms, bowel habits, diet, and medications, and will perform a physical exam, which may include a rectal exam. A rectal exam is performed in the health care providers office; anesthesia is not needed. To perform the exam, the health care provider asks the person to bend over a table or lie on one side while holding the knees close to the chest. The health care provider slides a gloved, lubricated finger into the rectum. The exam is used to check for pain, bleeding, or a blockage in the intestine.\n                \nThe health care provider may schedule one or more of the following tests:\n                \n- Blood test. A blood test involves drawing a persons blood at a health care providers office, a commercial facility, or a hospital and sending the sample to a lab for analysis. The blood test can show the presence of inflammation or anemiaa condition in which red blood cells are fewer or smaller than normal, which prevents the bodys cells from getting enough oxygen.  - Computerized tomography (CT) scan. A CT scan of the colon is the most common test used to diagnose diverticular disease. CT scans use a combination of x rays and computer technology to create three-dimensional (3D) images. For a CT scan, the person may be given a solution to drink and an injection of a special dye, called contrast medium. CT scans require the person to lie on a table that slides into a tunnel-shaped device where the x rays are taken. The procedure is performed in an outpatient center or a hospital by an x-ray technician, and the images are interpreted by a radiologista doctor who specializes in medical imaging. Anesthesia is not needed. CT scans can detect diverticulosis and confirm the diagnosis of diverticulitis.  - Lower gastrointestinal (GI) series. A lower GI series is an x-ray exam that is used to look at the large intestine. The test is performed at a hospital or an outpatient center by an x-ray technician, and the images are interpreted by a radiologist. Anesthesia is not needed. The health care provider may provide written bowel prep instructions to follow at home before the test. The person may be asked to follow a clear liquid diet for 1 to 3 days before the procedure. A laxative or enema may be used before the test. A laxative is medication that loosens stool and increases bowel movements. An enema involves flushing water or laxative into the rectum using a special squirt bottle. These medications cause diarrhea, so the person should stay close to a bathroom during the bowel prep.   - For the test, the person will lie on a table while the radiologist inserts a flexible tube into the persons anus. The colon is filled with barium, making signs of diverticular disease show up more clearly on x rays.  - For several days, traces of barium in the large intestine can cause stools to be white or light colored. Enemas and repeated bowel movements may cause anal soreness. A health care provider will provide specific instructions about eating and drinking after the test.  - Colonoscopy. The test is performed at a hospital or an outpatient center by a gastroenterologist. Before the test, the persons health care provider will provide written bowel prep instructions to follow at home. The person may need to follow a clear liquid diet for 1 to 3 days before the test. The person may also need to take laxatives and enemas the evening before the test.  - In most cases, light anesthesia, and possibly pain medication, helps people relax for the test. The person will lie on a table while the gastroenterologist inserts a flexible tube into the anus. A small camera on the tube sends a video image of the intestinal lining to a computer screen. The test can show diverticulosis and diverticular disease.  - Cramping or bloating may occur during the first hour after the test. Driving is not permitted for 24 hours after the test to allow the anesthesia time to wear off. Before the appointment, people should make plans for a ride home. Full recovery is expected by the next day, and people should be able to go back to their normal diet."}
{"_id":"403a6840-35b9-44fe-9b28-b9b34af5eb8f","text":"A health care provider may treat the symptoms of diverticulosis with a high-fiber diet or fiber supplements, medications, and possibly probiotics. Treatment for diverticular disease varies, depending on whether a person has diverticulitis or diverticular bleeding.\n                \nDiverticulosis\n                \nHigh-fiber diet. Studies have shown that a high-fiber diet can help prevent diverticular disease in people who already have diverticulosis.2 A health care provider may recommend a slow increase in dietary fiber to minimize gas and abdominal discomfort. For more information about fiber-rich foods, see Eating, Diet, and Nutrition.\n                \nFiber supplements. A health care provider may recommend taking a fiber product such as methylcellulose (Citrucel) or psyllium (Metamucil) one to three times a day. These products are available as powders, pills, or wafers and provide 0.5 to 3.5 grams of fiber per dose. Fiber products should be taken with at least 8 ounces of water.\n                \nMedications. A number of studies suggest the medication mesalazine (Asacol), given either continuously or in cycles, may be effective at reducing abdominal pain and GI symptoms of diverticulosis. Research has also shown that combining mesalazine with the antibiotic rifaximin (Xifaxan) can be significantly more effective than using rifaximin alone to improve a persons symptoms and maintain periods of remission, which means being free of symptoms.4\n                \nProbiotics. Although more research is needed, probiotics may help treat the symptoms of diverticulosis, prevent the onset of diverticulitis, and reduce the chance of recurrent symptoms. Probiotics are live bacteria, like those normally found in the GI tract. Probiotics can be found in dietary supplementsin capsules, tablets, and powdersand in some foods, such as yogurt.\n                \nTo help ensure coordinated and safe care, people should discuss their use of complementary and alternative medical practices, including their use of dietary supplements and probiotics, with their health care provider. Read more at www.nccam.nih.gov\/health\/probiotics.\n                \nTips for talking with health care providers are available at www.nccam.nih.gov\/timetotalk.\n                \nDiverticular Bleeding\n                \nDiverticular bleeding is rare. Bleeding can be severe; however, it may stop by itself and not require treatment. A person who has bleeding from the rectumeven a small amountshould see a health care provider right away.\n                \nTo treat the bleeding, a colonoscopy may be performed to identify the location of and stop the bleeding. A CT scan or angiogram also may be used to identify the site of the bleeding. A traditional angiogram is a special kind of x ray in which a thin, flexible tube called a catheter is threaded through a large artery, often from the groin, to the area of bleeding. Contrast medium is injected through the catheter so the artery shows up more clearly on the x ray. The procedure is performed in a hospital or an outpatient center by an x-ray technician, and the images are interpreted by a radiologist. Anesthesia is not needed, though a sedative may be given to lessen anxiety during the procedure.\n                \nIf the bleeding does not stop, abdominal surgery with a colon resection may be necessary. In a colon resection, the surgeon removes the affected part of the colon and joins the remaining ends of the colon together; general anesthesia is used. A blood transfusion may be needed if the person has lost a significant amount of blood.\n                \nDiverticulitis\n                \nDiverticulitis with mild symptoms and no complications usually requires a person to rest, take oral antibiotics, and be on a liquid diet for a period of time. If symptoms ease after a few days, the health care provider will recommend gradually adding solid foods back into the diet.\n                \nSevere cases of diverticulitis with acute pain and complications will likely require a hospital stay. Most cases of severe diverticulitis are treated with intravenous (IV) antibiotics and a few days without food or drink to help the colon rest. If the period without food or drink is longer, the person may be given parenteral nutritiona method of providing an IV liquid food mixture through a special tube in the chest. The mixture contains proteins, carbohydrates, fats, vitamins, and minerals."}
{"_id":"ad9fa3f9-bbb1-4934-bf02-1c4be98046fa","text":"Diverticulitis can attack suddenly and cause complications, such as\n                \n- an abscessa painful, swollen, pus-filled area just outside the colon wallcaused by infection  - a perforationa small tear or hole in the diverticula  - peritonitisinflammation of tissues inside the abdomen from pus and stool that leak through a perforation  - a fistulaan abnormal passage, or tunnel, between two organs, or between an organ and the outside of the body  - intestinal obstructionpartial or total blockage of movement of food or stool through the intestines\n                \nThese complications need to be treated to prevent them from getting worse and causing serious illness. In some cases, surgery may be needed.\n                \nAbscess, perforation, and peritonitis. Antibiotic treatment of diverticulitis usually prevents or treats an abscess. If the abscess is large or does not clear up with antibiotics, it may need to be drained. After giving the person numbing medication, a radiologist inserts a needle through the skin to the abscess and then drains the fluid through a catheter. The procedure is usually guided by an abdominal ultrasound or a CT scan. Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure.\n                \nA person with a perforation usually needs surgery to repair the tear or hole. Sometimes, a person needs surgery to remove a small part of the intestine if the perforation cannot be repaired.\n                \nA person with peritonitis may be extremely ill, with nausea, vomiting, fever, and severe abdominal tenderness. This condition requires immediate surgery to clean the abdominal cavity and possibly a colon resection at a later date after a course of antibiotics. A blood transfusion may be needed if the person has lost a significant amount of blood. Without prompt treatment, peritonitis can be fatal.\n                \nFistula. Diverticulitis-related infection may lead to one or more fistulas. Fistulas usually form between the colon and the bladder, small intestine, or skin. The most common type of fistula occurs between the colon and the bladder. Fistulas can be corrected with a colon resection and removal of the fistula.\n                \nIntestinal obstruction. Diverticulitis-related inflammation or scarring caused by past inflammation may lead to intestinal obstruction. If the intestine is completely blocked, emergency surgery is necessary, with possible colon resection. Partial blockage is not an emergency, so the surgery or other procedures to correct it can be scheduled.\n                \nWhen urgent surgery with colon resection is necessary for diverticulitis, two procedures may be needed because it is not safe to rejoin the colon right away. During the colon resection, the surgeon performs a temporary colostomy, creating an opening, or stoma, in the abdomen. The end of the colon is connected to the opening to allow normal eating while healing occurs. Stool is collected in a pouch attached to the stoma on the abdominal wall. In the second surgery, several months later, the surgeon rejoins the ends of the colon and closes the stoma."}
{"_id":"b906a1fc-3a28-4c08-8f56-bd3f41fb934f","text":"The Dietary Guidelines for Americans, 2010, recommends a dietary fiber intake of 14 grams per 1,000 calories consumed. For instance, for a 2,000-calorie diet, the fiber recommendation is 28 grams per day. The amount of fiber in a food is listed on the foods nutrition facts label. Some of the best sources of fiber include fruits; vegetables, particularly starchy ones; and whole grains. A health care provider or dietitian can help a person learn how to add more high-fiber foods into the diet.\n                \nFiber-rich Foods        Beans, cereals, and breads    Amount of fiber        1\/2 cup of navy beans    9.5 grams        1\/2 cup of kidney beans    8.2 grams        1\/2 cup of black beans    7.5 grams        Whole-grain cereal, cold        1\/2 cup of All-Bran    9.6 grams        3\/4 cup of Total    2.4 grams        3\/4 cup of Post Bran Flakes    5.3 grams        1 packet of whole-grain cereal, hot (oatmeal, Wheatena)    3.0 grams        1 whole-wheat English muffin    4.4 grams        Fruits        1 medium apple, with skin    3.3 grams        1 medium pear, with skin    4.3 grams        1\/2 cup of raspberries    4.0 grams        1\/2 cup of stewed prunes    3.8 grams        Vegetables        1\/2 cup of winter squash    2.9 grams         1 medium sweet potato, with skin    4.8 grams        1\/2 cup of green peas    4.4 grams        1 medium potato, with skin    3.8 grams        1\/2 cup of mixed vegetables    4.0 grams        1 cup of cauliflower    2.5 grams        1\/2 cup of spinach    3.5 grams        1\/2 cup of turnip greens    2.5 grams\n                \nScientists now believe that people with diverticular disease do not need to eliminate certain foods from their diet. In the past, health care providers recommended that people with diverticular disease avoid nuts, popcorn, and sunflower, pumpkin, caraway, and sesame seeds because they thought food particles could enter, block, or irritate the diverticula. However, recent data suggest that these foods are not harmful.5 The seeds in tomatoes, zucchini, cucumbers, strawberries, and raspberries, as well as poppy seeds, are also fine to eat. Nonetheless, people with diverticular disease may differ in the amounts and types of foods that worsen their symptoms."}
{"_id":"4c582eca-6d54-4d24-b803-0d3be8bb3140","text":"- Diverticular disease is a condition that occurs when a person has problems from small pouches, or sacs, that have formed and pushed outward through weak spots in the colon wall. The problems that occur with diverticular disease include diverticulitis and diverticular bleeding.  - When a person has diverticula that do not cause diverticulitis or diverticular bleeding, the condition is called diverticulosis.  - Scientists are not certain what causes diverticulosis and diverticular disease.  - Although diverticular disease is generally thought to be a condition found in older adults, it is becoming more common in people younger than age 50, most of whom are male.  - Health care providers often find diverticulosis during a routine x ray or a colonoscopy, a test used to look inside the rectum and entire colon to screen for colon cancer or polyps or to evaluate the source of rectal bleeding.  - To diagnose diverticular disease, a health care provider may schedule one or more of the following tests: blood test; computerized tomography (CT) scan; lower gastrointestinal (GI) series; colonoscopy.  - A health care provider may treat the symptoms of diverticulosis with a high-fiber diet or fiber supplements, medications, and possibly probiotics.  - Diverticular bleeding is rare. Bleeding can be severe; however, it may stop by itself and not require treatment. If the bleeding does not stop, abdominal surgery with a colon resection may be necessary.  - Diverticulitis with mild symptoms and no complications usually requires a person to rest, take oral antibiotics, and be on a liquid diet for a period of time.  - Diverticulitis can attack suddenly and cause complications, such as an abscess, a perforation, peritonitis, a fistula, or intestinal obstruction. These complications need to be treated to prevent them from getting worse and causing serious illness."}
{"_id":"6e3a9075-e7ac-4af2-9c5b-39b82652a6d7","text":"Intestinal pseudo-obstruction is a rare condition with symptoms that resemble those caused by a blockage, or obstruction, of the intestines, also called the bowel. However, when a health care provider examines the intestines, no blockage exists. Instead, the symptoms are due to nerve or muscle problems that affect the movement of food, fluid, and air through the intestines.\n                \nThe intestines are part of the gastrointestinal (GI) tract and include the small intestine and the large intestine. The small intestine is the organ where most digestion occurs. The small intestine measures about 20 feet and includes the\n                \n- duodenum, the first part of the small intestine  - jejunum, the middle section of the small intestine  - ileum, the lower end of the small intestine\n                \nThe large intestine absorbs water from stool and changes it from a liquid to a solid form, which passes out of the body during a bowel movement. The large intestine measures about 5 feet and includes the\n                \n- cecum, the first part of the large intestine, which is connected to the ileum  - colon, the part of the large intestine extending from the cecum to the rectum  - rectum, the lower end of the large intestine leading to the anus"}
{"_id":"2a9a7f4a-b9cd-4a50-901c-91a5ee871928","text":"Problems with nerves, muscles, or interstitial cells of Cajal cause intestinal pseudo-obstruction. Interstitial cells of Cajal are called pacemaker cells because they set the pace of intestinal contractions. These cells convey messages from nerves to muscles.\n                \nProblems with nerves, muscles, or interstitial cells of Cajal prevent normal contractions of the intestines and cause problems with the movement of food, fluid, and air through the intestines.\n                \nPrimary or idiopathic intestinal pseudo-obstruction is intestinal pseudo-obstruction that occurs by itself. In some people with primary intestinal pseudo-obstruction, mutations, or changes, in genestraits passed from parent to childcause the condition. However, health care providers do not typically order genetic testing for an intestinal pseudo-obstruction, as they dont commonly recognize gene mutations as a cause.\n                \nSome people have duplications or deletions of genetic material in the FLNA gene. Researchers believe that these genetic changes may impair the function of a protein, causing problems with the nerve cells in the intestines.1 As a result, the nerves cannot work with the intestinal muscles to produce normal contractions that move food, fluid, and air through the digestive tract. Also, these genetic changes may account for some of the other signs and symptoms that can occur with intestinal pseudo-obstruction, such as bladder symptoms and muscle weakness.\n                \nA condition called mitochondrial neurogastrointestinal encephalopathy may also cause primary intestinal pseudo-obstruction. In people with this condition, mitochondriastructures in cells that produce energydo not function normally. Mitochondrial neurogastrointestinal encephalopathy can also cause other symptoms, such as problems with nerves in the limbs and changes in the brain.\n                \nSecondary intestinal pseudo-obstruction develops as a complication of another medical condition. Causes of secondary intestinal pseudo-obstruction include\n                \n- abdominal or pelvic surgery  - diseases that affect muscles and nerves, such as lupus erythematosus, scleroderma, and Parkinsons disease  - infections  - medications, such as opiates and antidepressants, that affect muscles and nerves  - radiation to the abdomen  - certain cancers, including lung cancer"}
{"_id":"2d11bd80-ba3a-4873-ba85-e114274ee1ad","text":"Intestinal pseudo-obstruction symptoms may include\n                \n- abdominal swelling or bloating, also called distension  - abdominal pain  - nausea  - vomiting  - constipation  - diarrhea\n                \nOver time, the condition can cause malnutrition, bacterial overgrowth in the intestines, and weight loss. Malnutrition is a condition that develops when the body does not get the right amount of the vitamins, minerals, and other nutrients it needs to maintain healthy tissues and organ function.\n                \nSome people develop problems with their esophagus, stomach, or bladder."}
{"_id":"0ca0adb5-0c9b-4962-b6ee-085792117fa8","text":"To diagnose intestinal pseudo-obstruction, a health care provider may suggest the person consult a gastroenterologista doctor who specializes in digestive diseases. A health care provider will perform a physical exam; take a complete medical history, imaging studies, and a biopsy; and perform blood tests. A health care provider may order other tests to confirm the diagnosis. The health care provider also will look for the cause of the condition, such as an underlying illness.\n                \nIntestinal pseudo-obstruction can be difficult to diagnose, especially primary intestinal pseudo-obstruction. As a result, a correct diagnosis may take a long time.\n                \nPhysical Exam\n                \nA physical exam is one of the first things a health care provider may do to help diagnose intestinal pseudo-obstruction. During a physical exam, a health care provider usually\n                \n- examines a persons body  - uses a stethoscope to listen to bodily sounds  - taps on specific areas of the persons body\n                \nMedical History\n                \nThe health care provider will ask a person to provide a medical and family history to help diagnose intestinal pseudo-obstruction.\n                \nImaging Studies\n                \nA health care provider may order the following imaging studies:\n                \n- Abdominal x ray. An x ray is a picture recorded on film or a computer that a technician takes using low-level radiation. The amount of radiation used is small. An x-ray technician takes the x ray at a hospital or an outpatient center, and a radiologista doctor who specializes in medical imaginginterprets the images. A person does not need anesthesia. The person will lie on a table or stand during the x ray. The technician positions the x-ray machine over the abdominal area. The person will hold his or her breath as the technician takes the picture so that the picture will not be blurry. The technician may ask the person to change position for additional pictures. An x ray of the abdominal area will show whether symptoms are due to an intestinal blockage.  - Upper GI series. A health care provider may order an upper GI series to look at the small intestine. An x-ray technician performs the test at a hospital or an outpatient center, and a radiologist interprets the images; the health care provider may give infants and children anesthesia. A person should not eat or drink for 8 hours before the procedure, if possible. During the procedure, the person will stand or sit in front of an x-ray machine and drink barium, a chalky liquid. Infants lie on a table and the technician will give them barium through a tiny tube placed in the nose that runs into the stomach. Barium coats the lining of the small intestine, making signs of obstruction show up more clearly on x rays.  A person may experience bloating and nausea for a short time after the test. Barium liquid in the GI tract causes stools to be white or light colored for several days or longer in people with intestinal pseudo-obstruction. A health care provider will give the person specific instructions about eating and drinking after the test.  - Lower GI series. A health care provider may order a lower GI series, an x-ray exam to look at the large intestine. An x-ray technician performs the test at a hospital or an outpatient center, and a radiologist interprets the images. A person does not need anesthesia. The health care provider may provide written bowel prep instructions to follow at home before the test. The health care provider may ask the person to follow a clear liquid diet for 1 to 3 days before the procedure. A person may need to use a laxative or an enema before the test. A laxative is medication that loosens stool and increases bowel movements. An enema involves flushing water or laxative into the anus using a special squirt bottle.  For the test, the person will lie on a table while the health care provider inserts a flexible tube into the persons anus. The health care provider will fill the large intestine with barium, making signs of underlying problems show up more clearly on x rays. The test can show problems with the large intestine that are causing the persons symptoms.  Barium liquid in the GI tract causes stools to be white or light colored for several days or longer in people with intestinal pseudo-obstruction. Enemas and repeated bowel movements may cause anal soreness. A health care provider will provide specific instructions about eating and drinking after the test.  - Computerized tomography (CT) scan. CT scans use a combination of x rays and computer technology to create images. An x-ray technician performs the test at a hospital or an outpatient center, and a radiologist interprets the images. For a CT scan, a health care provider may give the person a solution to drink and an injection of a special dye, called contrast medium. CT scans require the person to lie on a table that slides into a tunnel-shaped device where the technician takes the x rays. CT scans can show both the internal and external intestinal wall. The health care provider may give children a sedative to help them fall asleep for the test.  - Upper GI endoscopy. This procedure involves using an endoscopea small, flexible tube with a lightto see the upper GI tract, which includes the esophagus, stomach, and duodenum. A gastroenterologist performs the test at a hospital or an outpatient center. The gastroenterologist carefully feeds the endoscope down the esophagus and into the stomach and duodenum. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining. A health care provider may give a person a liquid anesthetic to gargle or may spray anesthetic on the back of the persons throat. A health care provider will place an intravenous (IV) needle in a vein in the arm to administer sedation. Sedatives help patients stay relaxed and comfortable. This test can show blockages or other conditions in the upper small intestine. A gastroenterologist may obtain a biopsy of the lining of the small intestine during an upper GI endoscopy.\n                \nBiopsy\n                \nA gastroenterologist can obtain a biopsy of the intestinal wall during endoscopy or during surgery, if the person has surgery for intestinal pseudo-obstruction and the cause is unknown. If the health care provider needs to examine the nerves in the intestinal wall, a deeper biopsy, which a gastroenterologist can typically obtain only during surgery, is necessary.\n                \nA biopsy is a procedure that involves taking a piece of the intestinal wall tissue for examination with a microscope. A health care provider performs the biopsy in a hospital and uses light sedation and local anesthetic; the health care provider uses general anesthesia if performing the biopsy during surgery. A pathologista doctor who specializes in diagnosing diseasesexamines the intestinal tissue in a lab. Diagnosing problems in the nerve pathways of the intestinal tissue requires special techniques that are not widely available.\n                \nA health care provider can also use a biopsy obtained during endoscopy to rule out celiac disease. Celiac disease is an autoimmune disorder in which people cannot tolerate gluten because it damages the lining of their small intestine and prevents absorption of nutrients. Gluten is a protein found in wheat, rye, and barley and in products such as vitamin and nutrient supplements, lip balms, and certain medications.\n                \nBlood Tests\n                \nA blood test involves drawing blood at a health care providers office or a commercial facility and sending the sample to a lab for analysis. The blood test can show the presence of other diseases or conditions that may be causing a persons symptoms. The blood test also can show levels of essential vitamins and minerals to help detect malnutrition.\n                \nManometry\n                \nManometry is a test that measures muscle pressure and movements in the GI tract, such as how well the smooth muscles of the stomach and small intestine contract and relax. A gastroenterologist performs the test at a hospital or an outpatient center. While the person is under sedation, a health care provider places a thin tube, or manometry tube, into the stomach and moves it down into the small intestine. A gastroenterologist may use an endoscope to place this tube. A health care provider will move the person to a manometry room and connect the manometry tube to a computer. When the person wakes up from sedation, the computer records the pressure inside the intestine while the person is fasting and after the person has eaten a meal. Manometry can confirm the diagnosis of intestinal pseudo-obstruction and show the extent of the condition.\n                \nGastric Emptying Tests\n                \nGastric emptying tests can show if a disorder called gastroparesis is causing a persons symptoms. People with gastroparesis, which literally refers to a paralyzed stomach, have severely delayed gastric emptying, or the delayed movement of food from the stomach to the small intestine. Some patients with intestinal pseudo-obstruction also have gastroparesis.\n                \nTypes of gastric emptying tests include the following:\n                \n- Gastric emptying scintigraphy. This test involves eating a bland mealsuch as eggs or an egg substitutethat contains a small amount of radioactive material. A specially trained technician performs the test in a radiology center or hospital, and a radiologist interprets the results; the person does not need anesthesia. An external camera scans the abdomen to show where the radioactive material is located. The radiologist is then able to measure the rate of gastric emptying at 1, 2, 3, and 4 hours after the meal. Normal values depend on the composition of the meal. With some meals, if more than 10 percent of the meal is still in the stomach at 4 hours, a health care provider confirms the diagnosis of gastroparesis. Obtaining scans for 4 hours after the meal is essential. When the technician only obtains scans 1 to 2 hours after the meal, the results are often unreliable.  - Breath test. With this test, the person eats a meal containing a small amount of nonradioactive material. Then, the health care provider takes breath samples over a period of several hours to measure the amount of nonradioactive material in the exhaled breath. The results allow the health care provider to calculate how fast the stomach is emptying.  - SmartPill. The SmartPill is a small electronic device in capsule form. The SmartPill test is available at specialized outpatient centers. The person swallows the device so that it can move through the entire digestive tract and send information to a cell-phone-sized receiver worn around the persons waist or neck. The recorded information provides details about how quickly food travels through each part of the digestive tract."}
{"_id":"3d72d1a4-dff0-4b07-9717-eaaac07422c1","text":"A health care provider will treat intestinal pseudo-obstruction with nutritional support, medications, and, in some cases, decompression. Rarely, a person will need surgery. If an illness, a medication, or both cause intestinal pseudo-obstruction, a health care provider will treat the underlying illness, stop the medication, or do both.\n                \nNutritional Support\n                \nPeople with intestinal pseudo-obstruction often need nutritional support to prevent malnutrition and weight loss. Enteral nutrition provides liquid food through a feeding tube inserted through the nose into the stomach or placed directly into the stomach or small intestine. A health care provider inserts the feeding tube, sometimes using x ray or endoscopy for guidance, and teaches the person how to care for the tube after returning home. Enteral nutrition is sufficient for most people with intestinal pseudo-obstruction. In a severe case, a person may need IV feeding, also called parenteral nutrition, which provides liquid food through a tube placed in a vein.\n                \nEnteral nutrition is possible because the intestinal lining is normal in most people with intestinal pseudo-obstruction. Enteral nutrition is preferred over parenteral nutrition because it has a much lower risk of complications.\n                \nMedications\n                \nA health care provider prescribes medications to treat the different symptoms and complications of intestinal pseudo-obstruction, such as\n                \n- antibiotics to treat bacterial infections  - pain medication, which should be used sparingly, if at all, because most pain medications delay intestinal transit  - medication to make intestinal muscles contract  - antinausea medications  - antidiarrheal medications  - laxatives\n                \nDecompression\n                \nA person with acute colonic pseudo-obstruction and a greatly enlarged colon who does not respond to medications may need a procedure, called decompression, to remove gas from the colon. A gastroenterologist can perform the procedure in a hospital or an outpatient center. The gastroenterologist may choose to decompress the colon by using colonoscopy. During colonoscopy, the gastroenterologist inserts a flexible tube into the colon through the anus. A health care provider gives the person a light sedative, and possibly pain medication, to relax. If the person requires long-term decompression, the gastroenterologist also can decompress the colon through a surgical opening in the cecum. In this case, the health care provider gives the person local anesthesia.\n                \nSurgery\n                \nIn severe cases of intestinal pseudo-obstruction, a person may need surgery to remove part of the intestine. However, surgery should be performed rarely, if at all, because intestinal pseudo-obstruction is a generalized disorder that typically affects the entire intestine. Removing part of the intestine cannot cure the disease.\n                \nA surgeona doctor who specializes in surgerywill perform the surgery at a hospital; a person will need general anesthesia. A few highly specialized treatment centers offer small intestine transplantation. A health care provider may recommend small intestine transplantation when all other treatments have failed."}
{"_id":"215ee82b-84fe-4631-b5ad-53a84fdc114a","text":"Researchers have not found that eating, diet, and nutrition play a role in causing or preventing intestinal pseudo-obstruction. Following special diets usually does not help improve the disorder. However, eating frequent, small meals with pureed foods or liquids may ease digestion. Vitamin and trace mineral supplements may help a person who is malnourished."}
{"_id":"236144b6-17d7-4ba2-963b-22ee2fbc5ad3","text":"- Intestinal pseudo-obstruction is a rare condition with symptoms that resemble those caused by a blockage, or obstruction, of the intestines, also called the bowel. However, when a health care provider examines the intestines, no blockage exists. Instead, the symptoms are due to nerve or muscle problems that affect the movement of food, fluid, and air through the intestines.  - Intestinal pseudo-obstruction symptoms may include abdominal swelling or bloating, also called distension; abdominal pain; nausea; vomiting; constipation; and diarrhea. Over time, the condition can cause malnutrition, bacterial overgrowth in the intestines, and weight loss.  - To diagnose intestinal pseudo-obstruction, a health care provider may suggest the person consult a gastroenterologista doctor who specializes in digestive diseases. A health care provider will perform a physical exam; take a complete medical history, imaging studies, and a biopsy; and perform blood tests. A health care provider may order other tests to confirm the diagnosis.  - A health care provider will treat intestinal pseudo-obstruction with nutritional support, medications, and, in some cases, decompression. Rarely, a person will need surgery. If an illness, a medication, or both cause intestinal pseudo-obstruction, a health care provider will treat the underlying illness, stop the medication, or do both. A health care provider may recommend small intestine transplantation when all other treatments have failed."}
{"_id":"64e8c787-4007-4325-ba3f-3325eb6d4b8e","text":"Acromegaly is a hormonal disorder that results from too much growth hormone (GH) in the body. The pituitary, a small gland in the brain, makes GH. In acromegaly, the pituitary produces excessive amounts of GH. Usually the excess GH comes from benign, or noncancerous, tumors on the pituitary. These benign tumors are called adenomas.\n                \nAcromegaly is most often diagnosed in middle-aged adults, although symptoms can appear at any age. If not treated, acromegaly can result in serious illness and premature death. Acromegaly is treatable in most patients, but because of its slow and often \"sneaky\" onset, it often is not diagnosed early or correctly. The most serious health consequences of acromegaly are type 2 diabetes, high blood pressure, increased risk of cardiovascular disease, and arthritis. Patients with acromegaly are also at increased risk for colon polyps, which may develop into colon cancer if not removed.\n                \nWhen GH-producing tumors occur in childhood, the disease that results is called gigantism rather than acromegaly. A child's height is determined by the length of the so-called long bones in the legs. In response to GH, these bones grow in length at the growth platesareas near either end of the bone. Growth plates fuse after puberty, so the excessive GH production in adults does not result in increased height. However, prolonged exposure to excess GH before the growth plates fuse causes increased growth of the long bones and thus increased height. Pediatricians may become concerned about this possibility if a child's growth rate suddenly and markedly increases beyond what would be predicted by previous growth and how tall the child's parents are."}
{"_id":"178cc433-cdcc-437e-a6ba-0bd8a423089b","text":"The name acromegaly comes from the Greek words for \"extremities\" and \"enlargement,\" reflecting one of its most common symptomsthe abnormal growth of the hands and feet. Swelling of the hands and feet is often an early feature, with patients noticing a change in ring or shoe size, particularly shoe width. Gradually, bone changes alter the patient's facial features: The brow and lower jaw protrude, the nasal bone enlarges, and the teeth space out.\n                \nOvergrowth of bone and cartilage often leads to arthritis. When tissue thickens, it may trap nerves, causing carpal tunnel syndrome, which results in numbness and weakness of the hands. Body organs, including the heart, may enlarge.\n                \nOther symptoms of acromegaly include\n                \n- joint aches  - thick, coarse, oily skin  - skin tags  - enlarged lips, nose, and tongue  - deepening of the voice due to enlarged sinuses and vocal cords  - sleep apnea-breaks in breathing during sleep due to obstruction of the airway  - excessive sweating and skin odor  - fatigue and weakness  - headaches  - impaired vision  - abnormalities of the menstrual cycle and sometimes breast discharge in women  - erectile dysfunction in men  - decreased libido"}
{"_id":"a170c6f5-0d32-4022-a670-eeae0afa511f","text":"Acromegaly is caused by prolonged overproduction of GH by the pituitary gland. The pituitary produces several important hormones that control body functions such as growth and development, reproduction, and metabolism. But hormones never seem to act simply and directly. They usually \"cascade\" or flow in a series, affecting each other's production or release into the bloodstream.\n                \nGH is part of a cascade of hormones that, as the name implies, regulates the physical growth of the body. This cascade begins in a part of the brain called the hypothalamus. The hypothalamus makes hormones that regulate the pituitary. One of the hormones in the GH series, or \"axis,\" is growth hormone-releasing hormone (GHRH), which stimulates the pituitary gland to produce GH.\n                \nSecretion of GH by the pituitary into the bloodstream stimulates the liver to produce another hormone called insulin-like growth factor I (IGF-I). IGF-I is what actually causes tissue growth in the body. High levels of IGF-I, in turn, signal the pituitary to reduce GH production.\n                \nThe hypothalamus makes another hormone called somatostatin, which inhibits GH production and release. Normally, GHRH, somatostatin, GH, and IGF-I levels in the body are tightly regulated by each other and by sleep, exercise, stress, food intake, and blood sugar levels. If the pituitary continues to make GH independent of the normal regulatory mechanisms, the level of IGF-I continues to rise, leading to bone overgrowth and organ enlargement. High levels of IGF-I also cause changes in glucose (sugar) and lipid (fat) metabolism and can lead to diabetes, high blood pressure, and heart disease.\n                \nPituitary Tumors\n                \nIn more than 95 percent of people with acromegaly, a benign tumor of the pituitary gland, called an adenoma, produces excess GH. Pituitary tumors are labeled either micro- or macro-adenomas, depending on their size. Most GH-secreting tumors are macro-adenomas, meaning they are larger than 1 centimeter. Depending on their location, these larger tumors may compress surrounding brain structures. For example, a tumor growing upward may affect the optic chiasm-where the optic nerves crossleading to visual problems and vision loss. If the tumor grows to the side, it may enter an area of the brain called the cavernous sinus where there are many nerves, potentially damaging them.\n                \nCompression of the surrounding normal pituitary tissue can alter production of other hormones. These hormonal shifts can lead to changes in menstruation and breast discharge in women and erectile dysfunction in men. If the tumor affects the part of the pituitary that controls the thyroidanother hormone-producing glandthen thyroid hormones may decrease. Too little thyroid hormone can cause weight gain, fatigue, and hair and skin changes. If the tumor affects the part of the pituitary that controls the adrenal gland, the hormone cortisol may decrease. Too little cortisol can cause weight loss, dizziness, fatigue, low blood pressure, and nausea.\n                \nSome GH-secreting tumors may also secrete too much of other pituitary hormones. For example, they may produce prolactin, the hormone that stimulates the mammary glands to produce milk. Rarely, adenomas may produce thyroid-stimulating hormone. Doctors should assess all pituitary hormones in people with acromegaly.\n                \nRates of GH production and the aggressiveness of the tumor vary greatly among people with adenomas. Some adenomas grow slowly and symptoms of GH excess are often not noticed for many years. Other adenomas grow more rapidly and invade surrounding brain areas or the venous sinuses, which are located near the pituitary gland. Younger patients tend to have more aggressive tumors. Regardless of size, these tumors are always benign.\n                \nMost pituitary tumors develop spontaneously and are not genetically inherited. They are the result of a genetic alteration in a single pituitary cell, which leads to increased cell division and tumor formation. This genetic change, or mutation, is not present at birth, but happens later in life. The mutation occurs in a gene that regulates the transmission of chemical signals within pituitary cells. It permanently switches on the signal that tells the cell to divide and secrete GH. The events within the cell that cause disordered pituitary cell growth and GH oversecretion currently are the subject of intensive research.\n                \nNonpituitary Tumors\n                \nRarely, acromegaly is caused not by pituitary tumors but by tumors of the pancreas, lungs, and other parts of the brain. These tumors also lead to excess GH, either because they produce GH themselves or, more frequently, because they produce GHRH, the hormone that stimulates the pituitary to make GH. When these non-pituitary tumors are surgically removed, GH levels fall and the symptoms of acromegaly improve.\n                \nIn patients with GHRH-producing, non-pituitary tumors, the pituitary still may be enlarged and may be mistaken for a tumor. Physicians should carefully analyze all \"pituitary tumors\" removed from patients with acromegaly so they do not overlook the rare possibility that a tumor elsewhere in the body is causing the disorder."}
{"_id":"f1a820e9-cdcc-4409-bc26-ead3b62d6ac1","text":"Small pituitary adenomas are common, affecting about 17 percent of the population.1 However, research suggests most of these tumors do not cause symptoms and rarely produce excess GH.2 Scientists estimate that three to four out of every million people develop acromegaly each year and about 60 out of every million people suffer from the disease at any time.3 Because the clinical diagnosis of acromegaly is often missed, these numbers probably underestimate the frequency of the disease."}
{"_id":"70c67bd3-b01d-43dd-89d3-2e9f8b61f968","text":"Blood tests\n                \nIf acromegaly is suspected, a doctor must measure the GH level in a persons blood to determine if it is elevated. However, a single measurement of an elevated blood GH level is not enough to diagnose acromegaly: Because GH is secreted by the pituitary in impulses, or spurts, its concentration in the blood can vary widely from minute to minute. At a given moment, a person with acromegaly may have a normal GH level, whereas a GH level in a healthy person may even be five times higher.\n                \nMore accurate information is obtained when GH is measured under conditions that normally suppress GH secretion. Health care professionals often use the oral glucose tolerance test to diagnose acromegaly because drinking 75 to 100 grams of glucose solution lowers blood GH levels to less than 1 nanogram per milliliter (ng\/ml) in healthy people. In people with GH overproduction, this suppression does not occur. The oral glucose tolerance test is a highly reliable method for confirming a diagnosis of acromegaly.\n                \nPhysicians also can measure IGF-I levels, which increase as GH levels go up, in people with suspected acromegaly. Because IGF-I levels are much more stable than GH levels over the course of the day, they are often a more practical and reliable screening measure. Elevated IGF-I levels almost always indicate acromegaly. However, a pregnant womans IGF-I levels are two to three times higher than normal. In addition, physicians must be aware that IGF-I levels decline with age and may also be abnormally low in people with poorly controlled diabetes or liver or kidney disease.\n                \nImaging\n                \nAfter acromegaly has been diagnosed by measuring GH or IGF-I levels, a magnetic resonance imaging (MRI) scan of the pituitary is used to locate and detect the size of the tumor causing GH overproduction. MRI is the most sensitive imaging technique, but computerized tomography (CT) scans can be used if the patient should not have MRI. For example, people who have pacemakers or other types of implants containing metal should not have an MRI scan because MRI machines contain powerful magnets.\n                \nIf a head scan fails to detect a pituitary tumor, the physician should look for non-pituitary \"ectopic\" tumors in the chest, abdomen, or pelvis as the cause of excess GH. The presence of such tumors usually can be diagnosed by measuring GHRH in the blood and by a CT scan of possible tumor sites.\n                \nRarely, a pituitary tumor secreting GH may be too tiny to detect even with a sensitive MRI scan."}
{"_id":"2743581d-0ec7-46d3-81e4-870bca8d2e93","text":"Currently, treatment options include surgical removal of the tumor, medical therapy, and radiation therapy of the pituitary.\n                \nGoals of treatment are to\n                \n- reduce excess hormone production to normal levels  - relieve the pressure that the growing pituitary tumor may be exerting on the surrounding brain areas  - preserve normal pituitary function or treat hormone deficiencies  - improve the symptoms of acromegaly\n                \nSurgery\n                \nSurgery is the first option recommended for most people with acromegaly, as it is often a rapid and effective treatment. The surgeon reaches the pituitary via an incision through the nose or inside the upper lip and, with special tools, removes the tumor tissue in a procedure called transsphenoidal surgery. This procedure promptly relieves the pressure on the surrounding brain regions and leads to a rapid lowering of GH levels. If the surgery is successful, facial appearance and soft tissue swelling improve within a few days.\n                \nSurgery is most successful in patients with blood GH levels below 45 ng\/ml before the operation and with pituitary tumors no larger than 10 millimeters (mm) in diameter. Success depends in large part on the skill and experience of the surgeon, as well as the location of the tumor. Even with the most experienced neurosurgeon, the chance of a cure is small if the tumor has extended into critical brain structures or into the cavernous sinus where surgery could be risky.\n                \nThe success rate also depends on what level of GH is defined as a cure. The best measure of surgical success is normalization of GH and IGF-I levels. The overall rate of remission-control of the disease-after surgery ranges from 55 to 80 percent. (See For More Information to locate a board-certified neurosurgeon.)\n                \nA possible complication of surgery is damage to the surrounding normal pituitary tissue, which requires lifelong use of pituitary hormone replacement. The part of the pituitary that stores antidiuretic hormonea hormone important in water balancemay be temporarily or, rarely, permanently damaged and the patient may require medical therapy. Other potential problems include cerebrospinal fluid leaks and, rarely, meningitis. Cerebrospinal fluid bathes the brain and can leak from the nose if the incision area doesnt heal well. Meningitis is a bacterial or viral infection of the meninges, the outer covering of the brain.\n                \nEven when surgery is successful and hormone levels return to normal, people with acromegaly must be carefully monitored for years for possible recurrence of the disease. More commonly, hormone levels improve, but do not return to normal. Additional treatment, usually medications, may be required.\n                \nMedical Therapy\n                \nMedical therapy is most often used if surgery does not result in a cure and sometimes to shrink large tumors before surgery. Three medication groups are used to treat acromegaly.\n                \nSomatostatin analogs (SSAs) are the first medication group used to treat acromegaly. They shut off GH production and are effective in lowering GH and IGF-I levels in 50 to 70 percent of patients. SSAs also reduce tumor size in around 0 to 50 percent of patients but only to a modest degree. Several studies have shown that SSAs are safe and effective for long-term treatment and in treating patients with acromegaly caused by nonpituitary tumors. Long-acting SSAs are given by intramuscular injection once a month.\n                \nDigestive problems-such as loose stools, nausea, and gas-are a side effect in about half of people taking SSAs. However, the effects are usually temporary and rarely severe. About 10 to 20 percent of patients develop gallstones, but the gallstones do not usually cause symptoms. In rare cases, treatment can result in elevated blood glucose levels. More commonly, SSAs reduce the need for insulin and improve blood glucose control in some people with acromegaly who already have diabetes.\n                \nThe second medication group is the GH receptor antagonists (GHRAs), which interfere with the action of GH. They normalize IGF-I levels in more than 90 percent of patients. They do not, however, lower GH levels. Given once a day through injection, GHRAs are usually well-tolerated by patients. The long-term effects of these drugs on tumor growth are still under study. Side effects can include headaches, fatigue, and abnormal liver function.\n                \nDopamine agonists make up the third medication group. These drugs are not as effective as the other medications at lowering GH or IGF-I levels, and they normalize IGF-I levels in only a minority of patients. Dopamine agonists are sometimes effective in patients who have mild degrees of excess GH and have both acromegaly and hyperprolactinemiatoo much of the hormone prolactin. Dopamine agonists can be used in combination with SSAs. Side effects can include nausea, headache, and lightheadedness.\n                \nAgonist: A drug that binds to a receptor of a cell and triggers a response by the cell, mimicking the action of a naturally occurring substance.   Antagonist: A chemical that acts within the body to reduce the physiological activity of another chemical substance or hormone.\n                \nRadiation Therapy\n                \nRadiation therapy is usually reserved for people who have some tumor remaining after surgery and do not respond to medications. Because radiation leads to a slow lowering of GH and IGF-I levels, these patients often also receive medication to lower hormone levels. The full effect of this therapy may not occur for many years.\n                \nThe two types of radiation delivery are conventional and stereotactic. Conventional radiation delivery targets the tumor with external beams but can damage surrounding tissue. The treatment delivers small doses of radiation multiple times over 4 to 6 weeks, giving normal tissue time to heal between treatments.\n                \nStereotactic delivery allows precise targeting of a high-dose beam of radiation at the tumor from varying angles. The patient must wear a rigid head frame to keep the head still. The types of stereotactic radiation delivery currently available are proton beam, linear accelerator (LINAC), and gamma knife. With stereotactic delivery, the tumor must be at least 5 mm from the optic chiasm to prevent radiation damage. This treatment can sometimes be done in a single session, reducing the risk of damage to surrounding tissue.\n                \nAll forms of radiation therapy cause a gradual decline in production of other pituitary hormones over time, resulting in the need for hormone replacement in most patients. Radiation also can impair a patients fertility. Vision loss and brain injury are rare complications. Rarely, secondary tumors can develop many years later in areas that were in the path of the radiation beam."}
{"_id":"a0fbb77f-e324-487e-8b61-9095404748ff","text":"Currently, treatment options include surgical removal of the tumor, medical therapy, and radiation therapy of the pituitary.\n                \nGoals of treatment are to\n                \n- reduce excess hormone production to normal levels  - relieve the pressure that the growing pituitary tumor may be exerting on the surrounding brain areas  - preserve normal pituitary function or treat hormone deficiencies  - improve the symptoms of acromegaly\n                \nSurgery\n                \nSurgery is the first option recommended for most people with acromegaly, as it is often a rapid and effective treatment. The surgeon reaches the pituitary via an incision through the nose or inside the upper lip and, with special tools, removes the tumor tissue in a procedure called transsphenoidal surgery. This procedure promptly relieves the pressure on the surrounding brain regions and leads to a rapid lowering of GH levels. If the surgery is successful, facial appearance and soft tissue swelling improve within a few days.\n                \nSurgery is most successful in patients with blood GH levels below 45 ng\/ml before the operation and with pituitary tumors no larger than 10 millimeters (mm) in diameter. Success depends in large part on the skill and experience of the surgeon, as well as the location of the tumor. Even with the most experienced neurosurgeon, the chance of a cure is small if the tumor has extended into critical brain structures or into the cavernous sinus where surgery could be risky.\n                \nThe success rate also depends on what level of GH is defined as a cure. The best measure of surgical success is normalization of GH and IGF-I levels. The overall rate of remission-control of the disease-after surgery ranges from 55 to 80 percent. (See For More Information to locate a board-certified neurosurgeon.)\n                \nA possible complication of surgery is damage to the surrounding normal pituitary tissue, which requires lifelong use of pituitary hormone replacement. The part of the pituitary that stores antidiuretic hormonea hormone important in water balancemay be temporarily or, rarely, permanently damaged and the patient may require medical therapy. Other potential problems include cerebrospinal fluid leaks and, rarely, meningitis. Cerebrospinal fluid bathes the brain and can leak from the nose if the incision area doesnt heal well. Meningitis is a bacterial or viral infection of the meninges, the outer covering of the brain.\n                \nEven when surgery is successful and hormone levels return to normal, people with acromegaly must be carefully monitored for years for possible recurrence of the disease. More commonly, hormone levels improve, but do not return to normal. Additional treatment, usually medications, may be required.\n                \nMedical Therapy\n                \nMedical therapy is most often used if surgery does not result in a cure and sometimes to shrink large tumors before surgery. Three medication groups are used to treat acromegaly.\n                \nSomatostatin analogs (SSAs) are the first medication group used to treat acromegaly. They shut off GH production and are effective in lowering GH and IGF-I levels in 50 to 70 percent of patients. SSAs also reduce tumor size in around 0 to 50 percent of patients but only to a modest degree. Several studies have shown that SSAs are safe and effective for long-term treatment and in treating patients with acromegaly caused by nonpituitary tumors. Long-acting SSAs are given by intramuscular injection once a month.\n                \nDigestive problems-such as loose stools, nausea, and gas-are a side effect in about half of people taking SSAs. However, the effects are usually temporary and rarely severe. About 10 to 20 percent of patients develop gallstones, but the gallstones do not usually cause symptoms. In rare cases, treatment can result in elevated blood glucose levels. More commonly, SSAs reduce the need for insulin and improve blood glucose control in some people with acromegaly who already have diabetes.\n                \nThe second medication group is the GH receptor antagonists (GHRAs), which interfere with the action of GH. They normalize IGF-I levels in more than 90 percent of patients. They do not, however, lower GH levels. Given once a day through injection, GHRAs are usually well-tolerated by patients. The long-term effects of these drugs on tumor growth are still under study. Side effects can include headaches, fatigue, and abnormal liver function.\n                \nDopamine agonists make up the third medication group. These drugs are not as effective as the other medications at lowering GH or IGF-I levels, and they normalize IGF-I levels in only a minority of patients. Dopamine agonists are sometimes effective in patients who have mild degrees of excess GH and have both acromegaly and hyperprolactinemiatoo much of the hormone prolactin. Dopamine agonists can be used in combination with SSAs. Side effects can include nausea, headache, and lightheadedness.\n                \nAgonist: A drug that binds to a receptor of a cell and triggers a response by the cell, mimicking the action of a naturally occurring substance.   Antagonist: A chemical that acts within the body to reduce the physiological activity of another chemical substance or hormone.\n                \nRadiation Therapy\n                \nRadiation therapy is usually reserved for people who have some tumor remaining after surgery and do not respond to medications. Because radiation leads to a slow lowering of GH and IGF-I levels, these patients often also receive medication to lower hormone levels. The full effect of this therapy may not occur for many years.\n                \nThe two types of radiation delivery are conventional and stereotactic. Conventional radiation delivery targets the tumor with external beams but can damage surrounding tissue. The treatment delivers small doses of radiation multiple times over 4 to 6 weeks, giving normal tissue time to heal between treatments.\n                \nStereotactic delivery allows precise targeting of a high-dose beam of radiation at the tumor from varying angles. The patient must wear a rigid head frame to keep the head still. The types of stereotactic radiation delivery currently available are proton beam, linear accelerator (LINAC), and gamma knife. With stereotactic delivery, the tumor must be at least 5 mm from the optic chiasm to prevent radiation damage. This treatment can sometimes be done in a single session, reducing the risk of damage to surrounding tissue.\n                \nAll forms of radiation therapy cause a gradual decline in production of other pituitary hormones over time, resulting in the need for hormone replacement in most patients. Radiation also can impair a patients fertility. Vision loss and brain injury are rare complications. Rarely, secondary tumors can develop many years later in areas that were in the path of the radiation beam."}
{"_id":"db3c891d-e4ac-4962-ab3c-363491459282","text":"No single treatment is effective for all patients. Treatment should be individualized, and often combined, depending on patient characteristics such as age and tumor size.\n                \nIf the tumor has not yet invaded surrounding nonpituitary tissues, removal of the pituitary adenoma by an experienced neurosurgeon is usually the first choice. Even if a cure is not possible, surgery may be performed if the patient has symptoms of neurological problems such as loss of peripheral vision or cranial nerve problems. After surgery, hormone levels are measured to determine whether a cure has been achieved. This determination can take up to 8 weeks because IGF-I lasts a long time in the body's circulation. If cured, a patient must be monitored for a long time for increasing GH levels.\n                \nIf surgery does not normalize hormone levels or a relapse occurs, an endocrinologist should recommend additional drug therapy. With each medication, long-term therapy is necessary because their withdrawal can lead to rising GH levels and tumor re-expansion.\n                \nRadiation therapy is generally reserved for patients whose tumors are not completely removed by surgery, who are not good candidates for surgery because of other health problems, or who do not respond adequately to surgery and medication."}
{"_id":"99d71ab4-fbcb-408a-b100-c7765fc5a87c","text":"- Acromegaly is a hormonal disorder that results from too much growth hormone (GH) in the body.  - In most people with acromegaly, a benign tumor of the pituitary gland produces excess GH.  - Common features of acromegaly include abnormal growth of the hands and feet; bone growth in the face that leads to a protruding lower jaw and brow and an enlarged nasal bone; joint aches; thick, coarse, oily skin; and enlarged lips, nose, and tongue.  - Acromegaly can cause sleep apnea, fatigue and weakness, headaches, impaired vision, menstrual abnormalities in women, and erectile dysfunction in men.  - Acromegaly is diagnosed through a blood test. Magnetic resonance imaging (MRI) of the pituitary is then used to locate and detect the size of the tumor causing GH overproduction.  - The first line of treatment is usually surgical removal of the tumor. Medication or radiation may be used instead of or in addition to surgery."}
{"_id":"2b41cb8c-528c-42bd-b4b9-14d7d45de0b2","text":"Cirrhosis* is scarring of the liver. Scar tissue forms because of injury or long-term disease. Scar tissue replaces healthy liver tissue and blocks the normal flow of blood through the liver.\n                \nA healthy liver\n                \n- makes proteins  - helps fight infections  - cleans the blood  - helps digest food  - stores a form of sugar that your body uses for energy\n                \nA liver with too much scar tissue cannot work properly. You cannot live without a liver that works. But early treatment can control symptoms and keep cirrhosis from getting worse.\n                \n\n                \n*See the Pronunciation Guide for tips on how to say the words in bold type."}
{"_id":"5d713469-3662-42c4-a74e-11d3a6cbfd1e","text":"Causes of cirrhosis include\n                \n- heavy alcohol use  - some drugs, medicines, and harmful chemicals  - infections  - chronic hepatitis B, C, or Dviral infections that attack the liver  - autoimmune hepatitis, which causes the bodys immune system to destroy liver cells  - nonalcoholic fatty liver disease, which is often caused by obesity  - diseases that damage or destroy bile ductstubes that carry bile from the liver\n                \nSome inherited diseasesdiseases that are passed from parent to childcan cause cirrhosis:\n                \n- hemochromatosis, a disease that causes iron to collect in the liver  - Wilson disease, a condition that causes copper to build up in the liver  - porphyria, a disorder that affects the skin, bone marrow, and liver"}
{"_id":"98f660bc-db28-477d-ae3a-b11d8fee2bba","text":"You may have no symptoms in the early stages of cirrhosis. As cirrhosis gets worse you may\n                \n- feel tired or weak  - lose your appetite  - feel sick to your stomach  - lose weight  - notice red, spider-shaped blood vessels under your skin\n                \nCirrhosis can lead to other serious problems:\n                \n- You may bruise or bleed easily, or have nosebleeds.  - Bloating or swelling may occur as fluid builds up in your legs or abdomenthe area between your chest and hips. Fluid buildup in your legs is called edema; buildup in your abdomen is called ascites.  - Medicines, including those you can buy over the counter such as vitamins and herbal supplements, may have a stronger effect on you. Your liver does not break medicines down as quickly as a healthy liver would.   - Waste materials from food may build up in your blood or brain and cause confusion or difficulty thinking.   - Blood pressure may increase in the vein entering your liver, a condition called portal hypertension.   - Enlarged veins, called varices, may develop in your esophagus and stomach. Varices can bleed suddenly, causing you to throw up blood or pass blood in a bowel movement.   - Your kidneys may not work properly or may fail.   - Your skin and the whites of your eyes may turn yellow, a condition called jaundice.   - You may develop severe itching.   - You may develop gallstones.\n                \nIn the early stages, cirrhosis causes your liver to swell. Then, as more scar tissue replaces healthy tissue, your liver shrinks.\n                \nA small number of people with cirrhosis also get liver cancer."}
{"_id":"8e4c472d-87a3-45e5-9354-8258d02fc603","text":"Your doctor will examine you and may perform\n                \n- blood tests to see whether your liver is working properly   - imaging tests, which may show the size of your liver and show swelling or shrinkage   - a liver biopsy, in which a doctor uses a needle to take a small piece of liver tissue to view with a microscope to look for scar tissue"}
{"_id":"b19b63c4-5eb6-497e-9406-d831b3afeb71","text":"Once you have cirrhosis, nothing can make all the scar tissue go away. But treating the cause will keep cirrhosis from getting worse. For example, if cirrhosis is from heavy alcohol use, the treatment is to completely stop drinking alcohol. If cirrhosis is caused by hepatitis C, then the hepatitis C virus is treated with medicine.\n                \n\n                \nYour doctor will suggest treatment based on the cause of your cirrhosis and your symptoms. Being diagnosed early and carefully following a treatment plan can help many people with cirrhosis. In the late stages of cirrhosis, certain treatments may not be effective. In that case, your doctor will work with you to prevent or manage the problems that cirrhosis can cause.\n                \n\n                \nWhat if the cirrhosis treatment doesnt work?   If too much scar tissue forms, your liver could fail. Then you will need a liver transplant. A liver transplant can return you to good health. For information about liver transplantation, see the booklet What I need to know about Liver Transplantation from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)."}
{"_id":"e6dd4cf7-4091-4bb2-b57a-911705066efd","text":"If too much scar tissue forms, your liver could fail. Then you will need a liver transplant. A liver transplant can return you to good health. For information about liver transplantation, see the booklet What I need to know about Liver Transplantation from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)."}
{"_id":"b41fb916-b781-48ff-b174-2fccc71edf75","text":"To prevent cirrhosis,\n                \n- see your doctor for treatment of your liver disease. Many of the causes of cirrhosis are treatable. Early treatment may prevent cirrhosis.   - try to keep your weight in the normal range. Being overweight can make several liver diseases worse.   - do not drink any alcohol. Alcohol can harm liver cells. Drinking large amounts of alcohol over many years is one of the major causes of cirrhosis.   - do not use illegal drugs, which can increase your chances of getting hepatitis B or hepatitis C.   - see your doctor if you have hepatitis. Treatments for hepatitis B, C, and D are available. If you are on treatment, carefully follow your treatment directions.   - if you have autoimmune hepatitis, take your medicines and have regular checkups as recommended by your doctor or a liver specialist."}
{"_id":"29c7c4bc-90bc-43c1-8bb2-bdc400f68277","text":"- Cirrhosis is scarring of the liver. Scar tissue replaces healthy liver tissue.  - Some common causes of cirrhosis include heavy alcohol use, hepatitis infections, and nonalcoholic fatty liver disease.  - In the early stages of cirrhosis, you may have no symptoms. As the disease gets worse, cirrhosis can cause serious problems.  - Once you have cirrhosis, nothing can make all the scar tissue go away. But treatment can prevent cirrhosis from getting worse.  - If too much scar tissue forms and your liver fails, you will need a liver transplant.  - You can take steps to prevent cirrhosis or keep it from getting worse."}
{"_id":"1a651cef-f131-4cb6-8f37-4c51a1cacc4e","text":"NDM is a monogenic form of diabetes that occurs in the first 6 months of life. It is a rare condition occurring in only one in 100,000 to 500,000 live births. Infants with NDM do not produce enough insulin, leading to an increase in blood glucose. NDM can be mistaken for the much more common type 1 diabetes, but type 1 diabetes usually occurs later than the first 6 months of life. In about half of those with NDM, the condition is lifelong and is called permanent neonatal diabetes mellitus (PNDM). In the rest of those with NDM, the condition is transient and disappears during infancy but can reappear later in life; this type of NDM is called transient neonatal diabetes mellitus (TNDM). Specific genes that can cause NDM have been identified. More information about each type of NDM is provided in the appendix.\n                \nSymptoms of NDM include thirst, frequent urination, and dehydration. NDM can be diagnosed by finding elevated levels of glucose in blood or urine. In severe cases, the deficiency of insulin may cause the body to produce an excess of acid, resulting in a potentially life-threatening condition called ketoacidosis. Most fetuses with NDM do not grow well in the womb and newborns are much smaller than those of the same gestational age, a condition called intrauterine growth restriction. After birth, some infants fail to gain weight and grow as rapidly as other infants of the same age and sex. Appropriate therapy improves and may normalize growth and development."}
{"_id":"cc2aff99-8dc3-4011-95e6-bfbb66d44577","text":"MODY is a monogenic form of diabetes that usually first occurs during adolescence or early adulthood. However, MODY sometimes remains undiagnosed until later in life. A number of different gene mutations have been shown to cause MODY, all of which limit the ability of the pancreas to produce insulin. This process leads to the high blood glucose levels characteristic of diabetes and, in time, may damage body tissues, particularly the eyes, kidneys, nerves, and blood vessels. MODY accounts for about 1 to 5 percent of all cases of diabetes in the United States. Family members of people with MODY are at greatly increased risk for the condition.\n                \nPeople with MODY may have only mild or no symptoms of diabetes and their hyperglycemia may only be discovered during routine blood tests. MODY may be confused with type 1 or type 2 diabetes. People with MODY are generally not overweight and do not have other risk factors for type 2 diabetes, such as high blood pressure or abnormal blood fat levels. While both type 2 diabetes and MODY can run in families, people with MODY typically have a family history of diabetes in multiple successive generations, meaning that MODY is present in a grandparent, a parent, and a child. Unlike people with type 1 diabetes who always require insulin, people with MODY can often be treated with oral diabetes medications. Treatment varies depending on the genetic mutation that has caused the MODY. More information about each type of MODY is provided in the appendix."}
{"_id":"ed510b70-b764-4123-a3c4-824c8f12f8c3","text":"Testing for monogenic diabetes involves providing a blood sample from which DNA is isolated. The DNA is analyzed for changes in the genes that cause monogenic diabetes. Abnormal results can determine the gene responsible for diabetes in a particular individual or show whether someone is likely to develop a monogenic form of diabetes in the future. Genetic testing can also be helpful in selecting the most appropriate treatment for individuals with monogenic diabetes. Prenatal testing can diagnose these conditions in unborn children.\n                \nMost forms of monogenic diabetes are caused by dominant mutations, meaning that the condition can be passed on to children when only one parent is affected. In contrast, if the mutation is a recessive mutation, a disease gene must be inherited from both parents for diabetes to occur. For recessive forms of monogenic diabetes, testing can indicate whether parents or siblings without disease are carriers for recessive genetic conditions that could be inherited by their children.\n                \nIf you suspect that you or a member of your family may have a monogenic form of diabetes, you should seek help from health care professionals-physicians and genetic counselors-who have specialized knowledge and experience in this area. They can determine whether genetic testing is appropriate, select the genetic tests that should be performed, and provide information about the basic principles of genetics, genetic testing options, and confidentiality issues. They also can review the test results with the patient or parent after testing, make recommendations about how to proceed, and discuss testing options for other family members."}
{"_id":"145fba86-2c9e-4303-a4cf-729c46505b40","text":"- Mutations in single genes can cause rare forms of diabetes.  - Genetic testing can identify many forms of monogenic diabetes.  - A physician evaluates whether genetic testing is appropriate.  - A correct diagnosis aided by genetic testing can lead to optimal treatment.  - Recent research results show that people with certain forms of monogenic diabetes can be treated with oral diabetes medications instead of insulin injections."}
{"_id":"a7f45a06-9800-40f0-9302-56cfa883cbaa","text":"Gallstones are hard particles that develop in the gallbladder. The gallbladder is a small, pear-shaped organ located in the upper right abdomenthe area between the chest and hipsbelow the liver.\n                \nGallstones can range in size from a grain of sand to a golf ball. The gallbladder can develop a single large gallstone, hundreds of tiny stones, or both small and large stones. Gallstones can cause sudden pain in the upper right abdomen. This pain, called a gallbladder attack or biliary colic, occurs when gallstones block the ducts of the biliary tract."}
{"_id":"8aed8508-0086-4e53-8194-54077bd91644","text":"The biliary tract consists of the gallbladder and the bile ducts. The bile ducts carry bile and other digestive enzymes from the liver and pancreas to the duodenumthe fi rst part of the small intestine.\n                \nThe liver produces bilea fl uid that carries toxins and waste products out of the body and helps the body digest fats and the fat-soluble vitamins A, D, E, and K. Bile mostly consists of cholesterol, bile salts, and bilirubin. Bilirubin, a reddish-yellow substance, forms when hemoglobin from red blood cells breaks down. Most bilirubin is excreted through bile.\n                \n\n                \n\n                \nThe bile ducts of the biliary tract include the hepatic ducts, the common bile duct, the pancreatic duct, and the cystic duct. The gallbladder stores bile. Eating signals the gallbladder to contract and empty bile through the cystic duct and common bile duct into the duodenum to mix with food."}
{"_id":"e7349b8c-5b28-498e-b671-4befa3e9078a","text":"Imbalances in the substances that make up bile cause gallstones. Gallstones may form if bile contains too much cholesterol, too much bilirubin, or not enough bile salts. Scientists do not fully understand why these imbalances occur. Gallstones also may form if the gallbladder does not empty completely or often enough.\n                \nThe two types of gallstones are cholesterol and pigment stones:\n                \n- Cholesterol stones, usually yellow-green in color, consist primarily of hardened cholesterol. In the United States, more than 80 percent of gallstones are cholesterol stones.1  - Pigment stones, dark in color, are made of bilirubin."}
{"_id":"09ff23ec-499b-4561-b37c-94d4cc6d689c","text":"Certain people have a higher risk of developing gallstones than others:2\n                \n- Women are more likely to develop gallstones than men. Extra estrogen can increase cholesterol levels in bile and decrease gallbladder contractions, which may cause gallstones to form. Women may have extra estrogen due to pregnancy, hormone replacement therapy, or birth control pills.   - People over age 40 are more likely to develop gallstones than younger people.   - People with a family history of gallstones have a higher risk.   - American Indians have genetic factors that increase the amount of cholesterol in their bile. In fact, American Indians have the highest rate of gallstones in the United Statesalmost 65 percent of women and 30 percent of men have gallstones.   - Mexican Americans are at higher risk of developing gallstones.\n                \nOther factors that affect a persons risk of gallstones include2\n                \n- Obesity. People who are obese, especially women, have increased risk of developing gallstones. Obesity increases the amount of cholesterol in bile, which can cause stone formation.   - Rapid weight loss. As the body breaks down fat during prolonged fasting and rapid weight loss, the liver secretes extra cholesterol into bile. Rapid weight loss can also prevent the gallbladder from emptying properly. Low-calorie diets and bariatric surgerysurgery that limits the amount of food a person can eat or digestlead to rapid weight loss and increased risk of gallstones.   - Diet. Research suggests diets high in calories and refi ned carbohydrates and low in fi ber increase the risk of gallstones. Refi ned carbohydrates are grains processed to remove bran and germ, which contain nutrients and  fiber. Examples of refi ned carbohydrates include white bread and white rice.   - Certain intestinal diseases. Diseases that affect normal absorption of nutrients, such as Crohns disease, are associated with gallstones.   - Metabolic syndrome, diabetes, and insulin resistance. These conditions increase the risk of gallstones. Metabolic syndrome also increases the risk of gallstone complications. Metabolic syndrome is a group of traits and medical conditions linked to being overweight or obese that puts people at risk for heart disease and type 2 diabetes.\n                \nMore information about these conditions is provided in the NIDDK health topic, Insulin Resistance and Prediabetes.\n                \n- cirrhosisa condition in which the liver slowly deteriorates and malfunctions due to chronic, or long lasting, injury   - infections in the bile ducts   - severe hemolytic anemiasconditions in which red blood cells are continuously broken down, such as sickle cell anemia"}
{"_id":"9ea13f28-f41f-437c-bdf7-bbb142f529f7","text":"Many people with gallstones do not have symptoms. Gallstones that do not cause symptoms are called asymptomatic, or silent, gallstones. Silent gallstones do not interfere with the function of the gallbladder, liver, or pancreas.\n                \nIf gallstones block the bile ducts, pressure increases in the gallbladder, causing a gallbladder attack. The pain usually lasts from 1 to several hours.1 Gallbladder attacks often follow heavy meals, and they usually occur in the evening or during the night.\n                \nGallbladder attacks usually stop when gallstones move and no longer block the bile ducts. However, if any of the bile ducts remain blocked for more than a few hours, complications can occur. Complications include infl ammation, or swelling, of the gallbladder and severe damage or infection of the gallbladder, bile ducts, or liver.\n                \nA gallstone that becomes lodged in the common bile duct near the duodenum and blocks the pancreatic duct can cause gallstone pancreatitisin flammation of the pancreas.\n                \nLeft untreated, blockages of the bile ducts or pancreatic duct can be fatal."}
{"_id":"6f4568b2-5a1c-488e-980a-45a48e182273","text":"People who think they have had a gallbladder attack should notify their health care provider. Although these attacks usually resolve as gallstones move, complications can develop if the bile ducts remain blocked.\n                \nPeople with any of the following symptoms during or after a gallbladder attack should see a health care provider immediately:\n                \n- abdominal pain lasting more than 5 hours   - nausea and vomiting   - fevereven a low-grade feveror chills  - yellowish color of the skin or whites of the eyes, called jaundice   - tea-colored urine and light-colored stools\n                \nThese symptoms may be signs of serious infection or infl ammation of the gallbladder, liver, or pancreas."}
{"_id":"95dc6224-a3d3-4204-a56a-d1397a7322e0","text":"A health care provider will usually order an ultrasound exam to diagnose gallstones. Other imaging tests may also be used.\n                \n- Ultrasound exam. Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. A specially trained technician performs the procedure in a health care providers offi ce, outpatient center, or hospital, and a radiologista doctor who specializes in medical imaginginterprets the images. Anesthesia is not needed. If gallstones are present, they will be visible in the image. Ultrasound is the most accurate method to detect gallstones.  - Computerized tomography (CT) scan. A CT scan is an x ray that produces pictures of the body. A CT scan may include the injection of a special dye, called contrast medium. CT scans use a combination of x rays and computer technology to create three-dimensional (3-D) images. CT scans require the person to lie on a table that slides into a tunnel-shaped device where the x rays are taken. An x-ray technician performs the procedure in an outpatient center or hospital, and a radiologist interprets the images. Anesthesia is not needed. CT scans can show gallstones or complications, such as infection and blockage of the gallbladder or bile ducts. However, CT scans can miss gallstones that are present.  - Magnetic resonance imaging (MRI). MRI machines use radio waves and magnets to produce detailed pictures of the bodys internal organs and soft tissues without using x rays. A specially trained technician performs the procedure in an outpatient center or hospital, and a radiologist interprets the images. Anesthesia is not needed, though people with a fear of confi ned spaces may receive light sedation. An MRI may include the injection of contrast medium. With most MRI machines, the person lies on a table that slides into a tunnel-shaped device that may be open ended or closed at one end; some newer machines allow the person to lie in a more open space. MRIs can show gallstones in the ducts of the biliary system.  - Cholescintigraphy. Cholescintigraphyalso called a hydroxyl iminodiacetic acid scan, HIDA scan, or hepatobiliary scanuses an unharmful radioactive material to produce pictures of the biliary system. In cholescintigraphy, the person lies on an exam table and a health care provider injects a small amount of unharmful radioactive material into a vein in the persons arm. The health care provider may also inject a substance that causes the gallbladder to contract. A special camera takes pictures of the radioactive material as it moves through the biliary system. A specially trained technician performs the procedure in an outpatient center or hospital, and a radiologist interprets the images. Anesthesia is not needed. Cholescintigraphy is used to diagnose abnormal contractions of the gallbladder or obstruction of the bile ducts.   - Endoscopic retrograde cholangiopancreatography (ERCP). ERCP uses an x ray to look into the bile and pancreatic ducts. After lightly sedating the person, the health care provider inserts an endoscopea small,  flexible tube with a light and a camera on the endthrough the mouth into the duodenum and bile ducts. The endoscope is connected to a computer and video monitor. The health care provider injects contrast medium through the tube into the bile ducts, which makes the ducts show up on the monitor. The health care provider performs the procedure in an outpatient center or hospital. ERCP helps the health care provider locate the affected bile duct and the gallstone. The stone is captured in a tiny basket attached to the endoscope and removed. This test is more invasive than other tests and is used selectively.\n                \nHealth care providers also use blood tests to look for signs of infection or in flammation of the bile ducts, gallbladder, pancreas, or liver. A blood test involves drawing blood at a health care providers offi ce or commercial facility and sending the sample to a lab for analysis.\n                \nGallstone symptoms may be similar to those of other conditions, such as appendicitis, ulcers, pancreatitis, and gastroesophageal refl ux disease.\n                \nSometimes, silent gallstones are found when a person does not have any symptoms. For example, a health care provider may notice gallstones when performing ultrasound for a different reason."}
{"_id":"ef00d4d5-5a20-4ea4-bc00-49c7e8ec80ad","text":"If gallstones are not causing symptoms, treatment is usually not needed. However, if a person has a gallbladder attack or other symptoms, a health care provider will usually recommend treatment. A person may be referred to a gastroenterologista doctor who specializes in digestive diseasesfor treatment. If a person has had one gallbladder attack, more episodes will likely follow.\n                \nThe usual treatment for gallstones is surgery to remove the gallbladder. If a person cannot undergo surgery, nonsurgical treatments may be used to dissolve cholesterol gallstones. A health care provider may use ERCP to remove stones in people who cannot undergo surgery or to remove stones from the common bile duct in people who are about to have gallbladder removal surgery.\n                \nSurgery\n                \nSurgery to remove the gallbladder, called cholecystectomy, is one of the most common operations performed on adults in the United States.\n                \nThe gallbladder is not an essential organ, which means a person can live normally without a gallbladder. Once the gallbladder is removed, bile  flows out of the liver through the hepatic and common bile ducts and directly into the duodenum, instead of being stored in the gallbladder.\n                \nSurgeons perform two types of cholecystectomy:\n                \n-  Laparoscopic cholecystectomy. In a laparoscopic cholecystectomy, the surgeon makes several tiny incisions in the abdomen and inserts a laparoscopea thin tube with a tiny video camera attached. The camera sends a magni fied image from inside the body to a video monitor, giving the surgeon a close-up view of organs and tissues. While watching the monitor, the surgeon uses instruments to carefully separate the gallbladder from the liver, bile ducts, and other structures. Then the surgeon removes the gallbladder through one of the small incisions. Patients usually receive general anesthesia.   Most cholecystectomies are performed with laparoscopy. Many laparoscopic cholecystectomies are performed on an outpatient basis, meaning the person is able to go home the same day. Normal physical activity can usually be resumed in about a week.3   -  Open cholecystectomy. An open cholecystectomy is performed when the gallbladder is severely infl amed, infected, or scarred from other operations. In most of these cases, open cholecystectomy is planned from the start. However, a surgeon may perform an open cholecystectomy when problems occur during a laparoscopic cholecystectomy. In these cases, the surgeon must switch to open cholecystectomy as a safety measure for the patient.   To perform an open cholecystectomy, the surgeon creates an incision about 4 to 6 inches long in the abdomen to remove the gallbladder.4 Patients usually receive general anesthesia. Recovery from open cholecystectomy may require some people to stay in the hospital for up to a week. Normal physical activity can usually be resumed after about a month.3\n                \nA small number of people have softer and more frequent stools after gallbladder removal because bile fl ows into the duodenum more often. Changes in bowel habits are usually temporary; however, they should be discussed with a health care provider.\n                \nThough complications from gallbladder surgery are rare, the most common complication is injury to the bile ducts. An injured common bile duct can leak bile and cause a painful and possibly dangerous infection. One or more additional operations may be needed to repair the bile ducts. Bile duct injuries occur in less than 1 percent of cholecystectomies.5\n                \nNonsurgical Treatments for Cholesterol Gallstones\n                \nNonsurgical treatments are used only in special situations, such as when a person with cholesterol stones has a serious medical condition that prevents surgery. Gallstones often recur within 5 years after nonsurgical treatment.6\n                \nTwo types of nonsurgical treatments can be used to dissolve cholesterol gallstones:\n                \n- Oral dissolution therapy. Ursodiol (Actigall) and chenodiol (Chenix) are medications that contain bile acids that can dissolve gallstones. These medications are most effective in dissolving small cholesterol stones. Months or years of treatment may be needed to dissolve all stones.   - Shock wave lithotripsy. A machine called a lithotripter is used to crush the gallstone. The lithotripter generates shock waves that pass through the persons body to break the gallstone into smaller pieces. This procedure is used only rarely and may be used along with ursodiol."}
{"_id":"015fb447-2651-4794-8f43-770f69f10b30","text":"Factors related to eating, diet, and nutrition that increase the risk of gallstones include\n                \n- obesity   - rapid weight loss   - diets high in calories and refi ned carbohydrates and low in fi ber\n                \nPeople can decrease their risk of gallstones by maintaining a healthy weight through proper diet and nutrition.\n                \nUrsodiol can help prevent gallstones in people who rapidly lose weight through low-calorie diets or bariatric surgery. People should talk with their health care provider or dietitian about what diet is right for them."}
{"_id":"f757a0e0-36dd-4c53-97aa-05d4002223f9","text":"- Gallstones are hard particles that develop in the gallbladder.  - Imbalances in the substances that make up bile cause gallstones. Gallstones may form if bile contains too much cholesterol, too much bilirubin, or not enough bile salts. Scientists do not fully understand why these imbalances occur.   - Women, people over age 40, people with a family history of gallstones, American Indians, and Mexican Americans have a higher risk of developing gallstones.   - Many people with gallstones do not have symptoms. Gallstones that do not cause symptoms are called asymptomatic, or silent, gallstones.  - If gallstones block the bile ducts, pressure increases in the gallbladder, causing a gallbladder attack.  - Gallbladder attacks often follow heavy meals, and they usually occur in the evening or during the night.  - Gallstone symptoms may be similar to those of other conditions.   - If gallstones are not causing symptoms, treatment is usually not needed. However, if a person has a gallbladder attack or other symptoms, a health care provider will usually recommend treatment.   - The usual treatment for gallstones is surgery to remove the gallbladder. If a person cannot undergo surgery, nonsurgical treatments may be used to dissolve cholesterol gallstones. A health care provider may use endoscopic retrograde cholangiopancreatography (ERCP) to remove stones in people who cannot undergo surgery or to remove stones from the common bile duct in people who are about to have gallbladder removal surgery.   - The gallbladder is not an essential organ, which means a person can live normally without a gallbladder. Once the gallbladder is removed, bile  flows out of the liver through the hepatic and common bile ducts and directly into the duodenum, instead of being stored in the gallbladder."}
{"_id":"5b750a9c-2789-48c6-93c9-1ff3913b7994","text":"Microscopic colitis is an inflammation of the colon that a health care provider can see only with a microscope. Inflammation is the bodys normal response to injury, irritation, or infection of tissues. Microscopic colitis is a type of inflammatory bowel diseasethe general name for diseases that cause irritation and inflammation in the intestines.\n                \nThe two types of microscopic colitis are collagenous colitis and lymphocytic colitis. Health care providers often use the term microscopic colitis to describe both types because their symptoms and treatments are the same. Some scientists believe that collagenous colitis and lymphocytic colitis may be different phases of the same condition rather than separate conditions.\n                \nIn both types of microscopic colitis, an increase in the number of lymphocytes, a type of white blood cell, can be seen in the epitheliumthe layer of cells that lines the colon. An increase in the number of white blood cells is a sign of inflammation. The two types of colitis affect the colon tissue in slightly different ways:\n                \n- Lymphocytic colitis. The number of lymphocytes is higher, and the tissues and lining of the colon are of normal thickness.  - Collagenous colitis. The layer of collagen, a threadlike protein, underneath the epithelium builds up and becomes thicker than normal.\n                \nWhen looking through a microscope, the health care provider may find variations in lymphocyte numbers and collagen thickness in different parts of the colon. These variations may indicate an overlap of the two types of microscopic colitis."}
{"_id":"4a24404f-9bff-4ddf-a22a-fa1488604f18","text":"The colon is part of the gastrointestinal (GI) tract, a series of hollow organs joined in a long, twisting tube from the mouth to the anusa 1-inch-long opening through which stool leaves the body. Organs that make up the GI tract are the\n                \n- mouth  - esophagus  - stomach  - small intestine  - large intestine  - anus\n                \nThe first part of the GI tract, called the upper GI tract, includes the mouth, esophagus, stomach, and small intestine. The last part of the GI tract, called the lower GI tract, consists of the large intestine and anus. The intestines are sometimes called the bowel.\n                \nThe large intestine is about 5 feet long in adults and includes the colon and rectum. The large intestine changes waste from liquid to a solid matter called stool. Stool passes from the colon to the rectum. The rectum is 6 to 8 inches long in adults and is between the last part of the coloncalled the sigmoid colonand the anus. During a bowel movement, stool moves from the rectum to the anus and out of the body."}
{"_id":"8247a1c2-048c-4af8-aa70-6bc963d51854","text":"The exact cause of microscopic colitis is unknown. Several factors may play a role in causing microscopic colitis. However, most scientists believe that microscopic colitis results from an abnormal immune-system response to bacteria that normally live in the colon. Scientists have proposed other causes, including\n                \n- autoimmune diseases  - medications  - infections  - genetic factors  - bile acid malabsorption\n                \nAutoimmune Diseases\n                \nSometimes people with microscopic colitis also have autoimmune diseasesdisorders in which the bodys immune system attacks the bodys own cells and organs. Autoimmune diseases associated with microscopic colitis include\n                \n- celiac diseasea condition in which people cannot tolerate gluten because it damages the lining of the small intestine and prevents absorption of nutrients. Gluten is a protein found in wheat, rye, and barley.  - thyroid diseases such as      - Hashimotos diseasea form of chronic, or long lasting, inflammation of the thyroid.    - Graves diseasea disease that causes hyperthyroidism. Hyperthyroidism is a disorder that occurs when the thyroid gland makes more thyroid hormone than the body needs.    - rheumatoid arthritisa disease that causes pain, swelling, stiffness, and loss of function in the joints when the immune system attacks the membrane lining the joints.  - psoriasisa skin disease that causes thick, red skin with flaky, silver-white patches called scales.\n                \nMore information is provided in the NIDDK health topics:\n                \n- Celiac Disease  - Hashimotos Disease   - Graves Disease\n                \nMedications\n                \nResearchers have not found that medications cause microscopic colitis. However, they have found links between microscopic colitis and certain medications, most commonly\n                \n- nonsteroidal anti-inflammatory drugs such as aspirin, ibuprofen, and naproxen  - lansoprazole (Prevacid)  - acarbose (Prandase, Precose)  - ranitidine (Tritec, Zantac)  - sertraline (Zoloft)  - ticlopidine (Ticlid)\n                \nOther medications linked to microscopic colitis include\n                \n- carbamazepine  - clozapine (Clozaril, FazaClo)  - dexlansoprazole (Kapidex, Dexilant)  - entacapone (Comtan)  - esomeprazole (Nexium)  - flutamide (Eulexin)  - lisinopril (Prinivil, Zestril)  - omeprazole (Prilosec)  - pantoprazole (Protonix)  - paroxetine (Paxil, Pexeva)  - rabeprazole (AcipHex)  - simvastatin (Zocor)  - vinorelbine (Navelbine)\n                \nInfections\n                \nBacteria. Some people get microscopic colitis after an infection with certain harmful bacteria. Harmful bacteria may produce toxins that irritate the lining of the colon.\n                \nViruses. Some scientists believe that viral infections that cause inflammation in the GI tract may play a role in causing microscopic colitis.\n                \nGenetic Factors\n                \nSome scientists believe that genetic factors may play a role in microscopic colitis. Although researchers have not yet found a gene unique to microscopic colitis, scientists have linked dozens of genes to other types of inflammatory bowel disease, including\n                \n- Crohns diseasea disorder that causes inflammation and irritation of any part of the GI tract  - ulcerative colitisa chronic disease that causes inflammation and ulcers in the inner lining of the large intestine\n                \nMore information is provided in the NIDDK health topics:\n                \n- Crohns Disease  - Ulcerative Colitis\n                \nBile Acid Malabsorption\n                \nSome scientists believe that bile acid malabsorption plays a role in microscopic colitis. Bile acid malabsorption is the intestines inability to completely reabsorb bile acidsacids made by the liver that work with bile to break down fats. Bile is a fluid made by the liver that carries toxins and waste products out of the body and helps the body digest fats. Bile acids that reach the colon can lead to diarrhea."}
{"_id":"7ca026f9-3669-48db-a938-0bb099f98f64","text":"The most common symptom of microscopic colitis is chronic, watery, nonbloody diarrhea. Episodes of diarrhea can last for weeks, months, or even years. However, many people with microscopic colitis may have long periods without diarrhea. Other signs and symptoms of microscopic colitis can include\n                \n- a strong urgency to have a bowel movement or a need to go to the bathroom quickly  - pain, cramping, or bloating in the abdomenthe area between the chest and the hipsthat is usually mild  - weight loss  - fecal incontinenceaccidental passing of stool or fluid from the rectumespecially at night  - nausea  - dehydrationa condition that results from not taking in enough liquids to replace fluids lost through diarrhea\n                \nThe symptoms of microscopic colitis can come and go frequently. Sometimes, the symptoms go away without treatment."}
{"_id":"bea69c90-269b-4aef-a644-a8ae5a4aa3ab","text":"A pathologista doctor who specializes in examining tissues to diagnose diseasesdiagnoses microscopic colitis based on the findings of multiple biopsies taken throughout the colon. Biopsy is a procedure that involves taking small pieces of tissue for examination with a microscope. The pathologist examines the colon tissue samples in a lab. Many patients can have both lymphocytic colitis and collagenous colitis in different parts of their colon.\n                \nTo help diagnose microscopic colitis, a gastroenterologista doctor who specializes in digestive diseasesbegins with\n                \n- a medical and family history  - a physical exam\n                \nThe gastroenterologist may perform a series of medical tests to rule out other bowel diseasessuch as irritable bowel syndrome, celiac disease, Crohns disease, ulcerative colitis, and infectious colitisthat cause symptoms similar to those of microscopic colitis. These medical tests include\n                \n- lab tests  - imaging tests of the intestines  - endoscopy of the intestines\n                \nMedical and Family History\n                \nThe gastroenterologist will ask the patient to provide a medical and family history, a review of the symptoms, a description of eating habits, and a list of prescription and over-the-counter medications in order to help diagnose microscopic colitis. The gastroenterologist will also ask the patient about current and past medical conditions.\n                \nPhysical Exam\n                \nA physical exam may help diagnose microscopic colitis and rule out other diseases. During a physical exam, the gastroenterologist usually\n                \n- examines the patients body  - taps on specific areas of the patients abdomen\n                \nLab Tests\n                \nLab tests may include\n                \n- blood tests  - stool tests\n                \nBlood tests. A blood test involves drawing blood at a health care providers office or a commercial facility and sending the sample to a lab for analysis. A health care provider may use blood tests to help look for changes in red and white blood cell counts.\n                \n- Red blood cells. When red blood cells are fewer or smaller than normal, a person may have anemiaa condition that prevents the bodys cells from getting enough oxygen.  - White blood cells. When the white blood cell count is higher than normal, a person may have inflammation or infection somewhere in the body.\n                \nStool tests. A stool test is the analysis of a sample of stool. A health care provider will give the patient a container for catching and storing the stool. The patient returns the sample to the health care provider or a commercial facility that will send the sample to a lab for analysis. Health care providers commonly order stool tests to rule out other causes of GI diseases, such as different types of infectionsincluding bacteria or parasitesor bleeding, and help determine the cause of symptoms.\n                \nImaging Tests of the Intestines\n                \nImaging tests of the intestines may include the following:\n                \n- computerized tomography (CT) scan  - magnetic resonance imaging (MRI)  - upper GI series\n                \nSpecially trained technicians perform these tests at an outpatient center or a hospital, and a radiologista doctor who specializes in medical imaginginterprets the images. A patient does not need anesthesia. Health care providers use imaging tests to show physical abnormalities and to diagnose certain bowel diseases, in some cases.\n                \nCT scan. CT scans use a combination of x rays and computer technology to create images. For a CT scan, a health care provider may give the patient a solution to drink and an injection of a special dye, called contrast medium. CT scans require the patient to lie on a table that slides into a tunnel-shaped device where the technician takes the x rays.\n                \nMRI. MRI is a test that takes pictures of the bodys internal organs and soft tissues without using x rays. Although a patient does not need anesthesia for an MRI, some patients with a fear of confined spaces may receive light sedation, taken by mouth. An MRI may include a solution to drink and injection of contrast medium. With most MRI machines, the patient will lie on a table that slides into a tunnel-shaped device that may be open ended or closed at one end. Some machines allow the patient to lie in a more open space. During an MRI, the patient, although usually awake, must remain perfectly still while the technician takes the images, which usually takes only a few minutes. The technician will take a sequence of images to create a detailed picture of the intestines. During sequencing, the patient will hear loud mechanical knocking and humming noises.\n                \nUpper GI series. This test is an x-ray exam that provides a look at the shape of the upper GI tract. A patient should not eat or drink before the procedure, as directed by the health care provider. Patients should ask their health care provider about how to prepare for an upper GI series. During the procedure, the patient will stand or sit in front of an x-ray machine and drink barium, a chalky liquid. Barium coats the upper GI tract so the radiologist and gastroenterologist can see the organs shapes more clearly on x rays. A patient may experience bloating and nausea for a short time after the test. For several days afterward, barium liquid in the GI tract causes white or light-colored stools. A health care provider will give the patient specific instructions about eating and drinking after the test. More information is provided in the NIDDK health topic, Upper GI Series.\n                \nEndoscopy of the Intestines\n                \nEndoscopy of the intestines may include\n                \n- colonoscopy with biopsy  - flexible sigmoidoscopy with biopsy  - upper GI endoscopy with biopsy\n                \nA gastroenterologist performs these tests at a hospital or an outpatient center.\n                \nColonoscopy with biopsy. Colonoscopy is a test that uses a long, flexible, narrow tube with a light and tiny camera on one end, called a colonoscope or scope, to look inside the rectum and entire colon. In most cases, light anesthesia and pain medication help patients relax for the test. The medical staff will monitor a patients vital signs and try to make him or her as comfortable as possible. A nurse or technician places an intravenous (IV) needle in a vein in the arm or hand to give anesthesia.\n                \nFor the test, the patient will lie on a table while the gastroenterologist inserts a colonoscope into the anus and slowly guides it through the rectum and into the colon. The scope inflates the large intestine with air to give the gastroenterologist a better view. The camera sends a video image of the intestinal lining to a computer screen, allowing the gastroenterologist to carefully examine the tissues lining the colon and rectum. The gastroenterologist may move the patient several times and adjust the scope for better viewing. Once the scope has reached the opening to the small intestine, the gastroenterologist slowly withdraws it and examines the lining of the colon and rectum again. A colonoscopy can show irritated and swollen tissue, ulcers, and abnormal growths such as polypsextra pieces of tissue that grow on the lining of the intestine. If the lining of the rectum and colon appears normal, the gastroenterologist may suspect microscopic colitis and will biopsy multiple areas of the colon.\n                \nA health care provider will provide written bowel prep instructions to follow at home before the test. The health care provider will also explain what the patient can expect after the test and give discharge instructions.\n                \nFlexible sigmoidoscopy with biopsy. Flexible sigmoidoscopy is a test that uses a flexible, narrow tube with a light and tiny camera on one end, called a sigmoidoscope or scope, to look inside the rectum and the sigmoid colon. A patient does not usually need anesthesia.\n                \nFor the test, the patient will lie on a table while the gastroenterologist inserts the sigmoidoscope into the anus and slowly guides it through the rectum and into the sigmoid colon. The scope inflates the large intestine with air to give the gastroenterologist a better view. The camera sends a video image of the intestinal lining to a computer screen, allowing the gastroenterologist to carefully examine the tissues lining the sigmoid colon and rectum. The gastroenterologist may ask the patient to move several times and adjust the scope for better viewing. Once the scope reaches the end of the sigmoid colon, the gastroenterologist slowly withdraws it while carefully examining the lining of the sigmoid colon and rectum again.\n                \nThe gastroenterologist will look for signs of bowel diseases and conditions such as irritated and swollen tissue, ulcers, and polyps. If the lining of the rectum and colon appears normal, the gastroenterologist may suspect microscopic colitis and will biopsy multiple areas of the colon.\n                \nA health care provider will provide written bowel prep instructions to follow at home before the test. The health care provider will also explain what the patient can expect after the test and give discharge instructions.\n                \nUpper GI endoscopy with biopsy. Upper GI endoscopy is a test that uses a flexible, narrow tube with a light and tiny camera on one end, called an endoscope or a scope, to look inside the upper GI tract. The gastroenterologist carefully feeds the endoscope down the esophagus and into the stomach and first part of the small intestine, called the duodenum. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining. A health care provider may give a patient a liquid anesthetic to gargle or may spray anesthetic on the back of the patients throat. A health care provider will place an IV needle in a vein in the arm or hand to administer sedation. Sedatives help patients stay relaxed and comfortable. This test can show blockages or other conditions in the upper small intestine. A gastroenterologist may biopsy the lining of the small intestine during an upper GI endoscopy."}
{"_id":"6127ae73-0fce-44e8-8163-914c2bb5ae0a","text":"Treatment depends on the severity of symptoms. The gastroenterologist will\n                \n- review the medications the person is taking  - make recommendations to change or stop certain medications  - recommend that the person quit smoking\n                \nThe gastroenterologist may prescribe medications to help control symptoms. Medications are almost always effective in treating microscopic colitis. The gastroenterologist may recommend eating, diet, and nutrition changes. In rare cases, the gastroenterologist may recommend surgery.\n                \nMedications\n                \nThe gastroenterologist may prescribe one or more of the following:\n                \n- antidiarrheal medications such as bismuth subsalicylate (Kaopectate, Pepto-Bismol), diphenoxylate\/atropine (Lomotil), and loperamide  - corticosteroids such as budesonide (Entocort) and prednisone  - anti-inflammatory medications such as mesalamine and sulfasalazine (Azulfidine)  - cholestyramine resin (Locholest, Questran)a medication that blocks bile acids  - antibiotics such as metronidazole (Flagyl) and erythromycin  - immunomodulators such as mercaptopurine (Purinethol), azathioprine (Azasan, Imuran), and methotrexate (Rheumatrex, Trexall)  - anti-TNF therapies such as infliximab (Remicade) and adalimumab (Humira)\n                \nCorticosteroids are medications that decrease inflammation and reduce the activity of the immune system. These medications can have many side effects. Scientists have shown that budesonide is safer, with fewer side effects, than prednisone. Most health care providers consider budesonide the best medication for treating microscopic colitis.\n                \nPatients with microscopic colitis generally achieve relief through treatment with medications, although relapses can occur. Some patients may need long-term treatment if they continue to have relapses."}
{"_id":"db46fc6a-a6c3-49a8-a8e2-ae3529be4454","text":"To help reduce symptoms, a health care provider may recommend the following dietary changes:\n                \n- avoid foods and drinks that contain caffeine or artificial sugars  - drink plenty of liquids to prevent dehydration during episodes of diarrhea  - eat a milk-free diet if the person is also lactose intolerant  - eat a gluten-free diet\n                \nPeople should talk with their health care provider or dietitian about what type of diet is right for them.\n                \nSurgery\n                \nWhen the symptoms of microscopic colitis are severe and medications arent effective, a gastroenterologist may recommend surgery to remove the colon. Surgery is a rare treatment for microscopic colitis. The gastroenterologist will exclude other causes of symptoms before considering surgery."}
{"_id":"5fc05178-d35c-4409-88a6-41ab673c72f5","text":"Researchers do not know how to prevent microscopic colitis. However, researchers do believe that people who follow the recommendations of their health care provider may be able to prevent relapses of microscopic colitis."}
{"_id":"5cef8c9e-1aee-4e60-87a5-ef4558f88459","text":"No. Unlike the other inflammatory bowel diseases, such as Crohns disease and ulcerative colitis, microscopic colitis does not increase a persons risk of getting colon cancer."}
{"_id":"179fd65f-e8a8-4322-8fb9-2fd08665fdef","text":"- Microscopic colitis is an inflammation of the colon that a health care provider can see only with a microscope.  - The two types of microscopic colitis are collagenous colitis and lymphocytic colitis.  - The exact cause of microscopic colitis is unknown.  - Microscopic colitis is most common in females age 50 years or older.  - The most common symptom of microscopic colitis is chronic, watery, nonbloody diarrhea.  - A pathologista doctor who specializes in diagnosing diseasesdiagnoses microscopic colitis based on the findings of multiple biopsies taken throughout the colon.  - Treatment depends on the severity of symptoms.  - The gastroenterologist may prescribe medications to help control symptoms.  - Medications are almost always effective in treating microscopic colitis.  - The gastroenterologist may recommend eating, diet, and nutrition changes."}
{"_id":"0aacd839-0875-4b53-acf1-bcb37514ed44","text":"Fecal incontinence, also called a bowel control problem, is the accidental passing of solid or liquid stool or mucus from the rectum. Fecal incontinence includes the inability to hold a bowel movement until reaching a toilet as well as passing stool into ones underwear without being aware of it happening. Stool, also called feces, is solid waste that is passed as a bowel movement and includes undigested food, bacteria, mucus, and dead cells. Mucus is a clear liquid that coats and protects tissues in the digestive system.\n                \nFecal incontinence can be upsetting and embarrassing. Many people with fecal incontinence feel ashamed and try to hide the problem. However, people with fecal incontinence should not be afraid or embarrassed to talk with their health care provider. Fecal incontinence is often caused by a medical problem and treatment is available."}
{"_id":"8f1ea55a-6362-4b33-b255-d4a581344ce9","text":"Nearly 18 million U.S. adultsabout one in 12have fecal incontinence.1 People of any age can have a bowel control problem, though fecal incontinence is more common in older adults. Fecal incontinence is slightly more common among women. Having any of the following can increase the risk:\n                \n- diarrhea, which is passing loose, watery stools three or more times a day  - urgency, or the sensation of having very little time to get to the toilet for a bowel movement  - a disease or injury that damages the nervous system  - poor overall health from multiple chronic, or long lasting, illnesses  - a difficult childbirth with injuries to the pelvic floorthe muscles, ligaments, and tissues that support the uterus, vagina, bladder, and rectum"}
{"_id":"56e0f284-3d0f-4586-8b67-893ccbc622f8","text":"The GI tract is a series of hollow organs joined in a long, twisting tube from the mouth to the anus. The movement of muscles in the GI tract, along with the release of hormones and enzymes, allows for the digestion of food. Organs that make up the GI tract are the mouth, esophagus, stomach, small intestine, large intestinewhich includes the appendix, cecum, colon, and rectumand anus. The intestines are sometimes called the bowel. The last part of the GI tractcalled the lower GI tractconsists of the large intestine and anus.\n                \nThe large intestine absorbs water and any remaining nutrients from partially digested food passed from the small intestine. The large intestine then changes waste from liquid to stool. Stool passes from the colon to the rectum. The rectum is located between the last part of the coloncalled the sigmoid colonand the anus. The rectum stores stool prior to a bowel movement. During a bowel movement, stool moves from the rectum to the anus, the opening through which stool leaves the body."}
{"_id":"0ea5c51f-b2bc-48f7-9b49-29b9f0b94efd","text":"Fecal incontinence has many causes, including\n                \n- diarrhea  - constipation  - muscle damage or weakness  - nerve damage  - loss of stretch in the rectum  - childbirth by vaginal delivery  - hemorrhoids and rectal prolapse  - rectocele  - inactivity\n                \nDiarrhea\n                \nDiarrhea can cause fecal incontinence. Loose stools fill the rectum quickly and are more difficult to hold than solid stools. Diarrhea increases the chance of not reaching a bathroom in time.\n                \nConstipation\n                \nConstipation can lead to large, hard stools that stretch the rectum and cause the internal sphincter muscles to relax by reflex. Watery stool builds up behind the hard stool and may leak out around the hard stool, leading to fecal incontinence.\n                \nThe type of constipation that is most likely to lead to fecal incontinence occurs when people are unable to relax their external sphincter and pelvic floor muscles when straining to have a bowel movement, often mistakenly squeezing these muscles instead of relaxing them. This squeezing makes it difficult to pass stool and may lead to a large amount of stool in the rectum. This type of constipation, called dyssynergic defecation or disordered defecation, is a result of faulty learning. For example, children or adults who have pain when having a bowel movement may unconsciously learn to squeeze their muscles to delay the bowel movement and avoid pain.\n                \nMuscle Damage or Weakness\n                \nInjury to one or both of the sphincter muscles can cause fecal incontinence. If these muscles, called the external and internal anal sphincter muscles, are damaged or weakened, they may not be strong enough to keep the anus closed and prevent stool from leaking.\n                \nTrauma, childbirth injuries, cancer surgery, and hemorrhoid surgery are possible causes of injury to the sphincters. Hemorrhoids are swollen blood vessels in and around the anus and lower rectum.\n                \nNerve Damage\n                \nThe anal sphincter muscles wont open and close properly if the nerves that control them are damaged. Likewise, if the nerves that sense stool in the rectum are damaged, a person may not feel the urge to go to the bathroom. Both types of nerve damage can lead to fecal incontinence. Possible sources of nerve damage are childbirth; a long-term habit of straining to pass stool; spinal cord injury; and diseases, such as diabetes and multiple sclerosis, that affect the nerves that go to the sphincter muscles and rectum. Brain injuries from stroke, head trauma, or certain diseases can also cause fecal incontinence.\n                \nLoss of Stretch in the Rectum\n                \nNormally, the rectum stretches to hold stool until a person has a bowel movement. Rectal surgery, radiation treatment, and inflammatory bowel diseaseschronic disorders that cause irritation and sores on the lining of the digestive systemcan cause the rectal walls to become stiff. The rectum then cant stretch as much to hold stool, increasing the risk of fecal incontinence.\n                \nChildbirth by Vaginal Delivery\n                \nChildbirth sometimes causes injuries to muscles and nerves in the pelvic floor. The risk is greater if forceps are used to help deliver the baby or if an episiotomya cut in the vaginal area to prevent the babys head from tearing the vagina during birthis performed. Fecal incontinence related to childbirth can appear soon after delivery or many years later.\n                \nHemorrhoids and Rectal Prolapse\n                \nExternal hemorrhoids, which develop under the skin around the anus, can prevent the anal sphincter muscles from closing completely. Rectal prolapse, a condition that causes the rectum to drop down through the anus, can also prevent the anal sphincter muscles from closing well enough to prevent leakage. Small amounts of mucus or liquid stool can then leak through the anus.\n                \nRectocele\n                \nRectocele is a condition that causes the rectum to protrude through the vagina. Rectocele can happen when the thin layer of muscles separating the rectum from the vagina becomes weak. For women with rectocele, straining to have a bowel movement may be less effective because rectocele reduces the amount of downward force through the anus. The result may be retention of stool in the rectum. More research is needed to be sure rectocele increases the risk of fecal incontinence.\n                \nInactivity\n                \nPeople who are inactive, especially those who spend many hours a day sitting or lying down, have an increased risk of retaining a large amount of stool in the rectum. Liquid stool can then leak around the more solid stool. Frail, older adults are most likely to develop constipation-related fecal incontinence for this reason."}
{"_id":"e542784e-b4e8-438b-847e-15d8dc9ca834","text":"Health care providers diagnose fecal incontinence based on a persons medical history, physical exam, and medical test results. In addition to a general medical history, the health care provider may ask the following questions:\n                \n- When did fecal incontinence start?  - How often does fecal incontinence occur?  - How much stool leaks? Does the stool just streak the underwear? Does just a little bit of solid or liquid stool leak out or does complete loss of bowel control occur?  - Does fecal incontinence involve a strong urge to have a bowel movement or does it happen without warning?  - For people with hemorrhoids, do hemorrhoids bulge through the anus? Do the hemorrhoids pull back in by themselves, or do they have to be pushed in with a finger?  - How does fecal incontinence affect daily life?  - Is fecal incontinence worse after eating? Do certain foods seem to make fecal incontinence worse?  - Can passing gas be controlled?\n                \nPeople may want to keep a stool diary for several weeks before their appointment so they can answer these questions. A stool diary is a chart for recording daily bowel movement details. A sample stool diary is available on the Bowel Control Awareness Campaign website at www.bowelcontrol.nih.gov.\n                \nThe person may be referred to a doctor who specializes in problems of the digestive system, such as a gastroenterologist, proctologist, or colorectal surgeon, or a doctor who specializes in problems of the urinary and reproductive systems, such as a urologist or urogynecologist. The specialist will perform a physical exam and may suggest one or more of the following tests:\n                \n- anal manometry  - anal ultrasound  - magnetic resonance imaging (MRI)  - defecography  - flexible sigmoidoscopy or colonoscopy  - anal electromyography (EMG)\n                \nAnal manometry. Anal manometry uses pressure sensors and a balloon that can be inflated in the rectum to check the sensitivity and function of the rectum. Anal manometry also checks the tightness of the anal sphincter muscles around the anus. To prepare for this test, the person should use an enema and not eat anything 2 hours before the test. An enema involves flushing water or a laxative into the anus using a special squirt bottle. A laxative is medication that loosens stool and increases bowel movements. For this test, a thin tube with a balloon on its tip and pressure sensors below the balloon is inserted into the anus until the balloon is in the rectum and pressure sensors are located in the anal canal. The tube is slowly pulled back through the sphincter muscle to measure muscle tone and contractions. No anesthesia is needed for this test, which takes about 30 minutes.\n                \nAnal ultrasound. Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. An anal ultrasound is specific to the anus and rectum. The procedure is performed in a health care providers office, outpatient center, or hospital by a specially trained technician, and the images are interpreted by a radiologista doctor who specializes in medical imaging. Anesthesia is not needed. The images can show the structure of the anal sphincter muscles.\n                \nMRI. MRI machines use radio waves and magnets to produce detailed pictures of the bodys internal organs and soft tissues without using x rays. The procedure is performed in an outpatient center or hospital by a specially trained technician, and the images are interpreted by a radiologist. Anesthesia is not needed, though people with a fear of confined spaces may be given medication to help them relax. An MRI may include the injection of special dye, called contrast medium. With most MRI machines, the person lies on a table that slides into a tunnel-shaped device that may be open ended or closed at one end; some newer machines are designed to allow the person to lie in a more open space. MRIs can show problems with the anal sphincter muscles. MRI is an alternative to anal ultrasound that may provide more detailed information, especially about the external anal sphincter.\n                \nDefecography. This x ray of the area around the anus and rectum shows how well the person can hold and evacuate stool. The test also identifies structural changes in the rectum and anus such as rectocele and rectal prolapse. To prepare for the test, the person uses two enemas and does not eat anything 2 hours prior to the test. During the test, the health care provider fills the rectum with a soft paste that shows up on x rays and is the same consistency as stool. The person sits on a toilet inside an x-ray machine. The person is first asked to pull in and squeeze the sphincter muscles to prevent leakage and then to strain as if having a bowel movement. The radiologist studies the x rays to identify problems with the rectum, anus, and pelvic floor muscles.\n                \nFlexible sigmoidoscopy or colonoscopy. These tests are used to help diagnose problems causing fecal incontinence. The tests are similar, but colonoscopy is used to view the rectum and entire colon, while flexible sigmoidoscopy is used to view just the rectum and lower colon. These tests are performed at a hospital or outpatient center by a gastroenterologist. For both tests, a health care provider will provide written bowel prep instructions to follow at home. The person may be asked to follow a clear liquid diet for 1 to 3 days before either test. A laxative may be required the night before the test. One or more enemas may be required the night before and about 2 hours before the test.\n                \nIn most cases, people will be given light anesthesia, and possibly pain medication, to help them relax during flexible sigmoidoscopy. Anesthesia is used for colonoscopy. For either test, the person will lie on a table while the gastroenterologist inserts a flexible tube into the anus. A small camera on the tube sends a video image of the intestinal lining to a computer screen. The test can show problems in the lower GI tract that may be causing the bowel control problem. The gastroenterologist may also perform a biopsy, a procedure that involves taking a piece of tissue from the bowel lining for examination with a microscope.\n                \nThe person will not feel the biopsy. A pathologista doctor who specializes in diagnosing diseasesexamines the tissue in a lab to confirm the diagnosis.\n                \nCramping or bloating may occur during the first hour after these tests. Driving is not permitted for 24 hours after flexible sigmoidoscopy or colonoscopy to allow the anesthesia time to wear off. Before the appointment, a person should make plans for a ride home. Full recovery is expected by the next day and the person is able to go back to a normal diet.\n                \nAnal EMG. Anal EMG checks the health of the pelvic floor muscles and the nerves that control the muscles. The health care provider inserts a very thin needle electrode through the skin into the muscle. The electrode on the needle picks up the electrical activity given off by the muscles and shows it as images on a monitor or sounds through a speaker. An alternative type of anal EMG uses stainless steel plates attached to the sides of a plastic plug instead of a needle. The plug is inserted into the anal canal to measure the electrical activity of the external anal sphincter and other pelvic floor muscles. The average amount of electrical activity when the person relaxes quietly, squeezes to prevent a bowel movement, and strains to have a bowel movement shows whether there is damage to the nerves that control the external sphincter and pelvic floor muscles."}
{"_id":"feebbce9-d37f-459d-a3b8-666fe3b9fccf","text":"Treatment for fecal incontinence may include one or more of the following:\n                \n- eating, diet, and nutrition  - medications  - bowel training  - pelvic floor exercises and biofeedback  - surgery  - electrical stimulation"}
{"_id":"db5e9853-58fd-4c1a-8a83-ad3c916fb690","text":"Dietary changes that may improve fecal incontinence include\n                \n- Eating the right amount of fiber. Fiber can help with diarrhea and constipation. Fiber is found in fruits, vegetables, whole grains, and beans. Fiber supplements sold in a pharmacy or in a health food store are another common source of fiber to treat fecal incontinence. The Academy of Nutrition and Dietetics recommends consuming 20 to 35 grams of fiber a day for adults and age plus five grams for children. A 7-year-old child, for example, should get 7 plus five, or 12, grams of fiber a day. American adults consume only 15 grams a day on average.2 Fiber should be added to the diet slowly to avoid bloating.  - Getting plenty to drink. Drinking eight 8-ounce glasses of liquid a day may help prevent constipation. Water is a good choice. Drinks with caffeine, alcohol, milk, or carbonation should be avoided if they trigger diarrhea.\n                \nKeeping a Food Diary   A food diary can help identify foods that cause diarrhea and increase the risk of fecal incontinence. A food diary should list foods eaten, portion size, and when fecal incontinence occurs. After a few days, the diary may show a link between certain foods and fecal incontinence. Eating less of foods linked to fecal incontinence may improve symptoms. A food diary can also be helpful to a health care provider treating a person with fecal incontinence.   Common foods and drinks linked to fecal incontinence include   - dairy products such as milk, cheese, and ice cream   - drinks and foods containing caffeine   - cured or smoked meat such as sausage, ham, and turkey   - spicy foods   - alcoholic beverages   - fruits such as apples, peaches, and pears   - fatty and greasy foods   - sweeteners in diet drinks and sugarless gum and candy, including sorbitol, xylitol, mannitol, and fructose\n                \n\n                \nExamples of Foods That Have Fiber        Beans, cereals, and breads    Fiber         cup of beans (navy, pinto, kidney, etc.), cooked    6.29.6 grams         cup of shredded wheat, ready-to-eat cereal    2.73.8 grams         cup of 100% bran, ready-to-eat cereal    9.1 grams        1 small oat bran muffin    3.0 grams        1 whole-wheat English muffin    4.4 grams        Fruits        1 small apple, with skin    3.6 grams        1 medium pear, with skin    5.5 grams         cup of raspberries    4.0 grams         cup of stewed prunes    3.8 grams        Vegetables         cup of winter squash, cooked    2.9 grams         1 medium sweet potato, baked in skin    3.8 grams         cup of green peas, cooked    3.54.4 grams        1 small potato, baked, with skin    3.0 grams         cup of mixed vegetables, cooked    4.0 grams         cup of broccoli, cooked    2.62.8 grams          cup of greens (spinach, collards, turnip greens), cooked    2.53.5 grams\n                \n\n                \nMedications\n                \nIf diarrhea is causing fecal incontinence, medication may help. Health care providers sometimes recommend using bulk laxatives, such as Citrucel and Metamucil, to develop more solid stools that are easier to control. Antidiarrheal medications such as loperamide or diphenoxylate may be recommended to slow down the bowels and help control the problem.\n                \nBowel Training\n                \nDeveloping a regular bowel movement pattern can improve fecal incontinence, especially fecal incontinence due to constipation. Bowel training involves trying to have bowel movements at specific times of the day, such as after every meal. Over time, the body becomes used to a regular bowel movement pattern, thus reducing constipation and related fecal incontinence. Persistence is key to successful bowel training. Achieving a regular bowel control pattern can take weeks to months.\n                \nPelvic Floor Exercises and Biofeedback\n                \nExercises that strengthen the pelvic floor muscles may improve bowel control. Pelvic floor exercises involve squeezing and relaxing pelvic floor muscles 50 to 100 times a day. A health care provider can help with proper technique. Biofeedback therapy may also help a person perform the exercises properly. This therapy also improves a persons awareness of sensations in the rectum, teaching how to coordinate squeezing of the external sphincter muscle with the sensation of rectal filling. Biofeedback training uses special sensors to measure bodily functions. Sensors include pressure or EMG sensors in the anus, pressure sensors in the rectum, and a balloon in the rectum to produce graded sensations of rectal fullness. The measurements are displayed on a video screen as sounds or line graphs. The health care provider uses the information to help the person modify or change abnormal function. The person practices the exercises at home. Success with pelvic floor exercises depends on the cause of fecal incontinence, its severity, and the persons motivation and ability to follow the health care providers recommendations.\n                \nSurgery\n                \nSurgery may be an option for fecal incontinence that fails to improve with other treatments or for fecal incontinence caused by pelvic floor or anal sphincter muscle injuries.\n                \n- Sphincteroplasty, the most common fecal incontinence surgery, reconnects the separated ends of a sphincter muscle torn by childbirth or another injury. Sphincteroplasty is performed at a hospital by a colorectal, gynecological, or general surgeon.  - Artificial anal sphincter involves placing an inflatable cuff around the anus and implanting a small pump beneath the skin that the person activates to inflate or deflate the cuff. This surgery is much less common and is performed at a hospital by a specially trained colorectal surgeon.  - Nonabsorbable bulking agents can be injected into the wall of the anus to bulk up the tissue around the anus. The bulkier tissues make the opening of the anus narrower so the sphincters are able to close better. The procedure is performed in a health care providers office; anesthesia is not needed. The person can return to normal physical activities 1 week after the procedure.  - Bowel diversion is an operation that reroutes the normal movement of stool out of the body when part of the bowel is removed. The operation diverts the lower part of the small intestine or colon to an opening in the wall of the abdomenthe area between the chest and hips. An external pouch is attached to the opening to collect stool. The procedure is performed by a surgeon in a hospital and anesthesia is used. More information about these procedures can be found in the Bowel Diversion fact sheet.\n                \nElectrical Stimulation\n                \nElectrical stimulation, also called sacral nerve stimulation or neuromodulation, involves placing electrodes in the sacral nerves to the anus and rectum and continuously stimulating the nerves with electrical pulses. The sacral nerves connect to the part of the spine in the hip area. A battery-operated stimulator is placed beneath the skin. Based on the persons response, the health care provider can adjust the amount of stimulation so it works best for that person. The person can turn the stimulator on or off at any time. The procedure is performed in an outpatient center using local anesthesia."}
{"_id":"e81e57c0-eff0-49ff-8675-a9dd4e8657b4","text":"Fecal incontinence can cause embarrassment, fear, and loneliness. Taking steps to cope is important. The following tips can help:\n                \n- carrying a bag with cleanup supplies and a change of clothes when leaving the house.  - finding public restrooms before one is needed.  - using the toilet before leaving home.  - wearing disposable underwear or absorbent pads inserted in the underwear.  - using fecal deodorantspills that reduce the smell of stool and gas. Although fecal deodorants are available over the counter, a health care provider can help people find them.\n                \nEating tends to trigger contractions of the large intestine that push stool toward the rectum and also cause the rectum to contract for 30 to 60 minutes. Both these events increase the likelihood that a person will pass gas and have a bowel movement soon after eating. This activity may increase if the person is anxious. People with fecal incontinence may want to avoid eating in restaurants or at social gatherings, or they may want to take antidiarrheal medications before eating in these situations.\n                \nAnal Discomfort   The skin around the anus is delicate and sensitive. Constipation and diarrhea or contact between skin and stool can cause pain or itching. The following steps can help relieve anal discomfort:   - Washing the anal area after a bowel movement. Washing with water, but not soap, can help prevent discomfort. Soap can dry out the skin, making discomfort worse. Ideally, the anal area should be washed in the shower with lukewarm water or in a sitz batha special plastic tub that allows a person to sit in a few inches of warm water. No-rinse skin cleansers, such as Cavilon, are a good alternative. Wiping with toilet paper further irritates the skin and should be avoided. Premoistened, alcohol-free towelettes are a better choice.   - Keeping the anal area dry. The anal area should be allowed to air dry after washing. If time doesnt permit air drying, the anal area can be gently patted dry with a lint-free cloth.   - Creating a moisture barrier. A moisture barrier cream that contains ingredients such as dimethiconea type of siliconecan help form a barrier between skin and stool. The anal area should be cleaned before applying barrier cream. However, people should talk with their health care provider before using anal creams and ointments because some can irritate the anus.   - Using nonmedicated powders. Nonmedicated talcum powder or cornstarch can also relieve anal discomfort. As with moisture barrier creams, the anal area should be clean and dry before use.   - Using wicking pads or disposable underwear. Pads and disposable underwear with a wicking layer can pull moisture away from the skin.   - Wearing breathable clothes and underwear. Clothes and underwear should allow air to flow and keep skin dry. Tight clothes or plastic or rubber underwear that blocks air can worsen skin problems.   - Changing soiled underwear as soon as possible."}
{"_id":"bac2a26c-8ea2-426f-8e31-cb245ad61307","text":"- Fecal incontinence, also called a bowel control problem, is the accidental passing of solid or liquid stool or mucus from the rectum. Fecal incontinence includes the inability to hold a bowel movement until reaching a toilet as well as passing stool into ones underwear without being aware of it happening.  - Nearly 18 million U.S. adultsabout one in 12have fecal incontinence. People with fecal incontinence should not be afraid or embarrassed to talk with their health care provider.  - Fecal incontinence has many causes, including      - diarrhea    - constipation    - muscle damage or weakness    - nerve damage    - loss of stretch in the rectum    - childbirth by vaginal delivery    - hemorrhoids and rectal prolapse    - rectocele    - inactivity    - Health care providers diagnose fecal incontinence based on a persons medical history, physical exam, and medical test results.  - Treatment for fecal incontinence may include one or more of the following:      - eating, diet, and nutrition    - medications    - bowel training    - pelvic floor exercises and biofeedback    - surgery    - electrical stimulation    - A food diary can help identify foods that cause fecal incontinence.  - Fecal incontinence can occur in children because of a birth defect or disease, but in most cases it occurs because of constipation."}
{"_id":"26576697-922f-4117-ac79-67ae27dce3b6","text":"Diverticular* disease affects the colon. The colon is part of the large intestine that removes waste from your body. Diverticular disease is made up of two conditions: diverticulosis and diverticulitis. Diverticulosis occurs when pouches, called diverticula, form in the colon. These pouches bulge out like weak spots in a tire. Diverticulitis occurs if the pouches become inflamed.\n                \n*See the Pronunciation Guide for tips on how to say the words in bold type."}
{"_id":"0d20c1c3-6654-40b5-b72c-f551ac699a33","text":"Doctors are not sure what causes diverticular disease. Many think a diet low in fiber is the main cause. Fiber is a part of food that your body cannot digest. It is found in many fruits and vegetables. Fiber stays in the colon and absorbs water, which makes bowel movements easier to pass. Diets low in fiber may cause constipation, which occurs when stools are hard and difficult to pass. Constipation causes your muscles to strain when you pass stool. Straining may cause diverticula to form in the colon. If stool or bacteria get caught in the pouches, diverticulitis can occur."}
{"_id":"6e30a5a2-7373-4855-9a0f-3588b369a2d7","text":"The symptoms for diverticulosis and diverticulitis are different.\n                \nDiverticulosis. Many people don't have symptoms, but some people have cramping, bloating, and constipation. Some people also have bleeding, inflammation, and fistulas. If you are bleeding, bright red blood will pass through your rectum. The rectum is the end of the colon that connects to the anus. The rectum and anus are part of the gastrointestinal tract, which is the passage that food goes through. Rectal bleeding is usually painless, but it can be dangerous. You should see a doctor right away.\n                \nDiverticulitis. People with diverticulitis can have many symptoms. Often pain is felt in the lower part of the abdomen. If you have diverticulitis, you may have fevers, feel sick to your stomach, vomit, or have a change in your bowel habits."}
{"_id":"86024578-374d-4491-ac8b-123c42bb4b6f","text":"Many people get diverticular disease. Starting at age 40, the chance of getting it increases about every 10 years. About half of people between the ages of 60 and 80 have diverticular disease. Almost everyone over 80 has it."}
{"_id":"7b589933-5d43-4c71-885c-0d0d2d3c5199","text":"Treatment for diverticular disease depends on how serious the problem is and whether you are suffering from diverticulosis or diverticulitis. Most people get better by changing their diet. If you have rectal bleeding, you need to go to the hospital so a doctor can find the part of your colon that is bleeding. The doctor may use a special drug that makes the bleeding stop. The doctor may also decide to operate and remove the part of the colon that is bleeding."}
{"_id":"864395db-7722-4e74-a3db-312d4be336c6","text":"Eating high-fiber foods can help relieve symptoms. Sometimes mild pain medications also help."}
{"_id":"b5ecd6a3-46e5-4c10-86ad-fa0690df3f83","text":"A doctor may prescribe antibiotics and recommend following a liquid diet. Most people get better with this treatment. Some people may need surgery and other treatments.\n                \n- Surgery. Serious problems from diverticulitis are treated with surgery. Surgeons can clean the abdomen after infections and remove bleeding pouches and fistulas.  - Colon resection. If you get diverticulitis many times, your doctor might suggest taking out the part of the colon with diverticula. The healthy sections can be joined together. With the diverticula gone, you may avoid other infections.  - Emergency surgery. If you have severe problems, you may need emergency surgery to clear the infection and remove part of the colon. Later, a second surgery rejoins the healthy sections of the colon. The colon is separated for a brief time between surgeries, because rejoining the colon during the first surgery is not always safe. A temporary colostomy is needed between the two surgeries. A colostomy is an opening made on the abdomen where a plastic bag is connected to collect stool after food is digested. The surgeon makes the opening, called a stoma, and connects it to the end of the colon."}
{"_id":"9314499b-baef-4fa5-9f6f-96eb191809f6","text":"Eat a high-fiber diet to help prevent problems. Talk to your doctor about using fiber products like Benefiber, Citrucel, or Metamucil. Daily use can help you get the fiber you need if you do not get it through your diet.\n                \nAsk your doctor about which food choices are right for you.\n                \nEating foods high in fiber is simple and can help reduce diverticular disease symptoms and problems.\n                \nTry eating more of the following:\n                \n- Fruit. Raw apples, peaches, pears, and tangerines.  - Vegetables. Fresh broccoli, squash, carrots, and brussels sprouts.  - Starchy vegetables. Potatoes, baked beans, kidney beans, and lima beans.  - Grains. Whole-wheat bread, brown rice, bran flake cereal, and oatmeal.\n                \nTalk with your doctor about making diet changes. Learn what to eat and how to put more of these high-fiber foods in your diet."}
{"_id":"a6c1d237-05df-4f6e-b41a-300e76a00a8c","text":"- Diverticular disease is more common in people as they grow older.  - A low-fiber diet is the most likely cause of the disease.  - Most people are treated with a high-fiber diet and pain medication.  - Add whole grain foods, high-fiber fruits, and vegetables to your diet.  - Contact a doctor if you notice symptoms such as fever, chills, nausea, vomiting, abdominal pain, rectal bleeding, or change in bowel habits."}
{"_id":"51b5a12d-c4d9-4086-9288-9d078762dec1","text":"If you have advanced chronic kidney disease (CKD), you may soon need treatment to do the work your kidneys can no longer do. Learning about your treatment options for kidney failure will help you make the best choice for you. Each treatment has pros and cons. Your choice of treatment will have a big effect on your daily life, such as continuing to work if you do so currently. Talking with your doctor ahead of time about your options can help you take control of your care. Understanding the treatment you choose and getting used to the idea that you need to have this treatment takes time. If you find your choice of treatment does not fit your lifestyle, talk with your doctor about picking another treatment that fits your needs better."}
{"_id":"9d082149-4fba-4a3d-8a8b-9892368da42b","text":"The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the two kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra fluid. The urine flows from the kidneys to the bladder through two thin tubes of muscle called ureters, one on each side of the bladder. The bladder stores urine. The muscles of the bladder wall remain relaxed while the bladder fills with urine. As the bladder fills to capacity, signals sent to the brain tell a person to find a toilet soon. When the bladder empties, urine flows out of the body through a tube called the urethra, located at the bottom of the bladder. In men the urethra is long, while in women it is short."}
{"_id":"cc505664-da39-4a15-95f5-32f5058b7f51","text":"Chronic kidney disease means you have damaged kidneys that cannot filter blood normally. Wastes then build up in your blood, harming your body. Kidney disease usually does not get better and may lead to kidney failure. If your kidneys fail, current treatment options can help you live a longer, healthier life. Some people live with kidney disease for years without needing treatment. Others progress quickly to kidney failure."}
{"_id":"1cb4250b-0627-4dc3-becb-0bcab8be201f","text":"You have three treatment options to choose from to filter your blood. A fourth option offers care without replacing the work of the kidneys. None of these treatments helps the kidneys get better. However, they all can help you feel better.\n                \n- Hemodialysis uses a machine to move your blood through a filter outside your body, removing wastes.  - Peritoneal dialysis uses the lining of your belly to filter your blood inside your body, removing wastes.  - Kidney transplantation is surgery to place a healthy kidney from a person who has just died or a living person, usually a family member, into your body to take over the job of filtering your blood.  - Conservative management is the choice not to treat kidney failure with dialysis or a transplant. Instead, the focus is on using medicines to keep you comfortable, preserving kidney function through diet, and treating the problems of kidney failure, such as anemiaa shortage of red blood cells that can make you tiredand weak bones."}
{"_id":"c64c854b-cce5-4fc6-a679-672f9db20313","text":"Purpose of Hemodialysis\n                \nThe purpose of hemodialysis is to filter your blood. This type of dialysis uses a machine to remove harmful wastes and extra fluid, as your kidneys did when they were healthy. Hemodialysis helps control blood pressure and balance important minerals, such as potassium, sodium, calcium, and bicarbonate, in your blood. Hemodialysis is not a cure for kidney failure; however, it can help you feel better and live longer.\n                \nHow Hemodialysis Works\n                \nBefore you can begin dialysis, a surgeon will create a vascular access, usually in your arm. A vascular access lets high volumes of blood flow continuously during hemodialysis treatments to filter the largest possible amounts of blood per treatment.\n                \nHemodialysis uses a machine to move your blood through a filter, called a dialyzer, outside your body. A pump on the hemodialysis machine draws your blood through a needle into a tube, a few ounces at a time. Your blood then travels through the tube, which takes it to the dialyzer. Inside the dialyzer, your blood flows through thin fibers that filter out wastes and extra fluid. After the dialyzer filters your blood, another tube carries your blood back to your body. You can do hemodialysis at a dialysis center or in your home.\n                \nHemodialysis can replace part of your kidney function. You will also need dietary changes, medicines, and limits on water and other liquids you drink and get from food. Your dietary changes, the number of medicines you need, and limits on liquid will depend on where you receive your treatmentsat a dialysis center or at homeand how often you receive treatmentsthree or more times a week.\n                \nPros and Cons of Hemodialysis\n                \nThe pros and cons of hemodialysis differ for each person. What may be bad for one person may be good for another. Following is a list of the general pros and cons of dialysis center and home hemodialysis.\n                \nDialysis Center Hemodialysis\n                \nPros\n                \n- Dialysis centers are widely available.  - Trained health care providers are with you at all times and help administer the treatment.  - You can get to know other people with kidney failure who also need hemodialysis.  - You dont have to have a trained partner or keep equipment in your home.\n                \nCons\n                \n- The center arranges everyones treatments and allows few exceptions to the schedule.  - You need to travel to the center for treatment.  - This treatment has the strictest diet and limits on liquids because the longer time between treatments means wastes and extra fluid can build up in your body.  - You may have more frequent ups and downs in how you feel from day to day because of the longer time between sessions.  - Feeling better after a treatment may take a few hours.\n                \nHome Hemodialysis\n                \nPros\n                \n- You can do the treatment at the times you choose; however, you should follow your doctors orders about how many times a week you need treatment.  - You dont have to travel to a dialysis center.  - You gain a sense of control over your treatment.  - You will have fewer ups and downs in how you feel from day to day because of more frequent sessions.  - You can do your treatments at times that will let you work outside the home.  - You will have a more manageable diet and fewer limits on liquids because the shorter time between sessions prevents the buildup of wastes and extra fluid.  - You can take along a hemodialysis machine when traveling.  - You can spend more time with your loved ones because you dont have to go to the dialysis center three times a week.\n                \nCons\n                \n- Not all dialysis centers offer home hemodialysis training and support.  - You and a family member or friend will have to set aside a week or more at the beginning for training.  - Helping with treatments may be stressful for your family or friend.  - You need space for storing the hemodialysis machine and supplies at home.  - You will need to learn to put dialysis needles into your vascular access.  - Medicare and private insurance companies may limit the number of treatments they will pay for when you use home hemodialysis. Few people can afford the costs for additional treatments.\n                \nQuestions to Ask My Doctor\n                \nYou may want to ask your doctor these questions:\n                \n- Is hemodialysis the best treatment choice for me? Why?   - If Im treated at a dialysis center, can I go to the center of my choice?  - What should I look for in a dialysis center?  - Will my kidney doctor see me at the dialysis center?  - What does hemodialysis feel like?  - How will hemodialysis affect my ____ [blood pressure, diabetes, other conditions]?  - Is home hemodialysis available in my area? What type of training will I need? Who will train my partner and me?  - Will I be able to keep working? Can I have treatments at night? Will I be able to care for my children?  - How much should I exercise?   - Whom do I contact if I have problems?  - Who will be on my health care team? How can the members of my health care team help me?  - If I do home hemodialysis, will my insurance pay for more than three sessions a week?  - With whom can I talk about finances, sex, or family concerns?   - How\/where can I talk with other people who have faced this decision?\n                \nMore information about Hemodialysis and Home Hemodialysis is provided in the NIDDK health topics, Treatment Methods for Kidney Failure: Hemodialysis and Home Hemodialysis. See also the Kidney Failure Treatment Comparison Chart in this booklet, which compares hemodialysis, peritoneal dialysis, and transplantation."}
{"_id":"0725ea0e-87a8-4c04-a7f5-77bd0af9a430","text":"Purpose of Peritoneal Dialysis\n                \nThe purpose of peritoneal dialysis is to filter wastes and extra fluid from your body. This type of dialysis uses the lining of your bellythe space in your body that holds your stomach, bowels, and liverto filter your blood. This lining, called the peritoneum, acts to do the work of your kidneys.\n                \nHow Peritoneal Dialysis Works\n                \nA doctor will place a soft tube, called a catheter, in your belly a few weeks before you start treatment. The catheter stays in your belly permanently. When you start peritoneal dialysis, you will empty a kind of salty water, called dialysis solution, from a plastic bag through the catheter into your belly. When the bag is empty, you can disconnect your catheter from the bag so you can move around and do your normal activities. While the dialysis solution is inside your belly, it soaks up wastes and extra fluid from your body. After a few hours, you drain the used dialysis solution through another tube into a drain bag. You can throw away the used dialysis solution, now filled with wastes and extra fluid, in a toilet or tub. Then you start over with a fresh bag of dialysis solution. The process of emptying the used dialysis solution and refilling your belly with fresh solution is called an exchange. The process goes on continuously, so you always have dialysis solution in your belly soaking up wastes and extra fluid from your body.\n                \nTypes of Peritoneal Dialysis\n                \nTwo types of peritoneal dialysis are available. After you have learned about the types of peritoneal dialysis, you can choose the type that best fits your life. If one schedule or type of peritoneal dialysis does not suit you, talk with your doctor about trying the other type.\n                \n- Continuous ambulatory peritoneal dialysis does not require a machine and you can do it in any clean, well-lit place. The time period that the dialysis solution is in your belly is the dwell time. With continuous ambulatory peritoneal dialysis, the dialysis solution stays in your belly for a dwell time of 4 to 6 hours, or more. The process of draining the used dialysis solution and replacing it with fresh solution takes about 30 to 40 minutes. Most people change the dialysis solution at least four times a day and sleep with solution in their belly at night. With continuous ambulatory peritoneal dialysis, you do not have to wake up and perform dialysis tasks during the night.  - Continuous cycler-assisted peritoneal dialysis uses a machine called a cycler to fill and empty your belly three to five times during the night while you sleep. In the morning, you begin one exchange with a dwell time that lasts the entire day. You may do an additional exchange in the middle of the afternoon without the cycler to increase the amount of waste removed and to reduce the amount of fluid left behind in your body.\n                \nYou may need a combination of continuous ambulatory peritoneal dialysis and continuous cycler-assisted peritoneal dialysis if you weigh more than 175 pounds or if your peritoneum filters wastes slowly. For example, some people use a cycler at night and perform one exchange during the day. Others do four exchanges during the day and use a minicycler to perform one or more exchanges during the night. Youll work with your health care team to find the best schedule for you.\n                \nPros and Cons of Peritoneal Dialysis\n                \nEach type of peritoneal dialysis has pros and cons.\n                \nContinuous Ambulatory Peritoneal Dialysis\n                \nPros\n                \n- You can do continuous ambulatory peritoneal dialysis alone.  - You can do continuous ambulatory peritoneal dialysis at the times you choose, as long as you perform the required number of exchanges each day.  - You can do continuous ambulatory peritoneal dialysis in many locations.  - You can travel as long as you bring dialysis bags with you or have them delivered to your destination.  - You dont need a machine for continuous ambulatory peritoneal dialysis.  - You gain a sense of control over your treatment.\n                \nCons\n                \n- Continuous ambulatory peritoneal dialysis can disrupt your daily schedule.  - Continuous ambulatory peritoneal dialysis is a continuous treatment, and you should do all exchanges 7 days a week.  - Boxes of dialysis solution will take up space in your home.\n                \nContinuous Cycler-assisted Peritoneal Dialysis\n                \nPros\n                \n- You can do exchanges at night, while you sleep.  - You may not have to perform exchanges during the day.\n                \nCons\n                \n- You need a machine.  - Your connection to the cycler limits your movement at night.\n                \nQuestions to Ask My Doctor\n                \n- Is peritoneal dialysis the best treatment choice for me? Why? If yes, which type is best?   - What type of training do I need, and how long will it take?  - What does peritoneal dialysis feel like?   - How will peritoneal dialysis affect my ____ [blood pressure, diabetes, other conditions]?   - Will I be able to keep working? Will I be able to care for my children?   - How much should I exercise?   - Where do I store supplies?   - How often do I see my doctor?   - Who will be on my health care team? How can the members of my health care team help me?   - Whom do I contact if I have problems?   - With whom can I talk about finances, sex, or family concerns?   - How\/where can I talk with other people who have faced this decision?\n                \nMore information about Peritoneal Dialysis is provided in the NIDDK health topic, Treatment Methods for Kidney Failure: Peritoneal Dialysis. See also the Kidney Failure Treatment Comparison Chart, which compares peritoneal dialysis, hemodialysis, and transplantation."}
{"_id":"0fcc8832-9bc2-4cb4-89dd-bd887acf9eca","text":"What should I know about kidney transplantation?\n                \nThe purpose of kidney transplantation is to surgically place a healthy kidney from a donora person who has just died or a living person, most often a family memberinto your body. A kidney from someone who has just died is a deceased donor kidney. A kidney from a living person is a living donor kidney. A functioning kidney transplant does a better job of filtering wastes and keeping you healthy than dialysis.\n                \nHow Kidney Transplantation Works\n                \nSurgeonsdoctors who specialize in surgeryplace most transplanted kidneys in the lower front part of your abdomen. The kidney is connected to an artery, which brings unfiltered blood into the kidney, and a vein, which takes filtered blood out of the kidney. The surgeon also transplants the ureter from the donor to let urine from the new kidney flow to your bladder. Unless your damaged kidneys cause problems such as infection, they can remain in their normal position. The transplanted kidney takes over the job of filtering your blood. Your body normally attacks anything it sees as foreign, so to keep your body from attacking the kidney you need to take medicines called immunosuppressants for as long as the transplanted kidney functions.\n                \nPros and Cons of Kidney Transplantation\n                \nFollowing is a list of the pros and cons of kidney transplantation.\n                \nKidney Transplantation\n                \nPros\n                \n- A transplanted kidney works like a healthy kidney.  - If you have a living donor, you can choose the time of your operation.  - You may feel healthier and have an improved quality of life.  - You have fewer dietary restrictions.  - You wont need dialysis.  - People who receive a donated kidney have a greater chance of living a longer life than those who stay on dialysis.\n                \nCons\n                \n- Transplantation requires surgery.  - You will go through extensive medical testing at the transplant clinic.  - You may need to wait years for a deceased donor kidney.  - Your body may reject the new kidney, so one transplant may not last a lifetime.  - Youll need to take immunosuppressants, which may cause other health problems, for as long as the transplanted kidney functions.\n                \nQuestions to Ask My Doctor\n                \nYou may want to ask your doctor these questions:\n                \n- Is transplantation the best treatment choice for me? Why?  - What are my chances of having a successful transplant?  - How do I find out whether a family member or friend can donate?  - What are the risks to a family member or friend who donates?  - If a family member or friend does not donate, who will place me on a waiting list for a kidney? How long will I have to wait?  - How will I know if my donor kidney is working?  - How long does a transplanted kidney function?  - What side effects do immunosuppressants cause?  - Who will be on my transplant team? How can the members of my transplant team help me?  - With whom can I talk about finances, sex, or family concerns?  - How\/where can I talk with other people who have faced this decision?\n                \nMore information about Transplantation is provided in the NIDDK health topic, Treatment Methods for Kidney Failure: Transplantation. See also the Kidney Failure Treatment Comparison Chart, which compares peritoneal dialysis, hemodialysis, and transplantation."}
{"_id":"f5df24b6-e55d-4ace-ad98-82ff57f400b6","text":"Conservative management for kidney failure is the choice to say no to or stop dialysis treatments. For many people, dialysis not only extends life, it also improves the quality of life. For others who have serious conditions in addition to kidney failure, dialysis may seem like a burden that only prolongs suffering. If you have serious conditions in addition to kidney failure, dialysis may not prolong your life or improve the quality of your life.\n                \nYou have the right to say no to or stop dialysis. You may want to speak with your doctor, spouse, family, counselor, or renal social worker, who helps people with kidney disease, to help you make this decision.\n                \nIf you stop dialysis treatments or say you do not want to begin them, you may live for a few weeks or for several months, depending on your health and your remaining kidney function. You may choose to receive care from a hospicea facility or home program designed to meet the physical and emotional needs of the terminally illduring this time. Hospice care focuses on relief of pain and other symptoms. Whether or not you choose to use a hospice, your doctor can give you medicines to make you more comfortable. Your doctor can also give you medicines to treat the problems of kidney failure, such as anemia or weak bones. You may restart dialysis treatment if you change your mind.\n                \nAdvance Directives\n                \nAn advance directive is a statement or document in which you give instructions either to withhold certain treatments, such as dialysis, or to provide them, depending on your wishes and the specific circumstances. Even if you are happy with your quality of life on dialysis, you should think about circumstances that might make you want to stop dialysis treatments. At some point in a medical crisis, you might lose the ability to tell your health care team and loved ones what you want. Advance directives may include\n                \n- a living will  - a durable power of attorney for health care decisions  - a do not resuscitate (DNR) ordera legal form that tells your health care team you do not want cardiopulmonary resuscitation (CPR) or other life-sustaining treatment if your heart were to stop or if you were to stop breathing.\n                \nA living will is a document that details the conditions under which you would want to refuse treatment. You may state that you want your health care team to use all available means to sustain your life, or you may direct that you be withdrawn from dialysis if you fall into a coma from which you most likely wont wake up. In addition to dialysis, you may choose or refuse the following life-sustaining treatments:\n                \n- CPR  - feedings through a tube in your stomach  - mechanical or artificial means to help you breathe  - medicines to treat infections  - surgery  - receiving blood\n                \nRefusing to have CPR is the same as a DNR order. If you choose to have a DNR order, your doctor will place the order in your medical chart.\n                \nA durable power of attorney for health care decisions or a health care proxy is a document you use to assign a person to make health care decisions for you in the event you cannot make them for yourself. Make sure the person you name understands your values and will follow your instructions.\n                \nEach state has its own laws on advance directives. You can obtain a form for an advance medical directive thats valid in your state from the National Hospice and Palliative Care Organizationsee For More Information."}
{"_id":"ef9d9f0e-fc63-46da-954e-66310e64cf9a","text":"All of the treatment options for kidney failure require changes and restrictions in your diet.\n                \nHemodialysis\n                \nHemodialysis has the most restrictions. You should watch how much water and other liquids you get from food and drinks and avoid getting too much sodium, often from salt; potassium; and phosphorus. You may find it difficult to limit phosphorus because many foods that are high in phosphorus also provide the protein you need. Hemodialysis can remove protein from the body, so you should eat foods with high-quality protein, such as meat, fish, and eggs. Limit your phosphorus by avoiding foods such as beans, peas, nuts, tea, and colas. You may also need to take a pill called a phosphate binder that keeps phosphorus in your food from entering your bloodstream. Talk with your dialysis centers dietitian to find a hemodialysis meal plan that works for you.\n                \nMore information about nutrition for people who are on hemodialysis is provided in the NIDDK health topic, Eat Right to Feel Right on Hemodialysis.\n                \nPeritoneal Dialysis\n                \nLike hemodialysis, peritoneal dialysis requires limits on sodium and phosphorus. You may need to take a phosphate binder. The liquid limitations in peritoneal dialysis may not be as strict as those for hemodialysis. In fact, you may need to drink more water and other liquids if your peritoneal dialysis treatments remove too much fluid from your body. Peritoneal dialysis removes potassium from the body, so you may need to eat potassium-rich foods such as potatoes, tomatoes, oranges, and bananas. However, be careful not to eat too much potassium because it can cause an unsteady heartbeat. Peritoneal dialysis removes even more protein than hemodialysis, so eating foods with high-quality protein is important. You may need to limit calories because your body absorbs sugar from the dialysis solution.\n                \nKidney Transplantation\n                \nKidney transplantation has the fewest restrictions on your diet. You should limit sodium because it can raise your blood pressure. Medicines that you take after the transplant can cause you to gain weight, so you may need to limit calories.\n                \nConservative Management\n                \nThe diet for conservative management limits protein. Protein breaks down into waste products the kidneys must remove. Limiting protein may reduce the amount of work the kidneys have to do so they will last longer.\n                \n\n                \nHemodialysis    Peritoneal Dialysis    Kidney Transplantation                 In Center                 Home                 CAPD                 CCPD                 Deceased                 Living                     Schedule                 Three treatments a week for 3 to 5 hours or more.                 More flexibility in determining your schedule of treatments.                 Four to six exchanges a day, every day.                 Three to five exchanges a night, every night, with an additional exchange begun first thing in the morning.                 You may wait several years before a suitable kidney is available.                 If a friend or family member is donating, you can schedule the operation when you're both ready.                     After the operation, you'll have regular checkups with your doctor.                     Location                 Dialysis center.                 Home.                 Any clean environment that allows solution exchanges.                 The transplant operation takes place in a hospital.                     Availability                 Available in most communities; may require travel in some rural areas.                 Generally available, but not widely used because of equipment requirements.                 Widely available.                 Widely available.                 Transplant centers are located throughout the country. However, the demand for kidneys is far greater than the supply.                     Equipment      and Supplies                 No equipment or supplies in the home.                 Hemodialysis machine connected to plumbing; chair.                 Bags of dialysis solution take up storage space.                 Cycling machine; bags of dialysis solution.                 No equipment or supplies needed.                     Training Required                 Little training required; clinic staff perform most tasks.                 You and a helper must attend several training sessions.                 You'll need to attend several training sessions.                 You'll need to learn about your medications and when to take them.                     Diet                 Must limit fluids, sodium, potassium, and phosphorus.                 Must limit sodium and calories.                 Fewer dietary restrictions.                     Level of Freedom                 Little freedom during treatments. Greater freedom on non-treatment days.                 More freedom to set your own schedule. You're still linked to a machine for several hours a week.                 You can move around, exercise, work, drive, etc., with solution in your abdomen.                 You're linked to a machine during the night. You're free from exchanges during the day.                 Offers the greatest amount of freedom.                     Level of Responsibility                 Some patients prefer to let clinic staff perform all tasks.                 You and your helper are responsible for cleaning and setting up equipment and monitoring vital signs. Can be stressful on family helpers.                 You must perform exchanges four to six times a day, every day.                 You must set up your cycler every night.                 You must take immunosuppressants every day for as long as the transplanted kidney functions.\n                \nMore information about the treatments for kidney failure is provided in the NIDDK health communication program, National Kidney Disease Education Program."}
{"_id":"96817301-576f-4161-a15a-8c1b0bb0c128","text":"- You have three treatment options to choose from to filter your blood. A fourth option offers care without replacing the work of the kidneys.      - Hemodialysis    - Peritoneal dialysis    - Kidney transplantation    - Conservative management    - None of these treatments helps the kidneys get better. However, they all can help you feel better.  - Hemodialysis uses a machine to move your blood through a filter outside your body, removing wastes.  - Peritoneal dialysis uses the lining of your belly to filter your blood inside your body, removing wastes.  - Kidney transplantation is surgery to place a healthy kidney from a person who has just died or a living person, usually a family member, into your body to take over the job of filtering your blood.  - Conservative management is the choice not to treat kidney failure with dialysis or a transplant.  - All of the treatment options for kidney failure require changes and restrictions in your diet."}
{"_id":"f1319b7e-c7e2-471b-9322-a912eb6f96f8","text":"Hirschsprung* disease (HD) is a disease of the large intestine that causes severe constipation or intestinal obstruction. Constipation means stool moves through the intestines slower than usual. Bowel movements occur less often than normal and stools are difficult to pass. Some children with HD cant pass stool at all, which can result in the complete blockage of the intestines, a condition called intestinal obstruction. People with HD are born with it and are usually diagnosed when they are infants. Less severe cases are sometimes diagnosed when a child is older. An HD diagnosis in an adult is rare.\n                \n*See Pronunciation Guide for tips on how to say the words in bold type."}
{"_id":"e827be66-be06-48c1-a742-fb7cbc19ac67","text":"The large intestine, which includes the colon and rectum, is the last part of the digestive tract. The large intestines main job is to absorb water and hold stool. The rectum connects the colon to the anus. Stool passes out of the body through the anus. At birth, the large intestine is about 2 feet long. An adults large intestine is about 5 feet long."}
{"_id":"ae14ed4a-feff-4f6d-a317-71694e69ca0f","text":"People with HD have constipation because they lack nerve cells in a part or all of the large intestine. The nerve cells signal muscles in the large intestine to push stool toward the anus. Without a signal to push stool along, stool will remain in the large intestine.\n                \nHow severe HD is depends on how much of the large intestine is affected. Short-segment HD means only the last part of the large intestine lacks nerve cells. Long-segment HD means most or all of the large intestine, and sometimes the last part of the small intestine, lacks nerve cells.\n                \nIn a person with HD, stool moves through the large intestine until it reaches the part lacking nerve cells. At that point, the stool moves slowly or stops, causing an intestinal obstruction."}
{"_id":"5f5618cf-7ade-4739-87a5-a4e34423a471","text":"Before birth, a childs nerve cells normally grow along the intestines in the direction of the anus. With HD, the nerve cells stop growing too soon. Why the nerve cells stop growing is unclear. Some HD is inherited, meaning it is passed from parent to child through genes. HD is not caused by anything a mother did while pregnant."}
{"_id":"2983a5c6-8baf-435e-99f5-0105490619b9","text":"The main symptoms of HD are constipation or intestinal obstruction, usually appearing shortly after birth. Constipation in infants and children is common and usually comes and goes, but if your child has had ongoing constipation since birth, HD may be the problem.\n                \nSymptoms in Newborns\n                \nNewborns with HD almost always fail to have their first bowel movement within 48 hours after birth. Other symptoms include\n                \n- green or brown vomit  - explosive stools after a doctor inserts a finger into the rectum  - swelling of the belly, also known as the abdomen  - lots of gas  - bloody diarrhea\n                \n\n                \nSymptoms in Toddlers and Older Children\n                \nSymptoms of HD in toddlers and older children include\n                \n- not being able to pass stools without laxatives or enemas. A laxative is medicine that loosens stool and increases bowel movements. An enema is performed by flushing water, or sometimes a mild soap solution, into the anus using a special wash bottle.  - swelling of the abdomen.  - lots of gas.  - bloody diarrhea.  - slow growth or development.  - lack of energy because of a shortage of red blood cells, called anemia."}
{"_id":"504e5671-3e1a-4577-b2f2-6e84c641b26b","text":"HD is diagnosed based on symptoms and test results.\n                \nA doctor will perform a physical exam and ask questions about your childs bowel movements. HD is much less likely if parents can identify a time when their childs bowel habits were normal.\n                \nIf HD is suspected, the doctor will do one or more tests.\n                \nX rays\n                \nAn x ray is a black-and-white picture of the inside of the body. To make the large intestine show up better, the doctor may fill it with barium liquid. Barium liquid is inserted into the large intestine through the anus.\n                \nIf HD is the problem, the last segment of the large intestine will look narrower than normal. Just before this narrow segment, the intestine will look bulged. The bulging is caused by blocked stool stretching the intestine.\n                \nManometry\n                \nDuring manometry, the doctor inflates a small balloon inside the rectum. Normally, the rectal muscles will relax. If the muscles dont relax, HD may be the problem. This test is most often done in older children and adults.\n                \nBiopsy\n                \nBiopsy is the most accurate test for HD. The doctor removes a tiny piece of the large intestine and looks at it with a microscope. If nerve cells are missing, HD is the problem."}
{"_id":"5cd0d4a5-a560-4d6a-83b5-e627ca918de6","text":"Pull-through Procedure\n                \nHD is treated with surgery called a pull-through procedure. A surgeon removes the segment of the large intestine lacking nerve cells and connects the healthy segment to the anus. The pull-through procedure is usually done soon after diagnosis.\n                \nOstomy surgery\n                \nAn ostomy allows stool to leave the body through an opening in the abdomen. Although most children with HD do not need an ostomy, a child who has been very sick from HD may need an ostomy to get better before the pull-through procedure.\n                \nFor ostomy surgery, the surgeon first takes out the diseased segment of the large intestine. The end of the healthy intestine is moved to an opening in the abdomen where a stoma is created. A stoma is created by rolling the intestines end back on itself, like a shirt cuff, and stitching it to the abdominal wall. An ostomy pouch is attached to the stoma and worn outside the body to collect stool. The pouch will need to be emptied several times each day.\n                \n\n                \nIf the surgeon removes the entire large intestine and connects the small intestine to the stoma, the surgery is called an ileostomy. If the surgeon leaves part of the large intestine and connects it to the stoma, the surgery is called a colostomy.\n                \nLater, during the pull-through procedure, the surgeon removes the stoma and closes the abdomen with stitches."}
{"_id":"856e7da2-d6d6-4ad1-a80a-b6a296fde9dd","text":"- Hirschsprung disease (HD) is a disease of the large intestine that causes severe constipation or intestinal obstruction. People with HD are born with it.  - The large intestine, which includes the colon and rectum, is the last part of the digestive tract.  - The cause of HD is unclear. HD is not caused by anything a mother did while pregnant.  - The main symptoms of HD are constipation or intestinal obstruction, usually appearing shortly after birth.  - Newborns with HD almost always fail to have their first bowel movement within 48 hours after birth.  - HD is diagnosed based on symptoms and test results.  - HD is treated with surgery called a pull-through procedure.  - A child who has been very sick from HD may need an ostomy to get better before the pull-through procedure.  - Most children pass stool normally after the pull-through procedure.  - People with HD can suffer from an infection of the intestines, called enterocolitis, before or after surgery.  - If you have a child with HD, your chance of having more children with HD is greater."}
{"_id":"8f0c2164-4fb5-4526-8325-5f16b25d81a5","text":"- Starting a physical activity program can help you lose weight or keep a healthy weight and keep your blood glucose levels on target.  - Always talk with your health care team before you start a new physical activity program.  - Ask your health care team if you need to change the amount of medicine you take or the food you eat before any physical activity.  - Talk with your health care team about what types of physical activity are safe for you, such as walking, weightlifting, or housework.  - To make sure you stay active, find activities you like to do. Ask a friend or family member to be your exercise buddy.  - Write down your blood glucose levels and when and how long you are physically active in a record book.  - Doctors suggest that you aim for 30 to 60 minutes of moderate to vigorous physical activity most days of the week.  - Children and adolescents with type 2 diabetes who are 10 to 17 years old should aim for 60 minutes of moderate to vigorous activity every day.  - Not all physical activity has to take place at the same time. For example, you might take a walk for 20 minutes, lift hand weights for 10 minutes, and walk up and down the stairs for 5 minutes.  - Doing moderate to vigorous aerobic exercise for 30 to 60 minutes a day most days of the week provides many benefits. You can even split up these minutes into several parts.  - Start exercising slowly, with 5 to 10 minutes a day, and add a little more time each week. Try walking briskly, hiking, or climbing stairs.  - Whether youre a man or a woman, you can do strength training with hand weights, elastic bands, or weight machines two to three times a week.  - Stretching exercises are a light to moderate physical activity that both men and women can do. When you stretch, you increase your flexibility, lower your stress, and help prevent sore muscles.  - Increase daily activity by spending less time watching TV or at the computer.  - Try these simple ways to add light, moderate, or vigorous physical activities in your life every day:      - Walk around while you talk on the phone.    - Take a walk through your neighborhood.    - Do chores, such as work in the garden or rake leaves, clean the house, or wash the car.    - If you have type 1 diabetes, try not to do vigorous physical activity when you have ketones in your blood or urine."}
{"_id":"ba245a51-3099-44be-84a8-3cccf3d08156","text":"Hyperthyroidism is a disorder that occurs when the thyroid gland makes more thyroid hormone than the body needs. Hyperthyroidism is sometimes called thyrotoxicosis, the technical term for too much thyroid hormone in the blood. Thyroid hormones circulate throughout the body in the bloodstream and act on virtually every tissue and cell in the body. Hyperthyroidism causes many of the bodys functions to speed up. About 1 percent of the U.S. population has hyperthyroidism.1"}
{"_id":"7af56606-b6fb-4169-b361-f5f7deb1c1ce","text":"The thyroid is a 2-inch-long, butterfly-shaped gland weighing less than 1 ounce. Located in the front of the neck below the larynx, or voice box, it has two lobes, one on each side of the windpipe. The thyroid is one of the glands that make up the endocrine system. The glands of the endocrine system produce, store, and release hormones into the bloodstream. The hormones then travel through the body and direct the activity of the bodys cells.\n                \nThe thyroid gland makes two thyroid hormones, triiodothyronine (T3) and thyroxine (T4). T3 is made from T4 and is the more active hormone, directly affecting the tissues. Thyroid hormones affect metabolism, brain development, breathing, heart and nervous system functions, body temperature, muscle strength, skin dryness, menstrual cycles, weight, and cholesterol levels.\n                \nThyroid hormone production is regulated by thyroid-stimulating hormone (TSH), which is made by the pituitary gland in the brain. When thyroid hormone levels in the blood are low, the pituitary releases more TSH. When thyroid hormone levels are high, the pituitary responds by decreasing TSH production."}
{"_id":"a919ed37-f5d8-4ff2-b7f2-de6e48a6fbb8","text":"Hyperthyroidism has several causes, including\n                \n- Graves disease  - thyroid nodules  - thyroiditis, or inflammation of the thyroid  - consuming too much iodine  - overmedicating with synthetic thyroid hormone, which is used to treat underactive thyroid\n                \nRarely, hyperthyroidism is caused by a pituitary adenoma, which is a noncancerous tumor of the pituitary gland. In this case, hyperthyroidism is due to too much TSH.\n                \nGraves Disease\n                \nGraves disease, also known as toxic diffuse goiter, is the most common cause of hyperthyroidism in the United States. Graves disease is an autoimmune disorder. Normally, the immune system protects the body from infection by identifying and destroying bacteria, viruses, and other potentially harmful foreign substances. But in autoimmune diseases, the immune system attacks the bodys own cells and organs.\n                \nWith Graves disease, the immune system makes an antibody called thyroid stimulating immunoglobulin (TSI) that attaches to thyroid cells. TSI mimics the action of TSH and stimulates the thyroid to make too much thyroid hormone.\n                \nMore information is provided in the NIDDK health topic, Graves' disease.\n                \nThyroid Nodules\n                \nThyroid nodules, also called adenomas, are lumps in the thyroid. Thyroid nodules are common and usually noncancerous. About 3 to 7 percent of the U.S. population has them.2 However, nodules may become overactive and produce too much hormone.\n                \nA single overactive nodule is called a toxic adenoma. Multiple overactive nodules are called toxic multinodular goiter. Often found in older adults, toxic multinodular goiter can produce a large amount of excess thyroid hormone.\n                \nThyroiditis\n                \nThyroiditis is an inflammation of the thyroid that causes stored thyroid hormone to leak out of the thyroid gland. At first, the leakage raises hormone levels in the blood, leading to hyperthyroidism that lasts for 1 or 2 months. Most people then develop hypothyroidismwhen thyroid hormone levels are too lowbefore the thyroid is completely healed.\n                \nSeveral types of thyroiditis can cause hyperthyroidism followed by hypothyroidism:\n                \n- Subacute thyroiditis. This condition involves painful inflammation and enlargement of the thyroid. Experts are not sure what causes subacute thyroiditis, but it may be related to a viral or bacterial infection. The condition usually goes away on its own in a few months.  - Postpartum thyroiditis. This type of thyroiditis develops after a woman gives birth. For more information, see the section titled What happens with pregnancy and thyroid conditions?  - Silent thyroiditis. This type of thyroiditis is called silent because it is painless, as is postpartum thyroiditis, even though the thyroid may be enlarged. Like postpartum thyroiditis, silent thyroiditis is probably an autoimmune condition and sometimes develops into permanent hypothyroidism.\n                \nConsuming Too Much Iodine\n                \nThe thyroid uses iodine to make thyroid hormone, so the amount of iodine consumed influences the amount of thyroid hormone the thyroid makes. In some people, consuming large amounts of iodine may cause the thyroid to make excess thyroid hormone.\n                \nSometimes significant amounts of iodine are contained in medicationssuch as amiodarone, which is used to treat heart problemsor in supplements containing seaweed. Some cough syrups also contain large amounts of iodine. See Eating, Diet, and Nutrition for more information on iodine.\n                \nOvermedicating with Synthetic Thyroid Hormone\n                \nSome people who take synthetic thyroid hormone for hypothyroidism may take too much. People who take synthetic thyroid hormone should see their health care provider at least once a year to have their thyroid hormone levels checked and follow the health care providers instructions about the dosage.\n                \nSome other medications may also interact with synthetic thyroid hormone to raise hormone levels in the blood. People who take synthetic thyroid hormone should ask their health care provider about interactions when starting new medications."}
{"_id":"105c4a87-8367-41f6-bfcc-b5b7f6bba4fd","text":"Hyperthyroidism has many symptoms that can vary from person to person. Some common symptoms of hyperthyroidism are\n                \n- nervousness or irritability  - fatigue or muscle weakness  - heat intolerance  - trouble sleeping  - hand tremors  - rapid and irregular heartbeat  - frequent bowel movements or diarrhea  - weight loss  - mood swings  - goiter, which is an enlarged thyroid that may cause the neck to look swollen and can interfere with normal breathing and swallowing"}
{"_id":"3ec99970-6e72-4f0c-af35-cd1d56b1f584","text":"Many symptoms of hyperthyroidism are the same as those of other diseases, so hyperthyroidism usually cannot be diagnosed based on symptoms alone. With suspected hyperthyroidism, health care providers take a medical history and perform a thorough physical exam. Health care providers may then use several blood tests, such as the following, to confirm a diagnosis of hyperthyroidism and find its cause:\n                \nTSH test. The ultrasensitive TSH test is usually the first test a health care provider performs. This test detects even tiny amounts of TSH in the blood and is the most accurate measure of thyroid activity available. The TSH test is especially useful in detecting mild hyperthyroidism. Generally, a TSH reading below normal means a person has hyperthyroidism and a reading above normal means a person has hypothyroidism.\n                \nHealth care providers may conduct additional tests to help confirm the diagnosis or determine the cause of hyperthyroidism.\n                \nT3 and T4 test. This test shows the levels of T3 and T4 in the blood. With hyperthyroidism, the levels of one or both of these hormones in the blood are higher than normal.\n                \nThyroid-stimulating immunoglobulin (TSI) test. This test, also called a thyroidstimulating antibody test, measures the level of TSI in the blood. Most people with Graves disease have this antibody, but people whose hyperthyroidism is caused by other conditions do not.\n                \nRadioactive iodine uptake test. The radioactive iodine uptake test measures the amount of iodine the thyroid collects from the bloodstream. Measuring the amount of iodine in a persons thyroid helps the health care provider determine what is causing a persons hyperthyroidism. For example, low levels of iodine uptake might be a sign of thyroiditis, whereas high levels could indicate Graves disease.\n                \nThyroid scan. A thyroid scan shows how and where iodine is distributed in the thyroid. The images of nodules and other possible irregularities help the health care provider diagnose the cause of a persons hyperthyroidism.\n                \nMore information is provided in the NIDDK health topic, Thyroid Tests."}
{"_id":"eabbd650-5b22-4ccc-8740-5bc2a0c3c55e","text":"Health care providers treat hyperthyroidism with medications, radioiodine therapy, or thyroid surgery. The aim of treatment is to bring thyroid hormone levels to a normal state, thus preventing long-term complications, and to relieve uncomfortable symptoms. No single treatment works for everyone.\n                \nTreatment depends on the cause of hyperthyroidism and how severe it is. When choosing a treatment, health care providers consider a patients age, possible allergies to or side effects of the medications, other conditions such as pregnancy or heart disease, and the availability of an experienced thyroid surgeon.\n                \nFinding the right specialist for treatment is an important first step. Some professional societies, listed under For More Information, and endocrinology departments in local teaching hospitals can provide the names of local specialists.\n                \nMedications\n                \nBeta blockers. Health care providers may prescribe a medication called a beta blocker to reduce symptoms until other treatments take effect. Beta blockers act quickly to relieve many of the symptoms of hyperthyroidism, such as tremors, rapid heartbeat, and nervousness, but do not stop thyroid hormone production. Most people feel better within hours of taking these medications.\n                \nAntithyroid medications. Antithyroid therapy is the easiest way to treat hyperthyroidism. Antithyroid medications interfere with thyroid hormone production but dont usually have permanent results. Antithyroid medications are not used to treat thyroiditis.\n                \nOnce treatment with antithyroid medications begins, thyroid hormone levels may not move into the normal range for several weeks or months. The average treatment time is about 1 to 2 years, but treatment can continue for many years.\n                \nAntithyroid medications can cause side effects in some people, including\n                \n- allergic reactions such as rashes and itching  - a decrease in the number of white blood cells in the body, which can lower resistance to infection  - liver failure, in rare cases\n                \nStop your antithyroid medication and call your health care provider right away if you develop any of the following while taking antithyroid medications:   - fatigue   - weakness   - vague abdominal pain   - loss of appetite   - skin rash or itching   - easy bruising   - yellowing of the skin or whites of the eyes, called jaundice   - persistent sore throat   - fever\n                \nIn the United States, health care providers prescribe the antithyroid medication methimazole (Tapazole, Northyx) for most types of hyperthyroidism.\n                \nAntithyroid medications and pregnancy. Because pregnant and breastfeeding women cannot receive radioiodine therapy, they are usually treated with an antithyroid medication instead. However, experts agree that women in their first trimester of pregnancy should not take methimazole due to the rare occurrence of damage to the fetus. Another antithyroid medication, propylthiouracil (PTU), is available for women in this stage of pregnancy or for women who are allergic to or intolerant of methimazole and have no other treatment options.\n                \nHealth care providers may prescribe PTU for the first trimester of pregnancy and switch to methimazole for the second and third trimesters. Some women are able to stop taking antithyroid medications in the last 4 to 8 weeks of pregnancy due to the remission of hyperthyroidism that occurs during pregnancy. However these women should continue to be monitored for recurrence of thyroid problems following delivery.\n                \nStudies have shown that mothers taking antithyroid medications may safely breastfeed. However, they should take only moderate doses, less than 1020 milligrams daily, of the antithyroid medication methimazole. Doses should be divided and taken after feedings, and the infants should be monitored for side effects.4\n                \nWomen requiring higher doses of the antithyroid medication to control hyperthyroidism should not breastfeed.\n                \nRadioiodine Therapy\n                \nRadioactive iodine-131 is a common and effective treatment for hyperthyroidism. In radioiodine therapy, patients take radioactive iodine-131 by mouth. Because the thyroid gland collects iodine to make thyroid hormone, it will collect the radioactive iodine from the bloodstream in the same way. The radioactive iodine gradually destroys the cells that make up the thyroid gland but does not affect other body tissues.\n                \nMore than one round of radioiodine therapy may be needed to bring thyroid hormone production into the normal range. In the meantime, treatment with beta blockers can control symptoms.\n                \nAlmost everyone who receives radioactive iodine treatment eventually develops hypothyroidism. But health care providers consider this an acceptable outcome because hypothyroidism is easier to treat and has fewer long-term complications than hyperthyroidism. People who develop hypothyroidism must take synthetic thyroid hormone.\n                \nRadioiodine and pregnancy. Although iodine-131 is not known to cause birth defects or infertility, radioiodine therapy is not used in pregnant women or women who are breastfeeding. Radioactive iodine can be harmful to the fetus thyroid and can be passed from mother to child in breast milk. Experts recommend that women wait a year after treatment before becoming pregnant.\n                \nThyroid Surgery\n                \nThe least-used treatment is surgery to remove part or most of the thyroid gland. Sometimes surgery may be used to treat\n                \n- pregnant women who cannot tolerate antithyroid medications  - people with large goiters  - people who have cancerous thyroid nodules, though hyperthyroidism does not cause cancer\n                \nBefore surgery, the health care provider may prescribe antithyroid medications to temporarily bring a patients thyroid hormone levels into the normal range. This presurgical treatment prevents a condition called thyroid storma sudden, severe worsening of symptomsthat can occur when hyperthyroid patients have general anesthesia.\n                \nWhen part of the thyroid is removedas a treatment for toxic nodules, for examplethyroid hormone levels may return to normal. But some surgical patients may still develop hypothyroidism and need to take synthetic thyroxine, a medication that is identical to the hormone, T4, made by the thyroid. If the entire thyroid is removed, lifelong thyroid hormone medication is necessary. After surgery, health care providers will continue to monitor patients thyroid hormone levels.\n                \nAlthough uncommon, certain problems can occur in thyroid surgery. The parathyroid glands can be damaged because they are located very close to the thyroid. These glands help control calcium and phosphorus levels in the body. Damage to the laryngeal nerve, also located close to the thyroid, can lead to voice changes or breathing problems. But when surgery is performed by an experienced surgeon, less than 1 percent of patients have permanent complications.5 People who need help finding a surgeon can contact one of the organizations listed under For More Information."}
{"_id":"459273fc-5e4c-4aa8-9185-5152a0dd288a","text":"Experts recommend that people eat a balanced diet to obtain most nutrients. More information about diet and nutrition is provided by the National Agricultural Library at www.nutrition.gov.\n                \nDietary Supplements\n                \nIodine is an essential mineral for the thyroid. However, people with autoimmune thyroid disease may be sensitive to harmful side effects from iodine. Taking iodine drops or eating foods containing large amounts of iodinesuch as seaweed, dulse, or kelpmay cause or worsen hyperthyroidism. More information about iodine is provided by the National Library of Medicine in the fact sheet, Iodine in diet, available at www.nlm.nih.gov\/medlineplus.\n                \nWomen need more iodine when they are pregnantabout 250 micrograms a daybecause the baby gets iodine from the mothers diet. In the United States, about 7 percent of pregnant women may not get enough iodine in their diet or through prenatal vitamins.6 Choosing iodized saltsalt supplemented with iodineover plain salt and prenatal vitamins containing iodine will ensure this need is met.\n                \nTo help ensure coordinated and safe care, people should discuss their use of dietary supplements, such as iodine, with their health care provider. Tips for talking with health care providers are available through the National Center for Complementary and Integrative Health."}
{"_id":"f6069d58-eeb9-43cd-9080-770ab3030851","text":"- Hyperthyroidism is a disorder that occurs when the thyroid gland makes more thyroid hormone than the body needs.  - Hyperthyroidism is most often caused by Graves disease, an autoimmune disorder. Other causes include thyroid nodules, thyroiditis, consuming too much iodine, and overmedicating with synthetic thyroid hormone.  - Some symptoms of hyperthyroidism are nervousness or irritability, fatigue or muscle weakness, heat intolerance, trouble sleeping, hand tremors, rapid and irregular heartbeat, frequent bowel movements or diarrhea, weight loss, mood swings, and goiter.  - Hyperthyroidism is much more common in women than men.  - Hyperthyroidism is also more common in people older than age 60 and is often caused by thyroid nodules. Hyperthyroidism in this age group is sometimes misdiagnosed as depression or dementia. For people older than age 60, subclinical hyperthyroidism increases their chance of developing atrial fibrillation.  - Women with hyperthyroidism should discuss their condition with their health care provider before becoming pregnant.  - Hyperthyroidism is treated with medications, radioiodine therapy, or thyroid surgery. No single treatment works for everyone."}
{"_id":"fe6e8cde-0b58-4756-bdf5-5bfeb3a74135","text":"Polycystic kidney disease is a genetic disorder that causes numerous cysts to grow in the kidneys. A kidney cyst is an abnormal sac filled with fluid. PKD cysts can greatly enlarge the kidneys while replacing much of their normal structure, resulting in chronic kidney disease (CKD), which causes reduced kidney function over time. CKD may lead to kidney failure, described as end-stage kidney disease or ESRD when treated with a kidney transplant or blood-filtering treatments called dialysis. The two main types of PKD are autosomal dominant PKD and autosomal recessive PKD.\n                \nPKD cysts are different from the usually harmless simple cysts that often form in the kidneys later in life. PKD cysts are more numerous and cause complications, such as high blood pressure, cysts in the liver, and problems with blood vessels in the brain and heart."}
{"_id":"ee398bbd-8661-4ec8-9749-8b76b0f4b93c","text":"A gene mutation, or defect, causes polycystic kidney disease. Genes provide instructions for making proteins in the body. A gene mutation is a permanent change in the deoxyribonucleic acid (DNA) sequence that makes up a gene. In most cases of PKD, a person inherits the gene mutation, meaning a parent passes it on in his or her genes. In the remaining cases, the gene mutation develops spontaneously. In spontaneous cases, neither parent carries a copy of the mutated gene.\n                \nResearchers have found three different gene mutations associated with PKD. Two of the genes are associated with autosomal dominant PKD. The third gene is associated with autosomal recessive PKD. Gene mutations that cause PKD affect proteins that play a role in kidney development.\n                \n\n                \nGenetic Disorders   Each cell contains thousands of genes that provide the instructions for making proteins for growth and repair of the body. If a gene has a mutation, the protein made by that gene may not function properly, which sometimes creates a genetic disorder. Not all gene mutations cause a disorder.   People inherit two copies of most genes; one copy from each parent. A genetic disorder occurs when one or both parents pass a mutated gene to a child at conception. A genetic disorder can also occur through a spontaneous gene mutation, meaning neither parent carries a copy of the mutated gene. Once a spontaneous gene mutation has occurred, a person can pass it to his or her children.   Read more about genes and genetic conditions in the U.S. National Library of Medicines (NLMs) Genetics Home Reference."}
{"_id":"a76b6bb4-659a-4eb5-a1f1-3e883bfecdd4","text":"Estimates of PKDs prevalence range from one in 400 to one in 1,000 people.1 According to the United States Renal Data System, PKD accounts for 2.2 percent of new cases of kidney failure each year in the United States. Annually, eight people per 1 million have kidney failure as a result of PKD.2\n                \nPolycystic kidney disease exists around the world and in all races. The disorder occurs equally in women and men, although men are more likely to develop kidney failure from PKD. Women with PKD and high blood pressure who have had more than three pregnancies also have an increased chance of developing kidney failure."}
{"_id":"2e16f6a9-46e4-4b80-a19c-1ec7feca61b1","text":"Autosomal dominant PKD is the most common form of PKD and the most common inherited disorder of the kidneys.3 The term autosomal dominant means a child can get the disorder by inheriting the gene mutation from only one parent. Each child of a parent with an autosomal dominant mutation has a 50 percent chance of inheriting the mutated gene. About 10 percent of autosomal dominant PKD cases occur spontaneously.4\n                \nThe following chart shows the chance of inheriting an autosomal dominant gene mutation:\n                \n\n                \n\n                \nHealth care providers identify most cases of autosomal dominant PKD between the ages of 30 and 50.4 For this reason, health care providers often call autosomal dominant PKD adult PKD. However, the onset of kidney damage and how quickly the disorder progresses varies. In some cases, cysts may form earlier in life and grow quickly, causing symptoms in childhood.\n                \n\n                \n\n                \nThe cysts grow out of nephrons, the tiny filtering units inside the kidneys. The cysts eventually separate from the nephrons and continue to enlarge. The kidneys enlarge along with the cystswhich can number in the thousandswhile roughly retaining their kidney shape. In fully developed autosomal dominant PKD, a cyst-filled kidney can weigh as much as 20 to 30 pounds."}
{"_id":"6c86735a-c7d1-4343-90c0-19f487ed831b","text":"In many cases, PKD does not cause signs or symptoms until cysts are half an inch or larger. When present, the most common symptoms are pain in the back and sidesbetween the ribs and hipsand headaches. The pain can be temporary or persistent, mild or severe. Hematuriablood in the urinemay also be a sign of autosomal dominant PKD."}
{"_id":"29ff1ce4-8d31-4a97-b8e6-8ad5ba7c20e5","text":"The complications of autosomal dominant PKD include the following:\n                \n- Pain. Cyst infection, other types of urinary tract infections (UTIs), bleeding into cysts, kidney stones, or stretching of the fibrous tissue around the kidney because of cyst growth can cause pain in the area of the kidneys.  - High blood pressure. High blood pressure is present in about half of the people with autosomal dominant PKD and normal kidney function between the ages of 20 and 35.4 Almost 100 percent of people with kidney failure and autosomal dominant PKD have high blood pressure.1 High blood pressuregreater than 140\/90 mm Hgincreases the likelihood of heart disease and stroke, as well as adding to the damage already done to the kidneys by the cysts.  - Kidney failure. Kidney failure means the kidneys no longer work well enough to maintain health. A person with kidney failure may have the following symptoms:      - little or no urination    - edemaswelling, usually in the legs, feet, or ankles and less often in the hands or face    - drowsiness    - fatigue, or feeling tired    - generalized itching or numbness    - dry skin    - headaches    - weight loss    - appetite loss    - nausea    - vomiting    - sleep problems    - trouble concentrating    - darkened skin    - muscle cramps    - shortness of breath    - chest pain\n                \nUntreated kidney failure can lead to coma and death. More than half of people with autosomal dominant PKD progress to kidney failure by age 70.1\n                \n- UTIs. Kidney cysts block the flow of urine through the kidneys. Stagnant urine can set the stage for infection. Bacteria enter the urinary tract through the urethra and spread up to the kidneys. Sometimes, the kidney cysts become infected. UTIs may cause scarring in the kidneys.  - Kidney stones. About 20 percent of people with autosomal dominant PKD have kidney stones.1 Kidney stones can block the flow of urine and cause pain.  - Liver cysts. Liver cysts are the most common nonkidney complication of autosomal dominant PKD.1 Liver cysts generally cause no symptoms.  - Pancreatic cysts. PKD can also cause cysts in the pancreas. Pancreatic cysts rarely cause pancreatitisinflammation, or swelling, of the pancreas.  - Abnormal heart valves. Abnormal heart valves may occur in up to 25 percent of people with autosomal dominant PKD.1 Insufficient blood flow in the aortathe large artery that carries blood from the heartmay result from the abnormal heart valves.  - Diverticula. Diverticula are small pouches, or sacs, that push outward through weak spots in the colon wall. This complication is more common in people with PKD who have kidney failure.1  - Brain aneurysms. An aneurysm is a bulge in the wall of a blood vessel. Aneurysms in the brain might cause headaches that are severe or feel different from other headaches. Brain aneurysms can rupture, or break open, causing bleeding inside the skull. A ruptured aneurysm in the brain is a life-threatening condition and requires immediate medical attention."}
{"_id":"92c0fc60-4dc5-4e98-90fc-872a35fb6198","text":"Autosomal recessive PKD is a rare genetic disorder that affects the liver as well as the kidneys. The signs of autosomal recessive PKD frequently appear in the earliest months of life, even in the womb, so health care providers often call it infantile PKD. In an autosomal recessive disorder, the child has to inherit the gene mutation from both parents to have an increased likelihood for the disorder. The chance of a child inheriting autosomal recessive mutations from both parents with a gene mutation is 25 percent, or one in four. If only one parent carries the mutated gene, the child will not get the disorder, although the child may inherit the gene mutation. The child is a carrier of the disorder and can pass the gene mutation to the next generation. Genetic testing can show whether a parent or child is a carrier of the mutated gene. Autosomal recessive disorders do not typically appear in every generation of an affected family.\n                \nThe following chart shows the chance of inheriting an autosomal recessive mutation from parents who both carry the mutated gene:\n                \n\n                \n\n                \nRead more about how people inherit genetic conditions at the NLMs Genetics Home Reference."}
{"_id":"177880a2-8ec9-4f25-8700-f829fcb96b68","text":"An early sign of autosomal recessive PKD is an enlarged kidney, seen in a fetus or an infant using ultrasound. Kidney function is crucial for early physical development, so children with autosomal recessive PKD and decreased kidney function are usually smaller-than-average size, a condition called growth failure.\n                \nSome people with autosomal recessive PKD do not develop signs or symptoms until later in childhood or even adulthood."}
{"_id":"693128f9-8a8a-4fde-bb6e-eeb2c25e6b4f","text":"Babies with the most severe cases of autosomal recessive PKD often die hours or days after birth because they cannot breathe well enough to sustain life. Their lungs do not develop as they should during the prenatal period. Pressure from enlarged kidneys also contributes to breathing problems.\n                \nChildren born with autosomal recessive PKD often develop kidney failure before reaching adulthood.\n                \nLiver scarring occurs in all people with autosomal recessive PKD and is usually present at birth. However, liver problems tend to become more of a concern as people with autosomal recessive PKD grow older. Liver scarring can lead to progressive liver dysfunction and other problems.\n                \nAdditional complications of autosomal recessive PKD include high blood pressure and UTIs."}
{"_id":"a5b75fd6-3e74-44b8-af17-6b061e432bb3","text":"Scientists have not yet found a way to prevent PKD. However, people with PKD may slow the progression of kidney damage caused by high blood pressure through lifestyle changes, diet, and blood pressure medications. People with PKD should be physically active 30 minutes a day most days of the week. See Eating, Diet, and Nutrition for diet advice on lowering blood pressure and slowing the progression of kidney disease in general. If lifestyle and diet changes do not control a persons blood pressure, a health care provider may prescribe one or more blood pressure medications, including ACE inhibitors or ARBs."}
{"_id":"f91621b1-b221-4beb-85e3-e768b685aabe","text":"A dietitian specializes in helping people who have kidney disease choose the right foods and plan healthy meals. People with any kind of kidney disease, including PKD, should talk with a dietitian about foods that should be added to their diet and foods that might be harmful.\n                \nPKD may require diet changes for blood pressure control. Kidney disease in general also calls for certain diet changes.\n                \nFollowing a healthy eating plan can help lower blood pressure. A health care provider may recommend the Dietary Approaches to Stop Hypertension (DASH) eating plan, which focuses on fruits, vegetables, whole grains, and other foods that are heart healthy and lower in sodium, which often comes from salt. The DASH eating plan\n                \n- is low in fat and cholesterol  - features fat-free or low-fat milk and dairy products, fish, poultry, and nuts  - suggests less red meat, sweets, added sugars, and sugar-containing beverages  - is rich in nutrients, protein, and fiber\n                \nMore information about the DASH eating planis available from the National Heart, Lung, and Blood Institute.\n                \nAs your kidneys become more damaged, you may need to eat foods that are lower in phosphorus and potassium. The health care provider will use lab tests to watch your levels.\n                \nFoods high in potassium include\n                \n- bananas  - oranges  - potatoes  - tomatoes\n                \nLower-potassium foods include\n                \n- apples  - peaches  - carrots  - green beans\n                \nFoods higher in phosphorus include\n                \n- large portions of meat, fish and dairy foods  - bran cereals and oatmeal  - beans and nuts  - colas\n                \nLower-phosphorus alternatives include\n                \n- fresh fruits and vegetables  - breads  - pasta  - rice  - corn and rice cereals  - light-colored sodas\n                \nPeople with kidney disease and high blood pressure should also limit how much sodium they get to 2,300 mg or less each day.5\n                \nPeople with CKD may need to watch how much protein they eat. Everyone needs protein. However, protein breaks down into wastes the kidneys must remove. Large amounts of protein make the kidneys work harder. High-quality proteins such as meat, fish, and eggs create fewer wastes than other sources of protein. Beans, whole grains, soy products, nuts and nut butters, and dairy products can also be good sources of protein. Most people eat more protein than they need. Eating high-quality protein and smaller portions of protein can help protect the kidneys.\n                \nMore information about nutrition for kidney disease is provided in the NIDDK health topics:\n                \n- Nutrition for Children with Chronic Kidney Disease  - Nutrition for Adults with Early Chronic Kidney Disease  - Nutrition for Adults with Advanced Chronic Kidney Disease\n                \nThe National Kidney Disease Education Program offers a series of easy-to-read fact sheets about nutrition for people with CKD."}
{"_id":"ee3d5c94-45b1-4ab2-babe-0ebe47c10e31","text":"- Polycystic kidney disease (PKD) is a genetic disorder that causes numerous cysts to grow in the kidneys.  - A gene mutation, or defect, causes polycystic kidney disease.  - Autosomal dominant PKD is the most common form of PKD and the most common inherited disorder of the kidneys.  - Health care providers identify most cases of autosomal dominant PKD between the ages of 30 and 50.  - The most common symptoms of PKD are pain in the back and sidesbetween the ribs and hipsand headaches. The pain can be temporary or persistent, mild or severe. Hematuriablood in the urinemay also be a sign of autosomal dominant PKD.  - The complications of autosomal dominant PKD include the following:      - pain    - high blood pressure    - kidney failure    - urinary tract infections (UTIs)    - kidney stones    - liver cysts    - pancreatic cysts    - abnormal heart valves    - diverticula    - brain aneurysms    - A health care provider diagnoses autosomal dominant PKD using imaging tests and genetic testing.  - A radiologista doctor who specializes in medical imagingwill interpret the images produced by the following imaging tests:      - ultrasound    - computerized tomography scans    - magnetic resonance imaging    - Genetic testing can show whether a persons cells carry a gene mutation that causes autosomal dominant PKD. A health care provider may also use genetic testing results to determine whether someone with a family history of PKD is likely to develop the disorder in the future. Prenatal testing can diagnose autosomal recessive PKD in unborn children.  - Although a cure for autosomal dominant PKD is not currently available, treatment can ease symptoms and prolong life.  - Autosomal recessive PKD is a rare genetic disorder that affects the liver as well as the kidneys.  - The complications of autosomal recessive PKD include the following:      - death due to breathing problems    - kidney failure    - liver scarring    - high blood pressure    - UTIs    - A health care provider diagnoses autosomal recessive PKD with ultrasound imaging, even in a fetus or newborn.  - Treatments for autosomal recessive PKD focus on the symptoms and complications.  - Scientists have not yet found a way to prevent PKD. However, people with PKD may slow the progression of kidney damage caused by high blood pressure through lifestyle changes, diet, and blood pressure medications.  - People with any kind of kidney disease, including PKD, should talk with a dietitian about foods they should add to their diet and foods that might be harmful."}
{"_id":"58d26f7d-69ec-4dd6-a8b8-8fa73e25a47d","text":"CKD usually takes a long time to develop and does not go away. In CKD, the kidneys continue to workjust not as well as they should. Wastes may build up so gradually that the body becomes used to having those wastes in the blood. Salts containing phosphorus and potassium may rise to unsafe levels, causing heart and bone problems. Anemialow red blood cell countcan result from CKD because the kidneys stop making enough erythropoietin, a hormone that causes bone marrow to make red blood cells. After months or years, CKD may progress to permanent kidney failure, which requires a person to have a kidney transplant or regular blood filtering treatments called dialysis."}
{"_id":"ba682bdf-f956-40d3-8bbc-5787194f4413","text":"MNT is the use of nutrition counseling by a registered dietitian to help promote a medical or health goal. A health care provider may refer a patient to a registered dietitian to help with the patient's food plan. Many insurance policies cover MNT when recommended by a health care provider. Anyone who qualifies for Medicare can receive a benefit for MNT from a registered dietitian or nutrition professional when a health care provider provides a referral indicating that the person has diabetes or kidney disease.\n                \nOne way to locate a qualified dietitian is to contact the Academy of Nutrition and Dietetics at www.eatright.organd click on \"Find a Registered Dietitian.\" Users can enter their address or ZIP code for a list of dietitians in their area. A person looking for dietary advice to prevent kidney damage should click on \"Renal (Kidney) Nutrition\" in the specialty field. Dietitians who specialize in helping people with CKD are called renal dietitians.\n                \nTop"}
{"_id":"2e050e27-6e95-4af4-b38a-db10f034eb55","text":"As CKD progresses, people often lose their appetites because they find that foods do not taste the same. As a result, they consume fewer caloriesimportant units of energy in foodand may lose too much weight. Renal dietitians can help people with advanced CKD find healthy ways to add calories to their diet if they are losing too much weight.\n                \nTop"}
{"_id":"380b23a1-61e9-4bef-b1fc-f89c1ab11638","text":"Protein is an essential part of any diet. Proteins help build and maintain muscle, bone, skin, connective tissue, internal organs, and blood. They help fight disease and heal wounds. But proteins also break down into waste products that must be removed from the blood by the kidneys. Eating more protein than the body needs may put an extra burden on the kidneys and cause kidney function to decline faster.\n                \nHealth care providers recommend that people with CKD eat moderate or reduced amounts of protein. However, restricting protein could lead to malnutrition, so people with CKD need to be careful. The typical American diet contains more than enough protein. Learning about portion sizes can help people limit protein intake without endangering their health."}
{"_id":"cc645aea-a822-4779-9bec-81478e4497e5","text":"Most peoplewith or without CKDcan get the daily protein they need by eating two 3-ounce servings of meat or meat substitute. A 3-ounce serving of meat is about the size of a deck of cards or the palm of a persons hand.\n                \nA renal dietitian can help people learn about the amount and sources of protein in their diet. Animal protein in egg whites, cheese, chicken, fish, and red meats contain more of the essential nutrients a body needs. With careful meal planning, a well-balanced vegetarian diet can also provide these nutrients. A renal dietitian can help people with advanced CKD make small adjustments in their eating habits that can result in significant protein reduction. For example, people can lower their protein intake by making sandwiches using thinner slices of meat and adding lettuce, cucumber slices, apple slices, and other garnishes. The following table lists some higher-protein foods and suggestions for lower-protein alternatives that are better choices for people with CKD trying to limit their protein intake.\n                \nHigher- and Lower-protein Foods\n                \nBased on about a 3 oz. portion        Higher-Protein Foods    Lower-protein Alternatives        Ground beef Halibut Shrimp Salmon Tuna Chicken breast Roasted chicken     Chili con carne Beef stew Egg substitutes Tofu Imitation crab meat\n                \nWhen kidney function declines to the point where dialysis becomes necessary, patients should include more protein in their diet because dialysis removes large amounts of protein from the blood."}
{"_id":"7b06d19f-b70e-406e-b010-7570ae6d9817","text":"Everyone should know about fat sources because eating the wrong kinds of fat and too much fat increases the risk of clogged blood vessels and heart problems. Fat provides energy, helps produce hormonelike substances that regulate blood pressure and other heart functions, and carries fat-soluble vitamins. Everyone needs dietary fat, but some fats are healthier than others. People with CKD are at higher risk of having a heart attack or stroke. Therefore, people with CKD should be especially careful about how dietary fat affects their heart health.\n                \nPeople with advanced CKD should talk with a dietitian about healthy and unhealthy sources of fat. Saturated fats and trans-fatty acids can raise blood cholesterol levels and clog blood vessels. Saturated fats are found in animal products such as red meat, poultry, whole milk, and butter. These fats are usually solid at room temperature. Trans-fatty acids are often found in commercially baked goods such as cookies and cakes and in fried foods like doughnuts and french fries.\n                \nA dietitian can suggest healthy ways to include fat in the diet, especially if more calories are needed. Vegetable oils such as corn or safflower oil are healthier than animal fats such as butter or lard. Hydrogenated vegetable oils should be avoided because they are high in trans-fatty acids. Monounsaturated fatsolive, peanut, and canola oilsare healthy alternatives to animal fats. The table below shows the sources of fats, broken down into three types of fats that should be eaten less often and good fats that can be eaten more often.\n                \nSources of Fats\n                \nEat Less Often    Eat More Often        Saturated fats          - red meat      - poultry      - whole milk      - butter      - lard        Monounsaturated fats          - corn oil      - safflower oil      - olive oil      - peanut oil      - canola oil            Trans-fatty acids          - commercial baked goods      - french fries      - doughnuts            Hydrogenated vegetable oils          - margarine      - shortening"}
{"_id":"a858c1ba-bbe4-4fd3-bf25-f8170caed6ee","text":"Too much sodium in a person's diet can be harmful because it causes blood to hold fluid. People with CKD need to be careful not to let too much fluid build up in their bodies. The extra fluid raises blood pressure and puts a strain on the heart and kidneys. A dietitian can help people find ways to reduce the amount of sodium in their diet. Nutrition labels provide information about the sodium content in food. The U.S. Food and Drug Administration advises that healthy people should limit their daily sodium intake to no more than 2,300 milligrams (mg), the amount found in 1 teaspoon of table salt. People who are at risk for a heart attack or stroke because of a condition such as high blood pressure or kidney disease should limit their daily sodium intake to no more than 1,500 mg. Choosing sodium-free or low-sodium food products will help them reach that goal.\n                \nSodium is found in ordinary table salt and many salty seasonings such as soy sauce and teriyaki sauce. Canned foods, some frozen foods, and most processed meats have large amounts of salt. Snack foods such as chips and crackers are also high in salt.\n                \nAlternative seasonings such as lemon juice, salt-free seasoning mixes, and hot pepper sauce can help people reduce their salt intake. People with advanced CKD should avoid salt substitutes that use potassium, such as AlsoSalt or Nu-Salt, because CKD limits the body's ability to eliminate potassium from the blood. The table below provides some high-sodium foods and suggestions for low-sodium alternatives that are healthier for people with any level of CKD who have high blood pressure.\n                \nHigh- and Low-sodium Foods\n                \nHigh-sodium Foods    Low-sodium Alternatives        Salt Regular canned vegetables Hot dogs and canned meat Packaged rice with sauce Packaged noodles with sauce Frozen vegetables with sauce Frozen prepared meals Canned soup Regular tomato sauce Snack foods    Salt-free herb seasonings Low-sodium canned foods Frozen vegetables without sauce Fresh, cooked meat Plain rice without sauce Plain noodles without sauce Fresh vegetables without sauce Homemade soup with fresh ingredients Reduced-sodium tomato sauce Unsalted pretzels Unsalted popcorn"}
{"_id":"a2373298-3183-4bf0-ac6e-0dd731c3f911","text":"Keeping the proper level of potassium in the blood is essential. Potassium keeps the heart beating regularly and muscles working right. Problems can occur when blood potassium levels are either too low or too high. Damaged kidneys allow potassium to build up in the blood, causing serious heart problems. Potassium is found in many fruits and vegetables, such as bananas, potatoes, avocados, and melons. People with advanced CKD may need to avoid some fruits and vegetables. Blood tests can indicate when potassium levels have climbed above normal range. A renal dietitian can help people with advanced CKD find ways to limit the amount of potassium they eat. The potassium content of potatoes and other vegetables can be reduced by boiling them in water. The following table gives examples of some high-potassium foods and suggestions for low-potassium alternatives for people with advanced CKD.\n                \nHigh- and Low-potassium Foods\n                \nHigh-potassium Foods    Low-potassium Alternatives        Oranges and orange juice Melons Apricots Bananas Potatoes Tomatoes Sweet potatoes Cooked spinach Cooked broccoli Beans (baked, kidney, lima, pinto)    Apples and apple juice Cranberries and cranberry juice Canned pears Strawberries, blueberries, raspberries Plums Pineapple Cabbage Boiled Cauliflower"}
{"_id":"3c5f4664-4640-4e79-8007-93046f5656d7","text":"Damaged kidneys allow phosphorus, a mineral found in many foods, to build up in the blood. Too much phosphorus in the blood pulls calcium from the bones, making the bones weak and likely to break. Too much phosphorus may also make skin itch. Foods such as milk and cheese, dried beans, peas, colas, canned iced teas and lemonade, nuts, and peanut butter are high in phosphorus. A renal dietitian can help people with advanced CKD learn how to limit phosphorus in their diet.\n                \nAs CKD progresses, a person may need to take a phosphate binder such as sevelamer hydrochloride (Renagel), lanthanum carbonate (Fosrenol), calcium acetate (PhosLo), or calcium carbonate (Tums) to control the phosphorus in the blood. These medications act like sponges to soak up, or bind, phosphorus while it is in the stomach. Because it is bound, the phosphorus does not get into the blood. Instead, it is removed from the body in the stool.\n                \nThe table below lists some high-phosphorus foods and suggestions for low-phosphorus alternatives that are healthier for people with advanced CKD.\n                \nHigh- and Low-phosphorus Foods\n                \nHigh-phosphorus Foods    Low-phosphorus Alternatives        Dairy foods (milk, cheese, yogurt) Beans (baked, kidney, lima, pinto) Nuts and peanut butter Processed meats (hot dogs, canned meat) Cola Canned iced teas and lemonade Bran cereals Egg yolks     Liquid non-dairy creamer Sherbet Cooked rice Rice, wheat, and corn cereals Popcorn Peas Lemon-lime soda Root beer Powdered iced tea and lemonade mixes"}
{"_id":"d29f4346-6163-4101-9e20-e97d9811cc30","text":"- A person may prevent or delay some health problems from chronic kidney disease (CKD) by eating the right foods and avoiding foods high in sodium, potassium, and phosphorus.  - The kidneys remove wastes and extra water from the blood and make urine.  - Medical nutrition therapy (MNT) is the use of counseling by a registered dietitian to help promote a medical or health goal.  - Dietitians who specialize in helping people with CKD are called renal dietitians.  - People with advanced CKD often lose their appetites and consume fewer caloriesimportant units of energy in foodand may lose too much weight.  - Eating more protein than the body needs may put an extra burden on the kidneys and cause kidney function to decline faster. Most peoplewith or without CKDcan get the daily protein they need by eating two 3-ounce servings of meat or meat substitute.  - People with CKD are at higher risk of having a heart attack or stroke.  - Everyone needs dietary fat, but some fats are healthier than others.  - Too much sodium in a persons diet can be harmful because it causes blood to hold fluid. People with CKD need to be careful not to let too much fluid build up in their bodies.  - People with advanced CKD should avoid salt substitutes that use potassium because CKD limits the bodys ability to eliminate potassium from the blood.  - Damaged kidneys allow potassium to build up in the blood, causing serious heart problems. Potassium is found in many fruits and vegetables, such as bananas, potatoes, avocados, and melons.  - Too much phosphorus in the blood pulls calcium from the bones, making the bones weak and likely to break.  - People with advanced CKD may need to limit how much they drink because damaged kidneys can't remove extra fluid.  - Many patients find that keeping track of their test results helps them see how their treatment is working. Patients can ask their health care provider for copies of their lab reports and ask to have them explained, noting any results out of the normal range."}
{"_id":"52cc5354-b753-464d-bff2-f7351da27a70","text":"The NIDDK Nutrition for Chronic Kidney Disease Series includes three fact sheets:\n                \n- Nutrition for Early Chronic Kidney Disease in Adults  - Nutrition for Advanced Chronic Kidney Disease in Adults  - Nutrition for Chronic Kidney Disease in Children"}
{"_id":"756d1fc2-f02f-4fe8-959a-4fb359c928eb","text":"Diabetes is a complex group of diseases with a variety of causes. People with diabetes have high blood glucose, also called high blood sugar or hyperglycemia.\n                \nDiabetes is a disorder of metabolismthe way the body uses digested food for energy. The digestive tract breaks down carbohydratessugars and starches found in many foodsinto glucose, a form of sugar that enters the bloodstream. With the help of the hormone insulin, cells throughout the body absorb glucose and use it for energy. Diabetes develops when the body doesnt make enough insulin or is not able to use insulin effectively, or both.\n                \nInsulin is made in the pancreas, an organ located behind the stomach. The pancreas contains clusters of cells called islets. Beta cells within the islets make insulin and release it into the blood.\n                \nIf beta cells dont produce enough insulin, or the body doesnt respond to the insulin that is present, glucose builds up in the blood instead of being absorbed by cells in the body, leading to prediabetes or diabetes. Prediabetes is a condition in which blood glucose levels or A1C levelswhich reflect average blood glucose levelsare higher than normal but not high enough to be diagnosed as diabetes. In diabetes, the bodys cells are starved of energy despite high blood glucose levels.\n                \nOver time, high blood glucose damages nerves and blood vessels, leading to complications such as heart disease, stroke, kidney disease, blindness, dental disease, and amputations. Other complications of diabetes may include increased susceptibility to other diseases, loss of mobility with aging, depression, and pregnancy problems. No one is certain what starts the processes that cause diabetes, but scientists believe genes and environmental factors interact to cause diabetes in most cases.\n                \nThe two main types of diabetes are type 1 diabetes and type 2 diabetes. A third type, gestational diabetes, develops only during pregnancy. Other types of diabetes are caused by defects in specific genes, diseases of the pancreas, certain drugs or chemicals, infections, and other conditions. Some people show signs of both type 1 and type 2 diabetes."}
{"_id":"5390bc39-5890-4f3a-884e-4b9b8f61ac35","text":"Type 1 diabetes is caused by a lack of insulin due to the destruction of insulin-producing beta cells in the pancreas. In type 1 diabetesan autoimmune diseasethe bodys immune system attacks and destroys the beta cells. Normally, the immune system protects the body from infection by identifying and destroying bacteria, viruses, and other potentially harmful foreign substances. But in autoimmune diseases, the immune system attacks the bodys own cells. In type 1 diabetes, beta cell destruction may take place over several years, but symptoms of the disease usually develop over a short period of time.\n                \nType 1 diabetes typically occurs in children and young adults, though it can appear at any age. In the past, type 1 diabetes was called juvenile diabetes or insulin-dependent diabetes mellitus.\n                \nLatent autoimmune diabetes in adults (LADA) may be a slowly developing kind of type 1 diabetes. Diagnosis usually occurs after age 30. In LADA, as in type 1 diabetes, the bodys immune system destroys the beta cells. At the time of diagnosis, people with LADA may still produce their own insulin, but eventually most will need insulin shots or an insulin pump to control blood glucose levels.\n                \nGenetic Susceptibility\n                \nHeredity plays an important part in determining who is likely to develop type 1 diabetes. Genes are passed down from biological parent to child. Genes carry instructions for making proteins that are needed for the bodys cells to function. Many genes, as well as interactions among genes, are thought to influence susceptibility to and protection from type 1 diabetes. The key genes may vary in different population groups. Variations in genes that affect more than 1 percent of a population group are called gene variants.\n                \nCertain gene variants that carry instructions for making proteins called human leukocyte antigens (HLAs) on white blood cells are linked to the risk of developing type 1 diabetes. The proteins produced by HLA genes help determine whether the immune system recognizes a cell as part of the body or as foreign material. Some combinations of HLA gene variants predict that a person will be at higher risk for type 1 diabetes, while other combinations are protective or have no effect on risk.\n                \nWhile HLA genes are the major risk genes for type 1 diabetes, many additional risk genes or gene regions have been found. Not only can these genes help identify people at risk for type 1 diabetes, but they also provide important clues to help scientists better understand how the disease develops and identify potential targets for therapy and prevention.\n                \nGenetic testing can show what types of HLA genes a person carries and can reveal other genes linked to diabetes. However, most genetic testing is done in a research setting and is not yet available to individuals. Scientists are studying how the results of genetic testing can be used to improve type 1 diabetes prevention or treatment.\n                \nAutoimmune Destruction of Beta Cells\n                \nIn type 1 diabetes, white blood cells called T cells attack and destroy beta cells. The process begins well before diabetes symptoms appear and continues after diagnosis. Often, type 1 diabetes is not diagnosed until most beta cells have already been destroyed. At this point, a person needs daily insulin treatment to survive. Finding ways to modify or stop this autoimmune process and preserve beta cell function is a major focus of current scientific research.\n                \nRecent research suggests insulin itself may be a key trigger of the immune attack on beta cells. The immune systems of people who are susceptible to developing type 1 diabetes respond to insulin as if it were a foreign substance, or antigen. To combat antigens, the body makes proteins called antibodies. Antibodies to insulin and other proteins produced by beta cells are found in people with type 1 diabetes. Researchers test for these antibodies to help identify people at increased risk of developing the disease. Testing the types and levels of antibodies in the blood can help determine whether a person has type 1 diabetes, LADA, or another type of diabetes.\n                \nEnvironmental Factors\n                \nEnvironmental factors, such as foods, viruses, and toxins, may play a role in the development of type 1 diabetes, but the exact nature of their role has not been determined. Some theories suggest that environmental factors trigger the autoimmune destruction of beta cells in people with a genetic susceptibility to diabetes. Other theories suggest that environmental factors play an ongoing role in diabetes, even after diagnosis.\n                \nViruses and infections. A virus cannot cause diabetes on its own, but people are sometimes diagnosed with type 1 diabetes during or after a viral infection, suggesting a link between the two. Also, the onset of type 1 diabetes occurs more frequently during the winter when viral infections are more common. Viruses possibly associated with type 1 diabetes include coxsackievirus B, cytomegalovirus, adenovirus, rubella, and mumps. Scientists have described several ways these viruses may damage or destroy beta cells or possibly trigger an autoimmune response in susceptible people. For example, anti-islet antibodies have been found in patients with congenital rubella syndrome, and cytomegalovirus has been associated with significant beta cell damage and acute pancreatitisinflammation of the pancreas. Scientists are trying to identify a virus that can cause type 1 diabetes so that a vaccine might be developed to prevent the disease.\n                \nInfant feeding practices. Some studies have suggested that dietary factors may raise or lower the risk of developing type 1 diabetes. For example, breastfed infants and infants receiving vitamin D supplements may have a reduced risk of developing type 1 diabetes, while early exposure to cows milk and cereal proteins may increase risk. More research is needed to clarify how infant nutrition affects the risk for type 1 diabetes.\n                \nRead more in the Centers for Disease Control and Preventions (CDCs) publication  National Diabetes Statistics Report, 2014 at  www.cdc.gov for information about research studies related to type 1 diabetes."}
{"_id":"ac158051-9cdf-4c40-bdce-50c3d4588605","text":"Type 2 diabetesthe most common form of diabetesis caused by a combination of factors, including insulin resistance, a condition in which the bodys muscle, fat, and liver cells do not use insulin effectively. Type 2 diabetes develops when the body can no longer produce enough insulin to compensate for the impaired ability to use insulin. Symptoms of type 2 diabetes may develop gradually and can be subtle; some people with type 2 diabetes remain undiagnosed for years.\n                \nType 2 diabetes develops most often in middle-aged and older people who are also overweight or obese. The disease, once rare in youth, is becoming more common in overweight and obese children and adolescents. Scientists think genetic susceptibility and environmental factors are the most likely triggers of type 2 diabetes.\n                \nGenetic Susceptibility\n                \nGenes play a significant part in susceptibility to type 2 diabetes. Having certain genes or combinations of genes may increase or decrease a persons risk for developing the disease. The role of genes is suggested by the high rate of type 2 diabetes in families and identical twins and wide variations in diabetes prevalence by ethnicity. Type 2 diabetes occurs more frequently in African Americans, Alaska Natives, American Indians, Hispanics\/Latinos, and some Asian Americans, Native Hawaiians, and Pacific Islander Americans than it does in non-Hispanic whites.\n                \nRecent studies have combined genetic data from large numbers of people, accelerating the pace of gene discovery. Though scientists have now identified many gene variants that increase susceptibility to type 2 diabetes, the majority have yet to be discovered. The known genes appear to affect insulin production rather than insulin resistance. Researchers are working to identify additional gene variants and to learn how they interact with one another and with environmental factors to cause diabetes.\n                \nStudies have shown that variants of the TCF7L2 gene increase susceptibility to type 2 diabetes. For people who inherit two copies of the variants, the risk of developing type 2 diabetes is about 80 percent higher than for those who do not carry the gene variant.1 However, even in those with the variant, diet and physical activity leading to weight loss help delay diabetes, according to the Diabetes Prevention Program (DPP), a major clinical trial involving people at high risk.\n                \nGenes can also increase the risk of diabetes by increasing a persons tendency to become overweight or obese. One theory, known as the thrifty gene hypothesis, suggests certain genes increase the efficiency of metabolism to extract energy from food and store the energy for later use. This survival trait was advantageous for populations whose food supplies were scarce or unpredictable and could help keep people alive during famine. In modern times, however, when high-calorie foods are plentiful, such a trait can promote obesity and type 2 diabetes.\n                \nObesity and Physical Inactivity\n                \nPhysical inactivity and obesity are strongly associated with the development of type 2 diabetes. People who are genetically susceptible to type 2 diabetes are more vulnerable when these risk factors are present.\n                \nAn imbalance between caloric intake and physical activity can lead to obesity, which causes insulin resistance and is common in people with type 2 diabetes. Central obesity, in which a person has excess abdominal fat, is a major risk factor not only for insulin resistance and type 2 diabetes but also for heart and blood vessel disease, also called cardiovascular disease (CVD). This excess belly fat produces hormones and other substances that can cause harmful, chronic effects in the body such as damage to blood vessels.\n                \nThe DPP and other studies show that millions of people can lower their risk for type 2 diabetes by making lifestyle changes and losing weight. The DPP proved that people with prediabetesat high risk of developing type 2 diabetescould sharply lower their risk by losing weight through regular physical activity and a diet low in fat and calories. In 2009, a follow-up study of DPP participantsthe Diabetes Prevention Program Outcomes Study (DPPOS)showed that the benefits of weight loss lasted for at least 10 years after the original study began.2\n                \nRead more about the DPP, funded under National Institutes of Health (NIH) clinical trial number NCT00004992, and the DPPOS, funded under NIH clinical trial number NCT00038727 in  Diabetes Prevention Program.\n                \nInsulin Resistance\n                \nInsulin resistance is a common condition in people who are overweight or obese, have excess abdominal fat, and are not physically active. Muscle, fat, and liver cells stop responding properly to insulin, forcing the pancreas to compensate by producing extra insulin. As long as beta cells are able to produce enough insulin, blood glucose levels stay in the normal range. But when insulin production falters because of beta cell dysfunction, glucose levels rise, leading to prediabetes or diabetes.\n                \nAbnormal Glucose Production by the Liver\n                \nIn some people with diabetes, an abnormal increase in glucose production by the liver also contributes to high blood glucose levels. Normally, the pancreas releases the hormone glucagon when blood glucose and insulin levels are low. Glucagon stimulates the liver to produce glucose and release it into the bloodstream. But when blood glucose and insulin levels are high after a meal, glucagon levels drop, and the liver stores excess glucose for later, when it is needed. For reasons not completely understood, in many people with diabetes, glucagon levels stay higher than needed. High glucagon levels cause the liver to produce unneeded glucose, which contributes to high blood glucose levels. Metformin, the most commonly used drug to treat type 2 diabetes, reduces glucose production by the liver.\n                \nThe Roles of Insulin and Glucagon in Normal Blood Glucose Regulation\n                \nA healthy persons body keeps blood glucose levels in a normal range through several complex mechanisms. Insulin and glucagon, two hormones made in the pancreas, help regulate blood glucose levels:\n                \n- Insulin, made by beta cells, lowers elevated blood glucose levels.  - Glucagon, made by alpha cells, raises low blood glucose levels.\n                \n- Insulin helps muscle, fat, and liver cells absorb glucose from the bloodstream, lowering blood glucose levels.  - Insulin stimulates the liver and muscle tissue to store excess glucose. The stored form of glucose is called glycogen.  - Insulin also lowers blood glucose levels by reducing glucose production in the liver.\n                \n- Glucagon signals the liver and muscle tissue to break down glycogen into glucose, which enters the bloodstream and raises blood glucose levels.  - If the body needs more glucose, glucagon stimulates the liver to make glucose from amino acids.\n                \nMetabolic Syndrome\n                \nMetabolic syndrome, also called insulin resistance syndrome, refers to a group of conditions common in people with insulin resistance, including\n                \n- higher than normal blood glucose levels  - increased waist size due to excess abdominal fat  - high blood pressure  - abnormal levels of cholesterol and triglycerides in the blood\n                \nCell Signaling and Regulation\n                \nCells communicate through a complex network of molecular signaling pathways. For example, on cell surfaces, insulin receptor molecules capture, or bind, insulin molecules circulating in the bloodstream. This interaction between insulin and its receptor prompts the biochemical signals that enable the cells to absorb glucose from the blood and use it for energy.\n                \nProblems in cell signaling systems can set off a chain reaction that leads to diabetes or other diseases. Many studies have focused on how insulin signals cells to communicate and regulate action. Researchers have identified proteins and pathways that transmit the insulin signal and have mapped interactions between insulin and body tissues, including the way insulin helps the liver control blood glucose levels. Researchers have also found that key signals also come from fat cells, which produce substances that cause inflammation and insulin resistance.\n                \nThis work holds the key to combating insulin resistance and diabetes. As scientists learn more about cell signaling systems involved in glucose regulation, they will have more opportunities to develop effective treatments.\n                \nBeta Cell Dysfunction\n                \nScientists think beta cell dysfunction is a key contributor to type 2 diabetes. Beta cell impairment can cause inadequate or abnormal patterns of insulin release. Also, beta cells may be damaged by high blood glucose itself, a condition called glucose toxicity.\n                \nScientists have not determined the causes of beta cell dysfunction in most cases. Single gene defects lead to specific forms of diabetes called maturity-onset diabetes of the young (MODY). The genes involved regulate insulin production in the beta cells. Although these forms of diabetes are rare, they provide clues as to how beta cell function may be affected by key regulatory factors. Other gene variants are involved in determining the number and function of beta cells. But these variants account for only a small percentage of type 2 diabetes cases. Malnutrition early in life is also being investigated as a cause of beta cell dysfunction. The metabolic environment of the developing fetus may also create a predisposition for diabetes later in life.\n                \nRisk Factors for Type 2 Diabetes\n                \nPeople who develop type 2 diabetes are more likely to have the following characteristics:\n                \n- age 45 or older  - overweight or obese  - physically inactive  - parent or sibling with diabetes  - family background that is African American, Alaska Native, American Indian, Asian American, Hispanic\/Latino, or Pacific Islander American  - history of giving birth to a baby weighing more than 9 pounds  - history of gestational diabetes  - high blood pressure140\/90 or aboveor being treated for high blood pressure  - high-density lipoprotein (HDL), or good, cholesterol below 35 milligrams per deciliter (mg\/dL), or a triglyceride level above 250 mg\/dL  - polycystic ovary syndrome, also called PCOS  - prediabetesan A1C level of 5.7 to 6.4 percent; a fasting plasma glucose test result of 100125 mg\/dL, called impaired fasting glucose; or a 2-hour oral glucose tolerance test result of 140199, called impaired glucose tolerance  - acanthosis nigricans, a condition associated with insulin resistance, characterized by a dark, velvety rash around the neck or armpits  - history of CVD\n                \nThe American Diabetes Association (ADA) recommends that testing to detect prediabetes and type 2 diabetes be considered in adults who are overweight or obese and have one or more additional risk factors for diabetes. In adults without these risk factors, testing should begin at age 45."}
{"_id":"cb42b828-1df4-4194-9338-fefbf2b906df","text":"Insulin Resistance and Beta Cell Dysfunction\n                \nHormones produced by the placenta and other pregnancy-related factors contribute to insulin resistance, which occurs in all women during late pregnancy. Insulin resistance increases the amount of insulin needed to control blood glucose levels. If the pancreas cant produce enough insulin due to beta cell dysfunction, gestational diabetes occurs.\n                \nAs with type 2 diabetes, excess weight is linked to gestational diabetes. Overweight or obese women are at particularly high risk for gestational diabetes because they start pregnancy with a higher need for insulin due to insulin resistance. Excessive weight gain during pregnancy may also increase risk.\n                \nFamily History\n                \nHaving a family history of diabetes is also a risk factor for gestational diabetes, suggesting that genes play a role in its development. Genetics may also explain why the disorder occurs more frequently in African Americans, American Indians, and Hispanics\/Latinos. Many gene variants or combinations of variants may increase a womans risk for developing gestational diabetes. Studies have found several gene variants associated with gestational diabetes, but these variants account for only a small fraction of women with gestational diabetes.\n                \nFuture Risk of Type 2 Diabetes\n                \nBecause a womans hormones usually return to normal levels soon after giving birth, gestational diabetes disappears in most women after delivery. However, women who have gestational diabetes are more likely to develop gestational diabetes with future pregnancies and develop type 2 diabetes.3 Women with gestational diabetes should be tested for persistent diabetes 6 to 12 weeks after delivery and at least every 3 years thereafter.\n                \nAlso, exposure to high glucose levels during gestation increases a childs risk for becoming overweight or obese and for developing type 2 diabetes later on. The result may be a cycle of diabetes affecting multiple generations in a family. For both mother and child, maintaining a healthy body weight and being physically active may help prevent type 2 diabetes."}
{"_id":"420edf49-3e17-4037-a59c-d73b76311647","text":"Other types of diabetes have a variety of possible causes.\n                \nGenetic Mutations Affecting Beta Cells, Insulin, and Insulin Action\n                \nSome relatively uncommon forms of diabetes known as monogenic diabetes are caused by mutations, or changes, in a single gene. These mutations are usually inherited, but sometimes the gene mutation occurs spontaneously. Most of these gene mutations cause diabetes by reducing beta cells ability to produce insulin.\n                \nThe most common types of monogenic diabetes are neonatal diabetes mellitus (NDM) and MODY. NDM occurs in the first 6 months of life. MODY is usually found during adolescence or early adulthood but sometimes is not diagnosed until later in life. More information about NDM and MODY is provided in the NIDDK health topic, Monogenic Forms of Diabetes.\n                \nOther rare genetic mutations can cause diabetes by damaging the quality of insulin the body produces or by causing abnormalities in insulin receptors.\n                \nOther Genetic Diseases\n                \nDiabetes occurs in people with Down syndrome, Klinefelter syndrome, and Turner syndrome at higher rates than the general population. Scientists are investigating whether genes that may predispose people to genetic syndromes also predispose them to diabetes.\n                \nThe genetic disorders cystic fibrosis and hemochromatosis are linked to diabetes. Cystic fibrosis produces abnormally thick mucus, which blocks the pancreas. The risk of diabetes increases with age in people with cystic fibrosis. Hemochromatosis causes the body to store too much iron. If the disorder is not treated, iron can build up in and damage the pancreas and other organs.\n                \nDamage to or Removal of the Pancreas\n                \nPancreatitis, cancer, and trauma can all harm the pancreatic beta cells or impair insulin production, thus causing diabetes. If the damaged pancreas is removed, diabetes will occur due to the loss of the beta cells.\n                \nEndocrine Diseases\n                \nEndocrine diseases affect organs that produce hormones. Cushings syndrome and acromegaly are examples of hormonal disorders that can cause prediabetes and diabetes by inducing insulin resistance. Cushings syndrome is marked by excessive production of cortisolsometimes called the stress hormone. Acromegaly occurs when the body produces too much growth hormone. Glucagonoma, a rare tumor of the pancreas, can also cause diabetes. The tumor causes the body to produce too much glucagon. Hyperthyroidism, a disorder that occurs when the thyroid gland produces too much thyroid hormone, can also cause elevated blood glucose levels.\n                \nAutoimmune Disorders\n                \nRare disorders characterized by antibodies that disrupt insulin action can lead to diabetes. This kind of diabetes is often associated with other autoimmune disorders such as lupus erythematosus. Another rare autoimmune disorder called stiff-man syndrome is associated with antibodies that attack the beta cells, similar to type 1 diabetes.\n                \nMedications and Chemical Toxins\n                \nSome medications, such as nicotinic acid and certain types of diuretics, anti-seizure drugs, psychiatric drugs, and drugs to treat human immunodeficiency virus (HIV), can impair beta cells or disrupt insulin action. Pentamidine, a drug prescribed to treat a type of pneumonia, can increase the risk of pancreatitis, beta cell damage, and diabetes. Also, glucocorticoidssteroid hormones that are chemically similar to naturally produced cortisolmay impair insulin action. Glucocorticoids are used to treat inflammatory illnesses such as rheumatoid arthritis, asthma, lupus, and ulcerative colitis.\n                \nMany chemical toxins can damage or destroy beta cells in animals, but only a few have been linked to diabetes in humans. For example, dioxina contaminant of the herbicide Agent Orange, used during the Vietnam Warmay be linked to the development of type 2 diabetes. In 2000, based on a report from the Institute of Medicine, the U.S. Department of Veterans Affairs (VA) added diabetes to the list of conditions for which Vietnam veterans are eligible for disability compensation. Also, a chemical in a rat poison no longer in use has been shown to cause diabetes if ingested. Some studies suggest a high intake of nitrogen-containing chemicals such as nitrates and nitrites might increase the risk of diabetes. Arsenic has also been studied for possible links to diabetes.\n                \nLipodystrophy\n                \nLipodystrophy is a condition in which fat tissue is lost or redistributed in the body. The condition is associated with insulin resistance and type 2 diabetes."}
{"_id":"4ca475d2-6c01-4e30-adc6-bb41da55bb73","text":"Other types of diabetes have a variety of possible causes.\n                \nGenetic Mutations Affecting Beta Cells, Insulin, and Insulin Action\n                \nSome relatively uncommon forms of diabetes known as monogenic diabetes are caused by mutations, or changes, in a single gene. These mutations are usually inherited, but sometimes the gene mutation occurs spontaneously. Most of these gene mutations cause diabetes by reducing beta cells ability to produce insulin.\n                \nThe most common types of monogenic diabetes are neonatal diabetes mellitus (NDM) and MODY. NDM occurs in the first 6 months of life. MODY is usually found during adolescence or early adulthood but sometimes is not diagnosed until later in life. More information about NDM and MODY is provided in the NIDDK health topic, Monogenic Forms of Diabetes.\n                \nOther rare genetic mutations can cause diabetes by damaging the quality of insulin the body produces or by causing abnormalities in insulin receptors.\n                \nOther Genetic Diseases\n                \nDiabetes occurs in people with Down syndrome, Klinefelter syndrome, and Turner syndrome at higher rates than the general population. Scientists are investigating whether genes that may predispose people to genetic syndromes also predispose them to diabetes.\n                \nThe genetic disorders cystic fibrosis and hemochromatosis are linked to diabetes. Cystic fibrosis produces abnormally thick mucus, which blocks the pancreas. The risk of diabetes increases with age in people with cystic fibrosis. Hemochromatosis causes the body to store too much iron. If the disorder is not treated, iron can build up in and damage the pancreas and other organs.\n                \nDamage to or Removal of the Pancreas\n                \nPancreatitis, cancer, and trauma can all harm the pancreatic beta cells or impair insulin production, thus causing diabetes. If the damaged pancreas is removed, diabetes will occur due to the loss of the beta cells.\n                \nEndocrine Diseases\n                \nEndocrine diseases affect organs that produce hormones. Cushings syndrome and acromegaly are examples of hormonal disorders that can cause prediabetes and diabetes by inducing insulin resistance. Cushings syndrome is marked by excessive production of cortisolsometimes called the stress hormone. Acromegaly occurs when the body produces too much growth hormone. Glucagonoma, a rare tumor of the pancreas, can also cause diabetes. The tumor causes the body to produce too much glucagon. Hyperthyroidism, a disorder that occurs when the thyroid gland produces too much thyroid hormone, can also cause elevated blood glucose levels.\n                \nAutoimmune Disorders\n                \nRare disorders characterized by antibodies that disrupt insulin action can lead to diabetes. This kind of diabetes is often associated with other autoimmune disorders such as lupus erythematosus. Another rare autoimmune disorder called stiff-man syndrome is associated with antibodies that attack the beta cells, similar to type 1 diabetes.\n                \nMedications and Chemical Toxins\n                \nSome medications, such as nicotinic acid and certain types of diuretics, anti-seizure drugs, psychiatric drugs, and drugs to treat human immunodeficiency virus (HIV), can impair beta cells or disrupt insulin action. Pentamidine, a drug prescribed to treat a type of pneumonia, can increase the risk of pancreatitis, beta cell damage, and diabetes. Also, glucocorticoidssteroid hormones that are chemically similar to naturally produced cortisolmay impair insulin action. Glucocorticoids are used to treat inflammatory illnesses such as rheumatoid arthritis, asthma, lupus, and ulcerative colitis.\n                \nMany chemical toxins can damage or destroy beta cells in animals, but only a few have been linked to diabetes in humans. For example, dioxina contaminant of the herbicide Agent Orange, used during the Vietnam Warmay be linked to the development of type 2 diabetes. In 2000, based on a report from the Institute of Medicine, the U.S. Department of Veterans Affairs (VA) added diabetes to the list of conditions for which Vietnam veterans are eligible for disability compensation. Also, a chemical in a rat poison no longer in use has been shown to cause diabetes if ingested. Some studies suggest a high intake of nitrogen-containing chemicals such as nitrates and nitrites might increase the risk of diabetes. Arsenic has also been studied for possible links to diabetes.\n                \nLipodystrophy\n                \nLipodystrophy is a condition in which fat tissue is lost or redistributed in the body. The condition is associated with insulin resistance and type 2 diabetes."}
{"_id":"0ca3c068-a47b-4173-8f2d-99be8edd8ffe","text":"- Diabetes is a complex group of diseases with a variety of causes. Scientists believe genes and environmental factors interact to cause diabetes in most cases.  - People with diabetes have high blood glucose, also called high blood sugar or hyperglycemia. Diabetes develops when the body doesnt make enough insulin or is not able to use insulin effectively, or both.  - Insulin is a hormone made by beta cells in the pancreas. Insulin helps cells throughout the body absorb and use glucose for energy. If the body does not produce enough insulin or cannot use insulin effectively, glucose builds up in the blood instead of being absorbed by cells in the body, and the body is starved of energy.  - Prediabetes is a condition in which blood glucose levels or A1C levels are higher than normal but not high enough to be diagnosed as diabetes. People with prediabetes can substantially reduce their risk of developing diabetes by losing weight and increasing physical activity.  - The two main types of diabetes are type 1 diabetes and type 2 diabetes. Gestational diabetes is a third form of diabetes that develops only during pregnancy.  - Type 1 diabetes is caused by a lack of insulin due to the destruction of insulin-producing beta cells. In type 1 diabetesan autoimmune diseasethe bodys immune system attacks and destroys the beta cells.  - Type 2 diabetesthe most common form of diabetesis caused by a combination of factors, including insulin resistance, a condition in which the bodys muscle, fat, and liver cells do not use insulin effectively. Type 2 diabetes develops when the body can no longer produce enough insulin to compensate for the impaired ability to use insulin.  - Scientists believe gestational diabetes is caused by the hormonal changes and metabolic demands of pregnancy together with genetic and environmental factors. Risk factors for gestational diabetes include being overweight and having a family history of diabetes.  - Monogenic forms of diabetes are relatively uncommon and are caused by mutations in single genes that limit insulin production, quality, or action in the body.  - Other types of diabetes are caused by diseases and injuries that damage the pancreas; certain chemical toxins and medications; infections; and other conditions."}
{"_id":"8caecd2a-f5c5-49d6-9f99-b8a60b9e6ea8","text":"Childhood nephrotic syndrome is not a disease in itself; rather, it is a group of symptoms that\n                \n- indicate kidney damageparticularly damage to the glomeruli, the tiny units within the kidney where blood is filtered  - result in the release of too much protein from the body into the urine\n                \nWhen the kidneys are damaged, the protein albumin, normally found in the blood, will leak into the urine. Proteins are large, complex molecules that perform a number of important functions in the body.\n                \nThe two types of childhood nephrotic syndrome are\n                \n- primarythe most common type of childhood nephrotic syndrome, which begins in the kidneys and affects only the kidneys  - secondarythe syndrome is caused by other diseases\n                \nA health care provider may refer a child with nephrotic syndrome to a nephrologista doctor who specializes in treating kidney disease. A child should see a pediatric nephrologist, who has special training to take care of kidney problems in children, if possible. However, in many parts of the country, pediatric nephrologists are in short supply, so the child may need to travel. If traveling is not possible, some nephrologists who treat adults can also treat children."}
{"_id":"689f054d-45dd-4760-b7ec-0b1b4c72753e","text":"The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra fluid. Children produce less urine than adults and the amount produced depends on their age. The urine flows from the kidneys to the bladder through tubes called ureters. The bladder stores urine. When the bladder empties, urine flows out of the body through a tube called the urethra, located at the bottom of the bladder.\n                \nKidneys work at the microscopic level. The kidney is not one large filter. Each kidney is made up of about a million filtering units called nephrons. Each nephron filters a small amount of blood. The nephron includes a filter, called the glomerulus, and a tubule. The nephrons work through a two-step process. The glomerulus lets fluid and waste products pass through it; however, it prevents blood cells and large molecules, mostly proteins, from passing. The filtered fluid then passes through the tubule, which sends needed minerals back to the bloodstream and removes wastes."}
{"_id":"ba09e6f2-ff1d-4f3d-b43f-511d5f911655","text":"While idiopathic, or unknown, diseases are the most common cause of primary childhood nephrotic syndrome, researchers have linked certain diseases and some specific genetic changes that damage the kidneys with primary childhood nephrotic syndrome.\n                \nThe cause of secondary childhood nephrotic syndrome is an underlying disease or infection. Called a primary illness, its this underlying disease or infection that causes changes in the kidney function that can result in secondary childhood nephrotic syndrome.\n                \nCongenital diseasesdiseases that are present at birthcan also cause childhood nephrotic syndrome.\n                \nPrimary Childhood Nephrotic Syndrome\n                \nThe following diseases are different types of idiopathic childhood nephrotic syndrome:\n                \n- Minimal change disease involves damage to the glomeruli that can be seen only with an electron microscope. This type of microscope shows tiny details better than any other microscope. Scientists do not know the exact cause of minimal change disease. Minimal change disease is the most common cause of idiopathic childhood nephrotic syndrome.1  - Focal segmental glomerulosclerosis is scarring in scattered regions of the kidney:     - Focal means that only some of the glomeruli become scarred.    - Segmental means damage affects only part of an individual glomerulus.    - Membranoproliferative glomerulonephritis is a group of disorders involving deposits of antibodies that build up in the glomeruli, causing thickening and damage. Antibodies are proteins made by the immune system to protect the body from foreign substances such as bacteria or viruses.\n                \nSecondary Childhood Nephrotic Syndrome\n                \nSome common diseases that can cause secondary childhood nephrotic syndrome include\n                \n- diabetes, a condition that occurs when the body cannot use glucosea type of sugarnormally  - Henoch-Schnlein purpura, a disease that causes small blood vessels in the body to become inflamed and leak  - hepatitis, inflammation of the liver caused by a virus  - human immunodeficiency virus (HIV), a virus that alters the immune system  - lupus, an autoimmune disease that occurs when the body attacks its own immune system  - malaria, a disease of the blood that is spread by mosquitos  - streptococcal infection, an infection that results when the bacteria that causes strep throat or a skin infection is left untreated\n                \nOther causes of secondary childhood nephrotic syndrome can include certain medications, such as aspirin, ibuprofen, or other nonsteroidal anti-inflammatory drugs, and exposure to chemicals, such as mercury and lithium.\n                \nCongenital Diseases and Childhood Nephrotic Syndrome\n                \nCongenital nephrotic syndrome is rare and affects infants in the first 3 months of life.2 This type of nephrotic syndrome, sometimes called infantile nephrotic syndrome, can be caused by\n                \n- inherited genetic defects, which are problems passed from parent to child through genes  - infections at the time of birth\n                \nMore information about underlying diseases or infections that cause changes in kidney function is provided in the NIDDK health topic, Glomerular Diseases."}
{"_id":"b4464779-c222-4de5-a363-dbe252b91c8d","text":"The signs and symptoms of childhood nephrotic syndrome may include\n                \n- edemaswelling, most often in the legs, feet, or ankles and less often in the hands or face  - albuminuriawhen a childs urine has high levels of albumin  - hypoalbuminemiawhen a childs blood has low levels of albumin  - hyperlipidemiawhen a childs blood cholesterol and fat levels are higher than normal\n                \nIn addition, some children with nephrotic syndrome may have\n                \n- blood in their urine  - symptoms of infection, such as fever, lethargy, irritability, or abdominal pain  - loss of appetite  - diarrhea  - high blood pressure"}
{"_id":"0991386e-944c-4c0b-93e7-1e266c8dac83","text":"The complications of childhood nephrotic syndrome may include\n                \n- infection. When the kidneys are damaged, a child is more likely to develop infections because the body loses proteins that normally protect against infection. Health care providers will prescribe medications to treat infections. Children with childhood nephrotic syndrome should receive the pneumococcal vaccine and yearly flu shots to prevent those infections. Children should also receive age-appropriate vaccinations, although a health care provider may delay certain live vaccines while a child is taking certain medications.  - blood clots. Blood clots can block the flow of blood and oxygen through a blood vessel anywhere in the body. A child is more likely to develop clots when he or she loses proteins through the urine. The health care provider will treat blood clots with blood-thinning medications.  - high blood cholesterol. When albumin leaks into the urine, the albumin levels in the blood drop. The liver makes more albumin to make up for the low levels in the blood. At the same time, the liver makes more cholesterol. Sometimes children may need treatment with medications to lower blood cholesterol levels."}
{"_id":"a96a7d4a-6684-45f4-9c85-c2bff7d985f1","text":"A health care provider diagnoses childhood nephrotic syndrome with\n                \n- a medical and family history  - a physical exam  - urine tests  - a blood test  - ultrasound of the kidney  - kidney biopsy\n                \nMedical and Family History\n                \nTaking a medical and family history is one of the first things a health care provider may do to help diagnose childhood nephrotic syndrome.\n                \nPhysical Exam\n                \nA physical exam may help diagnose childhood nephrotic syndrome. During a physical exam, a health care provider most often\n                \n- examines a childs body  - taps on specific areas of the childs body\n                \nUrine Tests\n                \nA health care provider may order the following urine tests to help determine if a child has kidney damage from childhood nephrotic syndrome.\n                \nDipstick test for albumin. A dipstick test performed on a urine sample can detect the presence of albumin in the urine, which could mean kidney damage. The child or a caretaker collects a urine sample in a special container. For the test, a nurse or technician places a strip of chemically treated paper, called a dipstick, into the childs urine sample. Patches on the dipstick change color when albumin is present in urine.\n                \nUrine albumin-to-creatinine ratio. A health care provider uses this measurement to estimate the amount of albumin passed into the urine over a 24-hour period. The child provides a urine sample during an appointment with the health care provider. Creatinine is a waste product filtered in the kidneys and passed in the urine. A high urine albumin-to-creatinine ratio indicates that the kidneys are leaking large amounts of albumin into the urine.\n                \nBlood Test\n                \nA blood test involves drawing blood at a health care providers office or a commercial facility and sending the sample to a lab for analysis. The lab tests the sample to estimate how much blood the kidneys filter each minute, called the estimated glomerular filtration rate, or eGFR. The test results help the health care provider determine the amount of kidney damage. Health care providers may also order other blood tests to help determine the underlying disease that may be causing childhood nephrotic syndrome.\n                \nUltrasound of the Kidney\n                \nUltrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. A specially trained technician performs the procedure in a health care providers office, an outpatient center, or a hospital. A radiologista doctor who specializes in medical imaginginterprets the images to see if the kidneys look normal; a child does not need anesthesia.\n                \nKidney Biopsy\n                \nBiopsy is a procedure that involves taking a small piece of kidney tissue for examination with a microscope. A health care provider performs the biopsy in an outpatient center or a hospital. The health care provider will give the child light sedation and local anesthetic; however, in some cases, the child will require general anesthesia. A pathologista doctor who specializes in diagnosing diseasesexamines the tissue in a lab. The test can help diagnose childhood nephrotic syndrome.\n                \nWhen the health care provider suspects a child has minimal change disease, he or she often starts treatment with medications without performing a biopsy. If the medication is effective, the child does not need a biopsy. In most cases, a health care provider does not perform a biopsy on children younger than age 12 unless he or she thinks that another disease is the cause."}
{"_id":"80dbd52d-ba94-461f-b269-c588781014d1","text":"Health care providers will decide how to treat childhood nephrotic syndrome based on the type:\n                \n- primary childhood nephrotic syndrome: medications  - secondary childhood nephrotic syndrome: treat the underlying illness or disease  - congenital nephrotic syndrome: medications, surgery to remove one or both kidneys, and transplantation\n                \nPrimary Childhood Nephrotic Syndrome\n                \nHealth care providers treat idiopathic childhood nephrotic syndrome with several types of medications that control the immune system, remove extra fluid, and lower blood pressure.\n                \n- Control the immune system. Corticosteroids are a group of medications that reduce the activity of the immune system, decrease the amount of albumin lost in the urine, and decrease swelling. Health care providers commonly use prednisone or a related corticosteroid to treat idiopathic childhood nephrotic syndrome. About 90 percent of children achieve remission with daily corticosteroids for 6 weeks and then a slightly smaller dose every other day for 6 weeks.2 Remission is a period when the child is symptom-free.  Many children relapse after initial therapy, and health care providers treat them with a shorter course of corticosteroids until the disease goes into remission again. Children may have multiple relapses; however, they most often recover without long-term kidney damage.  When a child has frequent relapses or does not respond to treatment, a health care provider may prescribe other medications that reduce the activity of the immune system. These medications prevent the body from making antibodies that can damage kidney tissues. They include      - cyclophosphamide    - mycophenolate (CellCept, Myfortic)    - cyclosporine    - tacrolimus (Hecoria, Prograf)   A health care provider may use these other immune system medications with corticosteroids or in place of corticosteroids.  - Remove extra fluid. A health care provider may prescribe a diuretic, a medication that helps the kidneys remove extra fluid from the blood. Removing the extra fluid can often help to lower blood pressure.  - Lower blood pressure. Some children with childhood nephrotic syndrome develop high blood pressure and may need to take additional medications to lower their blood pressure. Two types of blood pressure-lowering medications, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, have the additional benefit of slowing the progression of kidney disease. Many children with nephrotic syndrome require two or more medications to control their blood pressure.\n                \nSecondary Childhood Nephrotic Syndrome\n                \nHealth care providers treat secondary childhood nephrotic syndrome by treating the underlying cause of the primary illness. For example, a health care provider may treat children by\n                \n- prescribing antibiotics for an infection  - adjusting medications to treat lupus, HIV, or diabetes  - changing or stopping medications that are known to cause secondary childhood nephrotic syndrome\n                \nWhile treating the underlying cause, the health care provider will also treat the child to improve or restore kidney function with the same medications used to treat primary childhood nephrotic syndrome.\n                \nCaretakers should make sure that children take all prescribed medications and follow the treatment plan recommended by their health care provider.\n                \nMore information about specific treatments for secondary childhood nephrotic syndrome is provided in the NIDDK health topic, Glomerular Diseases.\n                \nCongenital Nephrotic Syndrome\n                \nResearchers have found that medications are not effective in treating congenital nephrotic syndrome, and that most children will need a kidney transplant by the time they are 2 or 3 years old. A kidney transplant is surgery to place a healthy kidney from someone who has just died or a living donor, most often a family member, into a persons body to take over the job of the failing kidney. To keep the child healthy until the transplant, the health care provider may recommend the following:\n                \n- albumin injections to make up for the albumin lost in urine  - diuretics to help remove extra fluid that causes swelling  - antibiotics to treat the first signs of infection  - growth hormones to promote growth and help bones mature  - removal of one or both kidneys to decrease the loss of albumin in the urine  - dialysis to artificially filter wastes from the blood if the kidneys fail\n                \nMore information is provided in the NIDDK health topic, Treatment Methods for Kidney Failure in Children."}
{"_id":"d328ae4f-ef09-43a7-959d-bc2544b42456","text":"Researchers have not found a way to prevent childhood nephrotic syndrome when the cause is idiopathic or congenital."}
{"_id":"69eb2ca4-4e97-455b-a950-cee1f050ac04","text":"Children who have nephrotic syndrome may need to make changes to their diet, such as\n                \n- limiting the amount of sodium, often from salt, they take in each day  - reducing the amount of liquids they drink each day  - eating a diet low in saturated fat and cholesterol to help control elevated cholesterol levels\n                \nParents or caretakers should talk with the childs health care provider before making any changes to the childs diet.\n                \nMore information is provided in the NIDDK health topic, Nutrition for Chronic Kidney Disease in Children."}
{"_id":"f16b9411-7f61-48d8-bec0-42a4ecd0e2b9","text":"- Childhood nephrotic syndrome is not a disease in itself; rather, it is a group of symptoms that      - indicate kidney damageparticularly damage to the glomeruli, the tiny units within the kidney where blood is filtered    - result in the release of too much protein from the body into the urine    - The two types of childhood nephrotic syndrome are      - primarythe most common type of childhood nephrotic syndrome, which begins in the kidneys and affects only the kidneys    - secondarythe syndrome is caused by other diseases    - The signs and symptoms of childhood nephrotic syndrome may include      - edemaswelling, most often in the legs, feet, or ankles and less often in the hands or face    - albuminuriawhen a childs urine has high levels of albumin    - hypoalbuminemiawhen a childs blood has low levels of albumin    - hyperlipidemiawhen a childs blood cholesterol and fat levels are higher than normal    - A health care provider may order urine tests to help determine if a child has kidney damage from childhood nephrotic syndrome.  - Health care providers will decide how to treat childhood nephrotic syndrome based on the type:      - primary childhood nephrotic syndrome: medications    - secondary childhood nephrotic syndrome: treat the underlying illness or disease    - congenital nephrotic syndrome: medications, surgery to remove one or both kidneys, or transplantation"}
{"_id":"87b5fd3a-a544-4887-80e5-62132e22f174","text":"Renal tubular acidosis (RTA) is a disease that occurs when the kidneys fail to excrete acids into the urine, which causes a person's blood to remain too acidic. Without proper treatment, chronic acidity of the blood leads to growth retardation, kidney stones, bone disease, chronic kidney disease, and possibly total kidney failure.\n                \nThe body's cells use chemical reactions to carry out tasks such as turning food into energy and repairing tissue. These chemical reactions generate acids. Some acid in the blood is normal, but too much acidacidosiscan disturb many bodily functions. Healthy kidneys help maintain acid-base balance by excreting acids into the urine and returning bicarbonatean alkaline, or base, substanceto the blood. This \"reclaimed\" bicarbonate neutralizes much of the acid that is created when food is broken down in the body. The movement of substances like bicarbonate between the blood and structures in the kidneys is called transport.\n                \nOne researcher has theorized that Charles Dickens may have been describing a child with RTA in the character of Tiny Tim from A Christmas Carol. Tiny Tim's small stature, malformed limbs, and periods of weakness are all possible consequences of the chemical imbalance caused by RTA.1 In the story, Tiny Tim recovers when he receives medical treatment, which would likely have included sodium bicarbonate and sodium citrate, alkaline agents to neutralize acidic blood. The good news is that medical treatment can indeed reverse the effects of RTA."}
{"_id":"6b011ade-b555-46ed-b234-a071d6b0feb2","text":"Renal tubular acidosis (RTA) is a disease that occurs when the kidneys fail to excrete acids into the urine, which causes a person's blood to remain too acidic. Without proper treatment, chronic acidity of the blood leads to growth retardation, kidney stones, bone disease, chronic kidney disease, and possibly total kidney failure.\n                \nThe body's cells use chemical reactions to carry out tasks such as turning food into energy and repairing tissue. These chemical reactions generate acids. Some acid in the blood is normal, but too much acidacidosiscan disturb many bodily functions. Healthy kidneys help maintain acid-base balance by excreting acids into the urine and returning bicarbonatean alkaline, or base, substanceto the blood. This \"reclaimed\" bicarbonate neutralizes much of the acid that is created when food is broken down in the body. The movement of substances like bicarbonate between the blood and structures in the kidneys is called transport.\n                \nOne researcher has theorized that Charles Dickens may have been describing a child with RTA in the character of Tiny Tim from A Christmas Carol. Tiny Tim's small stature, malformed limbs, and periods of weakness are all possible consequences of the chemical imbalance caused by RTA.1 In the story, Tiny Tim recovers when he receives medical treatment, which would likely have included sodium bicarbonate and sodium citrate, alkaline agents to neutralize acidic blood. The good news is that medical treatment can indeed reverse the effects of RTA."}
{"_id":"f820e574-016a-40a4-a7a6-04a851295d0c","text":"To diagnose RTA, doctors check the acid-base balance in blood and urine samples. If the blood is more acidic than it should be and the urine less acidic than it should be, RTA may be the reason, but additional information is needed to rule out other causes. If RTA is the reason, additional information about the sodium, potassium, and chloride levels in the urine and the potassium level in the blood will help identify which type of RTA a person has. In all cases, the first goal of therapy is to neutralize acid in the blood, but different treatments may be needed to address the different underlying causes of acidosis."}
{"_id":"f3f39fc1-955c-48b2-a2fc-470382e43df3","text":"To diagnose RTA, doctors check the acid-base balance in blood and urine samples. If the blood is more acidic than it should be and the urine less acidic than it should be, RTA may be the reason, but additional information is needed to rule out other causes. If RTA is the reason, additional information about the sodium, potassium, and chloride levels in the urine and the potassium level in the blood will help identify which type of RTA a person has. In all cases, the first goal of therapy is to neutralize acid in the blood, but different treatments may be needed to address the different underlying causes of acidosis."}
{"_id":"77648ce2-26a0-43d2-8e03-e24ec91648a2","text":"Type 1: Classical Distal RTA\n                \nType 1 is also called classical distal RTA. \"Distal,\" which means distant, refers to the point in the urine-forming tube of the kidney where the defect occursrelatively distant from the point where fluid from the blood enters the tiny tube, or tubule, that collects fluid and wastes to form urine.\n                \nThis disorder may be inherited as a primary disorder or may be one symptom of a disease that affects many parts of the body. Researchers have discovered abnormal genes responsible for the inherited forms of the disease. More often, however, classical distal RTA occurs as a result of systemic diseasesdiseases that affect many organ systemslike the autoimmune disorders Sjgren's syndrome and lupus, which also attack the distal tubule.\n                \nOther diseases and conditions associated with classical distal RTA include sickle cell anemia, hyperparathyroidism, hyperthyroidism, chronic active hepatitis, primary biliary cirrhosis, a hereditary form of deafness, analgesic nephropathy, rejection of a transplanted kidney, renal medullary cystic disease, obstructive uropathy, and chronic urinary tract infections. Many of these conditions cause abnormal calcium deposits to build up in the kidney and impair distal tubule function.\n                \nA major consequence of classical distal RTA is a low blood potassium level. The level drops if the kidneys excrete too much potassium into urine instead of returning it to the blood supply. Because potassium helps regulate nerve and muscle health and heart rate, low levels can cause extreme weakness, irregular heartbeat, paralysis, and even death.\n                \nUntreated classical distal RTA causes growth retardation in children and progressive kidney and bone disease in adults. Restoring normal growth and preventing kidney stones are the major goals of therapy. If acidosis is corrected with sodium bicarbonate or sodium citrate, then low blood-potassium, salt depletion, and calcium leakage into urine will be corrected. This alkali therapy also helps decrease the development of kidney stones and stabilizes kidney function so kidney failure does not progress. Infants may need potassium supplements, but older children and adults rarely do because alkali therapy prevents the kidney from excreting potassium into the urine.\n                \nType 2: Proximal RTA\n                \nType 2 is also called proximal RTA. The word \"proximal,\" which means near, indicates that the defect is closer to the point where fluid and wastes from the blood enter the tubule.\n                \nThis form of RTA occurs most frequently in children as part of a disorder called Fanconi's syndrome. The features of Fanconi's syndrome include the abnormal excretion of glucose, amino acids, citrate, and phosphate into the urine, as well as vitamin D deficiency and low blood-potassium.\n                \nProximal RTA can also result from inherited disorders that disrupt the body's normal breakdown and use of nutrients. Examples include the rare disease cystinosis, in which cystine crystals are deposited in bones and other tissues; hereditary fructose intolerance; and Wilson disease.\n                \nProximal RTA also occurs in patients treated with ifosfamide, a drug used in chemotherapy. A few older drugssuch as acetazolamide or outdated tetracyclinecan also cause proximal RTA. In adults, proximal RTA may complicate diseases like multiple myeloma, or it may occur in people who experience chronic rejection of a transplanted kidney.\n                \nWhen possible, identifying and correcting the underlying causes are important steps in treating the acquired forms of proximal RTA. The diagnosis is based on the chemical analysis of blood and urine samples. Children with this disorder would likely receive large doses of an oral alkali, such as sodium bicarbonate or potassium citrate, to treat acidosis and prevent bone disorders, kidney stones, and growth failure. Correcting acidosis and low potassium levels restores normal growth patterns, allowing bone to mature while preventing further renal disease. Vitamin D supplements may also be needed to help prevent bone problems.\n                \nType 3\n                \nType 3 is rarely used as a classification because it is now thought to be a combination of type 1 and type 2.\n                \nType 4: Hyperkalemic RTA\n                \nType 4 is also called hyperkalemic RTA and is caused by a generalized transport abnormality of the distal tubule. The transport of electrolytes such as sodium, chloride, and potassium that normally occurs in the distal tubule is impaired. This form is distinguished from classical distal RTA and proximal RTA because it results in high levels of potassium in the blood instead of low levels. Either low potassiumhypokalemiaor high potassiumhyperkalemiacan be a problem because potassium is important in regulating heart rate.\n                \nType 4 RTA occurs when blood levels of the hormone aldosterone are low or when the kidneys do not respond to it. Aldosterone directs the kidneys to regulate the levels of sodium, potassium, and chloride in the blood. Type 4 RTA also occurs when the tubule transport of electrolytes such as sodium, chloride, and potassium is impaired due to an inherited disorder or the use of certain drugs.\n                \nDrugs that may cause type 4 RTA include\n                \n- diuretics used to treat congestive heart failure such as spironolactone or eplerenone  - blood pressure drugs called angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs)  - the antibiotic trimethoprim  - the antibiotic pentamidine, which is used to treat pneumonia  - an agent called heparin that keeps blood from clotting  - a class of painkillers called nonsteroidal anti-inflammatory drugs (NSAIDs)  - some immunosuppressive drugs used to prevent rejection\n                \nType 4 RTA may also result from diseases that alter kidney structure and function such as diabetic nephropathy, HIV\/AIDS, Addison's disease, sickle cell disease, urinary tract obstruction, lupus, amyloidosis, removal or destruction of both adrenal glands, and kidney transplant rejection.\n                \nFor people who produce aldosterone but cannot use it, researchers have identified the genetic basis for their body's resistance to the hormone. To treat type 4 RTA successfully, patients may require alkaline agents to correct acidosis and medication to lower the potassium in their blood.\n                \nIf treated early, most people with any type of RTA will not develop permanent kidney failure. Therefore, the goal is early recognition and adequate therapy, which will need to be maintained and monitored throughout the person's lifetime."}
{"_id":"b8f7e3f6-a4fe-4107-900b-901fed33309c","text":"Type 1: Classical Distal RTA\n                \nType 1 is also called classical distal RTA. \"Distal,\" which means distant, refers to the point in the urine-forming tube of the kidney where the defect occursrelatively distant from the point where fluid from the blood enters the tiny tube, or tubule, that collects fluid and wastes to form urine.\n                \nThis disorder may be inherited as a primary disorder or may be one symptom of a disease that affects many parts of the body. Researchers have discovered abnormal genes responsible for the inherited forms of the disease. More often, however, classical distal RTA occurs as a result of systemic diseasesdiseases that affect many organ systemslike the autoimmune disorders Sjgren's syndrome and lupus, which also attack the distal tubule.\n                \nOther diseases and conditions associated with classical distal RTA include sickle cell anemia, hyperparathyroidism, hyperthyroidism, chronic active hepatitis, primary biliary cirrhosis, a hereditary form of deafness, analgesic nephropathy, rejection of a transplanted kidney, renal medullary cystic disease, obstructive uropathy, and chronic urinary tract infections. Many of these conditions cause abnormal calcium deposits to build up in the kidney and impair distal tubule function.\n                \nA major consequence of classical distal RTA is a low blood potassium level. The level drops if the kidneys excrete too much potassium into urine instead of returning it to the blood supply. Because potassium helps regulate nerve and muscle health and heart rate, low levels can cause extreme weakness, irregular heartbeat, paralysis, and even death.\n                \nUntreated classical distal RTA causes growth retardation in children and progressive kidney and bone disease in adults. Restoring normal growth and preventing kidney stones are the major goals of therapy. If acidosis is corrected with sodium bicarbonate or sodium citrate, then low blood-potassium, salt depletion, and calcium leakage into urine will be corrected. This alkali therapy also helps decrease the development of kidney stones and stabilizes kidney function so kidney failure does not progress. Infants may need potassium supplements, but older children and adults rarely do because alkali therapy prevents the kidney from excreting potassium into the urine.\n                \nType 2: Proximal RTA\n                \nType 2 is also called proximal RTA. The word \"proximal,\" which means near, indicates that the defect is closer to the point where fluid and wastes from the blood enter the tubule.\n                \nThis form of RTA occurs most frequently in children as part of a disorder called Fanconi's syndrome. The features of Fanconi's syndrome include the abnormal excretion of glucose, amino acids, citrate, and phosphate into the urine, as well as vitamin D deficiency and low blood-potassium.\n                \nProximal RTA can also result from inherited disorders that disrupt the body's normal breakdown and use of nutrients. Examples include the rare disease cystinosis, in which cystine crystals are deposited in bones and other tissues; hereditary fructose intolerance; and Wilson disease.\n                \nProximal RTA also occurs in patients treated with ifosfamide, a drug used in chemotherapy. A few older drugssuch as acetazolamide or outdated tetracyclinecan also cause proximal RTA. In adults, proximal RTA may complicate diseases like multiple myeloma, or it may occur in people who experience chronic rejection of a transplanted kidney.\n                \nWhen possible, identifying and correcting the underlying causes are important steps in treating the acquired forms of proximal RTA. The diagnosis is based on the chemical analysis of blood and urine samples. Children with this disorder would likely receive large doses of an oral alkali, such as sodium bicarbonate or potassium citrate, to treat acidosis and prevent bone disorders, kidney stones, and growth failure. Correcting acidosis and low potassium levels restores normal growth patterns, allowing bone to mature while preventing further renal disease. Vitamin D supplements may also be needed to help prevent bone problems.\n                \nType 3\n                \nType 3 is rarely used as a classification because it is now thought to be a combination of type 1 and type 2.\n                \nType 4: Hyperkalemic RTA\n                \nType 4 is also called hyperkalemic RTA and is caused by a generalized transport abnormality of the distal tubule. The transport of electrolytes such as sodium, chloride, and potassium that normally occurs in the distal tubule is impaired. This form is distinguished from classical distal RTA and proximal RTA because it results in high levels of potassium in the blood instead of low levels. Either low potassiumhypokalemiaor high potassiumhyperkalemiacan be a problem because potassium is important in regulating heart rate.\n                \nType 4 RTA occurs when blood levels of the hormone aldosterone are low or when the kidneys do not respond to it. Aldosterone directs the kidneys to regulate the levels of sodium, potassium, and chloride in the blood. Type 4 RTA also occurs when the tubule transport of electrolytes such as sodium, chloride, and potassium is impaired due to an inherited disorder or the use of certain drugs.\n                \nDrugs that may cause type 4 RTA include\n                \n- diuretics used to treat congestive heart failure such as spironolactone or eplerenone  - blood pressure drugs called angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs)  - the antibiotic trimethoprim  - the antibiotic pentamidine, which is used to treat pneumonia  - an agent called heparin that keeps blood from clotting  - a class of painkillers called nonsteroidal anti-inflammatory drugs (NSAIDs)  - some immunosuppressive drugs used to prevent rejection\n                \nType 4 RTA may also result from diseases that alter kidney structure and function such as diabetic nephropathy, HIV\/AIDS, Addison's disease, sickle cell disease, urinary tract obstruction, lupus, amyloidosis, removal or destruction of both adrenal glands, and kidney transplant rejection.\n                \nFor people who produce aldosterone but cannot use it, researchers have identified the genetic basis for their body's resistance to the hormone. To treat type 4 RTA successfully, patients may require alkaline agents to correct acidosis and medication to lower the potassium in their blood.\n                \nIf treated early, most people with any type of RTA will not develop permanent kidney failure. Therefore, the goal is early recognition and adequate therapy, which will need to be maintained and monitored throughout the person's lifetime."}
{"_id":"94ee20a1-6c2b-4f53-98ba-20a296886273","text":"- Renal tubular acidosis (RTA) is a disease that occurs when the kidneys fail to excrete acids into the urine, which causes a person's blood to remain too acidic.  - Without proper treatment, chronic acidity of the blood leads to growth retardation, kidney stones, bone disease, chronic kidney disease, and possibly total kidney failure.  - If RTA is suspected, additional information about the sodium, potassium, and chloride levels in the urine and the potassium level in the blood will help identify which type of RTA a person has.  - In all cases, the first goal of therapy is to neutralize acid in the blood, but different treatments may be needed to address the different underlying causes of acidosis."}
{"_id":"f77a7e69-48d3-40f9-9060-ff73910b39fa","text":"- Renal tubular acidosis (RTA) is a disease that occurs when the kidneys fail to excrete acids into the urine, which causes a person's blood to remain too acidic.  - Without proper treatment, chronic acidity of the blood leads to growth retardation, kidney stones, bone disease, chronic kidney disease, and possibly total kidney failure.  - If RTA is suspected, additional information about the sodium, potassium, and chloride levels in the urine and the potassium level in the blood will help identify which type of RTA a person has.  - In all cases, the first goal of therapy is to neutralize acid in the blood, but different treatments may be needed to address the different underlying causes of acidosis."}
{"_id":"9cb47dc6-35b0-4d0e-a786-5564fd914a9d","text":"Diabetes problems are health problems that can happen when you have diabetes. If your diabetes is not under control, you will have too much glucose*, also called sugar, in your blood. Having too much glucose in your blood for a long time can affect many important parts of your body, such as your\n                \n- blood vessels and heart  - nerves  - kidneys  - mouth  - eyes  - feet\n                \nYou can do a lot to prevent or slow down these health problems if you keep your diabetes under control.\n                \nThis chart shows the body parts that can be affected by diabetes and the resulting health problems you may have.\n                \nAffected Body Part    Resulting Health Problems You May Have          Blood vessels and heart             - Heart disease      - Heart attack      - Stroke      - High blood pressure      - Poor blood circulation, or flow, throughout your body            Nerves             - Pain, tingling, weakness, or numbness in your hands, arms, feet, or legs      - Problems with your bladder, digestion, having sex, and keeping your heartbeats and blood pressure steady            Kidneys             - Protein loss through your urine      - Buildup of wastes and fluid in your blood            Mouth             - Gum disease and loss of teeth      - Dry mouth      - Thrush, or the growth of too much fungus in the mouth            Eyes             - Loss of vision and blindness            Feet             - Sores      - Infections      - Amputation\n                \n*See the Pronunciation Guide for tips on how to say the the words in bold type."}
{"_id":"a14bf904-31a9-420b-a6c7-bf3e3f9a3722","text":"The A1C test, also called the hemoglobin A1C test, HbA1C, or glycohemoglobin test, is a blood test that reflects the average level of glucose in your blood during the past 3 months. Your A1C test result is given in percents. Your doctor might use the A1C test to help diagnose your diabetes. Your doctor will draw a sample of your blood in the office or send you to a lab to have a sample of your blood drawn for the test. After being diagnosed with diabetes, you should have the A1C test at least twice a year.\n                \nYour A1C result plus your record of blood glucose numbers show whether your blood glucose is under control.\n                \n- If your A1C result is too high, you may need to change your diabetes care plan. Your health care team can help you decide what part of your plan to change. For instance, you might need to change your meal plan, your diabetes medicines, or your physical activity plan.  - If your A1C result is on target, then your diabetes treatment plan is working. The lower your A1C is, the lower your chance of having diabetes problems.\n                \nThis chart shows the A1C goals for different types of people with diabetes.\n                \nTypes of People    A1C Goals          Most people with diabetes    below 7%        Women with diabetes who want to get pregnant or who are pregnant    below 6%\n                \nA1C goals can also depend on\n                \n- how long you have had diabetes  - whether or not you have other health problems\n                \nAsk your doctor what goal is right for you.\n                \n\n                \nThis chart shows how your A1C result may match up to your average blood glucose number.\n                \nWhat Your A1C Result Means          My A1C Result    My Average Blood Glucose Number        6%    135        7%    170        8%    205        9%    240        10%    275        11%    310        12%    345"}
{"_id":"97c0e667-6121-4950-9d2b-cfd0b4cdeab2","text":"Following a healthy eating plan is a key step in living with diabetes and preventing diabetes problems. Your health care team will help you make a healthy eating plan.\n                \nMore information is provided in the NIDDK health topic, What I need to know about Eating and Diabetes or call 18008608747."}
{"_id":"87746351-ef7a-4900-8036-ed8c612bceb6","text":"You can take steps each day to prevent diabetes problems.\n                \nSteps          Healthy Eating                     - Follow the healthy eating plan that you and your doctor or dietitian have made.      - Learn what to eat to keep your blood glucose levels under control.      - Make wise food choices to help you feel good every day and to lose weight if needed.            Blood Glucose                     - Check your blood glucose every day.      - Each time you check your blood glucose, write the number in a record book to share with your health care team.      - Treat low blood glucose quickly.            Physical Activity                     - Even small amounts of physical activity help manage diabetes. Aim for 30 to 60 minutes of physical activity most days of the week. Children and adolescents with type 2 diabetes who are 10 to 17 years old should aim for 60 minutes of activity every day.      - Not all physical activity has to take place at the same time.      - Do aerobic activities, such as brisk walking, which use your large muscles to make your heart beat faster. The large muscles are those of the upper and lower arms and legs and those that control head, shoulder, and hip movements.      - Do activities to strengthen muscles and bone, such as lifting weights or sit-ups. Aim for two times a week.      - Stretch to increase your flexibility, lower stress, and help prevent muscle soreness after physical activity.      - Increase daily activity by decreasing time spent watching TV or at the computer. Children and adolescents should limit screen time not related to school to less than 2 hours per day. Limiting screen time can help you meet your physical activity goal.      - Always talk with your doctor before you start a new physical activity program.            Medicines                     - Take your medicines as directed, including insulin if ordered by your doctor.            Feet                     - Check your feet every day for cuts, blisters, sores, swelling, redness, or sore toenails.            Mouth                     - Brush and floss your teeth every day.            Blood Pressure                     - Control your blood pressure and cholesterol.            Smoking                     - Dont smoke."}
{"_id":"25e6b96a-c52e-48a6-91de-1f273f545bcd","text":"This chart lists important tests, exams, and vaccines to get at least once or twice a year.\n                \nTests, Exams, and Vaccines to Get at Least Once or Twice a Year    Make Sure to          A1C test             - Have this blood test at least twice a year. Your result will tell you what your average blood glucose level was for the past 3 months.            Cholesterol test             - Get a blood test to check your              - total cholesterol        - LDL        - HDL        - triglycerides                  Kidney tests             - Once a year, get a urine test to check for protein.      - At least once a year, get a blood test to check for creatinine, a waste product healthy kidneys remove from the body.            Eye exam             - See an eye doctor once a year for a complete eye exam that includes using drops in your eyes to dilate your pupils.      - If you are pregnant, have a complete eye exam in your first 3 months of pregnancy. Have another complete eye exam 1 year after your baby is born.            Dental exam             - See your dentist twice a year for a cleaning and checkup.            Flu vaccine             - Get a flu vaccine each year.            Pneumonia vaccine             - Get this vaccine if you are younger than 64.      - If youre older than 64 and your vaccine was more than 5 years ago, get another one.            Hepatitis B vaccine             - Get this vaccine if youre younger than 60 and you have not already had the vaccine.      - Prevent exposure to Hepatitis B by not sharing blood glucose monitors or other diabetes equipment."}
{"_id":"fe889aa1-f535-47b9-899f-177ef05ea00c","text":"Hepatitis B is a liver disease spread through contact with blood, semen, or other body fluids from a person infected with the hepatitis B virus. The disease is most commonly spread from an infected mother to her infant at birth. Hepatitis B is also spread through sex, wound-to-wound contact, and contact with items that may have blood on them, such as shaving razors, toothbrushes, syringes, and tattoo and body piercing needles.\n                \nHepatitis B is not spread through casual contact such as shaking hands or hugging; nor is it spread by sharing food or beverages, by sneezing and coughing, or through breastfeeding."}
{"_id":"963c9214-3b53-47f0-a156-0cc039979837","text":"Hepatitis B may start as a brief, flu-like illness. Most healthy adults and children older than 5 completely recover after the bodys immune system gets rid of the virus.\n                \nHepatitis B becomes chronic when the bodys immune system cant get rid of the virus. Over time, having the virus can lead to inflammation of the liver; scar tissue in the liver, called cirrhosis; or liver cancer. Inflammation is the painful red swelling that results when tissues of the body become infected. Young children and people with weakened immune systems are especially at risk. People who were infected as infants have a 90 percent chance of developing chronic hepatitis B.1"}
{"_id":"56863509-faa3-41ff-8d73-a68380138b47","text":"Since 1986, a hepatitis B vaccine has been available and should be given to newborns and children in the United States. The vaccine, however, is unavailableor has only recently become availablein many parts of the world. You are at higher risk for hepatitis B if you or your mother was born in a region of the world where hepatitis B is common, meaning 2 percent or more of the population is chronically infected with the hepatitis B virus.1 In most Asian and Pacific Island nations, 8 to 16 percent of the population is chronically infected.2"}
{"_id":"7b01440e-4362-45b3-99af-8faf66cfff78","text":"Hepatitis B is called a silent killer because many people have no symptoms, so the disease often progresses unnoticed for years. Unfortunately, many people first learn they have chronic hepatitis B when they develop symptoms of severe liver damage, which include\n                \n- yellowish eyes and skin, called jaundice  - a swollen stomach or ankles  - tiredness  - nausea  - weakness  - loss of appetite  - weight loss  - spiderlike blood vessels, called spider angiomas, that develop on the skin"}
{"_id":"32467a34-44e0-4001-b036-342219dbd30d","text":"Anyone can get hepatitis B, but some people are at higher risk, including\n                \n- people who were born to a mother with hepatitis B  - people who have close household contact with someone infected with the hepatitis B virus  - people who have lived in parts of the world where hepatitis B is common, including most Asian and Pacific Island nations  - people who are exposed to blood or body fluids at work  - people on hemodialysis  - people whose sex partner(s) has hepatitis B  - people who have had more than one sex partner in the last 6 months or have a history of sexually transmitted disease  - injection drug users  - men who have sex with men"}
{"_id":"17d8aec5-59f2-4e5c-b670-dbb68982e8bc","text":"Acquired cystic kidney disease happens when a person's kidneys develop fluid-filled sacs, called cysts, over time. Acquired cystic kidney disease is not the same as polycystic kidney disease (PKD), another disease that causes the kidneys to develop multiple cysts.\n                \nAcquired cystic kidney disease occurs in children and adults who have\n                \n- chronic kidney disease (CKD)a condition that develops over many years and may lead to end-stage kidney disease, or ESRD. The kidneys of people with CKD gradually lose their ability to filter wastes, extra salt, and fluid from the blood properly.  - end-stage kidney diseasetotal and permanent kidney failure that requires a kidney transplant or blood-filtering treatments called dialysis.\n                \nThe cysts are more likely to develop in people who are on kidney dialysis. The chance of developing acquired cystic kidney disease increases with the number of years a person is on dialysis. However, the cysts are caused by CKD or kidney failure, not dialysis treatments.\n                \nMore information is provided in the NIDDK health topics, kidney failureand dialysis."}
{"_id":"a102cd38-8eea-4af3-bf0c-22a318ae7324","text":"Acquired cystic kidney disease differs from PKD in several ways. Unlike acquired cystic kidney disease, PKD is a genetic, or inherited, disorder that can cause complications such as high blood pressure and problems with blood vessels in the brain and heart.\n                \nThe following chart lists the differences:\n                \nPeople with Polycystic Kidney Disease   - are born with a gene that causes the disease   - have enlarged kidneys   - develop cysts in the liver and other parts of the body   People with Acquired Cystic Kidney Disease   - do not have a disease-causing gene   - have kidneys that are normal-sized or smaller   - do not form cysts in other parts of the body\n                \nIn addition, for people with PKD, the presence of cysts marks the onset of their disease, while people with acquired cystic kidney disease already have CKD when they develop cysts.\n                \nMore information is provided in the NIDDK health topic, Polycystic Kidney Disease."}
{"_id":"dfa66923-c689-4779-a535-25d79bdccf02","text":"Acquired cystic kidney disease becomes more common the longer a person has CKD.\n                \n- About 7 to 22 percent of people with CKD already have acquired cystic kidney disease before starting dialysis treatments.  - Almost 60 percent of people on dialysis for 2 to 4 years develop acquired cystic kidney disease.1  - About 90 percent of people on dialysis for 8 years develop acquired cystic kidney disease.1"}
{"_id":"fb3919ed-a1c7-497d-9875-c5f20bd15983","text":"Researchers do not fully understand what causes cysts to grow in the kidneys of people with CKD. The fact that these cysts occur only in the kidneys and not in other parts of the body, as in PKD, indicates that the processes that lead to cyst formation take place primarily inside the kidneys.2"}
{"_id":"39f7ec3b-8b25-441f-a0b6-bd52fe9146ca","text":"A person with acquired cystic kidney disease often has no symptoms. However, the complications of acquired cystic kidney disease can have signs and symptoms."}
{"_id":"93db1b17-047f-43cb-af4d-ca099e0a2aed","text":"People with acquired cystic kidney disease may develop the following complications:\n                \n- an infected cyst, which can cause fever and back pain.  - blood in the urine, which can signal that a cyst in the kidney is bleeding.  - tumors in the kidneys. People with acquired cystic kidney disease are more likely than people in the general population to have cancerous kidney tumors. However, the chance of cancer spreading is lower in people with acquired cystic kidney disease than that of other kidney cancers not associated with acquired cystic kidney disease, and the long-term outlook is better.1"}
{"_id":"f019911d-9152-4cad-a993-10478ad3f040","text":"A health care provider may diagnose a person with acquired cystic kidney disease based on\n                \n- medical history  - imaging tests\n                \nMedical History\n                \nTaking a medical history may help a health care provider diagnose acquired cystic kidney disease. A health care provider may suspect acquired cystic kidney disease if a person who has been on dialysis for several years develops symptoms such as fever, back pain, or blood in the urine.\n                \nImaging Tests\n                \nTo confirm the diagnosis, the health care provider may order one or more imaging tests. A radiologista doctor who specializes in medical imaginginterprets the images from these tests, and the patient does not need anesthesia.\n                \n- Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. A specially trained technician performs the procedure in a health care provider's office, an outpatient center, or a hospital. The images can show cysts in the kidneys as well as the kidneys' size and shape.  - Computerized tomography (CT) scans use a combination of x rays and computer technology to create images. For a CT scan, a nurse or technician may give the patient a solution to drink and an injection of a special dye, called contrast medium. CT scans require the patient to lie on a table that slides into a tunnel-shaped device where an x-ray technician takes the x-rays. An x-ray technician performs the procedure in an outpatient center or a hospital. CT scans can show cysts and tumors in the kidneys.  - Magnetic resonance imaging (MRI) is a test that takes pictures of the body's internal organs and soft tissues without using x-rays. A specially trained technician performs the procedure in an outpatient center or a hospital. Although the patient does not need anesthesia, a health care provider may give people with a fear of confined spaces light sedation, taken by mouth. An MRI may include the injection of contrast medium. With most MRI machines, the patient will lie on a table that slides into a tunnel-shaped device that may be open-ended or closed at one end. Some machines allow the patient to lie in a more open space. During an MRI, the patient, although usually awake, must remain perfectly still while the technician takes the images, which usually takes only a few minutes. The technician will take a sequence of images from different angles to create a detailed picture of the kidneys. During the test, the patient will hear loud mechanical knocking and humming noises from the machine.\n                \nSometimes a health care provider may discover acquired cystic kidney disease during an imaging exam for another condition. Images of the kidneys may help the health care provider distinguish acquired cystic kidney disease from PKD."}
{"_id":"02f63665-f712-4ff2-815f-af4278265670","text":"If acquired cystic kidney disease is not causing complications, a person does not need treatment. A health care provider will treat infections with antibioticsmedications that kill bacteria. If large cysts are causing pain, a health care provider may drain the cyst using a long needle inserted into the cyst through the skin.\n                \nWhen a surgeon transplants a new kidney into a patient's body to treat kidney failure, acquired cystic kidney disease in the damaged kidneys, which usually remain in place after a transplant, often disappears.\n                \nA surgeon may perform an operation to remove tumors or suspected tumors. In rare cases, a surgeon performs an operation to stop cysts from bleeding.\n                \nHave Regular Screenings to Look for Cyst or Tumor Growth   Some health care providers recommend all people with end-stage kidney disease get screened for kidney cancer using CT scans or MRIs after 3 years of dialysis. People with acquired cystic kidney disease should talk with their health care provider about when to begin screening."}
{"_id":"6123d4a8-f076-4a0f-a293-17d7c3d2cf4e","text":"No specific diet will prevent or delay acquired cystic kidney disease. In general, a diet designed for people on hemodialysis or peritoneal dialysis reduces the amount of wastes that accumulate in the body between dialysis sessions.\n                \nMore information is provided in the NIDDK health topics, Eat Right to Feel Right on Hemodialysis and Nutrition for Advanced Chronic Kidney Disease in Adults."}
{"_id":"4a1d0e90-d6c0-4c45-a41c-57585d148d85","text":"- Acquired cystic kidney disease happens when a person's kidneys develop fluid-filled sacs, called cysts, over time.  - Acquired cystic kidney disease occurs in children and adults who have      - chronic kidney disease (CKD)    - end-stage kidney disease (ESRD)    - People with acquired cystic kidney disease may develop the following complications:      - an infected cyst, which can cause fever and back pain    - blood in the urine, which can signal that a cyst in the kidney is bleeding    - tumors in the kidneys    - To confirm the diagnosis, the health care provider may order one or more imaging tests:      - Ultrasound    - Computerized tomography (CT) scan    - Magnetic resonance imaging (MRI)    - If acquired cystic kidney disease is not causing complications, a person does not need treatment.  - A health care provider will treat infections with antibioticsmedications that kill bacteria.  - If large cysts are causing pain, a health care provider may drain the cyst using a long needle inserted into the cyst through the skin.  - A surgeon may perform an operation to remove tumors or suspected tumors. In rare cases, a surgeon performs an operation to stop cysts from bleeding."}
{"_id":"b0539eb9-d44b-4ce7-8e9b-8032e67ee072","text":"Benign prostatic hyperplasiaalso called BPHis a condition in men in which the prostate gland is enlarged and not cancerous. Benign prostatic hyperplasia is also called benign prostatic hypertrophy or benign prostatic obstruction.\n                \nThe prostate goes through two main growth periods as a man ages. The first occurs early in puberty, when the prostate doubles in size. The second phase of growth begins around age 25 and continues during most of a mans life. Benign prostatic hyperplasia often occurs with the second growth phase.\n                \nAs the prostate enlarges, the gland presses against and pinches the urethra. The bladder wall becomes thicker. Eventually, the bladder may weaken and lose the ability to empty completely, leaving some urine in the bladder. The narrowing of the urethra and urinary retentionthe inability to empty the bladder completelycause many of the problems associated with benign prostatic hyperplasia."}
{"_id":"19330476-9442-4dac-b339-b3582e7d82e4","text":"The prostate is a walnut-shaped gland that is part of the male reproductive system. The main function of the prostate is to make a fluid that goes into semen. Prostate fluid is essential for a mans fertility. The gland surrounds the urethra at the neck of the bladder. The bladder neck is the area where the urethra joins the bladder. The bladder and urethra are parts of the lower urinary tract. The prostate has two or more lobes, or sections, enclosed by an outer layer of tissue, and it is in front of the rectum, just below the bladder. The urethra is the tube that carries urine from the bladder to the outside of the body. In men, the urethra also carries semen out through the penis."}
{"_id":"f2e8a82a-a510-4b12-a208-96ea576d7287","text":"The cause of benign prostatic hyperplasia is not well understood; however, it occurs mainly in older men. Benign prostatic hyperplasia does not develop in men whose testicles were removed before puberty. For this reason, some researchers believe factors related to aging and the testicles may cause benign prostatic hyperplasia.\n                \nThroughout their lives, men produce testosterone, a male hormone, and small amounts of estrogen, a female hormone. As men age, the amount of active testosterone in their blood decreases, which leaves a higher proportion of estrogen. Scientific studies have suggested that benign prostatic hyperplasia may occur because the higher proportion of estrogen within the prostate increases the activity of substances that promote prostate cell growth.\n                \nAnother theory focuses on dihydrotestosterone (DHT), a male hormone that plays a role in prostate development and growth. Some research has indicated that even with a drop in blood testosterone levels, older men continue to produce and accumulate high levels of DHT in the prostate. This accumulation of DHT may encourage prostate cells to continue to grow. Scientists have noted that men who do not produce DHT do not develop benign prostatic hyperplasia."}
{"_id":"b4cda996-9e9c-4588-acc7-a8d8537718cc","text":"Benign prostatic hyperplasia is the most common prostate problem for men older than age 50. In 2010, as many as 14 million men in the United States had lower urinary tract symptoms suggestive of benign prostatic hyperplasia.1 Although benign prostatic hyperplasia rarely causes symptoms before age 40, the occurrence and symptoms increase with age. Benign prostatic hyperplasia affects about 50 percent of men between the ages of 51 and 60 and up to 90 percent of men older than 80.2"}
{"_id":"825efc71-2c1d-45ae-87fa-525f4ed40a9e","text":"Lower urinary tract symptoms suggestive of benign prostatic hyperplasia may include\n                \n- urinary frequencyurination eight or more times a day  - urinary urgencythe inability to delay urination  - trouble starting a urine stream  - a weak or an interrupted urine stream  - dribbling at the end of urination  - nocturiafrequent urination during periods of sleep  - urinary retention  - urinary incontinencethe accidental loss of urine  - pain after ejaculation or during urination  - urine that has an unusual color or smell\n                \nSymptoms of benign prostatic hyperplasia most often come from\n                \n- a blocked urethra  - a bladder that is overworked from trying to pass urine through the blockage\n                \nThe size of the prostate does not always determine the severity of the blockage or symptoms. Some men with greatly enlarged prostates have little blockage and few symptoms, while other men who have minimally enlarged prostates have greater blockage and more symptoms. Less than half of all men with benign prostatic hyperplasia have lower urinary tract symptoms.3\n                \nSometimes men may not know they have a blockage until they cannot urinate. This condition, called acute urinary retention, can result from taking over-the-counter cold or allergy medications that contain decongestants, such as pseudoephedrine and oxymetazoline. A potential side effect of these medications may prevent the bladder neck from relaxing and releasing urine. Medications that contain antihistamines, such as diphenhydramine, can weaken the contraction of bladder muscles and cause urinary retention, difficulty urinating, and painful urination. When men have partial urethra blockage, urinary retention also can occur as a result of alcohol consumption, cold temperatures, or a long period of inactivity."}
{"_id":"827cba09-2955-462f-a387-01bae2f3900a","text":"The complications of benign prostatic hyperplasia may include\n                \n- acute urinary retention  - chronic, or long lasting, urinary retention  - blood in the urine  - urinary tract infections (UTIs)  - bladder damage  - kidney damage  - bladder stones\n                \nMost men with benign prostatic hyperplasia do not develop these complications. However, kidney damage in particular can be a serious health threat when it occurs.\n                \n\n                \nWhen to Seek Medical Care   A person may have urinary symptoms unrelated to benign prostatic hyperplasia that are caused by bladder problems, UTIs, or prostatitisinflammation of the prostate. Symptoms of benign prostatic hyperplasia also can signal more serious conditions, including prostate cancer.   Men with symptoms of benign prostatic hyperplasia should see a health care provider.   Men with the following symptoms should seek immediate medical care:   - complete inability to urinate   - painful, frequent, and urgent need to urinate, with fever and chills   - blood in the urine   - great discomfort or pain in the lower abdomen and urinary tract"}
{"_id":"89858207-05dc-4dd5-91b0-95e1c5ceb33b","text":"A health care provider diagnoses benign prostatic hyperplasia based on\n                \n- a personal and family medical history  - a physical exam  - medical tests\n                \nPersonal and Family Medical History\n                \nTaking a personal and family medical history is one of the first things a health care provider may do to help diagnose benign prostatic hyperplasia. A health care provider may ask a man\n                \n- what symptoms are present  - when the symptoms began and how often they occur  - whether he has a history of recurrent UTIs  - what medications he takes, both prescription and over the counter  - how much liquid he typically drinks each day  - whether he consumes caffeine and alcohol  - about his general medical history, including any significant illnesses or surgeries\n                \nPhysical Exam\n                \nA physical exam may help diagnose benign prostatic hyperplasia. During a physical exam, a health care provider most often\n                \n- examines a patients body, which can include checking for      - discharge from the urethra    - enlarged or tender lymph nodes in the groin    - a swollen or tender scrotum    - taps on specific areas of the patients body  - performs a digital rectal exam\n                \nA digital rectal exam, or rectal exam, is a physical exam of the prostate. To perform the exam, the health care provider asks the man to bend over a table or lie on his side while holding his knees close to his chest. The health care provider slides a gloved, lubricated finger into the rectum and feels the part of the prostate that lies next to the rectum. The man may feel slight, brief discomfort during the rectal exam. A health care provider most often performs a rectal exam during an office visit, and men do not require anesthesia. The exam helps the health care provider see if the prostate is enlarged or tender or has any abnormalities that require more testing.\n                \nMany health care providers perform a rectal exam as part of a routine physical exam for men age 40 or older, whether or not they have urinary problems.\n                \nMedical Tests\n                \nA health care provider may refer men to a urologista doctor who specializes in urinary problems and the male reproductive systemthough the health care provider most often diagnoses benign prostatic hyperplasia on the basis of symptoms and a digital rectal exam. A urologist uses medical tests to help diagnose lower urinary tract problems related to benign prostatic hyperplasia and recommend treatment. Medical tests may include\n                \n- urinalysis  - a prostate-specific antigen (PSA) blood test  - urodynamic tests  - cystoscopy  - transrectal ultrasound  - biopsy\n                \nUrinalysis. Urinalysis involves testing a urine sample. The patient collects a urine sample in a special container in a health care providers office or a commercial facility. A health care provider tests the sample during an office visit or sends it to a lab for analysis. For the test, a nurse or technician places a strip of chemically treated paper, called a dipstick, into the urine. Patches on the dipstick change color to indicate signs of infection in urine.\n                \nPSA blood test. A health care provider may draw blood for a PSA test during an office visit or in a commercial facility and send the sample to a lab for analysis. Prostate cells create a protein called PSA. Men who have prostate cancer may have a higher amount of PSA in their blood. However, a high PSA level does not necessarily indicate prostate cancer. In fact, benign prostatic hyperplasia, prostate infections, inflammation, aging, and normal fluctuations often cause high PSA levels. Much remains unknown about how to interpret a PSA blood test, the tests ability to discriminate between cancer and prostate conditions such as benign prostatic hyperplasia, and the best course of action to take if the PSA level is high.\n                \nUrodynamic tests. Urodynamic tests include a variety of procedures that look at how well the bladder and urethra store and release urine. A health care provider performs urodynamic tests during an office visit or in an outpatient center or a hospital. Some urodynamic tests do not require anesthesia; others may require local anesthesia. Most urodynamic tests focus on the bladders ability to hold urine and empty steadily and completely and may include the following:\n                \n- uroflowmetry, which measures how rapidly the bladder releases urine  - postvoid residual measurement, which evaluates how much urine remains in the bladder after urination  - reduced urine flow or residual urine in the bladder, which often suggests urine blockage due to benign prostatic hyperplasia\n                \nMore information is provided in the NIDDK health topic, Urodynamic Testing.\n                \nCystoscopy. Cystoscopy is a procedure that uses a tubelike instrument, called a cystoscope, to look inside the urethra and bladder. A urologist inserts the cystoscope through the opening at the tip of the penis and into the lower urinary tract. A urologist performs cystoscopy during an office visit or in an outpatient center or a hospital. The urologist will give the patient local anesthesia; however, in some cases, the patient may require sedation and regional or general anesthesia. A urologist may use cystoscopy to look for blockage or stones in the urinary tract.\n                \nMore information is provided in the NIDDK health topic, Cystoscopy and Ureteroscopy.\n                \nTransrectal ultrasound. Transrectal ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. The health care provider can move the transducer to different angles to make it possible to examine different organs. A specially trained technician performs the procedure in a health care providers office, an outpatient center, or a hospital, and a radiologista doctor who specializes in medical imaginginterprets the images; the patient does not require anesthesia. Urologists most often use transrectal ultrasound to examine the prostate. In a transrectal ultrasound, the technician inserts a transducer slightly larger than a pen into the mans rectum, next to the prostate. The ultrasound image shows the size of the prostate and any abnormalities, such as tumors. Transrectal ultrasound cannot reliably diagnose prostate cancer.\n                \nBiopsy. Biopsy is a procedure that involves taking a small piece of prostate tissue for examination with a microscope. A urologist performs the biopsy in an outpatient center or a hospital. The urologist will give the patient light sedation and local anesthetic; however, in some cases, the patient will require general anesthesia. The urologist uses imaging techniques such as ultrasound, a computerized tomography scan, or magnetic resonance imaging to guide the biopsy needle into the prostate. A pathologista doctor who specializes in examining tissues to diagnose diseasesexamines the prostate tissue in a lab. The test can show whether prostate cancer is present.\n                \nMore information is provided in the NIDDK health topic, Medical Tests for Prostate Problems."}
{"_id":"b96b541b-13e6-40ec-87b2-31ca81c82156","text":"Treatment options for benign prostatic hyperplasia may include\n                \n- lifestyle changes  - medications  - minimally invasive procedures  - surgery\n                \nA health care provider treats benign prostatic hyperplasia based on the severity of symptoms, how much the symptoms affect a mans daily life, and a mans preferences.\n                \nMen may not need treatment for a mildly enlarged prostate unless their symptoms are bothersome and affecting their quality of life. In these cases, instead of treatment, a urologist may recommend regular checkups. If benign prostatic hyperplasia symptoms become bothersome or present a health risk, a urologist most often recommends treatment.\n                \nLifestyle Changes\n                \nA health care provider may recommend lifestyle changes for men whose symptoms are mild or slightly bothersome. Lifestyle changes can include\n                \n- reducing intake of liquids, particularly before going out in public or before periods of sleep  - avoiding or reducing intake of caffeinated beverages and alcohol  - avoiding or monitoring the use of medications such as decongestants, antihistamines, antidepressants, and diuretics  - training the bladder to hold more urine for longer periods  - exercising pelvic floor muscles  - preventing or treating constipation\n                \nMedications\n                \nA health care provider or urologist may prescribe medications that stop the growth of or shrink the prostate or reduce symptoms associated with benign prostatic hyperplasia:\n                \n- alpha blockers  - phosphodiesterase-5 inhibitors  - 5-alpha reductase inhibitors  - combination medications\n                \nAlpha blockers. These medications relax the smooth muscles of the prostate and bladder neck to improve urine flow and reduce bladder blockage:\n                \n- terazosin (Hytrin)  - doxazosin (Cardura)  - tamsulosin (Flomax)  - alfuzosin (Uroxatral)  - silodosin (Rapaflo)\n                \nPhosphodiesterase-5 inhibitors. Urologists prescribe these medications mainly for erectile dysfunction. Tadalafil (Cialis) belongs to this class of medications and can reduce lower urinary tract symptoms by relaxing smooth muscles in the lower urinary tract. Researchers are working to determine the role of erectile dysfunction drugs in the long-term treatment of benign prostatic hyperplasia.\n                \n5-alpha reductase inhibitors. These medications block the production of DHT, which accumulates in the prostate and may cause prostate growth:\n                \n- finasteride (Proscar)  - dutasteride (Avodart)\n                \nThese medications can prevent progression of prostate growth or actually shrink the prostate in some men. Finasteride and dutasteride act more slowly than alpha blockers and are useful for only moderately enlarged prostates.\n                \nCombination medications. Several studies, such as the Medical Therapy of Prostatic Symptoms (MTOPS) study, have shown that combining two classes of medications, instead of using just one, can more effectively improve symptoms, urinary flow, and quality of life. The combinations include\n                \n- finasteride and doxazosin  - dutasteride and tamsulosin (Jalyn), a combination of both medications that is available in a single tablet  - alpha blockers and antimuscarinics\n                \nA urologist may prescribe a combination of alpha blockers and antimuscarinics for patients with overactive bladder symptoms. Overactive bladder is a condition in which the bladder muscles contract uncontrollably and cause urinary frequency, urinary urgency, and urinary incontinence. Antimuscarinics are a class of medications that relax the bladder muscles.\n                \nMinimally Invasive Procedures\n                \nResearchers have developed a number of minimally invasive procedures that relieve benign prostatic hyperplasia symptoms when medications prove ineffective. These procedures include\n                \n- transurethral needle ablation  - transurethral microwave thermotherapy  - high-intensity focused ultrasound  - transurethral electrovaporization  - water-induced thermotherapy  - prostatic stent insertion\n                \nMinimally invasive procedures can destroy enlarged prostate tissue or widen the urethra, which can help relieve blockage and urinary retention caused by benign prostatic hyperplasia.\n                \nUrologists perform minimally invasive procedures using the transurethral method, which involves inserting a cathetera thin, flexible tubeor cystoscope through the urethra to reach the prostate. These procedures may require local, regional, or general anesthesia. Although destroying troublesome prostate tissue relieves many benign prostatic hyperplasia symptoms, tissue destruction does not cure benign prostatic hyperplasia. A urologist will decide which procedure to perform based on the mans symptoms and overall health.\n                \nTransurethral needle ablation. This procedure uses heat generated by radiofrequency energy to destroy prostate tissue. A urologist inserts a cystoscope through the urethra to the prostate. A urologist then inserts small needles through the end of the cystoscope into the prostate. The needles send radiofrequency energy that heats and destroys selected portions of prostate tissue. Shields protect the urethra from heat damage.\n                \nTransurethral microwave thermotherapy. This procedure uses microwaves to destroy prostate tissue. A urologist inserts a catheter through the urethra to the prostate, and a device called an antenna sends microwaves through the catheter to heat selected portions of the prostate. The temperature becomes high enough inside the prostate to destroy enlarged tissue. A cooling system protects the urinary tract from heat damage during the procedure.\n                \nHigh-intensity focused ultrasound. For this procedure, a urologist inserts a special ultrasound probe into the rectum, near the prostate. Ultrasound waves from the probe heat and destroy enlarged prostate tissue.\n                \nTransurethral electrovaporization. For this procedure, a urologist inserts a tubelike instrument called a resectoscope through the urethra to reach the prostate. An electrode attached to the resectoscope moves across the surface of the prostate and transmits an electric current that vaporizes prostate tissue. The vaporizing effect penetrates below the surface area being treated and seals blood vessels, which reduces the risk of bleeding.\n                \nWater-induced thermotherapy. This procedure uses heated water to destroy prostate tissue. A urologist inserts a catheter into the urethra so that a treatment balloon rests in the middle of the prostate. Heated water flows through the catheter into the treatment balloon, which heats and destroys the surrounding prostate tissue. The treatment balloon can target a specific region of the prostate, while surrounding tissues in the urethra and bladder remain protected.\n                \nProstatic stent insertion. This procedure involves a urologist inserting a small device called a prostatic stent through the urethra to the area narrowed by the enlarged prostate. Once in place, the stent expands like a spring, and it pushes back the prostate tissue, widening the urethra. Prostatic stents may be temporary or permanent. Urologists generally use prostatic stents in men who may not tolerate or be suitable for other procedures.\n                \nSurgery\n                \nFor long-term treatment of benign prostatic hyperplasia, a urologist may recommend removing enlarged prostate tissue or making cuts in the prostate to widen the urethra. Urologists recommend surgery when\n                \n- medications and minimally invasive procedures are ineffective  - symptoms are particularly bothersome or severe  - complications arise\n                \nAlthough removing troublesome prostate tissue relieves many benign prostatic hyperplasia symptoms, tissue removal does not cure benign prostatic hyperplasia.\n                \nSurgery to remove enlarged prostate tissue includes\n                \n- transurethral resection of the prostate (TURP)  - laser surgery  - open prostatectomy  - transurethral incision of the prostate (TUIP)\n                \nA urologist performs these surgeries, except for open prostatectomy, using the transurethral method. Men who have these surgical procedures require local, regional, or general anesthesia and may need to stay in the hospital.\n                \nThe urologist may prescribe antibiotics before or soon after surgery to prevent infection. Some urologists prescribe antibiotics only when an infection occurs.\n                \nImmediately after benign prostatic hyperplasia surgery, a urologist may insert a special catheter, called a Foley catheter, through the opening of the penis to drain urine from the bladder into a drainage pouch.\n                \nTURP. With TURP, a urologist inserts a resectoscope through the urethra to reach the prostate and cuts pieces of enlarged prostate tissue with a wire loop. Special fluid carries the tissue pieces into the bladder, and the urologist flushes them out at the end of the procedure. TURP is the most common surgery for benign prostatic hyperplasia and considered the gold standard for treating blockage of the urethra due to benign prostatic hyperplasia.\n                \nLaser surgery. With this surgery, a urologist uses a high-energy laser to destroy prostate tissue. The urologist uses a cystoscope to pass a laser fiber through the urethra into the prostate. The laser destroys the enlarged tissue. The risk of bleeding is lower than in TURP and TUIP because the laser seals blood vessels as it cuts through the prostate tissue. However, laser surgery may not effectively treat greatly enlarged prostates.\n                \nOpen prostatectomy. In an open prostatectomy, a urologist makes an incision, or cut, through the skin to reach the prostate. The urologist can remove all or part of the prostate through the incision. This surgery is used most often when the prostate is greatly enlarged, complications occur, or the bladder is damaged and needs repair. Open prostatectomy requires general anesthesia, a longer hospital stay than other surgical procedures for benign prostatic hyperplasia, and a longer rehabilitation period. The three open prostatectomy procedures are retropubic prostatectomy, suprapubic prostatectomy, and perineal prostatectomy. The recovery period for open prostatectomy is different for each man who undergoes the procedure. However, it typically takes anywhere from 3 to 6 weeks.4\n                \nTUIP. A TUIP is a surgical procedure to widen the urethra. During a TUIP, the urologist inserts a cystoscope and an instrument that uses an electric current or a laser beam through the urethra to reach the prostate. The urologist widens the urethra by making a few small cuts in the prostate and in the bladder neck. Some urologists believe that TUIP gives the same relief as TURP except with less risk of side effects.\n                \nAfter surgery, the prostate, urethra, and surrounding tissues may be irritated and swollen, causing urinary retention. To prevent urinary retention, a urologist inserts a Foley catheter so urine can drain freely out of the bladder. A Foley catheter has a balloon on the end that the urologist inserts into the bladder. Once the balloon is inside the bladder, the urologist fills it with sterile water to keep the catheter in place. Men who undergo minimally invasive procedures may not need a Foley catheter.\n                \nThe Foley catheter most often remains in place for several days. Sometimes, the Foley catheter causes recurring, painful, difficult-to-control bladder spasms the day after surgery. However, these spasms will eventually stop. A urologist may prescribe medications to relax bladder muscles and prevent bladder spasms. These medications include\n                \n- oxybutynin chloride (Ditropan)  - solifenacin (VESIcare)  - darifenacin (Enablex)  - tolterodine (Detrol)  - hyoscyamine (Levsin)  - propantheline bromide (Pro-Banthine)"}
{"_id":"390be0db-76de-4a3e-9a28-4e2a07cda205","text":"The complications of benign prostatic hyperplasia treatment depend on the type of treatment.\n                \nMedications\n                \nMedications used to treat benign prostatic hyperplasia may have side effects that sometimes can be serious. Men who are prescribed medications to treat benign prostatic hyperplasia should discuss possible side effects with a health care provider before taking the medications. Men who experience the following side effects should contact a health care provider right away or get emergency medical care:\n                \n- hives  - rash  - itching  - shortness of breath  - rapid, pounding, or irregular heartbeat  - painful erection of the penis that lasts for hours  - swelling of the eyes, face, tongue, lips, throat, arms, hands, feet, ankles, or lower legs  - difficulty breathing or swallowing  - chest pain  - dizziness or fainting when standing up suddenly  - sudden decrease or loss of vision  - blurred vision  - sudden decrease or loss of hearing  - chest pain, dizziness, or nausea during sexual activity\n                \nThese side effects are mostly related to phosphodiesterase-5 inhibitors. Side effects related to alpha blockers include\n                \n- dizziness or fainting when standing up suddenly  - decreased sexual drive  - problems with ejaculation\n                \nMinimally Invasive Procedures\n                \nComplications after minimally invasive procedures may include\n                \n- UTIs  - painful urination  - difficulty urinating  - an urgent or a frequent need to urinate  - urinary incontinence  - blood in the urine for several days after the procedure  - sexual dysfunction  - chronic prostatitislong-lasting inflammation of the prostate  - recurring problems such as urinary retention and UTIs\n                \nMost of the complications of minimally invasive procedures go away within a few days or weeks. Minimally invasive procedures are less likely to have complications than surgery.\n                \nSurgery\n                \nComplications after surgery may include\n                \n- problems urinating  - urinary incontinence  - bleeding and blood clots  - infection  - scar tissue  - sexual dysfunction  - recurring problems such as urinary retention and UTIs\n                \nProblems urinating. Men may initially have painful urination or difficulty urinating. They may experience urinary frequency, urgency, or retention. These problems will gradually lessen and, after a couple of months, urination will be easier and less frequent.\n                \nUrinary incontinence. As the bladder returns to normal, men may have some temporary problems controlling urination. However, long-term urinary incontinence rarely occurs. The longer urinary problems existed before surgery, the longer it takes for the bladder to regain its full function after surgery.\n                \nBleeding and blood clots. After benign prostatic hyperplasia surgery, the prostate or tissues around it may bleed. Blood or blood clots may appear in urine. Some bleeding is normal and should clear up within several days. However, men should contact a health care provider right away if\n                \n- they experience pain or discomfort  - their urine contains large clots  - their urine is so red it is difficult to see through\n                \nBlood clots from benign prostatic hyperplasia surgery can pass into the bloodstream and lodge in other parts of the bodymost often the legs. Men should contact a health care provider right away if they experience swelling or discomfort in their legs.\n                \nInfection. Use of a Foley catheter after benign prostatic hyperplasia surgery may increase the risk of a UTI. Anesthesia during surgery may cause urinary retention and also increase the risk of a UTI. In addition, the incision site of an open prostatectomy may become infected. A health care provider will prescribe antibiotics to treat infections.\n                \nScar tissue. In the year after the original surgery, scar tissue sometimes forms and requires surgical treatment. Scar tissue may form in the urethra and cause it to narrow. A urologist can solve this problem during an office visit by stretching the urethra. Rarely, the opening of the bladder becomes scarred and shrinks, causing blockage. This problem may require a surgical procedure similar to TUIP.\n                \nSexual dysfunction. Some men may experience temporary problems with sexual function after benign prostatic hyperplasia surgery. The length of time for restored sexual function depends on the type of benign prostatic hyperplasia surgery performed and how long symptoms were present before surgery. Many men have found that concerns about sexual function can interfere with sex as much as the benign prostatic hyperplasia surgery itself. Understanding the surgical procedure and talking about concerns with a health care provider before surgery often help men regain sexual function earlier. Many men find it helpful to talk with a counselor during the adjustment period after surgery. Even though it can take a while for sexual function to fully return, with time, most men can enjoy sex again.\n                \nMost health care providers agree that if men with benign prostatic hyperplasia were able to maintain an erection before surgery, they will probably be able to have erections afterward. Surgery rarely causes a loss of erectile function. However, benign prostatic hyperplasia surgery most often cannot restore function that was lost before the procedure. Some men find a slight difference in the quality of orgasm after surgery. However, most report no difference.\n                \nProstate surgery may make men sterile, or unable to father children, by causing retrograde ejaculationthe backward flow of semen into the bladder. Men flush the semen out of the bladder when they urinate. In some cases, medications such as pseudoephedrine, found in many cold medications, or imipramine can treat retrograde ejaculation. These medications improve muscle tone at the bladder neck and keep semen from entering the bladder.\n                \nRecurring problems. Men may require further treatment if prostate problems, including benign prostatic hyperplasia, return. Problems may arise when treatments for benign prostatic hyperplasia leave a good part of the prostate intact. About 10 percent of men treated with TURP or TUIP require additional surgery within 5 years. About 2 percent of men who have an open prostatectomy require additional surgery within 5 years.2\n                \nIn the years after benign prostatic hyperplasia surgery or treatment, men should continue having a digital rectal exam once a year and have any symptoms checked by a health care provider. In some cases, the health care provider may recommend a digital rectal exam and checkup more than once a year."}
{"_id":"6d42aee6-ecff-4bd1-8e3b-30b23f83852c","text":"Researchers have not found a way to prevent benign prostatic hyperplasia. Men with risk factors for benign prostatic hyperplasia should talk with a health care provider about any lower urinary tract symptoms and the need for regular prostate exams. Men can get early treatment and minimize benign prostatic hyperplasia effects by recognizing lower urinary tract symptoms and identifying an enlarged prostate."}
{"_id":"fe275f23-6650-45ca-9fc5-d03d5a03c81d","text":"Researchers have not found that eating, diet, and nutrition play a role in causing or preventing benign prostatic hyperplasia. However, a health care provider can give information about how changes in eating, diet, or nutrition could help with treatment. Men should talk with a health care provider or dietitian about what diet is right for them."}
{"_id":"5bc3b8eb-fe26-499a-8b57-0d1f83019052","text":"- Benign prostatic hyperplasiaalso called BPHis a condition in men in which the prostate gland is enlarged and not cancerous.  - The prostate is a walnut-shaped gland that is part of the male reproductive system.  - The cause of benign prostatic hyperplasia is not well understood; however, it occurs mainly in older men.  - Benign prostatic hyperplasia is the most common prostate problem for men older than age 50.  - Lower urinary tract symptoms suggestive of benign prostatic hyperplasia may include      - urinary frequencyurination eight or more times a day    - urinary urgencythe inability to delay urination    - trouble starting a urine stream    - a weak or an interrupted urine stream    - dribbling at the end of urination    - nocturiafrequent urination during periods of sleep    - urinary retentionthe inability to empty the bladder completely    - urinary incontinencethe accidental loss of urine    - pain after ejaculation or during urination    - urine that has an unusual color or smell    - The complications of benign prostatic hyperplasia may include      - acute urinary retention    - chronic, or long lasting, urinary retention    - blood in the urine    - urinary tract infections (UTIs)    - bladder damage    - kidney damage    - bladder stones    - A health care provider diagnoses benign prostatic hyperplasia based on      - a personal and family medical history    - a physical exam    - medical tests    - Treatment options for benign prostatic hyperplasia may include      - lifestyle changes    - medications    - minimally invasive procedures    - surgery    - The complications of benign prostatic hyperplasia treatment depend on the type of treatment.  - Researchers have not found a way to prevent benign prostatic hyperplasia.  - Researchers have not found that eating, diet, and nutrition play a role in causing or preventing benign prostatic hyperplasia."}
{"_id":"143cf2cf-2917-470f-90fc-8a5373fcac4d","text":"A UTI is an infection in the urinary tract. Infections are caused by microbesorganisms too small to be seen without a microscope. Bacteria * are the most common cause of UTIs. Normally, bacteria that enter the urinary tract are quickly removed by the body before they cause symptoms. But sometimes bacteria overcome the bodys natural defenses and cause infection.\n                \n*See the Pronunciation Guide for tips on how to say the underlined words."}
{"_id":"f233d5c0-b529-4038-9a93-71088aa4efb6","text":"Most UTIs are caused by bacteria that live in the bowel, the part of the digestive tract where stool is changed from liquid to solid. The bacterium Escherichia coli (E. coli) causes most UTIs. The urinary tract has several systems to prevent infection. The points where the ureters attach to the bladder act like one-way valves to prevent urine from backing up, or refluxing, toward the kidneys, and urination washes microbes out of the body. The bodys natural defenses also prevent infection. But despite these safeguards, infections still occur.\n                \nOther factors that may cause a child to get a UTI include the following:\n                \n- Waiting to urinate. Regular urination helps flush away bacteria. Holding urine allows bacteria to grow.  - Making too little urine. A child that doesnt drink enough fluids may not make enough urine to flush away bacteria.  - Constipation. Constipation is a condition in which a child has fewer than two bowel movements a week. Stools can be hard, dry, small, and difficult to pass. The hard stool in the bowel may press against the urinary tract and block the flow of urine, allowing bacteria to grow.\n                \nSome children are just more prone to UTIs than others, just as some children are more prone to getting coughs, colds, or ear infections."}
{"_id":"d328b0b4-71b5-495a-b0ac-c11fe910cfba","text":"Any child can get a UTI, though girls get UTIs more often than boys.\n                \nChildren with a condition called vesicoureteral reflux (VUR) are at higher risk for UTIs. VUR causes urine to reflux at the point where one or both ureters attach to the bladder. When urine stays in the urinary tract, bacteria have a chance to grow and spread. Infants and young children who get a UTI often have VUR.\n                \nBoys younger than 6 months who are not circumcised are at greater risk for a UTI than circumcised boys the same age. Boys who are circumcised have had the foreskin, which is the skin that covers the tip of the penis, removed."}
{"_id":"9458ee0c-fb15-45df-b8a2-f8e6235a5c90","text":"A child with a UTI may not have any symptoms. When symptoms are present, they can range from mild to severe. UTI symptoms can include\n                \n- fever  - pain or burning during urination with only a few drops of urine at a time  - irritability  - not eating  - nausea  - diarrhea  - vomiting  - cloudy, dark, bloody, or foul-smelling urine  - urinating often  - pain in the back or side below the ribs  - leaking urine into clothes or bedding in older children"}
{"_id":"372a30f0-f187-4d02-8793-51c317b01163","text":"A UTI is diagnosed by testing a sample of your childs urine. The way the urine is collected depends on your childs age:\n                \nThe health care provider looks at the urine sample with a microscope to check for bacteria or pus. The sample is also sent to a lab. The lab performs a urine culture by placing the sample in a tube or dish with a substance that encourages any bacteria present to grow. The bacteria that grow can be identified and tested to see which medicines will work best to treat the infection. A urine culture usually takes 1 to 3 days to complete."}
{"_id":"a06b638b-6d40-4101-888c-de0b50f452f1","text":"Bacteria-fighting medicines called antibiotics are used to treat a UTI. While the lab is doing the urine culture, the health care provider may begin treatment with an antibiotic that treats the bacteria most likely to be causing the infection. Once culture results are known, the health care provider may switch your child to a different antibiotic that targets the specific type of bacteria.\n                \nYour child will need to take antibiotics for at least 3 to 5 days and maybe as long as several weeks. Be sure your child takes every pill or every dose of liquid. Your child should feel better after a couple of days, but the infection might come back if your child stops taking the antibiotic too early.\n                \nYou should let your child drink as much as your child wants. But dont force your child to drink large amounts of fluid. Call your childs health care provider if your child doesnt want to or isnt able to drink. Also, talk with your childs health care provider if your child needs medicine for the pain of a UTI. The health care provider can recommend an over-the-counter pain medicine. A heating pad on the back or abdomen may also help."}
{"_id":"b3266943-b944-41be-b169-b69bc725c02b","text":"Talk with your childs health care provider after your childs UTI is gone. The health care provider may want to do more tests to check for VUR or a blockage in the urinary tract. Repeated infections in an abnormal urinary tract may cause kidney damage. The kinds of tests ordered will depend on the child and the type of infection. VUR and blockages in the urinary tract often go away as a child grows. In some cases, surgery may be needed to correct any defects in the urinary tract. More information about tests for VUR or a blockage in the urinary tract is provided in the NIDDK health topic, Urinary Tract Infections in Children."}
{"_id":"c28be4f0-1695-4a6e-aad1-56b45fa5d81c","text":"You can take the following steps to help prevent your child from getting a UTI:\n                \n- Teach your child not to hold in urine and to go to the bathroom whenever your child feels the urge.  - Teach your child how to properly clean himself or herself after using the bathroom to keep bacteria from entering the urinary tract.  - Have your child wear loose-fitting clothes. Tight clothes can trap moisture, which allows bacteria to grow.  - Buy your child cotton underwear. Cotton lets in air to dry the area.  - If your child has constipation, talk with a health care provider about the best treatment options."}
{"_id":"dbd76caa-0602-42da-890b-d91d5c6e6b20","text":"To help prevent a UTI, make sure your child drinks enough fluids each day. Talk with your childs health care provider to find out how much fluid your child should drink."}
{"_id":"846741d8-bd3c-4034-bb5c-18af5bf74e85","text":"- A urinary tract infection (UTI) is an infection in the urinary tract. Infections are caused by microbesorganisms too small to be seen without a microscope.  - Most UTIs are caused by bacteria that live in the bowel, the part of the digestive tract where stool is changed from liquid to solid.  - Any child can get a UTI, though girls get UTIs more often than boys.  - Most UTIs are not serious, but some infections can lead to serious problems.  - A child with a UTI may not have any symptoms. When symptoms are present, they can range from mild to severe.  - A UTI is diagnosed by testing a sample of your childs urine.  - Bacteria-fighting medicines called antibiotics are used to treat a UTI.  - Talk with your childs health care provider after your childs UTI is gone. The health care provider may want to do more tests to check for vesicoureteral reflux (VUR) or a blockage in the urinary tract.  - You can take steps to help prevent your child from getting a UTI."}
{"_id":"5c0f194b-cc78-443d-9d99-4a54058d500d","text":"Primary biliary cirrhosis is a chronic, or long lasting, disease that causes the small bile ducts in the liver to become inflamed and damaged and ultimately disappear.\n                \nThe bile ducts carry a fluid called bile from the liver to the gallbladder, where it is stored. When food enters the stomach after a meal, the gallbladder contracts, and the bile ducts carry bile to the duodenum, the first part of the small intestine, for use in digestion. The liver makes bile, which is made up of bile acids, cholesterol, fats, and fluids. Bile helps the body absorb fats, cholesterol, and fat-soluble vitamins. Bile also carries cholesterol, toxins, and waste products to the intestines, where the body removes them. When chronic inflammation, or swelling, damages the bile ducts, bile and toxic wastes build up in the liver, damaging liver tissue.\n                \nThis damage to the liver tissue can lead to cirrhosis, a condition in which the liver slowly deteriorates and is unable to function normally. In cirrhosis, scar tissue replaces healthy liver tissue, partially blocking the flow of blood through the liver.\n                \nThe liver is the bodys largest internal organ. The liver is called the bodys metabolic factory because of the important role it plays in metabolismthe way cells change food into energy after food is digested and absorbed into the blood. The liver has many functions, including\n                \n- taking up, storing, and processing nutrients from foodincluding fat, sugar, and proteinand delivering them to the rest of the body when needed  - making new proteins, such as clotting factors and immune factors  - producing bile  - removing waste products the kidneys cannot remove, such as fats, cholesterol, toxins, and medications\n                \nA healthy liver is necessary for survival. The liver can regenerate most of its own cells when they become damaged. However, if injury to the liver is too severe or long lasting, regeneration is incomplete, and the liver creates scar tissue. Scarring of the liver may lead to cirrhosis.\n                \nThe buildup of scar tissue that causes cirrhosis is usually a slow and gradual process. In the early stages of cirrhosis, the liver continues to function. However, as cirrhosis gets worse and scar tissue replaces more healthy tissue, the liver will begin to fail. Chronic liver failure, which is also called end-stage liver disease, progresses over months, years, or even decades. With end-stage liver disease, the liver can no longer perform important functions or effectively replace damaged cells.\n                \nPrimary biliary cirrhosis usually occurs between the ages of 30 and 65 and affects women more often than men.1"}
{"_id":"28c89bc0-bb57-40b4-a4ad-e4dc9c068a72","text":"The causes of primary biliary cirrhosis are unknown. Most research suggests it is an autoimmune disease. The immune system protects people from infection by identifying and destroying bacteria, viruses, and other potentially harmful foreign substances. An autoimmune disease is a disorder in which the bodys immune system attacks the bodys own cells and organs. In primary biliary cirrhosis, the immune system attacks the small bile ducts in the liver.\n                \nGenetics, or inherited genes, can make a person more likely to develop primary biliary cirrhosis. Primary biliary cirrhosis is more common in people who have a parent or siblingparticularly an identical twinwith the disease. In people who are genetically more likely to develop primary biliary cirrhosis, environmental factors may trigger or worsen the disease, including\n                \n- exposure to toxic chemicals  - smoking  - infections\n                \nGenetics can also make some people more likely to develop other autoimmune diseases, such as\n                \n- autoimmune hepatitis, a disease in which the bodys immune system attacks liver cells  - Sjgrens syndrome, a condition in which the immune system attacks the glands that produce tears and saliva  - autoimmune thyroid dysfunctions, conditions in which the immune system attacks the thyroid gland"}
{"_id":"191507b0-a859-45b3-b47f-d899856e471f","text":"The first and most common symptoms of primary biliary cirrhosis are\n                \n- fatigue, or feeling tired  - itching skin, and darkened skin in itching areas due to scratching  - dry eyes and mouth\n                \nSome people may have jaundice, a condition that causes the skin and whites of the eyes to turn yellow. Health care providers diagnose up to 60 percent of people with primary biliary cirrhosis before symptoms begin.2 Routine blood tests showing abnormal liver enzyme levels may lead a health care provider to suspect that a person without symptoms has primary biliary cirrhosis."}
{"_id":"9d72790b-8dcc-49a8-bde6-7524ba6a5de8","text":"Most complications of primary biliary cirrhosis are related to cirrhosis and start after primary biliary cirrhosis progresses to cirrhosis. In some cases, portal hypertension and esophageal varices may develop before cirrhosis.\n                \nPortal hypertension. The portal vein carries blood from the stomach, intestines, spleen, gallbladder, and pancreas to the liver. In cirrhosis, scar tissue partially blocks the normal flow of blood, which increases the pressure in the portal vein. This condition is called portal hypertension. Portal hypertension is a common complication of cirrhosis. This condition may lead to other complications, such as\n                \n- edemaswelling due to a buildup of fluidin the feet, ankles, or legs, and ascitesa buildup of fluid in the abdomen  - enlarged blood vessels, called varices, in the esophagus, stomach, or both  - an enlarged spleen, called splenomegaly  - mental confusion due to a buildup of toxins that are ordinarily removed by the liver, a condition called hepatic encephalopathy\n                \nEdema and ascites. Liver failure causes fluid buildup that results in edema and ascites. Ascites can lead to spontaneous bacterial peritonitis, a serious infection that requires immediate medical attention.\n                \nVarices. Portal hypertension may cause enlarged blood vessels in the esophagus, stomach, or both. These enlarged blood vessels, called esophageal or gastric varices, cause the vessel walls to become thin and blood pressure to increase, making the blood vessels more likely to burst. If they burst, serious bleeding can occur in the esophagus or upper stomach, requiring immediate medical attention.\n                \nSplenomegaly. Portal hypertension may cause the spleen to enlarge and retain white blood cells and platelets, reducing the numbers of these cells and platelets in the blood. A low platelet count may be the first evidence that a person has developed cirrhosis.\n                \nHepatic encephalopathy. A failing liver cannot remove toxins from the blood, so they eventually accumulate in the brain. The buildup of toxins in the brain is called hepatic encephalopathy. This condition can decrease mental function and cause stupor and even coma. Stupor is an unconscious, sleeplike state from which a person can only be aroused briefly by a strong stimulus, such as a sharp pain. Coma is an unconscious, sleeplike state from which a person cannot be aroused. Signs of decreased mental function include\n                \n- confusion  - personality changes  - memory loss  - trouble concentrating  - a change in sleep habits\n                \nMetabolic bone diseases. Some people with cirrhosis develop a metabolic bone disease, which is a disorder of bone strength usually caused by abnormalities of vitamin D, bone mass, bone structure, or minerals, such as calcium and phosphorous. Osteopenia is a condition in which the bones become less dense, making them weaker. When bone loss becomes more severe, the condition is referred to as osteoporosis. People with these conditions are more likely to develop bone fractures.\n                \nGallstones and bile duct stones. If cirrhosis prevents bile from flowing freely to and from the gallbladder, the bile hardens into gallstones. Symptoms of gallstones include abdominal pain and recurrent bacterial cholangitisirritated or infected bile ducts. Stones may also form in and block the bile ducts, causing pain, jaundice, and bacterial cholangitis.\n                \nSteatorrhea. Steatorrhea is a condition in which the body cannot absorb fat, causing a buildup of fat in the stool and loose, greasy, and foul-smelling bowel movements. Steatorrhea may be caused by impairment of bile delivery to the small intestine or by the pancreas not producing enough digestive enzymes.\n                \nLiver cancer. Liver cancer is common in people with cirrhosis. Liver cancer has a high mortality rate. Current treatments are limited and only fully successful if a health care provider detects the cancer early, before the tumor is too large. For this reason, health care providers should check people with cirrhosis for signs of liver cancer every 6 to 12 months. Health care providers use blood tests, ultrasound, or both to check for signs of liver cancer."}
{"_id":"abf55d06-fdf6-4d0c-942d-fce67259d405","text":"A health care provider may use the following tests to diagnose primary biliary cirrhosis:\n                \n- a medical and family history  - a physical exam  - blood tests  - imaging tests  - a liver biopsy\n                \nA health care provider usually bases a diagnosis of primary biliary cirrhosis on two out of three of the following criteria:\n                \n- a blood test showing elevated liver enzymes  - a blood test showing the presence of anti-mitochondrial antibodies (AMA)  - a liver biopsy showing signs of the disease\n                \nHealth care providers may order additional tests to rule out other causes of symptoms. Health care providers diagnose the majority of people with primary biliary cirrhosis early in the course of the disease.\n                \nMedical and family history. Taking a medical and family history is one of the first things a health care provider may do to help diagnose primary biliary cirrhosis. He or she will ask a patient to provide a medical and family history.\n                \nPhysical exam. A physical exam may help diagnose primary biliary cirrhosis. During a physical exam, a health care provider usually\n                \n- examines a patients body  - uses a stethoscope to listen to sounds in the abdomen  - taps on specific areas of the patients body\n                \nThe health care provider will perform a physical exam to look for signs of the disease. For example, the liver may feel hard or ascites may cause the abdomen to enlarge.\n                \nBlood test. A blood test involves drawing blood at a health care providers office or a commercial facility and sending the sample to a lab for analysis. The blood test can show elevated levels of liver enzymes, such as alkaline phosphatase. A routine blood test may show high levels of the liver enzyme alkaline phosphatase in people who have primary biliary cirrhosis and are not yet showing symptoms.\n                \nThe health care provider will perform an AMA blood test to help confirm the diagnosis. A blood test will detect the presence of AMA in 90 to 95 percent of people with primary biliary cirrhosis.3\n                \nImaging tests. A health care provider may use the following imaging tests to examine the bile ducts. These tests can distinguish between primary biliary cirrhosis and other conditions that affect the bile ducts.\n                \n- Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. A specially trained technician performs the procedure in a health care providers office, an outpatient center, or a hospital, and a radiologista doctor who specializes in medical imaging interprets the images. A patient does not need anesthesia. In addition to showing problems with the bile ducts, the images can show signs of advanced cirrhosis or complications.  - Magnetic resonance cholangiopancreatography uses magnetic resonance imaging (MRI) to examine the bile ducts. MRI machines use radio waves and magnets to produce detailed pictures of the bodys internal organs and soft tissues without using x rays. A specially trained technician performs magnetic resonance cholangiopancreatography in an outpatient center or a hospital, and a radiologist interprets the images. A patient does not need anesthesia, though a health care provider may use light sedation for patients with a fear of confined spaces. With most MRI machines, the patient lies on a table that slides into a tunnel-shaped device that may be open ended or closed at one end; some machines allow the patient to lie in a more open space.  - Endoscopic retrograde cholangiopancreatography uses an x ray to look at the bile ducts. A gastroenterologista doctor who specializes in digestive diseasesperforms the test at a hospital or an outpatient center. After lightly sedating the patient, the gastroenterologist inserts an endoscopea small, flexible tube with a light and a camera on the endthrough the mouth into the duodenum and bile ducts. The endoscope is connected to a computer and video monitor. The gastroenterologist injects a special dye, called contrast medium, through the tube into the bile ducts, which makes the ducts show up on the monitor. This test is more invasive than other imaging tests, and health care providers do not routinely need the test to make the diagnosis of primary biliary cirrhosis. A health care provider uses the test selectively when he or she is concerned that the blockage of the bile ducts has another cause, such as a gallstone or a narrowing of the large bile ducts due to inflammation or cancer. Patients may have pain, nausea, or vomiting after the test or may develop bacterial cholangitis or pancreatitisinflammation of the pancreas.\n                \nLiver biopsy. A liver biopsy is a procedure that involves taking a piece of liver tissue for examination with a microscope for signs of damage or disease. The health care provider may ask the patient to stop taking certain medications temporarily before the liver biopsy. The health care provider may ask the patient to fast for 8 hours before the procedure.\n                \nDuring the procedure, the patient lies on a table, right hand resting above the head. The health care provider applies a local anesthetic to the area where he or she will insert the biopsy needle. If needed, a health care provider will also give sedatives and pain medication. The health care provider uses a needle to take a small piece of liver tissue. He or she may use ultrasound, computerized tomography scans, or other imaging techniques to guide the needle. After the biopsy, the patient must lie on the right side for up to 2 hours and is monitored an additional 2 to 4 hours before being sent home.\n                \nA health care provider performs a liver biopsy at a hospital or an outpatient center. The health care provider sends the liver sample to a pathology lab, where the pathologista doctor who specializes in diagnosing diseaseslooks at the tissue with a microscope and sends a report to the patients health care provider.\n                \nA liver biopsy can confirm the diagnosis of primary biliary cirrhosis; however, a person does not always need this test. A health care provider will perform a biopsy if the AMA blood test is negative and the person shows other signs of primary biliary cirrhosis. Sometimes a health care provider finds a cause of liver damage other than primary biliary cirrhosis during biopsy."}
{"_id":"c4e74369-2071-4db7-9980-7d8c6482e4f7","text":"Treatment for primary biliary cirrhosis depends on how early a health care provider diagnoses the disease and whether complications are present. In the early stages of primary biliary cirrhosis, treatment can slow the progression of liver damage to cirrhosis. In the early stages of cirrhosis, the goals of treatment are to slow the progression of tissue scarring in the liver and prevent complications. As cirrhosis progresses, a person may need additional treatments and hospitalization to manage complications.\n                \nMedications\n                \nHealth care providers prescribe ursodiol (Actigall, Urso) to treat primary biliary cirrhosis. Ursodiol is a nontoxic bile acid that people can take orally. Ursodiol replaces the bile acids that are normally produced by the liver, which are more toxic and can harm the liver. Treatment with ursodiol can reduce levels of bilirubin and liver enzymes in the blood. Early treatment with this medication reduces the likelihood of needing a liver transplant and improves survival.3 Early treatment provides the most benefit; however, ursodiol treatment late in the course of the disease can still slow the progression of liver damage. While ursodiol treatment improves the outcome of primary biliary cirrhosis, it does not cure the disease.\n                \nResearchers are studying the effects of several other medications on the progression of primary biliary cirrhosis. To date, none has shown the positive effects of ursodiol.\n                \nAvoiding Alcohol and Other Substances\n                \nPeople with cirrhosis should not drink any alcohol or take any illegal substances, as both will cause more liver damage. People with cirrhosis should avoid complementary and alternative medications, such as herbs. People with cirrhosis should be careful about starting new medications and should consult a health care provider before taking prescription medications, over-the-counter medications, or vitamins. Many vitamins and prescription and over-the-counter medications can affect liver function.\n                \nTreatment of Symptoms and Complications\n                \nHealth care providers treat symptoms and complications as follows:\n                \nItching. Antihistamines may help with mild itching. However, antihistamines often cause drowsiness, and a person should take antihistamines just before bedtime to help with nighttime itching. A health care provider will treat more problematic itching with cholestyramine (Locholest, Questran), which reduces cholesterol in the blood. Experts believe high levels of cholesterol let substances that cause itching build up in tissues.\n                \nDry eyes and mouth. Health care providers usually treat dry eyes and mouth with artificial tears and saliva substitutes, respectively. These products are available without a prescription. A health care provider may treat people whose symptoms do not improve with pilocarpine (Salagen) or cevimeline (Evoxac). People who have difficulty with dry eyes should see an ophthalmologista doctor who diagnoses and treats all eye diseases and eye disordersregularly. People with dry mouth should have regular dental exams.\n                \nPortal hypertension. A health care provider may prescribe a beta-blocker or nitrate to treat portal hypertension. Beta-blockers lower blood pressure by helping the heart beat slower and with less force, and nitrates relax and widen blood vessels to let more blood flow to the heart and reduce the hearts workload.\n                \nVarices. Beta-blockers can lower the pressure in varices and reduce the likelihood of bleeding. Bleeding in the stomach or esophagus requires an immediate upper endoscopy. This procedure involves using an endoscope to look for varices. The health care provider may use the endoscope to perform a band ligation, a procedure that involves placing a special rubber band around the varices that causes the tissue to die and fall off. A gastroenterologist performs the procedure at a hospital or an outpatient center. People who have had varices in the past may need to take medication to prevent future episodes.\n                \nEdema and ascites. Health care providers prescribe diureticsmedications that remove fluid from the bodyto treat edema and ascites. A health care provider may remove large amounts of ascitic fluid from the abdomen and check for spontaneous bacterial peritonitis. A health care provider may prescribe bacteria-fighting medications called antibiotics to prevent infection. He or she may prescribe oral antibiotics; however, severe infection with ascites requires intravenous (IV) antibiotics.\n                \nHepatic encephalopathy. A health care provider will treat hepatic encephalopathy by cleansing the bowel with lactulose, a laxative given orally or as an enemaa liquid put into the rectum. A health care provider may also add antibiotics to the treatment. Hepatic encephalopathy may improve as other complications of cirrhosis are controlled.\n                \nOsteoporosis. A health care provider may prescribe bisphosphonate medications to improve bone density.\n                \nGallstones and bile duct stones. A health care provider may use surgery to remove gallstones. He or she may use endoscopic retrograde cholangiopancreatography, which uses balloons and basketlike devices, to retrieve the bile duct stones.\n                \nLiver cancer. A health care provider may recommend screening tests every 6 to 12 months to check for signs of liver cancer. Screening tests can find cancer before the person has symptoms of the disease. Cancer treatment is usually more effective when the health care provider finds the disease early. Health care providers use blood tests, ultrasound, or both to screen for liver cancer in people with cirrhosis. He or she may treat cancer with a combination of surgery, radiation, and chemotherapy."}
{"_id":"e12f35d0-4cb6-4ae3-9709-7da81d470098","text":"A healthy diet is important in all stages of cirrhosis because malnutrition is common in people with this disease. Malnutrition is a condition that occurs when the body does not get enough nutrients. Cirrhosis may lead to malnutrition because it can cause\n                \n- people to eat less because of symptoms such as loss of appetite  - changes in metabolism  - reduced absorption of vitamins and minerals\n                \nHealth care providers can recommend a meal plan that is well balanced and provides enough calories and protein. If ascites develops, a health care provider or dietitian may recommend a sodium-restricted diet. To improve nutrition, the health care provider may prescribe a liquid supplement. A person may take the liquid by mouth or through a nasogastric tubea tiny tube inserted through the nose and throat that reaches into the stomach.\n                \nA person with cirrhosis should not eat raw shellfish, which can contain a bacterium that causes serious infection. Cirrhosis affects the immune system, making people with cirrhosis more likely than healthy people to develop an infection after eating shellfish that contain this bacterium.\n                \nA health care provider may recommend calcium and vitamin D supplements to help prevent osteoporosis."}
{"_id":"c86140d3-e074-4789-8922-90ed1747e3c7","text":"- Primary biliary cirrhosis is a chronic disease that causes the small bile ducts in the liver to become inflamed and damaged and ultimately disappear.  - When chronic inflammation damages the bile ducts, bile and toxic wastes build up in the liver, damaging liver tissue. This damage to the liver tissue can lead to cirrhosis.  - The causes of primary biliary cirrhosis are unknown. Most research suggests it is an autoimmune disease.  - Primary biliary cirrhosis is more common in people who have a parent or siblingparticularly an identical twinwith the disease.  - The first and most common symptoms of primary biliary cirrhosis are fatigue, itching, and dry eyes and mouth. Some people may have jaundice, a condition that causes the skin and whites of the eyes to turn yellow. Health care providers diagnose up to 60 percent of people with primary biliary cirrhosis before symptoms begin.  - Most complications of primary biliary cirrhosis are related to cirrhosis and start after primary biliary cirrhosis progresses to cirrhosis.  - A health care provider may use the following tests to diagnose primary biliary cirrhosis:      - a medical and family history    - a physical exam    - blood tests    - imaging tests    - a liver biopsy    - Health care providers prescribe ursodiol (Actigall, Urso) to treat primary biliary cirrhosis. Early treatment with this medication reduces the likelihood of needing a liver transplant and improves survival.  - A health care provider may consider a liver transplant when cirrhosis leads to liver failure or treatment for complications is ineffective."}
{"_id":"e09fc148-7f98-4cde-aabd-4f9f468c0c09","text":"People with diabetes should be screened regularly for kidney disease. The two key markers for kidney disease are eGFR and urine albumin.\n                \n-  eGFR. eGFR stands for estimated glomerular filtration rate. Each kidney contains about 1 million tiny filters made up of blood vessels. These filters are called glomeruli. Kidney function can be checked by estimating how much blood the glomeruli filter in a minute. The calculation of eGFR is based on the amount of creatinine, a waste product, found in a blood sample. As the level of creatinine goes up, the eGFR goes down.  Kidney disease is present when eGFR is less than 60 milliliters per minute.  The American Diabetes Association (ADA) and the National Institutes of Health (NIH) recommend that eGFR be calculated from serum creatinine at least once a year in all people with diabetes.  -  Urine albumin. Urine albumin is measured by comparing the amount of albumin to the amount of creatinine in a single urine sample. When the kidneys are healthy, the urine will contain large amounts of creatinine but almost no albumin. Even a small increase in the ratio of albumin to creatinine is a sign of kidney damage.  Kidney disease is present when urine contains more than 30 milligrams of albumin per gram of creatinine, with or without decreased eGFR.  The ADA and the NIH recommend annual assessment of urine albumin excretion to assess kidney damage in all people with type 2 diabetes and people who have had type 1 diabetes for 5 years or more.\n                \nIf kidney disease is detected, it should be addressed as part of a comprehensive approach to the treatment of diabetes."}
{"_id":"fb89a2d4-aa6d-4531-ac5d-dfc049ceedc0","text":"People with diabetes should be screened regularly for kidney disease. The two key markers for kidney disease are eGFR and urine albumin.\n                \n-  eGFR. eGFR stands for estimated glomerular filtration rate. Each kidney contains about 1 million tiny filters made up of blood vessels. These filters are called glomeruli. Kidney function can be checked by estimating how much blood the glomeruli filter in a minute. The calculation of eGFR is based on the amount of creatinine, a waste product, found in a blood sample. As the level of creatinine goes up, the eGFR goes down.  Kidney disease is present when eGFR is less than 60 milliliters per minute.  The American Diabetes Association (ADA) and the National Institutes of Health (NIH) recommend that eGFR be calculated from serum creatinine at least once a year in all people with diabetes.  -  Urine albumin. Urine albumin is measured by comparing the amount of albumin to the amount of creatinine in a single urine sample. When the kidneys are healthy, the urine will contain large amounts of creatinine but almost no albumin. Even a small increase in the ratio of albumin to creatinine is a sign of kidney damage.  Kidney disease is present when urine contains more than 30 milligrams of albumin per gram of creatinine, with or without decreased eGFR.  The ADA and the NIH recommend annual assessment of urine albumin excretion to assess kidney damage in all people with type 2 diabetes and people who have had type 1 diabetes for 5 years or more.\n                \nIf kidney disease is detected, it should be addressed as part of a comprehensive approach to the treatment of diabetes."}
{"_id":"f4c345af-14a7-43a5-8fa0-8859ac5f4950","text":"Blood Pressure Medicines\n                \nScientists have made great progress in developing methods that slow the onset and progression of kidney disease in people with diabetes. Drugs used to lower blood pressure can slow the progression of kidney disease significantly. Two types of drugs, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), have proven effective in slowing the progression of kidney disease. Many people require two or more drugs to control their blood pressure. In addition to an ACE inhibitor or an ARB, a diuretic can also be useful. Beta blockers, calcium channel blockers, and other blood pressure drugs may also be needed.\n                \nAn example of an effective ACE inhibitor is lisinopril (Prinivil, Zestril), which doctors commonly prescribe for treating kidney disease of diabetes. The benefits of lisinopril extend beyond its ability to lower blood pressure: it may directly protect the kidneys' glomeruli. ACE inhibitors have lowered proteinuria and slowed deterioration even in people with diabetes who did not have high blood pressure.\n                \nAn example of an effective ARB is losartan (Cozaar), which has also been shown to protect kidney function and lower the risk of cardiovascular events.\n                \nPatients with even mild hypertension or persistent microalbuminuria should consult a health care provider about the use of antihypertensive medicines.\n                \nModerate-protein Diets\n                \nIn people with diabetes, excessive consumption of protein may be harmful. Experts recommend that people with kidney disease of diabetes consume the recommended dietary allowance for protein, but avoid high-protein diets. For people with greatly reduced kidney function, a diet containing reduced amounts of protein may help delay the onset of kidney failure. Anyone following a reduced-protein diet should work with a dietitian to ensure adequate nutrition.\n                \nIntensive Management of Blood Glucose\n                \nAntihypertensive drugs and low-protein diets can slow CKD. A third treatment, known as intensive management of blood glucose or glycemic control, has shown great promise for people with diabetes, especially for those in the early stages of CKD.\n                \nThe human body normally converts food to glucose, the simple sugar that is the main source of energy for the body's cells. To enter cells, glucose needs the help of insulin, a hormone produced by the pancreas. When a person does not make enough insulin, or the body does not respond to the insulin that is present, the body cannot process glucose, and it builds up in the bloodstream. High levels of glucose in the blood lead to a diagnosis of diabetes.\n                \nIntensive management of blood glucose is a treatment regimen that aims to keep blood glucose levels close to normal. The regimen includes testing blood glucose frequently, administering insulin throughout the day on the basis of food intake and physical activity, following a diet and activity plan, and consulting a health care team regularly. Some people use an insulin pump to supply insulin throughout the day.\n                \nA number of studies have pointed to the beneficial effects of intensive management of blood glucose. In the Diabetes Control and Complications Trial supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), researchers found a 50 percent decrease in both development and progression of early diabetic kidney disease in participants who followed an intensive regimen for controlling blood glucose levels. The intensively managed patients had average blood glucose levels of 150 milligrams per deciliterabout 80 milligrams per deciliter lower than the levels observed in the conventionally managed patients. The United Kingdom Prospective Diabetes Study, conducted from 1976 to 1997, showed conclusively that, in people with improved blood glucose control, the risk of early kidney disease was reduced by a third. Additional studies conducted over the past decades have clearly established that any program resulting in sustained lowering of blood glucose levels will be beneficial to patients in the early stages of CKD."}
{"_id":"efbc6812-bb9b-4ed5-a63a-fef2c62b91ee","text":"Blood Pressure Medicines\n                \nScientists have made great progress in developing methods that slow the onset and progression of kidney disease in people with diabetes. Drugs used to lower blood pressure can slow the progression of kidney disease significantly. Two types of drugs, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), have proven effective in slowing the progression of kidney disease. Many people require two or more drugs to control their blood pressure. In addition to an ACE inhibitor or an ARB, a diuretic can also be useful. Beta blockers, calcium channel blockers, and other blood pressure drugs may also be needed.\n                \nAn example of an effective ACE inhibitor is lisinopril (Prinivil, Zestril), which doctors commonly prescribe for treating kidney disease of diabetes. The benefits of lisinopril extend beyond its ability to lower blood pressure: it may directly protect the kidneys' glomeruli. ACE inhibitors have lowered proteinuria and slowed deterioration even in people with diabetes who did not have high blood pressure.\n                \nAn example of an effective ARB is losartan (Cozaar), which has also been shown to protect kidney function and lower the risk of cardiovascular events.\n                \nPatients with even mild hypertension or persistent microalbuminuria should consult a health care provider about the use of antihypertensive medicines.\n                \nModerate-protein Diets\n                \nIn people with diabetes, excessive consumption of protein may be harmful. Experts recommend that people with kidney disease of diabetes consume the recommended dietary allowance for protein, but avoid high-protein diets. For people with greatly reduced kidney function, a diet containing reduced amounts of protein may help delay the onset of kidney failure. Anyone following a reduced-protein diet should work with a dietitian to ensure adequate nutrition.\n                \nIntensive Management of Blood Glucose\n                \nAntihypertensive drugs and low-protein diets can slow CKD. A third treatment, known as intensive management of blood glucose or glycemic control, has shown great promise for people with diabetes, especially for those in the early stages of CKD.\n                \nThe human body normally converts food to glucose, the simple sugar that is the main source of energy for the body's cells. To enter cells, glucose needs the help of insulin, a hormone produced by the pancreas. When a person does not make enough insulin, or the body does not respond to the insulin that is present, the body cannot process glucose, and it builds up in the bloodstream. High levels of glucose in the blood lead to a diagnosis of diabetes.\n                \nIntensive management of blood glucose is a treatment regimen that aims to keep blood glucose levels close to normal. The regimen includes testing blood glucose frequently, administering insulin throughout the day on the basis of food intake and physical activity, following a diet and activity plan, and consulting a health care team regularly. Some people use an insulin pump to supply insulin throughout the day.\n                \nA number of studies have pointed to the beneficial effects of intensive management of blood glucose. In the Diabetes Control and Complications Trial supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), researchers found a 50 percent decrease in both development and progression of early diabetic kidney disease in participants who followed an intensive regimen for controlling blood glucose levels. The intensively managed patients had average blood glucose levels of 150 milligrams per deciliterabout 80 milligrams per deciliter lower than the levels observed in the conventionally managed patients. The United Kingdom Prospective Diabetes Study, conducted from 1976 to 1997, showed conclusively that, in people with improved blood glucose control, the risk of early kidney disease was reduced by a third. Additional studies conducted over the past decades have clearly established that any program resulting in sustained lowering of blood glucose levels will be beneficial to patients in the early stages of CKD."}
{"_id":"0feb724c-8678-43ee-b4cc-317fc9360195","text":"- Diabetes is the leading cause of chronic kidney disease (CKD) and kidney failure in the United States.  - People with diabetes should be screened regularly for kidney disease. The two key markers for kidney disease are estimated glomerular filtration rate (eGFR) and urine albumin.  - Drugs used to lower blood pressure can slow the progression of kidney disease significantly. Two types of drugs, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), have proven effective in slowing the progression of kidney disease.  - In people with diabetes, excessive consumption of protein may be harmful.  - Intensive management of blood glucose has shown great promise for people with diabetes, especially for those in the early stages of CKD."}
{"_id":"c22ffafd-c8ef-4e80-a430-439d05f736e2","text":"- Diabetes is the leading cause of chronic kidney disease (CKD) and kidney failure in the United States.  - People with diabetes should be screened regularly for kidney disease. The two key markers for kidney disease are estimated glomerular filtration rate (eGFR) and urine albumin.  - Drugs used to lower blood pressure can slow the progression of kidney disease significantly. Two types of drugs, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), have proven effective in slowing the progression of kidney disease.  - In people with diabetes, excessive consumption of protein may be harmful.  - Intensive management of blood glucose has shown great promise for people with diabetes, especially for those in the early stages of CKD."}
{"_id":"476347ec-759a-4481-ac04-8003a7a210bc","text":"Lactose\n                \n*\n                \nintestine\n                \nlactase\n                \n,\n                \nenzyme\n                \n*See the Pronunciation Guide for tips on how to say the words in bold type."}
{"_id":"8dcdaef3-e966-456b-ab2c-ae2da8fb2ad6","text":"Lactose intolerance means you have symptoms such as bloating, diarrhea, and gas after you have milk or milk products.\n                \nIf your small intestine does not produce much lactase, you cannot break down much lactose. Lactose that does not break down goes to your colon. The colon is an organ that absorbs water from stool and changes it from a liquid to a solid form. In your colon, bacteria that normally live in the colon break down the lactose and create fluid and gas, causing you to have symptoms.\n                \nThe causes of low lactase in your small intestine can include the following:\n                \n- In some people, the small intestine makes less lactase starting at about age 2, which may lead to symptoms of lactose intolerance. Other people start to have symptoms later, when they are teenagers or adults.  - Infection, disease, or other problems that harm the small intestine can cause low lactase levels. Low lactase levels can cause you to become lactose intolerant until your small intestine heals.  - Being born early may cause babies to be lactose intolerant for a short time after they are born.  - In a rare form of lactose intolerance, the small intestine produces little or no lactase enzyme from birth.\n                \nNot all people with low lactase levels have symptoms. If you have symptoms, you are lactose intolerant.\n                \nMost people who are lactose intolerant can have some milk or milk products and not have symptoms. The amount of lactose that causes symptoms is different from person to person.\n                \n\n                \nPeople sometimes confuse lactose intolerance with a milk allergy. While lactose intolerance is a digestive problem, a milk allergy is a reaction by the bodys immune system to one or more milk proteins. If you have a milk allergy, having even a small amount of milk or milk product can be life threatening. A milk allergy most commonly occurs in the first year of life. Lactose intolerance occurs more often during the teen years or adulthood."}
{"_id":"abb4e1e5-f7b1-45c2-9ba9-52bcf1b0e1db","text":"Common symptoms of lactose intolerance include\n                \n- bloating, a feeling of fullness or swelling, in your belly  - pain in your belly  - diarrhea  - gas  - nausea\n                \nYou may feel symptoms 30 minutes to 2 hours after you have milk or milk products. You may have mild or severe symptoms."}
{"_id":"5567997c-216f-4fae-a63b-305ed0d1d291","text":"Talk with your doctor about your dietary plan. A dietary plan can help you manage the symptoms of lactose intolerance and get enough nutrients. If you have a child with lactose intolerance, follow the diet plan that your childs doctor recommends.\n                \nMilk and milk products. You may be able to have milk and milk products without symptoms if you\n                \n- drink small amounts of milkhalf a cup or lessat a time  - drink small amounts of milk with meals, such as having milk with cereal or having cheese with crackers  - add small amounts of milk and milk products to your diet a little at a time and see how you feel  - eat milk products that are easier for people with lactose intolerance to break down:      - yogurt    - hard cheeses such as cheddar and Swiss\n                \n\n                \nLactose-free and lactose-reduced milk and milk products. You can find lactose-free and lactose-reduced milk and milk products at the grocery store. These products are just as healthy for you as regular milk and milk products.\n                \nLactase products. You can use lactase tablets and drops when you have milk and milk products. The lactase enzyme breaks down the lactose in food. Using lactase tablets or drops can help you prevent symptoms of lactose intolerance. Check with your doctor before using these products. Some people, such as young children and pregnant and breastfeeding women, may not be able to use these products.\n                \n\n                \n\n                \nCalcium and Vitamin D   If you are lactose intolerant, make sure you get enough calcium each day. Milk and milk products are the most common sources of calcium. Other foods that contain calcium include   - fish with soft bones, such as canned salmon or sardines   - broccoli and other leafy green vegetables   - oranges   - almonds, Brazil nuts, and dried beans   - tofu   - products with the label showing added calcium, such as cereals, fruit juices, and soy milk    Vitamin D helps the body absorb and use calcium. Be sure to eat foods that contain vitamin D, such as eggs, liver, and certain kinds of fish, such as salmon. Also, being outside in the sunlight helps your body make vitamin D. Some companies add vitamin D to milk and milk products. If you are able to drink small amounts of milk or eat yogurt, choose those that have vitamin D added.   Talk with your doctor about how to get enough nutrientsincluding calcium and vitamin Din your diet or your childs diet. Ask if you should also take a supplement to get enough calcium and vitamin D.   For safety reasons, talk with your doctor before using dietary supplements or any other nonmainstream medicine together with or in place of the treatment your doctor prescribes. Read more at www.ods.od.nih.gov and www.nccam.nih.gov."}
{"_id":"721d1165-4e82-4cac-9938-8fe473e17500","text":"- Lactose is a sugar found in milk and milk products.  - Lactose intolerance means you have symptoms such as bloating, diarrhea, and gas after you have milk or milk products.  - Your doctor will try to find out if you have lactose intolerance with a medical, family, and diet history; a physical exam; and medical tests.  - Most people with lactose intolerance can eat or drink some lactose without symptoms.  - If you have lactose intolerance, you can make changes to what you eat and drink. Some people may only need to have less lactose. Others may need to avoid lactose altogether.  - Talk with your doctor about how to get enough nutrientsincluding calcium and vitamin Din your diet or your childs diet. Ask if you should also take a supplement to get enough calcium and vitamin D. For safety reasons, talk with your doctor before using dietary supplements or any other nonmainstream medicine together with or in place of the treatment your doctor prescribes.  - Lactose is in many food products and in some medicines."}
{"_id":"f071113e-9e16-4cd2-9ff9-282bca73e564","text":"A cystocele, also called a prolapsed or dropped bladder, is the bulging or dropping of the bladder into the vagina. The bladder, located in the pelvis between the pelvic bones, is a hollow, muscular, balloon-shaped organ that expands as it fills with urine. During urination, also called voiding, the bladder empties through the urethra, located at the bottom of the bladder. The urethra is the tube that carries urine outside of the body. The vagina is the tube in a womans body that runs beside the urethra and connects the womb, or uterus, to the outside of the body."}
{"_id":"5da00e26-0271-4e31-a1bb-7cad6733b1d9","text":"A cystocele occurs when the muscles and supportive tissues between a womans bladder and vagina weaken and stretch, letting the bladder sag from its normal position and bulge into the vagina or through the vaginal opening. In a cystocele, the bladder tissue remains covered by the vaginal skin. A cystocele may result from damage to the muscles and tissues that hold the pelvic organs up inside the pelvis. A womans pelvic organs include the vagina, cervix, uterus, bladder, urethra, and small intestine. Damage to or weakening of the pelvic muscles and supportive tissues may occur after vaginal childbirth and with conditions that repeatedly strain or increase pressure in the pelvic area, such as\n                \n- repetitive straining for bowel movements  - constipation  - chronic or violent coughing  - heavy lifting  - being overweight or obese\n                \nA womans chances of developing a cystocele increase with age, possibly because of weakening muscles and supportive tissues from aging. Whether menopause increases a womans chances of developing a cystocele is unclear."}
{"_id":"b5061232-8fc6-4105-961c-301dcf60cbcd","text":"The symptoms of a cystocele may include\n                \n- a vaginal bulge  - the feeling that something is falling out of the vagina  - the sensation of pelvic heaviness or fullness  - difficulty starting a urine stream  - a feeling of incomplete urination  - frequent or urgent urination\n                \nWomen who have a cystocele may also leak some urine as a result of movements that put pressure on the bladder, called stress urinary incontinence. These movements can include coughing, sneezing, laughing, or physical activity, such as walking. Urinary retentionthe inability to empty the bladder completelymay occur with more severe cystoceles if the cystocele creates a kink in the womans urethra and blocks urine flow.\n                \nWomen with mild cystoceles often do not have any symptoms."}
{"_id":"fbf87c2d-2a64-4e55-962e-6b2a48c2850e","text":"Diagnosing a cystocele requires medical tests and a physical exam of the vagina. Medical tests take place in a health care providers office, an outpatient center, or a hospital. The health care provider will ask about symptoms and medical history. A health care provider uses a grading system to determine the severity of a womans cystocele. A cystocele receives one of three grades depending on how far a womans bladder has dropped into her vagina:\n                \n- grade 1mild, when the bladder drops only a short way into the vagina  - grade 2moderate, when the bladder drops far enough to reach the opening of the vagina  - grade 3most advanced, when the bladder bulges out through the opening of the vagina\n                \nIf a woman has difficulty emptying her bladder, a health care provider may measure the amount of urine left in the womans bladder after she urinates. The remaining urine is called the postvoid residual. A health care provider can measure postvoid residual with a bladder ultrasound. A bladder ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off the bladder to create an image and show the amount of remaining urine. A specially trained technician performs the procedure, and a radiologista doctor who specializes in medical imaginginterprets the images. A woman does not need anesthesia.\n                \nA health care provider can also use a cathetera thin, flexible tubeto measure a womans postvoid residual. The health care provider inserts the catheter through the womans urethra into her bladder to remove and measure the amount of remaining urine after the woman has urinated. A postvoid residual of 100 mL or more is a sign that the woman is not completely emptying her bladder. A woman receives local anesthesia.\n                \nA health care provider may use a voiding cystourethrograman x-ray exam of the bladderto diagnose a cystocele as well. A woman gets a voiding cystourethrogram while urinating. The x-ray images show the shape of the womans bladder and let the health care provider see any problems that might block normal urine flow. An x-ray technician performs a voiding cystourethrogram, and a radiologist interprets the images. A woman does not need anesthesia; however, some women may receive sedation. A health care provider may order additional tests to rule out problems in other parts of a womans urinary tract."}
{"_id":"38a7c733-f855-477e-a741-7715dc7f5a29","text":"Cystocele treatment depends on the severity of the cystocele and whether a woman has symptoms. If a womans cystocele does not bother her, a health care provider may recommend only that she avoid heavy lifting or straining, which could worsen her cystocele. If a woman has symptoms that bother her and wants treatment, the health care provider may recommend pelvic muscle exercises, a vaginal pessary, or surgery.\n                \nPelvic floor, or Kegel, exercises involve strengthening pelvic floor muscles. Strong pelvic floor muscles more effectively hold pelvic organs in place. A woman does not need special equipment for Kegel exercises.\n                \nThe exercises involve tightening and relaxing the muscles that support pelvic organs. A health care provider can help a woman learn proper technique.\n                \nMore information about pelvic muscle exercises is provided in the NIDDK health topic, Kegel Exercise Tips.\n                \nA vaginal pessary is a small, silicone medical device placed in the vagina that supports the vaginal wall and holds the bladder in place. Pessaries come in a number of shapes and sizes. A health care provider has many options to choose from to find the most comfortable pessary for a woman.\n                \nA heath care provider may recommend surgery to repair the vaginal wall support and reposition the womans bladder to its normal position. The most common cystocele repair is an anterior vaginal repairor anterior colporrhaphy. The surgeon makes an incision in the wall of the womans vagina and repairs the defect by folding over and sewing together extra supportive tissue between the vagina and bladder. The repair tightens the layers of tissue that separate the organs, creating more support for the bladder. A surgeon who specializes in the urinary tract or female reproductive system performs an anterior vaginal repair in a hospital. The woman receives either regional or general anesthesia. The woman may stay overnight in the hospital, and full recovery may take up to 4 to 6 weeks."}
{"_id":"6d178248-27b0-4be7-9c8c-77d92b2578b3","text":"Researchers have not found that eating, diet, and nutrition play a role in causing or preventing a cystocele."}
{"_id":"0da5b1c8-405e-4103-bc0c-95dc0f847088","text":"- A cystocele, also called a prolapsed or dropped bladder, is the bulging or dropping of the bladder into the vagina.  - A cystocele occurs when the muscles and supportive tissues between a womans bladder and vagina weaken and stretch, letting the bladder sag from its normal position and bulge into the vagina or through the vaginal opening.  - Diagnosing a cystocele requires medical tests and a physical exam of the vagina.  - Cystocele treatment depends on the severity of the cystocele and whether a woman has symptoms."}
{"_id":"38b21bfc-1312-413a-ad1c-b154d9f7f6a6","text":"Whipple disease is a rare bacterial infection that primarily affects the small intestine. The infection may spread to any organ in the body; however, it more commonly affects the\n                \n- joints  - central nervous system, which includes the brain, the spinal cord, and nerves located throughout the body  - heart  - eyes  - lungs\n                \nLeft untreated, Whipple disease gets worse and is usually life threatening."}
{"_id":"6fdff442-9881-4970-95bd-a8565cbbd645","text":"The small intestine is part of the upper gastrointestinal (GI) tract and is a tube-shaped organ between the stomach and large intestine. The upper GI tract also includes the mouth, esophagus, stomach, and duodenum, or the first part of the small intestine.\n                \nMost food digestion and nutrient absorption take place in the small intestine. The small intestine measures about 20 feet long and includes the duodenum, jejunum, and ileum. Villitiny, fingerlike protrusionsline the inside of the small intestine. Villi normally let nutrients from food be absorbed through the walls of the small intestine into the bloodstream."}
{"_id":"3371669c-8285-48ec-ab50-eba190ec2fdc","text":"Bacteria called Tropheryma whipplei (T. whipplei) cause Whipple disease. T. whipplei infection can cause internal sores, also called lesions, and thickening of tissues in the small intestine. The villi take on an abnormal, clublike appearance and the damaged intestinal lining does not properly absorb nutrients, causing diarrhea and malnutrition. Diarrhea is frequent, loose, and watery bowel movements. Malnutrition is a condition that develops when the body does not get the right amount of vitamins, minerals, and other nutrients it needs to maintain healthy tissues and organ function. Over time, the infection spreads to other parts of the persons body and will damage other organs."}
{"_id":"a7060c2e-d468-40fd-8370-c057ec925136","text":"Signs and symptoms of Whipple disease can vary widely from person to person. The most common symptoms of Whipple disease are\n                \n- diarrhea  - weight loss caused by malabsorption\n                \nA person may not have diarrhea. Instead, other signs and symptoms of Whipple disease may appear, such as\n                \n- abnormal yellow and white patches on the lining of the small intestine  - joint pain, with or without inflammation, that may appear off and on for years before other symptoms  - fatty or bloody stools  - abdominal cramps or bloating felt between the chest and groin  - enlarged lymph nodesthe small glands that make infection-fighting white blood cells  - loss of appetite  - fever  - fatigue, or feeling tired  - weakness  - darkening of the skin\n                \nPeople with a more advanced stage of Whipple disease may have neurologic symptomsthose related to the central nervous systemsuch as\n                \n- vision problems.  - memory problems or personality changes.  - facial numbness.  - headaches.  - muscle weakness or twitching.  - difficulty walking.  - hearing loss or ringing in the ears.  - dementiathe name for a group of symptoms caused by disorders that affect the brain. People with dementia may not be able to think well enough to do normal activities such as getting dressed or eating.\n                \nLess common symptoms of Whipple disease may include\n                \n- chronic cough.  - chest pain.  - pericarditisinflammation of the membrane surrounding the heart.  - heart failurea long-lasting condition in which the heart cannot pump enough blood to meet the bodys needs. Heart failure does not mean the heart suddenly stops working."}
{"_id":"747d6031-9de7-4fd3-8634-6bbe2bf13fd7","text":"People with Whipple disease may have complications caused by malnutrition, which is due to damaged villi in the small intestine. As a result of delayed diagnosis or treatment, people may experience the following complications in other areas of the body:\n                \n- long-lasting nutritional deficiencies  - heart and heart valve damage  - brain damage\n                \nA person with Whipple disease may experience a relapsea return of symptoms. Relapse can happen years after treatment and requires repeat treatments."}
{"_id":"5bad0b46-fb75-4993-97dc-e5943012ca0a","text":"A health care provider may use several tests and exams to diagnose Whipple disease, including the following:\n                \n- medical and family history  - physical exam  - blood tests  - upper GI endoscopy and enteroscopy\n                \nA patient may be referred to a gastroenterologista doctor who specializes in digestive diseases.\n                \nA health care provider may first try to rule out more common conditions with similar symptoms, including\n                \n- inflammatory rheumatic diseasecharacterized by inflammation and loss of function in one or more connecting or supporting structures of the body.  - celiac diseasea digestive disease that damages the small intestine and interferes with the absorption of nutrients from food. People who have celiac disease cannot tolerate gluten, a protein in wheat, rye, and barley.  - neurologic diseasesdisorders of the central nervous system.  - intra-abdominal lymphomaabdominal cancer in part of the immune system called the lymphatic system.  - Mycobacterium avium complexan infection that affects people with AIDS.\n                \nMedical and Family History\n                \nTaking a family and medical history can help a health care provider diagnose Whipple disease.\n                \nPhysical Exam\n                \nA physical exam may help diagnose Whipple disease. During a physical exam, a health care provider usually\n                \n- examines a patients body  - uses a stethoscope to listen to sounds related to the abdomen  - taps on specific areas of the patients body checking for pain or tenderness\n                \nBlood Tests\n                \nA technician or nurse draws a blood sample during an office visit or at a commercial facility and sends the sample to a lab for analysis. The health care provider may use blood tests to check for\n                \n- malabsorption. When the damaged villi do not absorb certain nutrients from food, the body has a shortage of protein, calories, and vitamins. Blood tests can show shortages of protein, calories, and vitamins in the body.  - abnormal levels of electrolytes. Electrolyteschemicals in body fluids, including sodium, potassium, magnesium, and chlorideregulate a persons nerve and muscle function. A patient who has malabsorption or a lot of diarrhea may lose fluids and electrolytes, causing an imbalance in the body.  - anemia. Anemia is a condition in which the body has fewer red blood cells than normal. A patient with Whipple disease does not absorb the proper nutrients to make enough red blood cells in the body, leading to anemia.  - T. whipplei DNA. Although not yet approved, rapid polymerase chain reaction diagnostic tests have been developed to detect T. whipplei DNA and may be useful in diagnosis.\n                \nUpper Gastrointestinal Endoscopy and Enteroscopy\n                \nAn upper GI endoscopy and enteroscopy are procedures that use an endoscopea small, flexible tube with a lightto see the upper GI tract. A health care provider performs these tests at a hospital or an outpatient center. The health care provider carefully feeds the endoscope down the esophagus and into the stomach and duodenum.\n                \nOnce the endoscope is in the duodenum, the health care provider will use smaller tools and a smaller scope to see more of the small intestine. These additional procedures may include\n                \n- push enteroscopy, which uses a long endoscope to examine the upper portion of the small intestine.  - double-balloon enteroscopy, which uses balloons to help move the endoscope through the entire small intestine.  - capsule enteroscopy, during which the patient swallows a capsule containing a tiny camera. As the capsule passes through the GI tract, the camera will transmit images to a video monitor. Using this procedure, the health care provider can examine the entire digestive tract.\n                \nA small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining. A health care provider may give a patient a liquid anesthetic to gargle or may spray anesthetic on the back of the patients throat. A health care provider will place an intravenous (IV) needle in a vein in the arm or hand to administer sedation. Sedatives help patients stay relaxed and comfortable. The test can show changes in the lining of the small intestine that can occur with Whipple disease.\n                \nThe health care provider can use tiny tools passed through the endoscope to perform biopsies. A biopsy is a procedure that involves taking a piece of tissue for examination with a microscope. A pathologista doctor who specializes in examining tissues to diagnose diseasesexamines the tissue from the stomach lining in a lab. The pathologist applies a special stain to the tissue and examines it for T. whipplei-infected cells with a microscope. Once the pathologist completes the examination of the tissue, he or she sends a report to the gastroenterologist for review. More information is provided in the NIDDK health topic, Upper GI Endoscopy."}
{"_id":"16e520b4-b1f4-4606-b8fe-45b1eee4aa5c","text":"The health care provider prescribes antibiotics to destroy the T. whipplei bacteria and treat Whipple disease. Health care providers choose antibiotics that treat the infection in the small intestine and cross the blood-brain barriera layer of tissue around the brain. Using antibiotics that cross the blood-brain barrier ensures destruction of any bacteria that may have entered the patients brain and central nervous system.\n                \nThe health care provider usually prescribes IV antibiotics for the first 2 weeks of treatment. Most patients feel relief from symptoms within the first week or two. A nurse or technician places an IV in the patients arm to give the antibiotics. IV antibiotics used to treat Whipple disease may include\n                \n- ceftriaxone (Rocephin)  - meropenem (Merrem I.V.)  - penicillin G (Pfizerpen)  - streptomycin (Streptomycin)\n                \nAfter a patient completes the IV antibiotics, the health care provider will prescribe long-term oral antibiotics. Patients receive long-term treatmentat least 1 to 2 yearsto cure the infection anywhere in the body. Oral antibiotics may include\n                \n- trimethoprim\/sulfamethoxazole (Septra, Bactrim)a combination antibiotic  - doxycycline (Vibramycin)\n                \nPatients should finish the prescribed course of antibiotics to ensure the medication destroyed all T. whipplei bacteria in the body. Patients who feel better may still have the bacteria in the small intestine or other areas of the body for 1 to 2 years. A health care provider will monitor the patient closely, repeat the blood tests, and repeat the upper GI endoscopy with biopsy during and after treatment to determine whether T. whipplei is still present.\n                \nPeople may relapse during or after treatment. A health care provider will prescribe additional or new antibiotics if a relapse occurs. Some people will relapse years after treatment, so it is important for patients to schedule routine follow-ups with the health care provider. Most patients have good outcomes with an early diagnosis and complete treatment.\n                \nHealth care providers treat patients with neurologic symptoms at diagnosis or during relapse more aggressively. Treatment may include\n                \n- a combination of antibiotics  - hydroxychloroquine (Plaquenil)an antimalarial medication  - weekly injections of interferon gammaa substance made by the body that activates the immune system  - corticosteroidsmedications that decrease inflammation"}
{"_id":"eb2045f2-9134-4814-a850-8930af1f7555","text":"Experts have not yet found a way to prevent Whipple disease."}
{"_id":"a3f3c2a9-7b59-416e-b43e-2c0f4d7950e6","text":"A person with Whipple disease and malabsorption may need\n                \n- a diet high in calories and protein  - vitamins  - nutritional supplements"}
{"_id":"76ea8f76-b73d-4b05-898b-8da4ee222a4b","text":"- Whipple disease is a rare bacterial infection that primarily affects the small intestine. Left untreated, Whipple disease gets worse and is usually life threatening.  - Bacteria called Tropheryma whipplei (T. whipplei) cause Whipple disease. T. whipplei infection can cause internal sores, also called lesions, and thickening of tissues in the small intestine.  - Anyone can get Whipple disease. However, it is more common in Caucasian men between 40 and 60 years old.  - Signs and symptoms of Whipple disease can vary widely from person to person. The most common symptoms of Whipple disease are      - diarrhea    - weight loss caused by malabsorption    - People with Whipple disease may have complications caused by malnutrition, which is due to damaged villi in the small intestine.  - The health care provider prescribes antibiotics to destroy the T. whipplei bacteria and treat Whipple disease.  - The health care provider usually prescribes intravenous (IV) antibiotics for the first 2 weeks of treatment. Most patients feel relief from symptoms within the first week or two.  - After a patient completes the IV antibiotics, the health care provider will prescribe long-term oral antibiotics.  - Most patients have good outcomes with an early diagnosis and complete treatment."}
{"_id":"36d80608-705e-491a-9da0-c4670bc860c1","text":"Risk factors are conditions that increase the chances of getting a particular disease. The more risk factors people have, the greater their chances of developing that disease or condition. Diabetic neuropathy and related sexual and urologic problems appear to be more common in people who\n                \n- have poor blood glucose control  - have high levels of blood cholesterol  - have high blood pressure  - are overweight  - are older than 40  - smoke  - are physically inactive"}
{"_id":"60504384-7c32-488f-8068-d35a5012e37d","text":"People with diabetes can lower their risk of sexual and urologic problems by keeping their blood glucose, blood pressure, and cholesterol levels close to the target numbers their health care provider recommends. Being physically active and maintaining a healthy weight can also help prevent the long-term complications of diabetes. For those who smoke, quitting will lower the risk of developing sexual and urologic problems due to nerve damage and also lower the risk for other health problems related to diabetes, including heart attack, stroke, and kidney disease.\n                \nMore information about preventing diabetes complications is provided in the NIDDK health topic, Prevent diabetes problems: Keep your diabetes under control, available from the National Diabetes Information Clearinghouse at 1-800-860-8747."}
{"_id":"8b35bdca-74c1-4c4d-b1d2-fbf711cc4d57","text":"The nerve damage of diabetes may cause sexual or urologic problems.\n                \n- Sexual problems in men with diabetes include      - erectile dysfunction    - retrograde ejaculation    - Sexual problems in women with diabetes include      - decreased vaginal lubrication and uncomfortable or painful intercourse    - decreased or no sexual desire    - decreased or absent sexual response    - Urologic problems in men and women with diabetes include      - bladder problems related to nerve damage, such as overactive bladder, poor control of sphincter muscles, and urine retention    - urinary tract infections    - Controlling diabetes through diet, physical activity, and medications as needed can help prevent sexual and urologic problems.  - Treatment is available for sexual and urologic problems."}
{"_id":"d7a3798f-3d95-4be7-b4c4-67b84267ae1e","text":"Nerves that work poorly can lead to three different kinds of bladder control problems.\n                \nOveractive bladder. Damaged nerves may send signals to the bladder at the wrong time, causing its muscles to squeeze without warning. The symptoms of overactive bladder include\n                \n- urinary frequencydefined as urination eight or more times a day or two or more times at night  - urinary urgencythe sudden, strong need to urinate immediately  - urge incontinenceleakage of urine that follows a sudden, strong urge to urinate\n                \nPoor control of sphincter muscles. Sphincter muscles surround the urethra and keep it closed to hold urine in the bladder. If the nerves to the sphincter muscles are damaged, the muscles may become loose and allow leakage or stay tight when you are trying to release urine.\n                \nUrine retention. For some people, nerve damage means their bladder muscles do not get the message that it is time to release urine or are too weak to completely empty the bladder. If the bladder becomes too full, urine may back up and the increasing pressure may damage the kidneys. Or urine that stays too long may lead to an infection in the kidneys or bladder. Urine retention may also lead to overflow incontinence."}
{"_id":"75d6a606-d8af-4953-83f2-6e54b8c81010","text":"Many events or conditions can damage nerves and nerve pathways. Some of the most common causes are\n                \n- vaginal childbirth  - infections of the brain or spinal cord  - diabetes  - stroke  - accidents that injure the brain or spinal cord  - multiple sclerosis  - heavy metal poisoning\n                \nIn addition, some children are born with nerve problems that can keep the bladder from releasing urine, leading to urinary infections or kidney damage."}
{"_id":"d23fc150-a552-4439-9c51-7426972acf46","text":"The treatment for a bladder control problem depends on the cause of the nerve damage and the type of voiding dysfunction that results.\n                \nIn the case of overactive bladder, your doctor may suggest a number of strategies, including bladder training, electrical stimulation, drug therapy, and, in severe cases where all other treatments have failed, surgery.\n                \nBladder training. Your doctor may ask you to keep a bladder diary-a record of your fluid intake, trips to the bathroom, and episodes of urine leakage. This record may indicate a pattern and suggest ways to avoid accidents by making a point of using the bathroom at certain times of the day-a practice called timed voiding. As you gain control, you can extend the time between trips to the bathroom. Bladder training also includes Kegel exercises to strengthen the muscles that hold in urine.\n                \nElectrical stimulation. Mild electrical pulses can be used to stimulate the nerves that control the bladder and sphincter muscles. Depending on which nerves the doctor plans to treat, these pulses can be given through the vagina or anus, or by using patches on the skin. Another method is a minor surgical procedure to place the electric wire near the tailbone. This procedure involves two steps. First, the wire is placed under the skin and connected to a temporary stimulator, which you carry with you for several days. If your condition improves during this trial period, then the wire is placed next to the tailbone and attached to a permanent stimulator under your skin. The Food and Drug Administration (FDA) has approved this device, marketed as the InterStim system, to treat urge incontinence, urgency-frequency syndrome, and urinary retention in patients for whom other treatments have not worked.\n                \nDrug therapy. Different drugs can affect the nerves and muscles of the urinary tract in different ways.\n                \n-  Drugs that relax bladder muscles and prevent bladder spasms include oxybutynin chloride (Ditropan), tolterodine (Detrol), hyoscyamine (Levsin), and propantheline bromide (Pro-Banthine), which belong to the class of drugs called anticholinergics. Their most common side effect is dry mouth, although large doses may cause blurred vision, constipation, a faster heartbeat, and flushing. A new patch delivery system for oxybutynin (Oxytrol) may decrease side effects. Ditropan XL and Detrol LA are timed-release formulations that deliver a low level of the drug continuously in the body. These drugs have the advantage of once-a-day administration. In 2004, the FDA approved trospium chloride (Sanctura), darifenacin (Enablex), and solifenacin succinate (VESIcare) for the treatment of overactive bladder.  -  Drugs for depression that also relax bladder muscles include imipramine hydrochloride (Tofranil), a tricyclic antidepressant. Side effects may include fatigue, dry mouth, dizziness, blurred vision, nausea, and insomnia.\n                \nAdditional drugs are being evaluated for the treatment of overactive bladder and may soon receive FDA approval.\n                \nSurgery. In extreme cases, when incontinence is severe and other treatments have failed, surgery may be considered. The bladder may be made larger through an operation known as augmentation cystoplasty, in which a part of the diseased bladder is replaced with a section taken from the patient's bowel. This operation may improve the ability to store urine but may make the bladder more difficult to empty, making regular catheterization necessary. Additional risks of surgery include the bladder breaking open and leaking urine into the body, bladder stones, mucus in the bladder, and infection."}
{"_id":"ca706102-4165-4856-9c10-d5e09b4a785b","text":"The job of the sphincter muscles is to hold urine in the bladder by squeezing the urethra shut. If the urethral sphincter fails to stay closed, urine may leak out of the bladder. When nerve signals are coordinated properly, the sphincter muscles relax to allow urine to pass through the urethra as the bladder contracts to push out urine. If the signals are not coordinated, the bladder and the sphincter may contract at the same time, so urine cannot pass easily.\n                \nDrug therapy for an uncoordinated bladder and urethra. Scientists have not yet found a drug that works selectively on the urethral sphincter muscles, but drugs used to reduce muscle spasms or tremors are sometimes used to help the sphincter relax. Baclofen (Lioresal) is prescribed for muscle spasms or cramping in patients with multiple sclerosis and spinal injuries. Diazepam (Valium) can be taken as a muscle relaxant or to reduce anxiety. Drugs called alpha-adrenergic blockers can also be used to relax the sphincter. Examples of these drugs are alfuzosin (UroXatral), tamsulosin (Flomax), terazosin (Hytrin), and doxazosin (Cardura). The main side effects are low blood pressure, dizziness, fainting, and nasal congestion. All of these drugs have been used to relax the urethral sphincter in people whose sphincter does not relax well on its own.\n                \nBotox injection. Botulinum toxin type A (Botox) is best known as a cosmetic treatment for facial wrinkles. Doctors have also found that botulinum toxin is useful in blocking spasms like eye ticks or relaxing muscles in patients with multiple sclerosis. Urologists have found that injecting botulinum toxin into the tissue surrounding the sphincter can help it to relax. Although the FDA has approved botulinum toxin only for facial cosmetic purposes, researchers are studying the safety and effectiveness of botulinum toxin injection into the sphincter for possible FDA approval in the future."}
{"_id":"72b0ccbe-d21b-425f-896a-5f2c3dd0d21b","text":"Urine retention may occur either because the bladder wall muscles cannot contract or because the sphincter muscles cannot relax.\n                \nCatheter. A catheter is a thin tube that can be inserted through the urethra into the bladder to allow urine to flow into a collection bag. If you are able to place the catheter yourself, you can learn to carry out the procedure at regular intervals, a practice called clean intermittent catheterization. Some patients cannot place their own catheters because nerve damage affects their hand coordination as well as their voiding function. These patients need to have a caregiver place the catheter for them at regular intervals. If regular catheter placement is not feasible, the patients may need to have an indwelling catheter that can be changed less often. Indwelling catheters have several risks, including infection, bladder stones, and bladder tumors. However, if the bladder cannot be emptied any other way, then the catheter is the only way to stop the buildup of urine in the bladder that can damage the kidneys.\n                \nUrethral stent. Stents are small tube-like devices inserted into the urethra and allowed to expand, like a spring, widening the opening for urine to flow out. Stents can help prevent urine backup when the bladder wall and sphincter contract at the same time because of improper nerve signals. However, stents can cause problems if they move or lead to infection.\n                \nSurgery. Men may consider a surgery that removes the external sphincter-a sphincterotomy-or a piece of it-a sphincter resection-to prevent urinary retention. The surgeon will pass a thin instrument through the urethra to deliver electrical or laser energy that burns away sphincter tissue. Possible complications include bleeding that requires a transfusion and, rarely, problems with erections. This procedure causes loss of urine control and requires the patient to collect urine by wearing an external catheter that fits over the penis like a condom. No external collection device is available for women.\n                \nUrinary diversion. If other treatments fail and urine regularly backs up and damages the kidneys, the doctor may recommend a urinary diversion, a procedure that may require an outside collection bag attached to a stoma, a surgically created opening where urine passes out of the body. Another form of urinary diversion replaces the bladder with a continent urinary reservoir, an internal pouch made from sections of the bowel or other tissue. This method allows the person to store urine inside the body until a catheter is used to empty it through a stoma."}
{"_id":"07b458c5-10c5-4a5a-b6cd-2d8435b56423","text":"For people who are on dialysis or approaching total kidney failure, adequate nutrition is important for maintaining energy, strength, healthy sleep patterns, bone health, heart health, and good mental health. A persons treatment will dictate the type of diet that should be followed:\n                \n- People on hemodialysis must watch how much fluid they drink and avoid eating foods with too much sodium, potassium, and phosphorus.  - In contrast, people on peritoneal dialysisa type of dialysis that uses the lining of the abdomen, or belly, to filter the blood inside the bodymay be able to eat more potassium-rich foods because peritoneal dialysis removes potassium from the body more efficiently than hemodialysis.  - Both hemodialysis and peritoneal dialysis can remove proteins from the body, so anyone on either form of dialysis should eat protein-rich foods such as meat, fish, and eggs.\n                \nAll dialysis centers and transplant clinics have a renal dietitian who specializes in helping people with kidney failure. People who are on dialysis or have a kidney transplant should talk with their clinics renal dietitian to develop a meal plan that will enhance the effectiveness of their treatment.\n                \nFor more information about nutrition for people with advanced CKD or who are on dialysis, see NIDDK health topics, Nutrition for Advanced Chronic Kidney Disease in Adults or Kidney Failure: Eat Right to Feel Right on Hemodialysis."}
{"_id":"f2e7d864-90f9-490b-878e-266a9b945e45","text":"- Kidney failure can affect a persons health in several ways.  - When the kidneys stop working, waste products build up in the blood, a condition known as uremia.  - People with kidney failure can avoid most of the problems of uremia by having regular dialysis treatments and limiting foods that contain sodium, potassium, and phosphorus.  - Anemia is common in people with chronic kidney disease (CKD), as well as those on dialysis, because the damaged kidneys slow the produc-tion of the hormone erythropoietin (EPO), which helps the bone marrow make red blood cells.  - People with kidney failure, particularly dialysis patients, have far higher rates of heart and blood vessel problems than people without kidney problems.  - People who have uremia often lose their appetite.  - Many people treated with hemodialysis complain of itchy skin.  - Kidney failure weakens the bones due to a condition called chronic kidney disease-mineral and bone disorder.  - Kidney failure can cause pain, stiffness, and fluid in the joints. These symptoms result from amyloidosis, a condition in which an abnormal protein in the blood called amyloid is deposited in tissues and organs, including the joints and tendons.  - People on dialysis often have insomnia, sleep apnea syndrome, and restless legs syndrome.  - People who have kidney failure and depression should tell their health care provider because depression can often be treated with adjustments to the diet and dialysis dose, medications, counseling, and cognitive behavioral therapy.  - For people who are on dialysis or approaching total kidney failure, adequate nutrition is important for maintaining energy, strength, healthy sleep patterns, bone health, heart health, and good mental health.  - All dialysis centers and transplant clinics have a renal dietitian who specializes in helping people with kidney failure. People who are on dialysis or have a kidney transplant should talk with their clinics renal dietitian to develop a meal plan that will enhance the effectiveness of their treatment."}
{"_id":"a9f007ff-a268-40b4-943a-158a03f30732","text":"Wilson disease is a genetic disease that prevents the body from removing extra copper. The body needs a small amount of copper from food to stay healthy; however, too much copper is poisonous. Normally, the liver filters extra copper and releases it into bile. Bile is a fluid made by the liver that carries toxins and wastes out of the body through the gastrointestinal tract. In Wilson disease, the liver does not filter copper correctly and copper builds up in the liver, brain, eyes, and other organs. Over time, high copper levels can cause life-threatening organ damage."}
{"_id":"2b2be5ee-d238-415d-b0d0-5732124c4cf4","text":"The liver is the bodys largest internal organ. The liver is called the bodys metabolic factory because of the important role it plays in metabolismthe way cells change food into energy after food is digested and absorbed into the blood. The liver has many important functions, including\n                \n- taking up, storing, and processing nutrients from foodincluding fat, sugar, and proteinand delivering them to the rest of the body when needed.  - making new proteins, such as clotting factors and immune factors.  - producing bile. In addition to carrying toxins and waste products out of the body, bile helps the body digest fats and the fat-soluble vitamins A, D, E, and K.  - removing waste products the kidneys cannot remove, such as fats, cholesterol, toxins, and medications.\n                \nA healthy liver is necessary for survival. The liver can regenerate most of its own cells when they become damaged. However, if injury to the liver is too severe or long lasting, regeneration is incomplete and the liver creates scar tissue."}
{"_id":"7be140ac-8bbd-4d64-b9df-ec4d08c44a3e","text":"Wilson disease is caused by an inherited autosomal recessive mutation, or change, in the ATP7B gene. In an autosomal recessive disease, the child has to inherit the gene mutation from both parents to have an increased likelihood for the disease. The chance of a child inheriting autosomal recessive mutations from both parents with a gene mutation is 25 percent, or one in four. If only one parent carries the mutated gene, the child will not get the disease, although the child may inherit one copy of the gene mutation. The child is called a carrier of the disease and can pass the gene mutation to the next generation. Genetic testing is a procedure that identifies changes in a patients genes and can show whether a parent or child is a carrier of a mutated gene. Autosomal recessive diseases are typically not seen in every generation of an affected family.\n                \nThe following chart shows the chance of inheriting an autosomal recessive mutation from parents who both carry the mutated gene.\n                \n\n                \nGenetic Diseases   Each cell contains thousands of genes that provide the instructions for making proteins for growth and repair of the body. If a gene has a mutation, the protein made by that gene may not function properly. Not all gene mutations cause a disease.   People have two copies of most genes; they inherit one copy from each parent. A genetic disease occurs when one or both parents pass a mutated gene to a child at conception. A genetic disease can also occur through a spontaneous gene mutation, meaning neither parent carries a copy of the mutated gene. Once a spontaneous gene mutation has occurred in a person, that person can pass the gene mutation on to a child.   Read more about genes and genetic conditions in the U.S. National Library of Medicines Genetics Home Reference at www.ghr.nlm.nih.gov."}
{"_id":"89ad2801-998a-4d3e-83b2-f5d6614bd01c","text":"The signs and symptoms of Wilson disease vary, depending on what organs of the body are affected. Wilson disease is present at birth; however, the signs and symptoms of the disease do not appear until the copper builds up in the liver, the brain, or other organs.\n                \nWhen people have signs and symptoms, they usually affect the liver, the central nervous system, or both. The central nervous system includes the brain, the spinal cord, and nerves throughout the body. Sometimes a person does not have symptoms and a health care provider discovers the disease during a routine physical exam or blood test, or during an illness. Children can have Wilson disease for several years before any signs and symptoms occur. People with Wilson disease may have\n                \n- liver-related signs and symptoms  - central nervous system-related signs and symptoms  - mental health-related signs and symptoms  - other signs and symptoms\n                \nLiver-related Signs and Symptoms\n                \nPeople with Wilson disease may develop signs and symptoms of chronic, or long lasting, liver disease:\n                \n- weakness  - fatigue, or feeling tired  - loss of appetite  - nausea  - vomiting  - weight loss  - pain and bloating from fluid accumulating in the abdomen  - edemaswelling, usually in the legs, feet, or ankles and less often in the hands or face  - itching  - spiderlike blood vessels, called spider angiomas, near the surface of the skin  - muscle cramps  - jaundice, a condition that causes the skin and whites of the eyes to turn yellow\n                \nSome people with Wilson disease may not develop signs or symptoms of liver disease until they develop acute liver failurea condition that develops suddenly.\n                \nCentral Nervous System-related Signs and Symptoms\n                \nCentral nervous system-related symptoms usually appear in people after the liver has retained a lot of copper; however, signs and symptoms of liver disease may not be present. Central nervous system-related symptoms occur most often in adults and sometimes occur in children.1 Signs and symptoms include\n                \n- tremors or uncontrolled movements  - muscle stiffness  - problems with speech, swallowing, or physical coordination\n                \nA health care provider may refer people with these symptoms to a neurologista doctor who specializes in nervous system diseases.\n                \nMental Health-related Signs and Symptoms\n                \nSome people will have mental health-related signs and symptoms when copper builds up in the central nervous system. Signs and symptoms may include\n                \n- personality changes  - depression  - feeling anxious, or nervous, about most things  - psychosiswhen a person loses contact with reality\n                \nOther Signs and Symptoms\n                \nOther signs and symptoms of Wilson disease may include\n                \n- anemia, a condition in which red blood cells are fewer or smaller than normal, which prevents the bodys cells from getting enough oxygen  - arthritis, a condition in which a person has pain and swelling in one or more joints  - high levels of amino acids, protein, uric acid, and carbohydrates in urine  - low platelet or white blood cell count  - osteoporosis, a condition in which the bones become less dense and more likely to fracture"}
{"_id":"c7f3f648-0fc3-459b-9f85-71d5924745ec","text":"People who have Wilson disease that is not treated or diagnosed early can have serious complications, such as\n                \n- cirrhosisscarring of the liver  - kidney damageas liver function decreases, the kidneys may be damaged  - persistent nervous system problems when nervous system symptoms do not resolve  - liver cancerhepatocellular carcinoma is a type of liver cancer that can occur in people with cirrhosis  - liver failurea condition in which the liver stops working properly  - death, if left untreated"}
{"_id":"0b537294-bcee-4c8a-8ebc-4f78b81f35d8","text":"A health care provider may use several tests and exams to diagnose Wilson disease, including the following:\n                \n- medical and family history  - physical exam  - blood tests  - urine tests  - liver biopsy  - imaging tests\n                \nHealth care providers typically see the same symptoms of Wilson disease in other conditions, and the symptoms of Wilson disease do not occur together often, making the disease difficult to diagnose.\n                \nMedical and Family History\n                \nA health care provider may take a medical and family history to help diagnose Wilson disease.\n                \nPhysical Exam\n                \nA physical exam may help diagnose Wilson disease. During a physical exam, a health care provider usually\n                \n- examines a patients body  - uses a stethoscope to listen to sounds related to the abdomen\n                \nA health care provider will use a special light called a slit lamp to look for Kayser-Fleischer rings in the eyes.\n                \nBlood Tests\n                \nA nurse or technician will draw blood samples at a health care providers office or a commercial facility and send the samples to a lab for analysis. A health care provider may\n                \n- perform liver enzyme or function testsblood tests that may indicate liver abnormalities.  - check copper levels in the blood. Since the copper is deposited into the organs and is not circulating in the blood, most people with Wilson disease have a lower-than-normal level of copper in the blood. In cases of acute liver failure caused by Wilson disease, the level of blood copper is often higher than normal.  - check the level of ceruloplasmina protein that carries copper in the bloodstream. Most people with Wilson disease have a lower-than-normal ceruloplasmin level.  - conduct genetic testing. A health care provider may recommend genetic testing in cases of a known family history of Wilson disease.\n                \nUrine Tests\n                \n24-hour urine collection. A patient will collect urine at home in a special container provided by a health care providers office or a commercial facility. A health care provider sends the sample to a lab for analysis. A 24-hour urine collection will show increased copper in the urine in most patients who have symptoms due to Wilson disease.\n                \nLiver Biopsy\n                \nA liver biopsy is a procedure that involves taking a small piece of liver tissue for examination with a microscope for signs of damage or disease. The health care provider may ask the patient to stop taking certain medications temporarily before the liver biopsy. He or she may also ask the patient to fasteat or drink nothingfor 8 hours before the procedure.\n                \nDuring the procedure, the patient lies on a table, right hand resting above the head. The health care provider applies a local anesthetic to the area where he or she will insert the biopsy needle. If needed, a health care provider will also give sedatives and pain medication. The health care provider uses the needle to take a small piece of liver tissue. He or she may use ultrasound, computerized tomography scans, or other imaging techniques to guide the needle. After the biopsy, the patient must lie on the right side for up to 2 hours and is monitored an additional 2 to 4 hours before being sent home.\n                \nA pathologista doctor who specializes in diagnosing diseasesexamines the liver tissue in a lab. The test can show cirrhosis of the liver. Sometimes the liver biopsy will show copper buildup in the liver cells; however, the results can vary because the copper does not always deposit evenly into the liver. Therefore, health care providers often find it more useful to analyze a piece of liver tissue for copper content. Most patients with Wilson disease have high levels of copper in the liver tissue when compared with carriers or with people who do not have Wilson disease.\n                \nMore information is provided in the NIDDK health topic, Liver Biopsy.\n                \nImaging Tests\n                \nA health care provider may order imaging tests to evaluate brain abnormalities in patients who have nervous system symptoms often seen with Wilson disease, or in patients diagnosed with Wilson disease. Health care providers do not use brain imaging tests to diagnose Wilson disease, though certain findings may suggest the patient has the disease.\n                \nMagnetic resonance imaging (MRI). An MRI is a test that takes pictures of the bodys internal organs and soft tissues without using x rays. A specially trained technician performs the procedure in an outpatient center or a hospital, and a radiologista doctor who specializes in medical imaginginterprets the images. The patient does not need anesthesia, though people with a fear of confined spaces may receive light sedation, taken by mouth. An MRI may include the injection of a special dye, called contrast medium. With most MRI machines, the patient will lie on a table that slides into a tunnel-shaped device that may be open ended or closed at one end. Some machines allow the patient to lie in a more open space. The technician will take a sequence of images from different angles to create a detailed picture of the brain. During sequencing, the patient will hear loud mechanical knocking and humming noises. MRI can show if other diseases or conditions are causing the patients neurological symptoms.\n                \nComputerized tomography (CT) scan. A CT scan uses a combination of x rays and computer technology to create images. For a CT scan, a health care provider may give the patient a solution to drink and an injection of contrast medium. CT scans require the patient to lie on a table that slides into a tunnel-shaped device where a technician takes the x rays. An x-ray technician performs the procedure in an outpatient center or a hospital. A radiologist interprets the images. The patient does not need anesthesia. A CT scan can show if other diseases or conditions are causing the patients neurological symptoms."}
{"_id":"cb007950-320b-435f-84e9-c517837c66a5","text":"A health care provider will treat Wilson disease with a lifelong effort to reduce and control the amount of copper in the body. Treatment may include\n                \n- medications  - changes in eating, diet, and nutrition  - a liver transplant\n                \nMedications\n                \nA health care provider will prescribe medications to treat Wilson disease. The medications have different actions that health care providers use during different phases of the treatment.\n                \nChelating agents. Chelating agents are medications that remove extra copper from the body by releasing it from organs into the bloodstream. Once the cooper is in the bloodstream, the kidneys then filter the copper and pass it into the urine. A health care provider usually recommends chelating agents at the beginning of treatment. A potential side effect of chelating agents is that nervous system symptoms may become worse during treatment. The two medications available for this type of treatment include\n                \n- trientine (Syprine)the risk for side effects and worsening nervous system symptoms appears to be lower with trientine than d-penicillamine. Researchers are still studying the side effects; however, some health care providers prefer to prescribe trientine as the first treatment of choice because it appears to be safer.  - d-penicillaminepeople taking d-penicillamine may have other reactions or side effects, such as      - fever    - a rash    - kidney problems    - bone marrow problems\n                \nA health care provider will prescribe a lower dose of a chelating agent to women who are pregnant to reduce the risk of birth defects. A health care provider should consider future screening on any newborn whose parent has Wilson disease.\n                \nZinc. A health care provider will prescribe zinc for patients who do not have symptoms, or after a person has completed successful treatment using a chelating agent and symptoms begin to improve. Zinc, taken by mouth as zinc salts such as zinc acetate (Galzin), blocks the digestive tracts absorption of copper from food. Although most people taking zinc usually do not experience side effects, some people may experience stomach upset. A health care provider may prescribe zinc for children with Wilson disease who show no symptoms. Women may take the full dosage of zinc safely during pregnancy.\n                \nMaintenance, or long term, treatment begins when symptoms improve and tests show that copper is at a safe level. Maintenance treatment typically includes taking zinc or a lower dose of a chelating agent. A health care provider closely monitors the person and reviews regular blood and urine tests to ensure maintenance treatment controls the copper level in the body.\n                \nTreatment for people with Wilson disease who have no symptoms may include a chelating agent or zinc in order to prevent symptoms from developing and stop or slow disease progression.\n                \nPeople with Wilson disease will take medications for the rest of their lives. Follow-up and adherence to the health care providers treatment plan is necessary to manage symptoms and prevent organ damage."}
{"_id":"dd5bffec-4839-48e6-ac37-84a850527b38","text":"People with Wilson disease should reduce their dietary copper intake by avoiding foods that are high in copper, such as\n                \n- shellfish  - liver  - mushrooms  - nuts  - chocolate\n                \nPeople should not eat these foods during the initial treatment and talk with the health care provider to discuss if they are safe to eat in moderation during maintenance treatment.\n                \nPeople with Wilson disease whose tap water runs through copper pipes or comes from a well should check the copper levels in the tap water. Water that sits in copper pipes may pick up copper residue, but running water lowers the level to within acceptable limits. People with Wilson disease should not use copper containers or cookware to store or prepare food or drinks.\n                \nTo help ensure coordinated and safe care, people should discuss their use of complementary and alternative medical practices, including their use of vitamins and dietary supplements, with their health care provider. Read more at www.nccam. nih.gov\/health. If the health care provider recommends taking any type of supplement or vitamin, a pharmacist can recommend types that do not contain copper.\n                \nPeople should talk with a health care provider about diet changes to reduce copper intake.\n                \nLiver Transplant\n                \nA liver transplant may be necessary in people when\n                \n- cirrhosis leads to liver failure  - acute liver failure happens suddenly  - treatment is not effective\n                \nA liver transplant is an operation to remove a diseased or an injured liver and replace it with a healthy one from another person, called a donor. A successful transplant is a life-saving treatment for people with liver failure.\n                \nMost liver transplants are successful. About 85 percent of transplanted livers are functioning after 1 year.2 Liver transplant surgery provides a cure for Wilson disease in most cases. More information is provided in the NIDDK health topic, Liver Transplantation."}
{"_id":"51f31e98-f3d2-4e90-95c8-e313ac426518","text":"A person cannot prevent Wilson disease; however, people with a family history of Wilson disease, especially those with an affected sibling or parent, should talk with a health care provider about testing. A health care provider may be able to diagnose Wilson disease before symptoms appear. Early diagnosis and treatment of Wilson disease can reduce or even prevent organ damage.\n                \nPeople with a family history of the disease may also benefit from genetic testing that can identify one or more gene mutations. A health care provider may refer a person with a family history of Wilson disease to a geneticista doctor who specializes in genetic diseases."}
{"_id":"61770786-dc38-47a0-8056-16784e3d482a","text":"- Wilson disease is a genetic disease that prevents the body from removing extra copper.  - Normally, the liver filters extra copper and releases it into bile. In Wilson disease, the liver does not filter copper correctly and copper builds up in the liver, brain, eyes, and other organs.  - Wilson disease is caused by an inherited autosomal recessive mutation, or change, in the ATP7B gene. In an autosomal recessive disease, the child has to inherit the gene mutation from both parents to have an increased likelihood for the disease.  - The signs and symptoms of Wilson disease vary, depending on what organs of the body are affected. People with Wilson disease may have      - liver-related signs and symptoms    - central nervous system-related signs and symptoms    - mental health-related signs and symptoms    - other signs and symptoms    - A health care provider will treat Wilson disease with a lifelong effort to reduce and control the amount of copper in the body. Treatment may include      - medications    - changes in eating, diet, and nutrition    - a liver transplant    - People with Wilson disease should reduce their dietary copper intake by avoiding foods that are high in copper, such as      - shellfish    - liver    - mushrooms    - nuts    - chocolate    - A person cannot prevent Wilson disease; however, people with a family history of Wilson disease, especially those with an affected sibling or parent, should talk with a health care provider about testing."}
{"_id":"56a4aebf-546a-4174-8253-8a7192d311b6","text":"Anemia is a condition in which a person has a lower than normal number of red blood cells or the amount of hemoglobin in the red blood cells drops below normal, which prevents the bodys cells from getting enough oxygen. Hemoglobin is an iron-rich protein that gives blood its red color and lets red blood cells transport oxygen from the lungs to the bodys tissues. Therefore, low numbers of red blood cells or low levels of hemoglobin also cause low blood iron levels.\n                \nPeople with anemia may feel tired because their blood does not supply enough oxygen to the bodys organs and tissues. If anemia becomes severe and prolonged, the lack of oxygen in the blood can lead to shortness of breath or exercise intolerancea condition in which a person becomes easily fatigued during or after physical activityand eventually can cause the heart and other organs to fail."}
{"_id":"2c59087e-d754-4b8b-849e-692681a5342d","text":"Anemia of inflammation and chronic disease is a type of anemia that commonly occurs with chronic, or long term, illnesses or infections. Cancer and inflammatory disorders, in which abnormal activation of the immune system occurs, can also cause AI\/ACD.\n                \nAI\/ACD is easily confused with iron-deficiency anemia because in both forms of anemia levels of iron circulating in the blood are low. Iron in the body is found both circulating in the blood and stored in body tissues. Circulating iron is necessary for red blood cell production. Low blood iron levels occur in iron-deficiency anemia because levels of the iron stored in the bodys tissues are depleted. In AI\/ACD, however, iron stores are normal or high. Low blood iron levels occur in AI\/ACD, despite normal iron stores, because inflammatory and chronic diseases interfere with the bodys ability to use stored iron and absorb iron from the diet. AI\/ACD is the second most common form of anemia, after iron-deficiency anemia.1"}
{"_id":"12240436-f7d3-49d7-af3f-879b3f778f23","text":"While AI\/ACD can affect people at any age, older adults are especially at risk because they have the highest rates of chronic disease. AI\/ACD is also common among hospitalized patients, particularly those with chronic illnesses.\n                \nMore than 130 million Americans live with at least one chronic illness.2 Addressing the causes of anemia in people with chronic disease can help improve their health and quality of life."}
{"_id":"deef3d92-ffd3-4e96-9018-5642d3f42db6","text":"Anemia of inflammation and chronic disease is caused by red blood cells not functioning normally, so they cannot absorb and use iron efficiently. In addition, the body cannot respond normally to erythropoietin (EPO), a hormone made by the kidneys that stimulates bone marrow to produce red blood cells. Over time, this abnormal functioning causes a lower than normal number of red blood cells in the body.\n                \nSome of the chronic diseases that lead to AI\/ACD include infectious and inflammatory diseases, kidney disease, and cancer. Certain treatments for chronic diseases may also impair red blood cell production and contribute to AI\/ACD.\n                \nInfectious and inflammatory diseases. As part of the immune system response that occurs with infectious and inflammatory diseases, cells of the immune system release proteins called cytokines. Cytokines help heal the body and defend it against infection. However, they can also affect normal body functions. In AI\/ACD, immune cytokines interfere with the bodys ability to absorb and use iron. Cytokines may also interfere with the production and normal activity of EPO.\n                \nInfectious diseases that cause AI\/ACD include\n                \n- tuberculosis, an infection in the lungs  - HIV\/AIDS, an infection that destroys the immune system  - endocarditis, an infection in the heart  - osteomyelitis, a bone infection\n                \nSometimes, acute infectionsthose that develop quickly and may not last longcan also cause AI\/ACD.\n                \nInflammatory diseases that can lead to AI\/ACD include\n                \n- rheumatoid arthritis, which causes pain, swelling, stiffness, and loss of function in the joints  - lupus, which causes damage to various body tissues, such as the joints, skin, kidneys, heart, lungs, blood vessels, and brain  - diabetes, in which levels of blood glucose, also called blood sugar, are above normal  - heart failure, in which the heart cannot pump enough blood to meet the bodys needs  - inflammatory bowel disease (IBD), diseases that cause inflammation and irritation in the intestines\n                \nIBD, including Crohns disease, can also cause iron deficiency due to poor absorption of iron by the diseased intestine and bleeding from the gastrointestinal (GI) tract.\n                \nKidney disease. People with kidney disease can develop anemia for several different reasons. Diseased kidneys often fail to make enough EPO. In addition, kidney disease results in abnormal absorption and use of iron, which is typical of AI\/ACD. Anemia worsens as kidney disease advances. Therefore, most people with kidney failure have anemia. Kidney failure is described as end-stage kidney disease, sometimes called ESRD, when treated with a kidney transplant or blood-filtering treatments called dialysis.\n                \nPeople with kidney failure can also develop iron deficiency due to blood loss during hemodialysis, a type of dialysis that uses a special filter called a dialyzer to remove wastes from the blood. Low levels of iron and folic acidanother nutrient required for normal red blood cell productionmay also contribute to anemia in people with kidney disease.\n                \nCancer. AI\/ACD can occur with certain types of cancer, including Hodgkins disease, non-Hodgkins lymphoma, and breast cancer. Like infectious and inflammatory diseases, these types of cancer cause inflammatory cytokines to be released in the body. Anemia can also be made worse by chemotherapy and radiation treatments that damage the bone marrow, and by the cancers invasion of bone marrow."}
{"_id":"1eaf6cd5-05fc-47cf-bf36-9023ccfaf7f1","text":"Anemia of inflammation and chronic disease typically develops slowly and, because it is usually mild, may cause few or no symptoms. Symptoms of anemia may also be masked by the symptoms of the underlying disease. Sometimes, AI\/ACD can cause or contribute to\n                \n- fatigue  - weakness  - pale skin  - a fast heartbeat  - shortness of breath  - exercise intolerance"}
{"_id":"fe6d0eb6-4b2c-417e-9fde-e13d70408d92","text":"To diagnose AI\/ACD, a health care provider orders a blood test called a complete blood count (CBC). A blood test involves drawing a persons blood at a health care providers office or commercial facility and sending the sample to a lab for analysis. The CBC includes a measurement of a persons hematocrit, the percentage of the blood that consists of red blood cells. The CBC also measures the amount of hemoglobin in the blood and can show whether a person has a lower than normal number of red blood cells.\n                \nIn addition to measuring hematocrit and hemoglobin, the CBC includes two other measurements to show whether a person has enough iron:\n                \n- The ferritin level indicates the amount of iron stored in the body. A ferritin score below 200 nanograms per liter is a sign that a person may have an iron deficiency.  - The transferrin saturation (TSAT) is a score that indicates how much iron is available, or circulating, to make red blood cells. A TSAT score below 20 percent is another sign of iron deficiency.3\n                \nA CBC result that shows low iron levels in the blood yet normal measures of iron stores in the body is a hallmark of AI\/ACD."}
{"_id":"3afc26b9-86b1-49ca-a766-a96c4105ed75","text":"Anemia of inflammation and chronic disease often is not treated separately from the condition with which it occurs. In general, health care providers focus on treating the underlying illness. If this treatment is successful, the anemia usually resolves. For example, antibiotics prescribed for infection and anti-inflammatory medications prescribed for rheumatoid arthritis or IBD can cause AI\/ACD to disappear. However, AI\/ACD is increasingly being viewed as a medical condition that merits direct treatment.\n                \nFor people with cancer or kidney disease who have low levels of EPO, a synthetic form of EPO may be prescribed. A health care provider usually injects EPO subcutaneouslyunder the skintwo or three times a week. A person may be taught how to inject the EPO at home. People on hemodialysis who cannot tolerate EPO shots may receive EPO intravenously during hemodialysis.\n                \nIf iron deficiency has a role in causing AI\/ACD, a person may need iron supplements to raise hematocrit to a target level. Iron supplements can be taken by pill, subcutaneously, or intravenously during hemodialysis.\n                \nPeople with kidney disease and AI\/ACD may also be advised to take vitamin B12 and folic acid supplements. A person should talk with a health care provider before taking any supplements.\n                \nMore information is provided in the NIDDK health topic, Anemia in Kidney Disease and Dialysis."}
{"_id":"8d8a95e4-4902-4c32-bd49-0f386e854859","text":"People with anemia caused by iron, vitamin B12, or folic acid deficiencies are usually advised to include sources of these nutrients in their diets.\n                \nDietary sources of iron include\n                \n- beans  - breakfast cereals  - chicken  - enriched bread  - spinach  - turkey\n                \nDietary sources of vitamin B12 include\n                \n- beef liver  - breakfast cereals  - chicken  - clams  - fish  - turkey\n                \nDietary sources of folic acid include\n                \n- beans  - breakfast cereals  - chicken  - enriched bread  - rice  - turkey"}
{"_id":"5c795486-c18b-4a3f-b4cd-74a80711c3c9","text":"- Anemia is a condition in which a person has a lower than normal number of red blood cells or the amount of hemoglobin in the red blood cells drops below normal, which prevents the bodys cells from getting enough oxygen.  - Anemia of inflammation and chronic disease (AI\/ACD) is a type of anemia that commonly occurs with chronic illnesses, infections, cancer, or inflammatory disorders.  - AI\/ACD typically develops slowly and, because it is usually mild, may cause few or no symptoms. Sometimes, AI\/ACD can cause or contribute to fatigue, weakness, pale skin, a fast heartbeat, shortness of breath, and exercise intolerance.  - To diagnose AI\/ACD, a health care provider orders a blood test called a complete blood count (CBC).  - AI\/ACD often is not treated separately from the condition with which it occurs. In general, health care providers focus on treating the underlying illness."}
{"_id":"1280d180-2b76-4ce8-9027-51385817f54f","text":"The urinary tract is the bodys drainage system for removing wastes and extra fluid. The urinary tract includes two kidneys, two ureters, a bladder, and a urethra. The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra fluid. Children produce less urine than adults. The amount produced depends on their age. The urine flows from the kidneys to the bladder through tubes called ureters. The bladder stores urine until releasing it through urination. When the bladder empties, urine flows out of the body through a tube called the urethra at the bottom of the bladder.\n                \nThe kidneys and urinary system keep fluids and natural chemicals in the body balanced. While a baby is developing in the mothers womb, called prenatal development, the placentaa temporary organ joining mother and babycontrols much of that balance. The babys kidneys begin to produce urine at about 10 to 12 weeks after conception. However, the mothers placenta continues to do most of the work until the last few weeks of the pregnancy. Wastes and extra water are removed from the babys body through the umbilical cord. The babys urine is released into the amniotic sac and becomes part of the amniotic fluid. This fluid plays a role in the babys lung development."}
{"_id":"c1c1364b-1ed2-4ad8-b6b9-d5e0582faad3","text":"Many types of defects in the urinary tract can cause urine blockage:\n                \n- Vesicoureteral reflux (VUR). Most children with VUR are born with a ureter that did not grow long enough during development in the womb. The valve formed by the ureter pressing against the bladder wall does not close properly, so urine backs uprefluxesfrom the bladder to the ureter and eventually to the kidney. Severe reflux may prevent a kidney from developing normally and may increase the risk for damage from infections after birth. VUR usually affects only one ureter and kidney, though it can affect both ureters and kidneys.  - Ureteropelvic junction (UPJ) obstruction. If urine is blocked where the ureter joins the kidney, only the kidney swells. The ureter remains a normal size. UPJ obstruction usually occurs in only one kidney.\n                \n- Bladder outlet obstruction (BOO). BOO describes any blockage in the urethra or at the opening of the bladder.Posterior urethral valves (PUV), the most common form of BOO seen in newborns and during prenatal ultrasound exams, is a birth defect in boys in which an abnormal fold of tissue in the urethra keeps urine from flowing freely out of the bladder. This defect may cause swelling in the entire urinary tract, including the urethra, bladder, ureters, and kidneys.  - Ureterocele. If the end of the ureter does not develop normally, it can bulge, creating a ureterocele. The ureterocele may obstruct part of the ureter or the bladder.\n                \nSome babies are born with genetic conditions that affect several different systems in the body, including the urinary tract:\n                \n- Prune belly syndrome (PBS). PBS is a group of birth defects involving poor development of the abdominal muscles, enlargement of the ureters and bladder, and both testicles remaining inside the body instead of descending into the scrotum. The skin over the abdomen is wrinkled, giving the appearance of a prune. PBS usually occurs in boys, and most children with PBS have hydronephrosisswelling in the kidneyand VUR.  - Esophageal atresia (EA). EA is a birth defect in which the esophagusthe muscular tube that carries food and liquids from the mouth to the stomachlacks the opening for food to pass into the stomach. Babies born with EA may also have problems with their spinal columns, digestive systems, hearts, and urinary tracts.  - Congenital heart defects. Heart defects range from mild to life threatening. Children born with heart defects also have a higher rate of problems in the urinary tract than children in the general population, suggesting that some types of heart and urinary defects may have a common genetic cause.\n                \nUrine blockage can also be caused by spina bifida and other birth defects that affect the spinal cord. These defects may interrupt nerve signals between the bladder, spinal cord, and brain, which are needed for urination, and lead to urinary retentionthe inability to empty the bladder completelyin newborns. Urine that remains in the bladder can reflux into the ureters and kidneys, causing swelling."}
{"_id":"ce7be19d-0d84-43b2-94b5-f700cec7fe39","text":"Before leaving the hospital, a baby with urine blockage may urinate only small amounts or may not urinate at all. As part of the routine newborn exam, the health care provider may feel an enlarged kidney or find a closed urethra, which may indicate urine blockage. Sometimes urine blockage is not apparent until a child develops symptoms of a urinary tract infection (UTI), including\n                \n- fever  - irritability  - not eating  - nausea  - diarrhea  - vomiting  - cloudy, dark, bloody, or foul-smelling urine  - urinating often\n                \nIf these symptoms persist, the child should see a health care provider. A child 2 months of age or younger with a fever should see a health care provider immediately. The health care provider will ask for a urine sample to test for bacteria."}
{"_id":"7a515b40-70ab-4d62-a25e-97bb3966de0f","text":"When a defect in the urinary tract blocks the flow of urine, the urine backs up and causes the ureters to swell, called hydroureter, and hydronephrosis.\n                \nHydronephrosis is the most common problem found during prenatal ultrasound of a baby in the womb. The swelling may be easy to see or barely detectable. The results of hydronephrosis may be mild or severe, yet the long-term outcome for the childs health cannot always be predicted by the severity of swelling. Urine blockage may damage the developing kidneys and reduce their ability to filter. In the most severe cases of urine blockage, where little or no urine leaves the babys bladder, the amount of amniotic fluid is reduced to the point that the babys lung development is threatened.\n                \nAfter birth, urine blockage may raise a childs risk of developing a UTI. Recurring UTIs can lead to more permanent kidney damage."}
{"_id":"6967e431-2190-49d3-8710-cba2da72baf7","text":"Defects of the urinary tract may be diagnosed before or after the baby is born.\n                \nDiagnosis before Birth\n                \nTests during pregnancy can help determine if the baby is developing normally in the womb.\n                \n- Ultrasound. Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. A prenatal ultrasound can show internal organs within the baby. The procedure is performed in a health care providers office, outpatient center, or hospital by a specially trained technician, and the images are interpreted by     - a radiologista doctor who specializes in medical imaging, or    - an obstetriciana doctor who delivers babies\n                \nThe images can show enlarged kidneys, ureters, or bladders in babies.\n                \n- Amniocentesis. Amniocentesis is a procedure in which amniotic fluid is removed from the mothers womb for testing. The procedure can be performed in the health care providers office, and local anesthetic may be used. The health care provider inserts a thin needle through the abdomen into the uterus to obtain a small amount of amniotic fluid. Cells from the fluid are grown in a lab and then analyzed. The health care provider usually uses ultrasound to find the exact location of the baby. The test can show whether the baby has certain birth defects and how well the babys lungs are developing.  - Chorionic villus sampling (CVS). CVS is the removal of a small piece of tissue from the placenta for testing. The procedure can be performed in the health care providers office; anesthesia is not needed. The health care provider uses ultrasound to guide a thin tube or needle through the vagina or abdomen into the placenta. Cells are removed from the placenta and then analyzed. The test can show whether the baby has certain genetic defects.\n                \nMost healthy women do not need all of these tests. Ultrasound exams during pregnancy are routine. Amniocentesis and CVS are recommended only when a risk of genetic problems exists because of family history or a problem is detected during an ultrasound. Amniocentesis and CVS carry a slight risk of harming the baby and mother or ending the pregnancy in miscarriage, so the risks should be carefully considered.\n                \nDiagnosis after Birth\n                \nDifferent imaging techniques can be used in infants and children to determine the cause of urine blockage.\n                \n- Ultrasound. Ultrasound can be used to view the childs urinary tract. For infants, the image is clearer than could be achieved while the baby was in the womb.  - Voiding cystourethrogram (VCUG). VCUG is an x-ray image of the bladder and urethra taken while the bladder is full and during urination, also called voiding. The procedure is performed in an outpatient center or hospital by an x-ray technician supervised by a radiologist, who then interprets the images. While anesthesia is not needed, sedation may be used for some children. The bladder and urethra are filled with a special dye, called contrast medium, to make the structures clearly visible on the x-ray images. The x-ray machine captures images of the contrast medium while the bladder is full and when the child urinates. The test can show reflux or blockage of the bladder due to an obstruction, such as PUV.  - Radionuclide scan. A radionuclide scan is an imaging technique that detects small amounts of radiation after a person is injected with radioactive chemicals. The dose of the radioactive chemicals is small; therefore, the risk of causing damage to cells is low. Radionuclide scans are performed in an outpatient center or hospital by a specially trained technician, and the images are interpreted by a radiologist. Anesthesia is not needed. Special cameras and computers are used to create images of the radioactive chemicals as they pass through the kidneys. Radioactive chemicals injected into the blood can provide information about kidney function."}
{"_id":"ddf5ab6c-a920-4c39-a810-6ea2ad212ac9","text":"Treatment for urine blockage depends on the cause and severity of the blockage. Hydronephrosis discovered before the baby is born rarely requires immediate action, especially if it is only on one side. The condition often goes away without any treatment before or after birth. The health care provider should keep track of the condition with frequent ultrasounds.\n                \nSurgery\n                \nIf the urine blockage threatens the life of the unborn baby, a fetal surgeon may recommend surgery to insert a shunt or correct the problem causing the blockage. A shunt is a small tube that can be inserted into the babys bladder to release urine into the amniotic sac. The procedure is similar to amniocentesis, in that a needle is inserted through the mothers abdomen. Ultrasound guides placement of the shunt, which is attached to the end of the needle. Alternatively, an endoscopea small, flexible tube with a lightcan be used to place a shunt or to repair the problem causing the blockage. Fetal surgery carries many risks, so it is performed only in special circumstances, such as when the amniotic fluid is absent and the babys lungs are not developing or when the kidneys are severely damaged.\n                \nIf the urinary defect does not correct itself after the child is born, and the child continues to have urine blockage, surgery may be needed to remove the obstruction and restore urine flow. The decision to operate depends on the degree of blockage. After surgery, a small tube, called a stent, may be placed in the ureter or urethra to keep it open temporarily while healing occurs.\n                \nAntibiotics\n                \nAntibiotics are bacteria-fighting medications. A child with possible urine blockage or VUR may be given antibiotics to prevent UTIs from developing until the urinary defect corrects itself or is corrected with surgery.\n                \nIntermittent Catheterization\n                \nIntermittent catheterization may be used for a child with urinary retention due to a nerve disease. The parent or guardian, and later the child, is taught to drain the bladder by inserting a thin tube, called a catheter, through the urethra to the bladder. Emptying the bladder in this way helps to decrease kidney damage, urine leakage, and UTIs."}
{"_id":"f66a1125-cde3-440b-8ef4-5db4157f50c8","text":"Researchers have not found that a mothers eating, diet, and nutrition play a role in causing or preventing urine blockage in newborns."}
{"_id":"c6102b60-73fb-469e-b24d-e2f242fa7a13","text":"- Many types of defects in the urinary tract can cause urine blockage:     - vesicoureteral reflux (VUR)    - ureteropelvic junction (UPJ) obstruction    - bladder outlet obstruction (BOO), such as posterior urethral valves (PUV)    - ureterocele    - Some babies are born with genetic conditions that affect several different systems in the body, including the urinary tract:     - prune belly syndrome (PBS)    - esophageal atresia (EA)    - congenital heart defects    - Urine blockage can also be caused by spina bifida and other birth defects that affect the spinal cord.  - Before leaving the hospital, a baby with urine blockage may urinate only small amounts or may not urinate at all. As part of the routine newborn exam, the health care provider may feel an enlarged kidney or find a closed urethra, which may indicate urine blockage. Sometimes urine blockage is not apparent until a child develops symptoms of a urinary tract infection (UTI).  - When a defect in the urinary tract blocks the flow of urine, the urine backs up and causes the ureters to swell, called hydroureter, and hydronephrosis.  - Defects of the urinary tract may be discovered before or after the baby is born.  - Prenatal tests include ultrasound, amniocentesis, and chorionic villus sampling (CVS).  - Different imaging techniques, including ultrasound, voiding cystourethrogram (VCUG), and radionuclide scan, can be used in infants and children to determine the cause of urine blockage.  - Treatment for urine blockage depends on the cause and severity of the blockage. Hydronephrosis discovered before the baby is born rarely requires immediate action, especially if it is only on one side. Treatments for more serious conditions include     - surgery    - antibiotics    - intermittent catheterization"}
{"_id":"59decc17-2964-4b44-acd5-b4a5054e2fc9","text":"Gas is air in the digestive tractthe large, muscular tube that extends from the mouth to the anus, where the movement of muscles, along with the release of hormones and enzymes, allows for the digestion of food. Gas leaves the body when people burp through the mouth or pass gas through the anus.\n                \nGas is primarily composed of carbon dioxide, oxygen, nitrogen, hydrogen, and sometimes methane. Flatus, gas passed through the anus, may also contain small amounts of gasses that contain sulfur. Flatus that contains more sulfur gasses has more odor.\n                \nEveryone has gas. However, many people think they burp or pass gas too often and that they have too much gas. Having too much gas is rare."}
{"_id":"4937bf4d-83c6-4838-b972-f25576fba410","text":"Gas in the digestive tract is usually caused by swallowing air and by the breakdown of certain foods in the large intestine by bacteria.\n                \nEveryone swallows a small amount of air when eating and drinking. The amount of air swallowed increases when people\n                \n- eat or drink too fast  - smoke  - chew gum  - suck on hard candy  - drink carbonated or fizzy drinks  - wear loose-fitting dentures\n                \nBurping allows some gas to leave the stomach. The remaining gas moves into the small intestine, where it is partially absorbed. A small amount travels into the large intestine for release through the anus.\n                \nThe stomach and small intestine do not fully digest some carbohydratessugars, starches, and fiber found in many foods. This undigested food passes through the small intestine to the large intestine. Once there, undigested carbohydrates are broken down by bacteria in the large intestine, which release hydrogen and carbon dioxide in the process. Other types of bacteria in the large intestine take in hydrogen gas and create methane gas or hydrogen sulfide, the most common sulfur gas in flatus.\n                \nStudies have detected methane in the breath of 30 to 62 percent of healthy adults.1 A larger percentage of adults may produce methane in the intestines, but the levels may be too low to be detected. Research suggests that people with conditions that cause constipation are more likely to produce detectable amounts of methane.1 More research is needed to find out the reasons for differences in methane production and to explore the relationship between methane and other health problems.\n                \nSome of the gas produced in the intestines is absorbed by the bloodstream and carried to the lungs, where it is released in the breath.\n                \nNormally, few bacteria live in the small intestine. Small intestinal bacterial overgrowth is an increase in the number of bacteria or a change in the type of bacteria in the small intestine. These bacteria can produce excess gas and may also cause diarrhea and weight loss. Small intestinal bacterial overgrowth is usually related to diseases or disorders that damage the digestive system or affect how it works, such as Crohns diseasean inflammatory bowel disease that causes inflammation, or swelling, and irritation of any part of the gastrointestinal (GI) tractor diabetes."}
{"_id":"fbd57dba-07dd-4226-a7dd-34d75127006e","text":"Most foods that contain carbohydrates can cause gas. In contrast, fats and proteins cause little gas. Foods that produce gas in one person may not cause gas in someone else, depending on how well individuals digest carbohydrates and the type of bacteria present in the intestines.\n                \nSome foods that may cause gas include\n                \n- beans  - vegetables such as broccoli, cauliflower, cabbage, brussels sprouts, onions, mushrooms, artichokes, and asparagus  - fruits such as pears, apples, and peaches  - whole grains such as whole wheat and bran  - sodas; fruit drinks, especially apple juice and pear juice; and other drinks that contain high-fructose corn syrup, a sweetener made from corn  - milk and milk products such as cheese, ice cream, and yogurt  - packaged foodssuch as bread, cereal, and salad dressingthat contain small amounts of lactose, a sugar found in milk and foods made with milk  - sugar-free candies and gums that contain sugar alcohols such as sorbitol, mannitol, and xylitol"}
{"_id":"cec59d31-3859-48fa-9a72-13a3caf7dfec","text":"The most common symptoms of gas are burping, passing gas, bloating, and abdominal pain or discomfort. However, not everyone experiences these symptoms.\n                \nBurping. Burping, or belching, once in a while, especially during and after meals, is normal. However, people who burp frequently may be swallowing too much air and releasing it before the air enters the stomach.\n                \nSome people who burp frequently may have an upper GI disorder, such as gastroesophageal reflux diseasea chronic condition in which stomach contents flow back up into the esophagus. People may believe that swallowing air and releasing it will relieve the discomfort, and they may intentionally or unintentionally develop a habit of burping to relieve discomfort.\n                \nPassing gas. Passing gas around 13 to 21 times a day is normal.2 Flatulence is excessive gas in the stomach or intestine that can cause bloating and flatus. Flatulence may be the result of problems digesting certain carbohydrates.\n                \nBloating. Bloating is a feeling of fullness and swelling in the abdomen, the area between the chest and hips. Problems digesting carbohydrates may cause increased gas and bloating. However, bloating is not always caused by too much gas. Bloating may result from diseases that affect how gas moves through the intestines, such as rapid gastric emptying, or from diseases that cause intestinal obstruction, such as colon cancer. People who have had many operations, internal hernias, or bands of internal scar tissue called adhesions may experience bloating.\n                \nDisorders such as irritable bowel syndrome (IBS) can affect how gas moves through the intestines or increase pain sensitivity in the intestines. IBS is a functional GI disorder, meaning that the symptoms are caused by changes in how the digestive tract works. The most common symptoms of IBS are abdominal pain or discomfort, often reported as cramping, along with diarrhea, constipation, or both. IBS may give a sensation of bloating because of increased sensitivity to normal amounts of gas.\n                \nEating a lot of fatty food can delay stomach emptying and cause bloating and discomfort, but not necessarily too much gas.\n                \nAbdominal pain and discomfort. People may feel abdominal pain or discomfort when gas does not move through the intestines normally. People with IBS may be more sensitive to gas and feel pain when gas is present in the intestines."}
{"_id":"6f946ddd-0847-4841-b725-980255682bc5","text":"People can try to find the cause of gas on their own by keeping a diary of what they eat and drink and how often they burp, pass gas, or have other symptoms. A diary may help identify specific foods that cause gas.\n                \nA health care provider should be consulted if\n                \n- symptoms of gas are bothersome  - symptoms change suddenly  - new symptoms occur, especially in people older than age 40  - gas is accompanied by other symptoms, such as constipation, diarrhea, or weight loss\n                \nThe health care provider will ask about dietary habits and symptoms and may ask a person to keep a food diary. Careful review of diet and the amount of burping or gas passed may help relate specific foods to symptoms and determine the severity of the problem. Recording gas symptoms can help determine whether the problem is too much gas in the intestines or increased sensitivity to normal amounts of gas.\n                \nIf milk or milk products are causing gas, the health care provider may perform blood or breath tests to check for lactose intolerance, the inability or insufficient ability to digest lactose. Lactose intolerance is caused by a deficiency of the enzyme lactase, which is needed to digest lactose. The health care provider may suggest avoiding milk products for a short time to see if symptoms improve.\n                \nThe health care provider may perform a physical exam and order other types of diagnostic tests, depending on a persons symptoms. These tests can rule out serious health problems that may cause gas or symptoms similar to those of gas."}
{"_id":"fb9c3c14-890d-43f2-86b0-73494804c658","text":"Gas can be treated by reducing swallowed air, making dietary changes, or taking over-the-counter or prescription medications. People who think they have too much gas can try to treat gas on their own before seeing a health care provider. Health care providers can provide advice about reducing gas and prescribe medications that may help.\n                \nReducing swallowed air. Swallowing less air may help reduce gas, especially for people who burp frequently. A health care provider may suggest eating more slowly, avoiding gum and hard candies, or checking with a dentist to make sure dentures fit correctly.\n                \nMaking dietary changes. People may be able to reduce gas by eating less of the foods that cause gas. However, many healthy foods may cause gas, such as fruits and vegetables, whole grains, and milk products. The amount of gas caused by certain foods varies from person to person. Effective dietary changes depend on learning through trial and error which foods cause a person to have gas and how much of the offending foods one can handle.\n                \nWhile fat does not cause gas, limiting high-fat foods can help reduce bloating and discomfort. Less fat in the diet helps the stomach empty faster, allowing gases to move more quickly into the small intestine.\n                \nTaking over-the-counter medications. Some over-the-counter medications can help reduce gas or the symptoms associated with gas:\n                \n- Alpha-galactosidase (Beano), an over-the-counter digestive aid, contains the sugar-digesting enzyme that the body lacks to digest the sugar in beans and many vegetables. The enzyme comes in liquid and tablet form. Five drops are added per serving or one tablet is swallowed just before eating to break down the gas-producing sugars. Beano has no effect on gas caused by lactose or fiber.  - Simethicone (Gas-X, Mylanta Gas) can relieve bloating and abdominal pain or discomfort caused by gas.  - Lactase tablets or drops can help people with lactose intolerance digest milk and milk products to reduce gas. Lactase tablets are taken just before eating foods that contain lactose; lactase drops can be added to liquid milk products. Lactose-free and lactose-reduced milk and milk products are available at most grocery stores.\n                \nTaking prescription medications. Health care providers may prescribe medications to help reduce symptoms, especially for people with small intestinal bacterial overgrowth or IBS. More information about IBS is provided in the NIDDK health topic, Irritable Bowel Syndrome fact sheet."}
{"_id":"d1502565-706f-4bdf-b94c-9350e95562d2","text":"Peoples eating habits and diet affect the amount of gas they have. For example, eating and drinking too fast may increase the amount of air swallowed, and foods that contain carbohydrates may cause some people to have more gas.\n                \nTracking eating habits and symptoms can help identify the foods that cause more gas. Avoiding or eating less of these foods may help reduce gas symptoms."}
{"_id":"ba2abd74-3f9d-47f4-8908-8609e78acc40","text":"- Gas is air in the digestive tract.  - Everyone has gas. However, many people think they pass gas too often and that they have too much gas. Having too much gas is rare.  - Gas in the digestive tract is usually caused by swallowing air and by the breakdown of certain foods in the large intestine by bacteria.  - Most foods that contain carbohydrates can cause gas. In contrast, fats and proteins cause little gas.  - Foods that produce gas in one person may not cause gas for someone else.  - The most common symptoms of gas are burping, passing gas, bloating, and abdominal pain or discomfort.  - Gas can be treated by reducing swallowed air, making dietary changes, or taking over-the-counter or prescription medications."}
{"_id":"a6a63529-dc0d-4a4e-8146-d9f373b2fde6","text":"Proctitis is inflammation of the lining of the rectum, the lower end of the large intestine leading to the anus. The large intestine and anus are part of the gastrointestinal (GI) tract. The GI tract is a series of hollow organs joined in a long, twisting tube from the mouth to the anus. The movement of muscles in the GI tract, along with the release of hormones and enzymes, allows for the digestion of food. With proctitis, inflammation of the rectal liningcalled the rectal mucosais uncomfortable and sometimes painful. The condition may lead to bleeding or mucous discharge from the rectum, among other symptoms."}
{"_id":"e780f0ff-a95a-44a4-bf2c-c61cb3ee02dc","text":"Proctitis is inflammation of the lining of the rectum, the lower end of the large intestine leading to the anus. The large intestine and anus are part of the gastrointestinal (GI) tract. The GI tract is a series of hollow organs joined in a long, twisting tube from the mouth to the anus. The movement of muscles in the GI tract, along with the release of hormones and enzymes, allows for the digestion of food. With proctitis, inflammation of the rectal liningcalled the rectal mucosais uncomfortable and sometimes painful. The condition may lead to bleeding or mucous discharge from the rectum, among other symptoms."}
{"_id":"2d565415-8816-4f12-bbe2-ccd541b8532e","text":"Proctitis has many causes, including acute, or sudden and short-term, and chronic, or long-lasting, conditions. Among the causes are the following:\n                \n- Sexually transmitted diseases (STDs). STDs that can be passed when a person is receiving anal sex are a common cause of proctitis. Common STD infections that can cause proctitis include gonorrhea, chlamydia, syphilis, and herpes. Herpes-induced proctitis may be particularly severe in people who are also infected with the HIV virus.  - Non-STD infections. Infections that are not sexually transmitted also can cause proctitis. Salmonella and Shigella are examples of foodborne bacteria that can cause proctitis. Streptococcal proctitis sometimes occurs in children who have strep throat.  - Anorectal trauma. Proctitis can be caused by trauma to the anorectal areawhich includes the rectum and anusfrom anal sex or the insertion of objects or harmful substances into the rectum, including the chemicals in some enemas.  - Ulcerative colitis and Crohns disease. Two forms of inflammatory bowel disease (IBD)ulcerative colitis and Crohns diseasecan cause proctitis. Ulcerative colitis causes irritation and ulcers, also called sores, in the inner lining of the colonpart of the large intestineand rectum. Crohns disease usually causes irritation in the lower small intestinealso called the ileumor the colon, but it can affect any part of the GI tract.  - Radiation therapy. People who have had radiation therapy that targets the pelvic area also may develop proctitis. Examples of those at risk are people with rectal, ovarian, or prostate cancer who have received radiation treatment directed to those areas. Symptoms of radiation proctitis, most commonly rectal bleeding, will typically occur within 6 weeks after beginning radiation therapy or more than 9 months after its completion.  - Antibiotics. Use of antibiotics may be associated with proctitis in some people. While meant to kill infectioncausing bacteria, antibiotics can also kill nonharmful, or commensal, bacteria in the GI tract. The loss of commensal bacteria can then allow other harmful bacteria known as Clostridium difficile to cause an infection in the colon and rectum."}
{"_id":"8c77371a-2228-4fcc-ac4f-cd0574ba1bf9","text":"Proctitis has many causes, including acute, or sudden and short-term, and chronic, or long-lasting, conditions. Among the causes are the following:\n                \n- Sexually transmitted diseases (STDs). STDs that can be passed when a person is receiving anal sex are a common cause of proctitis. Common STD infections that can cause proctitis include gonorrhea, chlamydia, syphilis, and herpes. Herpes-induced proctitis may be particularly severe in people who are also infected with the HIV virus.  - Non-STD infections. Infections that are not sexually transmitted also can cause proctitis. Salmonella and Shigella are examples of foodborne bacteria that can cause proctitis. Streptococcal proctitis sometimes occurs in children who have strep throat.  - Anorectal trauma. Proctitis can be caused by trauma to the anorectal areawhich includes the rectum and anusfrom anal sex or the insertion of objects or harmful substances into the rectum, including the chemicals in some enemas.  - Ulcerative colitis and Crohns disease. Two forms of inflammatory bowel disease (IBD)ulcerative colitis and Crohns diseasecan cause proctitis. Ulcerative colitis causes irritation and ulcers, also called sores, in the inner lining of the colonpart of the large intestineand rectum. Crohns disease usually causes irritation in the lower small intestinealso called the ileumor the colon, but it can affect any part of the GI tract.  - Radiation therapy. People who have had radiation therapy that targets the pelvic area also may develop proctitis. Examples of those at risk are people with rectal, ovarian, or prostate cancer who have received radiation treatment directed to those areas. Symptoms of radiation proctitis, most commonly rectal bleeding, will typically occur within 6 weeks after beginning radiation therapy or more than 9 months after its completion.  - Antibiotics. Use of antibiotics may be associated with proctitis in some people. While meant to kill infectioncausing bacteria, antibiotics can also kill nonharmful, or commensal, bacteria in the GI tract. The loss of commensal bacteria can then allow other harmful bacteria known as Clostridium difficile to cause an infection in the colon and rectum."}
{"_id":"87a1d499-7a86-420a-8d5c-c5e4adac2347","text":"Tenesmusan uncomfortable and frequent urge to have a bowel movementis one of the most common symptoms of proctitis. Other symptoms may include\n                \n- bloody bowel movements  - rectal bleeding  - a feeling of rectal fullness  - anal or rectal pain  - crampy abdominal pain  - rectal discharge of mucus or pus  - diarrhea or frequent passage of loose or liquid stools"}
{"_id":"80d487d1-b135-4094-aa57-9423f055e226","text":"To diagnose proctitis, a health care provider will take a complete medical history and do a physical exam. The health care provider will ask the patient about symptoms, current and past medical conditions, family history, and sexual behavior that increases the risk of STD-induced proctitis. The physical exam will include an assessment of the patients vital signs, an abdominal exam, and a rectal exam.\n                \nBased on the patients physical exam, symptoms, and other medical information, the doctor will decide which lab tests and diagnostic tests are needed. Lab tests may include blood tests such as a complete blood count to evaluate for blood loss or infection, stool tests to isolate and identify bacteria that may cause disease, and an STD screening. The doctor also may use one of the following diagnostic tests:\n                \n- Rectal culture. A cotton swab is inserted into the rectum to obtain a sample that can be used in tests that isolate and identify organisms that may cause disease.  - Anoscopy. This test allows examination of the anal canal and lower rectum by opening the anus using a special instrument called an anoscope.  - Flexible sigmoidoscopy and colonoscopy. These tests are used to help diagnose Crohns disease. The tests are similar, but colonoscopy is used to view the entire colon and rectum, while flexible sigmoidoscopy is used to view just the lower colon and rectum. For both tests, a health care provider will provide written bowel prep instructions to follow at home before the test. The person may be asked to follow a clear liquid diet for 1 to 3 days before the test. A laxative may be required the night before the test. One or more enemas may be required the night before and about 2 hours before the test."}
{"_id":"d1b49875-a93e-4b00-a7c8-8265f4cccb42","text":"Treatment of proctitis depends on its cause. The goal of treatment is to reduce inflammation, control symptoms, and eliminate infection, if it is present. Only a doctor can determine the cause of proctitis and the best course of treatment. With proper medical attention, proctitis can be successfully treated.\n                \nProctitis from Infection\n                \nIf lab tests confirm that an STD or non-STD infection is present, medication is prescribed based on the type of infection found. Antibiotics are prescribed to kill bacteria; antiviral medications are prescribed to treat viruses. Although some STD viruses cannot be eliminated, antivirals can control their symptoms.\n                \nProctitis from Other Causes\n                \nIf antibiotic use triggered proctitis, the doctor may prescribe a different antibiotic designed to destroy the harmful bacteria that have developed in the intestines.\n                \nIf proctitis is caused by anorectal trauma, the activity causing the inflammation should be stopped. Healing usually occurs in 4 to 6 weeks. The doctor may recommend over-the-counter medications such as antidiarrheals and those used for pain relief, such as aspirin and ibuprofen.\n                \nTreatment of radiation proctitis is based on symptoms. Radiation proctitis causing only mild symptoms such as occasional bleeding or tenesmus may heal without treatment. For people with persistent or severe bleeding, thermal therapy may be used to stop bleeding and inflammation. Thermal therapy is done during flexible sigmoidoscopy or colonoscopy and targets the rectal lining with a heat probe, electric current, or laser. Argon plasma coagulation is the most common thermal therapy used to control bleeding in radiation proctitis. In many cases, several treatments are required. Obstruction that results from a stricturea narrowing of the rectumcaused by radiation proctitis may be treated with stool softeners in mild cases. In people with narrower strictures, dilation to enlarge the narrow area may be required. Sucralfate, 5-aminosalicylic acidknown as 5-ASAor corticosteroid enemas can also be used to ease pain and reduce inflammation from radiation proctitis, although their effectiveness is limited.\n                \nWhen a chronic IBD such as ulcerative colitis or Crohns disease causes proctitis, treatment aims to reduce inflammation, control symptoms, and induce and maintain remissiona period when the person is symptom-free. Treatment depends on the extent and severity of the disease.\n                \nAnti-inflammation medications. Mild proctitis can often be effectively treated with topical mesalamine, either suppositories or enemas.\n                \nSome people with IBD and proctitis cannot tolerateor may have an incomplete response torectal therapy with 5-ASA suppositories or enemas. For these people, the doctor may prescribe oral medications alone or in combination with rectal therapy. Oral medications commonly used for proctitis contain salicylate. These include sulfasalazine- or mesalamine-containing medications, such as Asacol, Dipentum, or Pentasa. Possible side effects of oral administration of sulfasalazine- or mesalaminecontaining medications include nausea, vomiting, heartburn, diarrhea, and headache. Improvement in symptoms, including a decrease in bleeding, can occur within a few days, although complete healing requires 4 to 6 weeks of therapy.\n                \nCortisone or steroids. These medications, also called corticosteroids, are effective at reducing inflammation. Prednisone and budesonide are generic names of two medications in this group. Corticosteroids for proctitis may be taken in pill, suppository, or enema form. When symptoms are at their worst, corticosteroids are usually prescribed in a large dose. The dosage is then gradually lowered once symptoms are controlled. Corticosteroids can cause serious side effects, including greater susceptibility to infection and osteoporosis, or weakening of the bones.\n                \nImmune system suppressors. Medications that suppress the immune systemcalled immunosuppressive medicationsare also used to treat proctitis. The most commonly prescribed medication is 6-mercaptopurine or a related medication, azathioprine. Immunosuppressive medications work by blocking the immune reaction that contributes to inflammation. These medications may cause side effects such as nausea, vomiting, and diarrhea and may lower a persons resistance to infection. Some patients are treated with a combination of corticosteroids and immunosuppressive medications. Some studies suggest that immunosuppressive medications may enhance the effectiveness of corticosteroids.\n                \nInfliximab (Remicade). Researchers have found that high levels of a protein produced by the immune system, called tumor necrosis factor (TNF), are present in people with Crohns disease. Infliximab is the first of a group of medications that bind to TNF substances to block the bodys inflammation response. The U.S. Food and Drug Administration approved the medication for the treatment of moderate to severe Crohns disease that does not respond to standard therapiesmesalamine substances, corticosteroids, immunosuppressive medicationsand for the treatment of open, draining fistulas. The medication is also given to people who have Crohns disease with proctitis. Some studies suggest that infliximab may enhance the effectiveness of immunosuppressive medications.\n                \nBacterial infection can occur with flare-ups of ulcerative colitis or Crohns disease. Antibiotics may also be used to treat flare-ups in people with IBD and proctitis.\n                \nMore information about the treatment of IBD is provided in the NIDDK health topics, Ulcerative Colitis and Crohns Disease."}
{"_id":"6a1eed1e-d7c5-4a3f-962b-be9c48ea3498","text":"Drinking plenty of fluids is important when diarrhea or frequent passage of loose or liquid stools occurs.\n                \nAvoiding caffeine and foods that are greasy, high in fiber, or sweet may lessen diarrhea symptoms. Some people also have problems digesting lactosethe sugar found in milk and milk productsduring or after a bout of diarrhea. Yogurt, which has less lactose than milk, is often better tolerated. Yogurt with active, live bacterial cultures may even help people recover from diarrhea more quickly.\n                \nIf diarrhea symptoms improve, soft, bland foods can be added to the diet, including bananas, plain rice, boiled potatoes, toast, crackers, cooked carrots, and baked chicken without the skin or fat. If the diarrhea stops, a normal diet may be resumed if tolerated."}
{"_id":"6dcda6b2-06a7-4b6c-8368-52089b78d11f","text":"Proctitis that is not treated or does not respond to treatment may lead to complications, including\n                \n- severe bleeding and anemiaa condition in which red blood cells are fewer or smaller than normal, which means less oxygen is carried to the bodys cells  - abscessespainful, swollen, pus-filled areas caused by infection  - ulcers on the intestinal lining  - fistulasabnormal connections between two parts inside the body"}
{"_id":"c571bb15-9f76-40a2-a9c4-7bd5c41e4cb7","text":"People who receive anal sex can avoid getting STD-related proctitis by having their partner use a condom. If anorectal trauma caused proctitis, stopping the activity that triggered inflammation often will stop the inflammation and prevent recurrence.\n                \nOther causes of proctitis cannot always be prevented. However, their symptoms can be treated by a doctor."}
{"_id":"14c23aed-a8b9-44f1-a44b-afffe756d414","text":"- Proctitis is inflammation of the lining of the rectum, the lower end of the large intestine leading to the anus.  - Common causes of proctitis are sexually transmitted diseases (STDs), non-STD infections, anorectal trauma, ulcerative colitis and Crohns disease, radiation therapy, and antibiotic use.  - Treatment of proctitis depends on its cause; the goal of treatment is to reduce inflammation, control symptoms, and eliminate infection, if present.  - With proper medical attention, proctitis can be successfully treated.  - If infection is present with proctitis, antibiotics can be used to kill bacteria and antiviral medications can treat viral infections.  - People who receive anal sex can avoid getting STD-related proctitis by having their partner use a condom.  - If anorectal trauma caused proctitis, stopping the activity that triggered inflammation often will stop the inflammation and prevent recurrence.  - Some causes of proctitis cannot always be prevented, but their symptoms can be treated by a doctor."}
{"_id":"4a1fc2c3-2080-495b-8fa7-adadf7771a15","text":"Often, no symptoms appear during the early stages of diabetes retina problems. As retina problems worsen, your symptoms might include\n                \n- blurry or double vision  - rings, flashing lights, or blank spots in your vision  - dark or floating spots in your vision  - pain or pressure in one or both of your eyes  - trouble seeing things out of the corners of your eyes"}
{"_id":"b3503b96-e08c-443f-be47-eb1b82a7511d","text":"You can help your diabetes retina problems by controlling your\n                \n- blood glucose  - blood pressure  - cholesterol and triglycerides, or types of blood fat\n                \nIf your retinopathy still does not improve, then you may need other treatments. You will need to see an ophthalmologist who can decide whether you need one of these treatments:\n                \n- Medicines. Your doctor treats macular edema with injections of medicines into the eye. These medicines block a protein in the body that causes abnormal blood vessel growth and fluid leakage. Reducing the fluid leakage often allows the retina to return to normal thickness. The ophthalmologist will numb your eye and then insert a tiny needle to deliver the medicine.  - Laser treatment. Your doctor can also treat macular edema with focal laser treatment. In one visit, the ophthalmologist will numb your eye and place many small laser burns in the areas leaking fluid near the macula. These burns slow the leakage of fluid and reduce the amount of fluid in your retina.  Sometimes your doctor also treats diabetic retinopathy with scatter laser treatment. In two or more visits, the ophthalmologist will numb your eye and place thousands of laser burns around the new, weak blood vessels away from the macula, causing them to shrink.  Laser treatment can greatly reduce your chances of blindness from retina damage. However, laser treatment often cannot restore vision that has already been lost.  Treatment with medicines or lasers can be performed in your ophthalmologists office.  - Vitrectomy. If the bleeding in your eye is severe, you may need to go to the hospital for a surgery called a vitrectomy. Your ophthalmologist will numb your eye or give you general anesthesia to help you fall asleep. The ophthalmologist will make a tiny cut in your eye and remove the vitreous gel that is clouded with blood. The ophthalmologist replaces the vitreous gel with a salt solution."}
{"_id":"a46a0bb9-6e37-419e-af02-5c73cef2b785","text":"Gastroparesis, also called delayed gastric emptying, is a disorder that slows or stops the movement of food from the stomach to the small intestine. Normally, the muscles of the stomach, which are controlled by the vagus nerve, contract to break up food and move it through the gastrointestinal (GI) tract. The GI tract is a series of hollow organs joined in a long, twisting tube from the mouth to the anus. The movement of muscles in the GI tract, along with the release of hormones and enzymes, allows for the digestion of food. Gastroparesis can occur when the vagus nerve is damaged by illness or injury and the stomach muscles stop working normally. Food then moves slowly from the stomach to the small intestine or stops moving altogether."}
{"_id":"18e8aa1f-2ff2-42d1-82f6-485ba160c224","text":"Most people diagnosed with gastroparesis have idiopathic gastroparesis, which means a health care provider cannot identify the cause, even with medical tests. Diabetes is the most common known cause of gastroparesis. People with diabetes have high levels of blood glucose, also called blood sugar. Over time, high blood glucose levels can damage the vagus nerve. Other identifiable causes of gastroparesis include intestinal surgery and nervous system diseases such as Parkinsons disease or multiple sclerosis. For reasons that are still unclear, gastroparesis is more commonly found in women than in men."}
{"_id":"d3db6de5-5893-4044-9626-5d55ef648c61","text":"The most common symptoms of gastroparesis are nausea, a feeling of fullness after eating only a small amount of food, and vomiting undigested foodsometimes several hours after a meal. Other symptoms of gastroparesis include\n                \n- gastroesophageal reflux (GER), also called acid reflux or acid regurgitationa condition in which stomach contents flow back up into the esophagus, the organ that connects the mouth to the stomach  - pain in the stomach area  - abdominal bloating  - lack of appetite\n                \nSymptoms may be aggravated by eating greasy or rich foods, large quantities of foods with fibersuch as raw fruits and vegetablesor drinking beverages high in fat or carbonation. Symptoms may be mild or severe, and they can occur frequently in some people and less often in others. The symptoms of gastroparesis may also vary in intensity over time in the same individual. Sometimes gastroparesis is difficult to diagnose because people experience a range of symptoms similar to those of other diseases."}
{"_id":"02058ae5-e345-400f-b8be-a21b18cd8b70","text":"Gastroparesis is diagnosed through a physical exam, medical history, blood tests, tests to rule out blockage or structural problems in the GI tract, and gastric emptying tests. Tests may also identify a nutritional disorder or underlying disease. To rule out any blockage or other structural problems, the health care provider may perform one or more of the following tests:\n                \n- Upper gastrointestinal (GI) endoscopy. This procedure involves using an endoscopea small, flexible tube with a lightto see the upper GI tract, which includes the esophagus, stomach, and duodenumthe first part of the small intestine. The test is performed at a hospital or outpatient center by a gastroenterologista doctor who specializes in digestive diseases. The endoscope is carefully fed down the esophagus and into the stomach and duodenum. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining. A person may receive a liquid anesthetic that is gargled or sprayed on the back of the throat. An intravenous (IV) needle is placed in a vein in the arm if general anesthesia is given. The test may show blockage or large bezoarssolid collections of food, mucus, vegetable fiber, hair, or other material that cannot be digested in the stomachthat are sometimes softened, dissolved, or broken up during an upper GI endoscopy.  - Upper GI series. An upper GI series may be done to look at the small intestine. The test is performed at a hospital or outpatient center by an x-ray technician, and the images are interpreted by a radiologista doctor who specializes in medical imaging. Anesthesia is not needed. No eating or drinking is allowed for 8 hours before the procedure, if possible. If the person has diabetes, a health care provider may give different instructions about fasting before the test. During the procedure, the person will stand or sit in front of an x-ray machine and drink barium, a chalky liquid. Barium coats the small intestine, making signs of gastroparesis show up more clearly on x rays. Gastroparesis is likely if the x ray shows food in the stomach after fasting. A person may experience bloating and nausea for a short time after the test. For several days afterward, barium liquid in the GI tract causes stools to be white or light colored. A health care provider will give the person specific instructions about eating and drinking after the test.  - Ultrasound. Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. The procedure is performed in a health care providers office, outpatient center, or hospital by a specially trained technician, and the images are interpreted by a radiologist; anesthesia is not needed. The images can show whether gallbladder disease and pancreatitis could be the cause of a persons digestive symptoms, rather than gastroparesis.  - Gastric emptying scintigraphy. The test involves eating a bland mealsuch as eggs or an egg substitutethat contains a small amount of radioactive material. The test is performed in a radiology center or hospital by a specially trained technician and interpreted by a radiologist; anesthesia is not needed. An external camera scans the abdomen to show where the radioactive material is located. The radiologist is then able to measure the rate of gastric emptying at 1, 2, 3, and 4 hours after the meal. If more than 10 percent of the meal is still in the stomach at 4 hours, the diagnosis of gastroparesis is confirmed.  - SmartPill. The SmartPill is a small electronic device in capsule form. The SmartPill test is available at specialized outpatient centers. The images are interpreted by a radiologist. The device is swallowed and moves through the entire digestive tract, sending information to a cell-phone-sized receiver worn around the persons waist or neck. The recorded information provides a detailed record of how quickly food travels through each part of the digestive tract.  - Gastric emptying breath test. With this test, the person eats a special test meal that includes a natural material with a special type of carbon in it. Then, breath samples are taken over a period of several hours to measure the amount of the material in the exhaled breath. The results allow the health care provider to calculate how fast the stomach is emptying."}
{"_id":"96ee9d74-5638-471b-8512-14fded3f6f95","text":"Treatment of gastroparesis depends on the severity of the persons symptoms. In most cases, treatment does not cure gastroparesis, which is usually a chronic, or long-lasting, condition. Gastroparesis is also a relapsing conditionthe symptoms can come and go for periods of time. Treatment helps people manage the condition so they can be as comfortable and active as possible."}
{"_id":"6420f6fc-e527-4b83-a32b-61064627ee97","text":"Changing eating habits can sometimes help control the severity of gastroparesis symptoms. A health care provider may suggest eating six small meals a day instead of three large ones. If less food enters the stomach each time a person eats, the stomach may not become overly full, allowing it to empty more easily. Chewing food well, drinking noncarbonated liquids with a meal, and walking or sitting for 2 hours after a mealinstead of lying downmay assist with gastric emptying.\n                \nA health care provider may also recommend avoiding high-fat and fibrous foods. Fat naturally slows digestion and some raw vegetables and fruits are more difficult to digest than other foods. Some foods, such as oranges and broccoli, contain fibrous parts that do not digest well. People with gastroparesis should minimize their intake of large portions of these foods because the undigested parts may remain in the stomach too long. Sometimes, the undigested parts form bezoars.\n                \nWhen a person has severe symptoms, a liquid or pured diet may be prescribed. As liquids tend to empty more quickly from the stomach, some people may find a pured diet helps improve symptoms. Pured fresh or cooked fruits and vegetables can be incorporated into shakes and soups. A health care provider may recommend a dietitian to help a person plan meals that minimize symptoms and ensure all nutritional needs are met.\n                \nWhen the most extreme cases of gastroparesis lead to severe nausea, vomiting, and dehydration, urgent care may be required at a medical facility where IV fluids can be given.\n                \n\n                \nMedications\n                \nSeveral prescription medications are available to treat gastroparesis. A combination of medications may be used to find the most effective treatment.\n                \nMetoclopramide (Reglan). This medication stimulates stomach muscle contractions to help with gastric emptying. Metoclopramide also helps reduce nausea and vomiting. The medication is taken 20 to 30 minutes before meals and at bedtime. Possible side effects of metoclopramide include fatigue, sleepiness, and depression. Currently, this is the only medication approved by the FDA for treatment of gastroparesis. However, the FDA has placed a black box warning on this medication because of rare reports of it causing an irreversible neurologic side effect called tardive dyskinesiaa disorder that affects movement.\n                \nErythromycin. This antibiotic, prescribed at low doses, may improve gastric emptying. Like metaclopramide, erythromycin works by increasing the contractions that move food through the stomach. Possible side effects of erythromycin include nausea, vomiting, and abdominal cramps.\n                \nOther medications. Other medications may be used to treat symptoms and problems related to gastroparesis. For example, medications known as antiemetics are used to help control nausea and vomiting.\n                \nBotulinum Toxin\n                \nBotulinum toxin is a nerve blocking agent also known as Botox. After passing an endoscope into the stomach, a health care provider injects the Botox into the pylorus, the opening from the stomach into the duodenum. Botox is supposed to help keep the pylorus open for longer periods of time and improve symptoms of gastroparesis. Although some initial research trials showed modest improvement in gastroparesis symptoms and the rate of gastric emptying following the injections, other studies have failed to show the same degree of effectiveness of the Botox injections.1\n                \nGastric Electrical Stimulation\n                \nThis treatment alternative may be effective for some people whose nausea and vomiting do not improve with dietary changes or medications. A gastric neurostimulator is a surgically implanted battery-operated device that sends mild electrical pulses to the stomach muscles to help control nausea and vomiting. The procedure may be performed at a hospital or outpatient center by a gastroenterologist. General anesthesia may be required. The gastroenterologist makes several tiny incisions in the abdomen and inserts a laparoscopea thin tube with a tiny video camera attached. The camera sends a magnified image from inside the stomach to a video monitor, giving the gastroenterologist a close-up view of the tissues. Once implanted, the settings on the battery-operated device can be adjusted to determine the settings that best control symptoms.\n                \nJejunostomy\n                \nIf medications and dietary changes dont work, and the person is losing weight or requires frequent hospitalization for dehydration, a health care provider may recommend surgically placing a feeding tube through the abdominal wall directly into a part of the small intestine called the jejunum. The surgical procedure is known as a jejunostomy. The procedure is performed by a surgeon at a hospital or outpatient center. Anesthesia is needed. The feeding tube bypasses the stomach and delivers a special liquid food with nutrients directly into the jejunum. The jejunostomy is used only when gastroparesis is extremely severe.\n                \nParenteral Nutrition\n                \nWhen gastroparesis is so severe that dietary measures and other treatments are not helping, a health care provider may recommend parenteral nutritionan IV liquid food mixture supplied through a special tube in the chest. The procedure is performed by a surgeon at a hospital or outpatient center; anesthesia is needed. The surgeon inserts a thin, flexible tube called a catheter into a chest vein, with the catheter opening outside the skin. A bag containing liquid nutrients is attached to the catheter, and the nutrients are transported through the catheter into the chest vein and into the bloodstream. This approach is a less preferable alternative to a jejunostomy and is usually a temporary treatment to get through a difficult period of gastroparesis."}
{"_id":"a8ce2cf4-3865-44c3-8447-5e58ea35dde1","text":"An elevated blood glucose level directly interferes with normal stomach emptying, so good blood glucose control in people with diabetes is important. However, gastroparesis can make blood glucose control difficult. When food that has been delayed in the stomach finally enters the small intestine and is absorbed, blood glucose levels rise. Gastric emptying is unpredictable with gastroparesis, causing a persons blood glucose levels to be erratic and difficult to control.\n                \nThe primary treatment goals for gastroparesis related to diabetes are to improve gastric emptying and regain control of blood glucose levels. In addition to the dietary changes and treatments already described, a health care provider will likely adjust the persons insulin regimen.\n                \nTo better control blood glucose, people with diabetes and gastroparesis may need to\n                \n- take insulin more often or change the type of insulin they take  - take insulin after meals, instead of before  - check blood glucose levels frequently after eating and administer insulin when necessary\n                \nA health care provider will give specific instructions for taking insulin based on the individuals needs and the severity of gastroparesis.\n                \nIn some cases, the dietitian may suggest eating several liquid or pured meals a day until gastroparesis symptoms improve and blood glucose levels are more stable."}
{"_id":"afe3d048-e544-40d4-857b-bdb6f9ff32c9","text":"The problems of gastroparesis can include\n                \n- severe dehydration due to persistent vomiting  - gastroesophageal reflux disease (GERD), which is GER that occurs more than twice a week for a few weeks; GERD can lead to esophagitis irritation of the esophagus  - bezoars, which can cause nausea, vomiting, obstruction, or interfere with absorption of some medications in pill form  - difficulty managing blood glucose levels in people with diabetes  - malnutrition due to poor absorption of nutrients or a low calorie intake  - decreased quality of life, including work absences due to severe symptoms"}
{"_id":"7cafa287-1ea1-4d51-a6e4-5961bd51fed2","text":"- Gastroparesis, also called delayed gastric emptying, is a disorder that slows or stops the movement of food from the stomach to the small intestine.  - Gastroparesis can occur when the vagus nerve is damaged by illness or injury and the stomach muscles stop working normally. Food then moves slowly from the stomach to the small intestine or stops moving altogether.  - Most people diagnosed with gastroparesis have idiopathic gastroparesis, which means a health care provider cannot identify the cause, even with medical tests.  - Diabetes is the most common known cause of gastroparesis. People with diabetes have high levels of blood glucose, also called blood sugar. Over time, high blood glucose levels can damage the vagus nerve.  - The most common symptoms of gastroparesis are nausea, a feeling of fullness after eating only a small amount of food, and vomiting undigested food sometimes several hours after a meal. Other common symptoms include gastroesophageal reflux (GER), pain in the stomach area, abdominal bloating, and lack of appetite.  - Gastroparesis is diagnosed through a physical exam, medical history, blood tests, tests to rule out blockage or structural problems in the gastrointestinal (GI) tract, and gastric emptying tests.  - Changing eating habits can sometimes help control the severity of gastroparesis symptoms. A health care provider may suggest eating six small meals a day instead of three large ones. When a person has severe symptoms, a liquid or pured diet may be prescribed.  - Treatment of gastroparesis may include medications, botulinum toxin, gastric electrical stimulation, jejunostomy, and parenteral nutrition.  - For people with gastroparesis and diabetes, a health care provider will likely adjust the persons insulin regimen."}
{"_id":"7556a4c4-1c89-41e1-820b-84ebcf363d23","text":"Abdominal adhesions are bands of  fibrous tissue that can form between abdominal tissues and organs. Normally, internal tissues and organs have slippery surfaces, preventing them from sticking together as the body moves. However, abdominal adhesions cause tissues and organs in the abdominal cavity to stick together."}
{"_id":"ed82e719-0825-42ed-b83d-266568448f3c","text":"The abdominal cavity is the internal area of the body between the chest and hips that contains the lower part of the esophagus, stomach, small intestine, and large intestine. The esophagus carries food and liquids from the mouth to the stomach, which slowly pumps them into the small and large intestines. Abdominal adhesions can kink, twist, or pull the small and large intestines out of place, causing an intestinal obstruction. Intestinal obstruction, also called a bowel obstruction, results in the partial or complete blockage of movement of food or stool through the intestines."}
{"_id":"a5b2ee94-9619-4a22-a774-1926a04a55e6","text":"Abdominal surgery is the most frequent cause of abdominal adhesions. Surgery-related causes include\n                \n- cuts involving internal organs   - handling of internal organs  - drying out of internal organs and tissues  - contact of internal tissues with foreign materials, such as gauze, surgical gloves, and stitches  - blood or blood clots that were not rinsed away during surgery\n                \nAbdominal adhesions can also result from inflammation not related to surgery, including\n                \n- appendix rupture  - radiation treatment  - gynecological infections  - abdominal infections\n                \nRarely, abdominal adhesions form without apparent cause."}
{"_id":"6c8865b2-b7b0-4406-ae4f-3945edc0f116","text":"Of patients who undergo abdominal surgery, 93 percent develop abdominal adhesions.1 Surgery in the lower abdomen and pelvis, including bowel and gynecological operations, carries an even greater chance of abdominal adhesions. Abdominal adhesions can become larger and tighter as time passes, sometimes causing problems years after surgery."}
{"_id":"72220cd6-b442-4e34-8250-8d2535385671","text":"In most cases, abdominal adhesions do not cause symptoms. When symptoms are present, chronic abdominal pain is the most common."}
{"_id":"beada790-f1ff-4447-8638-d42afc5862d5","text":"Abdominal adhesions can cause intestinal obstruction and female infertilitythe inability to become pregnant after a year of trying.\n                \nAbdominal adhesions can lead to female infertility by preventing fertilized eggs from reaching the uterus, where fetal development takes place. Women with abdominal adhesions in or around their fallopian tubes have an increased chance of ectopic pregnancya fertilized egg growing outside the uterus. Abdominal adhesions inside the uterus may result in repeated miscarriagesa pregnancy failure before 20 weeks.\n                \n\n                \nSeek Help for Emergency Symptoms   A complete intestinal obstruction is life threatening and requires immediate medical attention and often surgery. Symptoms of an intestinal obstruction include   - severe abdominal pain or cramping   - nausea   - vomiting   - bloating    - loud bowel sounds   - abdominal swelling   - the inability to have a bowel movement or pass gas   - constipationa condition in which a person has fewer than three bowel movements a week; the bowel movements may be painful     A person with these symptoms should seek medical attention immediately."}
{"_id":"0fcc5388-e204-49fd-9e9a-27ac9e52c424","text":"A complete intestinal obstruction is life threatening and requires immediate medical attention and often surgery. Symptoms of an intestinal obstruction include\n                \n- severe abdominal pain or cramping  - nausea  - vomiting  - bloating   - loud bowel sounds  - abdominal swelling  - the inability to have a bowel movement or pass gas  - constipationa condition in which a person has fewer than three bowel movements a week; the bowel movements may be painful\n                \nA person with these symptoms should seek medical attention immediately."}
{"_id":"589efb1c-2ce4-4bdc-b6e2-86de39f2107b","text":"Abdominal adhesions cannot be detected by tests or seen through imaging techniques such as x rays or ultrasound. Most abdominal adhesions are found during surgery performed to examine the abdomen. However, abdominal x rays, a lower gastrointestinal (GI) series, and computerized tomography (CT) scans can diagnose intestinal obstructions.\n                \n- Abdominal x rays use a small amount of radiation to create an image that is recorded on  film or a computer. An x ray is performed at a hospital or an outpatient center by an x-ray technician, and the images are interpreted by a radiologista doctor who specializes in medical imaging. An x ray does not require anesthesia. The person will lie on a table or stand during the x ray. The x-ray machine is positioned over the abdominal area. The person will hold his or her breath as the picture is taken so that the picture will not be blurry. The person may be asked to change position for additional pictures.   - A lower GI series is an x-ray exam that is used to look at the large intestine. The test is performed at a hospital or an outpatient center by an x-ray technician, and the images are interpreted by a radiologist. Anesthesia is not needed. The health care provider may provide written bowel prep instructions to follow at home before the test. The person may be asked to follow a clear liquid diet for 1 to 3 days before the procedure. A laxative or an enema may be used before the test. A laxative is medication that loosens stool and increases bowel movements. An enema involves fl ushing water or laxative into the rectum using a special squirt bottle.  For the test, the person will lie on a table while the radiologist inserts a flexible tube into the persons anus. The large intestine is fi lled with barium, making signs of underlying problems show up more clearly on x rays.   - CT scans use a combination of x rays and computer technology to create images. The procedure is performed at a hospital or an outpatient center by an x-ray technician, and the images are interpreted by a radiologist. Anesthesia is not needed. A CT scan may include the injection of a special dye, called contrast medium. The person will lie on a table that slides into a tunnel-shaped device where the x rays are taken."}
{"_id":"f6df8489-2499-4985-aafb-f19f13ad771b","text":"Abdominal adhesions that do not cause symptoms generally do not require treatment. Surgery is the only way to treat abdominal adhesions that cause pain, intestinal obstruction, or fertility problems. More surgery, however, carries the risk of additional abdominal adhesions. People should speak with their health care provider about the best way to treat their abdominal adhesions.\n                \nComplete intestinal obstructions usually require immediate surgery to clear the blockage. Most partial intestinal obstructions can be managed without surgery."}
{"_id":"1d96a30c-3a0c-4ae2-b783-3d051a938b0c","text":"Abdominal adhesions are diffi cult to prevent; however, certain surgical techniques can minimize abdominal adhesions.\n                \nLaparoscopic surgery decreases the potential for abdominal adhesions because several tiny incisions are made in the lower abdomen instead of one large incision. The surgeon inserts a laparoscopea thin tube with a tiny video camera attachedinto one of the small incisions. The camera sends a magnified image from inside the body to a video monitor. Patients will usually receive general anesthesia during this surgery.\n                \nIf laparoscopic surgery is not possible and a large abdominal incision is required, at the end of surgery a special fi lmlike material can be inserted between organs or between the organs and the abdominal incision. The fi lmlike material, which looks similar to wax paper and is absorbed by the body in about a week, hydrates organs to help prevent abdominal adhesions.\n                \nOther steps taken during surgery to reduce abdominal adhesions include\n                \n- using starch- and latex-free gloves  - handling tissues and organs gently  - shortening surgery time   - using moistened drapes and swabs  - occasionally applying saline solution"}
{"_id":"b39d467d-8149-4222-9fe7-ff061fe8da09","text":"Researchers have not found that eating, diet, and nutrition play a role in causing or preventing abdominal adhesions. A person with a partial intestinal obstruction may relieve symptoms with a liquid or low- fiber diet, which is more easily broken down into smaller particles by the digestive system."}
{"_id":"1bc50197-94f6-43a1-879f-0e476281c0cc","text":"- Abdominal adhesions are bands of fibrous tissue that can form between abdominal tissues and organs. Abdominal adhesions cause tissues and organs in the abdominal cavity to stick together.  - Abdominal surgery is the most frequent cause of abdominal adhesions. Of patients who undergo abdominal surgery, 93 percent develop abdominal adhesions.  - In most cases, abdominal adhesions do not cause symptoms. When symptoms are present, chronic abdominal pain is the most common.  - A complete intestinal obstruction is life threatening and requires immediate medical attention and often surgery.  - Abdominal adhesions cannot be detected by tests or seen through imaging techniques such as x rays or ultrasound. However, abdominal x rays, a lower gastrointestinal (GI) series, and computerized tomography (CT) scans can diagnose intestinal obstructions.  - Surgery is the only way to treat abdominal adhesions that cause pain, intestinal obstruction, or fertility problems."}
{"_id":"631aee07-1060-4f26-b490-a7622f4b3b61","text":"What is diabetes?\n                \nThere are three main types of diabetes:\n                \n- Type 1 diabetes  Your body does not make insulin. This is a problem because you need insulin to take the sugar (glucose) from the foods you eat and turn it into energy for your body. You need to take insulin every day to live.   - Type 2 diabetes  Your body does not make or use insulin well. You may need to take pills or insulin to help control your diabetes. Type 2 is the most common type of diabetes.   - Gestational (jest-TAY-shun-al) diabetes  Some women get this kind of diabetes when they are pregnant. Most of the time, it goes away after the baby is born. But even if it goes away, these women and their children have a greater chance of getting diabetes later in life.\n                \nYou are the most important member of your health care team.\n                \nYou are the one who manages your diabetes day by day. Talk to your doctor about how you can best care for your diabetes to stay healthy. Some others who can help are:\n                \n\n                \n- dentist    - diabetes doctor    - diabetes educator    - dietitian    - eye doctor    - foot doctor     - friends and family    - mental health counselor    - nurse    - nurse practitioner    - pharmacist    - social worker\n                \nHow to learn more about diabetes.\n                \n- Take classes to learn more about living with diabetes. To find a class, check with your health care team, hospital, or area health clinic. You can also search online.   - Join a support group  in-person or online  to get peer support with managing your diabetes.   - Read about diabetes online. Go to National Diabetes Education Program.\n                \nTake diabetes seriously.\n                \nYou may have heard people say they have a touch of diabetes or that their sugar is a little high. These words suggest that diabetes is not a serious disease. That is not correct. Diabetes is serious, but you can learn to manage it.\n                \nPeople with diabetes need to make healthy food choices, stay at a healthy weight, move more every day, and take their medicine even when they feel good. Its a lot to do. Its not easy, but its worth it!\n                \nWhy take care of your diabetes?\n                \nTaking care of yourself and your diabetes can help you feel good today and in the future. When your blood sugar (glucose) is close to normal, you are likely to:\n                \n- have more energy   - be less tired and thirsty   - need to pass urine less often   - heal better   - have fewer skin or bladder infections\n                \nYou will also have less chance of having health problems caused by diabetes such as:\n                \n- heart attack or stroke   - eye problems that can lead to trouble seeing or going blind   - pain, tingling, or numbness in your hands and feet, also called nerve damage   - kidney problems that can cause your kidneys to stop working   - teeth and gum problems\n                \nActions you can take\n                \n-  Ask your health care team what type of diabetes you have.  -  Learn where you can go for support.  -  Learn how caring for your diabetes helps you feel good today and in the future."}
{"_id":"0be51cc3-3953-43f1-861a-865eb5892ece","text":"Diabetes is a complex group of diseases with a variety of causes. People with diabetes have high blood glucose, also called high blood sugar or hyperglycemia.\n                \nDiabetes is a disorder of metabolismthe way the body uses digested food for energy. The digestive tract breaks down carbohydratessugars and starches found in many foodsinto glucose, a form of sugar that enters the bloodstream. With the help of the hormone insulin, cells throughout the body absorb glucose and use it for energy. Diabetes develops when the body doesnt make enough insulin or is not able to use insulin effectively, or both.\n                \nInsulin is made in the pancreas, an organ located behind the stomach. The pancreas contains clusters of cells called islets. Beta cells within the islets make insulin and release it into the blood.\n                \nIf beta cells dont produce enough insulin, or the body doesnt respond to the insulin that is present, glucose builds up in the blood instead of being absorbed by cells in the body, leading to prediabetes or diabetes. Prediabetes is a condition in which blood glucose levels or A1C levelswhich reflect average blood glucose levelsare higher than normal but not high enough to be diagnosed as diabetes. In diabetes, the bodys cells are starved of energy despite high blood glucose levels.\n                \nOver time, high blood glucose damages nerves and blood vessels, leading to complications such as heart disease, stroke, kidney disease, blindness, dental disease, and amputations. Other complications of diabetes may include increased susceptibility to other diseases, loss of mobility with aging, depression, and pregnancy problems. No one is certain what starts the processes that cause diabetes, but scientists believe genes and environmental factors interact to cause diabetes in most cases.\n                \nThe two main types of diabetes are type 1 diabetes and type 2 diabetes. A third type, gestational diabetes, develops only during pregnancy. Other types of diabetes are caused by defects in specific genes, diseases of the pancreas, certain drugs or chemicals, infections, and other conditions. Some people show signs of both type 1 and type 2 diabetes."}
{"_id":"c4dac02d-4ce7-4210-b1d5-5e4ab21f0715","text":"Type 1 diabetes is caused by a lack of insulin due to the destruction of insulin-producing beta cells in the pancreas. In type 1 diabetesan autoimmune diseasethe bodys immune system attacks and destroys the beta cells. Normally, the immune system protects the body from infection by identifying and destroying bacteria, viruses, and other potentially harmful foreign substances. But in autoimmune diseases, the immune system attacks the bodys own cells. In type 1 diabetes, beta cell destruction may take place over several years, but symptoms of the disease usually develop over a short period of time.\n                \nType 1 diabetes typically occurs in children and young adults, though it can appear at any age. In the past, type 1 diabetes was called juvenile diabetes or insulin-dependent diabetes mellitus.\n                \nLatent autoimmune diabetes in adults (LADA) may be a slowly developing kind of type 1 diabetes. Diagnosis usually occurs after age 30. In LADA, as in type 1 diabetes, the bodys immune system destroys the beta cells. At the time of diagnosis, people with LADA may still produce their own insulin, but eventually most will need insulin shots or an insulin pump to control blood glucose levels.\n                \nGenetic Susceptibility\n                \nHeredity plays an important part in determining who is likely to develop type 1 diabetes. Genes are passed down from biological parent to child. Genes carry instructions for making proteins that are needed for the bodys cells to function. Many genes, as well as interactions among genes, are thought to influence susceptibility to and protection from type 1 diabetes. The key genes may vary in different population groups. Variations in genes that affect more than 1 percent of a population group are called gene variants.\n                \nCertain gene variants that carry instructions for making proteins called human leukocyte antigens (HLAs) on white blood cells are linked to the risk of developing type 1 diabetes. The proteins produced by HLA genes help determine whether the immune system recognizes a cell as part of the body or as foreign material. Some combinations of HLA gene variants predict that a person will be at higher risk for type 1 diabetes, while other combinations are protective or have no effect on risk.\n                \nWhile HLA genes are the major risk genes for type 1 diabetes, many additional risk genes or gene regions have been found. Not only can these genes help identify people at risk for type 1 diabetes, but they also provide important clues to help scientists better understand how the disease develops and identify potential targets for therapy and prevention.\n                \nGenetic testing can show what types of HLA genes a person carries and can reveal other genes linked to diabetes. However, most genetic testing is done in a research setting and is not yet available to individuals. Scientists are studying how the results of genetic testing can be used to improve type 1 diabetes prevention or treatment.\n                \nAutoimmune Destruction of Beta Cells\n                \nIn type 1 diabetes, white blood cells called T cells attack and destroy beta cells. The process begins well before diabetes symptoms appear and continues after diagnosis. Often, type 1 diabetes is not diagnosed until most beta cells have already been destroyed. At this point, a person needs daily insulin treatment to survive. Finding ways to modify or stop this autoimmune process and preserve beta cell function is a major focus of current scientific research.\n                \nRecent research suggests insulin itself may be a key trigger of the immune attack on beta cells. The immune systems of people who are susceptible to developing type 1 diabetes respond to insulin as if it were a foreign substance, or antigen. To combat antigens, the body makes proteins called antibodies. Antibodies to insulin and other proteins produced by beta cells are found in people with type 1 diabetes. Researchers test for these antibodies to help identify people at increased risk of developing the disease. Testing the types and levels of antibodies in the blood can help determine whether a person has type 1 diabetes, LADA, or another type of diabetes.\n                \nEnvironmental Factors\n                \nEnvironmental factors, such as foods, viruses, and toxins, may play a role in the development of type 1 diabetes, but the exact nature of their role has not been determined. Some theories suggest that environmental factors trigger the autoimmune destruction of beta cells in people with a genetic susceptibility to diabetes. Other theories suggest that environmental factors play an ongoing role in diabetes, even after diagnosis.\n                \nViruses and infections. A virus cannot cause diabetes on its own, but people are sometimes diagnosed with type 1 diabetes during or after a viral infection, suggesting a link between the two. Also, the onset of type 1 diabetes occurs more frequently during the winter when viral infections are more common. Viruses possibly associated with type 1 diabetes include coxsackievirus B, cytomegalovirus, adenovirus, rubella, and mumps. Scientists have described several ways these viruses may damage or destroy beta cells or possibly trigger an autoimmune response in susceptible people. For example, anti-islet antibodies have been found in patients with congenital rubella syndrome, and cytomegalovirus has been associated with significant beta cell damage and acute pancreatitisinflammation of the pancreas. Scientists are trying to identify a virus that can cause type 1 diabetes so that a vaccine might be developed to prevent the disease.\n                \nInfant feeding practices. Some studies have suggested that dietary factors may raise or lower the risk of developing type 1 diabetes. For example, breastfed infants and infants receiving vitamin D supplements may have a reduced risk of developing type 1 diabetes, while early exposure to cows milk and cereal proteins may increase risk. More research is needed to clarify how infant nutrition affects the risk for type 1 diabetes.\n                \nRead more in the Centers for Disease Control and Preventions (CDCs) publication  National Diabetes Statistics Report, 2014 at  www.cdc.gov for information about research studies related to type 1 diabetes."}
{"_id":"c3e4177c-022d-4d6a-b118-3b0249f99f61","text":"Type 2 diabetesthe most common form of diabetesis caused by a combination of factors, including insulin resistance, a condition in which the bodys muscle, fat, and liver cells do not use insulin effectively. Type 2 diabetes develops when the body can no longer produce enough insulin to compensate for the impaired ability to use insulin. Symptoms of type 2 diabetes may develop gradually and can be subtle; some people with type 2 diabetes remain undiagnosed for years.\n                \nType 2 diabetes develops most often in middle-aged and older people who are also overweight or obese. The disease, once rare in youth, is becoming more common in overweight and obese children and adolescents. Scientists think genetic susceptibility and environmental factors are the most likely triggers of type 2 diabetes.\n                \nGenetic Susceptibility\n                \nGenes play a significant part in susceptibility to type 2 diabetes. Having certain genes or combinations of genes may increase or decrease a persons risk for developing the disease. The role of genes is suggested by the high rate of type 2 diabetes in families and identical twins and wide variations in diabetes prevalence by ethnicity. Type 2 diabetes occurs more frequently in African Americans, Alaska Natives, American Indians, Hispanics\/Latinos, and some Asian Americans, Native Hawaiians, and Pacific Islander Americans than it does in non-Hispanic whites.\n                \nRecent studies have combined genetic data from large numbers of people, accelerating the pace of gene discovery. Though scientists have now identified many gene variants that increase susceptibility to type 2 diabetes, the majority have yet to be discovered. The known genes appear to affect insulin production rather than insulin resistance. Researchers are working to identify additional gene variants and to learn how they interact with one another and with environmental factors to cause diabetes.\n                \nStudies have shown that variants of the TCF7L2 gene increase susceptibility to type 2 diabetes. For people who inherit two copies of the variants, the risk of developing type 2 diabetes is about 80 percent higher than for those who do not carry the gene variant.1 However, even in those with the variant, diet and physical activity leading to weight loss help delay diabetes, according to the Diabetes Prevention Program (DPP), a major clinical trial involving people at high risk.\n                \nGenes can also increase the risk of diabetes by increasing a persons tendency to become overweight or obese. One theory, known as the thrifty gene hypothesis, suggests certain genes increase the efficiency of metabolism to extract energy from food and store the energy for later use. This survival trait was advantageous for populations whose food supplies were scarce or unpredictable and could help keep people alive during famine. In modern times, however, when high-calorie foods are plentiful, such a trait can promote obesity and type 2 diabetes.\n                \nObesity and Physical Inactivity\n                \nPhysical inactivity and obesity are strongly associated with the development of type 2 diabetes. People who are genetically susceptible to type 2 diabetes are more vulnerable when these risk factors are present.\n                \nAn imbalance between caloric intake and physical activity can lead to obesity, which causes insulin resistance and is common in people with type 2 diabetes. Central obesity, in which a person has excess abdominal fat, is a major risk factor not only for insulin resistance and type 2 diabetes but also for heart and blood vessel disease, also called cardiovascular disease (CVD). This excess belly fat produces hormones and other substances that can cause harmful, chronic effects in the body such as damage to blood vessels.\n                \nThe DPP and other studies show that millions of people can lower their risk for type 2 diabetes by making lifestyle changes and losing weight. The DPP proved that people with prediabetesat high risk of developing type 2 diabetescould sharply lower their risk by losing weight through regular physical activity and a diet low in fat and calories. In 2009, a follow-up study of DPP participantsthe Diabetes Prevention Program Outcomes Study (DPPOS)showed that the benefits of weight loss lasted for at least 10 years after the original study began.2\n                \nRead more about the DPP, funded under National Institutes of Health (NIH) clinical trial number NCT00004992, and the DPPOS, funded under NIH clinical trial number NCT00038727 in  Diabetes Prevention Program.\n                \nInsulin Resistance\n                \nInsulin resistance is a common condition in people who are overweight or obese, have excess abdominal fat, and are not physically active. Muscle, fat, and liver cells stop responding properly to insulin, forcing the pancreas to compensate by producing extra insulin. As long as beta cells are able to produce enough insulin, blood glucose levels stay in the normal range. But when insulin production falters because of beta cell dysfunction, glucose levels rise, leading to prediabetes or diabetes.\n                \nAbnormal Glucose Production by the Liver\n                \nIn some people with diabetes, an abnormal increase in glucose production by the liver also contributes to high blood glucose levels. Normally, the pancreas releases the hormone glucagon when blood glucose and insulin levels are low. Glucagon stimulates the liver to produce glucose and release it into the bloodstream. But when blood glucose and insulin levels are high after a meal, glucagon levels drop, and the liver stores excess glucose for later, when it is needed. For reasons not completely understood, in many people with diabetes, glucagon levels stay higher than needed. High glucagon levels cause the liver to produce unneeded glucose, which contributes to high blood glucose levels. Metformin, the most commonly used drug to treat type 2 diabetes, reduces glucose production by the liver.\n                \nThe Roles of Insulin and Glucagon in Normal Blood Glucose Regulation\n                \nA healthy persons body keeps blood glucose levels in a normal range through several complex mechanisms. Insulin and glucagon, two hormones made in the pancreas, help regulate blood glucose levels:\n                \n- Insulin, made by beta cells, lowers elevated blood glucose levels.  - Glucagon, made by alpha cells, raises low blood glucose levels.\n                \n- Insulin helps muscle, fat, and liver cells absorb glucose from the bloodstream, lowering blood glucose levels.  - Insulin stimulates the liver and muscle tissue to store excess glucose. The stored form of glucose is called glycogen.  - Insulin also lowers blood glucose levels by reducing glucose production in the liver.\n                \n- Glucagon signals the liver and muscle tissue to break down glycogen into glucose, which enters the bloodstream and raises blood glucose levels.  - If the body needs more glucose, glucagon stimulates the liver to make glucose from amino acids.\n                \nMetabolic Syndrome\n                \nMetabolic syndrome, also called insulin resistance syndrome, refers to a group of conditions common in people with insulin resistance, including\n                \n- higher than normal blood glucose levels  - increased waist size due to excess abdominal fat  - high blood pressure  - abnormal levels of cholesterol and triglycerides in the blood\n                \nCell Signaling and Regulation\n                \nCells communicate through a complex network of molecular signaling pathways. For example, on cell surfaces, insulin receptor molecules capture, or bind, insulin molecules circulating in the bloodstream. This interaction between insulin and its receptor prompts the biochemical signals that enable the cells to absorb glucose from the blood and use it for energy.\n                \nProblems in cell signaling systems can set off a chain reaction that leads to diabetes or other diseases. Many studies have focused on how insulin signals cells to communicate and regulate action. Researchers have identified proteins and pathways that transmit the insulin signal and have mapped interactions between insulin and body tissues, including the way insulin helps the liver control blood glucose levels. Researchers have also found that key signals also come from fat cells, which produce substances that cause inflammation and insulin resistance.\n                \nThis work holds the key to combating insulin resistance and diabetes. As scientists learn more about cell signaling systems involved in glucose regulation, they will have more opportunities to develop effective treatments.\n                \nBeta Cell Dysfunction\n                \nScientists think beta cell dysfunction is a key contributor to type 2 diabetes. Beta cell impairment can cause inadequate or abnormal patterns of insulin release. Also, beta cells may be damaged by high blood glucose itself, a condition called glucose toxicity.\n                \nScientists have not determined the causes of beta cell dysfunction in most cases. Single gene defects lead to specific forms of diabetes called maturity-onset diabetes of the young (MODY). The genes involved regulate insulin production in the beta cells. Although these forms of diabetes are rare, they provide clues as to how beta cell function may be affected by key regulatory factors. Other gene variants are involved in determining the number and function of beta cells. But these variants account for only a small percentage of type 2 diabetes cases. Malnutrition early in life is also being investigated as a cause of beta cell dysfunction. The metabolic environment of the developing fetus may also create a predisposition for diabetes later in life.\n                \nRisk Factors for Type 2 Diabetes\n                \nPeople who develop type 2 diabetes are more likely to have the following characteristics:\n                \n- age 45 or older  - overweight or obese  - physically inactive  - parent or sibling with diabetes  - family background that is African American, Alaska Native, American Indian, Asian American, Hispanic\/Latino, or Pacific Islander American  - history of giving birth to a baby weighing more than 9 pounds  - history of gestational diabetes  - high blood pressure140\/90 or aboveor being treated for high blood pressure  - high-density lipoprotein (HDL), or good, cholesterol below 35 milligrams per deciliter (mg\/dL), or a triglyceride level above 250 mg\/dL  - polycystic ovary syndrome, also called PCOS  - prediabetesan A1C level of 5.7 to 6.4 percent; a fasting plasma glucose test result of 100125 mg\/dL, called impaired fasting glucose; or a 2-hour oral glucose tolerance test result of 140199, called impaired glucose tolerance  - acanthosis nigricans, a condition associated with insulin resistance, characterized by a dark, velvety rash around the neck or armpits  - history of CVD\n                \nThe American Diabetes Association (ADA) recommends that testing to detect prediabetes and type 2 diabetes be considered in adults who are overweight or obese and have one or more additional risk factors for diabetes. In adults without these risk factors, testing should begin at age 45."}
{"_id":"4f94f8a2-b2d6-4fc9-98e6-4e37666eb270","text":"Insulin Resistance and Beta Cell Dysfunction\n                \nHormones produced by the placenta and other pregnancy-related factors contribute to insulin resistance, which occurs in all women during late pregnancy. Insulin resistance increases the amount of insulin needed to control blood glucose levels. If the pancreas cant produce enough insulin due to beta cell dysfunction, gestational diabetes occurs.\n                \nAs with type 2 diabetes, excess weight is linked to gestational diabetes. Overweight or obese women are at particularly high risk for gestational diabetes because they start pregnancy with a higher need for insulin due to insulin resistance. Excessive weight gain during pregnancy may also increase risk.\n                \nFamily History\n                \nHaving a family history of diabetes is also a risk factor for gestational diabetes, suggesting that genes play a role in its development. Genetics may also explain why the disorder occurs more frequently in African Americans, American Indians, and Hispanics\/Latinos. Many gene variants or combinations of variants may increase a womans risk for developing gestational diabetes. Studies have found several gene variants associated with gestational diabetes, but these variants account for only a small fraction of women with gestational diabetes.\n                \nFuture Risk of Type 2 Diabetes\n                \nBecause a womans hormones usually return to normal levels soon after giving birth, gestational diabetes disappears in most women after delivery. However, women who have gestational diabetes are more likely to develop gestational diabetes with future pregnancies and develop type 2 diabetes.3 Women with gestational diabetes should be tested for persistent diabetes 6 to 12 weeks after delivery and at least every 3 years thereafter.\n                \nAlso, exposure to high glucose levels during gestation increases a childs risk for becoming overweight or obese and for developing type 2 diabetes later on. The result may be a cycle of diabetes affecting multiple generations in a family. For both mother and child, maintaining a healthy body weight and being physically active may help prevent type 2 diabetes."}
{"_id":"4fdb25d1-da9e-411c-b522-285904d1d9df","text":"Other types of diabetes have a variety of possible causes.\n                \nGenetic Mutations Affecting Beta Cells, Insulin, and Insulin Action\n                \nSome relatively uncommon forms of diabetes known as monogenic diabetes are caused by mutations, or changes, in a single gene. These mutations are usually inherited, but sometimes the gene mutation occurs spontaneously. Most of these gene mutations cause diabetes by reducing beta cells ability to produce insulin.\n                \nThe most common types of monogenic diabetes are neonatal diabetes mellitus (NDM) and MODY. NDM occurs in the first 6 months of life. MODY is usually found during adolescence or early adulthood but sometimes is not diagnosed until later in life. More information about NDM and MODY is provided in the NIDDK health topic, Monogenic Forms of Diabetes.\n                \nOther rare genetic mutations can cause diabetes by damaging the quality of insulin the body produces or by causing abnormalities in insulin receptors.\n                \nOther Genetic Diseases\n                \nDiabetes occurs in people with Down syndrome, Klinefelter syndrome, and Turner syndrome at higher rates than the general population. Scientists are investigating whether genes that may predispose people to genetic syndromes also predispose them to diabetes.\n                \nThe genetic disorders cystic fibrosis and hemochromatosis are linked to diabetes. Cystic fibrosis produces abnormally thick mucus, which blocks the pancreas. The risk of diabetes increases with age in people with cystic fibrosis. Hemochromatosis causes the body to store too much iron. If the disorder is not treated, iron can build up in and damage the pancreas and other organs.\n                \nDamage to or Removal of the Pancreas\n                \nPancreatitis, cancer, and trauma can all harm the pancreatic beta cells or impair insulin production, thus causing diabetes. If the damaged pancreas is removed, diabetes will occur due to the loss of the beta cells.\n                \nEndocrine Diseases\n                \nEndocrine diseases affect organs that produce hormones. Cushings syndrome and acromegaly are examples of hormonal disorders that can cause prediabetes and diabetes by inducing insulin resistance. Cushings syndrome is marked by excessive production of cortisolsometimes called the stress hormone. Acromegaly occurs when the body produces too much growth hormone. Glucagonoma, a rare tumor of the pancreas, can also cause diabetes. The tumor causes the body to produce too much glucagon. Hyperthyroidism, a disorder that occurs when the thyroid gland produces too much thyroid hormone, can also cause elevated blood glucose levels.\n                \nAutoimmune Disorders\n                \nRare disorders characterized by antibodies that disrupt insulin action can lead to diabetes. This kind of diabetes is often associated with other autoimmune disorders such as lupus erythematosus. Another rare autoimmune disorder called stiff-man syndrome is associated with antibodies that attack the beta cells, similar to type 1 diabetes.\n                \nMedications and Chemical Toxins\n                \nSome medications, such as nicotinic acid and certain types of diuretics, anti-seizure drugs, psychiatric drugs, and drugs to treat human immunodeficiency virus (HIV), can impair beta cells or disrupt insulin action. Pentamidine, a drug prescribed to treat a type of pneumonia, can increase the risk of pancreatitis, beta cell damage, and diabetes. Also, glucocorticoidssteroid hormones that are chemically similar to naturally produced cortisolmay impair insulin action. Glucocorticoids are used to treat inflammatory illnesses such as rheumatoid arthritis, asthma, lupus, and ulcerative colitis.\n                \nMany chemical toxins can damage or destroy beta cells in animals, but only a few have been linked to diabetes in humans. For example, dioxina contaminant of the herbicide Agent Orange, used during the Vietnam Warmay be linked to the development of type 2 diabetes. In 2000, based on a report from the Institute of Medicine, the U.S. Department of Veterans Affairs (VA) added diabetes to the list of conditions for which Vietnam veterans are eligible for disability compensation. Also, a chemical in a rat poison no longer in use has been shown to cause diabetes if ingested. Some studies suggest a high intake of nitrogen-containing chemicals such as nitrates and nitrites might increase the risk of diabetes. Arsenic has also been studied for possible links to diabetes.\n                \nLipodystrophy\n                \nLipodystrophy is a condition in which fat tissue is lost or redistributed in the body. The condition is associated with insulin resistance and type 2 diabetes."}
{"_id":"1d24d83b-379b-47e9-8c46-cb322800a76f","text":"Other types of diabetes have a variety of possible causes.\n                \nGenetic Mutations Affecting Beta Cells, Insulin, and Insulin Action\n                \nSome relatively uncommon forms of diabetes known as monogenic diabetes are caused by mutations, or changes, in a single gene. These mutations are usually inherited, but sometimes the gene mutation occurs spontaneously. Most of these gene mutations cause diabetes by reducing beta cells ability to produce insulin.\n                \nThe most common types of monogenic diabetes are neonatal diabetes mellitus (NDM) and MODY. NDM occurs in the first 6 months of life. MODY is usually found during adolescence or early adulthood but sometimes is not diagnosed until later in life. More information about NDM and MODY is provided in the NIDDK health topic, Monogenic Forms of Diabetes.\n                \nOther rare genetic mutations can cause diabetes by damaging the quality of insulin the body produces or by causing abnormalities in insulin receptors.\n                \nOther Genetic Diseases\n                \nDiabetes occurs in people with Down syndrome, Klinefelter syndrome, and Turner syndrome at higher rates than the general population. Scientists are investigating whether genes that may predispose people to genetic syndromes also predispose them to diabetes.\n                \nThe genetic disorders cystic fibrosis and hemochromatosis are linked to diabetes. Cystic fibrosis produces abnormally thick mucus, which blocks the pancreas. The risk of diabetes increases with age in people with cystic fibrosis. Hemochromatosis causes the body to store too much iron. If the disorder is not treated, iron can build up in and damage the pancreas and other organs.\n                \nDamage to or Removal of the Pancreas\n                \nPancreatitis, cancer, and trauma can all harm the pancreatic beta cells or impair insulin production, thus causing diabetes. If the damaged pancreas is removed, diabetes will occur due to the loss of the beta cells.\n                \nEndocrine Diseases\n                \nEndocrine diseases affect organs that produce hormones. Cushings syndrome and acromegaly are examples of hormonal disorders that can cause prediabetes and diabetes by inducing insulin resistance. Cushings syndrome is marked by excessive production of cortisolsometimes called the stress hormone. Acromegaly occurs when the body produces too much growth hormone. Glucagonoma, a rare tumor of the pancreas, can also cause diabetes. The tumor causes the body to produce too much glucagon. Hyperthyroidism, a disorder that occurs when the thyroid gland produces too much thyroid hormone, can also cause elevated blood glucose levels.\n                \nAutoimmune Disorders\n                \nRare disorders characterized by antibodies that disrupt insulin action can lead to diabetes. This kind of diabetes is often associated with other autoimmune disorders such as lupus erythematosus. Another rare autoimmune disorder called stiff-man syndrome is associated with antibodies that attack the beta cells, similar to type 1 diabetes.\n                \nMedications and Chemical Toxins\n                \nSome medications, such as nicotinic acid and certain types of diuretics, anti-seizure drugs, psychiatric drugs, and drugs to treat human immunodeficiency virus (HIV), can impair beta cells or disrupt insulin action. Pentamidine, a drug prescribed to treat a type of pneumonia, can increase the risk of pancreatitis, beta cell damage, and diabetes. Also, glucocorticoidssteroid hormones that are chemically similar to naturally produced cortisolmay impair insulin action. Glucocorticoids are used to treat inflammatory illnesses such as rheumatoid arthritis, asthma, lupus, and ulcerative colitis.\n                \nMany chemical toxins can damage or destroy beta cells in animals, but only a few have been linked to diabetes in humans. For example, dioxina contaminant of the herbicide Agent Orange, used during the Vietnam Warmay be linked to the development of type 2 diabetes. In 2000, based on a report from the Institute of Medicine, the U.S. Department of Veterans Affairs (VA) added diabetes to the list of conditions for which Vietnam veterans are eligible for disability compensation. Also, a chemical in a rat poison no longer in use has been shown to cause diabetes if ingested. Some studies suggest a high intake of nitrogen-containing chemicals such as nitrates and nitrites might increase the risk of diabetes. Arsenic has also been studied for possible links to diabetes.\n                \nLipodystrophy\n                \nLipodystrophy is a condition in which fat tissue is lost or redistributed in the body. The condition is associated with insulin resistance and type 2 diabetes."}
{"_id":"1872db2d-0c6e-4be5-8b79-94e946a4d17a","text":"- Diabetes is a complex group of diseases with a variety of causes. Scientists believe genes and environmental factors interact to cause diabetes in most cases.  - People with diabetes have high blood glucose, also called high blood sugar or hyperglycemia. Diabetes develops when the body doesnt make enough insulin or is not able to use insulin effectively, or both.  - Insulin is a hormone made by beta cells in the pancreas. Insulin helps cells throughout the body absorb and use glucose for energy. If the body does not produce enough insulin or cannot use insulin effectively, glucose builds up in the blood instead of being absorbed by cells in the body, and the body is starved of energy.  - Prediabetes is a condition in which blood glucose levels or A1C levels are higher than normal but not high enough to be diagnosed as diabetes. People with prediabetes can substantially reduce their risk of developing diabetes by losing weight and increasing physical activity.  - The two main types of diabetes are type 1 diabetes and type 2 diabetes. Gestational diabetes is a third form of diabetes that develops only during pregnancy.  - Type 1 diabetes is caused by a lack of insulin due to the destruction of insulin-producing beta cells. In type 1 diabetesan autoimmune diseasethe bodys immune system attacks and destroys the beta cells.  - Type 2 diabetesthe most common form of diabetesis caused by a combination of factors, including insulin resistance, a condition in which the bodys muscle, fat, and liver cells do not use insulin effectively. Type 2 diabetes develops when the body can no longer produce enough insulin to compensate for the impaired ability to use insulin.  - Scientists believe gestational diabetes is caused by the hormonal changes and metabolic demands of pregnancy together with genetic and environmental factors. Risk factors for gestational diabetes include being overweight and having a family history of diabetes.  - Monogenic forms of diabetes are relatively uncommon and are caused by mutations in single genes that limit insulin production, quality, or action in the body.  - Other types of diabetes are caused by diseases and injuries that damage the pancreas; certain chemical toxins and medications; infections; and other conditions."}
{"_id":"d1c2e66e-1df2-4024-921c-11d4d152ed4f","text":"Renal artery stenosis is the narrowing of one or both renal arteries. Renal means kidney and stenosis means narrowing. The renal arteries are blood vessels that carry blood to the kidneys from the aortathe main blood vessel that carries blood from the heart to arteries throughout the body.\n                \nRVH is high blood pressure caused by RAS. Blood pressure is written with two numbers separated by a slash, 120\/80, and is said as 120 over 80. The top number is called the systolic pressure and represents the pressure as the heart beats and pushes blood through the blood vessels. The bottom number is called the diastolic pressure and represents the pressure as blood vessels relax between heartbeats. A persons blood pressure is considered normal if it stays at or below 120\/80. High blood pressure is a systolic pressure of 140 or above or a diastolic pressure of 90 or above.1"}
{"_id":"9bb4f968-f7ee-4f1b-b7ff-035fd337b489","text":"The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the two kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra fluid."}
{"_id":"e6840ea7-b2d8-4b5a-8ba1-03696dc2e9e0","text":"About 90 percent of RAS is caused by atherosclerosisclogging, narrowing, and hardening of the renal arteries.2 In these cases, RAS develops when plaquea sticky substance made up of fat, cholesterol, calcium, and other material found in the bloodbuilds up on the inner wall of one or both renal arteries. Plaque buildup is what makes the artery wall hard and narrow.\n                \nMost other cases of RAS are caused by fibromuscular dysplasia (FMD)the abnormal development or growth of cells on the renal artery wallswhich can cause blood vessels to narrow. Rarely, RAS is caused by other conditions."}
{"_id":"bfcbc2e0-8ef4-4e51-95e9-bad7b23e9642","text":"People at risk for artherosclerosis are also at risk for RAS. Risk factors for RAS caused by artherosclerosis include\n                \n- high blood cholesterol levels  - high blood pressure  - smoking  - insulin resistance  - diabetes  - being overweight or obese  - lack of physical activity  - a diet high in fat, cholesterol, sodium, and sugar  - being a man older than 45 or a woman older than 55  - a family history of early heart disease\n                \nThe risk factors for RAS caused by FMD are unknown, but FMD is most common in women and people 25 to 50 years of age.3 FMD can affect more than one person in a family, indicating that it may be caused by an inherited gene."}
{"_id":"af67268c-5269-4499-ae67-d5648be066b0","text":"In many cases, RAS has no symptoms until it becomes severe.\n                \nThe signs of RAS are usually either high blood pressure or decreased kidney function, or both, but RAS is often overlooked as a cause of high blood pressure. RAS should be considered as a cause of high blood pressure in people who\n                \n- are older than age 50 when they develop high blood pressure or have a marked increase in blood pressure  - have no family history of high blood pressure  - cannot be successfully treated with at least three or more different types of blood pressure medications\n                \nSymptoms of a significant decrease in kidney function include\n                \n- increase or decrease in urination  - edemaswelling, usually in the legs, feet, or ankles and less often in the hands or face  - drowsiness or tiredness  - generalized itching or numbness  - dry skin  - headaches  - weight loss  - appetite loss  - nausea  - vomiting  - sleep problems  - trouble concentrating  - darkened skin  - muscle cramps"}
{"_id":"fd6cf971-221f-47a6-be2c-a224806a4a7d","text":"People with RAS are at increased risk for complications resulting from loss of kidney function or atherosclerosis occurring in other blood vessels, such as\n                \n- chronic kidney disease (CKD)reduced kidney function over a period of time  - coronary artery diseasenarrowing and hardening of arteries that supply blood to the heart  - strokebrain damage caused by lack of blood flow to the brain  - peripheral vascular diseaseblockage of blood vessels that restricts flow of blood from the heart to other parts of the body, particularly the legs\n                \nRAS can lead to kidney failure, described as end-stage renal disease when treated with blood-filtering treatments called dialysis or a kidney transplant, though this is uncommon in people who receive ongoing treatment for RAS."}
{"_id":"76ad0993-9aeb-48dd-a54e-0ddcf6c92fb7","text":"A health care provider can diagnose RAS by listening to the abdomen with a stethoscope and performing imaging tests. When blood flows through a narrow artery, it sometimes makes a whooshing sound, called a bruit. The health care provider may place a stethoscope on the front or the side of the abdomen to listen for this sound. The absence of this sound, however, does not exclude the possibility of RAS.\n                \nIn some cases, RAS is found when a person has a test for another reason. For example, a health care provider may find RAS during a coronary angiogram for diagnosis of heart problems. A coronary angiogram is a procedure that uses a special dye, called contrast medium, and x rays to see how blood flows through the heart.\n                \nThe following imaging tests are used to diagnose RAS:\n                \n- Duplex ultrasound. Duplex ultrasound combines traditional ultrasound with Doppler ultrasonography. Traditional ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. Doppler ultrasonography records sound waves reflected off of moving objects, such as blood, to measure their speed and other aspects of how they flow. The procedure is performed in a health care providers office, outpatient center, or hospital by a specially trained technician, and the images are interpreted by a radiologista doctor who specializes in medical imaging. Anesthesia is not needed. The images can show blockage in the renal artery or blood moving through nearby arteries at a lower-than-normal speed. Ultrasound is noninvasive and low cost.  - Catheter angiogram. A catheter angiogram, also called a traditional angiogram, is a special kind of x ray in which a thin, flexible tube called a catheter is threaded through the large arteries, often from the groin, to the artery of interestin this case, the renal artery. The procedure is performed in a hospital or outpatient center by a radiologist. Anesthesia is not needed though a sedative may be given to lessen anxiety during the procedure. Contrast medium is injected through the catheter so the renal artery shows up more clearly on the x ray. Catheter angiogram is the gold standard for diagnosing RAS due to the high quality of the image produced. In addition, severe RAS can be treated during the same visit. However, a catheter angiogram is an invasive procedure, and a person may have side effects from the sedative or contrast medium or may have bleeding or injury to the artery from the catheter. The procedure is also more expensive than other imaging tests.  - Computerized tomographic angiography (CTA) scan. CTA scans use a combination of x rays and computer technology to create images. The procedure is performed in an outpatient center or hospital by an x-ray technician, and the images are interpreted by a radiologist. Anesthesia is not needed. Contrast medium is injected into a vein in the persons arm to better see the structure of the arteries. CTA scans require the person to lie on a table that slides into a tunnel-shaped device where the x rays are taken. CTA scans are less invasive than catheter angiograms and take less time. However, the risks from the x-ray radiation still exist, and the test often requires more contrast medium than a catheter angiogram, so it may not be recommended for a person with poor kidney function.  - Magnetic resonance angiogram (MRA). MRA uses radio waves and magnets to produce detailed pictures of the bodys internal organs and soft tissues without using x rays. The procedure is performed in an outpatient center or hospital by an x-ray technician, and the images are interpreted by a radiologist. Anesthesia is not needed though light sedation may be used for people with a fear of confined spaces. Contrast medium may be injected into a vein in the persons arm to better see the structure of the arteries. With most MRA scans, the person lies on a table that slides into a tunnel-shaped device that may be open ended or closed at one end; some newer machines are designed to allow the person to lie in a more open space. In addition to providing high-quality images noninvasively, MRA can provide a functional assessment of blood flow and organ function. However, the use of contrast medium for an MRA is not advised for people with poor kidney function because of the risk of complications to the skin and other organs if the kidneys do not remove the contrast medium well enough."}
{"_id":"ae3bafa8-7cb2-4d81-8c48-12f419a98d01","text":"Treatment for RAS includes lifestyle changes, medications, and surgery and aims to\n                \n- prevent RAS from getting worse  - treat RVH  - relieve the blockage of the renal arteries\n                \nRAS that has not led to RVH or caused a significant blockage of the artery may not need treatment. RAS that needs to be treated, also called critical RAS, is defined by the American Heart Association as a reduction by more than 60 percent in the diameter of the renal artery.1 However, health care providers are not exactly sure what degree of blockage will cause significant problems.\n                \nLifestyle Changes\n                \nThe first step in treating RAS is making lifestyle changes that promote healthy blood vessels throughout the body, including the renal arteries. The best ways to keep plaque from building up in the arteries are to exercise, maintain a healthy body weight, and choose healthy foods. People who smoke should quit to help protect their kidneys and other internal organs.\n                \nMedications\n                \nPeople with RVH may need to take medications thatwhen taken as prescribed by their health care providerlower blood pressure and can also significantly slow the progression of kidney disease. Two types of blood pressure-lowering medications, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), have proven effective in slowing the progression of kidney disease. Many people require two or more medications to control their blood pressure. In addition to an ACE inhibitor or an ARB, a diuretica medication that helps the kidneys remove fluid from the bloodmay be prescribed. Beta blockers, calcium channel blockers, and other blood pressure medications may also be needed. Some people with RAS cannot take an ACE inhibitor or ARB due to the effects on the kidneys. People with RAS who are prescribed an ACE inhibitor or ARB should have their kidney function checked within a few weeks of starting the medication.\n                \nA cholesterol-lowering medication to prevent plaque from building up in the arteries and a blood-thinner, such as aspirin, to help the blood flow more easily through the arteries may also be prescribed.\n                \nSurgery\n                \nAlthough surgery has been used in the past for treatment of RAS due to atherosclerosis, recent studies have not shown improved outcomes with surgery compared with medication. However, surgery may be recommended for people with RAS caused by FMD or RAS that does not improve with medication. Different types of surgery for RAS include the following. The procedures are performed in a hospital by a vascular surgeona doctor who specializes in repairing blood vessels. Anesthesia is needed.\n                \n- Angioplasty and stenting. Angioplasty is a procedure in which a catheter is put into the renal artery, usually through the groin, just as in a catheter angiogram. In addition, for angioplasty, a tiny balloon at the end of the catheter can be inflated to flatten the plaque against the artery wall. A small mesh tube, called a stent, may then be positioned inside the artery to keep plaque flattened and the artery open. People with RAS caused by FMD may be successfully treated with angioplasty alone, while angioplasty with stenting has a better outcome for people with RAS caused by atherosclerosis.  - Endarterectomy or bypass surgery. In an endarterectomy, the plaque is cleaned out of the artery, leaving the inside lining smooth and clear. To create a bypass, a vein or synthetic tube is used to connect the kidney to the aorta. This new path serves as an alternate route for blood to flow around the blocked artery into the kidney. These procedures are not performed as often as in the past due to a high risk of complications during and after the procedure."}
{"_id":"046cad63-160a-46d9-899b-57274d69c86a","text":"Limiting intake of fats, cholesterol, sodium, and sugar can help prevent atherosclerosis, which can lead to RAS. Most sodium in the diet comes from salt. A healthy diet that prevents people from becoming overweight or obese can also help prevent atherosclerosis. People with RAS that has caused decreased kidney function should limit their intake of protein, cholesterol, sodium, and potassium to slow the progression of kidney failure. More information about nutrition for CKD is provided in the NIDDK health topics, Nutrition for Early Chronic Kidney Disease in Adults and Nutrition for Advanced Chronic Kidney Disease in Adults. People should talk with their health care provider about what diet is right for them."}
{"_id":"84d83ebf-f426-4450-be36-68150f6b477a","text":"- Renal artery stenosis (RAS) is the narrowing of one or both renal arteries. The renal arteries are blood vessels that carry blood to the kidneys from the aortathe main blood vessel that carries blood from the heart to arteries throughout the body.  - Renovascular hypertension (RVH) is high blood pressure caused by RAS.  - About 90 percent of RAS is caused by atherosclerosis. Most other cases of RAS are caused by fibromuscular dysplasia (FMD), which can cause blood vessels to narrow.  - RAS often has no symptoms until it becomes severe. The first symptoms of RAS are usually either high blood pressure or decreased kidney function, or both, but RAS is often overlooked as a cause of high blood pressure.  - People with RAS are at increased risk for chronic kidney disease (CKD), coronary artery disease, stroke, and peripheral vascular disease.  - Imaging tests used to diagnose RAS include duplex ultrasound, catheter angiogram, computerized tomographic angiography (CTA) scan, and magnetic resonance angiogram (MRA).  - Treatment for RAS includes lifestyle changes, medications, and surgery."}
{"_id":"50f38a53-a976-4de9-a9f0-8e122c6ddc97","text":"Your kidneys are two bean-shaped organs, each about the size of a fist. They are located just below your rib cage, one on each side of your spine. Every day, your two kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine. Urine flows from your kidneys to your bladder through tubes called ureters. Your bladder stores urine until releasing it through urination."}
{"_id":"2526870a-0987-4917-83da-f22792c7efa0","text":"Blood pressure is the force of blood flow inside your blood vessels. Blood pressure is written with two numbers separated by a slash. For example, a blood pressure result of 130\/80 is said as 130 over 80. The first number is the pressure in your blood vessels as your heart beats and pushes blood through your blood vessels. The second number is the pressure as your blood vessels relax between heartbeats.\n                \nHigh blood pressure forces your heart to work harder to pump blood. High blood pressure can strain your heart, damage your blood vessels, and increase your risk of heart attack, stroke, eye problems, and kidney problems."}
{"_id":"7fa3c482-cf0e-4afc-bbbf-43b87a15446f","text":"In the early stages, diabetic kidney disease does not have any symptoms. Kidney disease happens so slowly that you may not feel sick at all for many years. You may not feel sick even when your kidneys do only half the job of healthy kidneys. Only your doctor can tell if you have kidney disease by checking the protein, or albumin, level in your urine at least once a year.\n                \nThe first symptom of diabetic kidney disease is often swelling in parts of your body, such as your hands, face, feet, or ankles. Also, large amounts of protein in your urine may cause urine to look foamy. Once your kidney function starts to decrease, other symptoms may include\n                \n- increased or decreased urination  - feeling drowsy or tired  - feeling itchy or numb  - dry skin  - headaches  - weight loss  - not feeling hungry  - feeling sick to your stomach  - vomiting  - sleep problems  - trouble staying focused  - darkened skin  - muscle cramps"}
{"_id":"353e7dfa-a80c-4e68-8faf-33acdea8d3e1","text":"Your dietitian or doctor may suggest a special eating plan for you. You may have to avoid a diet high in protein, fat, sodium, and potassium.\n                \n- Cut back on protein, especially animal products such as meat. Damaged kidneys may fail to remove protein waste products from your blood. Diets high in protein make your kidneys work harder and fail sooner.  - Avoid a high-fat diet. High-fat diets are high in cholesterol. Cholesterol is a type of fat found in your bodys cells, blood, and many foods. Your body needs some cholesterol to work the right way. For example, your body uses cholesterol to make certain essential hormones and maintain nerve function. However, your body makes all the cholesterol it needs. If you often eat foods that are high in cholesterol, or if high cholesterol runs in your family, extra cholesterol in your blood can build up over time in the walls of your blood vessels and arteries. High blood cholesterol can lead to heart disease and stroke, some of the biggest health problems for people with diabetes.  - Avoid high-sodium foods. Sodium is a mineral found in salt and other foods. High levels of sodium may raise your blood pressure. Some high-sodium foods include canned food, frozen dinners, and hot dogs. The amount of sodium is listed on the food label, so you can see which foods have the highest levels. Try to limit your sodium to less than a teaspoon a day, or about 2,300 milligrams (mg) a day. If you have high blood pressure or are African American, middle-aged, or older, aim for no more than 1,500 mg of sodium per day. Ask your doctor or your dietitian about how much sodium you can have.  - Ask your doctor about the amount of potassium you need. Potassium is a mineral that helps your heartbeat stay regular and muscles work right. Healthy kidneys keep the right amount of potassium in your body. However, if you have severe kidney damage, high levels of potassium may cause an abnormal heart rhythm or even make your heart stop, called cardiac arrest. Some high-potassium foods include apricots, bananas, oranges, and potatoes.\n                \nMore information about healthy eating and kidney disease is provided in the NIDDK health topics:   - Eat Right to Feel Right on Hemodialysis   - Nutrition for Advanced Chronic Kidney Disease in Adults   - Nutrition for Early Chronic Kidney Disease in Adults   - What I need to know about Eating and Diabetes"}
{"_id":"cf69250c-b5a5-4541-a03c-9d5aee794a87","text":"Kidney failure, also called end-stage kidney disease or ESRD, means your kidneys no longer work well enough to do their job. You will need treatment to replace the work your kidneys have stopped doing."}
{"_id":"d53dca65-3379-43f7-9a12-3fb7411e651f","text":"Crohn's disease is a chronic, or long lasting, disease that causes inflammationirritation or swellingin the gastrointestinal (GI) tract. Most commonly, Crohn's affects the small intestine and the beginning of the large intestine. However, the disease can affect any part of the GI tract, from the mouth to the anus.\n                \nCrohn's disease is a chronic inflammatory disease of the GI tract, called inflammatory bowel disease (IBD). Ulcerative colitis and microscopic colitis are the other common IBDs. More information is provided in the NIDDK health topics, Ulcerative Colitis and Microscopic Colitis: Collagenous Colitis and Lymphocytic Colitis.\n                \nCrohn's disease most often begins gradually and can become worse over time. Most people have periods of remissiontimes when symptoms disappearthat can last for weeks or years.\n                \nSome people with Crohn's disease receive care from a gastroenterologist, a doctor who specializes in digestive diseases."}
{"_id":"09839a0c-74f2-4eba-99d2-8d5dd3fca273","text":"The GI tract is a series of hollow organs joined in a long, twisting tube from the mouth to the anusa 1-inch-long opening through which stool leaves the body. The body digests food using the movement of muscles in the GI tract, along with the release of hormones and enzymes. Organs that make up the GI tract are the mouth, esophagus, stomach, small intestine, large intestinewhich includes the appendix, cecum, colon, and rectumand anus. The last part of the GI tractcalled the lower GI tractconsists of the large intestine and anus. The intestines are sometimes called the bowel."}
{"_id":"88e6d464-626a-40b2-9375-b6a22781510d","text":"The exact cause of Crohn's disease is unknown. Researchers believe the following factors may play a role in causing Crohn's disease:\n                \n- autoimmune reaction  - genes  - environment\n                \nAutoimmune reaction. Scientists believe one cause of Crohn's disease may be an autoimmune reactionwhen a person's immune system attacks healthy cells in the body by mistake. Normally, the immune system protects the body from infection by identifying and destroying bacteria, viruses, and other potentially harmful foreign substances. Researchers believe bacteria or viruses can mistakenly trigger the immune system to attack the inner lining of the intestines. This immune system response causes the inflammation, leading to symptoms.\n                \nGenes. Crohn's disease sometimes runs in families. Research has shown that people who have a parent or sibling with Crohn's disease may be more likely to develop the disease. Researchers continue to study the link between genes and Crohn's disease.\n                \nEnvironment. Some studies suggest that certain things in the environment may increase the chance of a person getting Crohn's disease, although the overall chance is low. Nonsteroidal anti-inflammatory drugs,1 antibiotics,2 and oral contraceptives2 may slightly increase the chance of developing Crohn's disease. A high-fat diet may also slightly increase the chance of getting Crohn's disease.3\n                \nSome people incorrectly believe that eating certain foods, stress, or emotional distress can cause Crohn's disease. Emotional distress and eating certain foods do not cause Crohn's disease. Sometimes the stress of living with Crohn's disease can make symptoms worse. Also, some people may find that certain foods can trigger or worsen their symptoms."}
{"_id":"1fa5c677-a574-4b71-8d3e-0257f33bc23f","text":"The most common signs and symptoms of Crohn's disease are\n                \n- diarrhea  - abdominal cramping and pain  - weight loss\n                \nOther general signs and symptoms include\n                \n- feeling tired  - nausea or loss of appetite  - fever  - anemiaa condition in which the body has fewer red blood cells than normal\n                \nSigns and symptoms of inflammation outside of the intestines include\n                \n- joint pain or soreness  - eye irritation  - skin changes that involve red, tender bumps under the skin\n                \nThe symptoms a person experiences can vary depending on the severity of the inflammation and where it occurs."}
{"_id":"b143596a-67cb-4fde-b671-896af138cb74","text":"A health care provider diagnoses Crohn's disease with the following:\n                \n- medical and family history  - physical exam  - lab tests  - upper GI series  - computerized tomography (CT) scan  - intestinal endoscopy\n                \nThe health care provider may perform a series of medical tests to rule out other bowel diseases, such as irritable bowel syndrome, ulcerative colitis, or celiac disease, that cause symptoms similar to those of Crohn's disease.\n                \nMedical and Family History\n                \nTaking a medical and family history can help a health care provider diagnose Crohn's disease and understand a patient's symptoms. He or she will ask the patient to describe his or her\n                \n- family history  - symptoms  - current and past medical conditions  - current medications\n                \nPhysical Exam\n                \nA physical exam may help diagnose Crohn's disease. During a physical exam, the health care provider most often\n                \n- checks for abdominal distension, or swelling  - listens to sounds within the abdomen using a stethoscope  - taps on the abdomen to check for tenderness and pain and establish if the liver or spleen is abnormal or enlarged\n                \nLab Tests\n                \nA health care provider may order lab tests, including blood and stool tests.\n                \nBlood tests. A blood test involves drawing blood at a health care provider's office or a lab. A lab technologist will analyze the blood sample. A health care provider may use blood tests to look for changes in\n                \n- red blood cells. When red blood cells are fewer or smaller than normal, a patient may have anemia.  - white blood cells. When the white blood cell count is higher than normal, a person may have inflammation or infection somewhere in his or her body.\n                \nStool tests. A stool test is the analysis of a sample of stool. A health care provider will give the patient a container for catching and storing the stool at home. The patient returns the sample to the health care provider or to a lab. A lab technologist will analyze the stool sample. Health care providers commonly order stool tests to rule out other causes of GI diseases.\n                \nUpper Gastrointestinal Series\n                \nAn upper GI series, also called a barium swallow, uses x-rays and fluoroscopy to help diagnose problems of the upper GI tract. Fluoroscopy is a form of x-ray that makes it possible to see the internal organs and their motion on a video monitor. An x-ray technician performs this test at a hospital or an outpatient center, and a radiologista doctor who specializes in medical imaginginterprets the images.\n                \nThis test does not require anesthesia. A patient should not eat or drink before the procedure, as directed by the health care provider. Patients should ask their health care provider about how to prepare for an upper GI series.\n                \nDuring the procedure, the patient will stand or sit in front of an x-ray machine and drink barium, a chalky liquid. Barium coats the esophagus, stomach, and small intestine so the radiologist and a health care provider can see the shape of these organs more clearly on x-rays.\n                \nA patient may experience bloating and nausea for a short time after the test. For several days afterward, barium liquid in the GI tract causes white or light-colored stools. A health care provider will give the patient specific instructions about eating and drinking after the test.\n                \nComputerized Tomography Scan\n                \nComputerized tomography scans use a combination of x-rays and computer technology to create images. For a CT scan, a health care provider may give the patient a solution to drink and an injection of a special dye, called contrast medium. CT scans require the patient to lie on a table that slides into a tunnel-shaped device where the x-rays are taken. An x-ray technician performs the procedure in an outpatient center or a hospital, and a radiologist interprets the images. The patient does not need anesthesia. CT scans can diagnose both Crohn's disease and the complications seen with the disease.\n                \nIntestinal Endoscopy\n                \nIntestinal endoscopies are the most accurate methods for diagnosing Crohn's disease and ruling out other possible conditions, such as ulcerative colitis, diverticular disease, or cancer. Intestinal endoscopies include\n                \n- upper GI endoscopy and enteroscopy  - capsule endoscopy  - colonoscopy\n                \nUpper GI endoscopy and enteroscopy. An upper GI endoscopy is a procedure that uses an endoscopea small, flexible tube with a lightto directly visualize the lining of the upper GI tract. A health care provider performs the procedure at a hospital or an outpatient center. A nurse or technician may give the patient a liquid anesthetic to gargle or will spray the anesthetic on the back of a patient's throat. The anesthetic numbs the throat and calms the gag reflex. The nurse or technician will then place an intravenous (IV) needle in the person's arm or hand to provide a sedative. The health care provider carefully feeds the endoscope down the patient's esophagus and into the stomach. A small camera on the endoscope sends a video image to a monitor, allowing close examination of the GI tract.\n                \nDuring an enteroscopy, the health care provider examines the small intestine with a special, longer endoscope. The health care provider carefully feeds the endoscope into the small intestine using one of the following procedures:\n                \n- push enteroscopy, which uses a long endoscope to examine the upper portion of the small intestine  - single- or double-balloon enteroscopy, which use small balloons to help move the endoscope into the small intestine  - spiral enteroscopy, which uses a tube attached to an endocope that acts as a cork screw to move the instrument into the small intestine\n                \nThe procedure most often takes between 15 and 60 minutes. The endoscope does not interfere with the patient's breathing, and many patients fall asleep during the procedure.\n                \nCapsule endoscopy. Although this procedure can examine the entire digestive tract, health care providers use it mostly to examine the small intestine. The patient swallows a capsule containing a tiny camera. As the capsule passes through the GI tract, the camera will record and transmit images to a small receiver device worn by the patient. When the recording is done, the health care provider downloads the images and reviews them on a video monitor. The camera capsule leaves the patient's body during a bowel movement and is safely flushed down the toilet.\n                \nColonoscopy. Colonoscopy is a test that uses a long, flexible, narrow tube with a light and tiny camera on one end, called a colonoscope or scope, to look inside a patient's rectum and entire colon. In most cases, light anesthesia and pain medication help patients relax for the test. The medical staff will monitor a patient's vital signs and try to make him or her as comfortable as possible. A nurse or technician will place an IV needle in a vein in the patient's arm or hand to give anesthesia.\n                \nFor the test, the patient will lie on a table or stretcher while the gastroenterologist inserts a colonoscope into the patient's anus and slowly guides it through the rectum and into the colon. The scope inflates the large intestine with air to give the gastroenterologist a better view. The camera sends a video image of the intestinal lining to a monitor, allowing the gastroenterologist to examine the tissues lining the colon and rectum. The gastroenterologist may move the patient several times and adjust the scope for better viewing. Once the scope has reached the opening to the small intestine, the gastroenterologist slowly withdraws it and examines the lining of the colon and rectum again.\n                \nA colonoscopy can show inflamed and swollen tissue, ulcers, and abnormal growths such as polypsextra pieces of tissue that grow on the inner lining of the intestine. If the gastroenterologist suspects Crohn's disease, he or she will biopsy the patient's colon and rectum. A biopsy is a procedure that involves taking small pieces of tissue for examination with a microscope.\n                \nA health care provider will give patients written bowel prep instructions to follow at home before the test. The health care provider will also give patients information about how to care for themselves following the procedure."}
{"_id":"2efc3cf2-2122-4912-bbed-d3ed0972385f","text":"A health care provider treats Crohn's disease with\n                \n- medications  - bowel rest  - surgery\n                \nWhich treatment a person needs depends on the severity of the disease and symptoms. Each person experiences Crohn's disease differently, so health care providers adjust treatments to improve the person's symptoms and induce, or bring about, remission.\n                \nMedications\n                \nWhile no medication cures Crohn's disease, many can reduce symptoms. The goals of medication therapy are\n                \n- inducing and maintaining remission  - improving the person's quality of life\n                \nMany people with Crohn's disease require medication therapy. Health care providers will prescribe medications depending on the person's symptoms:\n                \n- aminosalicylates  - corticosteroids  - immunomodulators  - biologic therapies  - other medications\n                \nAminosalicylates are medications that contain 5-aminosalicyclic acid (5-ASA), which helps control inflammation. Health care providers use aminosalicylates to treat people newly diagnosed with Crohn's disease who have mild symptoms. Aminosalicylates include\n                \n- balsalazide  - mesalamine  - olsalazine  - sulfasalazinea combination of sulfapyridine and 5-ASA\n                \nSome of the common side effects of aminosalicylates include\n                \n- abdominal pain  - diarrhea  - headaches  - heartburn  - nausea and vomiting\n                \nCorticosteroids, also known as steroids, help reduce the activity of the immune system and decrease inflammation. Health care providers prescribe corticosteroids for people with moderate to severe symptoms. Corticosteroids include\n                \n- budesonide  - hydrocortisone  - methylprednisone  - prednisone\n                \nSide effects of corticosteroids include\n                \n- acne  - a higher chance of developing infections  - bone mass loss  - high blood glucose  - high blood pressure  - mood swings  - weight gain\n                \nIn most cases, health care providers do not prescribe corticosteroids for long-term use.\n                \nImmunomodulators reduce immune system activity, resulting in less inflammation in the GI tract. These medications can take several weeks to 3 months to start working. Immunomodulators include\n                \n- 6-mercaptopurine, or 6-MP  - azathioprine  - cyclosporine  - methotrexate\n                \nHealth care providers prescribe these medications to help people with Crohn's disease go into remission or to help people who do not respond to other treatments. People taking these medications may have the following side effects:\n                \n- a low white blood cell count, which can lead to a higher chance of infection  - fatigue, or feeling tired  - nausea and vomiting  - pancreatitis\n                \nHealth care providers most often prescribe cyclosporine only to people with severe Crohn's disease because of the medication's serious side effects. People should talk with their health care provider about the risks and benefits of cyclosporine.\n                \nBiologic therapies are medications that target a protein made by the immune system. Neutralizing this protein decreases inflammation in the intestine. Biologic therapies work quickly to bring on remission, especially in people who do not respond to other medications. Biologic therapies include\n                \n- adalimumab  - certolizumab  - infliximab  - natalizumab  - vedolizumab\n                \nHealth care providers most often give patients infliximab every 6 to 8 weeks at a hospital or an outpatient center. Side effects may include a toxic reaction to the medication and a higher chance of developing infections, particularly tuberculosis.\n                \nOther medications to treat symptoms or complications may include\n                \n- acetaminophen for mild pain. People with Crohn's disease should avoid using ibuprofen, naproxen, and aspirin since these medications can make symptoms worse.  - antibiotics to prevent or treat infections and fistulas.  - loperamide to help slow or stop severe diarrhea. In most cases, people only take this medication for short periods of time since it can increase the chance of developing megacolon.\n                \nBowel Rest\n                \nSometimes Crohn's disease symptoms are severe and a person may need to rest his or her bowel for a few days to several weeks. Bowel rest involves drinking only clear liquids or having no oral intake. To provide the patient with nutrition, a health care provider will deliver IV nutrition through a special catheter, or tube, inserted into a vein in the patient's arm. Some patients stay in the hospital, while other patients are able to receive the treatment at home. In most cases, the intestines are able to heal during bowel rest.\n                \nSurgery\n                \nEven with medication treatments, up to 20 percent of people will need surgery to treat their Crohn's disease.1 Although surgery will not cure Crohn's disease, it can treat complications and improve symptoms. Health care providers most often recommend surgery to treat\n                \n- fistulas  - bleeding that is life threatening  - bowel obstructions  - side effects from medications when they threaten a person's health  - symptoms when medications do not improve a person's condition\n                \nA surgeon can perform different types of operations to treat Crohn's disease:\n                \n- small bowel resection  - subtotal colectomy  - proctocolectomy and ileostomy\n                \nPatients will receive general anesthesia. Most patients will stay in the hospital for 3 to 7 days after the surgery. Full recovery may take 4 to 6 weeks.\n                \nSmall bowel resection. Small bowel resection is surgery to remove part of a patient's small intestine. When a patient with Crohn's disease has a blockage or severe disease in the small intestine, a surgeon may need to remove that section of intestine. The two types of small bowel resection are\n                \n- laparoscopicwhen a surgeon makes several small, half-inch incisions in the patient's abdomen. The surgeon inserts a laparoscopea thin tube with a tiny light and video camera on the endthrough the small incisions. The camera sends a magnified image from inside the body to a video monitor, giving the surgeon a close-up view of the small intestine. While watching the monitor, the surgeon inserts tools through the small incisions and removes the diseased or blocked section of small intestine. The surgeon will reconnect the ends of the intestine.  - open surgerywhen a surgeon makes one incision about 6 inches long in the patient's abdomen. The surgeon will locate the diseased or blocked section of small intestine and remove or repair that section. The surgeon will reconnect the ends of the intestine.\n                \nSubtotal colectomy. A subtotal colectomy, also called a large bowel resection, is surgery to remove part of a patient's large intestine. When a patient with Crohn's disease has a blockage, a fistula, or severe disease in the large intestine, a surgeon may need to remove that section of intestine. A surgeon can perform a subtotal colectomy by\n                \n- laparoscopic colectomywhen a surgeon makes several small, half-inch incisions in the abdomen. While watching the monitor, the surgeon removes the diseased or blocked section of the large intestine. The surgeon will reconnect the ends of the intestine.  - open surgerywhen a surgeon makes one incision about 6 to 8 inches long in the abdomen. The surgeon will locate the diseased or blocked section of small intestine and remove that section. The surgeon will reconnect the ends of the intestine.\n                \nProctocolectomy and ileostomy. A proctocolectomy is surgery to remove a patient's entire colon and rectum. An ileostomy is a stoma, or opening in the abdomen, that a surgeon creates from a part of the ileumthe last section of the small intestine. The surgeon brings the end of the ileum through an opening in the patient's abdomen and attaches it to the skin, creating an opening outside of the patient's body. The stoma is about three-fourths of an inch to a little less than 2 inches wide and is most often located in the lower part of the patient's abdomen, just below the beltline.\n                \nA removable external collection pouch, called an ostomy pouch or ostomy appliance, connects to the stoma and collects intestinal contents outside the patient's body. Intestinal contents pass through the stoma instead of passing through the anus. The stoma has no muscle, so it cannot control the flow of intestinal contents, and the flow occurs whenever peristalsis occurs. Peristalsis is the movement of the organ walls that propels food and liquid through the GI tract.\n                \nPeople who have this type of surgery will have the ileostomy for the rest of their lives."}
{"_id":"2492f21f-439b-4552-aa23-b66b26d5ebaf","text":"Researchers have not found that eating, diet, and nutrition cause Crohn's disease symptoms. Good nutrition is important in the management of Crohn's disease, however. Dietary changes can help reduce symptoms. A health care provider may recommend that a person make dietary changes such as\n                \n- avoiding carbonated drinks  - avoiding popcorn, vegetable skins, nuts, and other high-fiber foods  - drinking more liquids  - eating smaller meals more often  - keeping a food diary to help identify troublesome foods\n                \nHealth care providers may recommend nutritional supplements and vitamins for people who do not absorb enough nutrients.\n                \nTo help ensure coordinated and safe care, people should discuss their use of complementary and alternative medical practices, including their use of dietary supplements and probiotics, with their health care provider. Read more at www.nccam.nih.gov\/health\/probiotics.\n                \nDepending on a person's symptoms or medications, a health care provider may recommend a specific diet, such as a\n                \n- high-calorie diet  - lactose-free diet  - low-fat diet  - low-fiber diet  - low-salt diet\n                \nPeople should speak with a health care provider about specific dietary recommendations and changes."}
{"_id":"0d4888ac-f125-47af-8e9c-7ec8e2930c51","text":"Complications of Crohn's disease can include\n                \n- bowel obstruction. Crohn's disease can thicken the wall of the intestine. Over time, the thickened areas of the intestine can narrow, which can block the intestine. A partial or complete obstruction, also called a bowel blockage, can block the movement of food or stool through the intestines. A complete bowel obstruction is life threatening and requires immediate medical attention and often surgery.  - fistulasabnormal passages, or tunnels, between two organs, or between an organ and the outside of the body. How a health care provider treats fistulas depends on their type and severity. For some people, fistulas heal with medication and diet changes, while other people will need to have surgery.  - anal fissuressmall tears in the anus that may cause itching, pain, or bleeding. Most anal fissures heal with medical treatment, including ointments, warm baths, and dietary changes.  - ulcers. Inflammation anywhere along the GI tract can lead to ulcers or open sores in a person's mouth, intestines, anus, and perineumthe area between the anus and the sex organs. In most cases, the treatment a health care provider prescribes for Crohn's disease will also treat the ulcers.  - malnutritiona condition that develops when the body does not get the right amount of vitamins, minerals, and nutrients it needs to maintain healthy tissues and organ function. Some people may need IV fluids or feeding tubes to replace lost nutrients and fluids.  - inflammation in other areas of the body. The immune system can trigger inflammation in the      - joints    - eyes    - skin\n                \nHealth care providers can treat inflammation by adjusting medications or prescribing new medications.\n                \n\n                \nCrohn's Disease and Colon Cancer   People with Crohn's disease in the large intestine may be more likely to develop colon cancer. People who receive ongoing treatment and remain in remission may reduce their chances of developing colon cancer.   People with Crohn's disease should talk with their health care provider about how often they should get screened for colon cancer. Screening can include colonoscopy with biopsies. Such screening does not reduce a person's chances of developing colon cancer. Instead, screening can help diagnose cancer early and improve chances for recovery."}
{"_id":"a7c74e8d-678f-468f-a046-14810ae28a59","text":"- Crohn's disease is a chronic, or long lasting, disease that causes inflammationirritation or swellingin the gastrointestinal (GI) tract.  - The exact cause of Crohn's disease is unknown. Researchers believe that factors such as an autoimmune reaction, genes, and environment may play a role in causing Crohn's disease.  - Crohn's disease can occur in people of any age. However, it is more likely to develop in people      - between the ages of 20 and 29    - who have a family member, most often a sibling or parent, with inflammatory bowel disease (IBD)    - who smoke cigarettes    - The most common signs and symptoms of Crohn's disease are diarrhea, abdominal cramping and pain, and weight loss.  - A health care provider diagnoses Crohn's disease with the following:      - medical and family history    - physical exam    - lab tests    - upper GI series    - computerized tomography (CT) scan    - intestinal endoscopy    - Which treatment a person needs depends on the severity of the disease and symptoms.  - Good nutrition is important in the management of Crohn's disease. A health care provider may recommend that a person make dietary changes.  - People with Crohn's disease should talk with their health care provider about how often they should get screened for colon cancer."}
{"_id":"754533f9-5309-4896-a4f2-21bfe189dd75","text":"Diabetes management and treatment is expensive. According to the American Diabetes Association (ADA), the average cost of health care for a person with diabetes is $13,741 a yearmore than twice the cost of health care for a person without diabetes.1\n                \nMany people who have diabetes need help paying for their care. For those who qualify, a variety of government and nongovernment programs can help cover health care expenses. This publication is meant to help people with diabetes and their family members find and access such resources."}
{"_id":"092becf3-2d89-4dff-8936-3f0d5d98f528","text":"Health insurance helps pay for medical care, including the cost of diabetes care. Health insurance options include the following:\n                \n- private health insurance, which includes group and individual health insurance  - government health insurance, such as Medicare, Medicaid, the Childrens Health Insurance Program (CHIP), TRICARE, and veterans health care programs\n                \nStarting in 2014, the Affordable Care Act (ACA) prevents insurers from denying coverage or charging higher premiums to people with preexisting conditions, such as diabetes. The ACA also requires most people to have health insurance or pay a fee. Some people may be exempt from this fee. Read more about the ACA at HealthCare.gov or call 18003182596, TTY 18558894325."}
{"_id":"7f79b44e-e5aa-4599-a5d5-c90bc74295c0","text":"Insurance companies sell private health insurance plans. Two types of private health insurance are\n                \n- Group health insurance. People may be eligible to purchase group health insurance through their employer or union or through a family members employer or union. Other organizations, such as professional or alumni organizations, may also offer group health insurance.  - Individual health insurance. People may purchase individual health insurance for themselves and their families. The website HealthCare.gov provides information about individual insurance plans. The website also provides a search function, called the Health Insurance Marketplace, to find health insurance options by state. Depending on their income and family size, some people may qualify for lower-cost premiums through the Health Insurance Marketplace. People can select or change individual health insurance plans during the open enrollment period each year. HealthCare.gov lists open enrollment period dates. The website also provides information about life events that may allow people to enroll outside the open enrollment period.\n                \nEmployers may have a waiting period before an employee and his or her family members can enroll in the company health plan. Under the ACA, the waiting period can be no longer than 90 days. Certain health plans called health maintenance organizations (HMOs) may have an affiliation perioda time that must pass before health insurance coverage becomes effective. An affiliation period can be no longer than 3 months.\n                \nThe ACA expanded coverage of preventive services. For example, adults with sustained high blood pressure may have access to diabetes screening at no cost. Adults and children may have access to obesity screening and counseling at no cost.\n                \nEach states insurance regulatory office, sometimes called the state insurance department or commission, provides more information about health insurance laws. This office can also help identify an insurance company that offers individual coverage. The National Association of Insurance Commissioners website, www.naic.org\/state_web_map.htm , provides a membership list with contact information and a link to the website for each states insurance regulatory office.\n                \nThe ADA also provides information about health insurance options at www.diabetes.org\/living-with-diabetes\/health-insurance .\n                \nKeeping Group Health Insurance after Leaving a Job\n                \nWhen leaving a job, a person may be able to continue the group health insurance provided by his or her employer for up to 18 months under a federal law called the Consolidated Omnibus Budget Reconciliation Act, or COBRA. Although people pay more for group health insurance through COBRA than they did as employees, group coverage may be cheaper than individual coverage. People who have a disability before becoming eligible for COBRA or who are determined by the Social Security Administration to be disabled within the first 60 days of COBRA coverage may be able to extend COBRA coverage an additional 11 months, for up to 29 months of coverage. COBRA may also cover young adults who were insured under a parents policy after they have reached the age limit and are trying to obtain their own insurance.\n                \nRead more at www.dol.gov\/dol\/topic\/health-plans\/cobra.htm or call the U.S. Department of Labor at 18664USADOL (18664872365).\n                \nIf a person doesnt qualify for coverage or if COBRA coverage has expired, other options may be available:\n                \n- Some states require employers to offer conversion policies, in which people stay with their insurance company and buy individual coverage.  - Some professional and alumni organizations offer group coverage for members.  - Some insurance companies offer short-term stopgap policies designed for people who are between jobs. However, these policies may not meet ACA requirements. For example, they may not cover preexisting conditions.  - People can purchase individual health insurance policies.\n                \nEach states insurance regulatory office can provide more information about these and other options. Information about consumer health plans is also available at the U.S. Department of Labors website at www.dol.gov\/dol\/topic\/health-plans\/consumerinfhealth.htm."}
{"_id":"8f47a7ec-0a1d-4ebe-a109-301176d8d964","text":"Medicare is a federal health insurance program that pays health care costs for eligible people who are\n                \n- age 65 or older  - under age 65 with certain disabilities  - of any age with end-stage renal diseasetotal and permanent kidney failure that requires a kidney transplant or blood-filtering treatments called dialysis\n                \nWhat health plans does Medicare offer?\n                \nMedicare has four parts:\n                \n- Part A (hospital insurance) covers inpatient care, skilled nursing home residence, hospice care, and home health care. Part A has no premium for those who have paid enough Medicare taxes. A premium is an amount a person must pay periodicallymonthly or quarterlyfor Medicare, other health plan, or drug plan coverage. Part A does have a deductible, an amount a person must pay for health care or prescriptions before the health plan will pay. A person must pay a daily amount for hospital stays that last longer than 60 days.  - Part B (medical insurance) covers services from health care providers, outpatient care, home health care, durable medical equipment, and some preventative services. Part B has a monthly premium based on a persons income. Rates change each year. After a person pays the deductible each year, Part B pays 80 percent for most covered services as a primary payer. The billing staff of the service providerhospital or cliniccan calculate how much a person will owe.  - Part C (Medicare Advantage Plans) are part of Medicare and are sometimes called MA Plans. Medicare must approve Medicare Advantage Plans. Each Medicare Advantage Plan must cover Part A and Part B services and may cover other services, too. Medicare Advantage Plans may have Part D prescription coverage. If not, a person can buy a Part D plan separately. Medicare Advantage Plans are not all the same. A person who is thinking of choosing a Medicare Advantage Plan should ask about the rules of the plan. The rules may specify which health care providers or hospitals a person may use. The plan may require a referral from a primary care provider to see a specialist. The plan may not cover medical expenses incurred during travel. How much a person has to pay out-of-pocket each year will vary by plan. People who have a Medicare Advantage Plan cannot have a Medigap plan to help pay out of-pocket costs. See the section on Medigap.  Four types of Medicare Advantage Plans are available:      - HMOs    - preferred provider organizations (PPOs)    - private fee for service plans    - special needs plans for certain groups    - Part D (prescription drug coverage) has a premium and covers some medications. Private insurance companies offer different Part D plans approved by Medicare. Costs and coverage vary by plan. A person who has few assets and earns less than 150 percent of the federal poverty level may qualify for extra help to pay Part D premiums and medication costs. People can apply for this help by calling the Social Security Administration, visiting www.socialsecurity.gov to apply online, visiting their local Social Security office, or contacting their state medical assistance (Medicaid) office. People can find the current-year guidelines at www.aspe.hhs.gov\/poverty or by calling Social Security at 18007721213, TTY 18003250778. People can find information and applications for Part D plans at www.medicare.gov. A person can also apply for Part D with an insurance company that sells one of these plans.\n                \nOther Medicare health plans are for certain groups, such as frail people living in the community and people with multiple chronic illnesses, and include hospital and medical coverage. Some pay for prescribed medications, too. State health insurance programscalled Medicaidpartially finance and administer these services. The plans include the following:\n                \n- Medicare Cost Plans are HMOs, like the ones offered as Medicare Advantage plans, only out-of-network providers are paid as if the policyholder had Original Medicare. Original Medicare is Medicare Part A and Part B.  - Program of All-Inclusive Care for the Elderly (PACE) combines medical, social, and long-term care services for frail people who live and get health care in the community.  - Medicare Innovation Projects are special projects that test improvements in Medicare coverage, payment, and quality of care.\n                \nRead more about Medicare Cost Plans and Demonstration or Pilot Programs on the state Medicaid website at www.medicaid.gov or call 1800MEDICARE (18006334227). State Medicaid offices can provide more information about PACE. See the section on Medicaid.\n                \nDoes Medicare cover diabetes services and supplies?\n                \nMedicare helps pay for the diabetes services, supplies, and equipment listed below and for some preventive services for people who are at risk for diabetes. However, coinsurance or deductibles may apply. A person must have Medicare Part B or Medicare Part D to receive these covered services and supplies.\n                \nMedicare Part B helps pay for\n                \n- diabetes screening tests for people at risk of developing diabetes  - diabetes self-management training  - diabetes supplies such as glucose monitors, test strips, and lancets  - insulin pumps and insulin if used with an insulin pump  - counseling to help people who are obese lose weight  - flu and pneumonia shots  - foot exams and treatment for people with diabetes  - eye exams to check for glaucoma and diabetic retinopathy  - medical nutrition therapy services for people with diabetes or kidney disease, when referred by a health care provider  - therapeutic shoes or inserts, in some cases\n                \nMedicare Part D helps pay for\n                \n- diabetes medications  - insulin, excluding insulin used with an insulin pump  - diabetes supplies such as needles and syringes for injecting insulin\n                \nPeople who are in a Medicare Advantage Plan or other Medicare health plan should check their plans membership materials and call for details about how the plan provides the diabetes services, supplies, and medications covered by Medicare.\n                \nRead more at www.medicare.gov\/publications\/pubs\/pdf\/11022.pdf (PDF, 1,023 KB) or call 1800MEDICARE (18006334227) to request the free booklet Medicares Coverage of Diabetes Supplies & Services.\n                \nWhere can a person find more information about Medicare?\n                \nA person can find more information about Medicare by\n                \n- visiting the Medicare website  - calling 1800MEDICARE\n                \nMedicare website. Read more about Medicare at www.medicare.gov, the official U.S. Government website for people with Medicare. The website has a full range of information about Medicare, including free publications such as Medicare & You, which is the official Government handbook about Medicare, and Medicare BasicsA Guide for Families and Friends of People with Medicare.\n                \nThrough the Medicare website, people can also\n                \n- find out if they are eligible for Medicare and when they can enroll  - learn about their Medicare health plan options  - find out what Medicare covers  - find a Medicare Prescription Drug Plan  - compare Medicare health plan options in their area  - find a health care provider who participates in Medicare  - get information about the quality of care provided by hospitals, home health agencies, and dialysis facilities\n                \nCalling Medicare. Calling 1800MEDICARE (18006334227) is another way to get help with Medicare questions, order free publications, and more. Help is available 24 hours a day, every day, and is available in English, Spanish, and other languages. TTY users should call 18774862048.\n                \nAccess Personal Medicare Information   People who enroll in Medicare can register with www.MyMedicare.gov, a secure online service, and use the site to access their personal Medicare information at any time. People can view their claims and order history, and see a description of covered preventive services.\n                \n\n                \nWhat is Medigap?\n                \nA Medigap plan, also known as a Medicare supplement plan, can help pay what Original Medicare does not pay for covered services. Insurance companies sell Medigap coverage. People who have a Medicare Advantage plan cannot also have a Medigap plan. A person can buy a Medigap policy from any insurance company licensed to sell the policy in the persons home state.\n                \nFor people who are 65 and older, federal law says that in the first 6 months a person has Part B, companies cannot deny an application or limit payment for anything Original Medicare covers. Some states make insurance companies sell at least one Medigap coverage plan to those under 65 with Medicare. State insurance offices can explain the plans in their state. Find local offices on a map at www.naic.org\/state_web_map.htm ."}
{"_id":"23cb7429-a9b7-4a19-be73-92dd358f81fa","text":"People who enroll in Medicare can register with www.MyMedicare.gov, a secure online service, and use the site to access their personal Medicare information at any time. People can view their claims and order history, and see a description of covered preventive services."}
{"_id":"f1fda057-5f47-400b-b0e8-af38d0f3570c","text":"Medicaid is a state health insurance program for those with low incomes and few assets. Each state runs its own program. The Federal Government requires that Medicaid programs cover a specific set of services; however, states can choose to cover more services in addition to the ones required. A person may have Medicaid alone or Medicare and Medicaid. If a person has both types of coverage, Medicare pays first and Medicaid pays second. Medicaid may pay for things Medicare does not. A person can apply for Medicaid at a city or county department of social services office. The state medical assistance (Medicaid) office can help people find out whether they qualify for Medicaid and can provide more information about Medicaid programs. A social worker can also explain a states Medicaid program and help a person apply.\n                \nTo contact a state Medicaid office, people can\n                \n- search for Medicaid information for a state at www.medicaid.gov or call 18772672323  - search online or check the government pages of the phone book for the local department of human services or department of social services\n                \nCHIP gives free or low-cost Medicaid to children whose parents earn too much for Medicaid, though not enough to pay for a health plan. CHIP may also provide assistance to parents. CHIP is a federal and state program. Read more at www.insurekidsnow.gov or call 18775437669."}
{"_id":"2ff77424-016c-4b03-b8e8-e457a12cb98b","text":"Assistive technology is any device that assists, adapts, or helps to rehabilitate someone with a disability so he or she may function more safely, effectively, and independently at home, at work, and in the community. Assistive technology may include\n                \n- computers with features that make them accessible to people with disabilities  - adaptive equipment, such as wheelchairs  - bathroom modifications, such as grab bars or shower seats\n                \nThe following organizations may be able to provide information, awareness, and training in the use of technology to assist people with disabilities:\n                \nAlliance for Technology Access 1119 Old Humboldt Road Jackson, TN 38305 Phone: 18009143017 or 7315545ATA (7315545282) TTY: 7315545284 Fax: 7315545283 Email: atainfo@ataccess.org Internet: www.ataccess.org\n                \nNational Assistive Technology Technical Assistance Partnership 1700 North Moore Street, Suite 1540 Arlington, VA 222091903 Phone: 7035246686 Fax: 7035246630 TTY: 7035246639 Email: resnaTA@resna.org Internet: www.resnaprojects.org\/nattap\n                \nUnited Cerebral Palsy 1825 K Street NW, Suite 600 Washington, D.C. 20006 Phone: 18008725827 or 2027760406 Internet: www.ucp.org\/resources\/assistive-technology"}
{"_id":"d8e54e58-1099-4da3-abce-142761c9dfcd","text":"- Diabetes management and treatment is expensive. Many people who have diabetes need help paying for their care. For those who qualify, a variety of government and nongovernment programs can help cover health care expenses.  - Health insurance helps pay for medical care, including the cost of diabetes care. Health insurance options include private health insurance and government health insurance.  - Insurance companies sell private health insurance plans. Two types of private health insurance are group health insurance and individual health insurance.  - Medicare is a federal health insurance program that pays health care costs for eligible people who are age 65 or older, under age 65 with certain disabilities, or of any age with end-stage renal disease.  - Medicaid is a state health insurance program for those with low incomes and few assets. Each state runs its own program.  - The Childrens Health Insurance Program (CHIP) gives free or low-cost Medicaid to children whose parents earn too much for Medicaid, though not enough to pay for a health plan.  - Many local governments have public health departments that can help people who need medical care. Local resources such as charitable groups may offer financial help for some expenses related to diabetes.  - People should talk with their health care providers if they have problems paying for diabetes medications. Less expensive generic medications for diabetes, blood pressure, and cholesterol are available. If a health care provider prescribes medications that a person cannot afford, the person should ask the health care provider about cheaper alternatives.  - Health care providers may also be able to assist people who need help paying for their medications and diabetes testing supplies, such as glucose test strips, by providing free samples or referring them to local programs. Drug companies that sell insulin or diabetes medications often have patient assistance programs."}
{"_id":"36e68d42-ade6-4d99-9dda-6f9b45f268e6","text":"Viral hepatitis is inflammation of the liver caused by a virus. Several different viruses, named the hepatitis A, B, C, D, and E viruses, cause viral hepatitis.\n                \nAll of these viruses cause acute, or short-term, viral hepatitis. The hepatitis B, C, and D viruses can also cause chronic hepatitis, in which the infection is prolonged, sometimes lifelong. Chronic hepatitis can lead to cirrhosis, liver failure, and liver cancer.\n                \nResearchers are looking for other viruses that may cause hepatitis, but none have been identified with certainty. Other viruses that less often affect the liver include cytomegalovirus; Epstein-Barr virus, also called infectious mononucleosis; herpesvirus; parvovirus; and adenovirus."}
{"_id":"036cbab9-612f-4dea-a635-94288ccabaa1","text":"Symptoms include\n                \n- jaundice, which causes a yellowing of the skin and eyes  - fatigue  - abdominal pain  - loss of appetite  - nausea  - vomiting  - diarrhea  - low grade fever  - headache\n                \nHowever, some people do not have symptoms."}
{"_id":"2b09194b-e3b7-4262-8e2a-1a3ae8bba053","text":"- Viral hepatitis is inflammation of the liver caused by the hepatitis A, B, C, D, or E viruses.  - Depending on the type of virus, viral hepatitis is spread through contaminated food or water, contact with infected blood, sexual contact with an infected person, or from mother to child during childbirth.  - Vaccines offer protection from hepatitis A and hepatitis B.  - No vaccines are available for hepatitis C, D, and E. Reducing exposure to the viruses offers the best protection.  - Hepatitis A and E usually resolve on their own. Hepatitis B, C, and D can be chronic and serious. Drugs are available to treat chronic hepatitis."}
{"_id":"b49bfb20-37b1-4798-aa24-d0d0c8cc5d08","text":"Some cases of viral hepatitis cannot be attributed to the hepatitis A, B, C, D, or E viruses, or even the less common viruses that can infect the liver, such as cytomegalovirus, Epstein-Barr virus, herpesvirus, parvovirus, and adenovirus. These cases are called non-AE hepatitis. Scientists continue to study the causes of non-AE hepatitis."}
{"_id":"b6f239ff-712f-4c83-9372-35923340d216","text":"Diabetic neuropathies are a family of nerve disorders caused by diabetes. People with diabetes can, over time, develop nerve damage throughout the body. Some people with nerve damage have no symptoms. Others may have symptoms such as pain, tingling, or numbnessloss of feelingin the hands, arms, feet, and legs. Nerve problems can occur in every organ system, including the digestive tract, heart, and sex organs.\n                \nAbout 60 to 70 percent of people with diabetes have some form of neuropathy. People with diabetes can develop nerve problems at any time, but risk rises with age and longer duration of diabetes. The highest rates of neuropathy are among people who have had diabetes for at least 25 years. Diabetic neuropathies also appear to be more common in people who have problems controlling their blood glucose, also called blood sugar, as well as those with high levels of blood fat and blood pressure and those who are overweight."}
{"_id":"a6b4d5ee-1a73-49a3-ae90-1583b7aba894","text":"The causes are probably different for different types of diabetic neuropathy. Researchers are studying how prolonged exposure to high blood glucose causes nerve damage. Nerve damage is likely due to a combination of factors:\n                \n- metabolic factors, such as high blood glucose, long duration of diabetes, abnormal blood fat levels, and possibly low levels of insulin  - neurovascular factors, leading to damage to the blood vessels that carry oxygen and nutrients to nerves  - autoimmune factors that cause inflammation in nerves  - mechanical injury to nerves, such as carpal tunnel syndrome  - inherited traits that increase susceptibility to nerve disease  - lifestyle factors, such as smoking or alcohol use"}
{"_id":"edceb4fa-9b51-4af4-be04-219d6b3b86f3","text":"Symptoms depend on the type of neuropathy and which nerves are affected. Some people with nerve damage have no symptoms at all. For others, the first symptom is often numbness, tingling, or pain in the feet. Symptoms are often minor at first, and because most nerve damage occurs over several years, mild cases may go unnoticed for a long time. Symptoms can involve the sensory, motor, and autonomicor involuntarynervous systems. In some people, mainly those with focal neuropathy, the onset of pain may be sudden and severe.\n                \nSymptoms of nerve damage may include\n                \n- numbness, tingling, or pain in the toes, feet, legs, hands, arms, and fingers  - wasting of the muscles of the feet or hands  - indigestion, nausea, or vomiting  - diarrhea or constipation  - dizziness or faintness due to a drop in blood pressure after standing or sitting up  - problems with urination  - erectile dysfunction in men or vaginal dryness in women  - weakness\n                \nSymptoms that are not due to neuropathy, but often accompany it, include weight loss and depression."}
{"_id":"fd9b1069-33dc-4044-8efa-155d8fce0cfa","text":"Diabetic neuropathy can be classified as peripheral, autonomic, proximal, or focal. Each affects different parts of the body in various ways.\n                \n- Peripheral neuropathy, the most common type of diabetic neuropathy, causes pain or loss of feeling in the toes, feet, legs, hands, and arms.  - Autonomic neuropathy causes changes in digestion, bowel and bladder function, sexual response, and perspiration. It can also affect the nerves that serve the heart and control blood pressure, as well as nerves in the lungs and eyes. Autonomic neuropathy can also cause hypoglycemia unawareness, a condition in which people no longer experience the warning symptoms of low blood glucose levels.  - Proximal neuropathy causes pain in the thighs, hips, or buttocks and leads to weakness in the legs.  - Focal neuropathy results in the sudden weakness of one nerve or a group of nerves, causing muscle weakness or pain. Any nerve in the body can be affected.\n                \n\n                \nNeuropathy Affects Nerves Throughout the Body  Peripheral neuropathy affects   - toes   - feet   - legs   - hands   - arms   Autonomic neuropathy affects   - heart and blood vessels   - digestive system   - urinary tract   - sex organs   - sweat glands   - eyes   - lungs   Proximal neuropathy affects   - thighs   - hips   - buttocks   - legs   Focal neuropathy affects   - eyes   - facial muscles   - ears   - pelvis and lower back   - chest   - abdomen   - thighs   - legs   - feet"}
{"_id":"7c8ae112-7012-4b7d-90df-a24882ca3130","text":"Peripheral neuropathy, also called distal symmetric neuropathy or sensorimotor neuropathy, is nerve damage in the arms and legs. Feet and legs are likely to be affected before hands and arms. Many people with diabetes have signs of neuropathy that a doctor could note but feel no symptoms themselves. Symptoms of peripheral neuropathy may include\n                \n- numbness or insensitivity to pain or temperature  - a tingling, burning, or prickling sensation  - sharp pains or cramps  - extreme sensitivity to touch, even light touch  - loss of balance and coordination\n                \nThese symptoms are often worse at night.\n                \nPeripheral neuropathy may also cause muscle weakness and loss of reflexes, especially at the ankle, leading to changes in the way a person walks. Foot deformities, such as hammertoes and the collapse of the midfoot, may occur. Blisters and sores may appear on numb areas of the foot because pressure or injury goes unnoticed. If an infection occurs and is not treated promptly, the infection may spread to the bone, and the foot may then have to be amputated. Many amputations are preventable if minor problems are caught and treated in time."}
{"_id":"815d4b26-6071-4eab-856c-1dba68d974f1","text":"Autonomic neuropathy affects the nerves that control the heart, regulate blood pressure, and control blood glucose levels. Autonomic neuropathy also affects other internal organs, causing problems with digestion, respiratory function, urination, sexual response, and vision. In addition, the system that restores blood glucose levels to normal after a hypoglycemic episode may be affected, resulting in loss of the warning symptoms of hypoglycemia.\n                \nHypoglycemia Unawareness\n                \nNormally, symptoms such as shakiness, sweating, and palpitations occur when blood glucose levels drop below 70 mg\/dL. In people with autonomic neuropathy, symptoms may not occur, making hypoglycemia difficult to recognize. Problems other than neuropathy can also cause hypoglycemia unawareness.\n                \nHeart and Blood Vessels\n                \nThe heart and blood vessels are part of the cardiovascular system, which controls blood circulation. Damage to nerves in the cardiovascular system interferes with the body's ability to adjust blood pressure and heart rate. As a result, blood pressure may drop sharply after sitting or standing, causing a person to feel light-headed or even to faint. Damage to the nerves that control heart rate can mean that the heart rate stays high, instead of rising and falling in response to normal body functions and physical activity.\n                \nDigestive System\n                \nNerve damage to the digestive system most commonly causes constipation. Damage can also cause the stomach to empty too slowly, a condition called gastroparesis. Severe gastroparesis can lead to persistent nausea and vomiting, bloating, and loss of appetite. Gastroparesis can also make blood glucose levels fluctuate widely, due to abnormal food digestion.\n                \nNerve damage to the esophagus may make swallowing difficult, while nerve damage to the bowels can cause constipation alternating with frequent, uncontrolled diarrhea, especially at night. Problems with the digestive system can lead to weight loss.\n                \nUrinary Tract and Sex Organs\n                \nAutonomic neuropathy often affects the organs that control urination and sexual function. Nerve damage can prevent the bladder from emptying completely, allowing bacteria to grow in the bladder and kidneys and causing urinary tract infections. When the nerves of the bladder are damaged, urinary incontinence may result because a person may not be able to sense when the bladder is full or control the muscles that release urine.\n                \nAutonomic neuropathy can also gradually decrease sexual response in men and women, although the sex drive may be unchanged. A man may be unable to have erections or may reach sexual climax without ejaculating normally. A woman may have difficulty with arousal, lubrication, or orgasm.\n                \nSweat Glands\n                \nAutonomic neuropathy can affect the nerves that control sweating. When nerve damage prevents the sweat glands from working properly, the body cannot regulate its temperature as it should. Nerve damage can also cause profuse sweating at night or while eating.\n                \nEyes\n                \nFinally, autonomic neuropathy can affect the pupils of the eyes, making them less responsive to changes in light. As a result, a person may not be able to see well when a light is turned on in a dark room or may have trouble driving at night."}
{"_id":"24832cca-bffd-4dbf-84f4-80914bb3bb5f","text":"Proximal neuropathy, sometimes called lumbosacral plexus neuropathy, femoral neuropathy, or diabetic amyotrophy, starts with pain in the thighs, hips, buttocks, or legs, usually on one side of the body. This type of neuropathy is more common in those with type 2 diabetes and in older adults with diabetes. Proximal neuropathy causes weakness in the legs and the inability to go from a sitting to a standing position without help. Treatment for weakness or pain is usually needed. The length of the recovery period varies, depending on the type of nerve damage."}
{"_id":"07c59b94-9554-4f6a-a727-ab5169ac7604","text":"Focal neuropathy appears suddenly and affects specific nerves, most often in the head, torso, or leg. Focal neuropathy may cause\n                \n- inability to focus the eye  - double vision  - aching behind one eye  - paralysis on one side of the face, called Bell's palsy  - severe pain in the lower back or pelvis  - pain in the front of a thigh  - pain in the chest, stomach, or side  - pain on the outside of the shin or inside of the foot  - chest or abdominal pain that is sometimes mistaken for heart disease, a heart attack, or appendicitis\n                \nFocal neuropathy is painful and unpredictable and occurs most often in older adults with diabetes. However, it tends to improve by itself over weeks or months and does not cause long-term damage.\n                \nPeople with diabetes also tend to develop nerve compressions, also called entrapment syndromes. One of the most common is carpal tunnel syndrome, which causes numbness and tingling of the hand and sometimes muscle weakness or pain. Other nerves susceptible to entrapment may cause pain on the outside of the shin or the inside of the foot."}
{"_id":"41003232-d1b3-43bb-aa8a-552246182d93","text":"The best way to prevent neuropathy is to keep blood glucose levels as close to the normal range as possible. Maintaining safe blood glucose levels protects nerves throughout the body."}
{"_id":"a7a2e8c8-3cb7-4d66-8509-7e5759151e66","text":"Doctors diagnose neuropathy on the basis of symptoms and a physical exam. During the exam, the doctor may check blood pressure, heart rate, muscle strength, reflexes, and sensitivity to position changes, vibration, temperature, or light touch.\n                \nFoot Exams\n                \nExperts recommend that people with diabetes have a comprehensive foot exam each year to check for peripheral neuropathy. People diagnosed with peripheral neuropathy need more frequent foot exams. A comprehensive foot exam assesses the skin, muscles, bones, circulation, and sensation of the feet. The doctor may assess protective sensation or feeling in the feet by touching them with a nylon monofilamentsimilar to a bristle on a hairbrushattached to a wand or by pricking them with a pin. People who cannot sense pressure from a pinprick or monofilament have lost protective sensation and are at risk for developing foot sores that may not heal properly. The doctor may also check temperature perception or use a tuning fork, which is more sensitive than touch pressure, to assess vibration perception.\n                \nOther Tests\n                \nThe doctor may perform other tests as part of the diagnosis.\n                \n- Nerve conduction studies or electromyography are sometimes used to help determine the type and extent of nerve damage. Nerve conduction studies check the transmission of electrical current through a nerve. Electromyography shows how well muscles respond to electrical signals transmitted by nearby nerves. These tests are rarely needed to diagnose neuropathy.  - A check of heart rate variability shows how the heart responds to deep breathing and to changes in blood pressure and posture.  - Ultrasound uses sound waves to produce an image of internal organs. An ultrasound of the bladder and other parts of the urinary tract, for example, can be used to assess the structure of these organs and show whether the bladder empties completely after urination."}
{"_id":"db838c9e-8ada-4647-a8cf-636bf0fb96b9","text":"The first treatment step is to bring blood glucose levels within the normal range to help prevent further nerve damage. Blood glucose monitoring, meal planning, physical activity, and diabetes medicines or insulin will help control blood glucose levels. Symptoms may get worse when blood glucose is first brought under control, but over time, maintaining lower blood glucose levels helps lessen symptoms. Good blood glucose control may also help prevent or delay the onset of further problems. As scientists learn more about the underlying causes of neuropathy, new treatments may become available to help slow, prevent, or even reverse nerve damage.\n                \nAs described in the following sections, additional treatment depends on the type of nerve problem and symptom.\n                \nPain Relief\n                \nDoctors usually treat painful diabetic neuropathy with oral medications, although other types of treatments may help some people. People with severe nerve pain may benefit from a combination of medications or treatments and should consider talking with a health care provider about treatment options.\n                \nMedications used to help relieve diabetic nerve pain include\n                \n- tricyclic antidepressants, such as amitriptyline, imipramine, and desipramine (Norpramin, Pertofrane)  - other types of antidepressants, such as duloxetine (Cymbalta), venlafaxine, bupropion (Wellbutrin), paroxetine (Paxil), and citalopram (Celexa)  - anticonvulsants, such as pregabalin (Lyrica), gabapentin (Gabarone, Neurontin), carbamazepine, and lamotrigine (Lamictal)  - opioids and opioidlike drugs, such as controlled-release oxycodone, an opioid; and tramadol (Ultram), an opioid that also acts as an antidepressant\n                \nDuloxetine and pregabalin are approved by the U.S. Food and Drug Administration specifically for treating painful diabetic peripheral neuropathy.\n                \nPeople do not have to be depressed for an antidepressant to help relieve their nerve pain. All medications have side effects, and some are not recommended for use in older adults or those with heart disease. Because over-the-counter pain medicines such as acetaminophen and ibuprofen may not work well for treating most nerve pain and can have serious side effects, some experts recommend avoiding these medications.\n                \nTreatments that are applied to the skintypically to the feetinclude capsaicin cream and lidocaine patches (Lidoderm, Lidopain). Studies suggest that nitrate sprays or patches for the feet may relieve pain. Studies of alpha-lipoic acid, an antioxidant, and evening primrose oil suggest they may help relieve symptoms and improve nerve function in some patients.\n                \nA device called a bed cradle can keep sheets and blankets from touching sensitive feet and legs. Acupuncture, biofeedback, or physical therapy may help relieve pain in some people. Treatments that involve electrical nerve stimulation, magnetic therapy, and laser or light therapy may be helpful but need further study. Researchers are also studying several new therapies in clinical trials.\n                \nGastrointestinal Problems\n                \nTo relieve mild symptoms of gastroparesisindigestion, belching, nausea, or vomitingdoctors suggest eating small, frequent meals; avoiding fats; and eating less fiber. When symptoms are severe, doctors may prescribe erythromycin to speed digestion, metoclopramide to speed digestion and help relieve nausea, or other medications to help regulate digestion or reduce stomach acid secretion.\n                \nTo relieve diarrhea or other bowel problems, doctors may prescribe an antibiotic such as tetracycline, or other medications as appropriate.\n                \nDizziness and Weakness\n                \nSitting or standing slowly may help prevent the light-headedness, dizziness, or fainting associated with blood pressure and circulation problems. Raising the head of the bed or wearing elastic stockings may also help. Some people benefit from increased salt in the diet and treatment with salt-retaining hormones. Others benefit from high blood pressure medications. Physical therapy can help when muscle weakness or loss of coordination is a problem.\n                \nUrinary and Sexual Problems\n                \nTo clear up a urinary tract infection, the doctor will probably prescribe an antibiotic. Drinking plenty of fluids will help prevent another infection. People who have incontinence should try to urinate at regular intervalsevery 3 hours, for examplebecause they may not be able to tell when the bladder is full.\n                \nTo treat erectile dysfunction in men, the doctor will first do tests to rule out a hormonal cause. Several methods are available to treat erectile dysfunction caused by neuropathy. Medicines are available to help men have and maintain erections by increasing blood flow to the penis. Some are oral medications and others are injected into the penis or inserted into the urethra at the tip of the penis. Mechanical vacuum devices can also increase blood flow to the penis. Another option is to surgically implant an inflatable or semirigid device in the penis.\n                \nVaginal lubricants may be useful for women when neuropathy causes vaginal dryness. To treat problems with arousal and orgasm, the doctor may refer women to a gynecologist.\n                \nFoot Care\n                \nPeople with neuropathy need to take special care of their feet. The nerves to the feet are the longest in the body and are the ones most often affected by neuropathy. Loss of sensation in the feet means that sores or injuries may not be noticed and may become ulcerated or infected. Circulation problems also increase the risk of foot ulcers. Smoking increases the risk of foot problems and amputation. A health care provider may be able to provide help with quitting smoking.\n                \nMore than 60 percent of all nontraumatic lower-limb amputations in the United States occur in people with diabetes. Nontraumatic amputations are those not caused by trauma such as severe injuries from an accident. In 2004, about 71,000 nontraumatic amputations were performed in people with diabetes. Comprehensive foot care programs can reduce amputation rates by 45 to 85 percent.\n                \nCareful foot care involves\n                \n- cleaning the feet daily using warmnot hotwater and a mild soap. Soaking the feet should be avoided. A soft towel can be used to dry the feet and between the toes.  - inspecting the feet and toes every day for cuts, blisters, redness, swelling, calluses, or other problems. Using a mirrorhandheld or placed on the floormay be helpful in checking the bottoms of the feet, or another person can help check the feet. A health care provider should be notified of any problems.  - using lotion to moisturize the feet. Getting lotion between the toes should be avoided.  - filing corns and calluses gently with a pumice stone after a bath or shower.  - cutting toenails to the shape of the toes and filing the edges with an emery board each week or when needed.  - always wearing shoes or slippers to protect feet from injuries. Wearing thick, soft, seamless socks can prevent skin irritation.  - wearing shoes that fit well and allow the toes to move. New shoes can be broken in gradually by first wearing them for only an hour at a time.  - looking shoes over carefully before putting them on and feeling the insides to make sure the shoes are free of tears, sharp edges, or objects that might injure the feet.\n                \nPeople who need help taking care of their feet should consider making an appointment to see a foot doctor, also called a podiatrist."}
{"_id":"e73e10e8-b0a9-4f69-a9fc-97c8beceacfb","text":"- Diabetic neuropathies are nerve disorders caused by many of the abnormalities common to diabetes, such as high blood glucose.  - Neuropathy can affect nerves throughout the body, causing numbness and sometimes pain in the hands, arms, feet, or legs, and problems with the digestive tract, heart, sex organs, and other body systems.  - Treatment first involves bringing blood glucose levels within the normal range. Good blood glucose control may help prevent or delay the onset of further problems.  - Foot care is an important part of treatment. People with neuropathy need to inspect their feet daily for any injuries. Untreated injuries increase the risk of infected foot sores and amputation.  - Treatment also includes pain relief and other medications as needed, depending on the type of nerve damage.  - Smoking increases the risk of foot problems and amputation. A health care provider may be able to provide help with quitting."}
{"_id":"ef6cb283-5bbe-4fe6-b298-ff15624bee56","text":"Hepatitis* A is a virus, or infection, that causes liver disease and inflammation of the liver. Viruses can cause sickness. For example, the flu is caused by a virus. People can pass viruses to each other.\n                \nInflammation is swelling that occurs when tissues of the body become injured or infected. Inflammation can cause organs to not work properly."}
{"_id":"56858dd3-44dc-4ea9-99cf-8d8fc9c43677","text":"The liver is an organ that does many important things. You cannot live without a liver.\n                \n*See the Pronunciation Guide for tips on how to say the words in bold type.\n                \nThe liver\n                \n- removes harmful chemicals from your blood  - fights infection  - helps digest food  - stores nutrients and vitamins  - stores energy"}
{"_id":"5210115f-9e60-4e12-9478-f7b6c450d73b","text":"Anyone can get hepatitis A, but those more likely to are people who\n                \n- travel to developing countries  - live with someone who currently has an active hepatitis A infection  - use illegal drugs, including noninjection drugs  - have unprotected sex with an infected person  - provide child care\n                \nAlso, men who have sex with men are more likely to get hepatitis A."}
{"_id":"85b40e3e-5c8b-460b-abba-9e81e59debab","text":"Most people do not have any symptoms of hepatitis A. If symptoms of hepatitis A occur, they include\n                \n- feeling tired  - muscle soreness  - upset stomach  - fever  - loss of appetite  - stomach pain  - diarrhea  - dark-yellow urine  - light-colored stools  - yellowish eyes and skin, called jaundice\n                \nSymptoms of hepatitis A can occur 2 to 7 weeks after coming into contact with the virus. Children younger than age 6 may have no symptoms. Older children and adults often get mild, flulike symptoms. See a doctor right away if you or a child in your care has symptoms of hepatitis A."}
{"_id":"c4126f37-660e-43ae-8dc1-363ae7862703","text":"A blood test will show if you have hepatitis A. Blood tests are done at a doctors office or outpatient facility. A blood sample is taken using a needle inserted into a vein in your arm or hand. The blood sample is sent to a lab to test for hepatitis A."}
{"_id":"bc4724ed-b700-468e-b220-5433bbcedd96","text":"Hepatitis A usually gets better in a few weeks without treatment. However, some people can have symptoms for up to 6 months. Your doctor may suggest medicines to help relieve your symptoms. Talk with your doctor before taking prescription and over-the-counter medicines.\n                \nSee your doctor regularly to make sure your body has fully recovered. If symptoms persist after 6 months, then you should see your doctor again.\n                \nWhen you recover, your body will have learned to fight off a future hepatitis A infection. However, you can still get other kinds of hepatitis."}
{"_id":"2a42c67b-c173-40d9-acd5-87d7335e674e","text":"If you have hepatitis A, you should do things to take care of yourself, including eating a healthy diet. Avoid drinking alcohol, which can harm the liver. Talk with your doctor before taking vitamins and other supplements."}
{"_id":"382f44c3-5206-4891-8c8a-2703945a042e","text":"- Hepatitis A is a virus, or infection, that causes inflammation of the liver.  - Anyone can get hepatitis A, but some people are more likely to than others.  - You could get hepatitis A through contact with an infected persons stool.  - Most people do not have any symptoms of hepatitis A.  - Children younger than age 6 may have no symptoms of hepatitis A.  - Hepatitis A may cause mild, flulike symptoms in older children and adults.  - See a doctor right away if you or a child in your care has symptoms of hepatitis A.  - A blood test will show if you have hepatitis A.  - Hepatitis A usually gets better in a few weeks without treatment.  - You can avoid getting hepatitis A by receiving the hepatitis A vaccine.  - Tell your doctor and your dentist if you have hepatitis A.  - See your doctor right away if you think you have been in contact with the hepatitis A virus."}
{"_id":"9d871fb6-cb4d-43f1-b335-9c57d9ef30c7","text":"Before scientists learned how to make synthetic hormones, many animal hormones, such as insulin, were used to treat human disorders. Growth hormone from animals did not work in humans. Human growth hormone (pituitary hGH) was therefore made from human pituitary glands by the National Hormone and Pituitary Program (NHPP), funded by the U.S. Department of Health and Human Services (HHS). From 1963 to 1985, the NHPP sent pituitary hGH to hundreds of doctors across the country. As a part of research studies, doctors used the hormone to treat nearly 7,700 children for failure to grow.\n                \nIn 1985, the HHS learned that three young men treated with pituitary hGH died of Creutzfeldt-Jakob disease (CJD), a rare and incurable brain disease. The HHS believed these illnesses were related to pituitary hGH. The HHS immediately stopped the distribution of the hormone and began a national study to learn more about how pituitary hGH treatment may have caused this problem. The HHS continues to monitor individuals who received pituitary hGH through the NHPP for CJD."}
{"_id":"6376a2a5-fb7a-42bf-96bf-3943bf060638","text":"The HHS has identified 29 cases of CJD among the nearly 7,700 people in the United States who received NHPP pituitary hGH. None of the 29 people who got CJD began treatment with pituitary hGH after 1977, the year that the NHPP began producing pituitary hGH in a laboratory (headed by Dr. Albert Parlow) using a new purification step. Today, the growth hormone used to treat patients is made biosynthetically and not from human pituitary glands. Biosynthetic growth hormone (bGH), also known as recombinant human growth hormone (rhGH), poses no threat of infection with CJD.\n                \nBased on NHPP records, the HHS estimated 7,700 people were treated with pituitary hGH from the NHPP. Of these, the HHS got the names and addresses of 6,272 from their doctors and treatment centers so that their health could be monitored. Another 1,400 people are believed to have been treated with pituitary hGH; however, the HHS does not have their names and addresses. The HHS hoped to learn about CJD and other health problems in the unmonitored group of 1,400 and notified many doctors about the problem of CJD, asking them to report CJD among people treated with pituitary hGH. The HHS has learned that five of the 29 people with confirmed CJD were among the 1,400 people the HHS was not able to identify and study.\n                \nSome U.S. laboratories that made pituitary hGH for the NHPP also made hGH for use in other countries. The HHS learned that six people in New Zealand and two people in Brazil who received U.S.-made pituitary hGH may also have gotten CJD. A total of 37 people who were treated with pituitary hGH made in the United States may have gotten CJD.\n                \nBefore bGH was available, several pharmaceutical companies made pituitary hGH. Some children treated in the U.S. received hormone produced by these companies when NHPP hGH was not available to them. Some of the 29 people with confirmed CJD received hGH from both the NHPP and a pharmaceutical company. Recently, the HHS has learned of an individual treated in the U.S. who developed CJD and received only commercial pituitary hGH. That person was not eligible for NHPP hGH and received pituitary hGH made by two pharmaceutical companies."}
{"_id":"7592a1f2-8bd8-48fe-bba6-3cbeabc5bfee","text":"People treated with pituitary hGH in other countries also got CJD. HHS doctors share information with doctors around the world about health issues such as CJD and read reports about CJD and other health problems related to pituitary hGH treatment.\n                \nCountry    Number of CJD Cases Reported*    Number of Individuals Treated    Source of hGH in Reported Cases        New Zealand***    6    159    United States        France    119    1,700    France        United Kingdom    75    1,849    United Kingdom        Holland    2    unpublished    Holland        Brazil    2    unpublished    United States         Australia    1**    608    Australia        Austria    1    unpublished    pharmaceutical (commercial)        Qatar    1    unpublished    France        Ireland    1    unpublished    Not known\n                \n*as of November 2014\n                \n**This case has been recognized by the Australian surveillance authorities as a \"possible\" (albeit unlikely) CJD case.\n                \n***New Zealand has reported six people with CJD among 159 who received pituitary hGH. All six were among 49 people who received pituitary hGH made by the U.S. lab that supplied most NHPP pituitary hGH before 1977. We don't know why this ratesix out of 49 (12.2 percent)is so high in those in New Zealand who received American hormone. HHS scientists believe that this U.S.-made hormone did not undergo the same filtering process used in the United States when the hormone was put into vials. In addition, some hormone preparations sent to New Zealand were not distributed in the United States.\n                \nNew Zealand has little information on the hormone preparations used to treat the people who got CJD. Information provided to the HHS from medical authorities in New Zealand indicated the following dates of pituitary hGH treatment for the six New Zealand patients who developed CJD: 1964 to 1966, 1964 to 1970, 1965 to 1972, 1966 to 1972, 1967 to 1969, and 1970 to 1973. With no common period of treatment, it is unlikely that a single preparation exposed all six patients to CJD.\n                \nThere is some information on the hormone sent to New Zealand from the lab that also produced hormone for the NHPP before 1977. Some preparations and components of preparations were used in both countries and others were distributed only in the United States or in New Zealand.\n                \nThe time between the start of pituitary hGH treatment and the first sign of CJD symptoms was similar in the 29 United States patients (14 to 44 years) and the six New Zealand patients (17 to 37 years). The New Zealand patients who got CJD were treated with pituitary hGH for an average of 4.3 years. In the United States, average treatment time was 8.4 years in patients who got CJD.\n                \nIn France, 119 people with CJD were among the 1,700 treated with pituitary hGH. The pattern of exposure to CJD in France is very different from the pattern in the United States. In France, people who received pituitary hGH in 1984 and 1985 appear to be at highest risk for CJD. We have learned from animal studies that when scientists injected a greater amount of CJD infectious agent into an animal, it took less time for CJD to develop. Because of the larger number of people with CJD and shorter times between treatment and CJD onset in France, the level of infection in French hormone was probably higher than in the U.S. hormone. The purification procedure used in France differed from that begun in 1977 in the United States.\n                \nThe United Kingdom has reported 75 people with CJD among 1,849 who received pituitary hGH. Experts have also found CJD in two people in Holland, two people in Brazil, and one each in Australia, Austria, Qatar, and Ireland. France, the United Kingdom, Holland, and Australia made their own hormone. The Brazilian patients got pituitary hGH from a U.S. lab that also made NHPP hormone before 1977. This was a different lab than the U.S. lab that made hormone for New Zealand. The Qatar patient received pituitary hGH made in France. The Austrian patient received pituitary hGH made by a pharmaceutical company. Four Australian women developed CJD after receiving other human pituitary hormones as fertility treatments."}
{"_id":"324287bd-4fc6-4bb2-8bad-09f94e638991","text":"Most people were treated with pituitary hGH because their pituitary glands did not make enough of their own GH. Some of these people also had problems making other pituitary hormones. One of these hormones tells the adrenal glands to make cortisol, a hormone needed for life. People lacking this hormone are at risk of death from adrenal crisis, but adrenal crisis can be prevented. More pituitary hGH recipients have died from adrenal crisis than from CJD. Pituitary hGH did not cause adrenal problems, but some people who received hGH have a pituitary problem that puts them at risk for adrenal crisis. Please read the health alert and discuss this information with your doctor.\n                \nBesides CJD, no other serious or fatal health risks from pituitary hGH treatment have been found.\n                \nMad Cow Disease\n                \nStarting in 1996, reports of a new form of CJD in young people who lived in the United Kingdom have raised concerns worldwide.\n                \nSince at least 1985, some cattle in the United Kingdom have developed a disease called bovine spongiform encephalopathy (BSE), or \"mad cow\" disease. \"Mad cow\" disease is a sickness in cattle that is caused by an agent that is similar, but not identical, to the agents that cause the most common forms of CJD in people. Individuals who consume products made from cattle infected with the agent that causes \"mad cow\" disease can become infected with the agent themselves and develop the human form of \"mad cow\" disease, called variant CJD (vCJD). In humans, vCJD and the more common forms of CJD (those without the word \"variant\") are separate diseases. As of November 2012, 227 cases of vCJD were confirmed worldwide, mostly from the United Kingdom. Researchers believe all but three of these 227 individuals got vCJD by eating beef from animals with \"mad cow\" disease. The three exceptions were persons who are believed to have developed vCJD because they received infected blood from a donor who had acquired the agent by eating beef from animals with \"mad cow\" disease.\n                \nIn the United States, three cases of vCJD have been found. According to the Centers for Disease Control and Prevention (CDC), the investigation of these three cases indicated that they most likely acquired their infection in the United Kingdom (two cases) and Saudi Arabia (one case).\n                \nPeople who received pituitary hGH are not at higher risk for vCJD.\n                \nAIDS\n                \nHIV, also known as the human immunodeficiency virus, causes AIDS. Pituitary hGH does not cause AIDS. HIV is destroyed by the methods used to make pituitary hGH. People who have been treated with pituitary hGH do not have a higher risk for AIDS.\n                \nLow Levels of GH in Adults\n                \nSome people who received pituitary hGH as children may have low levels of GH as adults and might therefore benefit from bGH as adults. People with low levels of growth hormone as adults may have symptoms or changes like these:\n                \n- more body fat  - less muscle  - less bone mass  - less strength  - less energy\n                \nIf you lacked GH as a child and have these problems as an adult, ask your doctor whether they might be due to low GH. Because these conditions are common in many people, they are not always due to low GH. Studies have shown that GH treatment in adults with low GH reduces fat and increases muscle mass. Effects on strength, energy, and bone fractures in GH-deficient adults receiving GH replacement are not as clear.\n                \nToday, GH is completely synthetic. It is not made from human pituitaries. It poses no threat of contamination. The Human Growth Foundation (HGF) is one source of information about growth-related disorders. The Foundation can be reached at 18004516434.\n                \nCancer\n                \nHHS studies of people treated with pituitary hGH supplied by the NHPP show no increased risk of cancer in those who did not have tumors before pituitary hGH treatment. Many people who received NHPP pituitary hGH had brain tumors that caused their lack of GH. People who have had one tumor have an increased risk for getting other tumors.\n                \nIn previous updates, we reported that in 1988, Japanese doctors reported an increased risk of leukemia in people treated with GH. Subsequent studies of individuals who were given pituitary hGH in the United States, Japan, and the United Kingdom found no higher rate of leukemia among those who did not have tumors and\/or radiation before treatment with pituitary hGH.\n                \nEmotional Problems\n                \nNo studies have shown that pituitary hGH causes changes in personality, emotional problems, or suicide."}
{"_id":"ad72cd9f-5312-44fb-9257-6ca3d5790101","text":"CJD does not cause the same symptoms in everyone. In most people who got CJD from pituitary hGH, the first signs they noticed were difficulty with walking and balance, dizziness, and\/or clumsiness. Later, some began to slur words and have jerky movements. They also had trouble seeing, remembering, and\/or thinking clearly. The disease becomes worse very quickly. When individuals have symptoms like these over a long period of time (such as a year) without getting much worse, they do not have CJD. Occasional forgetfulness, clumsiness, or headaches do not mean one has CJD. You should discuss concerns with your doctor if you are not sure.\n                \nCJD is a rare disease. Most cases of CJD are not linked to pituitary hGH. When CJD is not linked to pituitary hGH, the first symptoms are usually mental changes such as confusion, problems thinking clearly, memory loss, behavior changes, and dementia. Though symptoms may differ, there are similar changes in the brain tissue of all patients with CJD."}
{"_id":"b02c4c87-f19b-4ee8-b927-6a22c3744d20","text":"No one can say what an individual person's risk is. Of the approximately 7,700 people who received NHPP pituitary hGH, 29 people got CJD. The two things that seem to be connected with getting CJD after pituitary hGH treatment are\n                \n1. How long a person was treated:\n                \n- In the United States, the average length of time for pituitary hGH treatment through the NHPP was about 3 years. For those individuals who developed CJD, the average length of treatment was about 8.4 years.  - Even though longer treatment time increased the risk for CJD in the United States, in other countries CJD has developed after shorter treatment periods.\n                \n2. When a person was treated:\n                \n- All of the 29 individuals treated with NHPP hGH who got CJD in the United States started pituitary hGH before 1977. No CJD has been reported in Americans who began treatment with NHPP hormone after 1977, when production of NHPP hormone was moved to a laboratory (headed by Dr. Albert Parlow) that used a new method of purifying pituitary hGH. Research in animals showed the newer purification steps introduced in 1977 reduced the risk of CJD transmission. Recently, an analysis of NHPP hGH recipients was completed taking into account the differences in follow-up time and the duration of treatment of recipients starting treatment before or after 1977. That analysis found that the new purification steps greatly reduced and may have eliminated the risk for CJD infection.  - Two cases of CJD have been reported in individuals who received commercially prepared pituitary hGH. An Austrian person was treated with pituitary hGH (Crescormon, from Kabi Pharma) for 14 months and died from CJD 22 years later. An American who was too tall to be eligible for NHPP hormone was treated with pituitary hGH made by two pharmaceutical companies (Asellacrin, from Serono, and Crescormon, from Kabi Pharma). This individual was treated with commercial hGH for 23 months and died just over 26 years later. The methods used to produce these commercial hormone preparations were not identical to the method used in Dr. Parlow's laboratory but did include a version of the important new purification step that has been shown to reduce CJD infectivity.  - Overall, one out of about 265 people (29 out of about 7,700 people) who were treated with NHPP pituitary hGH got CJD.  - However, one in about 91 people who began treatment before 1977 got CJD.  - People who started treatment before 1970 are at even higher risk. In that early group, one in about every 48 people (about 2.1 percent) got CJD.  - The appearance of new cases is decreasing, as there has only been one new case in the past 5 years."}
{"_id":"48afacdb-2345-43a6-b013-7e6c1873a603","text":"The best source for details on your treatment is the doctor or center that gave you pituitary hGH. To protect patient privacy, the HHS did not ask for the names of those treated with pituitary hGH until 1985, when the first CJD cases were reported. In 1985, the HHS asked doctors and treatment centers for the names and addresses of recipients to inform them of the risk of CJD.\n                \nWe know which pituitary hGH preparations were sent to each treatment center and when they were sent. However, because individual doctors administered the pituitary hGH, we don't know which preparation each person might have gotten. We have tried to find this information in the medical records of patients who developed CJD, but many doctors did not note the specific preparation in their records. When records were incomplete, it was assumed that patients who got CJD might have been exposed to all preparations sent to their treatment center during the time they were treated. Since it is impossible to confidently identify high-risk or risk-free hormone, we do not think that details on the hormone preparations that individuals received will help to clarify individual level of risk."}
{"_id":"e5c05b4a-1d1a-48cb-971b-2f25964d5260","text":"We have not found any particular preparation of pituitary hGH that is especially likely to carry CJD. We believe that CJD did not come from a single infected pituitary gland or preparation. Prior to 1977, in an effort to extract as much hormone as possible from the pituitary glands, the glands were often processed repeatedly. Hormone extracted from the same pituitaries was often included in many hormone preparations. Also, patients who got CJD were treated on average for 8.4 years and received many different hormone preparations. This makes it very difficult to identify any preparation associated with transmitting CJD.\n                \nDoctors wanted to see if a specific preparation of pituitary hGH could transmit CJD. To try to find the pituitary hGH that could have caused CJD, HHS researchers did two things:\n                \n1. They set up a test in animals, injecting samples of all available preparations of pituitary hGH directly into the brains of monkeys. CJD develops more rapidly if injected into the brain than under the skin, as hGH was used in people. The animals were watched for 10 years. The brains of all animals were examined for signs of CJD. If an animal got sick with CJD, it would help researchers to understand which vials of pituitary hGH were contaminated with the agent that causes CJD.\n                \n2. They studied people treated with pituitary hGH to see who got CJD and which hormone preparation they might have received based on which preparations were sent to their doctor.\n                \nResults:\n                \n- The animal tests did not help find the pituitary hGH that might have caused CJD. One animal developed the disease 5 years after injection of pituitary hGH. Two other animals that received injections from different vials of the same pituitary hGH preparation did not develop CJD.  - None of the people who developed CJD are known to have received the hormone preparation that made the animal sick. At most, two patients (whose records are incomplete) may have received this pituitary hGH preparation. Because of this, we do not believe that the patients who received the hormone preparation that transmitted CJD to the animal have a greater risk of developing CJD than others treated with pituitary hGH. Because each preparation of pituitary hGH was used to fill multiple vials, it is not known if CJD contamination was spread evenly among all vials of pituitary hGH that came from a particular preparation. It's possible that one vial got more contamination and another got little or none from the same preparation of pituitary hGH. It is believed that multiple preparations of pituitary hGH probably had very low levels of the CJD infectious agent. With such low levels of contamination, some vials of a preparation might carry CJD while other vials would not. Further, most of the people who got CJD received pituitary hGH for long periods of time and received many different preparations."}
{"_id":"631dacca-bf02-452f-b6e5-c2919b43c616","text":"CJD is usually diagnosed based on signs and symptoms of the illness, how severe they are, and how quickly they become worse. However, doctors must study brain tissue from a biopsy or autopsy in order to make a definite diagnosis of CJD.\n                \nOther tests can suggest CJD. In 1996, researchers developed a test that helps doctors diagnose CJD in patients with symptoms. This test detects an abnormal protein in a sample of spinal fluid. When this protein is found, it helps make a diagnosis of CJD. It is much easier and safer to take a sample of spinal fluid than to do a brain biopsy. Unfortunately, this test cannot identify CJD in patients who do not have symptoms. The test cannot predict who may develop CJD in the future.\n                \nResearchers from many countries, including the United States, have reported success using MRI to diagnose CJD and vCJD in people with symptoms of the disease. MRI is a safe and painless tool that allows doctors to look at images of the brain and does not involve the collection of brain or spinal fluid samples."}
{"_id":"b7dc1028-3614-499e-af76-f4c8fe43c75a","text":"Although CJD is a rare disorder, some of the world's leading researchers are working hard to learn more about this disease.\n                \nAbout 10 percent of the people who get CJD have the inherited type. Some people have gotten CJD from medical procedures such as pituitary hGH injections, tissue grafts, or corneal transplants. Scientists don't fully understand what causes CJD. Evidence suggests that a unique infectious agent called a prion [PREE-on] may be the cause. A prion is an unusual infectious agent because it contains no genetic material. It is a protein that takes on different forms. In its normal, harmless form, the protein is curled into a spiral. In its infectious form, the protein folds into an abnormal shape. Somehow, these abnormal proteins change the shape of normal proteins. This change begins a serious chain reaction that results in brain problems.\n                \nPeople with inherited CJD have an abnormal gene that leads to changes in their prion protein. This gene makes the protein likely to assume the abnormal shape. Exposure to the abnormal form of the protein can also occur through injection of contaminated pituitary hGH, tissue grafts, and corneal transplants and through exposures to infected brain tissue.\n                \nIf CJD results from a defect in protein folding, it may be possible to identify drugs that can help the prion protein assume its proper shape. Such drugs would slow or stop the progress of the disease. Treatments like these are being studied by researchers. Researchers in both Europe and the United States are also trying to develop a test that will identify CJD before symptoms appear.\n                \nMore information and medical journal articles about CJD and growth hormone therapy can be found on the National Endocrine and Metabolic Diseases Information Service web page Human Growth Hormone and Creutzfeldt-Jakob Disease Resource List."}
{"_id":"29ca36b3-6579-43f6-9752-ce1ce5739cd4","text":"Some parents did not tell their children about receiving treatment with pituitary hGH and the possible risk of CJD. These children are now adults. Although the HHS no longer sends annual information about the problem of CJD in pituitary hGH recipients, the HHS does maintain a mailing list should any important new information become available. If parents are no longer available to receive HHS mailings, their adult children may not have access to important new information. Some pituitary hGH recipients have learned about the risk of CJD from newspaper stories. Others heard about it when they tried to give blood. Those who were not told by their parents are often angry when they hear about it outside the family. Any parent of an individual who received pituitary hGH who has not received any mailings from the HHSthe last correspondence was sent in June 1999should contact the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) with the adult child's current address. Knowledgeable staff members are glad to answer any questions that parents or recipients may have."}
{"_id":"93ef5add-5ccc-43ab-88cc-fa782989b3e7","text":"The Creutzfeldt-Jakob Disease Foundation, Inc. (www.cjdfoundation.org) was created in 1993 by two families who lost relatives to CJD and the neurologist who treated their family members. This nonprofit corporation seeks to promote awareness of CJD through research and education and to reach out to people who have lost loved ones to this illness. For information on CJD from the NIH, see www.ninds.nih.gov.\n                \nThe Human Growth Foundation (HGF) (www.hgfound.org) is a nonprofit organization concerned with children's growth disorders and adult GH deficiency. The HGF has information available online and through its toll-free number, 18004516434. The HGF also supports an Internet mailing list to help the exchange of information about adult GH deficiency and adult GH replacement therapy."}
{"_id":"8a8fd49a-7e45-401a-bef9-d8cb02071b4a","text":"Foodborne illnesses are infections or irritations of the gastrointestinal (GI) tract caused by food or beverages that contain harmful bacteria, parasites, viruses, or chemicals. The GI tract is a series of hollow organs joined in a long, twisting tube from the mouth to the anus. Common symptoms of foodborne illnesses include vomiting, diarrhea, abdominal pain, fever, and chills.\n                \nMost foodborne illnesses are acute, meaning they happen suddenly and last a short time, and most people recover on their own without treatment. Rarely, foodborne illnesses may lead to more serious complications. Each year, an estimated 48 million people in the United States experience a foodborne illness. Foodborne illnesses cause about 3,000 deaths in the United States annually.1"}
{"_id":"a20568fb-fe0b-4c1f-bc64-adcebe6e51e0","text":"The majority of foodborne illnesses are caused by harmful bacteria and viruses.2 Some parasites and chemicals also cause foodborne illnesses.\n                \nBacteria\n                \nBacteria are tiny organisms that can cause infections of the GI tract. Not all bacteria are harmful to humans.\n                \nSome harmful bacteria may already be present in foods when they are purchased. Raw foods including meat, poultry, fish and shellfish, eggs, unpasteurized milk and dairy products, and fresh produce often contain bacteria that cause foodborne illnesses. Bacteria can contaminate foodmaking it harmful to eatat any time during growth, harvesting or slaughter, processing, storage, and shipping.\n                \nFoods may also be contaminated with bacteria during food preparation in a restaurant or home kitchen. If food preparers do not thoroughly wash their hands, kitchen utensils, cutting boards, and other kitchen surfaces that come into contact with raw foods, cross-contaminationthe spread of bacteria from contaminated food to uncontaminated foodmay occur.\n                \nIf hot food is not kept hot enough or cold food is not kept cold enough, bacteria may multiply. Bacteria multiply quickly when the temperature of food is between 40 and 140 degrees. Cold food should be kept below 40 degrees and hot food should be kept above 140 degrees. Bacteria multiply more slowly when food is refrigerated, and freezing food can further slow or even stop the spread of bacteria. However, bacteria in refrigerated or frozen foods become active again when food is brought to room temperature. Thoroughly cooking food kills bacteria.\n                \nMany types of bacteria cause foodborne illnesses. Examples include\n                \n- Salmonella, a bacterium found in many foods, including raw and undercooked meat, poultry, dairy products, and seafood. Salmonella may also be present on egg shells and inside eggs.  - Campylobacter jejuni (C. jejuni), found in raw or undercooked chicken and unpasteurized milk.  - Shigella, a bacterium spread from person to person. These bacteria are present in the stools of people who are infected. If people who are infected do not wash their hands thoroughly after using the bathroom, they can contaminate food that they handle or prepare. Water contaminated with infected stools can also contaminate produce in the field.  - Escherichia coli (E. coli), which includes several different strains, only a few of which cause illness in humans. E. coli O157:H7 is the strain that causes the most severe illness. Common sources of E. coli include raw or undercooked hamburger, unpasteurized fruit juices and milk, and fresh produce.  - Listeria monocytogenes (L. monocytogenes), which has been found in raw and undercooked meats, unpasteurized milk, soft cheeses, and ready-to-eat deli meats and hot dogs.  - Vibrio, a bacterium that may contaminate fish or shellfish.  - Clostridium botulinum (C. botulinum), a bacterium that may contaminate improperly canned foods and smoked and salted fish.\n                \nViruses\n                \nViruses are tiny capsules, much smaller than bacteria, that contain genetic material. Viruses cause infections that can lead to sickness. People can pass viruses to each other. Viruses are present in the stool or vomit of people who are infected. People who are infected with a virus may contaminate food and drinks, especially if they do not wash their hands thoroughly after using the bathroom.\n                \nCommon sources of foodborne viruses include\n                \n- food prepared by a person infected with a virus  - shellfish from contaminated water  - produce irrigated with contaminated water\n                \nCommon foodborne viruses include\n                \n- norovirus, which causes inflammation of the stomach and intestines  - hepatitis A, which causes inflammation of the liver\n                \nParasites\n                \nParasites are tiny organisms that live inside another organism. In developed countries such as the United States, parasitic infections are relatively rare.\n                \nCryptosporidium parvum and Giardia intestinalis are parasites that are spread through water contaminated with the stools of people or animals who are infected. Foods that come into contact with contaminated water during growth or preparation can become contaminated with these parasites. Food preparers who are infected with these parasites can also contaminate foods if they do not thoroughly wash their hands after using the bathroom and before handling food.\n                \nTrichinella spiralis is a type of roundworm parasite. People may be infected with this parasite by consuming raw or undercooked pork or wild game.\n                \nChemicals\n                \nHarmful chemicals that cause illness may contaminate foods such as\n                \n- fish or shellfish, which may feed on algae that produce toxins, leading to high concentrations of toxins in their bodies. Some types of fish, including tuna and mahi mahi, may be contaminated with bacteria that produce toxins if the fish are not properly refrigerated before they are cooked or served.  - certain types of wild mushrooms.  - unwashed fruits and vegetables that contain high concentrations of pesticides."}
{"_id":"c5bbe7ef-9802-4d75-8c42-0c4034ca8dff","text":"Anyone can get a foodborne illness. However, some people are more likely to develop foodborne illnesses than others, including\n                \n- infants and children  - pregnant women and their fetuses  - older adults  - people with weak immune systems\n                \nThese groups also have a greater risk of developing severe symptoms or complications of foodborne illnesses."}
{"_id":"6e39adfb-670f-4b3b-b49b-1d997ef60a8c","text":"Symptoms of foodborne illnesses depend on the cause. Common symptoms of many foodborne illnesses include\n                \n- vomiting  - diarrhea or bloody diarrhea  - abdominal pain  - fever  - chills\n                \nSymptoms can range from mild to serious and can last from a few hours to several days.\n                \nC. botulinum and some chemicals affect the nervous system, causing symptoms such as\n                \n- headache  - tingling or numbness of the skin  - blurred vision  - weakness  - dizziness  - paralysis"}
{"_id":"3d1ca64a-8d69-4631-af47-f315fdcf1832","text":"Foodborne illnesses may lead to dehydration, hemolytic uremic syndrome (HUS), and other complications. Acute foodborne illnesses may also lead to chronicor long lastinghealth problems.\n                \nDehydration\n                \nWhen someone does not drink enough fluids to replace those that are lost through vomiting and diarrhea, dehydration can result. When dehydrated, the body lacks enough fluid and electrolytesminerals in salts, including sodium, potassium, and chlorideto function properly. Infants, children, older adults, and people with weak immune systems have the greatest risk of becoming dehydrated.\n                \nSigns of dehydration are\n                \n- excessive thirst  - infrequent urination  - dark-colored urine  - lethargy, dizziness, or faintness\n                \nSigns of dehydration in infants and young children are\n                \n- dry mouth and tongue  - lack of tears when crying  - no wet diapers for 3 hours or more  - high fever  - unusually cranky or drowsy behavior  - sunken eyes, cheeks, or soft spot in the skull\n                \nAlso, when people are dehydrated, their skin does not flatten back to normal right away after being gently pinched and released.\n                \nSevere dehydration may require intravenous fluids and hospitalization. Untreated severe dehydration can cause serious health problems such as organ damage, shock, or comaa sleeplike state in which a person is not conscious.\n                \nHUS\n                \nHemolytic uremic syndrome is a rare disease that mostly affects children younger than 10 years of age. HUS develops when E. coli bacteria lodged in the digestive tract make toxins that enter the bloodstream. The toxins start to destroy red blood cells, which help the blood to clot, and the lining of the blood vessels.\n                \nIn the United States, E. coli O157:H7 infection is the most common cause of HUS, but infection with other strains of E. coli, other bacteria, and viruses may also cause HUS. A recent study found that about 6 percent of people with E. coli O157:H7 infections developed HUS. Children younger than age 5 have the highest risk, but females and people age 60 and older also have increased risk.3\n                \nSymptoms of E. coli O157:H7 infection include diarrhea, which may be bloody, and abdominal pain, often accompanied by nausea, vomiting, and fever. Up to a week after E. coli symptoms appear, symptoms of HUS may develop, including irritability, paleness, and decreased urination. HUS may lead to acute renal failure, which is a sudden and temporary loss of kidney function. HUS may also affect other organs and the central nervous system. Most people who develop HUS recover with treatment. Research shows that in the United States between 2000 and 2006, fewer than 5 percent of people who developed HUS died of the disorder. Older adults had the highest mortality rateabout one-third of people age 60 and older who developed HUS died.3\n                \nStudies have shown that some children who recover from HUS develop chronic complications, including kidney problems, high blood pressure, and diabetes.\n                \nOther Complications\n                \nSome foodborne illnesses lead to other serious complications. For example, C. botulinum and certain chemicals in fish and seafood can paralyze the muscles that control breathing. L. monocytogenes can cause spontaneous abortion or stillbirth in pregnant women.\n                \nResearch suggests that acute foodborne illnesses may lead to chronic disorders, including\n                \n- reactive arthritis, a type of joint inflammation that usually affects the knees, ankles, or feet. Some people develop this disorder following foodborne illnesses caused by certain bacteria, including C. jejuni and Salmonella. Reactive arthritis usually lasts fewer than 6 months, but this condition may recur or become chronic arthritis.4  - irritable bowel syndrome (IBS), a disorder of unknown cause that is associated with abdominal pain, bloating, and diarrhea or constipation or both. Foodborne illnesses caused by bacteria increase the risk of developing IBS.5  - Guillain-Barr syndrome, a disorder characterized by muscle weakness or paralysis that begins in the lower body and progresses to the upper body. This syndrome may occur after foodborne illnesses caused by bacteria, most commonly C. jejuni. Most people recover in 6 to 12 months.6\n                \nA recent study found that adults who had recovered from E. coli O157:H7 infections had increased risks of high blood pressure, kidney problems, and cardiovascular disease.7"}
{"_id":"52881c2b-d861-40a3-8ff3-f3fdd4ac3076","text":"To diagnose foodborne illnesses, health care providers ask about symptoms, foods and beverages recently consumed, and medical history. Health care providers will also perform a physical examination to look for signs of illness.\n                \nDiagnostic tests for foodborne illnesses may include a stool culture, in which a sample of stool is analyzed in a laboratory to check for signs of infections or diseases. A sample of vomit or a sample of the suspected food, if available, may also be tested. A health care provider may perform additional medical tests to rule out diseases and disorders that cause symptoms similar to the symptoms of foodborne illnesses.\n                \nIf symptoms of foodborne illnesses are mild and last only a short time, diagnostic tests are usually not necessary."}
{"_id":"9dc726f8-4e96-4c64-9833-9e0305b44db4","text":"The only treatment needed for most foodborne illnesses is replacing lost fluids and electrolytes to prevent dehydration.\n                \nOver-the-counter medications such as loperamide (Imodium) and bismuth subsalicylate (Pepto-Bismol and Kaopectate) may help stop diarrhea in adults. However, people with bloody diarrheaa sign of bacterial or parasitic infectionshould not use these medications. If diarrhea is caused by bacteria or parasites, over-the-counter medications may prolong the problem. Medications to treat diarrhea in adults can be dangerous for infants and children and should only be given with a health care providers guidance.\n                \nIf the specific cause of the foodborne illness is diagnosed, a health care provider may prescribe medications, such as antibiotics, to treat the illness.\n                \nHospitalization may be required to treat lifethreatening symptoms and complications, such as paralysis, severe dehydration, and HUS."}
{"_id":"26adecde-a5f5-4893-8e5b-d861e3d5d4d2","text":"The following steps may help relieve the symptoms of foodborne illnesses and prevent dehydration in adults:\n                \n- drinking plenty of liquids such as fruit juices, sports drinks, caffeine-free soft drinks, and broths to replace fluids and electrolytes  - sipping small amounts of clear liquids or sucking on ice chips if vomiting is still a problem  - gradually reintroducing food, starting with bland, easy-to-digest foods such as rice, potatoes, toast or bread, cereal, lean meat, applesauce, and bananas  - avoiding fatty foods, sugary foods, dairy products, caffeine, and alcohol until recovery is complete\n                \nInfants and children present special concerns. Infants and children are likely to become dehydrated more quickly from diarrhea and vomiting because of their smaller body size. The following steps may help relieve symptoms and prevent dehydration in infants and children:\n                \n- giving oral rehydration solutions such as Pedialyte, Naturalyte, Infalyte, and CeraLyte to prevent dehydration  - giving food as soon as the child is hungry  - giving infants breast milk or fullstrength formula, as usual, along with oral rehydration solutions\n                \nOlder adults and adults with weak immune systems should also drink oral rehydration solutions to prevent dehydration."}
{"_id":"52bbbb62-f0da-4649-9da6-1f78b268b26e","text":"Foodborne illnesses can be prevented by properly storing, cooking, cleaning, and handling foods.\n                \n- Raw and cooked perishable foodsfoods that can spoilshould be refrigerated or frozen promptly. If perishable foods stand at room temperature for more than 2 hours, they may not be safe to eat. Refrigerators should be set at 40 degrees or lower and freezers should be set at 0 degrees.  - Foods should be cooked long enough and at a high enough temperature to kill the harmful bacteria that cause illnesses. A meat thermometer should be used to ensure foods are cooked to the appropriate internal temperature:      - 145 degrees for roasts, steaks, and chops of beef, veal, pork, and lamb, followed by 3 minutes of rest time after the meat is removed from the heat source    - 160 degrees for ground beef, veal, pork, and lamb    - 165 degrees for poultry    - Cold foods should be kept cold and hot foods should be kept hot.  - Fruits and vegetables should be washed under running water just before eating, cutting, or cooking. A produce brush can be used under running water to clean fruits and vegetables with firm skin.  - Raw meat, poultry, seafood, and their juices should be kept away from other foods.  - People should wash their hands for at least 20 seconds with warm, soapy water before and after handling raw meat, poultry, fish, shellfish, produce, or eggs. People should also wash their hands after using the bathroom, changing diapers, or touching animals.  - Utensils and surfaces should be washed with hot, soapy water before and after they are used to prepare food. Diluted bleach1 teaspoon of bleach to 1 quart of hot watercan also be used to sanitize utensils and surfaces.\n                \nMore information about preventing foodborne illnesses is available at www.foodsafety.gov."}
{"_id":"bcfa6f99-efac-446a-bc8c-df262cf5a651","text":"- Foodborne illnesses are infections or irritations of the gastrointestinal (GI) tract caused by food or beverages that contain harmful bacteria, parasites, viruses, or chemicals.  - Anyone can get a foodborne illness. However, some people are more likely to develop foodborne illnesses than others, including infants and children, pregnant women and their fetuses, older adults, and people with weakened immune systems.  - Symptoms of foodborne illnesses depend on the cause. Common symptoms of many foodborne illnesses include vomiting, diarrhea or bloody diarrhea, abdominal pain, fever, and chills.  - Foodborne illnesses may lead to dehydration, hemolytic uremic syndrome (HUS), and other complications. Acute foodborne illnesses may also lead to chronicor long lastinghealth problems.  - The only treatment needed for most foodborne illnesses is replacing lost fluids and electrolytes to prevent dehydration.  - Foodborne illnesses can be prevented by properly storing, cooking, cleaning, and handling foods."}
{"_id":"8b013b14-b49b-49a6-9547-f3d7ad72b197","text":"If you have been taking analgesics regularly to control chronic pain, you may be advised to find new ways to treat your pain, such as behavior modification or relaxation techniques. Depending on how much your kidney function has declined, you may be advised to change your diet, limit the fluids you drink, or take medications to avoid anemia and bone problems caused by kidney disease. Your doctor will monitor your kidney function with regular urine and blood tests."}
{"_id":"00055e54-c1eb-459d-b05e-c583bfcaca47","text":"Cyclic vomiting syndrome, sometimes referred to as CVS, is an increasingly recognized disorder with sudden, repeated attacksalso called episodesof severe nausea, vomiting, and physical exhaustion that occur with no apparent cause. The episodes can last from a few hours to several days. Episodes can be so severe that a person has to stay in bed for days, unable to go to school or work. A person may need treatment at an emergency room or a hospital during episodes. After an episode, a person usually experiences symptom-free periods lasting a few weeks to several months. To people who have the disorder, as well as their family members and friends, cyclic vomiting syndrome can be disruptive and frightening.\n                \nThe disorder can affect a person for months, years, or decades. Each episode of cyclic vomiting syndrome is usually similar to previous ones, meaning that episodes tend to start at the same time of day, last the same length of time, and occur with the same symptoms and level of intensity."}
{"_id":"4943aaee-0663-4504-840d-3ff3386f33f2","text":"The GI tract is a series of hollow organs joined in a long, twisting tube from the mouth to the anusthe opening through which stool leaves the body. The body digests food using the movement of muscles in the GI tract, along with the release of hormones and enzymes. Cyclic vomiting syndrome affects the upper GI tract, which includes the mouth, esophagus, stomach, small intestine, and duodenum, the first part of the small intestine. The esophagus is the muscular tube that carries food and liquids from the mouth to the stomach. The stomach slowly pumps the food and liquids through the duodenum and into the rest of the small intestine, which absorbs nutrients from food particles. This process is automatic and people are usually not aware of it, though people sometimes feel food in their esophagus when they swallow something too large, try to eat too quickly, or drink hot or cold liquids."}
{"_id":"2f410a16-e656-4da5-905e-83c4db0cd5f8","text":"The cause of cyclic vomiting syndrome is unknown. However, some experts believe that some possible problems with bodily functions may contribute to the cause, such as the following:\n                \n- gastrointestinal motilitythe way food moves through the digestive system  - central nervous system functionincludes the brain, spinal cord, and nerves that control bodily responses  - autonomic nervous system functionnerves that control internal organs such as the heart  - hormone imbalanceshormones are a chemical produced in one part of the body and released into the blood to trigger or regulate particular bodily functions  - in children, an abnormal inherited gene may also contribute to the condition\n                \nSpecific conditions or events may trigger an episode of cyclic vomiting:\n                \n- emotional stress, anxiety, or panic attacksfor example, in children, common triggers of anticipatory anxiety are school exams or events, birthday parties, holidays, family conflicts, or travel  - infections, such as a sinus infection, a respiratory infection, or the flu  - eating certain foods, such as chocolate or cheese, or additives such as caffeine, nitritescommonly found in cured meats such as hot dogsand monosodium glutamate, also called MSG  - hot weather  - menstrual periods  - motion sickness  - overeating, fasting, or eating right before bedtime  - physical exhaustion or too much exercise"}
{"_id":"9b9d3f8f-c314-4ab7-94d7-f50815b6f7f8","text":"Cyclic vomiting syndrome is more common in children than adults, although reports of the syndrome in adults have increased in recent years.1 Usually, children are about 5 years old when diagnosed with cyclic vomiting syndrome, which occurs in every three out of 100,000 children.2"}
{"_id":"35435fee-0617-41de-a126-dc4d69d060e8","text":"The main symptoms of cyclic vomiting syndrome are severe nausea and sudden vomiting lasting hours to days. A person may also experience one or more of the following symptoms:\n                \n- retching, or making an attempt to vomit  - heaving or gagging  - lack of appetite  - abdominal pain  - diarrhea  - fever  - dizziness  - headache  - sensitivity to light\n                \nIntensity of symptoms will vary as a person cycles through four distinct phases of an episode:\n                \n- Prodrome phase. During the prodrome phase, the person feels that an episode of nausea and vomiting is about to start. Often marked by intense sweating and nauseawith or without abdominal painthis phase can last from a few minutes to several hours. The person may appear unusually pale.  - Vomiting phase. This phase consists of intense nausea, vomiting, and retching. Periods of vomiting and retching can last 20 to 30 minutes at a time. The person may be subdued and responsive, immobile and unresponsive, or writhing and moaning with intense abdominal pain. An episode can last from hours to days.  - Recovery phase. This phase begins when the vomiting and retching stop and the nausea subsides. Improvement of symptoms during the recovery phase can vary. Healthy color, appetite, and energy return gradually or right away.  - Well phase. This phase occurs between episodes when no symptoms are present."}
{"_id":"d0f452bd-4438-4ef8-8139-396c010ec5ed","text":"The severe vomiting and retching that define cyclic vomiting syndrome increase the chance of developing several complications, including dehydration, esophagitis, a Mallory-Weiss tear, and tooth decay.\n                \n- Dehydration may occur when a person does not replace fluids that were lost because of vomiting and diarrhea. When dehydrated, the body lacks enough fluid and electrolytesminerals in salts, including sodium, potassium, and chlorideto function properly. Severe dehydration may require intravenous (IV) fluids and hospitalization.  - Esophagitisinflammation or irritation of the esophaguscan result from the stomach acid that exits through the esophagus during vomiting.  - A Mallory-Weiss teara tear in the lower end of the esophagusis caused by severe vomiting. A person with bloody vomit and stool should see a health care provider right away.  - Tooth decay or corroding tooth enamel is damage caused by stomach acid.\n                \n\n                \nSeek Help for Signs or Symptoms of Severe Dehydration   People who have any signs or symptoms of severe dehydration should call or see a health care provider right away:   - excessive thirst   - dark-colored urine   - infrequent urination   - lethargy, dizziness, or faintness   - dry skin    Infants, children, older adults, and people with weak immune systems have the greatest chance of becoming dehydrated. People should watch for the following signs and symptoms of dehydration in infants, young children, and people who are unable to communicate their symptoms:   - dry mouth and tongue   - lack of tears when crying   - infants with no wet diapers for 3 hours or more   - infants with a sunken soft spot   - unusually cranky or drowsy behavior   - sunken eyes or cheeks   - fever    If left untreated, severe dehydration can cause serious health problems, such as organ damage, shock, or comaa sleeplike state in which a person is not conscious."}
{"_id":"af9d0762-89ab-4a0b-81b3-072ccaeeb13b","text":"People who have any signs or symptoms of severe dehydration should call or see a health care provider right away:\n                \n- excessive thirst  - dark-colored urine  - infrequent urination  - lethargy, dizziness, or faintness  - dry skin\n                \nInfants, children, older adults, and people with weak immune systems have the greatest chance of becoming dehydrated. People should watch for the following signs and symptoms of dehydration in infants, young children, and people who are unable to communicate their symptoms:\n                \n- dry mouth and tongue  - lack of tears when crying  - infants with no wet diapers for 3 hours or more  - infants with a sunken soft spot  - unusually cranky or drowsy behavior  - sunken eyes or cheeks  - fever\n                \nIf left untreated, severe dehydration can cause serious health problems, such as organ damage, shock, or comaa sleeplike state in which a person is not conscious."}
{"_id":"707d60ea-470b-4b02-b7dc-ead69331820b","text":"A specific test to diagnose cyclic vomiting syndrome does not exist; instead, a health care provider will rule out other conditions and diagnose the syndrome based upon\n                \n- a medical and family history  - a physical exam  - a pattern or cycle of symptoms  - blood tests  - urine tests  - imaging tests  - upper GI endoscopy  - a gastric emptying test\n                \nOften, it is suspected that one of the following is causing their symptoms:\n                \n- gastroparesisa disorder that slows or stops the movement of food from the stomach to the small intestine  - gastroenteritisinflammation of the lining of the stomach, small intestine, and large intestine\n                \nA diagnosis of cyclic vomiting syndrome may be difficult to make until the person sees a health care provider. A health care provider will suspect cyclic vomiting syndrome if the person suffers from repeat episodes of vomiting.\n                \nMedical and Family History\n                \nTaking a medical and family history is one of the first things a health care provider may do to help diagnose cyclic vomiting syndrome. He or she will ask the patient to provide a medical and family history.\n                \nPhysical Exam\n                \nA physical exam may help diagnose other conditions besides cyclic vomiting syndrome. During a physical exam, a health care provider usually\n                \n- examines a patients body  - taps on specific areas of the patients body\n                \nPattern or Cycle of Symptoms in Children3\n                \nA health care provider will often suspect cyclic vomiting syndrome in a child when the child\n                \n- has at least five separate episodes, or at least three separate episodes over 6 months  - has episodes of intense nausea and vomiting lasting 1 hour to 10 days and occurring at least 1 week apart  - has episodes that are similar to previous onesthey tend to start at the same time of day, last the same length of time, and occur with the same symptoms and level of intensity  - vomits during episodes at least four times per hour for at least 1 hour  - vomits and it is not attributed to another disorder  - has absence of nausea and vomiting between episodes\n                \nPattern or Cycle of Symptoms in Adults4,5\n                \nA health care provider will often suspect cyclic vomiting syndrome in adults when the following is present for at least 3 months and the symptoms started more than 6 months ago:\n                \n- Each episode of cyclic vomiting syndrome is usually similar to previous ones, meaning that episodes tend to start at the same time of day and last the same length of timeless than 1 week.  - Three or more separate episodes in the past year.  - Absence of nausea or vomiting between episodes.\n                \nBlood Tests\n                \nA nurse or technician will draw blood samples at a health care providers office or a commercial facility and send the samples to a lab for analysis. The blood test can tell the health care provider if the patient has any signs of dehydration or other problems.\n                \nUrine Tests\n                \nUrinalysis involves testing a urine sample. The patient collects a urine sample in a special container in a health care providers office or a commercial facility. A health care provider tests the sample in the same location or sends the sample to a lab for analysis. A urinalysis can rule out kidney problems or an infection.\n                \nImaging Tests\n                \nThe health care provider decides which test to order based on the symptoms, medical history, and physical exam.\n                \nUpper GI series. A health care provider may order an upper GI series to look at the upper GI tract. A radiologista doctor who specializes in medical imagingperforms this test at a hospital or an outpatient center. This test does not require anesthesia. The patient should not eat or drink for 8 hours before the procedure, if possible. During the procedure, the patient will stand or sit in front of an x-ray machine and drink barium, a chalky liquid. Infants lie on a table and a health care provider gives them barium through a tiny tube placed in the nose that runs into the stomach. Barium coats the GI tract, making signs of obstruction or other problems that can cause vomiting show up more clearly on x rays. A patient may experience bloating and nausea for a short time after the test. The upper GI series can show other problems that may be causing symptoms, such as an ulcer or obstruction.\n                \nAbdominal ultrasound. A health care provider may order an ultrasound to look at the organs in the abdomen. A technician uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. The technician performs the procedure in a health care providers office, an outpatient center, or a hospital. A radiologist interprets the images. A patient does not need anesthesia. The abdominal ultrasound can show other problems that may be causing symptoms, such as gallstones.\n                \nUpper Gastrointestinal Endoscopy\n                \nThis procedure involves using an endoscopea small, flexible tube with a lightto see the upper GI tract. A gastroenterologista doctor who specializes in digestive diseasesperforms the test at a hospital or an outpatient center. A health care provider may give a patient a liquid anesthetic to gargle or may spray anesthetic on the back of the patients throat. A nurse or technician will place an IV needle in a vein in the arm to administer sedation or anesthesia. Sedatives or anesthesia help a patient stay relaxed and comfortable. The gastroenterologist carefully inserts the endoscope into the mouth and feeds the endoscope down the esophagus and into the stomach and duodenum. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining. The upper GI endoscopy can show other problems that may be causing symptoms, such as an ulcer. A gastroenterologist may obtain a biopsya procedure that involves taking a small piece of tissue for examination with a microscopeof the small-intestinal lining during an upper GI endoscopy. The patient will not feel the biopsy.\n                \nGastric Emptying Test\n                \nAlso called gastric emptying scintigraphy, this test involves eating a bland mealsuch as eggs or an egg substitutethat contains a small amount of radioactive material. A specially trained technician performs the test in a radiology center or hospital, and a radiologist interprets the results; the patient does not need anesthesia. An external camera scans the abdomen to show where the radioactive material is located. The radiologist is then able to measure the rate of gastric emptying at 1, 2, 3, and 4 hours after the meal."}
{"_id":"7a8c5fc2-a0d5-44f8-9804-d3a1a91995c4","text":"A health care provider may refer patients to a gastroenterologist for treatment.\n                \nPeople with cyclic vomiting syndrome should get plenty of rest and take medications to prevent a vomiting episode, stop an episode in progress, speed up recovery, or relieve associated symptoms.\n                \nThe health care team tailors treatment to the symptoms experienced during each of the four cyclic vomiting syndrome phases:\n                \n- Prodrome phase treatment. The goal during the prodrome phase is to stop an episode before it progresses. Taking medication early in the phase can help stop an episode from moving to the vomiting phase or becoming severe; however, people do not always realize an episode is coming. For example, a person may wake up in the morning and begin vomiting. A health care provider may recommend the following medications for both children and adults:      - ondansetron (Zofran) or lorazepam (Ativan) for nausea    - ibuprofen for abdominal pain    - ranitidine (Zantac), lansoprazole (Prevacid), or omeprazole (Prilosec, Zegerid) to control stomach acid production    - sumatriptan (Imitrex)prescribed as a nasal spray, an injection, or a pill that dissolves under the tonguefor migraines    - Vomiting phase treatment. Once vomiting begins, people should call or see a health care provider as soon as possible. Treatment usually requires the person to stay in bed and sleep in a dark, quiet room. A health care provider may recommend the following for both children and adults:      - medication for pain, nausea, and reducing stomach acid and anxiety    - anti-migraine medications such as sumatriptan to stop symptoms of a migraine or possibly stop an episode in progress    - hospitalization for severe nausea and vomiting    - IV fluids and medications to prevent dehydration and treat symptoms    - IV nutrition if an episode continues for several days    - Recovery phase treatment. During the recovery phase, drinking and eating will replace lost electrolytes. A person may need IV fluids for a period of time. Some people find their appetite returns to normal right away, while others start by drinking clear liquids and then moving slowly to other liquids and solid food. A health care provider may prescribe medications during the recovery phase and well phase to prevent future episodes.  - Well phase treatment. During the well phase, a health care provider may use medications to treat people whose episodes are frequent and long lasting in an effort to prevent or ease future episodes. A person may need to take a medication daily for 1 to 2 months before evaluating whether it helps prevent episodes. A health care provider may prescribe the following medications for both children and adults during the well phase to prevent cyclic vomiting syndrome episodes, lessen their severity, and reduce their frequency:      - amitriptyline (Elavil)    - propranolol (Inderal)    - cyproheptadine (Periactin)"}
{"_id":"8fe73bc6-b220-468a-9391-20989aeb779e","text":"A person should stay away from known triggers, especially during the well phase, as well as\n                \n- get adequate sleep to prevent exhaustion  - treat sinus problems or allergies  - seek help on reducing stress and anxiety  - avoid foods that trigger episodes or foods with additives\n                \nA health care provider may refer people with cyclic vomiting syndrome and anxiety to a stress management specialist for relaxation therapy or other treatments.\n                \nA health care provider may prescribe medications to prevent migraines for people with cyclic vomiting syndrome."}
{"_id":"ab344e62-8906-485d-a185-d555fc09d2c3","text":"During the prodrome and vomiting phases of cyclic vomiting syndrome, a person will generally take in little or no nutrition by mouth. During the recovery phase, the person may be quite hungry as soon as the vomiting stops. As eating resumes, a person or his or her family should watch for the return of nausea. In some cases, a person can start with clear liquids and proceed slowly to a regular diet.\n                \nDuring the well phase, a balanced diet and regular meals are important. People should avoid any trigger foods and foods with additives. Eating small, carbohydrate-containing snacks between meals, before exercise, and at bedtime may help prevent future attacks. A health care provider will assist with planning a return to a regular diet."}
{"_id":"f523348b-6702-4303-a3dd-9acd98a0ff0b","text":"- Cyclic vomiting syndrome, sometimes referred to as CVS, is an increasingly recognized disorder with sudden, repeated attacksalso called episodesof severe nausea, vomiting, and physical exhaustion that occur with no apparent cause.  - The disorder can affect a person for months, years, or decades.  - The cause of cyclic vomiting syndrome is unknown.  - The severe vomiting and retching that define cyclic vomiting syndrome increase the chance of developing several complications, including dehydration, esophagitis, a Mallory-Weiss tear, and tooth decay.  - Intensity of symptoms will vary as a person cycles through four distinct phases of an episode.  - The main symptoms of cyclic vomiting syndrome are severe nausea and sudden vomiting lasting hours to days.  - People with cyclic vomiting syndrome should get plenty of rest and take medications to prevent a vomiting episode, stop an episode in progress, speed up recovery, or relieve associated symptoms.  - During the well phase, a balanced diet and regular meals are important. A health care provider will assist with planning a return to a regular diet."}
{"_id":"95c8f482-c3c7-485a-81bd-8335e2136843","text":"Diabetes is a complex group of diseases with a variety of causes. People with diabetes have high blood glucose, also called high blood sugar or hyperglycemia.\n                \nDiabetes is a disorder of metabolismthe way the body uses digested food for energy. The digestive tract breaks down carbohydratessugars and starches found in many foodsinto glucose, a form of sugar that enters the bloodstream. With the help of the hormone insulin, cells throughout the body absorb glucose and use it for energy. Diabetes develops when the body doesnt make enough insulin or is not able to use insulin effectively, or both.\n                \nInsulin is made in the pancreas, an organ located behind the stomach. The pancreas contains clusters of cells called islets. Beta cells within the islets make insulin and release it into the blood.\n                \nIf beta cells dont produce enough insulin, or the body doesnt respond to the insulin that is present, glucose builds up in the blood instead of being absorbed by cells in the body, leading to prediabetes or diabetes. Prediabetes is a condition in which blood glucose levels or A1C levelswhich reflect average blood glucose levelsare higher than normal but not high enough to be diagnosed as diabetes. In diabetes, the bodys cells are starved of energy despite high blood glucose levels.\n                \nOver time, high blood glucose damages nerves and blood vessels, leading to complications such as heart disease, stroke, kidney disease, blindness, dental disease, and amputations. Other complications of diabetes may include increased susceptibility to other diseases, loss of mobility with aging, depression, and pregnancy problems. No one is certain what starts the processes that cause diabetes, but scientists believe genes and environmental factors interact to cause diabetes in most cases.\n                \nThe two main types of diabetes are type 1 diabetes and type 2 diabetes. A third type, gestational diabetes, develops only during pregnancy. Other types of diabetes are caused by defects in specific genes, diseases of the pancreas, certain drugs or chemicals, infections, and other conditions. Some people show signs of both type 1 and type 2 diabetes."}
{"_id":"e6807718-d30a-4c5a-809e-969c0a2a1c3b","text":"Type 1 diabetes is caused by a lack of insulin due to the destruction of insulin-producing beta cells in the pancreas. In type 1 diabetesan autoimmune diseasethe bodys immune system attacks and destroys the beta cells. Normally, the immune system protects the body from infection by identifying and destroying bacteria, viruses, and other potentially harmful foreign substances. But in autoimmune diseases, the immune system attacks the bodys own cells. In type 1 diabetes, beta cell destruction may take place over several years, but symptoms of the disease usually develop over a short period of time.\n                \nType 1 diabetes typically occurs in children and young adults, though it can appear at any age. In the past, type 1 diabetes was called juvenile diabetes or insulin-dependent diabetes mellitus.\n                \nLatent autoimmune diabetes in adults (LADA) may be a slowly developing kind of type 1 diabetes. Diagnosis usually occurs after age 30. In LADA, as in type 1 diabetes, the bodys immune system destroys the beta cells. At the time of diagnosis, people with LADA may still produce their own insulin, but eventually most will need insulin shots or an insulin pump to control blood glucose levels.\n                \nGenetic Susceptibility\n                \nHeredity plays an important part in determining who is likely to develop type 1 diabetes. Genes are passed down from biological parent to child. Genes carry instructions for making proteins that are needed for the bodys cells to function. Many genes, as well as interactions among genes, are thought to influence susceptibility to and protection from type 1 diabetes. The key genes may vary in different population groups. Variations in genes that affect more than 1 percent of a population group are called gene variants.\n                \nCertain gene variants that carry instructions for making proteins called human leukocyte antigens (HLAs) on white blood cells are linked to the risk of developing type 1 diabetes. The proteins produced by HLA genes help determine whether the immune system recognizes a cell as part of the body or as foreign material. Some combinations of HLA gene variants predict that a person will be at higher risk for type 1 diabetes, while other combinations are protective or have no effect on risk.\n                \nWhile HLA genes are the major risk genes for type 1 diabetes, many additional risk genes or gene regions have been found. Not only can these genes help identify people at risk for type 1 diabetes, but they also provide important clues to help scientists better understand how the disease develops and identify potential targets for therapy and prevention.\n                \nGenetic testing can show what types of HLA genes a person carries and can reveal other genes linked to diabetes. However, most genetic testing is done in a research setting and is not yet available to individuals. Scientists are studying how the results of genetic testing can be used to improve type 1 diabetes prevention or treatment.\n                \nAutoimmune Destruction of Beta Cells\n                \nIn type 1 diabetes, white blood cells called T cells attack and destroy beta cells. The process begins well before diabetes symptoms appear and continues after diagnosis. Often, type 1 diabetes is not diagnosed until most beta cells have already been destroyed. At this point, a person needs daily insulin treatment to survive. Finding ways to modify or stop this autoimmune process and preserve beta cell function is a major focus of current scientific research.\n                \nRecent research suggests insulin itself may be a key trigger of the immune attack on beta cells. The immune systems of people who are susceptible to developing type 1 diabetes respond to insulin as if it were a foreign substance, or antigen. To combat antigens, the body makes proteins called antibodies. Antibodies to insulin and other proteins produced by beta cells are found in people with type 1 diabetes. Researchers test for these antibodies to help identify people at increased risk of developing the disease. Testing the types and levels of antibodies in the blood can help determine whether a person has type 1 diabetes, LADA, or another type of diabetes.\n                \nEnvironmental Factors\n                \nEnvironmental factors, such as foods, viruses, and toxins, may play a role in the development of type 1 diabetes, but the exact nature of their role has not been determined. Some theories suggest that environmental factors trigger the autoimmune destruction of beta cells in people with a genetic susceptibility to diabetes. Other theories suggest that environmental factors play an ongoing role in diabetes, even after diagnosis.\n                \nViruses and infections. A virus cannot cause diabetes on its own, but people are sometimes diagnosed with type 1 diabetes during or after a viral infection, suggesting a link between the two. Also, the onset of type 1 diabetes occurs more frequently during the winter when viral infections are more common. Viruses possibly associated with type 1 diabetes include coxsackievirus B, cytomegalovirus, adenovirus, rubella, and mumps. Scientists have described several ways these viruses may damage or destroy beta cells or possibly trigger an autoimmune response in susceptible people. For example, anti-islet antibodies have been found in patients with congenital rubella syndrome, and cytomegalovirus has been associated with significant beta cell damage and acute pancreatitisinflammation of the pancreas. Scientists are trying to identify a virus that can cause type 1 diabetes so that a vaccine might be developed to prevent the disease.\n                \nInfant feeding practices. Some studies have suggested that dietary factors may raise or lower the risk of developing type 1 diabetes. For example, breastfed infants and infants receiving vitamin D supplements may have a reduced risk of developing type 1 diabetes, while early exposure to cows milk and cereal proteins may increase risk. More research is needed to clarify how infant nutrition affects the risk for type 1 diabetes.\n                \nRead more in the Centers for Disease Control and Preventions (CDCs) publication  National Diabetes Statistics Report, 2014 at  www.cdc.gov for information about research studies related to type 1 diabetes."}
{"_id":"11ebde33-72e3-457a-b42d-0839066ce622","text":"Type 2 diabetesthe most common form of diabetesis caused by a combination of factors, including insulin resistance, a condition in which the bodys muscle, fat, and liver cells do not use insulin effectively. Type 2 diabetes develops when the body can no longer produce enough insulin to compensate for the impaired ability to use insulin. Symptoms of type 2 diabetes may develop gradually and can be subtle; some people with type 2 diabetes remain undiagnosed for years.\n                \nType 2 diabetes develops most often in middle-aged and older people who are also overweight or obese. The disease, once rare in youth, is becoming more common in overweight and obese children and adolescents. Scientists think genetic susceptibility and environmental factors are the most likely triggers of type 2 diabetes.\n                \nGenetic Susceptibility\n                \nGenes play a significant part in susceptibility to type 2 diabetes. Having certain genes or combinations of genes may increase or decrease a persons risk for developing the disease. The role of genes is suggested by the high rate of type 2 diabetes in families and identical twins and wide variations in diabetes prevalence by ethnicity. Type 2 diabetes occurs more frequently in African Americans, Alaska Natives, American Indians, Hispanics\/Latinos, and some Asian Americans, Native Hawaiians, and Pacific Islander Americans than it does in non-Hispanic whites.\n                \nRecent studies have combined genetic data from large numbers of people, accelerating the pace of gene discovery. Though scientists have now identified many gene variants that increase susceptibility to type 2 diabetes, the majority have yet to be discovered. The known genes appear to affect insulin production rather than insulin resistance. Researchers are working to identify additional gene variants and to learn how they interact with one another and with environmental factors to cause diabetes.\n                \nStudies have shown that variants of the TCF7L2 gene increase susceptibility to type 2 diabetes. For people who inherit two copies of the variants, the risk of developing type 2 diabetes is about 80 percent higher than for those who do not carry the gene variant.1 However, even in those with the variant, diet and physical activity leading to weight loss help delay diabetes, according to the Diabetes Prevention Program (DPP), a major clinical trial involving people at high risk.\n                \nGenes can also increase the risk of diabetes by increasing a persons tendency to become overweight or obese. One theory, known as the thrifty gene hypothesis, suggests certain genes increase the efficiency of metabolism to extract energy from food and store the energy for later use. This survival trait was advantageous for populations whose food supplies were scarce or unpredictable and could help keep people alive during famine. In modern times, however, when high-calorie foods are plentiful, such a trait can promote obesity and type 2 diabetes.\n                \nObesity and Physical Inactivity\n                \nPhysical inactivity and obesity are strongly associated with the development of type 2 diabetes. People who are genetically susceptible to type 2 diabetes are more vulnerable when these risk factors are present.\n                \nAn imbalance between caloric intake and physical activity can lead to obesity, which causes insulin resistance and is common in people with type 2 diabetes. Central obesity, in which a person has excess abdominal fat, is a major risk factor not only for insulin resistance and type 2 diabetes but also for heart and blood vessel disease, also called cardiovascular disease (CVD). This excess belly fat produces hormones and other substances that can cause harmful, chronic effects in the body such as damage to blood vessels.\n                \nThe DPP and other studies show that millions of people can lower their risk for type 2 diabetes by making lifestyle changes and losing weight. The DPP proved that people with prediabetesat high risk of developing type 2 diabetescould sharply lower their risk by losing weight through regular physical activity and a diet low in fat and calories. In 2009, a follow-up study of DPP participantsthe Diabetes Prevention Program Outcomes Study (DPPOS)showed that the benefits of weight loss lasted for at least 10 years after the original study began.2\n                \nRead more about the DPP, funded under National Institutes of Health (NIH) clinical trial number NCT00004992, and the DPPOS, funded under NIH clinical trial number NCT00038727 in  Diabetes Prevention Program.\n                \nInsulin Resistance\n                \nInsulin resistance is a common condition in people who are overweight or obese, have excess abdominal fat, and are not physically active. Muscle, fat, and liver cells stop responding properly to insulin, forcing the pancreas to compensate by producing extra insulin. As long as beta cells are able to produce enough insulin, blood glucose levels stay in the normal range. But when insulin production falters because of beta cell dysfunction, glucose levels rise, leading to prediabetes or diabetes.\n                \nAbnormal Glucose Production by the Liver\n                \nIn some people with diabetes, an abnormal increase in glucose production by the liver also contributes to high blood glucose levels. Normally, the pancreas releases the hormone glucagon when blood glucose and insulin levels are low. Glucagon stimulates the liver to produce glucose and release it into the bloodstream. But when blood glucose and insulin levels are high after a meal, glucagon levels drop, and the liver stores excess glucose for later, when it is needed. For reasons not completely understood, in many people with diabetes, glucagon levels stay higher than needed. High glucagon levels cause the liver to produce unneeded glucose, which contributes to high blood glucose levels. Metformin, the most commonly used drug to treat type 2 diabetes, reduces glucose production by the liver.\n                \nThe Roles of Insulin and Glucagon in Normal Blood Glucose Regulation\n                \nA healthy persons body keeps blood glucose levels in a normal range through several complex mechanisms. Insulin and glucagon, two hormones made in the pancreas, help regulate blood glucose levels:\n                \n- Insulin, made by beta cells, lowers elevated blood glucose levels.  - Glucagon, made by alpha cells, raises low blood glucose levels.\n                \n- Insulin helps muscle, fat, and liver cells absorb glucose from the bloodstream, lowering blood glucose levels.  - Insulin stimulates the liver and muscle tissue to store excess glucose. The stored form of glucose is called glycogen.  - Insulin also lowers blood glucose levels by reducing glucose production in the liver.\n                \n- Glucagon signals the liver and muscle tissue to break down glycogen into glucose, which enters the bloodstream and raises blood glucose levels.  - If the body needs more glucose, glucagon stimulates the liver to make glucose from amino acids.\n                \nMetabolic Syndrome\n                \nMetabolic syndrome, also called insulin resistance syndrome, refers to a group of conditions common in people with insulin resistance, including\n                \n- higher than normal blood glucose levels  - increased waist size due to excess abdominal fat  - high blood pressure  - abnormal levels of cholesterol and triglycerides in the blood\n                \nCell Signaling and Regulation\n                \nCells communicate through a complex network of molecular signaling pathways. For example, on cell surfaces, insulin receptor molecules capture, or bind, insulin molecules circulating in the bloodstream. This interaction between insulin and its receptor prompts the biochemical signals that enable the cells to absorb glucose from the blood and use it for energy.\n                \nProblems in cell signaling systems can set off a chain reaction that leads to diabetes or other diseases. Many studies have focused on how insulin signals cells to communicate and regulate action. Researchers have identified proteins and pathways that transmit the insulin signal and have mapped interactions between insulin and body tissues, including the way insulin helps the liver control blood glucose levels. Researchers have also found that key signals also come from fat cells, which produce substances that cause inflammation and insulin resistance.\n                \nThis work holds the key to combating insulin resistance and diabetes. As scientists learn more about cell signaling systems involved in glucose regulation, they will have more opportunities to develop effective treatments.\n                \nBeta Cell Dysfunction\n                \nScientists think beta cell dysfunction is a key contributor to type 2 diabetes. Beta cell impairment can cause inadequate or abnormal patterns of insulin release. Also, beta cells may be damaged by high blood glucose itself, a condition called glucose toxicity.\n                \nScientists have not determined the causes of beta cell dysfunction in most cases. Single gene defects lead to specific forms of diabetes called maturity-onset diabetes of the young (MODY). The genes involved regulate insulin production in the beta cells. Although these forms of diabetes are rare, they provide clues as to how beta cell function may be affected by key regulatory factors. Other gene variants are involved in determining the number and function of beta cells. But these variants account for only a small percentage of type 2 diabetes cases. Malnutrition early in life is also being investigated as a cause of beta cell dysfunction. The metabolic environment of the developing fetus may also create a predisposition for diabetes later in life.\n                \nRisk Factors for Type 2 Diabetes\n                \nPeople who develop type 2 diabetes are more likely to have the following characteristics:\n                \n- age 45 or older  - overweight or obese  - physically inactive  - parent or sibling with diabetes  - family background that is African American, Alaska Native, American Indian, Asian American, Hispanic\/Latino, or Pacific Islander American  - history of giving birth to a baby weighing more than 9 pounds  - history of gestational diabetes  - high blood pressure140\/90 or aboveor being treated for high blood pressure  - high-density lipoprotein (HDL), or good, cholesterol below 35 milligrams per deciliter (mg\/dL), or a triglyceride level above 250 mg\/dL  - polycystic ovary syndrome, also called PCOS  - prediabetesan A1C level of 5.7 to 6.4 percent; a fasting plasma glucose test result of 100125 mg\/dL, called impaired fasting glucose; or a 2-hour oral glucose tolerance test result of 140199, called impaired glucose tolerance  - acanthosis nigricans, a condition associated with insulin resistance, characterized by a dark, velvety rash around the neck or armpits  - history of CVD\n                \nThe American Diabetes Association (ADA) recommends that testing to detect prediabetes and type 2 diabetes be considered in adults who are overweight or obese and have one or more additional risk factors for diabetes. In adults without these risk factors, testing should begin at age 45."}
{"_id":"d00201bf-f405-47b8-a8fb-eeb57c0deb48","text":"Insulin Resistance and Beta Cell Dysfunction\n                \nHormones produced by the placenta and other pregnancy-related factors contribute to insulin resistance, which occurs in all women during late pregnancy. Insulin resistance increases the amount of insulin needed to control blood glucose levels. If the pancreas cant produce enough insulin due to beta cell dysfunction, gestational diabetes occurs.\n                \nAs with type 2 diabetes, excess weight is linked to gestational diabetes. Overweight or obese women are at particularly high risk for gestational diabetes because they start pregnancy with a higher need for insulin due to insulin resistance. Excessive weight gain during pregnancy may also increase risk.\n                \nFamily History\n                \nHaving a family history of diabetes is also a risk factor for gestational diabetes, suggesting that genes play a role in its development. Genetics may also explain why the disorder occurs more frequently in African Americans, American Indians, and Hispanics\/Latinos. Many gene variants or combinations of variants may increase a womans risk for developing gestational diabetes. Studies have found several gene variants associated with gestational diabetes, but these variants account for only a small fraction of women with gestational diabetes.\n                \nFuture Risk of Type 2 Diabetes\n                \nBecause a womans hormones usually return to normal levels soon after giving birth, gestational diabetes disappears in most women after delivery. However, women who have gestational diabetes are more likely to develop gestational diabetes with future pregnancies and develop type 2 diabetes.3 Women with gestational diabetes should be tested for persistent diabetes 6 to 12 weeks after delivery and at least every 3 years thereafter.\n                \nAlso, exposure to high glucose levels during gestation increases a childs risk for becoming overweight or obese and for developing type 2 diabetes later on. The result may be a cycle of diabetes affecting multiple generations in a family. For both mother and child, maintaining a healthy body weight and being physically active may help prevent type 2 diabetes."}
{"_id":"03a48d7f-a436-4b78-a6b9-e070f052a151","text":"Other types of diabetes have a variety of possible causes.\n                \nGenetic Mutations Affecting Beta Cells, Insulin, and Insulin Action\n                \nSome relatively uncommon forms of diabetes known as monogenic diabetes are caused by mutations, or changes, in a single gene. These mutations are usually inherited, but sometimes the gene mutation occurs spontaneously. Most of these gene mutations cause diabetes by reducing beta cells ability to produce insulin.\n                \nThe most common types of monogenic diabetes are neonatal diabetes mellitus (NDM) and MODY. NDM occurs in the first 6 months of life. MODY is usually found during adolescence or early adulthood but sometimes is not diagnosed until later in life. More information about NDM and MODY is provided in the NIDDK health topic, Monogenic Forms of Diabetes.\n                \nOther rare genetic mutations can cause diabetes by damaging the quality of insulin the body produces or by causing abnormalities in insulin receptors.\n                \nOther Genetic Diseases\n                \nDiabetes occurs in people with Down syndrome, Klinefelter syndrome, and Turner syndrome at higher rates than the general population. Scientists are investigating whether genes that may predispose people to genetic syndromes also predispose them to diabetes.\n                \nThe genetic disorders cystic fibrosis and hemochromatosis are linked to diabetes. Cystic fibrosis produces abnormally thick mucus, which blocks the pancreas. The risk of diabetes increases with age in people with cystic fibrosis. Hemochromatosis causes the body to store too much iron. If the disorder is not treated, iron can build up in and damage the pancreas and other organs.\n                \nDamage to or Removal of the Pancreas\n                \nPancreatitis, cancer, and trauma can all harm the pancreatic beta cells or impair insulin production, thus causing diabetes. If the damaged pancreas is removed, diabetes will occur due to the loss of the beta cells.\n                \nEndocrine Diseases\n                \nEndocrine diseases affect organs that produce hormones. Cushings syndrome and acromegaly are examples of hormonal disorders that can cause prediabetes and diabetes by inducing insulin resistance. Cushings syndrome is marked by excessive production of cortisolsometimes called the stress hormone. Acromegaly occurs when the body produces too much growth hormone. Glucagonoma, a rare tumor of the pancreas, can also cause diabetes. The tumor causes the body to produce too much glucagon. Hyperthyroidism, a disorder that occurs when the thyroid gland produces too much thyroid hormone, can also cause elevated blood glucose levels.\n                \nAutoimmune Disorders\n                \nRare disorders characterized by antibodies that disrupt insulin action can lead to diabetes. This kind of diabetes is often associated with other autoimmune disorders such as lupus erythematosus. Another rare autoimmune disorder called stiff-man syndrome is associated with antibodies that attack the beta cells, similar to type 1 diabetes.\n                \nMedications and Chemical Toxins\n                \nSome medications, such as nicotinic acid and certain types of diuretics, anti-seizure drugs, psychiatric drugs, and drugs to treat human immunodeficiency virus (HIV), can impair beta cells or disrupt insulin action. Pentamidine, a drug prescribed to treat a type of pneumonia, can increase the risk of pancreatitis, beta cell damage, and diabetes. Also, glucocorticoidssteroid hormones that are chemically similar to naturally produced cortisolmay impair insulin action. Glucocorticoids are used to treat inflammatory illnesses such as rheumatoid arthritis, asthma, lupus, and ulcerative colitis.\n                \nMany chemical toxins can damage or destroy beta cells in animals, but only a few have been linked to diabetes in humans. For example, dioxina contaminant of the herbicide Agent Orange, used during the Vietnam Warmay be linked to the development of type 2 diabetes. In 2000, based on a report from the Institute of Medicine, the U.S. Department of Veterans Affairs (VA) added diabetes to the list of conditions for which Vietnam veterans are eligible for disability compensation. Also, a chemical in a rat poison no longer in use has been shown to cause diabetes if ingested. Some studies suggest a high intake of nitrogen-containing chemicals such as nitrates and nitrites might increase the risk of diabetes. Arsenic has also been studied for possible links to diabetes.\n                \nLipodystrophy\n                \nLipodystrophy is a condition in which fat tissue is lost or redistributed in the body. The condition is associated with insulin resistance and type 2 diabetes."}
{"_id":"c0f62ddc-d318-496b-a7b4-bdc4663d79e1","text":"Other types of diabetes have a variety of possible causes.\n                \nGenetic Mutations Affecting Beta Cells, Insulin, and Insulin Action\n                \nSome relatively uncommon forms of diabetes known as monogenic diabetes are caused by mutations, or changes, in a single gene. These mutations are usually inherited, but sometimes the gene mutation occurs spontaneously. Most of these gene mutations cause diabetes by reducing beta cells ability to produce insulin.\n                \nThe most common types of monogenic diabetes are neonatal diabetes mellitus (NDM) and MODY. NDM occurs in the first 6 months of life. MODY is usually found during adolescence or early adulthood but sometimes is not diagnosed until later in life. More information about NDM and MODY is provided in the NIDDK health topic, Monogenic Forms of Diabetes.\n                \nOther rare genetic mutations can cause diabetes by damaging the quality of insulin the body produces or by causing abnormalities in insulin receptors.\n                \nOther Genetic Diseases\n                \nDiabetes occurs in people with Down syndrome, Klinefelter syndrome, and Turner syndrome at higher rates than the general population. Scientists are investigating whether genes that may predispose people to genetic syndromes also predispose them to diabetes.\n                \nThe genetic disorders cystic fibrosis and hemochromatosis are linked to diabetes. Cystic fibrosis produces abnormally thick mucus, which blocks the pancreas. The risk of diabetes increases with age in people with cystic fibrosis. Hemochromatosis causes the body to store too much iron. If the disorder is not treated, iron can build up in and damage the pancreas and other organs.\n                \nDamage to or Removal of the Pancreas\n                \nPancreatitis, cancer, and trauma can all harm the pancreatic beta cells or impair insulin production, thus causing diabetes. If the damaged pancreas is removed, diabetes will occur due to the loss of the beta cells.\n                \nEndocrine Diseases\n                \nEndocrine diseases affect organs that produce hormones. Cushings syndrome and acromegaly are examples of hormonal disorders that can cause prediabetes and diabetes by inducing insulin resistance. Cushings syndrome is marked by excessive production of cortisolsometimes called the stress hormone. Acromegaly occurs when the body produces too much growth hormone. Glucagonoma, a rare tumor of the pancreas, can also cause diabetes. The tumor causes the body to produce too much glucagon. Hyperthyroidism, a disorder that occurs when the thyroid gland produces too much thyroid hormone, can also cause elevated blood glucose levels.\n                \nAutoimmune Disorders\n                \nRare disorders characterized by antibodies that disrupt insulin action can lead to diabetes. This kind of diabetes is often associated with other autoimmune disorders such as lupus erythematosus. Another rare autoimmune disorder called stiff-man syndrome is associated with antibodies that attack the beta cells, similar to type 1 diabetes.\n                \nMedications and Chemical Toxins\n                \nSome medications, such as nicotinic acid and certain types of diuretics, anti-seizure drugs, psychiatric drugs, and drugs to treat human immunodeficiency virus (HIV), can impair beta cells or disrupt insulin action. Pentamidine, a drug prescribed to treat a type of pneumonia, can increase the risk of pancreatitis, beta cell damage, and diabetes. Also, glucocorticoidssteroid hormones that are chemically similar to naturally produced cortisolmay impair insulin action. Glucocorticoids are used to treat inflammatory illnesses such as rheumatoid arthritis, asthma, lupus, and ulcerative colitis.\n                \nMany chemical toxins can damage or destroy beta cells in animals, but only a few have been linked to diabetes in humans. For example, dioxina contaminant of the herbicide Agent Orange, used during the Vietnam Warmay be linked to the development of type 2 diabetes. In 2000, based on a report from the Institute of Medicine, the U.S. Department of Veterans Affairs (VA) added diabetes to the list of conditions for which Vietnam veterans are eligible for disability compensation. Also, a chemical in a rat poison no longer in use has been shown to cause diabetes if ingested. Some studies suggest a high intake of nitrogen-containing chemicals such as nitrates and nitrites might increase the risk of diabetes. Arsenic has also been studied for possible links to diabetes.\n                \nLipodystrophy\n                \nLipodystrophy is a condition in which fat tissue is lost or redistributed in the body. The condition is associated with insulin resistance and type 2 diabetes."}
{"_id":"0d88caa2-7eb9-469b-af9f-819507d6c2a6","text":"- Diabetes is a complex group of diseases with a variety of causes. Scientists believe genes and environmental factors interact to cause diabetes in most cases.  - People with diabetes have high blood glucose, also called high blood sugar or hyperglycemia. Diabetes develops when the body doesnt make enough insulin or is not able to use insulin effectively, or both.  - Insulin is a hormone made by beta cells in the pancreas. Insulin helps cells throughout the body absorb and use glucose for energy. If the body does not produce enough insulin or cannot use insulin effectively, glucose builds up in the blood instead of being absorbed by cells in the body, and the body is starved of energy.  - Prediabetes is a condition in which blood glucose levels or A1C levels are higher than normal but not high enough to be diagnosed as diabetes. People with prediabetes can substantially reduce their risk of developing diabetes by losing weight and increasing physical activity.  - The two main types of diabetes are type 1 diabetes and type 2 diabetes. Gestational diabetes is a third form of diabetes that develops only during pregnancy.  - Type 1 diabetes is caused by a lack of insulin due to the destruction of insulin-producing beta cells. In type 1 diabetesan autoimmune diseasethe bodys immune system attacks and destroys the beta cells.  - Type 2 diabetesthe most common form of diabetesis caused by a combination of factors, including insulin resistance, a condition in which the bodys muscle, fat, and liver cells do not use insulin effectively. Type 2 diabetes develops when the body can no longer produce enough insulin to compensate for the impaired ability to use insulin.  - Scientists believe gestational diabetes is caused by the hormonal changes and metabolic demands of pregnancy together with genetic and environmental factors. Risk factors for gestational diabetes include being overweight and having a family history of diabetes.  - Monogenic forms of diabetes are relatively uncommon and are caused by mutations in single genes that limit insulin production, quality, or action in the body.  - Other types of diabetes are caused by diseases and injuries that damage the pancreas; certain chemical toxins and medications; infections; and other conditions."}
{"_id":"068d492b-0ca2-492f-ae31-5c79a94ff37c","text":"Urinary retention is the inability to empty the bladder completely. Urinary retention can be acute or chronic. Acute urinary retention happens suddenly and lasts only a short time. People with acute urinary retention cannot urinate at all, even though they have a full bladder. Acute urinary retention, a potentially life-threatening medical condition, requires immediate emergency treatment. Acute urinary retention can cause great discomfort or pain.\n                \nChronic urinary retention can be a long-lasting medical condition. People with chronic urinary retention can urinate. However, they do not completely empty all of the urine from their bladders. Often people are not even aware they have this condition until they develop another problem, such as urinary incontinenceloss of bladder control, resulting in the accidental loss of urineor a urinary tract infection (UTI), an illness caused by harmful bacteria growing in the urinary tract."}
{"_id":"087d73c9-57d5-4510-9f4a-05d2f25b5fea","text":"The urinary tract is the bodys drainage system for removing urine, which is composed of wastes and extra fluid. In order for normal urination to occur, all body parts in the urinary tract need to work together in the correct order.\n                \nKidneys. The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine. The kidneys work around the clock; a person does not control what they do.\n                \nUreters. Ureters are the thin tubes of muscleone on each side of the bladderthat carry urine from each of the kidneys to the bladder.\n                \nBladder. The bladder, located in the pelvis between the pelvic bones, is a hollow, muscular, balloon-shaped organ that expands as it fills with urine. Although a person does not control kidney function, a person does control when the bladder empties. Bladder emptying is known as urination. The bladder stores urine until the person finds an appropriate time and place to urinate. A normal bladder acts like a reservoir and can hold 1.5 to 2 cups of urine. How often a person needs to urinate depends on how quickly the kidneys produce the urine that fills the bladder. The muscles of the bladder wall remain relaxed while the bladder fills with urine. As the bladder fills to capacity, signals sent to the brain tell a person to find a toilet soon. During urination, the bladder empties through the urethra, located at the bottom of the bladder.\n                \nThree sets of muscles work together like a dam, keeping urine in the bladder.\n                \nThe first set is the muscles of the urethra itself. The area where the urethra joins the bladder is the bladder neck. The bladder neck, composed of the second set of muscles known as the internal sphincter, helps urine stay in the bladder. The third set of muscles is the pelvic floor muscles, also referred to as the external sphincter, which surround and support the urethra.\n                \nTo urinate, the brain signals the muscular bladder wall to tighten, squeezing urine out of the bladder. At the same time, the brain signals the sphincters to relax. As the sphincters relax, urine exits the bladder through the urethra."}
{"_id":"2850a351-1a18-46d4-8300-152ae088040d","text":"Urinary retention can result from\n                \n- obstruction of the urethra  - nerve problems  - medications  - weakened bladder muscles\n                \nObstruction of the Urethra\n                \nObstruction of the urethra causes urinary retention by blocking the normal urine flow out of the body. Conditions such as benign prostatic hyperplasiaalso called BPHurethral stricture, urinary tract stones, cystocele, rectocele, constipation, and certain tumors and cancers can cause an obstruction.\n                \nBenign prostatic hyperplasia. For men in their 50s and 60s, urinary retention is often caused by prostate enlargement due to benign prostatic hyperplasia. Benign prostatic hyperplasia is a medical condition in which the prostate gland is enlarged and not cancerous. The prostate is a walnut-shaped gland that is part of the male reproductive system. The gland surrounds the urethra at the neck of the bladder. The bladder neck is the area where the urethra joins the bladder. The prostate goes through two main periods of growth. The first occurs early in puberty, when the prostate doubles in size. The second phase of growth begins around age 25 and continues during most of a mans life. Benign prostatic hyperplasia often occurs with the second phase of growth.\n                \nAs the prostate enlarges, the gland presses against and pinches the urethra. The bladder wall becomes thicker. Eventually, the bladder may weaken and lose the ability to empty completely, leaving some urine in the bladder.\n                \nMore information is provided in the NIDDK health topic, Prostate Enlargement: Benign Prostatic Hyperplasia.\n                \nUrethral stricture. A urethral stricture is a narrowing or closure of the urethra. Causes of urethral stricture include inflammation and scar tissue from surgery, disease, recurring UTIs, or injury. In men, a urethral stricture may result from prostatitis, scarring after an injury to the penis or perineum, or surgery for benign prostatic hyperplasia and prostate cancer. Prostatitis is a frequently painful condition that involves inflammation of the prostate and sometimes the areas around the prostate. The perineum is the area between the anus and the sex organs. Since men have a longer urethra than women, urethral stricture is more common in men than women.1\n                \nMore information is provided in the NIDDK health topic, Prostatitis: Inflammation of the Prostate.\n                \nSurgery to correct pelvic organ prolapse, such as cystocele and rectocele, and urinary incontinence can also cause urethral stricture. The urethral stricture often gets better a few weeks after surgery.\n                \nUrethral stricture and acute or chronic urinary retention may occur when the muscles surrounding the urethra do not relax. This condition happens mostly in women.\n                \nUrinary tract stones. Urinary tract stones develop from crystals that form in the urine and build up on the inner surfaces of the kidneys, ureters, or bladder. The stones formed or lodged in the bladder may block the opening to the urethra.\n                \nCystocele. A cystocele is a bulging of the bladder into the vagina. A cystocele occurs when the muscles and supportive tissues between a womans bladder and vagina weaken and stretch, letting the bladder sag from its normal position and bulge into the vagina. The abnormal position of the bladder may cause it to press against and pinch the urethra.\n                \nMore information is provided in the NIDDK health topic, Cystocele.\n                \nRectocele. A rectocele is a bulging of the rectum into the vagina. A rectocele occurs when the muscles and supportive tissues between a womans rectum and vagina weaken and stretch, letting the rectum sag from its normal position and bulge into the vagina. The abnormal position of the rectum may cause it to press against and pinch the urethra.\n                \nConstipation. Constipation is a condition in which a person has fewer than three bowel movements a week or has bowel movements with stools that are hard, dry, and small, making them painful or difficult to pass. A person with constipation may feel bloated or have pain in the abdomen the area between the chest and hips. Some people with constipation often have to strain to have a bowel movement. Hard stools in the rectum may push against the bladder and urethra, causing the urethra to be pinched, especially if a rectocele is present.\n                \nMore information is provided in the NIDDK health topic, Constipation.\n                \nTumors and cancers. Tumors and cancerous tissues in the bladder or urethra can gradually expand and obstruct urine flow by pressing against and pinching the urethra or by blocking the bladder outlet. Tumors may be cancerous or noncancerous.\n                \nNerve Problems\n                \nUrinary retention can result from problems with the nerves that control the bladder and sphincters. Many events or conditions can interfere with nerve signals between the brain and the bladder and sphincters. If the nerves are damaged, the brain may not get the signal that the bladder is full. Even when a person has a full bladder, the bladder muscles that squeeze urine out may not get the signal to push, or the sphincters may not get the signal to relax. People of all ages can have nerve problems that interfere with bladder function. Some of the most common causes of nerve problems include\n                \n- vaginal childbirth  - brain or spinal cord infections or injuries  - diabetes  - stroke  - multiple sclerosis  - pelvic injury or trauma  - heavy metal poisoning\n                \nIn addition, some children are born with defects that affect the coordination of nerve signals among the bladder, spinal cord, and brain. Spina bifida and other birth defects that affect the spinal cord can lead to urinary retention in newborns.\n                \nMore information is provided in the NIDDK health topics, Nerve Disease and Bladder Control and Urine Blockage in Newborns.\n                \nMany patients have urinary retention right after surgery. During surgery, anesthesia is often used to block pain signals in the nerves, and fluid is given intravenously to compensate for possible blood loss. The combination of anesthesia and intravenous (IV) fluid may result in a full bladder with impaired nerve function, causing urinary retention. Normal bladder nerve function usually returns once anesthesia wears off. The patient will then be able to empty the bladder completely.\n                \nMedications\n                \nVarious classes of medications can cause urinary retention by interfering with nerve signals to the bladder and prostate. These medications include\n                \n- antihistamines to treat allergies      - cetirizine (Zyrtec)    - chlorpheniramine (Chlor-Trimeton)    - diphenhydramine (Benadryl)    - fexofenadine (Allegra)    - anticholinergics\/antispasmodics to treat stomach cramps, muscle spasms, and urinary incontinence      - hyoscyamine (Levbid)    - oxybutynin (Ditropan)    - propantheline (Pro-Banthine)    - tolterodine (Detrol)    - tricyclic antidepressants to treat anxiety and depression      - amitriptyline (Elavil)    - doxepin (Adapin)    - imipramine (Tofranil)    - nortriptyline (Pamelor)\n                \nOther medications associated with urinary retention include\n                \n- decongestants      - ephedrine    - phenylephrine    - pseudoephedrine    - nifedipine (Procardia), a medication to treat high blood pressure and chest pain  - carbamazepine (Tegretol), a medication to control seizures in people with epilepsy  - cyclobenzaprine (Flexeril), a muscle relaxant medication  - diazepam (Valium), a medication used to relieve anxiety, muscle spasms, and seizures  - nonsteroidal anti-inflammatory drugs  - amphetamines  - opioid analgesics\n                \nOver-the-counter cold and allergy medications that contain decongestants, such as pseudoephedrine, and antihistamines, such as diphenhydramine, can increase symptoms of urinary retention in men with prostate enlargement.\n                \nWeakened Bladder Muscles\n                \nAging is a common cause of weakened bladder muscles. Weakened bladder muscles may not contract strongly enough or long enough to empty the bladder completely, resulting in urinary retention."}
{"_id":"1423f97a-781e-49bc-8128-b105a49c9d1c","text":"Urinary retention in men becomes more common with age.\n                \n- In men 40 to 83 years old, the overall incidence of urinary retention is 4.5 to 6.8 per 1,000 men.2  - For men in their 70s, the overall incidence increases to 100 per 1,000 men.2  - For men in their 80s, the incidence of acute urinary retention is 300 per 1,000 men.2\n                \nUrinary retention in women is less common, though not rare.3 The incidence of urinary retention in women has not been well studied because researchers have primarily thought of urinary retention as a mans problem related to the prostate.4"}
{"_id":"690218cb-cca4-49b6-8a03-5c64ab49b794","text":"The symptoms of acute urinary retention may include the following and require immediate medical attention:\n                \n- inability to urinate  - painful, urgent need to urinate  - pain or discomfort in the lower abdomen  - bloating of the lower abdomen\n                \nThe symptoms of chronic urinary retention may include\n                \n- urinary frequencyurination eight or more times a day  - trouble beginning a urine stream  - a weak or an interrupted urine stream  - an urgent need to urinate with little success when trying to urinate  - feeling the need to urinate after finishing urination  - mild and constant discomfort in the lower abdomen and urinary tract\n                \nSome people with chronic urinary retention may not have symptoms that lead them to seek medical care. People who are unaware they have chronic urinary retention may have a higher chance of developing complications.\n                \n\n                \nWhen to Seek Medical Care   A person who has any of the following symptoms should see a health care provider right away:   - complete inability to urinate   - great discomfort or pain in the lower abdomen and urinary tract"}
{"_id":"08d0558d-b5e6-40e9-bdd9-f80d18f55c50","text":"A health care provider diagnoses acute or chronic urinary retention with\n                \n- a physical exam  - postvoid residual measurement\n                \nA health care provider may use the following medical tests to help determine the cause of urinary retention:\n                \n- cystoscopy  - computerized tomography (CT) scans  - urodynamic tests  - electromyography\n                \nPhysical Exam\n                \nA health care provider may suspect urinary retention because of a patients symptoms and, therefore, perform a physical exam of the lower abdomen. The health care provider may be able to feel a distended bladder by lightly tapping on the lower belly.\n                \nPostvoid Residual Measurement\n                \nThis test measures the amount of urine left in the bladder after urination. The remaining urine is called the postvoid residual. A specially trained technician performs an ultrasound, which uses harmless sound waves to create a picture of the bladder, to measure the postvoid residual. The technician performs the bladder ultrasound in a health care providers office, a radiology center, or a hospital, and a radiologista doctor who specializes in medical imaginginterprets the images. The patient does not need anesthesia.\n                \nA health care provider may use a cathetera thin, flexible tubeto measure postvoid residual. The health care provider inserts the catheter through the urethra into the bladder, a procedure called catheterization, to drain and measure the amount of remaining urine. A postvoid residual of 100 mL or more indicates the bladder does not empty completely. A health care provider performs this test during an office visit. The patient often receives local anesthesia.\n                \nMedical Tests\n                \nCystoscopy. Cystoscopy is a procedure that requires a tubelike instrument, called a cystoscope, to look inside the urethra and bladder. A health care provider performs cystoscopy during an office visit or in an outpatient center or a hospital. The patient will receive local anesthesia. However, in some cases, the patient may receive sedation and regional or general anesthesia. A health care provider may use cystoscopy to diagnose urethral stricture or look for a bladder stone blocking the opening of the urethra.\n                \nMore information is provided in the NIDDK health topic, Cystoscopy and Ureteroscopy.\n                \nCT scans. CT scans use a combination of x rays and computer technology to create images. For a CT scan, a health care provider may give the patient a solution to drink and an injection of a special dye, called contrast medium. CT scans require the patient to lie on a table that slides into a tunnel-shaped device where a technician takes the x rays. An x-ray technician performs the procedure in an outpatient center or a hospital, and a radiologist interprets the images. The patient does not need anesthesia. A health care provider may give infants and children a sedative to help them fall asleep for the test. CT scans can show\n                \n- urinary tract stones  - UTIs  - tumors  - traumatic injuries  - abnormal, fluid-containing sacs called cysts\n                \nUrodynamic tests. Urodynamic tests include a variety of procedures that look at how well the bladder and urethra store and release urine. A health care provider may use one or more urodynamic tests to diagnose urinary retention. The health care provider will perform these tests during an office visit. For tests that use a catheter, the patient often receives local anesthesia.\n                \n- Uroflowmetry. Uroflowmetry measures urine speed and volume. Special equipment automatically measures the amount of urine and the flow ratehow fast urine comes out. Uroflowmetry equipment includes a device for catching and measuring urine and a computer to record the data. The equipment creates a graph that shows changes in flow rate from second to second so the health care provider can see the highest flow rate and how many seconds it takes to get there. A weak bladder muscle or blocked urine flow will yield an abnormal test result.  - Pressure flow study. A pressure flow study measures the bladder pressure required to urinate and the flow rate a given pressure generates. A health care provider places a catheter with a manometer into the bladder. The manometer measures bladder pressure and flow rate as the bladder empties. A pressure flow study helps diagnose bladder outlet obstruction.  - Video urodynamics. This test uses x rays or ultrasound to create real-time images of the bladder and urethra during the filling or emptying of the bladder. For x rays, a health care provider passes a catheter through the urethra into the bladder. He or she fills the bladder with contrast medium, which is visible on the video images. Video urodynamic images can show the size and shape of the urinary tract, the flow of urine, and causes of urinary retention, such as bladder neck obstruction.\n                \nMore information is provided in the NIDDK health topic, Urodynamic Testing.\n                \nElectromyography. Electromyography uses special sensors to measure the electrical activity of the muscles and nerves in and around the bladder and sphincters. A specially trained technician places sensors on the skin near the urethra and rectum or on a urethral or rectal catheter. The sensors record, on a machine, muscle and nerve activity. The patterns of the nerve impulses show whether the messages sent to the bladder and sphincters coordinate correctly. A technician performs electromyography in a health care providers office, an outpatient center, or a hospital. The patient does not need anesthesia if the technician uses sensors placed on the skin. The patient will receive local anesthesia if the technician uses sensors placed on a urethral or rectal catheter."}
{"_id":"4f116789-1a05-487b-8124-e8ea8a838088","text":"A health care provider treats urinary retention with\n                \n- bladder drainage  - urethral dilation  - urethral stents  - prostate medications  - surgery\n                \nThe type and length of treatment depend on the type and cause of urinary retention.\n                \nBladder Drainage\n                \nBladder drainage involves catheterization to drain urine. Treatment of acute urinary retention begins with catheterization to relieve the immediate distress of a full bladder and prevent bladder damage. A health care provider performs catheterization during an office visit or in an outpatient center or a hospital. The patient often receives local anesthesia. The health care provider can pass a catheter through the urethra into the bladder. In cases of a blocked urethra, he or she can pass a catheter directly through the lower abdomen, just above the pubic bone, directly into the bladder. In these cases, the health care provider will use anesthesia.\n                \nFor chronic urinary retention, the patient may require intermittentoccasional, or not continuousor long-term catheterization if other treatments do not work. Patients who need to continue intermittent catheterization will receive instruction regarding how to selfcatheterize to drain urine as necessary.\n                \nUrethral Dilation\n                \nUrethral dilation treats urethral stricture by inserting increasingly wider tubes into the urethra to widen the stricture. An alternative dilation method involves inflating a small balloon at the end of a catheter inside the urethra. A health care provider performs a urethral dilation during an office visit or in an outpatient center or a hospital. The patient will receive local anesthesia. In some cases, the patient will receive sedation and regional anesthesia.\n                \nUrethral Stents\n                \nAnother treatment for urethral stricture involves inserting an artificial tube, called a stent, into the urethra to the area of the stricture. Once in place, the stent expands like a spring and pushes back the surrounding tissue, widening the urethra. Stents may be temporary or permanent. A health care provider performs stent placement during an office visit or in an outpatient center or a hospital. The patient will receive local anesthesia. In some cases, the patient will receive sedation and regional anesthesia.\n                \nProstate Medications\n                \nMedications that stop the growth of or shrink the prostate or relieve urinary retention symptoms associated with benign prostatic hyperplasia include\n                \n- dutasteride (Avodart)  - finasteride (Proscar)\n                \nThe following medications relax the muscles of the bladder outlet and prostate to help relieve blockage:\n                \n- alfuzosin (Uroxatral)  - doxazosin (Cardura)  - silodosin (Rapaflo)  - tadalafil (Cialis)  - tamsulosin (Flomax)  - terazosin (Hytrin)\n                \nSurgery\n                \nProstate surgery. To treat urinary retention caused by benign prostatic hyperplasia, a urologista doctor who specializes in the urinary tractmay surgically destroy or remove enlarged prostate tissue by using the transurethral method. For transurethral surgery, the urologist inserts a catheter or surgical instruments through the urethra to reach the prostate. Removal of the enlarged tissue usually relieves the blockage and urinary retention caused by benign prostatic hyperplasia. A urologist performs some procedures on an outpatient basis. Some men may require a hospital stay. In some cases, the urologist will remove the entire prostate using open surgery. Men will receive general anesthesia and have a longer hospital stay than for other surgical procedures. Men will also have a longer rehabilitation period for open surgery.\n                \nMore information is provided in the NIDDK health topic, Prostate Enlargement: Benign Prostatic Hyperplasia.\n                \nInternal urethrotomy. A urologist can repair a urethral stricture by performing an internal urethrotomy. For this procedure, the urologist inserts a special catheter into the urethra until it reaches the stricture. The urologist then uses a knife or laser to make an incision that opens the stricture. The urologist performs an internal urethrotomy in an outpatient center or a hospital. The patient will receive general anesthesia.\n                \nCystocele or rectocele repair. Women may need surgery to lift a fallen bladder or rectum into its normal position. The most common procedure for cystocele and rectocele repair involves a urologist, who also specializes in the female reproductive system, making an incision in the wall of the vagina. Through the incision, the urologist looks for a defect or hole in the tissue that normally separates the vagina from the other pelvic organs. The urologist places stitches in the tissue to close up the defect and then closes the incision in the vaginal wall with more stitches, removing any extra tissue. These stitches tighten the layers of tissue that separate the organs, creating more support for the pelvic organs. A urologist or gynecologista doctor who specializes in the female reproductive systemperforms the surgery to repair a cystocele or rectocele in a hospital. Women will receive anesthesia.\n                \nTumor and cancer surgery. Removal of tumors and cancerous tissues in the bladder or urethra may reduce urethral obstruction and urinary retention."}
{"_id":"387092a2-9843-4a0a-8370-aace5298a222","text":"Complications of urinary retention and its treatments may include\n                \n- UTIs  - bladder damage  - kidney damage  - urinary incontinence after prostate, tumor, or cancer surgery\n                \nUTIs. Urine is normally sterile, and the normal flow of urine usually prevents bacteria from infecting the urinary tract. With urinary retention, the abnormal urine flow gives bacteria at the opening of the urethra a chance to infect the urinary tract.\n                \nBladder damage. If the bladder becomes stretched too far or for long periods, the muscles may be permanently damaged and lose their ability to contract.\n                \nKidney damage. In some people, urinary retention causes urine to flow backward into the kidneys. This backward flow, called reflux, may damage or scar the kidneys.\n                \nUrinary incontinence after prostate, tumor, or cancer surgery. Transurethral surgery to treat benign prostatic hyperplasia may result in urinary incontinence in some men. This problem is often temporary. Most men recover their bladder control in a few weeks or months after surgery. Surgery to remove tumors or cancerous tissue in the bladder, prostate, or urethra may also result in urinary incontinence."}
{"_id":"77cbd755-b161-47f6-9889-e834fb43da8a","text":"People can prevent urinary retention before it occurs by treating some of the potential causes. For example, men with benign prostatic hyperplasia should take prostate medications as prescribed by their health care provider. Men with benign prostatic hyperplasia should avoid medications associated with urinary retention, such as over-the-counter cold and allergy medications that contain decongestants. Women with mild cystocele or rectocele may prevent urinary retention by doing exercises to strengthen the pelvic muscles. In most cases, dietary and lifestyle changes will help prevent urinary retention caused by constipation. People whose constipation continues should see a health care provider.\n                \nMore information about exercises to strengthen the pelvic muscles is provided in the NIDDK health topic, Kegel Exercise Tips."}
{"_id":"67454039-b46d-4efb-9071-f6d6720953a6","text":"Researchers have not found that eating, diet, and nutrition play a role in causing or preventing urinary retention."}
{"_id":"fb8301a2-7f9e-430f-957a-6c028e781061","text":"- Urinary retention is the inability to empty the bladder completely.  - Urinary retention can be acute or chronic.  - Urinary retention can result from      - obstruction of the urethra    - nerve problems    - medications    - weakened bladder muscles    - The symptoms of acute urinary retention may include the following and require immediate medical attention:      - inability to urinate    - painful, urgent need to urinate    - pain or discomfort in the lower abdomen    - bloating of the lower abdomen    - The symptoms of chronic urinary retention may include      - urinary frequencyurination eight or more times a day    - trouble beginning a urine stream    - a weak or an interrupted urine stream    - an urgent need to urinate with little success when trying to urinate    - feeling the need to urinate after finishing urination    - mild and constant discomfort in the lower abdomen and urinary tract    - A health care provider diagnoses acute or chronic urinary retention with      - a physical exam    - postvoid residual measurement    - A health care provider may use the following medical tests to help determine the cause of urinary retention:      - cystoscopy    - computerized tomography (CT) scans    - urodynamic tests    - electromyography    - A health care provider treats urinary retention with      - bladder drainage    - urethral dilation    - urethral stents    - prostate medications    - surgery    - Complications of urinary retention and its treatments may include      - urinary tract infections (UTIs)    - bladder damage    - kidney damage    - urinary incontinence after prostate, tumor, or cancer surgery    - People can prevent urinary retention before it occurs by treating some of the potential causes."}
{"_id":"a796792b-9414-4f4c-acd3-97955d6602b2","text":"Proteinuriaalso called albuminuria or urine albuminis a condition in which urine contains an abnormal amount of protein. Albumin is the main protein in the blood. Proteins are the building blocks for all body parts, including muscles, bones, hair, and nails. Proteins in the blood also perform a number of important functions. They protect the body from infection, help blood clot, and keep the right amount of fluid circulating throughout the body.\n                \nAs blood passes through healthy kidneys, they filter out the waste products and leave in the things the body needs, like albumin and other proteins. Most proteins are too big to pass through the kidneys' filters into the urine. However, proteins from the blood can leak into the urine when the filters of the kidney, called glomeruli, are damaged.\n                \nProteinuria is a sign of chronic kidney disease (CKD), which can result from diabetes, high blood pressure, and diseases that cause inflammation in the kidneys. For this reason, testing for albumin in the urine is part of a routine medical assessment for everyone. Kidney disease is sometimes called renal disease. If CKD progresses, it can lead to end-stage renal disease (ESRD), when the kidneys fail completely. A person with ESRD must receive a kidney transplant or regular blood-cleansing treatments called dialysis."}
{"_id":"51ce861e-9fe0-4a31-8d2c-f39bff2a6e7b","text":"People with diabetes, hypertension, or certain family backgrounds are at risk for proteinuria. In the United States, diabetes is the leading cause of ESRD.1 In both type 1 and type 2 diabetes, albumin in the urine is one of the first signs of deteriorating kidney function. As kidney function declines, the amount of albumin in the urine increases.\n                \nAnother risk factor for developing proteinuria is hypertension, or high blood pressure. Proteinuria in a person with high blood pressure is an indicator of declining kidney function. If the hypertension is not controlled, the person can progress to full kidney failure.\n                \nAfrican Americans are more likely than Caucasians to have high blood pressure and to develop kidney problems from it, even when their blood pressure is only mildly elevated. In fact, African Americans are six times more likely than Caucasians to develop hypertension-related kidney failure.2\n                \nOther groups at risk for proteinuria are American Indians, Hispanics\/Latinos, Pacific Islander Americans, older adults, and overweight people. These at-risk groups and people who have a family history of kidney disease should have their urine tested regularly."}
{"_id":"245edd98-06f0-4793-af4a-9aa5ce323abc","text":"Proteinuria has no signs or symptoms in the early stages. Large amounts of protein in the urine may cause it to look foamy in the toilet. Also, because protein has left the body, the blood can no longer soak up enough fluid, so swelling in the hands, feet, abdomen, or face may occur. This swelling is called edema. These are signs of large protein loss and indicate that kidney disease has progressed. Laboratory testing is the only way to find out whether protein is in a persons urine before extensive kidney damage occurs.\n                \nSeveral health organizations recommend regular urine checks for people at risk for CKD. A 1996 study sponsored by the National Institutes of Health determined that proteinuria is the best predictor of progressive kidney failure in people with type 2 diabetes. The American Diabetes Association recommends regular urine testing for proteinuria for people with type 1 or type 2 diabetes. The National Kidney Foundation recommends that routine checkups include testing for excess protein in the urine, especially for people in high-risk groups."}
{"_id":"8aa2012d-475b-4b46-a133-03947b0bc041","text":"Until recently, an accurate protein measurement required a 24-hour urine collection. In a 24-hour collection, the patient urinates into a container, which is kept refrigerated between trips to the bathroom. The patient is instructed to begin collecting urine after the first trip to the bathroom in the morning. Every drop of urine for the rest of the day is to be collected in the container. The next morning, the patient adds the first urination after waking and the collection is complete.\n                \nIn recent years, researchers have found that a single urine sample can provide the needed information. In the newer technique, the amount of albumin in the urine sample is compared with the amount of creatinine, a waste product of normal muscle breakdown. The measurement is called a urine albumin-to-creatinine ratio (UACR). A urine sample containing more than 30 milligrams of albumin for each gram of creatinine (30 mg\/g) is a warning that there may be a problem. If the laboratory test exceeds 30 mg\/g, another UACR test should be done 1 to 2 weeks later. If the second test also shows high levels of protein, the person has persistent proteinuria, a sign of declining kidney function, and should have additional tests to evaluate kidney function."}
{"_id":"1961557d-7a03-4f44-91e9-1000d03697fa","text":"Tests that measure the amount of creatinine in the blood will show whether a persons kidneys are removing wastes efficiently. Having too much creatinine in the blood is a sign that a person has kidney damage. The doctor can use the creatinine measurement to estimate how efficiently the kidneys are filtering the blood. This calculation is called the estimated glomerular filtration rate, or eGFR. CKD is present when the eGFR is less than 60 milliliters per minute (mL\/min)."}
{"_id":"345832ca-a42f-4f38-9545-620ee016be2f","text":"- Proteinuria is a condition in which urine contains a detectable amount of protein.  - Proteinuria is a sign of chronic kidney disease (CKD).  - Groups at risk for proteinuria include African Americans, American Indians, Hispanics\/Latinos, Pacific Islander Americans, older people, overweight people, people with diabetes or hypertension, and people who have a family history of kidney disease.  - Proteinuria may have no signs or symptoms. Laboratory testing is the only way to find out whether protein is in a person's urine.  - Several health organizations recommend regular checks for proteinuria so kidney disease can be detected and treated before it progresses.  - A person with diabetes, hypertension, or both should work to control blood glucose and blood pressure."}
{"_id":"0f387c0d-0963-42ad-b7a5-24c3db65e78e","text":"Nephrotic syndrome is a collection of symptoms that indicate kidney damage. Nephrotic syndrome includes the following:\n                \n- proteinurialarge amounts of protein in the urine  - hyperlipidemiahigher than normal fat and cholesterol levels in the blood  - edema, or swelling, usually in the legs, feet, or ankles and less often in the hands or face  - hypoalbuminialow levels of albumin in the blood\n                \nAlbumin is a protein that acts like a sponge, drawing extra fluid from the body into the bloodstream where it remains until removed by the kidneys. When albumin leaks into the urine, the blood loses its capacity to absorb extra fluid from the body, causing edema.\n                \nNephrotic syndrome results from a problem with the kidneys filters, called glomeruli. Glomeruli are tiny blood vessels in the kidneys that remove wastes and excess fluids from the blood and send them to the bladder as urine.\n                \nAs blood passes through healthy kidneys, the glomeruli filter out the waste products and allow the blood to retain cells and proteins the body needs. However, proteins from the blood, such as albumin, can leak into the urine when the glomeruli are damaged. In nephrotic syndrome, damaged glomeruli allow 3 grams or more of protein to leak into the urine when measured over a 24-hour period, which is more than 20 times the amount that healthy glomeruli allow."}
{"_id":"2ace57ff-b08f-4823-a2db-840f3cdd82dc","text":"Nephrotic syndrome can be caused by diseases that affect only the kidneys, such as focal segmental glomerulosclerosis (FSGS) or membranous nephropathy. Diseases that affect only the kidneys are called primary causes of nephrotic syndrome. The glomeruli are usually the targets of these diseases for reasons that are not fully understood. In FSGSthe most common primary cause of nephrotic syndromescar tissue forms in parts of the glomeruli. In membranous nephropathy, immune molecules form harmful deposits on the glomeruli.\n                \nNephrotic syndrome can also be caused by systemic diseases, which are diseases that affect many parts of the body, such as diabetes or lupus. Systemic diseases that affect the kidneys are called secondary causes of nephrotic syndrome. More than 50 percent of nephrotic syndrome cases in adults have secondary causes, with diabetes being the most common.1"}
{"_id":"0db55369-b4b3-44b1-b358-7b82a0c00aea","text":"In addition to proteinuria, hyperlipidemia, edema, and hypoalbumina, people with nephrotic syndrome may experience\n                \n- weight gain  - fatigue  - foamy urine  - loss of appetite"}
{"_id":"cf3b86a6-cb50-421c-833d-9f1cb360d1e9","text":"The loss of different proteins from the body can lead to a variety of complications in people with nephrotic syndrome. Blood clots can form when proteins that normally prevent them are lost through the urine. Blood clots can block the flow of blood and oxygen through a blood vessel. Loss of immunoglobulinsimmune system proteins that help fight disease and infectionleads to an increased risk of infections. These infections include pneumonia, a lung infection; cellulitis, a skin infection; peritonitis, an abdominal infection; and meningitis, a brain and spine infection. Medications given to treat nephrotic syndrome can also increase the risk of these infections. Other complications of nephrotic syndrome include\n                \n- hypothyroidisma condition in which the thyroid gland does not produce enough thyroid hormone to meet the bodys needs  - anemiaa condition in which red blood cells are fewer or smaller than normal, which means less oxygen is carried to the bodys cells  - coronary artery disease, also called coronary heart diseaseheart disease caused by narrowing of the arteries that supply blood to the heart  - high blood pressure, also called hypertensiona condition in which blood flows through the blood vessels with a force greater than normal  - acute kidney injurysudden and temporary loss of kidney function"}
{"_id":"47e40f38-4676-43c6-bf43-08f20607fcb1","text":"Urine samples are taken to diagnose people suspected of having nephrotic syndrome.\n                \nNephrotic syndrome is diagnosed when large amounts of protein are found in the urine. The blood protein albumin makes up much of the protein that is lost, though many other important proteins are also lost in nephrotic syndrome.\n                \nThe presence of albumin in the urine can be detected with a dipstick test performed on a urine sample. The urine sample is collected in a special container in a health care providers office or commercial facility and can be tested in the same location or sent to a lab for analysis. For the test, a nurse or technician places a strip of chemically treated paper, called a dipstick, into the urine. Patches on the dipstick change color when protein is present in urine.\n                \nA more precise measurement is usually needed to confirm the diagnosis. Either a single urine sample or a 24-hour collection of urine can be sent to a lab for analysis. With the single urine sample, the lab measures both albumin and creatinine, a waste product of normal muscle breakdown. The comparison of the measurements is called a urine albumin-to-creatinine ratio. A urine sample containing more than 30 milligrams of albumin for each gram of creatinine may signal a problem. With a 24-hour collection of urine, the lab measures only the amount of albumin present. The single urine sample is easier to collect than the 24-hour sample and is usually sufficient to confirm diagnosis, though the 24-hour collection may be used in some cases.\n                \nOnce nephrotic syndrome is diagnosed, blood tests are usually needed to check for systemic diseases that may be causing the nephrotic syndrome and to find out how well the kidneys are working overall. A blood test involves drawing blood at a health care providers office or commercial facility and sending the sample to a lab for analysis.\n                \nThough blood tests can point toward systemic diseases, a kidney biopsy is usually needed to diagnose the specific underlying disease causing the nephrotic syndrome and to determine the best treatment. A kidney biopsy is a procedure that involves taking a piece of kidney tissue for examination with a microscope. Kidney biopsies are performed by a health care provider in a hospital with light sedation and local anesthetic. A biopsy is often not needed for a person with diabetes because the persons medical history and lab tests may be enough to diagnose the problem as being a result of diabetes."}
{"_id":"92a3d4cb-f7b7-4495-8bbf-0ac20aab5774","text":"Treating nephrotic syndrome includes addressing the underlying cause as well as taking steps to reduce high blood pressure, edema, high cholesterol, and the risks of infection. Treatment usually includes medications and changes in diet.\n                \nMedications that lower blood pressure can also significantly slow the progression of kidney disease causing nephrotic syndrome. Two types of blood pressure lowering medications, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), have proven effective in slowing the progression of kidney disease by reducing the pressure inside the glomeruli and thereby reducing proteinuria. Many people require two or more medications to control their blood pressure. In addition to an ACE inhibitor or an ARB, a diuretica medication that aids the kidneys in removing fluid from the bloodcan also be useful in helping to reduce blood pressure as well as edema. Beta blockers, calcium channel blockers, and other blood pressure medications may also be needed.\n                \nStatin medications may be given to lower cholesterol.\n                \nPeople with nephrotic syndrome should receive the pneumococcal vaccine, which helps protect against a bacterium that commonly causes infection, and yearly flu shots.\n                \nBlood thinning medications are usually only given to people with nephrotic syndrome who develop a blood clot; these medications are not used as a preventive measure.\n                \nNephrotic syndrome may go away once the underlying cause has been treated. More information about treating the underlying causes of nephrotic syndrome is provided in the NIDDK health topic, Glomerular Diseases."}
{"_id":"9239f5f7-23d8-43e3-94ef-895dfd964d74","text":"Eating, diet, and nutrition have not been shown to play a role in causing or preventing nephrotic syndrome in adults. For people who have developed nephrotic syndrome, limiting intake of dietary sodium, often from salt, and fluid may be recommended to help reduce edema. A diet low in saturated fat and cholesterol may also be recommended to help control hyperlipidemia."}
{"_id":"8060997a-35a8-4a23-8a43-e7805924cac2","text":"- Nephrotic syndrome includes the following:      - proteinurialarge amounts of protein in the urine    - hyperlipidemiahigher than normal fat and cholesterol levels in the blood    - edema, or swelling, usually in the legs, feet, or ankles and less often in the hands or face    - hypoalbuminialow levels albumin in the blood    - Primary causes of nephrotic syndrome are diseases that affect only the kidneys, such as focal segmental glomerulosclerosis (FSGS). Secondary causes of nephrotic syndrome are diseases that affect many parts of the body, such as diabetes.  - In addition to proteinuria, hyperlipidemia, edema, and hypoalbumina, people with nephrotic syndrome may experience      - weight gain    - fatigue    - foamy urine    - loss of appetite    - The loss of different proteins from the body can lead to a variety of complications in people with nephrotic syndrome.  - Treating nephrotic syndrome includes addressing the underlying cause and taking steps to reduce high blood pressure, edema, high cholesterol, and the risks of infection. Treatment usually includes medications and changes in diet."}
{"_id":"b16d5159-c3e8-4958-bc48-bdca7c958a46","text":"Diarrhea is frequent, loose, and watery bowel movements. Bowel movements, also called stools, are body wastes passed through the rectum and anus. Stools contain what is left after your digestive system absorbs nutrients and fluids from what you eat and drink. If your body does not absorb the fluids, or if your digestive system produces extra fluids, stools will be loose and watery. Loose stools contain more water, salts, and minerals and weigh more than solid stools.\n                \nDiarrhea that lasts a short time is called acute diarrhea. Acute diarrhea is a common problem and usually lasts only 1 or 2 days, but it may last longer. Diarrhea that lasts for at least 4 weeks is called chronic diarrhea. Chronic diarrhea symptoms may be continual or they may come and go.\n                \n*See the Pronunciation Guide for tips on how to say the words in bold type."}
{"_id":"5e0b46c3-cab4-4e8e-9775-6bcf28ca3604","text":"Causes of diarrhea include\n                \n- bacteria from contaminated food or water  - viruses that cause illnesses such as the flu  - parasites, which are tiny organisms found in contaminated food or water  - medicines such as antibiotics  - problems digesting certain foods  - diseases that affect the stomach, small intestine, or colon, such as Crohns disease  - problems with how the colon functions, caused by disorders such as irritable bowel syndrome\n                \nSometimes no cause can be found. As long as diarrhea goes away within 1 to 2 days, finding the cause is not usually necessary."}
{"_id":"7d95eb03-14c1-419c-8a6e-e24d27a67616","text":"In addition to passing frequent, loose stools, other possible symptoms include\n                \n- cramps or pain in the abdomenthe area between the chest and hips  - an urgent need to use the bathroom  - loss of bowel control\n                \nYou may feel sick to your stomach or become dehydrated. If a virus or bacteria is the cause of your diarrhea, you may have fever and chills and bloody stools.\n                \nDehydration\n                \nBeing dehydrated means your body does not have enough fluid to work properly. Every time you have a bowel movement, you lose fluids. Diarrhea causes you to lose even more fluids. You also lose salts and minerals such as sodium, chloride, and potassium. These salts and minerals affect the amount of water that stays in your body.\n                \nDehydration can be serious, especially for children, older adults, and people with weakened immune systems.\n                \nSigns of dehydration in adults are\n                \n- being thirsty  - urinating less often than usual  - having dark-colored urine  - having dry skin  - feeling tired  - feeling dizzy or fainting\n                \nSigns of dehydration in babies and young children are\n                \n- having a dry mouth and tongue  - crying without tears  - having no wet diapers for 3 hours or more  - having sunken eyes, cheeks, or soft spot in the skull  - having a high fever  - being more cranky or drowsy than usual\n                \nAlso, when people are dehydrated, their skin does not flatten back to normal right away after being gently pinched and released."}
{"_id":"f61447e5-b7eb-4baa-83b4-f6f034a764ae","text":"To find the cause of diarrhea, the health care provider may\n                \n- perform a physical exam  - ask about any medicines you are taking  - test your stool or blood to look for bacteria, parasites, or other signs of disease or infection  - ask you to stop eating certain foods to see whether your diarrhea goes away\n                \nIf you have chronic diarrhea, your health care provider may perform other tests to look for signs of disease."}
{"_id":"293f9a68-5b4b-4074-a808-1d931c945a9e","text":"Diarrhea is treated by replacing lost fluids, salts, and minerals to prevent dehydration.\n                \nTaking medicine to stop diarrhea can be helpful in some cases. Medicines you can buy over the counter without a prescription include loperamide (Imodium) and bismuth subsalicylate (Pepto-Bismol, Kaopectate). Stop taking these medicines if symptoms get worse or if the diarrhea lasts more than 2 days. If you have bloody diarrhea, you should not use over-the-counter diarrhea medicines. These medicines may make diarrhea last longer. The health care provider will usually prescribe antibiotics instead.\n                \nOver-the-counter medicines for diarrhea may be dangerous for babies and children. Talk with the health care provider before giving your child these medicines."}
{"_id":"c71a7e16-c05f-4c3f-85c2-88d601a07963","text":"To prevent dehydration when you have diarrhea, it is important to drink plenty of water, but you also need to drink fluids that contain sodium, chloride, and potassium.\n                \n- Adults should drink water, fruit juices, sports drinks, sodas without caffeine, and salty broths.  - Children should drink oral rehydration solutionsspecial drinks that contain salts and minerals to prevent dehydration. These drinks include Pedialyte, Naturalyte, Infalyte, and CeraLyte. These drinks are sold in most grocery stores and drugstores.\n                \n- bananas  - plain rice  - boiled potatoes  - toast  - crackers  - cooked carrots  - baked chicken without the skin or fat\n                \nIf a certain food is the cause of diarrhea, try to avoid it.\n                \n- drinks with caffeine, such as coffee and cola  - high-fat or greasy foods, such as fried foods  - foods with a lot of fiber, such as citrus fruits  - sweet foods, such as cakes and cookies\n                \nDuring or after an episode of diarrhea, some people have trouble digesting lactose, the sugar in milk and milk products. However, you may be able to digest yogurt. Eating yogurt with active, live bacterial cultures may even help you feel better faster.\n                \nWhen babies have diarrhea, continue breastfeeding or formula feeding as usual.\n                \nAfter you have had diarrhea caused by a virus, problems digesting lactose may last up to 4 to 6 weeks. You may have diarrhea for a short time after you eat or drink milk or milk products."}
{"_id":"88f7de8e-8d41-4917-bd5e-1d4ec5909e7d","text":"Two types of diarrhea can be preventedrotavirus diarrhea and travelers diarrhea.\n                \nRotavirus Diarrhea\n                \nTwo vaccines, RotaTeq and Rotarix, protect against rotavirusa common virus that causes diarrhea in babies and children. RotaTeq is given to babies in three doses at 2, 4, and 6 months of age. Rotarix is given in two doses. The first dose is given when the baby is 6 weeks old, and the second is given at least 4 weeks later but before the baby is 24 weeks old. To learn more about rotavirus vaccines, talk with your childs health care provider. You can also find more information at the Centers for Disease Control and Prevention rotavirus vaccination webpage at www.cdc.gov\/vaccines\/vpd-vac\/rotavirus.\n                \nRotaTeq and Rotarix only prevent diarrhea caused by rotavirus. Children who have been vaccinated may still get diarrhea from another cause.\n                \nTravelers Diarrhea\n                \n\n                \nPeople may develop travelers diarrhea while visiting developing areas of the world such as Latin America, Africa, and southern Asia. Travelers diarrhea is caused by eating food or drinking water that contains harmful bacteria, viruses, or parasites.\n                \nYou can prevent travelers diarrhea by being careful:\n                \n- Do not drink tap water, use tap water to brush your teeth, or use ice cubes made from tap water.  - Do not eat or drink unpasteurized milk or milk products.  - Do not eat raw fruits and vegetables unless they can be peeled and you peel them yourself.  - Do not eat raw or rare meat and fish.  - Do not eat meat or shellfish that is not hot when served to you.  - Do not eat food sold by street vendors.\n                \nYou can drink bottled water, carbonated soft drinks, and hot drinks such as coffee and tea.\n                \nBefore traveling outside the United States, talk with your health care provider. Your health care provider may suggest taking medicine with you. In some cases, taking antibiotics before traveling can help prevent travelers diarrhea. And early treatment with antibiotics can shorten an episode of travelers diarrhea."}
{"_id":"8e93f32e-30b3-41bc-9546-f33eb5c86ae6","text":"- Diarrhea is frequent, loose, and watery bowel movements.  - Acute diarrhea is a common problem. It usually lasts only 1 or 2 days, but it may last longer.  - Being dehydrated means your body does not have enough fluid to work properly. Dehydration can be serious, especially for children, older adults, and people with weakened immune systems.  - Diarrhea is treated by replacing lost fluids, salts, and minerals.  - See your health care provider if you have signs of dehydration, diarrhea for more than 2 days, severe pain in your abdomen or rectum, a fever of 102 degrees or higher, stools containing blood or pus, or stools that are black and tarry.  - Take your child to a health care provider right away if your child has signs of dehydration, diarrhea for more than 24 hours, a fever of 102 degrees or higher, stools containing blood or pus, or stools that are black and tarry.  - Two types of diarrhea can be prevented rotavirus diarrhea and travelers diarrhea."}
{"_id":"d6a059a9-b813-4eb6-a49e-1785903f0d8c","text":"Alagille syndrome is a genetic condition that results in various symptoms in different parts of the body, including the liver. A person with Alagille syndrome has fewer than the normal number of small bile ducts inside the liver. The liver is the organ in the abdomenthe area between the chest and hipsthat makes blood proteins and bile, stores energy and nutrients, fights infection, and removes harmful chemicals from the blood.\n                \nBile ducts are tubes that carry bile from the liver cells to the gallbladder for storage and to the small intestine for use in digestion. Bile is fluid made by the liver that carries toxins and waste products out of the body and helps the body digest fats and the fat-soluble vitamins A, D, E, and K. In people with Alagille syndrome, the decreased number of bile ducts causes bile to build up in the liver, a condition also called cholestasis, leading to liver damage and liver disease."}
{"_id":"f83c892e-93b6-4a42-b000-a02a70c3ad73","text":"The digestive system is made up of the gastrointestinal (GI) tractalso called the digestive tractand the liver, pancreas, and gallbladder. The GI tract is a series of hollow organs joined in a long, twisting tube from the mouth to the anus. The hollow organs that make up the GI tract are the mouth, esophagus, stomach, small intestine, large intestinewhich includes the colon and rectumand anus. Food enters the mouth and passes to the anus through the hollow organs of the digestive system. The liver, pancreas, and gallbladder are the solid organs of the digestive system. The digestive system helps the body digest food."}
{"_id":"8863db95-9cdd-4262-9e3d-0c49d7e493d6","text":"Alagille syndrome is caused by a gene mutation, or defect. Genes provide instructions for making proteins in the body. A gene mutation is a permanent change in the DNA sequence that makes up a gene. DNA, or deoxyribonucleic acid, is the material inside cells that carries genetic information and passes genes from parent to child. Approximately 30 to 50 percent of people with Alagille syndrome have an inherited gene mutation, meaning it has been passed on by a parent. In the remaining cases, the gene mutation develops spontaneously.1 In spontaneous cases, neither parent carries a copy of the mutated gene.\n                \nMost cases of Alagille syndrome are caused by a mutation in the JAGGED1 (JAG1) gene. In less than 1 percent of cases, a mutation in the NOTCH2 gene is the cause.2\n                \n\n                \nGenetic Disorders   Each cell contains thousands of genes that provide the instructions for making proteins for growth and repair of the body. If a gene has a mutation, the protein made by that gene may not function properly, which sometimes creates a genetic disorder. Not all gene mutations cause a disorder.   People have two copies of most genes; one copy is inherited from each parent. A genetic disorder occurs when one or both parents pass a mutated gene to a child at conception. A genetic disorder can also occur through a spontaneous gene mutation, meaning neither parent carries a copy of the mutated gene. Once a spontaneous gene mutation has occurred in a person, it can be passed to the person's children.   Read more about genes and genetic conditions at the U.S. National Library of Medicine's (NLM's) Genetics Home Reference at www.ghr.nlm.nih.gov."}
{"_id":"4d3df789-f9c6-4638-99b7-1d3bdcca31a5","text":"Alagille syndrome occurs in about one of every 30,000 live births.3 The disorder affects both sexes equally and shows no geographical, racial, or ethnic preferences.\n                \nJAG1 and NOTCH2 gene mutations are inherited in an autosomal dominant way, which means a child can get Alagille syndrome by inheriting either of the gene mutations from only one parent. Each child of a parent with an autosomal dominant mutation has a 50 percent chance of inheriting the mutated gene.\n                \nThe following chart shows the chance of inheriting an autosomal dominant gene mutation:\n                \nThe gene mutations that cause Alagille syndrome may cause mild or subtle symptoms. Some people may not know they are affected, while others with the gene mutation may develop more serious characteristics of Alagille syndrome. A person with a gene mutation, whether showing serious symptoms or not, has Alagille syndrome and can pass the gene mutation to a child.\n                \nRead more about how genetic conditions are inherited at the NLM's Genetics Home Reference website at www.ghr.nlm.nih.gov."}
{"_id":"7794839f-e8d1-42c7-889f-b893204175cd","text":"The signs and symptoms of Alagille syndrome and their severity vary, even among people in the same family sharing the same gene mutation.\n                \nLiver\n                \nIn some people, problems in the liver may be the first signs and symptoms of the disorder. These signs and symptoms can occur in children and adults with Alagille syndrome, and in infants as early as the first 3 months of life.\n                \nJaundice. Jaundicewhen the skin and whites of the eyes turn yellowis a result of the liver not removing bilirubin from the blood. Bilirubin is a reddish-yellow substance formed when hemoglobin breaks down. Hemoglobin is an iron-rich protein that gives blood its red color. Bilirubin is absorbed by the liver, processed, and released into bile. Blockage of the bile ducts forces bilirubin and other elements of bile to build up in the blood.\n                \nJaundice may be difficult for parents and even health care providers to detect. Many healthy newborns have mild jaundice during the first 1 to 2 weeks of life due to an immature liver. This normal type of jaundice disappears by the second or third week of life, whereas the jaundice of Alagille syndrome deepens. Newborns with jaundice after 2 weeks of life should be seen by a health care provider to check for a possible liver problem.\n                \nDark urine and gray or white stools. High levels of bilirubin in the blood that pass into the urine can make the urine darker, while stool lightens from a lack of bilirubin reaching the intestines. Gray or white bowel movements after 2 weeks of age are a reliable sign of a liver problem and should prompt a visit to a health care provider.\n                \nPruritus. The buildup of bilirubin in the blood may cause itching, also called pruritus. Pruritus usually starts after 3 months of age and can be severe.\n                \nXanthomas. Xanthomas are fatty deposits that appear as yellow bumps on the skin. They are caused by abnormally high cholesterol levels in the blood, common in people with liver disease. Xanthomas may appear anywhere on the body. However, xanthomas are usually found on the elbows, joints, tendons, knees, hands, feet, or buttocks.\n                \nOther Signs and Symptoms of Alagille Syndrome\n                \nCertain signs of Alagille syndrome are unique to the disorder, including those that affect the vertebrae and facial features.\n                \nFace. Many children with Alagille syndrome have deep-set eyes, a straight nose, a small and pointed chin, large ears, and a prominent, wide forehead. These features are not usually recognized until after infancy. By adulthood, the chin is more prominent.\n                \nEyes. Posterior embryotoxon is a condition in which an opaque ring is present in the cornea, the transparent covering of the eyeball. The abnormality is common in people with Alagille syndrome, though it usually does not affect vision.\n                \nSkeleton. The most common skeletal defect in a person with Alagille syndrome is when the shape of the vertebraebones of the spinegives the appearance of flying butterflies. This defect, known as \"butterfly\" vertebrae, rarely causes medical problems or requires treatment.\n                \nHeart and blood vessels. People with Alagille syndrome may have the following signs and symptoms having to do with the heart and blood vessels:\n                \n- heart murmuran extra or unusual sound heard during a heartbeat. A heart murmur is the most common sign of Alagille syndrome other than the general symptoms of liver disease.1 Most people with Alagille syndrome have a narrowing of the blood vessels that carry blood from the heart to the lungs.1 This narrowing causes a murmur that can be heard with a stethoscope. Heart murmurs usually do not cause problems.  - heart walls and valve problems. A small number of people with Alagille syndrome have serious problems with the walls or valves of the heart. These conditions may need treatment with medications or corrective surgery.  - blood vessel problems. People with Alagille syndrome may have abnormalities of the blood vessels in the head and neck. This serious complication can lead to internal bleeding or stroke. Alagille syndrome can also cause narrowing or bulging of other blood vessels in the body.\n                \nKidney disease. A wide range of kidney diseases can occur in Alagille syndrome. The kidneys are two bean-shaped organs, each about the size of a fist, that filter wastes and extra fluid from the blood. Some people have small kidneys or have cystsfluid-filled sacsin the kidneys. Kidney function can also decrease."}
{"_id":"08eff129-5d0a-47ee-b3c3-f6ad9c806380","text":"The complications of Alagille syndrome include liver failure, portal hypertension, and growth problems. People with Alagille syndrome usually have a combination of complications, and may not have every complication listed below.\n                \nLiver failure. Over time, the decreased number of bile ducts may lead to chronic liver failure, also called end-stage liver disease. This condition progresses over months, years, or even decades. The liver can no longer perform important functions or effectively replace damaged cells. A person may need a liver transplant. A liver transplant is surgery to remove a diseased or an injured liver and replace it with a healthy whole liver or a segment of a liver from another person, called a donor.\n                \nPortal hypertension. The spleen is the organ that cleans blood and makes white blood cells. White blood cells attack bacteria and other foreign cells. Blood flow from the spleen drains directly into the liver. When a person with Alagille syndrome has advanced liver disease, the blood flow backs up into the spleen and other blood vessels. This condition is called portal hypertension. The spleen may become larger in the later stages of liver disease. A person with an enlarged spleen should avoid contact sports to protect the organ from injury. Advanced portal hypertension can lead to serious bleeding problems.\n                \nGrowth problems. Alagille syndrome can lead to poor growth in infants and children, as well as delayed puberty in older children. Liver disease can cause malabsorption, which can result in growth problems. Malabsorption is the inability of the small intestine to absorb nutrients from foods, which results in protein, calorie, and vitamin deficiencies. Serious heart problems, if present in Alagille syndrome, can also affect growth.\n                \nMalabsorption. People with Alagille syndrome may have diarrhealoose, watery stoolsdue to malabsorption. The condition occurs because bile is necessary for the digestion of food. Malabsorption can lead to bone fractures, eye problems, blood-clotting problems, and learning delays.\n                \nLong-term Outlook\n                \nThe long-term outlook for people with Alagille syndrome depends on several factors, including the severity of liver damage and heart problems. Predicting who will experience improved bile flow and who will progress to chronic liver failure is difficult. Ten to 30 percent of people with Alagille syndrome will eventually need a liver transplant.3\n                \nMany adults with Alagille syndrome whose symptoms improve with treatment lead normal, productive lives. Deaths in people with Alagille syndrome are most often caused by chronic liver failure, heart problems, and blood vessel problems."}
{"_id":"fa7f5524-83f0-43a4-8ceb-b4f31370cf2e","text":"A health care provider diagnoses Alagille syndrome by performing a thorough physical exam and ordering one or more of the following tests and exams:\n                \n- blood test  - urinalysis  - x ray  - abdominal ultrasound  - cardiology exam  - slit-lamp exam  - liver biopsy  - genetic testing\n                \nAlagille syndrome can be difficult to diagnose because the signs and symptoms vary and the syndrome is so rare.\n                \nFor a diagnosis of Alagille syndrome, three of the following symptoms typically should be present:\n                \n- liver symptoms, such as jaundice, pruritus, malabsorption, and xanthomas  - heart abnormalities or murmurs  - skeletal abnormalities  - posterior embryotoxon  - facial features typical of Alagille syndrome  - kidney disease  - blood vessel problems\n                \nA health care provider may perform a liver biopsy to diagnose Alagille syndrome; however, it is not necessary to make a diagnosis. A diagnosis can be made in a person who does not meet the clinical criteria of Alagille syndrome yet does have a gene mutation of JAG1. The health care provider may have a blood sample tested to look for the JAG1 gene mutation. The gene mutation can be identified in 94 percent of people with a diagnosis of Alagille syndrome.2\n                \nBlood test. A blood test involves drawing blood at a health care provider's office or a commercial facility and sending the sample to a lab for analysis. The blood test can show nutritional status and the presence of liver disease and kidney function.\n                \nUrinalysis. Urinalysis is the testing of a urine sample. The urine sample is collected in a special container in a health care provider's office or a commercial facility and can be tested in the same location or sent to a lab for analysis. Urinalysis can show many problems of the urinary tract and other body systems. The sample may be observed for color, cloudiness, or concentration; signs of drug use; chemical composition, including glucose; the presence of protein, blood cells, or bacteria; or other signs of disease.\n                \nX ray. An x ray is a picture created by using radiation and recorded on film or on a computer. The amount of radiation used is small. An x-ray technician performs the x ray at a hospital or an outpatient center, and a radiologista doctor who specializes in medical imaginginterprets the images. Anesthesia is not needed. The patient will lie on a table or stand during the x ray. The technician positions the x-ray machine over the spine area to look for \"butterfly\" vertebrae. The patient will hold his or her breath as the picture is taken so that the picture will not be blurry. The patient may be asked to change position for additional pictures.\n                \nAbdominal ultrasound. Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. The transducer can be moved to different angles to make it possible to examine different organs. In abdominal ultrasound, the health care provider applies a gel to the patient's abdomen and moves a handheld transducer over the skin. The gel allows the transducer to glide easily, and it improves the transmission of the signals. A specially trained technician performs the procedure in a health care provider's office, an outpatient center, or a hospital, and a radiologist interprets the images; anesthesia is not needed. The images can show an enlarged liver or rule out other conditions.\n                \nCardiology exam. A cardiologista doctor who treats people who have heart problemsperforms a cardiology exam in a health care provider's office, an outpatient center, or a hospital. During a full exam, a cardiologist may inspect the patient's physical appearance, measure pulse rate and blood pressure, observe the jugular vein, check for rapid or skipped heartbeats, listen for variations in heart sounds, and listen to the lungs.\n                \nSlit-lamp exam. An ophthalmologista doctor who diagnoses and treats all eye diseases and eye disordersperforms a slit-lamp exam to diagnose posterior embryotoxon. The ophthalmologist examines the eye with a slit lamp, a microscope combined with a high-intensity light that shines a thin beam on the eye. While sitting in a chair, the patient will rest his or her head on the slit lamp. A yellow dye may be used to examine the cornea and tear layer. The dye is applied as a drop, or the specialist may touch a strip of paper stained with the dye to the white of the patient's eye. The specialist will also use drops in the patient's eye to dilate the pupil.\n                \nLiver biopsy. A liver biopsy is a procedure that involves taking a piece of liver tissue for examination with a microscope for signs of damage or disease. The health care provider may ask the patient to stop taking certain medications temporarily before the liver biopsy. The patient may be asked to fast for 8 hours before the procedure.\n                \nDuring the procedure, the patient lies on a table, right hand resting above the head. A local anesthetic is applied to the area where the biopsy needle will be inserted. If needed, sedatives and pain medication are also given. The health care provider uses a needle to take a small piece of liver tissue. The health care provider may use ultrasound, computerized tomography scans, or other imaging techniques to guide the needle. After the biopsy, the patient should lie on the right side for up to 2 hours and is monitored an additional 2 to 4 hours before being sent home.\n                \nGenetic testing. The health care provider may refer a person suspected of having Alagille syndrome to a geneticista doctor who specializes in genetic disorders. For a genetic test, the geneticist takes a blood or saliva sample and analyzes the DNA for the JAG1 gene mutation. The geneticist tests for the JAG1 gene mutation first, since it is more common in Alagille syndrome than NOTCH2. Genetic testing is often done only by specialized labs. The results may not be available for several months because of the complexity of the testing.\n                \nThe usefulness of genetic testing for Alagille syndrome is limited by two factors:\n                \n- Detection of a mutated gene cannot predict the onset of symptoms or how serious the disorder will be.  - Even if a mutated gene is found, no specific cure for the disorder exists.\n                \n\n                \nWhen to Consider Genetic Counseling   People who are considering genetic testing may want to consult a genetics counselor. Genetic counseling can help family members understand how test results may affect them individually and as a family. Genetic counseling is provided by genetics professionalshealth care professionals with specialized degrees and experience in medical genetics and counseling. Genetics professionals include geneticists, genetics counselors, and genetics nurses.   Genetics professionals work as members of health care teams, providing information and support to individuals or families who have genetic disorders or a higher chance of having an inherited condition. Genetics professionals   - assess the likelihood of a genetic disorder by researching a family's history, evaluating medical records, and conducting a physical exam of the patient and other family members   - weigh the medical, social, and ethical decisions surrounding genetic testing   - provide support and information to help a person make a decision about testing   - interpret the results of genetic tests and medical data   - provide counseling or refer individuals and families to support services   - serve as patient advocates   - explain possible treatments or preventive measures   - discuss reproductive options    Genetic counseling may be useful when a family member is deciding whether to have genetic testing and again later when test results are available."}
{"_id":"57ba372d-c72b-4110-91cc-98769a9d49a1","text":"Treatment for Alagille syndrome includes medications and therapies that increase the flow of bile from the liver, promote growth and development in infants' and children's bodies, correct nutritional deficiencies, and reduce the person's discomfort. Ursodiol (Actigall, Urso) is a medication that increases bile flow. Other treatments address specific symptoms of the disorder.\n                \nLiver failure. People with Alagille syndrome who develop end-stage liver failure need a liver transplant with a whole liver from a deceased donor or a segment of a liver from a living donor. People with Alagille syndrome who also have heart problems may not be candidates for a transplant because they could be more likely to have complications during and after the procedure. A liver transplant surgical team performs the transplant in a hospital.\n                \nMore information is provided in the NIDDK health topic, Liver Transplantation.\n                \nPruritus. Itching may decrease when the flow of bile from the liver is increased. Medications such as cholestyramine (Prevalite), rifampin (Rifadin, Rimactane), naltrexone (Vivitrol), or antihistamines may be prescribed to relieve pruritus. People should hydrate their skin with moisturizers and keep their fingernails trimmed to prevent skin damage from scratching. People with Alagille syndrome should avoid baths and take short showers to prevent the skin from drying out.\n                \nIf severe pruritus does not improve with medication, a procedure called partial external biliary diversion may provide relief from itching. The procedure involves surgery to connect one end of the small intestine to the gallbladder and the other end to an opening in the abdomencalled a stomathrough which bile leaves the body and is collected in a pouch. A surgeon performs partial external biliary diversion in a hospital. The patient will need general anesthesia.\n                \nMalabsorption and growth problems. Infants with Alagille syndrome are given a special formula that helps the small intestine absorb much-needed fat. Infants, children, and adults can benefit from a high-calorie diet, calcium, and vitamins A, D, E, and K. They may also need additional zinc. If someone with Alagille syndrome does not tolerate oral doses of vitamins, a health care provider may give the person injections for a period of time. A child may receive additional calories through a tiny tube that is passed through the nose into the stomach. If extra calories are needed for a long time, a health care provider may place a tube, called a gastrostomy tube, directly into the stomach through a small opening made in the abdomen. A child's growth may improve with increased nutrition and flow of bile from the liver.\n                \nXanthomas. For someone who has Alagille syndrome, these fatty deposits typically worsen over the first few years of life and then improve over time. They may eventually disappear in response to partial external biliary diversion or the medications used to increase bile flow."}
{"_id":"3510293c-3d2b-46d4-a8ad-a14de1cbc848","text":"Scientists have not yet found a way to prevent Alagille syndrome. However, complications of the disorder can be managed with the help of health care providers. Routine visits with a health care team are needed to prevent complications from becoming worse."}
{"_id":"08842448-8b98-489d-8711-30bd78790d81","text":"Researchers have not found that eating, diet, and nutrition play a role in causing or preventing Alagille syndrome. However, these factors are important for people with Alagille syndrome, particularly children, who are malnourished, growing poorly, or have delayed puberty. Caregivers and parents of children with Alagille syndrome should try to maximize their children's potential for growth through good eating, diet, and nutrition.\n                \nA nutritionist or a dietitiana person with training in nutrition and dietcan work with someone with Alagille syndrome and his or her health care team to build an appropriate healthy eating plan. A person with Alagille syndrome may need to take dietary supplements or vitamins in addition to eating a set number of calories, based on the type of complications the person has. Researchers consider good nutrition to be one of the most important aspects of managing the disorder.\n                \nIf potential liver problems are present, a person with Alagille syndrome should not drink alcoholic beverages without talking with his or her health care provider first.\n                \nAdditionally, eating, diet, and nutrition play a part in overall health and preventing further health problems."}
{"_id":"cf1ee1df-6d25-4581-9f5e-7dc37987a0ed","text":"- Alagille syndrome is a genetic condition that results in various symptoms in different parts of the body, including the liver.  - A person with Alagille syndrome has fewer than the normal number of small bile ducts inside the liver.  - In people with Alagille syndrome, the decreased number of bile ducts causes bile to build up in the liver, a condition also called cholestasis, leading to liver damage and liver disease.  - Alagille syndrome is caused by a gene mutation, or defect. Approximately 30 to 50 percent of people with Alagille syndrome have an inherited gene mutation, meaning it has been passed on by a parent.  - Alagille syndrome occurs in about one of every 30,000 live births. The disorder affects both sexes equally and shows no geographical, racial, or ethnic preferences.  - The gene mutations that cause Alagille syndrome may cause mild or subtle symptoms. Some people may not know they are affected.  - The signs and symptoms of Alagille syndrome and their severity vary, even among people in the same family sharing the same gene mutation.  - In some people, problems in the liver may be the first signs and symptoms of the disorder.  - The complications of Alagille syndrome include liver failure, portal hypertension, and growth problems.  - Ten to 30 percent of people with Alagille syndrome will eventually need a liver transplant.  - A health care provider diagnoses Alagille syndrome by performing a thorough physical exam and other tests.  - Genetic counseling can help family members understand how genetic test results may affect them individually and as a family.  - Treatment for Alagille syndrome includes medications and therapies that increase the flow of bile from the liver, promote growth and development in infants' and children's bodies, correct nutritional deficiencies, and reduce the person's discomfort.  - Scientists have not yet found a way to prevent Alagille syndrome.  - Caregivers and parents of children with Alagille syndrome should try to maximize their children's potential for growth through good eating, diet, and nutrition."}
{"_id":"77e1cb56-d08d-4356-a6c2-5482df878c6f","text":"Too much glucose in the blood for a long time can cause diabetes problems. This high blood glucose, also called blood sugar, can damage many parts of the body, such as the heart, blood vessels, eyes, and kidneys. Heart and blood vessel disease can lead to heart attacks and strokes, the leading causes of death for people with diabetes. You can do a lot to prevent or slow down diabetes problems.\n                \nThis booklet is about heart and blood vessel problems caused by diabetes. You will learn the things you can do each day and during each year to stay healthy and prevent diabetes problems."}
{"_id":"cbe87f50-ed6b-44ec-95e4-3e8822705559","text":"You can do a lot to prevent heart disease and stroke.\n                \n- Keep your blood glucose under control. You can see if your blood glucose is under control by having an A1C test at least twice a year. The A1C test tells you your average blood glucose for the past 2 to 3 months. The target for most people with diabetes is below 7. In some people with heart disease or other special circumstances, their doctor may recommend slightly higher levels of A1C.  - Keep your blood pressure under control. Have it checked at every doctor visit. The target for most people with diabetes is below 140\/80, unless their doctor sets a different target.  - Keep your cholesterol under control. Have it checked at least once a year. The targets for most people with diabetes are      - LDLbadcholesterol: below 100    - HDLgoodcholesterol: above 40 in men and above 50 in women    - triglyceridesanother type of fat in the blood: below 150    - Make sure the foods you eat are \"heart-healthy.\" Include foods high in fiber, such as oat bran, oatmeal, whole-grain breads and cereals, fruits, and vegetables. Cut back on foods high in saturated fat or cholesterol, such as meats, butter, dairy products with fat, eggs, shortening, lard, and foods with palm oil or coconut oil. Limit foods with trans fat, such as snack foods and commercial baked goods.  - If you smoke, quit. Your doctor can tell you about ways to help you quit smoking.  - Ask your doctor whether you should take an aspirin every day. Studies have shown that taking a low dose of aspirin every day can help reduce your risk of heart disease and stroke.  - Take your medicines as directed."}
{"_id":"259beb2d-b874-4897-a287-3a39b87d8f88","text":"You may have one or more of the following warning signs:\n                \n- chest pain or discomfort  - pain or discomfort in your arms, back, jaw, or neck  - indigestion or stomach pain  - shortness of breath  - sweating  - nausea  - light-headedness\n                \nOr, you may have no warning signs at all. Warning signs may come and go. If you have any of these warning signs, call 911 right away. Getting prompt treatment can reduce damage to the heart."}
{"_id":"c1f2b7ef-eccc-4d10-868a-12cc3409672d","text":"Narrowed blood vessels leave a smaller opening for blood to flow through. Having narrowed blood vessels is like turning on a garden hose and holding your thumb over the opening. The smaller opening makes the water shoot out with more pressure. In the same way, narrowed blood vessels lead to high blood pressure. Other factors, such as kidney problems and being overweight, also can lead to high blood pressure.\n                \nMany people with diabetes also have high blood pressure. If you have heart, eye, or kidney problems from diabetes, high blood pressure can make them worse.\n                \nYou will see your blood pressure written with two numbers separated by a slash. For example, your reading might be 120\/70, said as \"120 over 70.\" For most people with diabetes, the target is to keep the first number below 140 and the second number below 80, unless their doctor sets a different target.\n                \nIf you have high blood pressure, ask your doctor how to lower it. Your doctor may ask you to take blood pressure medicine every day. Some types of blood pressure medicine can also help keep your kidneys healthy.\n                \nYou may also be able to control your blood pressure by\n                \n- eating more fruits and vegetables  - eating less salt and high-sodium foods  - losing weight if you need to  - being physically active  - not smoking  - limiting alcoholic drinks"}
{"_id":"7e037937-5751-4da8-bdea-4a110648f256","text":"A stroke happens when part of your brain is not getting enough blood and stops working. Depending on the part of the brain that is damaged, a stroke can cause\n                \n- sudden weakness or numbness of your face, arm, or leg on one side of your body  - sudden confusion, trouble talking, or trouble understanding  - sudden dizziness, loss of balance, or trouble walking  - sudden trouble seeing in one or both eyes or sudden double vision  - sudden severe headache\n                \nSometimes, one or more of these warning signs may happen and then disappear. You might be having a \"mini-stroke,\" also called a TIA or a transient ischemic attack. If you have any of these warning signs, call 911 right away. Getting care for a TIA may reduce or prevent a stroke. Getting prompt treatment for a stroke can reduce the damage to the brain and improve chances for recovery."}
{"_id":"48ddb411-04bd-4d71-8637-7faf487b2dbc","text":"- Don't smoke.  - Keep blood glucose and blood pressure under control.  - Keep blood fats close to normal.  - Be physically active.  - Ask your doctor if you should take aspirin every day.\n                \nYou also may need surgery to treat PAD."}
{"_id":"5120b8f1-527e-4f32-b714-676d21b67d46","text":"Primary hyperparathyroidism is a disorder of the parathyroid glands, also called parathyroids. Primary means this disorder originates in the parathyroid glands. In primary hyperparathyroidism, one or more of the parathyroid glands are overactive. As a result, the gland releases too much parathyroid hormone (PTH). The disorder includes the problems that occur in the rest of the body as a result of too much PTHfor example, loss of calcium from bones.\n                \nIn the United States, about 100,000 people develop primary hyperparathyroidism each year.1 The disorder is diagnosed most often in people between age 50 and 60, and women are affected about three times as often as men.2\n                \nSecondary, or reactive, hyperparathyroidism can occur if a problem such as kidney failure causes the parathyroid glands to be overactive."}
{"_id":"769fb867-dd01-40c6-8e03-470e9f8127de","text":"The parathyroid glands are four pea-sized glands located on or near the thyroid gland in the neck. Occasionally, a person is born with one or more of the parathyroid glands in another location. For example, a gland may be embedded in the thyroid, in the thymusan immune system organ located in the chestor elsewhere around this area. In most such cases, however, the parathyroid glands function normally.\n                \nThe parathyroid glands are part of the bodys endocrine system. Endocrine glands produce, store, and release hormones, which travel in the bloodstream to target cells elsewhere in the body and direct the cells activity.\n                \nThough their names are similar, the thyroid and parathyroid glands are entirely different glands, each producing distinct hormones with specific functions. The parathyroid glands produce PTH, a hormone that helps maintain the correct balance of calcium in the body. PTH regulates the level of calcium in the blood, release of calcium from bone, absorption of calcium in the small intestine, and excretion of calcium in the urine.\n                \nWhen the level of calcium in the blood falls too low, normal parathyroid glands release just enough PTH to restore the blood calcium level."}
{"_id":"9ff06cc5-883e-4708-a35f-80fe4add3be2","text":"High PTH levels trigger the bones to release increased amounts of calcium into the blood, causing blood calcium levels to rise above normal. The loss of calcium from bones may weaken the bones. Also, the small intestine may absorb more calcium from food, adding to the excess calcium in the blood. In response to high blood calcium levels, the kidneys excrete more calcium in the urine, which can lead to kidney stones.\n                \nHigh blood calcium levels might contribute to other problems, such as heart disease, high blood pressure, and difficulty with concentration. However, more research is needed to better understand how primary hyperparathyroidism affects the cardiovascular systemthe heart and blood vesselsand the central nervous systemthe brain and spinal cord."}
{"_id":"eeadd2c7-38fe-4388-9a19-c0ce816db5eb","text":"In about 80 percent of people with primary hyperparathyroidism, a benign, or noncancerous, tumor called an adenoma has formed in one of the parathyroid glands.2 The tumor causes the gland to become overactive. In most other cases, the excess hormone comes from two or more overactive parathyroid glands, a condition called multiple tumors or hyperplasia. Rarely, primary hyperparathyroidism is caused by cancer of a parathyroid gland.\n                \nIn most cases, health care providers dont know why adenoma or multiple tumors occur in the parathyroid glands. Most people with primary hyperparathyroidism have no family history of the disorder, but some cases can be linked to an inherited problem. For example, familial multiple endocrine neoplasia type 1 is a rare, inherited syndrome that causes multiple tumors in the parathyroid glands as well as in the pancreas and the pituitary gland. Another rare genetic disorder, familial hypocalciuric hypercalcemia, causes a kind of hyperparathyroidism that is atypical, in part because it does not respond to standard parathyroid surgery."}
{"_id":"de4d3d99-b2d6-47b4-85f2-98c8676ee56a","text":"Most people with primary hyperparathyroidism have no symptoms. When symptoms appear, they are often mild and nonspecific, such as\n                \n- muscle weakness  - fatigue and an increased need for sleep  - feelings of depression  - aches and pains in bones and joints\n                \nPeople with more severe disease may have\n                \n- loss of appetite  - nausea  - vomiting  - constipation  - confusion or impaired thinking and memory  - increased thirst and urination\n                \nThese symptoms are mainly due to the high blood calcium levels that result from excessive PTH."}
{"_id":"0d646b23-5847-4a74-b50b-5bb34c626a27","text":"Health care providers diagnose primary hyperparathyroidism when a person has high blood calcium and PTH levels. High blood calcium is usually the first sign that leads health care providers to suspect parathyroid gland overactivity. Other diseases can cause high blood calcium levels, but only in primary hyperparathyroidism is the elevated calcium the result of too much PTH.\n                \nRoutine blood tests that screen for a wide range of conditions, including high blood calcium levels, are helping health care providers diagnose primary hyperparathyroidism in people who have mild forms of the disorder and are symptom-free. For a blood test, blood is drawn at a health care providers office or commercial facility and sent to a lab for analysis."}
{"_id":"075aea33-9fbd-47b7-bfb8-4d7d0c9ea25d","text":"Once the diagnosis of primary hyperparathyroidism is established, other tests may be done to assess complications:\n                \n- Bone mineral density test. Dual energy x-ray absorptiometry, sometimes called a DXA or DEXA scan, uses low-dose x rays to measure bone density. During the test, a person lies on a padded table while a technician moves the scanner over the persons body. DXA scans are performed in a health care providers office, outpatient center, or hospital by a specially trained technician and may be interpreted by a metabolic bone disease expert or radiologista doctor who specializes in medical imagingor other specialists; anesthesia is not needed. The test can help assess bone loss and risk of fractures.  - Ultrasound. Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. The procedure is performed in a health care providers office, outpatient center, or hospital by a specially trained technician, and the images are interpreted by a radiologist; anesthesia is not needed. The images can show the presence of kidney stones.  - Computerized tomography (CT) scan. CT scans use a combination of x rays and computer technology to create three-dimensional (3-D) images. A CT scan may include the injection of a special dye, called contrast medium. CT scans require the person to lie on a table that slides into a tunnel-shaped device where the x rays are taken. The procedure is performed in an outpatient center or hospital by an x-ray technician, and the images are interpreted by a radiologist; anesthesia is not needed. CT scans can show the presence of kidney stones.  - Urine collection. A 24-hour urine collection may be done to measure selected chemicals, such as calcium and creatinine, which is a waste product healthy kidneys remove. The person collects urine over a 24-hour period, and the urine is sent to a laboratory for analysis. The urine collection may provide information on kidney damage, the risk of kidney stone formation, and the risk of familial hypocalciuric hypercalcemia.  - 25-hydroxy-vitamin D blood test. This test is recommended because vitamin D deficiency is common in people with primary hyperparathyroidism."}
{"_id":"33672b90-bc1a-4f57-a828-9ff1096a1b63","text":"Surgery\n                \nSurgery to remove the overactive parathyroid gland or glands is the only definitive treatment for the disorder, particularly if the patient has a very high blood calcium level or has had a fracture or a kidney stone. In patients without any symptoms, guidelines are used to identify who might benefit from parathyroid surgery.3\n                \nWhen performed by experienced endocrine surgeons, surgery cures primary hyperparathyroidism in more than 95 percent of operations.2\n                \nSurgeons often use imaging tests before surgery to locate the overactive gland to be removed. The most commonly used tests are sestamibi and ultrasound scans. In a sestamibi scan, the patient receives an injection of a small amount of radioactive dye that is absorbed by overactive parathyroid glands. The overactive glands can then be viewed using a special camera.\n                \nSurgeons use two main strategies to remove the overactive gland or glands:\n                \n- Minimally invasive parathyroidectomy. This type of surgery, which can be done on an outpatient basis, may be used when only one of the parathyroid glands is likely to be overactive. Guided by a tumor-imaging test, the surgeon makes a small incision in the neck to remove the gland. The small incision means that patients typically have less pain and a quicker recovery than with more invasive surgery. Local or general anesthesia may be used for this type of surgery.  - Standard neck exploration. This type of surgery involves a larger incision that allows the surgeon to access and examine all four parathyroid glands and remove the overactive ones. This type of surgery is more extensive and typically requires a hospital stay of 1 to 2 days. Surgeons use this approach if they plan to inspect more than one gland. General anesthesia is used for this type of surgery.\n                \nAlmost all people with primary hyperparathyroidism who have symptoms can benefit from surgery. Experts believe that those without symptoms but who meet guidelines for surgery will also benefit from surgery. Surgery can lead to improved bone density and fewer fractures and can reduce the chance of forming kidney stones. Other potential benefits are being studied by researchers.\n                \nSurgery for primary hyperparathyroidism has a complication rate of 13 percent when performed by experienced endocrine surgeons.4 Rarely, patients undergoing surgery experience damage to the nerves controlling the vocal cords, which can affect speech. A small number of patients lose all their healthy parathyroid tissue and thus develop chronic low calcium levels, requiring lifelong treatment with calcium and some form of vitamin D. This complication is called hypoparathyroidism. The complication rate is slightly higher for operations on multiple tumors than for a single adenoma because more extensive surgery is needed.\n                \nPeople with primary hyperparathyroidism due to familial hypocalciuric hypercalcemia should not have surgery.\n                \nMonitoring\n                \nSome people who have mild primary hyperparathyroidism may not need immediate or even any surgery and can be safely monitored. People may wish to talk with their health care provider about long-term monitoring if they\n                \n- are symptom-free  - have only slightly elevated blood calcium levels  - have normal kidneys and bone density\n                \nLong-term monitoring should include periodic clinical evaluations, annual serum calcium measurements, annual serum creatinine measurements to check kidney function, and bone density measurements every 1 to 2 years.\n                \nVitamin D deficiency should be corrected if present. Patients who are monitored need not restrict calcium in their diets.\n                \nIf the patient and health care provider choose long-term monitoring, the patient should\n                \n- drink plenty of water  - exercise regularly  - avoid certain diuretics, such as thiazides\n                \nEither immobilizationthe inability to move due to illness or injuryor gastrointestinal illness with vomiting or diarrhea that leads to dehydration can cause blood calcium levels to rise further in someone with primary hyperparathyroidism. People with primary hyperparathyroidism should seek medical attention if they find themselves immobilized or dehydrated due to vomiting or diarrhea.\n                \nMedications\n                \nCalcimimetics are a new class of medications that decrease parathyroid gland secretion of PTH. The calcimimetic, cinacalcet (Sensipar), has been approved by the U.S. Food and Drug Administration for the treatment of secondary hyperparathyroidism caused by dialysisa blood-filtering treatment for kidney failureand primary hyperparathyroidism caused by parathyroid cancer. Cinacalcet has also been approved for the management of hypercalcemia associated with primary hyperparathyroidism.\n                \nA number of other medications are being studied to learn whether they may be helpful in treating primary hyperparathyroidism. These medications include bisphosphonates and selective estrogen receptor modulators."}
{"_id":"8df33652-2765-40c7-9df0-e7317f8dd9d0","text":"Eating, diet, and nutrition have not been shown to play a role in causing or preventing primary hyperparathyroidism.\n                \nVitamin D. Experts suggest correcting vitamin D deficiency in people with primary hyperparathyroidism to achieve a serum level of 25-hydroxy-vitamin D greater than 20 nanograms per deciliter (50 nanomoles per liter). Research is ongoing to determine optimal doses and regimens of vitamin D supplementation for people with primary hyperparathyroidism.\n                \nFor the healthy public, the Institute of Medicine (IOM) guidelines for vitamin D intake are\n                \n- people ages 1 to 70 years may require 600 International Units (IUs)  - people age 71 and older may require as much as 800 IUs\n                \nThe IOM also recommends that no more than 4,000 IUs of vitamin D be taken per day.\n                \nCalcium. People with primary hyperparathyroidism without symptoms who are being monitored do not need to restrict calcium in their diet. People with low calcium levels due to loss of all parathyroid tissue from surgery will need to take calcium supplements for the rest of their life.\n                \nTo help ensure coordinated and safe care, people should discuss their use of complementary and alternative medicine practices, including their use of dietary supplements, with their health care provider. Tips for talking with health care providers are available through the National Center for Complementary and Integrative Health."}
{"_id":"615426ca-ff29-49c9-bb7a-3d66c06a2582","text":"- Primary hyperparathyroidism is a disorder of the parathyroid glands, in which one or more of the parathyroid glands are overactive. As a result, the gland releases too much parathyroid hormone (PTH).  - High PTH levels trigger the bones to release increased calcium into the blood, causing blood calcium levels to rise above normal. T he loss of calcium from bones may weaken the bones. In response to high blood calcium levels, the kidneys excrete more calcium in the urine, which can lead to kidney stones.  - Most people with primary hyperparathyroidism have no symptoms. When symptoms appear, they are often mild and nonspecific, such as muscle weakness, fatigue, increased need for sleep, feelings of depression, or aches and pains in bones and joints.  - People with more severe primary hyperparathyroidism may have symptoms such as loss of appetite, nausea, vomiting, constipation, confusion or impaired thinking and memory, and increased thirst and urination.  - Health care providers diagnose primary hyperparathyroidism when a person has high blood calcium and PTH levels.  - Surgery to remove the overactive parathyroid gland or glands is the only definitive treatment for the disorder. When performed by experienced endocrine surgeons, surgery cures primary hyperparathyroidism in more than 95 percent of operations. Some people who have mild primary hyperparathyroidism may not need immediate or even any surgery and can be safely monitored. People with primary hyperparathyroidism due to familial hypocalciuric hypercalcemia should not have surgery."}
{"_id":"11d83fcf-cb8e-48e6-9b47-e7344dd77e72","text":"Urinary incontinence is the loss of bladder control, resulting in the accidental leakage of urine from the body. For example, a man may feel a strong, sudden need, or urgency, to urinate just before losing a large amount of urine, called urgency incontinence.\n                \nUI can be slightly bothersome or totally debilitating. For some men, the chance of embarrassment keeps them from enjoying many activities, including exercising, and causes emotional distress. When people are inactive, they increase their chances of developing other health problems, such as obesity and diabetes."}