Druvith/medqa1 huggingface dataset:
Question:  What is (are) Wilson Disease ?
Answer: 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.
Question:  What are the treatments for Wilson Disease ?
Answer: 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.
Question:  What is the outlook for Wilson Disease ?
Answer: 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.
Question:  what research (or clinical trials) is being done for Wilson Disease ?
Answer: 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.
Question:  What is (are) Cerebral Aneurysms ?
Answer: 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.
Question:  What are the treatments for Cerebral Aneurysms ?
Answer: 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.
Question:  What is the outlook for Cerebral Aneurysms ?
Answer: 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.
Question:  what research (or clinical trials) is being done for Cerebral Aneurysms ?
Answer: 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.
Question:  What is (are) Charcot-Marie-Tooth Disease ?
Answer: 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.
Question:  What are the treatments for Charcot-Marie-Tooth Disease ?
Answer: 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.
Question:  What is the outlook for Charcot-Marie-Tooth Disease ?
Answer: 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.
Question:  what research (or clinical trials) is being done for Charcot-Marie-Tooth Disease ?
Answer: 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.
Question:  What is (are) Alternating Hemiplegia ?
Answer: 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.
Question:  What are the treatments for Alternating Hemiplegia ?
Answer: 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
Question:  What is the outlook for Alternating Hemiplegia ?
Answer: 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.
Question:  what research (or clinical trials) is being done for Alternating Hemiplegia ?
Answer: 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.
Question:  What is (are) Meralgia Paresthetica ?
Answer: 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.
Question:  What are the treatments for Meralgia Paresthetica ?
Answer: 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.
Question:  What is the outlook for Meralgia Paresthetica ?
Answer: 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.
Question:  what research (or clinical trials) is being done for Meralgia Paresthetica ?
Answer: 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.
Question:  What is (are) Neurosyphilis ?
Answer: 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:
                
- asymptomatic neurosyphilis - meningeal neurosyphilis - meningovascular neurosyphilis - general paresis, and - tabes dorsalis.
                
Asymptomatic 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.
Question:  What are the treatments for Neurosyphilis ?
Answer: 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.
Question:  What is the outlook for Neurosyphilis ?
Answer: 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.
Question:  what research (or clinical trials) is being done for Neurosyphilis ?
Answer: 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.
Question:  What is (are) Neuromyelitis Optica ?
Answer: 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.
                
NMO 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.
Question:  What are the treatments for Neuromyelitis Optica ?
Answer: 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.
Question:  What is the outlook for Neuromyelitis Optica ?
Answer: 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.
Question:  what research (or clinical trials) is being done for Neuromyelitis Optica ?
Answer: 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.
Question:  What is (are) Tay-Sachs Disease ?
Answer: 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.
Question:  What are the treatments for Tay-Sachs Disease ?
Answer: 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.
Question:  What is the outlook for Tay-Sachs Disease ?
Answer: Even with the best of care, children with Tay-Sachs disease usually die by age 4, from recurring infection.