bowang0911/MedQuAD huggingface dataset:
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.
                
More 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.
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.
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.
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.
                
With 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.
                
Depending 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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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..
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.
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.
                
Symptoms 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.
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.
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.
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.
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.
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.
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.