Druvith/medqa huggingface dataset:
What is (are) Reye's Syndrome ? 

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.
What are the treatments for Reye's Syndrome ? 

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.
What is the outlook for Reye's Syndrome ? 

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.
what research (or clinical trials) is being done for Reye's Syndrome ? 

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.
What is (are) Cerebral Arteriosclerosis ? 

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.
                
Cerebral 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.
                
Cerebral 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.
What are the treatments for Cerebral Arteriosclerosis ? 

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.
What is the outlook for Cerebral Arteriosclerosis ? 

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.
what research (or clinical trials) is being done for Cerebral Arteriosclerosis ? 

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.
What is (are) Schizencephaly ? 

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.
What are the treatments for Schizencephaly ? 

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.
What is the outlook for Schizencephaly ? 

The prognosis for individuals with schizencephaly varies depending on the size of the clefts and the extent of neurological disabilities.
what research (or clinical trials) is being done for Schizencephaly ? 

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.
What is (are) Inflammatory Myopathies ? 

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.
What are the treatments for Inflammatory Myopathies ? 

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.
What is the outlook for Inflammatory Myopathies ? 

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.
what research (or clinical trials) is being done for Inflammatory Myopathies ? 

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.
What is (are) Stiff-Person Syndrome ? 

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.
What are the treatments for Stiff-Person Syndrome ? 

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.
What is the outlook for Stiff-Person Syndrome ? 

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.
what research (or clinical trials) is being done for Stiff-Person Syndrome ? 

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.
What is (are) Hereditary Spastic Paraplegia ? 

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.
What are the treatments for Hereditary Spastic Paraplegia ? 

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.
What is the outlook for Hereditary Spastic Paraplegia ? 

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.
what research (or clinical trials) is being done for Hereditary Spastic Paraplegia ? 

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.
What is (are) Leukodystrophy ? 

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.
What are the treatments for Leukodystrophy ? 

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.
What is the outlook for Leukodystrophy ? 

The prognosis for the leukodystrophies varies according to the specific type of leukodystrophy.
what research (or clinical trials) is being done for Leukodystrophy ? 

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.
What is (are) Canavan Disease ? 

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.
                
Symptoms 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.
What are the treatments for Canavan Disease ? 

Canavan disease causes progressive brain atrophy. There is no cure, nor is there a standard course of treatment. Treatment is symptomatic and supportive.
What is the outlook for Canavan Disease ? 

The prognosis for Canavan disease is poor. Death usually occurs before age 10, although some children may survive into their teens and twenties.
what research (or clinical trials) is being done for Canavan Disease ? 

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.
What is (are) Alexander Disease ? 

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.
What are the treatments for Alexander Disease ? 

There is no cure for Alexander disease, nor is there a standard course of treatment. Treatment of Alexander disease is symptomatic and supportive.
What is the outlook for Alexander Disease ? 

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.