randomani/MedicalQnA-llama2 huggingface dataset:
This is a medical question of type : research 
 what research (or clinical trials) is being done for Shingles ? 
 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.
This is a medical question of type : information 
 What is (are) Leigh's Disease ? 
 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.
                
In 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.
                
There 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.
This is a medical question of type : treatment 
 What are the treatments for Leigh's Disease ? 
 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.
This is a medical question of type : outlook 
 What is the outlook for Leigh's Disease ? 
 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.
This is a medical question of type : research 
 what research (or clinical trials) is being done for Leigh's Disease ? 
 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.
This is a medical question of type : information 
 What is (are) Kuru ? 
 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.
                
Kuru 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.
This is a medical question of type : treatment 
 What are the treatments for Kuru ? 
 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.
This is a medical question of type : outlook 
 What is the outlook for Kuru ? 
 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.
This is a medical question of type : research 
 what research (or clinical trials) is being done for Kuru ? 
 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.
This is a medical question of type : information 
 What is (are) Neurodegeneration with Brain Iron Accumulation ? 
 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.
This is a medical question of type : treatment 
 What are the treatments for Neurodegeneration with Brain Iron Accumulation ? 
 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.
This is a medical question of type : outlook 
 What is the outlook for Neurodegeneration with Brain Iron Accumulation ? 
 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.
This is a medical question of type : research 
 what research (or clinical trials) is being done for Neurodegeneration with Brain Iron Accumulation ? 
 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..
This is a medical question of type : information 
 What is (are) Pompe Disease ? 
 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.
                
Early 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.
                
Late 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.
This is a medical question of type : treatment 
 What are the treatments for Pompe Disease ? 
 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.
This is a medical question of type : outlook 
 What is the outlook for Pompe Disease ? 
 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.
This is a medical question of type : research 
 what research (or clinical trials) is being done for Pompe Disease ? 
 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.
This is a medical question of type : information 
 What is (are) Dysgraphia ? 
 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.
This is a medical question of type : treatment 
 What are the treatments for Dysgraphia ? 
 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.
This is a medical question of type : outlook 
 What is the outlook for Dysgraphia ? 
 Some individuals with dysgraphia improve their writing ability, but for others, the disorder persists.
This is a medical question of type : research 
 what research (or clinical trials) is being done for Dysgraphia ? 
 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.
This is a medical question of type : information 
 What is (are) Orthostatic Hypotension ? 
 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).
This is a medical question of type : treatment 
 What are the treatments for Orthostatic Hypotension ? 
 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.
This is a medical question of type : outlook 
 What is the outlook for Orthostatic Hypotension ? 
 The prognosis for individuals with orthostatic hypotension depends on the underlying cause of the condition.
This is a medical question of type : research 
 what research (or clinical trials) is being done for Orthostatic Hypotension ? 
 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.
This is a medical question of type : information 
 What is (are) Huntington's Disease ? 
 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.
This is a medical question of type : treatment 
 What are the treatments for Huntington's Disease ? 
 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.
This is a medical question of type : outlook 
 What is the outlook for Huntington's Disease ? 
 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.
This is a medical question of type : research 
 what research (or clinical trials) is being done for Huntington's Disease ? 
 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.
                
The 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.
This is a medical question of type : treatment 
 What are the treatments for Transmissible Spongiform Encephalopathies ? 
 TSEs tend to progress rapidly and usually culminate in death over the course of a few months to a few years.
This is a medical question of type : outlook 
 What is the outlook for Transmissible Spongiform Encephalopathies ? 
 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.