Input: What is (are) Carpal Tunnel Syndrome ?

Output: Carpal tunnel syndrome (CTS) occurs when the median nerve, which runs from the forearm into the palm of the hand, becomes pressed or squeezed at the wrist. The carpal tunnel is a narrow, rigid passageway of ligament and bones at the base of the hand that houses the median nerve and the tendons that bend the fingers. The median nerve provides feeling to the palm side of the thumb and to most of the fingers. Symptoms usually start gradually, with numbness, tingling, weakness, and sometimes pain in the hand and wrist. People might have difficulty with tasks such as driving or reading a book. Decreased hand strength may make it difficult to grasp small objects or perform other manual tasks. In some cases no direct cause of the syndrome can be identified. Contributing factors include trauma or injury to the wrist that causes swelling, thyroid disease, rheumatoid arthritis, and fluid retention during pregnancy. Women are three times more likely than men to develop carpal tunnel syndrome. The disorder usually occurs only in adults. </s>


Input: What are the treatments for Carpal Tunnel Syndrome ?

Output: Initial treatment generally involves immobilizing the wrist in a splint, nonsteroidal anti-inflammatory drugs to temporarily reduce swelling, and injections of corticosteroid drugs (such as prednisone). For more severe cases, surgery may be recommended. </s>


Input: What is the outlook for Carpal Tunnel Syndrome ?

Output: In general, carpal tunnel syndrome responds well to treatment, but less than half of individuals report their hand(s) feeling completely normal following surgery. Some residual numbness or weakness is common. At work, people can perform stretching exercises, take frequent rest breaks, wear splints to keep wrists straight, and use correct posture and wrist position to help prevent or worsen symptoms. Wearing fingerless gloves can help keep hands warm and flexible. </s>


Input: what research (or clinical trials) is being done for Carpal Tunnel Syndrome ?

Output: The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to conduct fundamental research on the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. NINDS-funded scientists are studying the factors that lead to long-lasting nerve pain disorders, and how the affected nerves are related to symptoms of numbness, loss of function, and pain. Researchers also are examining biomechanical stresses that contribute to the nerve damage responsible for symptoms of carpal tunnel syndrome in order to better understand, treat, and prevent it. </s>


Input: What is (are) Opsoclonus Myoclonus ?

Output: Opsoclonus myoclonus is a rare neurological disorder characterized by an unsteady, trembling gait, myoclonus (brief, shock-like muscle spasms), and opsoclonus (irregular, rapid eye movements). Other symptoms may include difficulty speaking, poorly articulated speech, or an inability to speak. A decrease in muscle tone, lethargy, irritability, and malaise (a vague feeling of bodily discomfort) may also be present. Opsoclonus myoclonus may occur in association with tumors or viral infections. It is often seen in children with tumors. </s>


Input: What are the treatments for Opsoclonus Myoclonus ?

Output: Treatment for opsoclonus myoclonus may include corticosteroids or ACTH (adrenocorticotropic hormone). In cases where there is a tumor present, treatment such as chemotherapy, surgery, or radiation may be required. </s>


Input: What is the outlook for Opsoclonus Myoclonus ?

Output: The prognosis for opsoclonus myoclonus varies depending on the symptoms and the presence and treatment of tumors. With treatment of the underlying cause of the disorder, there may be an improvement of symptoms. The symptoms sometimes recur without warning. Generally the disorder is not fatal. </s>


Input: what research (or clinical trials) is being done for Opsoclonus Myoclonus ?

Output: The NINDS supports and conducts research on movement disorders such as opsoclonus myoclonus. These studies are aimed at increasing knowledge about these disorders and finding ways to prevent, treat, and cure them. </s>


Input: What is (are) Dysautonomia ?

Output: Dysautonomia refers to a disorder of autonomic nervous system (ANS) function that generally involves failure of the sympathetic or parasympathetic components of the ANS, but dysautonomia involving excessive or overactive ANS actions also can occur. Dysautonomia can be local, as in reflex sympathetic dystrophy, or generalized, as in pure autonomic failure. It can be acute and reversible, as in Guillain-Barre syndrome, or chronic and progressive. Several common conditions such as diabetes and alcoholism can include dysautonomia. Dysautonomia also can occur as a primary condition or in association with degenerative neurological diseases such as Parkinson's disease. Other diseases with generalized, primary dysautonomia include multiple system atrophy and familial dysautonomia. Hallmarks of generalized dysautonomia due to sympathetic failure are impotence (in men) and a fall in blood pressure during standing (orthostatic hypotension). Excessive sympathetic activity can present as hypertension or a rapid pulse rate. </s>


Input: What are the treatments for Dysautonomia ?

Output: There is usually no cure for dysautonomia. Secondary forms may improve with treatment of the underlying disease. In many cases treatment of primary dysautonomia is symptomatic and supportive. Measures to combat orthostatic hypotension include elevation of the head of the bed, water bolus (rapid infusion of water given intravenously), a high-salt diet, and drugs such as fludrocortisone and midodrine. </s>


Input: What is the outlook for Dysautonomia ?

Output: The outlook for individuals with dysautonomia depends on the particular diagnostic category. People with chronic, progressive, generalized dysautonomia in the setting of central nervous system degeneration have a generally poor long-term prognosis. Death can occur from pneumonia, acute respiratory failure, or sudden cardiopulmonary arrest. </s>


Input: what research (or clinical trials) is being done for Dysautonomia ?

Output: The NINDS supports and conducts research on dysautonomia. This research aims to discover ways to diagnose, treat, and, ultimately, prevent these disorders. </s>


Input: What is (are) Metachromatic Leukodystrophy ?

Output: Metachromatic leukodystrophy (MLD) is one of a group of genetic disorders called the leukodystrophies, which are characterized by the toxic buildup of lipids (fatty materials such as oils and waxes) and other storage materials in cells in the white matter of the central nervous system and peripheral nerves. The buildup of storage materials impairs the growth or development of the myelin sheath, the fatty covering that acts as an insulator around nerve fibers. (Myelin, which lends its color to the white matter of the brain, is a complex substance made up of a mixture of fats and proteins.) MLD is one of several lipid storage diseases, which result in the harmful buildup of lipids in brain cells and other cells and tissues in the body. People with lipid storage diseases either do not produce enough of one of the enzymes needed to break down (metabolize) lipids or they produce enzymes that do not work properly. Some leukodystrophies are caused by genetic defects of enzymes that regulate the metabolism of fats needed in myelin synthesis. MLD, which affects males and females, is cause by a deficiency of the enzyme arylsulfatase A. MLD has three characteristic forms: late infantile, juvenile, and adult. Late infantile MLD typically begins between 12 and 20 months following birth. Infants appear normal at first but develop difficulty walking after the first year of life and eventually lose the ability to walk. Other symptoms include muscle wasting and weakness,developmental delays, progressive loss of vision leading to blindness, impaired swallowing, and dementia before age 2. Most children with this form of MLD die by age 5. Symptoms of the juvenile form of MLD (which begins between 3-10 years of age) include impaired school performance, mental deterioration, an inability to control movements, seizures, and dementia. Symptoms continue to get worse, and death eventually occurs 10 to 20 years following disease onset.. The adult form commonly begins after age 16, with symptoms that include psychiatric disturbances, seizures, tremor, impaired concentration, depression, and dementia. Death generally occurs within 6 to 14 years after onset of symptoms. </s>


Input: What are the treatments for Metachromatic Leukodystrophy ?

Output: There is no cure for MLD. Bone marrow transplantation may delay progression of the disease in some infantile-onset cases. Other treatment is symptomatic and supportive. Considerable progress has been made with regard to gene therapy in an animal model of MLD and in clinical trials. </s>


Input: What is the outlook for Metachromatic Leukodystrophy ?

Output: The prognosis for MLD is poor. Most children within the infantile form die by age 5. Symptoms of the juvenile form progress with death occurring 10 to 20 years following onset. Those persons affected by the adult form typically die withing 6 to 14 years following onset of symptoms. </s>


Input: what research (or clinical trials) is being done for Metachromatic Leukodystrophy ?

Output: The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS is a part of the National Institutes of Health (NIH), the leading supporter of biomedical research in the world. Research funded by the NINDS focuses on better understanding how neurological defects arise in lipid storage disorders and on the development of new treatments targeting disease mechanisms, including gene therapies, cell-based therapies, and pharmacological approaches. NINDS-funded preclinical research aims to study the effectiveness and safety of virus-based delivery of the normal ARSA gene to promote gene expression throughout the central nervous system and overcome the mutation-caused deficiency. If successful, the project could lead to trials in humans. Other research hopes to study the use of patient-specific induced pluripotent stem cells (cells that are capable of becoming other types of cells) in correcting the gene deficiency in metachromatic leukodystrophy. </s>


Input: What is (are) Atrial Fibrillation and Stroke ?

Output: Atrial fibrillation (AF) describes the rapid, irregular beating of the left atrium (upper chamber) of the heart. These rapid contractions of the heart are weaker than normal contractions, resulting in slow flow of blood in the atrium. The blood pools and becomes sluggish and can result in the formation of blood clots. If a clot leaves the heart and travels to the brain, it can cause a stroke by blocking the flow of blood through cerebral arteries. Some people with AF have no symptoms, but others may experience a fluttering feeling in the area of the chest above the heart, chest pain, lightheadness or fainting, shortness of breath, and fatigue. AF is diagnosed by an electrocardiogram (ECG), a device that records the hearts electrical activity. Other tests are often performed to rule out contributing causes, such as high blood pressure, an overactive thyroid gland, heart failure, faulty heart valves, lung disease, and stimulant or alcohol abuse. Some people will have no identifiable cause for their AF. </s>


Input: What are the treatments for Atrial Fibrillation and Stroke ?

Output: Within a few hours after onset of a stroke, treatment with drugs or devices that dissolve or break up the clot can restore blood flow to the brain and lead to a better recovery. To prevent strokes related to AF, doctors often prescribe medications to prevent formation of clots in the heart, which can travel to the brain and cause stroke. Immediately after a stroke, doctors may temporarily administer heparin by injection, while starting an oral medication for long-term protection from clots. The most commonly used drug has been warfarin. People taking warfarin must be closely monitored to make sure their blood is thin enough to prevent clots, but not so thin as to promote bleeding. Since some foods, vitamin supplements, and medications can affect warfarin action, keeping the blood just thin enough can be tricky. More recently, a number of new blood thinners, including dabigatran, rivaroxaban, and apixaban, have been shown to be as effective as warfarin in stroke prevention. These newer medications do not require regular blood test monitoring and may have less tendency to cause bleeding due to making the blood too thin. Some individuals with AF may have a lower risk of stroke and may be treated with aspirin, either alone or with another antiplatelet agency like clopidogrel. Other treatments for AF include medications such as beta blockers or calcium channel blockers to slow the heartbeat, and anti-arrhythmic drugs or electrical cardioversion (which delivers an electrical shock to the heart) to normalize the heartbeat. </s>


Input: What is the outlook for Atrial Fibrillation and Stroke ?

Output: AF, which affects as many as 2.2 million Americans, increases an individuals risk of stroke by 4 to 6 times on average. The risk increases with age. In people over 80 years old, AF is the direct cause of 1 in 4 strokes. Treating individuals with warfarin or new blood thinners reduces the rate of stroke for those who have AF by approximately one-half to two- thirds. People with AF can have multiple strokes, including silent strokes (strokes that don't show physical symptoms but show up on a brain scan) that, over time, can cause dementia, so prevention is important. </s>


Input: what research (or clinical trials) is being done for Atrial Fibrillation and Stroke ?

Output: The National Institute of Neurological Disorders and Stroke (NINDS) is the leading Federal agency directing and funding research relevant to AF and stroke prevention. The NINDS conducts basic and clinical research in its laboratories and clinics at the National Institutes of Health (NIH), and also supports additional research through grants to major research institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders such as AF that can increase the risk of stroke. </s>


Input: What is (are) Migraine ?

Output: The pain of a migraine headache is often described as an intense pulsing or throbbing pain in one area of the head. However, it is much more; the International Headache Society diagnoses a migraine by its pain and number of attacks (at least 5, lasting 4-72 hours if untreated), and additional symptoms including nausea and/or vomiting, or sensitivity to both light and sound. Migraine is three times more common in women than in men and affects more than 10 percent of people worldwide. Roughly one-third of affected individuals can predict the onset of a migraine because it is preceded by an "aura," visual disturbances that appear as flashing lights, zig-zag lines or a temporary loss of vision. People with migraine tend to have recurring attacks triggered by a number of different factors, including stress, anxiety, hormonal changes, bright or flashing lights, lack of food or sleep, and dietary substances. Migraine in some women may relate to changes in hormones and hormonal levels during their menstrual cycle. For many years, scientists believed that migraines were linked to the dilation and constriction of blood vessels in the head. Investigators now believe that migraine has a genetic cause. </s>


Input: What are the treatments for Migraine ?

Output:
There is no absolute cure for migraine since its pathophysiology has yet to be fully understood. There are two ways to approach the treatment of migraine headache with drugs: prevent the attacks, or relieve the symptoms during the attacks. Prevention involves the use of medications and behavioral changes. Drugs originally developed for epilepsy, depression, or high blood pressure to prevent future attacks have been shown to be extremely effective in treating migraine. Botulinum toxin A has been shown to be effective in prevention of chronic migraine. Behaviorally, stress management strategies, such as exercise, relaxation techniques, biofeedback mechanisms, and other therapies designed to limit daily discomfort, may reduce the number and severity of migraine attacks. Making a log of personal triggers of migraine can also provide useful information for trigger-avoiding lifestyle changes, including dietary considerations, eating regularly scheduled meals with adequate hydration, stopping certain medications, and establishing a consistent sleep schedule. Hormone therapy may help some women whose migraines seem to be linked to their menstrual cycle. A weight loss program is recommended for obese individuals with migraine.

Relief of symptoms, or acute treatments, during attacks consists of sumatriptan, ergotamine drugs, and analgesics such as ibuprofen and aspirin. The sooner these treatments are administered, the more effective they are. </s>


Input: What is the outlook for Migraine ?

Output: Responsive prevention and treatment of migraine is incredibly important. Evidence shows an increased sensitivity after each successive attack, eventually leading to chronic daily migraine in some individuals With proper combination of drugs for prevention and treatment of migraine attacks most individuals can overcome much of the discomfort from this debilitating disorder. Women whose migraine attacks occur in association with their menstrual cycle are likely to have fewer attacks and milder symptoms after menopause. </s>


Input: what research (or clinical trials) is being done for Migraine ?

Output:
Researchers believe that migraine is the result of fundamental neurological abnormalities caused by genetic mutations at work in the brain. New models are aiding scientists in studying the basic science involved in the biological cascade, genetic components and mechanisms of migraine. Understanding the causes of migraine as well as the events that effect them will give researchers the opportunity to develop and test drugs that could be more targeted to preventing or interrupting attacks entirely. Therapies currently being tested for their effectiveness in treating migraine include magnesium, coenzyme Q10, vitamin B12, riboflavin, fever-few, and butterbur.

In 2010, a team of researchers found a common mutation in the gene TRESK which contains instructions for a certain potassium ion channel. Potassium channels are important for keeping a nerve cell at rest and mutations in them can lead to overactive cells that respond to much lower levels of pain. Large genetic analyses similar to the one used to identify TRESK will most likely lead to the identification of a number of other genes linked to migraine. </s>


Input: What is (are) Aicardi Syndrome ?

Output:
Aicardi syndrome is a rare genetic disorder that primarily affects newborn girls. The condition is sporadic, meaning it is not known to pass from parent to child. (An exception is a report of two sisters and a pair of identical twins, all of whom were affected.) The mutation that causes Aicardi syndrome has not been identified, but it is thought to be caused by a dominant mutation that appears for the first time in a family in an x-linked gene that may be lethal in certain males.. Aicardi syndrome can be seen in boys born with an extra "X" chromosome. (Females have two X chromosomes, while males normally have an X and a Y chromosome.) The precise gene or genetic mechanism causing Aicardi syndrome is not yet known.

Originally, Aicardi syndrome was characterized by three main features: 1) partial or complete absence of the structure (corpus callosum) that links the two halves of the brain (2) infantile spasms (a type of seizure disorder), and 3) chorioretinal lacunae, lesions on the retina that look like yellowish spots. However, Aicardi syndrome is now known to have a much broader spectrum of abnormalities than was initially described. Not all girls with the condition have the three features described above and many girls have additional feature such as lower tone around the head and trunk, microcephaly (small head circumference), and spasticity in the limbs.

Typical findings in the brain of girls with Aicardi syndrome include heterotopias, which are groups of brain cells that, during development, migrated to the wrong area of brain; polymicrogyria or pachygyria, which are numerous small, or too few, brain folds; and cysts, (fluid filled cavities) in the brain. Girls with Aicardi syndrome have varying degrees of intellectual disability and developmental delay. Many girls also have developmental abnormalities of their optic nerves and some have microphthalmia (small eyes). Skeletal problems such as absent or abnormal ribs and abnormalities of vertebrae in the spinal column (including hemivertebrae and butterfly vertebrae) have also been reported. Some girls also have skin problems, facial asymmetry, small hands, and an increased incidence of tumors.

(Aicardi syndrome is distinct from Aicardi-Goutieres syndrome, which is an inherited encephalopathy that affects newborn infants.) </s>


Input: What are the treatments for Aicardi Syndrome ?

Output: There is no cure for Aicardi syndrome nor is there a standard course of treatment. Treatment generally involves medical management of seizures and programs to help parents and children cope with developmental delays. Long-term management by a pediatric neurologist with expertise in the management of infantile spasms is recommended. </s>


Input: What is the outlook for Aicardi Syndrome ?

Output: The prognosis for girls with Aicardi syndrome varies according to the severity of their symptoms. There is an increased risk for death in childhood and adolescence, but survivors into adulthood have been described. </s>


Input: what research (or clinical trials) is being done for Aicardi Syndrome ?

Output: The NINDS supports and conducts research on neurogenetic disorders such as Aicardi syndrome. The goals of this research are to locate and understand the genes involved and to develop techniques to diagnose, treat, prevent, and ultimately cure disorders such as Aicardi syndrome. </s>


Input: What is (are) Refsum Disease ?

Output: Adult Refsum disease (ARD) is a rare genetic disease that causes weakness or numbness of the hands and feet (peripheral neuropathy). Due to a genetic abnormality, people with ARD disease lack the enzyme in peroxisomes that break down phytanic acid, a type of fat found in certain foods. As a result, toxic levels of phytanic acid build up in the brain, blood, and other tissues. The disease usually begins in late childhood or early adulthood with increasing night blindness due to degeneration of the retina (retinitis pigmentosa). If the disease progresses, other symptoms may include deafness, loss of the sense of smell (anosmia), problems with balance and coordination (ataxia), dry and scaly skin (ichthyosis), and heartbeat abnormalities (cardiac arrhythmias). Some individuals will have shortened bones in their fingers or toes, or a visibly shortened fourth toe. Although the disease usually appears in early childhood, some people will not develop symptoms until their 40s or 50s. </s>


Input: What are the treatments for Refsum Disease ?

Output: The primary treatment for ARD is to restrict or avoid foods that contain phytanic acid, including dairy products; beef and lamb; and fatty fish such as tuna, cod, and haddock. Some individuals may also require plasma exchange (plasmapheresis) in which blood is drawn, filtered, and reinfused back into the body, to control the buildup of phytanic acid. </s>


Input: What is the outlook for Refsum Disease ?

Output: ARD is treatable because phytanic acid is not produced by the body, but is only found in foods. With treatment, muscle weakness, numbness, and dry and scaly skin generally disappear. However, vision and hearing problems may persist and the sense of smell may not return. Untreated, ARD can lead to sudden death caused by heartbeat abnormalities. </s>


Input: what research (or clinical trials) is being done for Refsum Disease ?

Output: The National Institute of Neurological Disorders and Stroke (NINDS) supports research related to Adult Refsum Disease through grants to major research institutions across the country. Research is focused on finding better ways to prevent, treat, and ultimately cure ARD and other peroxisomal disorders. </s>


Input: What is (are) Frontotemporal Dementia ?

Output: Frontotemporal dementia (FTD) describes a clinical syndrome associated with shrinking of the frontal and temporal anterior lobes of the brain. Originally known as Picks disease, the name and classification of FTD has been a topic of discussion for over a century. The current designation of the syndrome groups together Picks disease, primary progressive aphasia, and semantic dementia as FTD. Some doctors propose adding corticobasal degeneration and progressive supranuclear palsy to FTD and calling the group Pick Complex. These designations will continue to be debated. As it is defined today, the symptoms of FTD fall into two clinical patterns that involve either (1) changes in behavior, or (2) problems with language. The first type features behavior that can be either impulsive (disinhibited) or bored and listless (apathetic) and includes inappropriate social behavior; lack of social tact; lack of empathy; distractability; loss of insight into the behaviors of oneself and others; an increased interest in sex; changes in food preferences; agitation or, conversely, blunted emotions; neglect of personal hygiene; repetitive or compulsive behavior, and decreased energy and motivation. The second type primarily features symptoms of language disturbance, including difficulty making or understanding speech, often in conjunction with the behavioral types symptoms. Spatial skills and memory remain intact. There is a strong genetic component to the disease; FTD often runs in families. </s>


Input: What are the treatments for Frontotemporal Dementia ?

Output: No treatment has been shown to slow the progression of FTD. Behavior modification may help control unacceptable or dangerous behaviors. Aggressive, agitated, or dangerous behaviors could require medication. Anti-depressants have been shown to improve some symptoms. </s>


Input: What is the outlook for Frontotemporal Dementia ?

Output: The outcome for people with FTD is poor. The disease progresses steadily and often rapidly, ranging from less than 2 years in some individuals to more than 10 years in others. Eventually some individuals with FTD will need 24-hour care and monitoring at home or in an institutionalized care setting. </s>


Input: what research (or clinical trials) is being done for Frontotemporal Dementia ?

Output: The National Institute of Neurological Disorders and Stroke (NINDS), and other institutes of the National Institutes of Health (NIH), conduct research related to FTD in laboratories at the NIH, and also support additional research through grants to major medical institutions across the country. </s>


Input: What is (are) Shaken Baby Syndrome ?

Output: Shaken baby syndrome is a type of inflicted traumatic brain injury that happens when a baby is violently shaken. A baby has weak neck muscles and a large, heavy head. Shaking makes the fragile brain bounce back and forth inside the skull and causes bruising, swelling, and bleeding, which can lead to permanent, severe brain damage or death. The characteristic injuries of shaken baby syndrome are subdural hemorrhages (bleeding in the brain), retinal hemorrhages (bleeding in the retina), damage to the spinal cord and neck, and fractures of the ribs and bones. These injuries may not be immediately noticeable. Symptoms of shaken baby syndrome include extreme irritability, lethargy, poor feeding, breathing problems, convulsions, vomiting, and pale or bluish skin. Shaken baby injuries usually occur in children younger than 2 years old, but may be seen in children up to the age of 5. </s>


Input: What are the treatments for Shaken Baby Syndrome ?

Output: Emergency treatment for a baby who has been shaken usually includes life-sustaining measures such as respiratory support and surgery to stop internal bleeding and bleeding in the brain. Doctors may use brain scans, such as MRI and CT, to make a more definite diagnosis. </s>


Input: What is the outlook for Shaken Baby Syndrome ?

Output: In comparison with accidental traumatic brain injury in infants, shaken baby injuries have a much worse prognosis. Damage to the retina of the eye can cause blindness. The majority of infants who survive severe shaking will have some form of neurological or mental disability, such as cerebral palsy or cognitive impairment, which may not be fully apparent before 6 years of age. Children with shaken baby syndrome may require lifelong medical care. </s>


Input: what research (or clinical trials) is being done for Shaken Baby Syndrome ?

Output: The National Institute of Neurological Disorders and Stroke (NINDS), and other institutes of the National Institutes of Health (NIH), conduct research related to shaken baby syndrome in laboratories at the NIH and also support additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to treat and heal medical conditions such as shaken baby syndrome. </s>


Input: What is (are) Gerstmann-Straussler-Scheinker Disease ?

Output: Gerstmann-Straussler-Scheinker disease (GSS) is an extremely rare, neurodegenerative brain disorder. It is almost always inherited and is found in only a few families around the world. Onset of the disease usually occurs between the ages of 35 and 55. In the early stages, patients may experience varying levels of ataxia (lack of muscle coordination), including clumsiness, unsteadiness, and difficulty walking. As the disease progresses, the ataxia becomes more pronounced and most patients develop dementia. Other symptoms may include dysarthria (slurring of speech), nystagmus (involuntary movements of the eyes), spasticity (rigid muscle tone), and visual disturbances, sometimes leading to blindness. Deafness also can occur. In some families, parkinsonian features are present. GSS belongs to a family of human and animal diseases known as the transmissible spongiform encephalopathies (TSEs). Other TSEs include Creutzfeldt-Jakob disease, kuru, and fatal familial insomnia. </s>


Input: What are the treatments for Gerstmann-Straussler-Scheinker Disease ?

Output: There is no cure for GSS, nor are there any known treatments to slow progression of the disease. Current therapies are aimed at alleviating symptoms and making the patient as comfortable as possible. </s>


Input: What is the outlook for Gerstmann-Straussler-Scheinker Disease ?

Output: GSS is a slowly progressive condition usually lasting from 2 to 10 years. The disease ultimately causes severe disability and finally death, often after the patient goes into a coma or has a secondary infection such as aspiration pneumonia due to an impaired ability to swallow. </s>


Input: what research (or clinical trials) is being done for Gerstmann-Straussler-Scheinker Disease ?

Output: The NINDS supports and conducts research on TSEs, including GSS. Much of this research is aimed at characterizing the agents that cause these disorders, clarifying the mechanisms underlying them, and, ultimately, finding ways to prevent, treat, and cure them. </s>


Input: What is (are) Syringomyelia ?

Output: Syringomyelia (sear-IN-go-my-EEL-ya) is a disorder in which a fluid-filled cyst forms within the spinal cord. This cyst, called a syrinx, expands and elongates over time, destroying the center of the spinal cord. Since the spinal cord connects the brain to nerves in the extremities, this damage results in pain, weakness, and stiffness in the back, shoulders, arms, or legs. Symptoms vary among individuals. Other symptoms may include headaches and a loss of the ability to feel extremes of hot or cold, especially in the hands.Signs of the disorder tend to develop slowly, although sudden onset may occur with coughing or straining. If not treated surgically, syringomyelia often leads to progressive weakness in the arms and legs, loss of hand sensation, and chronic, severe pain. In most cases, the disorder is related to a congenital abnormality of the brain called a Chiari I malformation. This malformation causes the lower part of the cerebellum to protrude from its normal location in the back of the head, through the hole connecting the skull and spine, and into the cervical or neck portion of the spinal canal. Syringomyelia may also occur as a complication of trauma, meningitis, hemorrhage, a tumor, or other condition. Symptoms may appear months or even years after the initial injury, starting with pain, weakness, and sensory impairment originating at the site of trauma. Some cases of syringomyelia are familial, although this is rare. </s>


Input: What are the treatments for Syringomyelia ?

Output:
Surgery is usually recommended for individuals with syringomyelia, with the type of surgery and its location dependent on the type of syrinx. In persons with syringomyelia that is associated with the Chiara I malformation, a procedure that removes skulll bone and expands the space around the malformation usually prevents new symptoms from developing and results in the syrinx becoming smaller. In some individuals it may be necessary to drain the syrinx, which can be accomplished using a catheter, drainage tubes, and valves. Recurrence of syringomyelia after surgery may make additional operations necessary; these may not be completely successful over the long term.

In the absence of symptoms, syringomyelia is usually not treated. In addition, a physician may recommend not treating the condition in individuals of advanced age or in cases where there is no progression of symptoms. Whether treated or not, many individuals are told to avoid activities that involve straining. </s>


Input: What is the outlook for Syringomyelia ?

Output: Symptoms usually begin in young adulthood, with symptoms of one form usually beginning between the ages of 25 and 40. If not treated surgically (when needed), syringomyelia often leads to progressive weakness in the arms and legs, loss of hand sensation, and chronic, severe pain. Symptoms may worsen with straining or any activity that causes cerebrospinal fluid pressure to fluctuate. Some individuals may have long periods of stability. Surgery results in stabilization or modest improvement in symptoms for most individuals. Delay in treatment may result in irreversible spinal cord injury. </s>


Input: what research (or clinical trials) is being done for Syringomyelia ?

Output:
The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. NINDS investigators are studying how syrinxes first form, as well as the mechanisms of the disorders. NINDS investigators have found that the normal flow of cerebrospinal fluid that occurs with each heartbeat is obstructed in people with syringomyelia. Surgical procedures that relieve this obstruction usually result in the syrinx becoming much smaller in size. Studies are also underway to identify and better understand genetic factors that influence the development of Chiari I malformations and syringomyelia. Researchers hope to better understand the role of birth defects of the skull and brain in the development of hindbrain malformations that can lead to syringomyelia. Diagnostic technology is another area for continued research.

NINDS scientists are examining individuals who either have syringomyelia or are at risk of developing the disorder. They are investigating the factors that influence its development, progression, and treatment by recording more than 5 years of symptoms, muscle strength, overall function, and magnetic resonance imaging (MRI) scan findings from individuals who receive standard treatment for syringomyelia. Study results may allow scientists to provide more accurate recommendations to future individuals with syringomyelia regarding optimal surgical or non-surgical treatments. </s>


Input: What is (are) Dandy-Walker Syndrome ?

Output: Dandy-Walker Syndrome is a congenital brain malformation involving the cerebellum (an area of the back of the brain that coordinates movement) and the fluid-filled spaces around it. The key features of this syndrome are an enlargement of the fourth ventricle (a small channel that allows fluid to flow freely between the upper and lower areas of the brain and spinal cord), a partial or complete absence of the area of the brain between the two cerebellar hemispheres (cerebellar vermis), and cyst formation near the lowest part of the skull. An increase in the size and pressure of the fluid spaces surrounding the brain (hydrocephalus) may also be present. The syndrome can appear dramatically or develop unnoticed. Symptoms, which often occur in early infancy, include slow motor development and progressive enlargement of the skull. In older children, symptoms of increased intracranial pressure (pressure within the skull) such as irritability and vomiting, and signs of cerebellar dysfunction such as unsteadiness, lack of muscle coordination, or jerky movements of the eyes may occur. Other symptoms include increased head circumference, bulging at the back of the skull, abnormal breathing problems, and problems with the nerves that control the eyes, face and neck. Dandy-Walker Syndrome is sometimes associated with disorders of other areas of the central nervous system, including absence of the area made up of nerve fibers connecting the two cerebral hemispheres (corpus callosum) and malformations of the heart, face, limbs, fingers and toes. </s>


Input: What are the treatments for Dandy-Walker Syndrome ?

Output: Treatment for individuals with Dandy-Walker Syndrome generally consists of treating the associated problems, if needed. A surgical procedure called a shunt may be required to drain off excess fluid within the brain, which will reduce pressure inside the skull and improve symptoms. Treatment may also include various forms of therapy (physicial, occupational) and specialized education. </s>


Input: What is the outlook for Dandy-Walker Syndrome ?

Output: The effect of Dandy-Walker Syndrome on intellectual development is variable, with some children having normal cognition and others never achieving normal intellectual development even when the excess fluid buildup is treated early and correctly. Longevity depends on the severity of the syndrome and associated malformations. The presence of multiple congenital defects may shorten life span. </s>


Input: what research (or clinical trials) is being done for Dandy-Walker Syndrome ?

Output: The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. The NINDS conducts and supports a wide range of studies that explore the complex mechanisms of normal brain development. Researchers are studying DNA samples from individuals with Dandy-Walker syndrome to identify genes involved with the syndrome, as well as to better understand its causes and improve diagnosis and treatment options. Other research indicates that mothers with diabetes and those with rubella (German measles) during pregnancy are more likely to have a child with Dandy-Walker syndrome. </s>


Input: What is (are) Spina Bifida ?

Output: Spina bifida (SB) is a neural tube defect (a disorder involving incomplete development of the brain, spinal cord, and/or their protective coverings) caused by the failure of the fetus's spine to close properly during the first month of pregnancy. Infants born with SB sometimes have an open lesion on their spine where significant damage to the nerves and spinal cord has occurred. Although the spinal opening can be surgically repaired shortly after birth, the nerve damage is permanent, resulting in varying degrees of paralysis of the lower limbs. Even when there is no lesion present there may be improperly formed or missing vertebrae and accompanying nerve damage. In addition to physical and mobility difficulties, most individuals have some form of learning disability. The types of SB are: myelomeningocele, the severest form, in which the spinal cord and its protective covering (the meninges) protrude from an opening in the spine; meningocele in which the spinal cord develops normally but the meninges and spinal fluid) protrude from a spinal opening; closed neural tube defects, which consist of a group of defects in which development of the spinal cord is affected by malformations of the fat, bone, or meninges; and and occulta, the mildest form, in which one or more vertebrae are malformed and covered by a layer of skin. SB may also cause bowel and bladder complications, and many children with SB have hydrocephalus (excessive accumulation of cerebrospinal fluid in the brain). </s>


Input: What are the treatments for Spina Bifida ?

Output: There is no cure for SB because the nerve tissue cannot be replaced or repaired. Treatment for the variety of effects of SB may include surgery, medication, and physiotherapy. Many individuals with SB will need assistive devices such as braces, crutches, or wheelchairs. Ongoing therapy, medical care, and/or surgical treatments may be necessary to prevent and manage complications throughout the individual's life. Surgery to close the newborn's spinal opening is generally performed within 24 hours after birth to minimize the risk of infection and to preserve existing function in the spinal cord. </s>


Input: What is the outlook for Spina Bifida ?

Output: The prognosis for individuals with SB depends on the number and severity of abnormalities. Prognosis is poorest for those with complete paralysis, hydrocephalus, and other congenital defects. With proper care, most children with SB live well into adulthood. </s>


Input: what research (or clinical trials) is being done for Spina Bifida ?

Output: The NINDS supports a broad range of research on neural tube defects such as SB aimed at finding ways to treat, prevent, and, ultimately, cure these disorders. Recent studies have shown that the addition of folic acid to the diet of women of child-bearing age may significantly reduce the incidence of neural tube defects. Therefore it is recommended that all women of child-bearing age consume 400 micrograms of folic acid daily. </s>


Input: What is (are) Back Pain ?

Output: Acute or short-term low back pain generally lasts from a few days to a few weeks. Most acute back pain is the result of trauma to the lower back or a disorder such as arthritis. Pain from trauma may be caused by a sports injury, work around the house or in the garden, or a sudden jolt such as a car accident or other stress on spinal bones and tissues. Symptoms may range from muscle ache to shooting or stabbing pain, limited flexibility and range of motion, or an inability to stand straight. Chronic back pain is pain that persists for more than 3 months. It is often progressive and the cause can be difficult to determine. </s>


Input: What are the treatments for Back Pain ?

Output: Most low back pain can be treated without surgery. Treatment involves using over-the-counter pain relievers to reduce discomfort and anti-inflammatory drugs to reduce inflammation. The goal of treatment is to restore proper function and strength to the back, and prevent recurrence of the injury. Medications are often used to treat acute and chronic low back pain. Effective pain relief may involve a combination of prescription drugs and over-the-counter remedies. Although the use of cold and hot compresses has never been scientifically proven to quickly resolve low back injury, compresses may help reduce pain and inflammation and allow greater mobility for some individuals. Bed rest is recommended for only 12 days at most. Individuals should resume activities as soon as possible. Exercise may be the most effective way to speed recovery from low back pain and help strengthen back and abdominal muscles. In the most serious cases, when the condition does not respond to other therapies, surgery may relieve pain caused by back problems or serious musculoskeletal injuries. </s>


Input: What is the outlook for Back Pain ?

Output: Most patients with back pain recover without residual functional loss, but individuals should contact a doctor if there is not a noticeable reduction in pain and inflammation after 72 hours of self-care. Recurring back pain resulting from improper body mechanics or other nontraumatic causes is often preventable. Engaging in exercises that don't jolt or strain the back, maintaining correct posture, and lifting objects properly can help prevent injuries. Many work-related injuries are caused or aggravated by stressors such as heavy lifting, vibration, repetitive motion, and awkward posture. Applying ergonomic principles  designing furniture and tools to protect the body from injury  at home and in the workplace can greatly reduce the risk of back injury and help maintain a healthy back. </s>


Input: what research (or clinical trials) is being done for Back Pain ?

Output: The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct pain research in laboratories at the NIH and also support pain research through grants to major medical institutions across the country. Currently, researchers are examining the use of different drugs to effectively treat back pain, in particular, chronic pain that has lasted at least 6 months. Other studies are comparing different health care approaches to the management of acute low back pain (standard care versus chiropractic, acupuncture, or massage therapy). These studies are measuring symptom relief, restoration of function, and patient satisfaction. Other research is comparing standard surgical treatments to the most commonly used standard nonsurgical treatments to measure changes in health-related quality of life among patients suffering from spinal stenosis. </s>


Input: What is (are) Neuroleptic Malignant Syndrome ?

Output: Neuroleptic malignant syndrome is a life-threatening, neurological disorder most often caused by an adverse reaction to neuroleptic or antipsychotic drugs. Symptoms include high fever, sweating, unstable blood pressure, stupor, muscular rigidity, and autonomic dysfunction. In most cases, the disorder develops within the first 2 weeks of treatment with the drug; however, the disorder may develop any time during the therapy period. The syndrome can also occur in people taking anti-Parkinsonism drugs known as dopaminergics if those drugs are discontinued abruptly. </s>


Input: What are the treatments for Neuroleptic Malignant Syndrome ?

Output: Generally, intensive care is needed. The neuroleptic or antipsychotic drug is discontinued, and the fever is treated aggressively. A muscle relaxant may be prescribed. Dopaminergic drugs, such as a dopamine agonist, have been reported to be useful. </s>


Input: What is the outlook for Neuroleptic Malignant Syndrome ?

Output: Early identification of and treatment for individuals with neuroleptic malignant syndrome improves outcome. If clinically indicated, a low potency neuroleptic can be reintroduced very slowly when the individual recovers, although there is a risk that the syndrome might recur. Another alternative is to substitute another class of drugs for the neuroleptic. Anesthesia may be a risk to individuals who have experienced neuroleptic malignant syndrome. </s>


Input: what research (or clinical trials) is being done for Neuroleptic Malignant Syndrome ?

Output: The NINDS supports research on neurological disorders such as neuroleptic malignant syndrome. Much of this research focuses on finding ways to prevent and treat the disorder. </s>


Input: What is (are) Antiphospholipid Syndrome ?

Output: Antiphospholipid syndrome (APS) is an autoimmune disorder caused when antibodies -- immune system cells that fight off bacteria and viruses -- mistakenly attack healthy body tissues and organs. In APS, specific antibodies activate the inner lining of blood vessels, which leads to the formation of blood clots in arteries or veins. APS is sometimes called sticky blood syndrome, because of the increased tendency to form blood clots in the veins and arteries. The symptoms of APS are due to the abnormal blood clotting. Clots can develop in the veins of the legs and lungs, or in the placenta of pregnant women. One of the most serious complications of APS occurs when a clot forms in the brain and causes a stroke. Other neurological symptoms include chronic headaches, dementia (similar to the dementia of Alzheimers disease), and seizures. Infrequently, individuals will develop chorea (a movement disorder in which the body and limbs writhe uncontrollably), cognitive dysfunction (such as poor memory), transverse myelitis, depression or psychosis, optic neuropathy, or sudden hearing loss. In pregnant women, clots in the placenta can cause miscarriages. APS is diagnosed by the presence of a positive antiphospholipid antibody and either a history of blood clots in an artery or vein or a history of multiple miscarriages or other pregnancy problems. Some individuals will have a characteristic lacy, net-like red rash called livedo reticularis over their wrists and knees. </s>


Input: What are the treatments for Antiphospholipid Syndrome ?

Output: The main goal of treatment is to thin the blood to reduce clotting. At present, the recommended treatment is low-dose aspirin. For individuals who have already had a stroke or experience recurrent clots, doctors recommend treatment with the anticoagulant warfarin. Pregnant women are treated with either aspirin or another anticoagulant -- heparin -- since warfarin can cause birth defects. </s>


Input: What is the outlook for Antiphospholipid Syndrome ?

Output: APS improves significantly with anticoagulation therapy, which reduces the risk of further clots in veins and arteries. Treatment should be lifelong, since there is a high risk of further clots in individuals who stop warfarin treatment. Doctors often recommend that individuals stop smoking, exercise regularly, and eat a healthy diet to prevent high blood pressure and diabetes, which are diseases that increase the risk for stroke. Treating pregnant women with aspirin or heparin usually prevents miscarriages related to APS. </s>


Input: what research (or clinical trials) is being done for Antiphospholipid Syndrome ?

Output: The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) support research on APS through grants to major medical institutions across the country.NINDS-funded research is looking at ways to reduce clotting and prevent stroke. Among other NIH-funded research efforts, scientists are examining the role of antiphospholipid antibodies in clotting and pregnancy loss, which is commonly seen in individuals with lupus. Another project hopes to identify potential inherited risk factors for the development of APS. </s>


Input: What is (are) Kearns-Sayre Syndrome ?

Output: Kearns-Sayre syndrome (KSS) is a rare neuromuscular disorder with onset usually before the age of 20 years. It is the result of abnormalities in the DNA of mitochondria - small rod-like structures found in every cell of the body that produce the energy that drives cellular functions. The mitochondrial diseases correlate with specific DNA mutations that cause problems with many of the organs and tissues in the body. KSS is characterized by progressive limitation of eye movements until there is complete immobility, accompanied by eyelid droop. It is also associated with abnormal accumulation of pigmented material on the membrane lining the eyes. Additional symptoms may include mild skeletal muscle weakness, heart block (a cardiac conduction defect), short stature, hearing loss, an inability to coordinate voluntary movements (ataxia), impaired cognitive function, and diabetes. Seizures are infrequent. Several endocrine disorders can be associated with KSS. </s>


Input: What are the treatments for Kearns-Sayre Syndrome ?

Output: There is currently no effective way to treat mitochondria abnormalities in KSS. Treatment is generally symptomatic and supportive. Management of KSS involves multiple specialties depending on the organs involved. The most essential is a regular and long-term follow-up with cardiologists. Conduction problems of heart impulse like heart block may be treated with a pacemaker. Other consultations may include audiology, ophthalmology, endocrinology, neurology, and neuropsychiatry. Hearing aids may be required. There is typically no treatment for limitation in eye movement. Endocrinology abnormalities can be treated with drugs. </s>


Input: What is the outlook for Kearns-Sayre Syndrome ?

Output: KSS is a slowly progressive disorder. The prognosis for individuals with KSS varies depending on the severity and the number of organs involved. Early diagnosis and periodic electrocardiogram (ECG) are important since heart block can cause death in 20 percent of patients. Early pacemaker implantation can be of great benefit and offer a longer life expectancy in many patients. </s>


Input: what research (or clinical trials) is being done for Kearns-Sayre Syndrome ?

Output: The NINDS supports research on neuromuscular disorders such as KSS. The goals of this research are to increase understanding of these disorders, and to find ways to prevent, treat, and, ultimately, cure them. The most promising approach for treatment in the future will be to alter replication or destroy abnormal mitochondria. </s>


Input: What is (are) Restless Legs Syndrome ?

Output: Restless legs syndrome (RLS) is a neurological disorder characterized by unpleasant sensations in the legs and an uncontrollable, and sometimes overwhelming, urge to move them for relief. Individuals affected with the disorder often describe the sensations as throbbing, polling, or creeping. The sensations range in severity from uncomfortable to irritating to painful. </s>


Input: What are the treatments for Restless Legs Syndrome ?

Output:
For those with mild to moderate symptoms, many physicians suggest certain lifestyle changes and activities to reduce or eliminate symptoms. Decreased use of caffeine, alcohol, and tobacco may provide some relief. Physicians may suggest that certain individuals take supplements to correct deficiencies in iron, folate, and magnesium. Taking a hot bath, massaging the legs, or using a heating pad or ice pack can help relieve symptoms in some patients.

Physicians also may suggest a variety of medications to treat RLS, including dopaminergics, benzodiazepines (central nervous system depressants), opioids, and anticonvulsants. The drugs ropinirole, pramipexole, gabapentin enacarbil, and rotigotine have been approved by the U.S. Food and Drug Administration for treating moderate to severe RLS. The Relaxis pad, which the person can place at the site of discomfort when in bed and provides 30 minutes of vibrations (counterstimulation) that ramp off after 30 minutes, also has been approved by the FDA. </s>


Input: What is the outlook for Restless Legs Syndrome ?

Output: RLS is generally a life-long condition for which there is no cure. Symptoms may gradually worsen with age. Nevertheless, current therapies can control the disorder, minimizing symptoms and increasing periods of restful sleep. In addition, some individuals have remissions, periods in which symptoms decrease or disappear for days, weeks, or months, although symptoms usually eventually reappear. </s>


Input: what research (or clinical trials) is being done for Restless Legs Syndrome ?

Output: The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct and support RLS research in laboratories at the NIH and at major medical institutions across the country. The goal of this research is to increase scientific understanding of RLS, find improved methods of diagnosing and treating the syndrome, and discover ways to prevent it. </s>


Input: What is (are) Infantile Refsum Disease ?

Output: Infantile Refsum disease (IRD) is a medical condition within the Zellweger spectrum of perixisome biogenesis disorders (PBDs), inherited genetic disorders that damage the white matter of the brain and affect motor movements. PBDs are part of a larger group of disorders called the leukodystrophies. The Zellweger spectrum of PBDs include related, but not more severe, disorders referred to as Zellweger syndrome (ZS) and neonatal adrenoleukodystrophy. Collectively, these disorders are caused by inherited defects in any one of 12 genes, called PEX genes, which are required for the normal formation and function of peroxisomes. Peroxisomes are cell structures required for the normal formation and function of the brain, eyes, liver, kidneys, and bone. They contain enzymes that break down toxic substances in the cells, including very long chain fatty acids and phytanic acid (a type of fat found in certain foods), and synthesize certain fatty materials (lipids) that are required for cell function. When peroxisomes are not functioning, there is over-accumulation of very long chain fatty acids and phytanic acid, and a lack of bile acids and plasmalogens--specialized lipids found in cell membranes and the myelin sheaths and encase and protect nerve fibers.. IRD has some residual perixisome function, resulting in less severe disease than in Zellweger syndrome. Symptoms of IRD begin in infancy with retinitis pigmentosa, a visual impairment that often leads to blindness, and hearing problems that usually progress to deafness by early childhood. Other symptoms may include rapid, jerky eye movements (nystagmus); floppy muscle tone (hypotonia) and lack of muscle coordination (ataxia); mental and growth disabilities; abnormal facial features; enlarged liver; and white matter abnormalities of brain myelin. At the mildest extreme of the disorder, intellect may be preserved. Although Adult Refsum disease and IRD have similar names, they are separate disorders caused by different gene defects. </s>


Input: What are the treatments for Infantile Refsum Disease ?

Output: The primary treatment for IRD is to avoid foods that contain phytanic acid, including dairy products; beef and lamb; and fatty fish such as tuna, cod, and haddock. Although this prevents the accumulation of phytanic acid, it does not address the accumulation of very long chain fatty acids, and the deficiency of bile acids and plasmalogens. </s>


Input: What is the outlook for Infantile Refsum Disease ?

Output: IRD is a fatal disease, but some children will survive into their teens and twenties, and possibly even beyond. </s>


Input: what research (or clinical trials) is being done for Infantile Refsum Disease ?

Output: The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to IRDin its laboratories at the National Institutes of Health (NIH), and also supports additional research through grants to major medical institutions across the country. Research is focused on finding better ways to prevent, treat, and ultimately cure disorders such as the PBDs. </s>


Input: What is (are) Reye's Syndrome ?

Output: 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. </s>


Input: What are the treatments for Reye's Syndrome ?

Output: 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. </s>


Input: What is the outlook for Reye's Syndrome ?

Output: 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. </s>


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

Output: 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. </s>


Input: What is (are) Cerebral Arteriosclerosis ?

Output:
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. </s>


Input: What are the treatments for Cerebral Arteriosclerosis ?

Output: 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. </s>


Input: What is the outlook for Cerebral Arteriosclerosis ?

Output: 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. </s>


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

Output: 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. </s>


Input: What is (are) Schizencephaly ?

Output: 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. </s>


Input: What are the treatments for Schizencephaly ?

Output: 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. </s>


Input: What is the outlook for Schizencephaly ?

Output: The prognosis for individuals with schizencephaly varies depending on the size of the clefts and the extent of neurological disabilities. </s>


Input: what research (or clinical trials) is being done for Schizencephaly ?

Output: 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. </s>


Input: What is (are) Inflammatory Myopathies ?

Output: 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. </s>


Input: What are the treatments for Inflammatory Myopathies ?

Output: 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. </s>


Input: What is the outlook for Inflammatory Myopathies ?

Output: 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. </s>


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

Output: 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. </s>


Input: What is (are) Stiff-Person Syndrome ?

Output: 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. </s>


Input: What are the treatments for Stiff-Person Syndrome ?

Output: 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. </s>


Input: What is the outlook for Stiff-Person Syndrome ?

Output: 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. </s>


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

Output: 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. </s>


Input: What is (are) Hereditary Spastic Paraplegia ?

Output: 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. </s>


Input: What are the treatments for Hereditary Spastic Paraplegia ?

Output: 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. </s>


Input: What is the outlook for Hereditary Spastic Paraplegia ?

Output: 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. </s>


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

Output: 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. </s>


Input: What is (are) Leukodystrophy ?

Output: 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. </s>


Input: What are the treatments for Leukodystrophy ?

Output: 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. </s>


Input: What is the outlook for Leukodystrophy ?

Output: The prognosis for the leukodystrophies varies according to the specific type of leukodystrophy. </s>


Input: what research (or clinical trials) is being done for Leukodystrophy ?

Output: 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. </s>


Input: What is (are) Canavan Disease ?

Output:
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. </s>


Input: What are the treatments for Canavan Disease ?

Output: Canavan disease causes progressive brain atrophy. There is no cure, nor is there a standard course of treatment. Treatment is symptomatic and supportive. </s>


Input: What is the outlook for Canavan Disease ?

Output: The prognosis for Canavan disease is poor. Death usually occurs before age 10, although some children may survive into their teens and twenties. </s>


Input: what research (or clinical trials) is being done for Canavan Disease ?

Output: 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. </s>


Input: What is (are) Alexander Disease ?

Output: 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. </s>


Input: What are the treatments for Alexander Disease ?

Output: There is no cure for Alexander disease, nor is there a standard course of treatment. Treatment of Alexander disease is symptomatic and supportive. </s>


Input: What is the outlook for Alexander Disease ?

Output: 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. </s>


Input: what research (or clinical trials) is being done for Alexander Disease ?

Output: Recent discoveries show that most individuals (approximately 90 percent) with Alexander disease have a mutation in the gene that makes glial fibrillary acidic protein (GFAP). GFAP is a normal component of the brain, but it is unclear how the mutations in this genecauses the disease. In most cases mutations occur spontaneously are not inherited from parents.A small number of people thought to have Alexander disease do not have identifiable mutations in GFAP, which leads researchers to believe that there may be other genetic or perhaps even non-genetic causes of Alexander disease. Current research is aimed at understanding the mechanisms by which the mutations cause disease, developing better animal models for the disorder, and exploring potential strategies for treatment. At present, there is no exact animal model for the disease; however, mice have been engineered to produce the same mutant forms of GFAP found in individuals with Alexander disease. These mice form Rosenthal fibers and have a predisposition for seizures, but do not yet mimic all features of human disease (such as the leukodystrophies). One clinical study is underway to identify biomarkers of disease severity or progression in samples of blood or cerebrospinal fluid. Such biomarkers, if found, would be a major advantage for evaluating the response to any treatments that are developed in the future. </s>


Input: What is (are) Narcolepsy ?

Output: Narcolepsy is a chronic neurological disorder caused by the brain's inability to regulate sleep-wake cycles normally. At various times throughout the day, people with narcolepsy experience irresistable bouts ofsleep. If the urge becomes overwhelming, individuals will fall asleep for periods lasting from a few seconds to several minutes. In rare cases, some people may remain asleep for an hour or longer. In addition to excessive daytime sleepiness (EDS), three other major symptoms frequently characterize narcolepsy: cataplexy, or the sudden loss of voluntary muscle tone; vivid hallucinations during sleep onset or upon awakening; and brief episodes of total paralysis at the beginning or end of sleep. Narcolepsy is not definitively diagnosed in most patients until 10 to 15 years after the first symptoms appear. The cause of narcolepsy remains unknown. It is likely that narcolepsy involves multiple factors interacting to cause neurological dysfunction and sleep disturbances. </s>


Input: What are the treatments for Narcolepsy ?

Output: There is no cure for narcolepsy. In 1999, after successful clinical trial results, the U.S. Food and Drug Administration (FDA) approved a drug called modafinil for the treatment of EDS. Two classes of antidepressant drugs have proved effective in controlling cataplexy in many patients: tricyclics (including imipramine, desipramine, clomipramine, and protriptyline) and selective serotonin reuptake inhibitors (including fluoxetine and sertraline). Drug therapy should be supplemented by behavioral strategies. For example, many people with narcolepsy take short, regularly scheduled naps at times when they tend to feel sleepiest. Improving the quality of nighttime sleep can combat EDS and help relieve persistent feelings of fatigue. Among the most important common-sense measures people with narcolepsy can take to enhance sleep quality are actions such as maintaining a regular sleep schedule, and avoiding alcohol and caffeine-containing beverages before bedtime. The drug Xyrem (sodium oxybate or gamma hydroxybutyrate, also known as GHB) was approved in July 2002 for treating cataplexy and in November 2005 for EDS in people who have narcolepsy. Due to safety concerns associated with the use of this drug, the distribution of Xyrem is tightly restricted. </s>


Input: What is the outlook for Narcolepsy ?

Output: None of the currently available medications enables people with narcolepsy to consistently maintain a fully normal state of alertness. But EDS and cataplexy, the most disabling symptoms of the disorder, can be controlled in most patients with drug treatment. Often the treatment regimen is modified as symptoms change. Whatever the age of onset, patients find that the symptoms tend to get worse over the two to three decades after the first symptoms appear. Many older patients find that some daytime symptoms decrease in severity after age 60. </s>


Input: what research (or clinical trials) is being done for Narcolepsy ?

Output: The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research into narcolepsy and other sleep disorders in laboratories at the NIH and also support additional research through grants to major medical institutions across the country. The NINDS continues to support investigations into the basic biology of sleep, including the brain mechanisms involved in generating and regulating sleep. Within the National Heart, Lung, and Blood Institute, also a component of the NIH, the       National        Center   on Sleep Disorders Research (NCSDR) coordinates Federal government sleep research activities and shares information with private and nonprofit groups. </s>


Input: What are the complications of Neurological Complications of AIDS ?

Output:
AIDS is primarily an immune system disorder caused by the human immunodeficiency virus (HIV), but it can also affect the nervous system. HIV does not appear to directly invade nerve cells but it jeopardizes their health and function, causing symptoms such as confusion, forgetfulness, behavioral changes, headaches, progressive weakness and loss of sensation in the arms and legs, cognitive motor impairment, or damage to the peripheral nerves. Other complications that can occur as a result of HIV infection or the drugs used to treat it include pain, seizures, shingles, spinal cord problems, lack of coordination, difficult or painful swallowing, anxiety disorder, depression, fever, vision loss, gait disorders, destruction of brain tissue, and coma. Other AIDS-related nervous system disorders may be caused by certain cancers or by illnesses that would not otherwise affect people with healthy immune systems.

Among the most common neurological complications are: AIDS dementia complex, causing symptoms such as encephalitis (inflammation of the brain), behavioral changes, and a gradual decline in cognitive function; central nervous system lymphomas, cancerous tumors that either begin in the brain or result from a cancer that has spread from another site in the body; cryptococcal meningitis; cytomegalovirus infections; herpes virus infections; neuropathy; neurosyphilis; progressive multifocal leukoencephalopathy (PML); and psychological and neuropsychiatric disorders. </s>


Input: What are the treatments for Neurological Complications of AIDS ?

Output:
No single treatment can cure the neurological complications of AIDS. Some disorders require aggressive therapy while others are treated symptomatically.

Medicines range from analgesics sold over the counter to antiepileptic drugs, opiates, corticosteroids, and some classes of antidepressants. Other treatments include radiation therapy or chemotherapy to kill or shrink cancerous brain tumors that may be caused by HIV, antifungal or antimalarial drugs to combat certain bacterial infections, and penicillin to treat neurosyphilis. Aggressive antiretroviral therapy is used to treat AIDS dementia complex, PML, and cytomegalovirus encephalitis. HAART, or highly active antiretroviral therapy, combines at least three drugs to reduce the amount of virus circulating in the blood and may also delay the start of some infections. </s>


Input: What is the outlook for Neurological Complications of AIDS ?

Output: The overall prognosis for individuals with AIDS in recent years has improved significantly because of new drugs and treatments. AIDS clinicians often fail to recognize neurological complications of AIDS. Those who suspect they are having neurological complications should be sure to discuss these with their doctor. </s>


Input: what research (or clinical trials) is being done for Neurological Complications of AIDS ?

Output: Within the Federal government, the National Institute of Neurological Disorders and Stroke (NINDS), one part of the National Institutes of Health (NIH), supports research on the neurological consequences of AIDS. The NINDS works closely with its sister agency, the National Institute of Allergy and Infectious Diseases (NIAID), which has primary responsibility for research related to HIV and AIDS. </s>


Input: What is (are) Tabes Dorsalis ?

Output: Tabes dorsalis is a slow degeneration of the nerve cells and nerve fibers that carry sensory information to the brain. The degenerating nerves are in the dorsal columns of the spinal cord (the portion closest to the back of the body) and carry information that help maintain a person's sense of position. Tabes dorsalis is the result of an untreated syphilis infection. Symptoms may not appear for some decades after the initial infection and include weakness, diminished reflexes, unsteady gait, progressive degeneration of the joints, loss of coordination, episodes of intense pain and disturbed sensation, personality changes, dementia, deafness, visual impairment, and impaired response to light. The disease is more frequent in males than in females. Onset is commonly during mid-life. The incidence of tabes dorsalis is rising, in part due to co-associated HIV infection. </s>


Input: What are the treatments for Tabes Dorsalis ?

Output: Penicillin, administered intravenously, is the treatment of choice. Associated pain can be treated with opiates, valproate, or carbamazepine. Patients may also require physical or rehabilitative therapy to deal with muscle wasting and weakness. Preventive treatment for those who come into sexual contact with an individual with tabes dorsalis is important. </s>


Input: What is the outlook for Tabes Dorsalis ?

Output: If left untreated, tabes dorsalis can lead to paralysis, dementia, and blindness. Existing nerve damage cannot be reversed. </s>


Input: what research (or clinical trials) is being done for Tabes Dorsalis ?

Output: The NINDS supports and conducts research on neurodegenerative disorders, such as tabes dorsalis, in an effort to find ways to prevent, treat, and, ultimately, cure these disorders. </s>


Input: What is (are) Herpes Zoster Oticus ?

Output: Herpes zoster oticus, also called Ramsay Hunt Syndrome or Ramsay Hunt Syndrome type II, is a common complication of shingles. Shingles is an infection caused by the varicella-zoster virus, which is the virus that causes chickenpox. Shingles occurs in people who have had chickenpox and represents a reactivation of the dormant varicella-zoster virus. Herpes zoster oticus, which is caused by the spread of the varicella-zoster virus to facial nerves, is characterized by intense ear pain, a rash around the ear, mouth, face, neck, and scalp, and paralysis of facial nerves. Other symptoms may include hearing loss, vertigo (abnormal sensation of movement), and tinnitus (abnormal sounds). Taste loss in the tongue and dry mouth and eyes may also occur. </s>


Input: What are the treatments for Herpes Zoster Oticus ?

Output: Some cases of herpes zoster oticus do not require treatment. When treatment is needed, medications such as antiviral drugs or corticosteroids may be prescribed. Vertigo may be treated with the drug diazepam </s>


Input: What is the outlook for Herpes Zoster Oticus ?

Output: Generally, the prognosis of herpes zoster oticus is good. However, in some cases, hearing loss may be permanent. Vertigo may last for days or weeks. Facial paralysis may be temporary or permanent. </s>


Input: what research (or clinical trials) is being done for Herpes Zoster Oticus ?

Output: The NINDS supports research on shingles and shingles-related conditions. Current studies focus on the relationship between the persistence of neurotropic viruses and development of neurological diseases including herpes simplex and varicella-zoster viruses. </s>


Input: What is (are) Hemicrania Continua ?

Output: Hemicrania continua is a chronic and persistent form of headache marked by continuous pain that varies in severity, always occurs on the same side of the face and head, and is superimposed with additional debilitating symptoms. on the continuous but fluctuating pain are occasional attacks of more severe pain. A small percentage of individuals with hemicrania continua have bilateral pain, or pain on both sides of the head. A headache is considered hemicrania continua if the person has had a one-sided daily or continuous headache of moderate intensity with occasional short, piercing head pain for more than 3 months without shifting sides or pain-free periods. The headache must also be completely responsive to treatment with the non-steroidal anti-inflammatory drug drug indomethacin. It must have at least one of the following symptoms: eye redness and/or tearing, nasal congestion and/or runny nose, ptosis (drooping eyelid) and miosis (contracture of the iris). Occasionally, individuals will also have forehead sweating and migraine symptoms, such as throbbing pain, nausea and/or vomiting, or sensitivity to light and sound. The disorder has two forms: chronic, with daily headaches, and remitting, in which headaches may occur for a period as long as 6 months and are followed by a pain-free period of weeks to months until the pain returns. Most patients experience attacks of increased pain three to five times per 24-hour cycle. This disorder is more common in women than in men. Physical exertion and alcohol use may increase the severity of headache pain in some patients. The cause of this disorder is unknown. </s>


Input: What are the treatments for Hemicrania Continua ?

Output: Indomethacin provides rapid relief from symptoms. Patients must take between 25 and 300 milligrams of indomethacin daily and indefinitely to decrease symptoms. Some individuals may need to take acid-suppression medicine due to a gastrointestinal side effect. For those who cannot tolerate the side effects, another NSAID, celecoxib, has been shown to have less complications and can be prescribed. Amitriptyline and other tricyclic antidepressants are also effective in some individuals with hemicrania continua as a preventative treatment. </s>


Input: What is the outlook for Hemicrania Continua ?

Output: Individuals may obtain complete to near-complete relief of symptoms with proper medical attention and daily medication. Some people may not be able to tolerate long-term use of indomethacin and may have to rely on less effective NSAIDs. </s>


Input: what research (or clinical trials) is being done for Hemicrania Continua ?

Output: The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) support research related to hemicrania continua through grants to medical research institutions across the country. Much of this research focuses on understanding hemicrania continua in order to finding better ways to prevent, treat, and ultimately cure the disorder. </s>