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What is (are) Transient Ischemic Attack ?
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A transient ischemic attack (TIA) is a transient stroke that lasts only a few minutes. It occurs when the blood supply to part of the brain is briefly interrupted. TIA symptoms, which usually occur suddenly, are similar to those of stroke but do not last as long. Most symptoms of a TIA disappear within an hour, although they may persist for up to 24 hours. Symptoms can include: numbness or weakness in the face, arm, or leg, especially on one side of the body; confusion or difficulty in talking or understanding speech; trouble seeing in one or both eyes; and difficulty with walking, dizziness, or loss of balance and coordination.
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What are the treatments for Transient Ischemic Attack ?
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Because there is no way to tell whether symptoms are from a TIA or an acute stroke, patients should assume that all stroke-like symptoms signal an emergency and should not wait to see if they go away. A prompt evaluation (within 60 minutes) is necessary to identify the cause of the TIA and determine appropriate therapy. Depending on a patient's medical history and the results of a medical examination, the doctor may recommend drug therapy or surgery to reduce the risk of stroke in people who have had a TIA. The use of antiplatelet agents, particularly aspirin, is a standard treatment for patients at risk for stroke. People with atrial fibrillation (irregular beating of the heart) may be prescribed anticoagulants.
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What is the outlook for Transient Ischemic Attack ?
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TIAs are often warning signs that a person is at risk for a more serious and debilitating stroke. About one-third of those who have a TIA will have an acute stroke some time in the future. Many strokes can be prevented by heeding the warning signs of TIAs and treating underlying risk factors. The most important treatable factors linked to TIAs and stroke are high blood pressure, cigarette smoking, heart disease, carotid artery disease, diabetes, and heavy use of alcohol. Medical help is available to reduce and eliminate these factors. Lifestyle changes such as eating a balanced diet, maintaining healthy weight, exercising, and enrolling in smoking and alcohol cessation programs can also reduce these factors.
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what research (or clinical trials) is being done for Transient Ischemic Attack ?
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NINDS is the leading supporter of research on stroke and TIA in the U.S. and sponsors studies ranging from clinical trials to investigations of basic biological mechanisms as well as studies with animals.
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What is (are) Hemicrania Continua ?
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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.
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What are the treatments for Hemicrania Continua ?
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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.
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What is the outlook for Hemicrania Continua ?
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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.
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what research (or clinical trials) is being done for Hemicrania Continua ?
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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.
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What is (are) Essential Tremor ?
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Tremor is an unintentional, somewhat rhythmic, muscle movement involving to-and-fro movements (oscillations) of one or more parts of the body. Essential tremor (previously called benign essential tremor) is the most common form of abnormal tremor. (In some people, tremor is a symptom of a neurological disorder or appears as a side effect of certain drugs.) Although it may be mild and nonprogressive in some people, in others the tremor is slowly progressive, starting on one side of the body but eventually affecting both sides. Hand tremor is most common but the head, arms, voice, tongue, legs, and trunk may also be involved. Hand tremor may cause problems with purposeful movements such as eating, writing, sewing, or shaving. Head tremor may be seen as a "yes-yes" or "no-no" motion. Essential tremor may be accompanied by mild gait disturbance. Heightened emotion, stress, fever, physical exhaustion, or low blood sugar may trigger tremors or increase their severity. There may be mild degeneration in the certain parts of the cerebellum in persons with essential tremor. Onset is most common after age 40, although symptoms can appear at any age. Children of a parent who has essential tremor have up to a 50 percent chance of inheriting the condition. Essential tremor is not associated with any known pathology.
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What are the treatments for Essential Tremor ?
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There is no definitive cure for essential tremor. Symptomatic drug therapy may include propranolol or other beta blockers and primidone, an anticonvulsant drug. Eliminating tremor "triggers" such as caffeine and other stimulants from the diet is often recommended. Physical and occupational therapy may help to reduce tremor and improve coordination and muscle control for some individuals. Deep brain stimulation uses a surgically implanted, battery-operated medical device called a neurostimulator to delivery electrical stimulation to targeted areas of the brain that control movement, temporarily blocking the nerve signals that cause tremor. Other surgical intervention is effective but may have side effects.
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What is the outlook for Essential Tremor ?
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Although essential tremor is not life-threatening, it can make it harder to perform daily tasks and is embarrassing to some people. Tremor frequency may decrease as the person ages, but the severity may increase, affecting the person's ability to perform certain tasks or activities of daily living. In many people the tremor may be mild throughout life.
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what research (or clinical trials) is being done for Essential Tremor ?
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The National Institute of Neurological Disorders and Stroke, a unit of the National Institutes of Health (NIH) within the U.S. Department of Health and Human Services, is the nation's leading federal funder of research on disorders of the brain and nervous system. The NINDS sponsors research on tremor both at its facilities at the NIH and through grants to medical centers.
Scientists at the NINDS are evaluating the effectiveness of 1-octanol, a substance similar to alcohol but less intoxicating, for treating essential tremor. Results of two previous NIH studies have shown this agent to be promising as a potential new treatment.
Scientists are also studying the effectiveness of botulinum toxin as a treatment for a variety of involuntary movement disorders, including essential tremor of the hand.
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What is (are) CADASIL ?
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CADASIL (Cerebral Autosomal Dominant Arteriopathy with Sub-cortical Infarcts and Leukoencephalopathy) is an inherited form of cerebrovascular disease that occurs when the thickening of blood vessel walls blocks the flow of blood to the brain. The disease primarily affects small blood vessels in the white matter of the brain. A mutation in the Notch3 gene alters the muscular walls in these small arteries. CADASIL is characterized by migraine headaches and multiple strokes progressing to dementia. Other symptoms include cognitive deterioration, seizures, vision problems, and psychiatric problems such as severe depression and changes in behavior and personality. Individuals may also be at higher risk of heart attack. Symptoms and disease onset vary widely, with signs typically appearing in the mid-30s. Some individuals may not show signs of the disease until later in life. CADASIL formerly known by several names, including hereditary multi-infarct dementia is one cause of vascular cognitive impairment (dementia caused by lack of blood to several areas of the brain). It is an autosomal dominant inheritance disorder, meaning that one parent carries and passes on the defective gene. Most individuals with CADASIL have a family history of the disorder. However, because the genetic test for CADASIL was not available before 2000, many cases were misdiagnosed as multiple sclerosis, Alzheimer's disease, or other neurodegenerative diseases.
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What are the treatments for CADASIL ?
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There is no treatment to halt this genetic disorder. Individuals are given supportive care. Migraine headaches may be treated by different drugs and a daily aspirin may reduce stroke and heart attack risk. Drug therapy for depression may be given. Affected individuals who smoke should quit as it can increase the risk of stroke in CADASIL. Other stroke risk factors such as hypertension, hyperlipidemia, diabetes, blood clotting disorders and obstructive sleep apnea also should be aggressively treated..
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What is the outlook for CADASIL ?
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Symptoms usually progress slowly. By age 65, the majority of persons with CADASIL have cognitive problems and dementia. Some will become dependent due to multiple strokes.
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what research (or clinical trials) is being done for CADASIL ?
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The National Institute of Neurological Disorders and Stroke (NINDS) conducts stroke research and clinical trials at its laboratories and clinics at the National Institutes of Health (NIH) and through grants to major medical institutions across the country. Scientists are currently studying different drugs to reduce cognitive problems seen in patients with CADASIL. Researchers are also looking at ways to overcome an over-reaction to hormones that lead to high blood pressure and poor blood supply in patients with CADASIL.
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What is (are) Central Pontine Myelinolysis ?
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Central pontine myelinolysis (CPM) is a neurological disorder that most frequently occurs after too rapid medical correction of sodium deficiency (hyponatremia). The rapid rise in sodium concentration is accompanied by the movement of small molecules and pulls water from brain cells. Through a mechanism that is only partly understood, the shift in water and brain molecules leads to the destruction of myelin, a substance that surrounds and protects nerve fibers. Nerve cells (neurons) can also be damaged. Certain areas of the brain are particularly susceptible to myelinolysis, especially the part of the brain stem called the pons. Some individuals will also have damage in other areas of the brain, which is called extrapontine myelinolysis (EPM). Experts estimate that 10 percent of those with CPM will also have areas of EPM.
The initial symptoms of myelinolysis, which begin to appear 2 to 3 days after hyponatremia is corrected, include a depressed level of awareness, difficulty speaking (dysarthria or mutism), and difficulty swallowing (dysphagia). Additional symptoms often arise over the next 1-2 weeks, including impaired thinking, weakness or paralysis in the arms and legs, stiffness, impaired sensation, and difficulty with coordination. At its most severe, myelinolysis can lead to coma, locked-in syndrome (which is the complete paralysis of all of the voluntary muscles in the body except for those that control the eyes), and death.
Although many affected people improve over weeks to months, some have permanent disability. Some also develop new symptoms later, including behavioral or intellectual impairment or movement disorders like parkinsonism or tremor.
Anyone, including adults and children, who undergoes a rapid rise in serum sodium is at risk for myelinolysis. Some individuals who are particularly vulnerable are those with chronic alcoholism and those who have had a liver transplant. Myelinolysis has occurred in individuals undergoing renal dialysis, burn victims, people with HIV-AIDS, people over-using water loss pills (diuretics), and women with eating disorders such as anorexia or bulimia. The risk for CPM is greater if the serum (blood) sodium was low for at least 2 days before correction.
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What are the treatments for Central Pontine Myelinolysis ?
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The ideal treatment for myelinolysis is to prevent the disorder by identifying individuals at risk and following careful guidelines for evaluation and correction of hyponatremia. These guidelines aim to safely restore the serum sodium level, while protecting the brain. For those who have hyponatremia for at least 2 days, or for whom the duration is not known, the rate of rise in the serum sodium concentration should be kept below 10 mmol/L during any 24-hour period, if possible.
For those who develop myelinolysis, treatment is supportive. Some physicians have tried to treat myelinolysis with steroid medication or other experimental therapies, but none has been proven effective. Individuals are likely to require extensive and prolonged physical therapy and rehabilitation. Those individuals who develop parkinsonian symptoms may respond to the dopaminergic drugs that work for individuals with Parkinsons disease.
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What is the outlook for Central Pontine Myelinolysis ?
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The prognosis for myelinolysis varies. Some individuals die and others recover completely. Although the disorder was originally considered to have a mortality rate of 50 percent or more, improved imaging techniques and early diagnosis have led to a better prognosis for many people. Most individuals improve gradually, but still continue to have challenges with speech, walking, emotional ups and downs, and forgetfulness.
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what research (or clinical trials) is being done for Central Pontine Myelinolysis ?
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The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS is a component of the National Institutes of Health, the leading supporter of biomedical research in the world.
The NINDS conducts and supports research to better understand conditions that affect the protective myelin coating around nerve fibers and ways to prevent and treat the destruction of myelin. Scientists hope to develop drugs that can prevent brain cells from dying or help them produce new myelin. Research funded by the NIH's National Institute of Diabetes and Digestive and Kidney Diseases aims to understand the biological mechanisms involved in water balance in the body.
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What is (are) Kuru ?
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Kuru is a rare and fatal brain disorder that occurred at epidemic levels during the 1950s-60s among the Fore people in the highlands of New Guinea. The disease was the result of the practice of ritualistic cannibalism among the Fore, in which relatives prepared and consumed the tissues (including brain) of deceased family members. Brain tissue from individuals with kuru was highly infectious, and the disease was transmitted either through eating or by contact with open sores or wounds. Government discouragement of the practice of cannibalism led to a continuing decline in the disease, which has now mostly disappeared.
Kuru belongs to a class of infectious diseases called transmissible spongiform encephalopathies (TSEs), also known as prion diseases. The hallmark of a TSE disease is misshapen protein molecules that clump together and accumulate in brain tissue. Scientists believe that misshapen prion proteins have the ability to change their shape and cause other proteins of the same type to also change shape. Other TSEs include Creutzfeldt-Jakob disease and fatal familial insomnia in humans, bovine spongiform encephalopathy in cattle (also known as mad cow disease), scrapie in sheep and goats, and chronic wasting disease in deer and elk.
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What are the treatments for Kuru ?
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There were no treatments that could control or cure kuru, other than discouraging the practice of cannibalism. Currently, there are no cures or treatments for any of the other TSE diseases.
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What is the outlook for Kuru ?
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Similar to other the TSEs, kuru had a long incubation period; it was years or even decades before an infected person showed symptoms. Because kuru mainly affected the cerebellum, which is responsible for coordination, the usual first symptoms were an unsteady gait, tremors, and slurred speech. (Kuru is the Fore word for shiver.) Unlike most of the other TSEs, dementia was either minimal or absent. Mood changes were often present. Eventually, individuals became unable to stand or eat, and they died in a comatose state from 6 to 12 months after the first appearance of symptoms.
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what research (or clinical trials) is being done for Kuru ?
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The NINDS funds research to better understand the genetic, molecular, and cellular mechanisms that underlie the TSE diseases. Findings from this research will lead to ways to diagnose, treat, prevent, and ultimately cure these diseases.
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What is (are) Spinal Muscular Atrophy ?
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Spinal Muscular Atrophy (SMA) Types I, II, and III belong to a group of hereditary diseases that cause weakness and wasting of the voluntary muscles in the arms and legs of infants and children. The disorders are caused by an abnormal or missing gene known as the survival motor neuron gene 1 (SMN1), which is responsible for the production of a protein essential to motor neurons. Without this protein, lower motor neurons in the spinal cord degenerate and die. The type of SMA (I, II, or III) is determined by the age of onset and the severity of symptoms. Type I (also known as Werdnig-Hoffman disease, or infantile-onset SMA) is evident at birth or within the first few months. Symptoms include floppy limbs and trunk, feeble movements of the arms and legs, swallowing and feeding difficulties, and impaired breathing. Type II (the intermediate form) usually begins 6 and 18 months of age. Legs tend to be more impaired than arms. Children with Type II may able to sit and some may be able to stand or walk with help. Symptoms of Type III (also called Kugelberg-Welander disease) appear between 2 and 17 years of age and include difficulty running, climbing steps, or rising from a chair. The lower extremities are most often affected. Complications include scoliosis and chronic shortening of muscles or tendons around joints.
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What are the treatments for Spinal Muscular Atrophy ?
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There is no cure for SMA. Treatment consists of managing the symptoms and preventing complications.
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What is the outlook for Spinal Muscular Atrophy ?
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The prognosis is poor for babies with SMA Type I. Most die within the first two years. For children with SMA Type II, the prognosis for life expectancy or for independent standing or walking roughly correlates with how old they are when they first begin to experience symptoms - older children tend to have less severe symptoms Life expectancy is reduced but some individuals live into adolescence or young adulthood. Individuals with SMA type III may be prone to respiratory infections but with care may have a normal lifespan.
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what research (or clinical trials) is being done for Spinal Muscular Atrophy ?
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Between 2003 and 2012, the NINDS piloted the Spinal Muscular Atrophy Project to expedite therapeutics development for this hereditary neurodegenerative disease. The Project was designed to accelerate the research process by identifying drugs that increase the level of SMN protein in cultured cells, so that they could be used as potential leads for further drug discovery and clinical testing. Read more about the history of this pioneering effort and how it led to collaboration with several pharmaceutical and biotechnology companies.
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What is (are) Motor Neuron Diseases ?
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The motor neuron diseases (MNDs) are a group of progressive neurological disorders that destroy cells that control essential muscle activity such as speaking, walking, breathing, and swallowing. Normally, messages from nerve cells in the brain (called upper motor neurons) are transmitted to nerve cells in the brain stem and spinal cord (called lower motor neurons) and from them to particular muscles. When there are disruptions in these signals, the result can be gradual muscle weakening, wasting away, and uncontrollable twitching (called fasciculations). Eventually, the ability to control voluntary movement can be lost. MNDs may be inherited or acquired, and they occur in all age groups. MNDs occur more commonly in men than in women, and symptoms may appear after age 40. In children, particularly in inherited or familial forms of the disease, symptoms can be present at birth or appear before the child learns to walk.
The causes of sporadic (noninherited) MNDs are not known, but environmental, toxic, viral, or genetic factors may be implicated. Common MNDs include amyotrophic lateral sclerosis (ALS), progressive bulbar palsy, primary lateral sclerosis, and progressive muscular atrophy. Other MNDs include the many inherited forms of spinal muscular atrophy and post-polio syndrome, a condition that can strike polio survivors decades after their recovery from poliomyelitis.
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What are the treatments for Motor Neuron Diseases ?
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There is no cure or standard treatment for the MNDs. Symptomatic and supportive treatment can help patients be more comfortable while maintaining their quality of life. The drug riluzole (Rilutek), which as of this date is the only drug approved by the U.S. Food and Drug Administration to treat ALS, prolongs life by 2-3 months but does not relieve symptoms. Other medicines that may help reduce symptoms include muscle relaxants such as baclofen, tizanidine, and the benzodiazepines for spasticity; glycopyrrolate and atropine to treat excessive saliva; and anticonvulsants and nonsteroidal anti-inflammatory drugs to relieve pain. Panic attacks can be treated with benzodiazepines. Some patients may require stronger medicines such as morphine to cope with musculoskeletal abnormalities or pain in later stages of the disorders, and opiates are used to provide comfort care in terminal stages of the disease.
Physical and speech therapy, occupational therapy, and rehabilitation may help to improve posture, prevent joint immobility, slow muscle weakness and atrophy, and cope with swallowing difficulties. Applying heat may relieve muscle pain. Assistive devices such as supports or braces, orthotics, speech synthesizers, and wheelchairs help some patients retain independence. Proper nutrition and a balanced diet are essential to maintaining weight and strength.
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What is the outlook for Motor Neuron Diseases ?
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Prognosis varies depending on the type of MND and the age of onset. Some MNDs, such as primary lateral sclerosis and Kennedy disease, are not fatal and progress slowly. Patients with spinal muscular atrophy may appear to be stable for long periods, but improvement should not be expected. Some MNDs, such as ALS and some forms of spinal muscular atrophy, are fatal.
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what research (or clinical trials) is being done for Motor Neuron Diseases ?
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The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS is a component of the National Institutes of Health (NIH), the leading supporter of biomedical research in the world. Researchers are testing whether different drugs, agents, or interventions are safe and effective in slowing the progression of motor neuron diseasess. NIH is also conducting clinical trials to study drugs to stimulate muscle growth in Kennedys disease and to suppress endogenous retroviruses in individuals with ALS. A large NIH-led collaborative study is investigating the genes and gene activity, proteins, and modifications of adult stem cell models from both healthy people and those with ALS,spinal muscular atrophy, and other neurodegenerative diseases to better understand the function of neurons and other support cells and identify candidate therapeutic compounds.
conducts research related to the MNDs in its laboratories at the National Institutes of Health (NIH), and also supports additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders such as the MNDs.
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What is (are) Alternating Hemiplegia ?
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Alternating hemiplegia is a rare neurological disorder that develops in childhood, most often before the child is 18 months old. The disorder is characterized by recurrent episodes of paralysis that involve one or both sides of the body, multiple limbs, or a single limb. The paralysis may affect different parts of the body at different times and may be brief or last for several days. Oftentimes these episodes will resolve after sleep. Affected children may also have abnormal movements involving stiffening or "dance-like" movements of a limb, as well as walking and balance problems. Some children have seizures. Children may have normal or delayed development. There are both benign and more serious forms of the disorder. Most children do not have a family history of the disorder; however, recent studies have show that some children with a family history have mutations in the genes CACNA1A, SCN1A, and ATP1A2. Mutations in the ATP1A2 gene have previously been associated with families affect by familial hemiplegic migraine.
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What are the treatments for Alternating Hemiplegia ?
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Drug therapy including verapamil may help to reduce the severity and duration of attacks of paralysis associated with the more serious form of alternating hemiplegia
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What is the outlook for Alternating Hemiplegia ?
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Children with the benign form of alternating hemiplegia have a good prognosis. Those who experience the more severe form have a poor prognosis because intellectual and mental capacities do not respond to drug therapy, and balance and gait problems continue. Over time, walking unassisted becomes difficult or impossible.
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what research (or clinical trials) is being done for Alternating Hemiplegia ?
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The NINDS supports research on paralytic disorders such as alternating hemiplegia, with the goals of learning more about these disorders and finding ways to prevent, treat and, ultimately cure them.
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What is (are) Troyer Syndrome ?
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Troyer syndrome is one of more than 40 genetically-distinct neurological disorders known collectively as the hereditary spastic paraplegias. These disorders are characterized by their paramount feature of progressive muscle weakness and spasticity in the legs. Additional symptoms of Troyer syndrome (also called SPG20) include leg contractures, difficulty walking, speech disorders, drooling, atrophy of the hand muscles, developmental delays, fluctuating emotions, and short stature. Onset is typically in early childhood, and symptoms gradually worsen over time. Troyer syndrome is an autosomal recessive disorder (meaning that both parents must carry and pass on the defective gene that produces the illness) that results from a mutation in the spastic paraplegia gene (SPGP20) located in chromosome 13 that results in loss of the spartin proteins. The disease was first observed in Amish families in Ohio. Diagnosis is made by specialized genetic testing.
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What are the treatments for Troyer Syndrome ?
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There are no specific treatments to prevent or slow the progressive degeneration seen in Troyer syndrome. Symptomatic therapy includes antispasmodic drugs and physical therapy to improve muscle strength and maintain range of motion in the legs. Assistive devices may be needed to help with walking.
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What is the outlook for Troyer Syndrome ?
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Prognosis varies, although the disease is progressive. Some patients may have a mild form of the disease while others eventually lose the ability to walk normally. Troyer syndrome does not shorten the normal life span.
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what research (or clinical trials) is being done for Troyer Syndrome ?
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The NINDS supports research on genetic disorders such as the hereditary spastic paraplegias. A gene for Troyer syndrome has been identified and others may be identified in the future. Understanding how these genes cause Troyer syndrome and the hereditary spastic paraplegias in general will lead to ways to prevent, treat, and cure these disorders.
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What is (are) Niemann-Pick Disease ?
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Niemann-Pick disease (NP) refers to a group of inherited metabolic disorders known as lipid storage diseases. Lipids (fatty materials such as waxes, fatty acids, oils, and cholesterol) and proteins are usually broken down into smaller components to provide energy for the body. In Niemann-Pick disease, harmful quantities of lipids accumulate in the brain, spleen, liver, lungs, and bone marrow. Neurological symptoms may include ataxia (lack of muscle control during voluntary movements such as walking), loss of muscle tone, brain degeneration, increased sensitivity to touch, spasticity (stiff muscles and awkward movement), and slurred speech. Other symptoms may include feeding and swallowing difficulties, eye paralysis, learning problems, and an enlarged liver and spleen. There may be clouding of the cornea and a characteristic cherry-red halo develops around the center of the retina. The disease has three categories. Type A, the most severe form, occurs in early infancy and is seen primarily in Jewish families. It is characterized by progressive weakness, an enlarged liver and spleen, swollen lymph nodes, and profound brain damage by six months of age. Children with this type rarely live beyond 18 months. Type B usually occurs in the pre-teen years, with symptoms that include ataxia and peripheral neuropathy. The brain is generally not affected. Other symptoms include enlarged liver and spleen, and pulmonary difficulties. In types A and B, insufficient activity of an enzyme called sphingomyelinase causes the build up of toxic amounts of sphingomyelin, a fatty substance present in every cell of the body. Type C may appear early in life or develop in the teen or adult years. It is caused by a lack of the NPC1 or NPC2 proteins. Affected individuals may have extensive brain damage that can cause an inability to look up and down, difficulty in walking and swallowing, and progressive loss of vision and hearing. There may be moderate enlargement of the spleen and liver. Individuals wit Type C who share a common ancestral background in Nova Scotia were previously referred to as Type D.
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What are the treatments for Niemann-Pick Disease ?
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There is currently no cure for Niemann-Pick disease. Treatment is supportive. Children usually die from infection or progressive neurological loss. There is currently no effective treatment for persons with type A. Bone marrow transplantation has been attempted in a few individuals with type B. The development of enzyme replacement and gene therapies might also be helpful for those with type B. restricting one's diet does not prevent the buildup of lipids in cells and tissues.
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What is the outlook for Niemann-Pick Disease ?
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Infants with type A die in infancy. Children with Type B may live a comparatively long time, but may require supplemental oxygen because of lung impairment. The life expectancy of persons with type C varies: some individuals die in childhood while others who appear to be less severely affected can live into adulthood.
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what research (or clinical trials) is being done for Niemann-Pick Disease ?
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The National Institute of Neurological Disorders and Stroke (NINDS), a part of the National Institutes of Health (NIH), conducts and supports research about Niemann-Pick disease through research grants to research institutions across the country. Investigators at the NINDS have identified two different genes that, when defective, contribute to Niemann-Pick disease type C. NINDS scientists are studying the mechanisms by which lipids accumulating in these storage diseases causes harm to the body. Additional research studies hope to identify biomarkers (signs that may indicate risk of a disease and improve diagnosis) for the lipid storage disorders.
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What is (are) Spinal Cord Injury ?
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A spinal cord injury usually begins with a sudden, traumatic blow to the spine that fractures or dislocates vertebrae. The damage begins at the moment of injury when displaced bone fragments, disc material, or ligaments bruise or tear into spinal cord tissue. Most injuries to the spinal cord don't completely sever it. Instead, an injury is more likely to cause fractures and compression of the vertebrae, which then crush and destroy axons -- extensions of nerve cells that carry signals up and down the spinal cord between the brain and the rest of the body. An injury to the spinal cord can damage a few, many, or almost all of these axons. Some injuries will allow almost complete recovery. Others will result in complete paralysis.
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What are the treatments for Spinal Cord Injury ?
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Improved emergency care for people with spinal cord injuries and aggressive treatment and rehabilitation can minimize damage to the nervous system and even restore limited abilities. Respiratory complications are often an indication of the severity of spinal cord injury About one-third of those with injury to the neck area will need help with breathing and require respiratory support. The steroid drug methylprednisolone appears to reduce the damage to nerve cells if it is given within the first 8 hours after injury. Rehabilitation programs combine physical therapies with skill-building activities and counseling to provide social and emotional support.Electrical simulation of nerves by neural prosthetic devices may restore specific functions, including bladder, breathing, cough, and arm or leg movements, though eligibility for use of these devices depends on the level and type of the spinal cord injury.
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What is the outlook for Spinal Cord Injury ?
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Spinal cord injuries are classified as either complete or incomplete. An incomplete injury means that the ability of the spinal cord to convey messages to or from the brain is not completely lost. People with incomplete injuries retain some motor or sensory function below the injury. A complete injury is indicated by a total lack of sensory and motor function below the level of injury. People who survive a spinal cord injury will most likely have medical complications such as chronic pain and bladder and bowel dysfunction, along with an increased susceptibility to respiratory and heart problems. Successful recovery depends upon how well these chronic conditions are handled day to day.
Surgery to relieve compression of the spinal tissue by surrounding bones broken or dislocated by the injury is often necessary, through timing of such surgery may vary widely. A recent prospective multicenter trial called STASCIS is exploring whether performing decompression surgery early (less than 24 hours following injury) can improve outcomes for patients with bone fragments or other tissues pressing on the spinal cord.
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what research (or clinical trials) is being done for Spinal Cord Injury ?
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The National Institute of Neurological Disorders and Stroke (NINDS) conducts spinal cord research in its laboratories at the National Institutes of Health (NIH) and also supports additional research through grants to major research institutions across the country. Advances in research are giving doctors and patients hope that repairing injured spinal cords is a reachable goal. Advances in basic research are also being matched by progress in clinical research, especially in understanding the kinds of physical rehabilitation that work best to restore function. Some of the more promising rehabilitation techniques are helping spinal cord injury patients become more mobile.
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What is (are) Congenital Myasthenia ?
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All forms of myasthenia are due to problems in the communication between nerve cells and muscles. Most involve the activities of neurotransmitters. Neurotransmitters are chemicals that allow neurons to relay information from one cell to the next. For neurotransmitters to be effective, the nerve cell must release the neurotransmitter properly, and the muscle cell must be able to detect the neurotransmitter and respond to its signal properly.
The most common type of myasthenia, myasthenia gravis, is caused by an abnormal immune response in which antibodies block the ability of the muscle to detect the neurotransmitter. Congenital myasthenia, however, differs from myasthenia gravis because the disrupted communication isn't caused by antibodies, but by genetic defects.
There are several different subtypes of congenital myasthenia, each the result of a specific genetic mutation. Since all types of myasthenia are due to the inability of nerves to trigger muscle activity, they all involve weakness, although there is some variability in the specific muscles affected.
Symptoms of congenital myasthenia usually appear in the first few years of childhood, but may not be noticeable until much later, occasionally remaining unrecognized until adulthood. If the symptoms begin in infancy, they usually appear as "floppiness" and a failure to meet developmental milestones, such as rolling over or sitting up. Some infants may also have episodes of choking or pauses in breathing. If the symptoms begin in toddlers or preschool children, they appear as weakness during physical activities or an inability to perform age-appropriate actions, such as running or climbing. In addition, if eye muscles are involved, children may have droopy eyelids, "lazy eye," or double vision. If mouth or throat muscles are involved, children may have difficulty speaking or swallowing. An important characteristic of myasthenia is that the weakness worsens during continuous activity, with strength returning, at least partially, after resting.
Congenital myasthenia is an inherited (genetic) disorder. All but one known subtype are recessive disorders, which means that a child will have to have two copies of the abnormal gene (one from each parent) in order to develop the disease. To diagnose congenital myasthenia, a neurologist will test various muscles to determine if they grow weaker with repeated activity. The doctor will also test the electrical activity of nerves and muscles using electromyography (EMG) and nerve conduction tests (NCS). Blood tests are often used to determine if antibodies could be causing the symptoms. Genetic tests may be ordered.
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What are the treatments for Congenital Myasthenia ?
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The possibilities for treatment depend on the specific subtype of congenital myasthenia. Most treatments attempt to improve the signaling between nerve cell and muscle. These drugs include pyridostigmine, fluoxetine, ephedrine, and 3,4-diaminopyridine. Treatments to alter the immune system are not used for this form of myasthenia. There are no treatments to cure the underlying genetic abnormality.
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What is the outlook for Congenital Myasthenia ?
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The prognosis depends on the specific subtype of congenital myasthenia, the muscles involved, and the age at onset of symptoms. If a child has difficulty breathing, feeding, or swallowing, they may be vulnerable to pneumonia or respiratory failure. In other cases, weakness is stable and does not worsen over time. In one subtype, weakness improves with time. Life-span is normal in most cases in which respiratory function is not compromised.
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what research (or clinical trials) is being done for Congenital Myasthenia ?
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The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) support research related to congenital myasthenia 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 congenital myasthenia.
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What is (are) Tabes Dorsalis ?
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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.
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What are the treatments for Tabes Dorsalis ?
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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.
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What is the outlook for Tabes Dorsalis ?
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If left untreated, tabes dorsalis can lead to paralysis, dementia, and blindness. Existing nerve damage cannot be reversed.
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what research (or clinical trials) is being done for Tabes Dorsalis ?
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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.
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What is (are) Batten Disease ?
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Batten disease is a fatal, inherited disorder of the nervous system that begins in childhood. In some cases, the early signs are subtle, taking the form of personality and behavior changes, slow learning, clumsiness, or stumbling. Symptoms of Batten disease are linked to a buildup of substances called lipopigments in the body's tissues. Lipopigments are made up of fats and proteins. Because vision loss is often an early sign, Batten disease may be first suspected during an eye exam. Often, an eye specialist or other physician may refer the child to a neurologist. Diagnostic tests for Batten disease include blood or urine tests, skin or tissue sampling, an electroencephalogram (EEG), electrical studies of the eyes, and brain scans.
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What are the treatments for Batten Disease ?
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As yet, no specific treatment is known that can halt or reverse the symptoms of Batten disease. However, seizures can sometimes be reduced or controlled with anticonvulsant drugs, and other medical problems can be treated appropriately as they arise. Physical therapy and occupational therapy may help patients retain functioning as long as possible.
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What is the outlook for Batten Disease ?
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Over time, affected children suffer cognitive impairment, worsening seizures, and progressive loss of sight and motor skills. Eventually, children with Batten disease become blind, bedridden, and demented. Batten disease is often fatal by the late teens or twenties.
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what research (or clinical trials) is being done for Batten Disease ?
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The biochemical defects that underlie several NCLs have recently been discovered. An enzyme called palmitoyl-protein thioesterase has been shown to be insufficiently active in the infantile form of Batten disease (this condition is now referred to as CLN1). In the late infantile form (CLN2), a deficiency of an acid protease, an enzyme that hydrolyzes proteins, has been found as the cause of this condition. A mutated gene has been identified in juvenile Batten disease (CLN3), but the protein for which this gene codes has not been identified. In addition, research scientists are working with NCL animal models to improve understanding and treatment of these disorders. One research team, for example, is testing the usefulness of bone marrow transplantation in a sheep model, while other investigators are working to develop mouse models. Mouse models will make it easier for scientists to study the genetics of these diseases.
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What is (are) Attention Deficit-Hyperactivity Disorder ?
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Attention deficit-hyperactivity disorder (ADHD) is a neurobehavioral disorder that affects 3-5 percent of all American children. It interferes with a person's ability to stay on a task and to exercise age-appropriate inhibition (cognitive alone or both cognitive and behavioral). Some of the warning signs of ADHD include failure to listen to instructions, inability to organize oneself and school work, fidgeting with hands and feet, talking too much, leaving projects, chores and homework unfinished, and having trouble paying attention to and responding to details. There are several types of ADHD: a predominantly inattentive subtype, a predominantly hyperactive-impulsive subtype, and a combined subtype. ADHD is usually diagnosed in childhood, although the condition can continue into the adult years.
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What are the treatments for Attention Deficit-Hyperactivity Disorder ?
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The usual course of treatment may include medications such as methylphenidate (Ritalin) or dextroamphetamine (Dexedrine), which are stimulants that decrease impulsivity and hyperactivity and increase attention. Most experts agree that treatment for ADHD should address multiple aspects of the individual's functioning and should not be limited to the use of medications alone. Treatment should include structured classroom management, parent education (to address discipline and limit-setting), and tutoring and/or behavioral therapy for the child.
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What is the outlook for Attention Deficit-Hyperactivity Disorder ?
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There is no "cure" for ADHD. Children with the disorder seldom outgrow it; however, some may find adaptive ways to accommodate the ADHD as they mature.
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what research (or clinical trials) is being done for Attention Deficit-Hyperactivity Disorder ?
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Several components of the NIH support research on developmental disorders such as ADHD. Research programs of the NINDS, the National Institute of Mental Health (NIMH), and the National Institute of Child Health and Human Development (NICHD) seek to address unanswered questions about the causes of ADHD, as well as to improve diagnosis and treatment.
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What is (are) Gerstmann-Straussler-Scheinker Disease ?
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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.
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What are the treatments for Gerstmann-Straussler-Scheinker Disease ?
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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.
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What is the outlook for Gerstmann-Straussler-Scheinker Disease ?
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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.
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what research (or clinical trials) is being done for Gerstmann-Straussler-Scheinker Disease ?
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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.
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What is (are) Septo-Optic Dysplasia ?
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Septo-optic dysplasia (SOD) is a rare disorder characterized by abnormal development of the optic disk, pituitary deficiencies, and often agenesis (absence) of the septum pellucidum (the part of the brain that separates the anterior horns or the lateral ventricles of the brain). Symptoms may include blindness in one or both eyes, pupil dilation in response to light, nystagmus (a rapid, involuntary to-and-fro movement of the eyes), inward and outward deviation of the eyes, hypotonia (low muscle tone), and hormonal problems. Seizures may also occur. In a few cases, jaundice (prolonged yellow skin discoloration) may occur at birth. Intellectual problems vary in severity among individuals. While some children with SOD have normal intelligence, others have learning disabilities. Most, however, are developmentally delayed due to vision impairment or neurological problems.
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What are the treatments for Septo-Optic Dysplasia ?
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Treatment for SOD is symptomatic. Hormone deficiencies may be treated with hormone replacement therapy. The optical problems associated with SOD are generally not treatable. Vision, physical, and occupational therapies may be required.
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What is the outlook for Septo-Optic Dysplasia ?
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The prognosis for individuals with SOD varies according to the presence and severity of symptoms.
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what research (or clinical trials) is being done for Septo-Optic Dysplasia ?
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The NINDS supports and conducts neurogenetic research which focuses on identifying and studying the genes involved in normal brain development. The knowledge gained from these fundamental studies provides the foundation for understanding how this process can go awry and, thus, may eventually give clues to understanding disorders such as SOD.
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What is (are) Paroxysmal Hemicrania ?
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Paroxysmal hemicrania is a rare form of headache that usually begins in adulthood. Patients experience severe throbbing, claw-like, or boring pain usually on one side of the face; in, around, or behind the eye; and occasionally reaching to the back of the neck. This pain may be accompanied by red and tearing eyes, a drooping or swollen eyelid on the affected side of the face, and nasal congestion. Patients may also feel dull pain, soreness, or tenderness between attacks. Attacks of paroxysmal hemicrania typically occur from 5 to 40 times per day and last 2 to 30 minutes. The disorder has two forms: chronic, in which patients experience attacks on a daily basis for a year or more, and episodic, in which the headaches may remit for months or years. Certain movements of the head or neck or external pressure to the neck may trigger these headaches in some patients. The disorder is more common in women than in men.
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What are the treatments for Paroxysmal Hemicrania ?
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The nonsteroidal anti-inflammatory drug (NSAID) indomethacin often provides complete relief from symptoms. Other less effective NSAIDs, calcium-channel blocking drugs (such as verapamil), and corticosteroids may be used to treat the disorder. Patients with both paroxysmal hemicrania and trigeminal neuralgia (a condition of the 5th cranial nerve that causes sudden, severe pain typically felt on one side of the jaw or cheek) should receive treatment for each disorder.
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What is the outlook for Paroxysmal Hemicrania ?
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Many patients experience complete to near-complete relief of symptoms following physician-supervised medical treatment. Paroxysmal hemicrania may last indefinitely but has been known to go into remission or stop spontaneously.
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what research (or clinical trials) is being done for Paroxysmal Hemicrania ?
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The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) support research related to paroxysmal hemicrania through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure headache disorders such as paroxysmal hemicrania.
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What is (are) Hydranencephaly ?
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Hydranencephaly is a rare condition in which the brain's cerebral hemispheres are absent and replaced by sacs filled with cerebrospinal fluid. An infant with hydranencephaly may appear normal at birth. The infant's head size and spontaneous reflexes such as sucking, swallowing, crying, and moving the arms and legs may all seem normal. However, after a few weeks the infant usually becomes irritable and has increased muscle tone. After a few months of life, seizures and hydrocephalus (excessive accumulation of cerebrospinal fluid in the brain) may develop. Other symptoms may include visual impairment, lack of growth, deafness, blindness, spastic quadriparesis (paralysis), and intellectual deficits. Hydranencephaly is considered to be an extreme form of porencephaly (a rare disorder characterized by a cyst or cavity in the cerebral hemispheres) and may be caused by vascular infections or traumatic disorders after the 12th week of pregnancy. Diagnosis may be delayed for several months because early behavior appears to be relatively normal. Some infants may have additional abnormalities at birth including seizures, myoclonus (spasm or twitching of a muscle or group of muscles), and respiratory problems.
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What are the treatments for Hydranencephaly ?
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There is no definitive treatment for hydranencephaly. Treatment is symptomatic and supportive. Hydrocephalus may be treated with a shunt (a surgically implanted tube that diverts fluid from one pathway to another).
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What is the outlook for Hydranencephaly ?
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The outlook for children with hydranencephaly is generally poor, and many children with this disorder die before age 1. However, in rare cases, children with hydranencephaly may survive for several years or more.
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what research (or clinical trials) is being done for Hydranencephaly ?
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The NINDS conducts and supports a wide range of studies that explore the complex mechanisms of normal brain development. The knowledge gained from these fundamental studies provides the foundation for understanding how this process can go awry and, thus, offers hope for new means to treat and prevent developmental brain disorders, including hydranencephaly.
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What is (are) Hydromyelia ?
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Hydromyelia refers to an abnormal widening of the central canal of the spinal cord that creates a cavity in which cerebrospinal fluid (commonly known as spinal fluid) can accumulate. As spinal fluid builds up, it may put abnormal pressure on the spinal cord and damage nerve cells and their connections. Hydromyelia is sometimes used interchangeably with syringomyelia, the name for a condition that also involves cavitation in the spinal cord. In hydromyelia, the cavity that forms is connected to the fourth ventricle in the brain, and is almost always associated in infants and children with hydrocephalus or birth defects such as Chiari Malformation II and Dandy-Walker syndrome. Syringomyelia, however, features a closed cavity and occurs primarily in adults, the majority of whom have Chiari Malformation type 1 or have experienced spinal cord trauma. Symptoms, which may occur over time, include weakness of the hands and arms, stiffness in the legs; and sensory loss in the neck and arms. Some individuals have severe pain in the neck and arms. Diagnosis is made by magnetic resonance imaging (MRI), which reveals abnormalities in the anatomy of the spinal cord..
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What are the treatments for Hydromyelia ?
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Generally, physicians recommend surgery for children with hydromyelia if they have moderate or severe neurological deficits. Surgical treatment re-establishes the normal flow of spinal fluid.
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What is the outlook for Hydromyelia ?
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Surgery may permanently or temporarily relieve symptoms, but it can also cause a number of severe complications. In rare cases, hydromyelia may resolve on its own without any medical intervention.
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what research (or clinical trials) is being done for Hydromyelia ?
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The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to hydromyelia in its clinics and laboratories at The National Institutes of Health (NIH) and 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 abnormalities of the spinal cord such as hydromyelia.
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What is (are) Neuroleptic Malignant Syndrome ?
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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.
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What are the treatments for Neuroleptic Malignant Syndrome ?
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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.
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What is the outlook for Neuroleptic Malignant Syndrome ?
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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.
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what research (or clinical trials) is being done for Neuroleptic Malignant Syndrome ?
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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.
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What is (are) Peripheral Neuropathy ?
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Peripheral neuropathy describes damage to the peripheral nervous system, which transmits information from the brain and spinal cord to every other part of the body.
More than 100 types of peripheral neuropathy have been identified, each with its own characteristic set of symptoms, pattern of development, and prognosis. Impaired function and symptoms depend on the type of nerves -- motor, sensory, or autonomic -- that are damaged. Some people may experience temporary numbness, tingling, and pricking sensations, sensitivity to touch, or muscle weakness. Others may suffer more extreme symptoms, including burning pain (especially at night), muscle wasting, paralysis, or organ or gland dysfunction. Peripheral neuropathy may be either inherited or acquired. Causes of acquired peripheral neuropathy include physical injury (trauma) to a nerve, tumors, toxins, autoimmune responses, nutritional deficiencies, alcoholism, medical procedures, and vascular and metabolic disorders. Acquired peripheral neuropathies are caused by systemic disease, trauma from external agents, or infections or autoimmune disorders affecting nerve tissue. Inherited forms of peripheral neuropathy are caused by inborn mistakes in the genetic code or by new genetic mutations.
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What are the treatments for Peripheral Neuropathy ?
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No medical treatments exist that can cure inherited peripheral neuropathy. However, there are therapies for many other forms. In general, adopting healthy habits -- such as maintaining optimal weight, avoiding exposure to toxins, following a physician-supervised exercise program, eating a balanced diet, correcting vitamin deficiencies, and limiting or avoiding alcohol consumption -- can reduce the physical and emotional effects of peripheral neuropathy. Systemic diseases frequently require more complex treatments.
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What is the outlook for Peripheral Neuropathy ?
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In acute neuropathies, such as Guillain-Barr syndrome, symptoms appear suddenly, progress rapidly, and resolve slowly as damaged nerves heal. In chronic forms, symptoms begin subtly and progress slowly. Some people may have periods of relief followed by relapse. Others may reach a plateau stage where symptoms stay the same for many months or years. Some chronic neuropathies worsen over time, but very few forms prove fatal unless complicated by other diseases. Occasionally the neuropathy is a symptom of another disorder.
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what research (or clinical trials) is being done for Peripheral Neuropathy ?
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The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to peripheral neuropathies in laboratories at the NIH and also support additional research through grants to major medical institutions across the country. Current research projects funded by the NINDS involve investigations of genetic factors associated with hereditary neuropathies, studies of biological mechanisms involved in diabetes-associated neuropathies, and investigations exploring how the immune system contributes to peripheral nerve damage. Neuropathic pain is a primary target of NINDS-sponsored studies aimed at developing more effective therapies for symptoms of peripheral neuropathy. Some scientists hope to identify substances that will block the brain chemicals that generate pain signals, while others are investigating the pathways by which pain signals reach the brain.
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What is (are) Dermatomyositis ?
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Dermatomyositis is one of a group of muscle diseases known as the inflammatory myopathies, which are characterized by chronic muscle inflammation accompanied by muscle weakness. Dermatomyositis cardinal symptom is a skin rash that precedes, accompanies, or follows progressive muscle weakness. The rash looks patchy, with purple or red discolorations, and characteristically develops on the eyelids and on muscles used to extend or straighten joints, including knuckles, elbows, knees, and toes. Red rashes may also occur on the face, neck, shoulders, upper chest, back, and other locations, and there may be swelling in the affected areas. The rash sometimes occurs without obvious muscle involvement. Adults with dermatomyositis may experience weight loss, a low-grade fever, inflamed lungs, and be sensitive to light such that the rash or muscle disease gets worse. Children and adults with dermatomyositis may develop calcium deposits, which appear as hard bumps under the skin or in the muscle (called calcinosis). Calcinosis most often occurs 1-3 years after the disease begins. These deposits are seen more often in children with dermatomyositis than in adults. In some cases of dermatomyositis, distal muscles (muscles located away from the trunk of the body, such as those in the forearms and around the ankles and wrists) may be affected as the disease progresses. Dermatomyositis may be associated with collagen-vascular or autoimmune diseases, such as lupus.
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What are the treatments for Dermatomyositis ?
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There is no cure for dermatomyositis, but the symptoms can be treated. Options include medication, physical therapy, exercise, heat therapy (including microwave and ultrasound), orthotics and assistive devices, and rest. The standard treatment for dermatomyositis is a corticosteroid drug, given either in pill form or intravenously. Immunosuppressant drugs, such as azathioprine and methotrexate, may reduce inflammation in people who do not respond well to prednisone. Periodic treatment using intravenous immunoglobulin can also improve recovery. Other immunosuppressive agents used to treat the inflammation associated with dermatomyositis include cyclosporine A, cyclophosphamide, and tacrolimus. Physical therapy is usually recommended to prevent muscle atrophy and to regain muscle strength and range of motion. Many individuals with dermatomyositis may need a topical ointment, such as topical corticosteroids, for their skin disorder. They should wear a high-protection sunscreen and protective clothing. Surgery may be required to remove calcium deposits that cause nerve pain and recurrent infections.
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What is the outlook for Dermatomyositis ?
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Most cases of dermatomyositis respond to therapy. The disease is usually more severe and resistant to therapy in individuals with cardiac or pulmonary problems.
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what research (or clinical trials) is being done for Dermatomyositis ?
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The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research relating to dermatomyositis in laboratories at the NIH and support additional research through grants to major medical institutions across the country. Currently funded research is exploring patterns of gene expression among the inflammatory myopathies, the role of viral infection as a precursor to the disorders, and the safety and efficacy of various treatment regimens.
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What is (are) Whiplash ?
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Whiplash-a soft tissue injury to the neck-is also called neck sprain or neck strain. It is characterized by a collection of symptoms that occur following damage to the neck, usually because of sudden extension and flexion. The disorder commonly occurs as the result of an automobile accident and may include injury to intervertebral joints, discs, and ligaments, cervical muscles, and nerve roots. Symptoms such as neck pain may be present directly after the injury or may be delayed for several days. In addition to neck pain, other symptoms may include neck stiffness, injuries to the muscles and ligaments (myofascial injuries), headache, dizziness, abnormal sensations such as burning or prickling (paresthesias), or shoulder or back pain. In addition, some people experience cognitive, somatic, or psychological conditions such as memory loss, concentration impairment, nervousness/irritability, sleep disturbances, fatigue, or depression.
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What are the treatments for Whiplash ?
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Treatment for individuals with whiplash may include pain medications, nonsteroidal anti-inflammatory drugs, antidepressants, muscle relaxants, and a cervical collar (usually worn for 2 to 3 weeks). Range of motion exercises, physical therapy, and cervical traction may also be prescribed. Supplemental heat application may relieve muscle tension.
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What is the outlook for Whiplash ?
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Generally, prognosis for individuals with whiplash is good. The neck and head pain clears within a few days or weeks. Most patients recover within 3 months after the injury, however, some may continue to have residual neck pain and headaches.
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what research (or clinical trials) is being done for Whiplash ?
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The NINDS conducts and supports research on trauma-related disorders such as whiplash. Much of this research focuses on increasing scientific understanding of these disorders and finding ways to prevent and treat them.
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