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What is (are) Wernicke-Korsakoff Syndrome ?
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Wernicke's encephalopathy is a degenerative brain disorder caused by the lack of thiamine (vitamin B1). It may result from alcohol abuse, dietary deficiencies, prolonged vomiting, eating disorders, or the effects of chemotherapy. B1 deficiency causes damage to the brain's thalamus and hypothalamus. Symptoms include mental confusion, vision problems, coma, hypothermia, low blood pressure, and lack of muscle coordination (ataxia). Korsakoff syndrome (also called Korsakoff's amnesic syndrome) is a memory disorder that results from vitamin B1 deficiency and is associated with alcoholism. Korsakoff's syndrome damages nerve cells and supporting cells in the brain and spinal cord, as well as the part of the brain involved with memory. Symptoms include amnesia, tremor, coma, disorientation, and vision problems, The disorder's main features are problems in acquiring new information or establishing new memories, and in retrieving previous memories. Although Wernicke's and Korsakoff's are related disorders, some scientists believe them to be different stages of the same disorder, which is called Wernicke-Korsakoff syndrome. Wernicke's encephalopathy represents the "acute" phase of the disorder and Korsakoff's amnesic syndrome represents the disorder progressing to a "chronic" or long-lasting stage.
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What are the treatments for Wernicke-Korsakoff Syndrome ?
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Treatment involves replacement of thiamine and providing proper nutrition and hydration. In some cases, drug therapy is also recommended.Stopping alcohol use may prevent further nerve and brain damage. In individuals with Wernicke's encephalopathy, it is very important to start thiamine replacement before beginning nutritional replenishment.
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What is the outlook for Wernicke-Korsakoff Syndrome ?
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Most symptoms of Wernicke's encephalopathy can be reversed if detected and treated promptly and completely. Stopping alcohol use may prevent further nerve and brain damage. However, improvement in memory function is slow and, usually, incomplete. Without treatment, these disorders can be disabling and life-threatening.
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what research (or clinical trials) is being done for Wernicke-Korsakoff Syndrome ?
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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 supports research on neurological disorders such as Wernicke's encephalopathy, Korsakoff's amnesic syndrome, and Wernicke-Korsakoff syndrome, to expand our understanding of the functional changes of the diseases and ways to treat them..One areas of research is studying how exercise can improve cognitive functioning based on modulation of certain nerve cells in a rodent model of amnesia produced by by thiamine deficiency. The National Institute of Alcohol Abuse and Alcoholism also supports research on these disorders.
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What is (are) Multiple System Atrophy with Orthostatic Hypotension ?
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Multiple system atrophy with orthostatic hypotension is the current classification for a neurological disorder that was once called Shy-Drager syndrome. A progressive disorder of the central and autonomic nervous systems, it is characterized by orthostatic hypotension (an excessive drop in blood pressure when standing up) which causes dizziness or fainting. Multiple system atrophy can occur without orthostatic hypotension, but instead have urinary involvement (urgency/incontinence). Doctors classify the disorder into 3 types: the Parkinsonian-type includes symptoms of Parkinson's disease such as slow movement, stiff muscles, and tremor; the cerebellar-type, which causes problems with coordination and speech; and the combined-type, which includes symptoms of both parkinsonism and cerebellar failure. Problems with urinary incontinence, constipation, and sexual impotence in men happen early in the course of the disease. Other symptoms include generalized weakness, double vision or other vision disturbances, difficulty breathing and swallowing, sleep disturbances, and decreased sweating. Because the disease resembles others, a correct diagnosis may take years.
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What are the treatments for Multiple System Atrophy with Orthostatic Hypotension ?
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There is no cure for multiple system atrophy with orthostatic hypotension. Treatment is aimed at controlling symptoms. Anti-Parkinson medication such as Sinemet may improve the general sense of well-being. Medications to elevate blood pressure while standing are often used, but may cause high blood pressure when lying down. Individuals should sleep with the head of the bed elevated. An artificial feeding tube or breathing tube may be required for problems with swallowing and breathing.
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What is the outlook for Multiple System Atrophy with Orthostatic Hypotension ?
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Most individuals with multiple system atrophy with orthostatic hypotension die within 7 to 10 years after the onset of symptoms. A problem with the respiratory system is the most common cause of death.
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what research (or clinical trials) is being done for Multiple System Atrophy with Orthostatic Hypotension ?
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The NINDS supports research on disorders of the autonomic nervous system, including multiple system atrophy with orthostatic hypotension. This research is aimed at developing techniques to diagnose, treat, and prevent these disorders. Currently there are ongoing treatment trials of drugs to treat MSA.
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What is (are) Transverse Myelitis ?
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Transverse myelitis is a neurological disorder caused by inflammation across both sides of one level, or segment, of the spinal cord. The segment of the spinal cord at which the damage occurs determines which parts of the body are affected. Damage at one segment will affect function at that segment and segments below it. In people with transverse myelitis, inflammation usually occurs at the thoracic (upper back) level, causing problems with leg movement and bowel and bladder control, which require signals from the lower segments of the spinal cord. What usually begins as a sudden onset of lower back pain, muscle weakness, or abnormal sensations in the toes and feet can rapidly progress to more severe symptoms, including paralysis, urinary retention, and loss of bowel control.
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What are the treatments for Transverse Myelitis ?
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No effective cure currently exists for people with transverse myelitis. Physicians often prescribe corticosteroid therapy during the first few weeks of illness to decrease inflammation. Following initial therapy, the most critical part of the treatment for this disorder consists of keeping the patients body functioning while hoping for either complete or partial spontaneous recovery of the nervous system. If an individual begins to recover limb control, physical therapy begins to help improve muscle strength, coordination, and range of motion.
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What is the outlook for Transverse Myelitis ?
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Most individuals will have only one episode of transverse myelitis. Recovery usually begins within 2 to 12 weeks of the onset of symptoms and may continue for up to 2 years and in some cases longer--requiring aggressive physical therapy and rehabilitation. However, if there is no improvement within the first 3 to 6 months, complete recovery is unlikely (although some recovery can occur). Historic data, shows that about one-third of people affected with transverse myelitis experience good or full recovery from their symptoms. Another one-third show only fair recovery and are left with significant deficits. The remaining one-third show no recovery at all, with marked dependence on others for basic functions of daily living. New, more aggressive treatment protocols may result in greater recovery statistics.
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what research (or clinical trials) is being done for Transverse Myelitis ?
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The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to transverse myelitis in its laboratories at the National Institutes of Health (NIH), and also supports additional transverse myelitis research through grants to major medical institutions across the country. Some studies focus on strategies to repair the spinal cord, including approaches using cell transplantation. The NINDS also funds researchers who are using animal models of spinal cord injury to study strategies for replacement or regeneration of spinal cord nerve cells. The knowledge gained from such research should lead to a greater knowledge of the mechanisms responsible for transverse myelitis and may ultimately provide a means to prevent and treat this disorder.
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What are the complications of Neurological Complications of AIDS ?
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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.
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What are the treatments for Neurological Complications of AIDS ?
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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.
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What is the outlook for Neurological Complications of AIDS ?
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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.
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what research (or clinical trials) is being done for Neurological Complications of AIDS ?
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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.
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What is (are) Neurodegeneration with Brain Iron Accumulation ?
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Neurodegeneration with brain iron accumulation (NBIA) is a rare, inherited, neurological movement disorder characterized by an abnormal accumulation of iron in the brain and progressive degeneration of the nervous system. Symptoms, which vary greatly among patients and usually develop during childhood, may include dystonia (slow writhing, distorting muscle contractions of the limbs, face, or trunk), dysarthria (slurred or slow speech) choreoathetosis (involuntary, purposeless jerky muscle movements), muscle rigidity (uncontrolled tightness of the muscles), spasticity (sudden, involuntary muscle spasms), and/or ataxia (inability to coordinate movements), confusion, disorientation, seizures, stupor, and dementia. Visual changes are also common, most often due to atrophy of the optic nerve (optic atrophy) or degeneration of the retinal layer in the back of the eye (retinal degeneration Cognitive decline occurs in some forms of NBIA; the majority of individuals with NBIA do not have cognitive impairment. Several genes have been found that cause NBIA.
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What are the treatments for Neurodegeneration with Brain Iron Accumulation ?
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There is no cure for NBIA, nor is there a standard course of treatment. Treatment is symptomatic and supportive, and may include physical or occupational therapy, exercise physiology, and/or speech pathology. Many medications are available to treat the primary symptoms of dystonia and spasticity, including oral medications, intrathecal baclofen pump (in which a small pump is implanted under the skin and is programmed to deliver a specific amount of medication on a regular basis), deep brain stimulation, and botulinum toxin injection.
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What is the outlook for Neurodegeneration with Brain Iron Accumulation ?
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NBIA is a progressive condition. Most individuals experience periods of rapid decline lasting weeks to months, with relatively stable periods in between. The rate of progression correlates with the age at onset, meaning that children with early symptoms tend to fare more poorly. For those with early onset, dystonia and spasticity can eventually limit the ability to walk, usually leading to use of a wheelchair by the midteens. Life expectancy is variable, although premature death does occur in NBIA. Premature death usually occurs due to secondary complications such as impaired swallowing or confinement to a bed or wheelchair, which can lead to poor nutrition or aspiration pneumonia. With improved medical care, however, a greater number of affected individuals reach adulthood. For those with atypical, late-onset NBIA, many are diagnosed as adults and live well into adulthood.
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what research (or clinical trials) is being done for Neurodegeneration with Brain Iron Accumulation ?
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The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. NINDS-funded researchers are developing a mouse model of an NBIA disorder to gain insight into the causes of the disease and accelerate ongoing efforts to identify therapeutics to treat it..
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What is (are) Occipital Neuralgia ?
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Occipital neuralgia is a distinct type of headache characterized by piercing, throbbing, or electric-shock-like chronic pain in the upper neck, back of the head, and behind the ears, usually on one side of the head. Typically, the pain of occipital neuralgia begins in the neck and then spreads upwards. Some individuals will also experience pain in the scalp, forehead, and behind the eyes. Their scalp may also be tender to the touch, and their eyes especially sensitive to light. The location of pain is related to the areas supplied by the greater and lesser occipital nerves, which run from the area where the spinal column meets the neck, up to the scalp at the back of the head. The pain is caused by irritation or injury to the nerves, which can be the result of trauma to the back of the head, pinching of the nerves by overly tight neck muscles, compression of the nerve as it leaves the spine due to osteoarthritis, or tumors or other types of lesions in the neck. Localized inflammation or infection, gout, diabetes, blood vessel inflammation (vasculitis), and frequent lengthy periods of keeping the head in a downward and forward position are also associated with occipital neuralgia. In many cases, however, no cause can be found. A positive response (relief from pain) after an anesthetic nerve block will confirm the diagnosis.
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What are the treatments for Occipital Neuralgia ?
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Treatment is generally symptomatic and includes massage and rest. In some cases, antidepressants may be used when the pain is particularly severe. Other treatments may include local nerve blocks and injections of steroids directly into the affected area.
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What is the outlook for Occipital Neuralgia ?
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Occipital neuralgia is not a life-threatening condition. Many individuals will improve with therapy involving heat, rest, anti-inflammatory medications, and muscle relaxants. Recovery is usually complete after the bout of pain has ended and the nerve damage repaired or lessened.
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what research (or clinical trials) is being done for Occipital Neuralgia ?
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The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes at the National Institutes of Health conduct research related to pain and occipital neuralgia in their clinics and laboratories and support additional research through grants to major medical institutions across the country. Much of this research focuses on understanding the basic mechanisms of pain and testing treatments in order to find better ways to treat occipital neuralgia.
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What is (are) Congenital Myopathy ?
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A myopathy is a disorder of the muscles that usually results in weakness. Congenital myopathy refers to a group of muscle disorders that appear at birth or in infancy. Typically, an infant with a congenital myopathy will be "floppy," have difficulty breathing or feeding, and will lag behind other babies in meeting normal developmental milestones such as turning over or sitting up.
Muscle weakness can occur for many reasons, including a problem with the muscle, a problem with the nerve that stimulates the muscle, or a problem with the brain. Therefore, to diagnose a congenital myopathy, a neurologist will perform a detailed physical exam as well as tests to determine the cause of weakness. If a myopathy is suspected, possible tests include a blood test for a muscle enzyme called creatine kinase, an electromyogram (EMG) to evaluate the electrical activity of the muscle, a muscle biopsy, and genetic testing.
There are currently seven distinct types of congenital myopathy, with some variation in symptoms, complications, treatment options, and outlook.
Nemaline myopathy is the most common congenital myopathy. Infants usually have problems with breathing and feeding. Later, some skeletal problems may arise, such as scoliosis (curvature of the spine). In general, the weakness does not worsen during life.
Myotubular myopathy is rare and only affects boys. Weakness and floppiness are so severe that a mother may notice reduced movements of the baby in her womb during pregnancy. There are usually significant breathing and swallowing difficulties; many children do not survive infancy. Osteopenia (weakening of the bones) is also associated with this disorder.
Centronuclear myopathy is rare and begins in infancy or early childhood with weakness of the arms and legs, droopy eyelids, and problems with eye movements. Weakness often gets worse with time.
Central core disease varies among children with regard to the severity of problems and the degree of worsening over time. Usually, there is mild floppiness in infancy, delayed milestones, and moderate limb weakness, which do not worsen much over time. Children with central core disease may have life-threatening reactions to general anesthesia. Treatment with the drug salbutamol has been shown to reduce weakness significantly, although it does not cure the disorder.
Multi-minicore disease has several different subtypes. Common to most is severe weakness of the limbs and scoliosis. Often breathing difficulties occur as well. Some children have weakened eye movements.
Congenital fiber-type disproportion myopathy is a rare disorder that begins with floppiness, limb and facial weakness, and breathing problems.
Hyaline body myopathy is a disorder characterized by the specific appearance under the microscope of a sample of muscle tissue. It probably includes several different causes. Because of this, the symptoms are quite variable.
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What are the treatments for Congenital Myopathy ?
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Currently, only central core disease has an effective treatment (see above). There are no known cures for any of these disorders. Supportive treatment may involve orthopedic treatments, as well as physical, occupational or speech therapy.
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What is the outlook for Congenital Myopathy ?
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When breathing difficulties are severe, and particularly if there is also a problem with feeding and swallowing, infants may die of respiratory failure or complications such as pneumonia. Sometimes muscle weakness can lead to skeletal problems, such as scoliosis, reduced mobility of joints, or hip problems. The heart muscle is rarely involved.
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what research (or clinical trials) is being done for Congenital Myopathy ?
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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 congenital myopathies in their 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 prevent, treat, and ultimately cure the disorders that make up the congenital myopathies.
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What is (are) Corticobasal Degeneration ?
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Corticobasal degeneration is a progressive neurological disorder characterized by nerve cell loss and atrophy (shrinkage) of multiple areas of the brain including the cerebral cortex and the basal ganglia. Corticobasal degeneration progresses gradually. Initial symptoms, which typically begin at or around age 60, may first appear on one side of the body (unilateral), but eventually affect both sides as the disease progresses. Symptoms are similar to those found in Parkinson disease, such as poor coordination, akinesia (an absence of movements), rigidity (a resistance to imposed movement), disequilibrium (impaired balance); and limb dystonia (abnormal muscle postures). Other symptoms such as cognitive and visual-spatial impairments, apraxia (loss of the ability to make familiar, purposeful movements), hesitant and halting speech, myoclonus (muscular jerks), and dysphagia (difficulty swallowing) may also occur. An individual with corticobasal degeneration eventually becomes unable to walk.
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What are the treatments for Corticobasal Degeneration ?
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There is no treatment available to slow the course of corticobasal degeneration, and the symptoms of the disease are generally resistant to therapy. Drugs used to treat Parkinson disease-type symptoms do not produce any significant or sustained improvement. Clonazepam may help the myoclonus. Occupational, physical, and speech therapy can help in managing disability.
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What is the outlook for Corticobasal Degeneration ?
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Corticobasal degeneration usually progresses slowly over the course of 6 to 8 years. Death is generally caused by pneumonia or other complications of severe debility such as sepsis or pulmonary embolism.
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what research (or clinical trials) is being done for Corticobasal Degeneration ?
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The NINDS supports and conducts research studies on degenerative disorders such as corticobasal degeneration. The goals of these studies are to increase scientific understanding of these disorders and to find ways to prevent, treat, and cure them.
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What is (are) Central Cord Syndrome ?
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Central cord syndrome is the most common form of incomplete spinal cord injury characterized by impairment in the arms and hands and to a lesser extent in the legs. The brain's ability to send and receive signals to and from parts of the body below the site of injury is reduced but not entirely blocked. This syndrome is associated with damage to the large nerve fibers that carry information directly from the cerebral cortex to the spinal cord. These nerves are particularly important for hand and arm function. Symptoms may include paralysis or loss of fine control of movements in the arms and hands, with relatively less impairment of leg movements. Sensory loss below the site of the injury and loss of bladder control may also occur, as well as painful sensations such as tinging, burning, or dull ache. The overall amount and type of functional loss is dependent upon the severity of nerve damage. Central cord syndrome is usually the result of trauma that causes damage to the vertebrae in the neck or herniation of the vertebral discs. It also may develop in persons over the age of 50 due to gradual weakening of the vertebrae and discs, which narrows the spinal column and may contribute to compression of the spinal cord when the neck is hyper-extended.
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What are the treatments for Central Cord Syndrome ?
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There is no cure for central cord syndrome although some people recover near-normal function. There is no standard course of treatment, although drug therapy, surgery, and rest are often part of the program. Magnetic resonance imaging (MRI) is used to indicate the degree of spinal cord compression and vertebral instability. Vertebral instability due to acute traumatic injury or cervical disc herniation is often treated by surgery to prevent further damage to the spinal cord. Recent reports indicate that earlier surgery may improve chances for recovery. Numerous recent studies suggest that surgery also can be beneficial in individuals with persistent compression of the spinal cord and ongoing neurological deterioration.
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What is the outlook for Central Cord Syndrome ?
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The prognosis for central cord syndrome varies, but most people whose syndrome is caused by trauma have some recovery of neurological function. Evaluation of abnormal signals on MRI images can help predict he likelihood that neurological recovery may occur naturally. Those who receive medical intervention soon after their injury often have good outcomes. Many people with the disorder recover substantial function after their initial injury, and the ability to walk is recovered in most cases, although some impairment may remain. Improvement occurs first in the legs, then the bladder, and may be seen in the arms. Hand function recovers last, if at all. Recovery is generally better in younger patients, compared to those over the age of 50.
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what research (or clinical trials) is being done for Central Cord Syndrome ?
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Our understanding of central cord syndrome has increased greatly in recent decades as a result of research funded conducted by the National Institute of Neurological Disorders and Stroke (NINDS). Much of this research focuses on finding better ways to prevent, treat, and ultimately cure neurological disorders such as central cord syndrome.
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What is (are) Tay-Sachs Disease ?
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Tay-Sachs disease is a inherited metabolic disease caused by the harmful buildup of lipids (fatty materials such as oils and acids) in various cells and tissues in the body. It is part of a group of genetic disorders called the GM2 gangliosidoses. Tay-Sachs and its variant form are caused by a deficiency in the enzyme hexosaminidase A. Affected children appear to develop normally until about age 6 months. Then, symptoms begin and include progressive loss of mental ability, dementia, blindness, increased startle reflex to noise, progressive loss of hearing leading to deafness, and difficulty with swallowing. Seizures may begin in the child's second year. Persons with Tay-Sachs also have "cherry-red" spots in their eyes.A much rarer form of the disorder, called late-onset Tay-Sachs disease, occurs in individuals in their twenties and early thirties and is characterized by an unsteady gait and progressive neurological deterioration. The incidence of Tay-Sachs has been particularly high among people of Eastern European and Askhenazi Jewish descent., as well as in certain French Canadians and Louisiana Cajuns. Affected individuals and carriers of Tay-Sachs disease can be identified by a blood test that measures hexosaminidase A activity. Both parents must carry the mutated gene in order to have an affected child. In these instances, there is a 25 percent chance with each pregnancy that the child will be affected with Tay-Sachs disease. Prenatal diagnosis is available if desired. A very severe form of Tay-Sachs disease is know as Sandhoff disease, which is not limited to any ethnic group.
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What are the treatments for Tay-Sachs Disease ?
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Presently there is no specific treatment for Tay-Sachs disease. Anticonvulsant medicine may initially control seizures. Other supportive treatment includes proper nutrition and hydration and techniques to keep the airway open. Children may eventually need a feeding tube.
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What is the outlook for Tay-Sachs Disease ?
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Even with the best of care, children with Tay-Sachs disease usually die by age 4, from recurring infection.
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what research (or clinical trials) is being done for Tay-Sachs Disease ?
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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 is a part of the National Institutes of Health (NIH), the leading supporter of biomedical research in the world. the NINDS and other NIH Institutes supports the Lysosomal Diseases Netowrk, which addresses some of the major challenges in the diagnosis, management, and therapy of rare diseases, including the lipid storage diseases. Additional 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 research on the gangliosidoses includes using variations of magnetic resonance imaging to develop a biomarker (a sign that may indicate risk of a disease and improve diagnosis) to effectively evaluate brain biochemistry and disease progression. Other research is expanding the use of virus-delivered gene therapy seen in an animall model of Tay-Sachs disease for use in humans.
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What is (are) Empty Sella Syndrome ?
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Empty Sella Syndrome (ESS) is a disorder that involves the sella turcica, a bony structure at the base of the brain that surrounds and protects the pituitary gland. ESS is often discovered during radiological imaging tests for pituitary disorders. ESS occurs n up to 25 percent of the population.An individual with ESS may have no symptoms or may have symptoms resulting from partial or complete loss of pituitary function (including headaches, low sex drive, and impotence).There are two types of ESS: primary and secondary. Primary ESS happens when a small anatomical defect above the pituitary gland allows spinal fluid to partially or completely fill the sella turcica. This causes the gland to flatten out along the interior walls of the sella turcica cavity. Individuals with primary ESS may have high levels of the hormone prolactin, which can interfere with the normal function of the testicles and ovaries. Primary ESS is most common in adults and women, and is often associated with obesity and high blood pressure. In some instances the pituitary gland may be smaller than usual; this may be due to a condition called pseudotumor cerebri (which means "false brain tumor," brought on by high pressure within the skull), In rare instances this high fluid pressure can be associated with drainage of spinal fluid through the nose. Secondary ESS is the result of the pituitary gland regressing within the cavity after an injury, surgery, or radiation therapy. Individuals with secondary ESS can sometimes have symptoms that reflect the loss of pituitary functions, such as the ceasing of menstrual periods, infertility, fatigue, and intolerance to stress and infection. In children, ESS may be associated with early onset of puberty, growth hormone deficiency, pituitary tumors, or pituitary gland dysfunction. Magnetic resonance imaging (MRI) scans are useful in evaluating ESS and for identifying underlying disorders that may be the cause of high fluid pressure.
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What are the treatments for Empty Sella Syndrome ?
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Unless the syndrome results in other medical problems, treatment for endocrine dysfunction associated with pituitary malfunction is symptomatic and supportive. Individuals with primary ESS who have high levels of prolactin may be given bromocriptine. In some cases, particularly when spinal fluid drainage is observed, surgery may be needed.
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What is the outlook for Empty Sella Syndrome ?
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ESS is not a life-threatening condition. Most often, and particularly among those with primary ESS, the disorder does not cause health problems and does not affect life expectancy.
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what research (or clinical trials) is being done for Empty Sella Syndrome ?
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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 supports and conducts fundamental studies that explore the complex mechanisms of normal brain development and to better understand neurological conditions such as ESS. The knowledge gained from these fundamental studies helps researchers understand neurodevelopment and provides opportunities to more effectively treat and perhaps even prevent, such disorders.
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What is (are) Foot Drop ?
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Foot drop describes the inability to raise the front part of the foot due to weakness or paralysis of the muscles that lift the foot. As a result, individuals with foot drop scuff their toes along the ground or bend their knees to lift their foot higher than usual to avoid the scuffing, which causes what is called a steppage gait. Foot drop can be unilateral (affecting one foot) or bilateral (affecting both feet). Foot drop is a symptom of an underlying problem and is either temporary or permanent, depending on the cause. Causes include: neurodegenerative disorders of the brain that cause muscular problems, such as multiple sclerosis, stroke, and cerebral palsy; motor neuron disorders such as polio, some forms of spinal muscular atrophy and amyotrophic lateral sclerosis (commonly known as Lou Gehrigs disease); injury to the nerve roots, such as in spinal stenosis; peripheral nerve disorders such as Charcot-Marie-Tooth disease or acquired peripheral neuropathy; local compression or damage to the peroneal nerve as it passes across the fibular bone below the knee; and muscle disorders, such as muscular dystrophy or myositis.
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What are the treatments for Foot Drop ?
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Treatment depends on the specific cause of foot drop. The most common treatment is to support the foot with light-weight leg braces and shoe inserts, called ankle-foot orthotics. Exercise therapy to strengthen the muscles and maintain joint motion also helps to improve gait. Devices that electrically stimulate the peroneal nerve during footfall are appropriate for a small number of individuals with foot drop. In cases with permanent loss of movement, surgery that fuses the foot and ankle joint or that transfers tendons from stronger leg muscles is occasionally performed.
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What is the outlook for Foot Drop ?
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The prognosis for foot drop depends on the cause. Foot drop caused by trauma or nerve damage usually shows partial or even complete recovery. For progressive neurological disorders, foot drop will be a symptom that is likely to continue as a lifelong disability, but it will not shorten life expectancy.
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what research (or clinical trials) is being done for Foot Drop ?
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The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to the neurological conditions that cause foot drop 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 the kinds of neurological disorders that cause foot drop.
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What is (are) Autism ?
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Autistic disorder (sometimes called autism or classical ASD) is the most common condition in a group of developmental disorders known as the autism spectrum disorders (ASDs).
Autistic children have difficulties with social interaction, display problems with verbal and nonverbal communication, and exhibit repetitive behaviors or narrow, obsessive interests. These behaviors can range in impact from mild to disabling. Autism varies widely in its severity and symptoms and may go unrecognized, especially in mildly affected children or when more debilitating handicaps mask it. Scientists arent certain what causes autism, but its likely that both genetics and environment play a role.
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What are the treatments for Autism ?
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There is no cure for autism. Therapies and behavioral interventions are designed to remedy specific symptoms and can bring about substantial improvement. The ideal treatment plan coordinates therapies and interventions that meet the specific needs of individual children. Treatment options include educational/bahavioral interventions, medications, and other therapies. Most professionals agree that the earlier the intervention, the better.
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What is the outlook for Autism ?
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For many children, autism symptoms improve with treatment and with age. Some children with autism grow up to lead normal or near-normal lives. Children whose language skills regress early in life, usually before the age of 3, appear to be at risk of developing epilepsy or seizure-like brain activity. During adolescence, some children with autism may become depressed or experience behavioral problems. Parents of these children should be ready to adjust treatment for their child as needed. People with an ASD usually continue to need services and support as they get older but many are able to work successfully and live independently or within a supportive environment.
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what research (or clinical trials) is being done for Autism ?
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The National Institute of Neurological Disorders and Stroke (NINDS) conducts research in its laboratories at the National Institutes of Health (NIH) and also supports additional research through grants to major medical institutions across the country. As part of the Childrens Health Act of 2000, the NINDS and three sister institutes have formed the NIH Autism Coordinating Committee to expand, intensify, and coordinate NIHs autism research. As part of the Childrens Health Act of 2000, the NINDS and three sister institutes have formed the NIH Autism Coordinating Committee to expand, intensify, and coordinate NIHs autism research. Eight dedicated research centers across the country have been established as Centers of Excellence in Autism Research to bring together researchers and the resources they need. The Centers are conducting basic and clinical research, including investigations into causes, diagnosis, early detection, prevention, and treatment of autism.
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What is (are) Kleine-Levin Syndrome ?
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Kleine-Levin syndrome is a rare disorder that primarily affects adolescent males (approximately 70 percent of those with Kleine-Levin syndrome are male). It is characterized by recurring but reversible periods of excessive sleep (up to 20 hours per day). Symptoms occur as "episodes," typically lasting a few days to a few weeks. Episode onset is often abrupt, and may be associated with flu-like symptoms. Excessive food intake, irritability, childishness, disorientation, hallucinations, and an abnormally uninhibited sex drive may be observed during episodes. Mood can be depressed as a consequence, but not a cause, of the disorder. Affected individuals are completely normal between episodes, although they may not be able to remember afterwards everything that happened during the episode. It may be weeks or more before symptoms reappear. Symptoms may be related to malfunction of the hypothalamus and thalamus, parts of the brain that govern appetite and sleep.
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What are the treatments for Kleine-Levin Syndrome ?
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There is no definitive treatment for Kleine-Levin syndrome and watchful waiting at home, rather than pharmacotherapy, is most often advised. Stimulant pills, including amphetamines, methylphenidate, and modafinil, are used to treat sleepiness but may increase irritability and will not improve cognitive abnormalities. Because of similarities between Kleine-Levin syndrome and certain mood disorders, lithium and carbamazepine may be prescribed and, in some cases, have been shown to prevent further episodes. This disorder should be differentiated from cyclic re-occurrence of sleepiness during the premenstrual period in teen-aged girls, which may be controlled with birth control pills. It also should be differentiated from encephalopathy, recurrent depression, or psychosis.
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What is the outlook for Kleine-Levin Syndrome ?
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Episodes eventually decrease in frequency and intensity over the course of eight to 12 years.
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what research (or clinical trials) is being done for Kleine-Levin Syndrome ?
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NINDS supports a broad range of clinical and basic research on diseases causing sleep disorders in an effort to clarify the mechanisms of these conditions and to develop better treatments for them.
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What is (are) Pelizaeus-Merzbacher Disease ?
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Pelizaeus-Merzbacher disease (PMD) is a rare, progressive, degenerative central nervous system disorder in which coordination, motor abilities, and intellectual function deteriorate. The disease is one of a group of gene-linked disorders known as the leukodystrophies, which affect growth of the myelin sheath -- the fatty covering that wraps around and protects nerve fibers in the brain. The disease is caused by a mutation in the gene that controls the production of a myelin protein called proteolipid protein-1 (PLP1). PMD is inherited as an X-linked recessive trait; the affected individuals are male and the mothers are carriers of the PLP1 mutation. Severity and onset of the disease ranges widely, depending on the type of PLP1 mutation. PMD is one of a spectrum of diseases associated with PLP1, which also includes Spastic Paraplegia Type 2 (SPG2). The PLP1-related disorders span a continuum of neurologic symptoms that range from severe central nervous system involvement (PMD) to progressive weakness and stiffness of the legs (SPG2). There are four general classifications within this spectrum of diseases. In order of severity, they are:
- Connatal PMD, which is the most severe type and involves delayed mental and physical development and severe neurological symptoms; - Classic PMD, in which the early symptoms include muscle weakness, involuntary movements of the eyes (nystagmus), and delays in motor development within the first year of life; - Complicated SPG2, which features motor development issues and brain involvement, and, - Pure SPG2, which includes cases of PMD that do not have neurologic complications.
Noticeable changes in the extent of myelination can be detected by MRI analyses of the brain. Additional symptoms of PMD may include slow growth, tremor, failure to develop normal control of head movement, and deteriorating speech and cognitive function.
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What are the treatments for Pelizaeus-Merzbacher Disease ?
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There is no cure for Pelizaeus-Merzbacher disease, nor is there a standard course of treatment. Treatment is symptomatic and supportive and may include medication for movement disorders.
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What is the outlook for Pelizaeus-Merzbacher Disease ?
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The prognosis for those with the severe forms of Pelizaeus-Merzbacher disease is poor, with progressive deterioration until death. On the other end of the disease spectrum, individuals with the mild form, in which spastic paraplegia is the chief symptom, may have nearly normal activity and life span.
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what research (or clinical trials) is being done for Pelizaeus-Merzbacher Disease ?
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NINDS supports research on gene-linked 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.
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What is (are) Dysautonomia ?
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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.
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What are the treatments for Dysautonomia ?
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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.
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What is the outlook for Dysautonomia ?
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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.
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what research (or clinical trials) is being done for Dysautonomia ?
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The NINDS supports and conducts research on dysautonomia. This research aims to discover ways to diagnose, treat, and, ultimately, prevent these disorders.
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What is (are) Neurofibromatosis ?
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The neurofibromatoses are genetic disorders that cause tumors to grow in the nervous system. The tumors begin in the supporting cells that make up the nerves and the myelin sheath--the thin membrane that envelops and protects the nerves. These disorders cause tumors to grow on nerves and, less frequently, in the brain and spinal cord, and produce other abnormalities such as skin changes and bone deformities. Although many affected persons inherit the disorder, between 30 and 50 percent of new cases arise spontaneously through mutation (change) in an individual's genes. Once this change has taken place, the mutant gene can be passed on to succeeding generations. There are three forms of neurofibromatosis (NF):
- NF1 is the more common type of the disorder. Symptoms of NF1, which may be evident at birth and nearly always by the time the child is 10 years old, may include light brown spots on the skin ("cafe-au-lait" spots), two or more growths on the iris of the eye, a tumor on the optic nerve, a larger than normal head circumference, and abnormal development of the spine, a skull bone, or the tibia. - NF2 is less common and is characterized by slow-growing tumors on the vestibular branch of the right and left eighth cranial nerves, which are called vestibular schwannomas or acoustic neuromas.. The tumors press on and damage neighboring nerves and reduce hearing. - The distinctive feature of schwannomatosis is the development of multiple schwannomas (tumors made up of certain cells) everywhere in the body except on the vestibular branch of the 8th cranial nerve. The dominant symptom is pain, which develops as a schwannoma enlarges or compresses nerves or adjacent tissue. Some people may develop numbness, tingling, or weakness in the fingers and toes.
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What are the treatments for Neurofibromatosis ?
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Treatment may include surgery, focused radiation, or chemotherapy. Surgery to remove NF2 tumors completely is one option. Surgery for vestibular schwannomas does not restore hearing and usually reduces hearing. Sometimes surgery is not performed until functional hearing is lost completely. Surgery may result in damage to the facial nerve and some degree of facial paralysis. Focused radiation of vestibular schwannoma carries of a lower risk of facial paralysis than open surgery, but is more effective o shrinking small to moderate tumors than larger tumors. Chemotherapy with a drug that targets the blood vessels of vestibular schwannoma can reduce the size of the tumor and improves hearing, but some tumors do not respond at all and sometimes respond only temporarily. Bone malformations can often be corrected surgically, and surgery can also correct cataracts and retinal abnormalities. Pain usually subsides when tumors are removed completely.
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What is the outlook for Neurofibromatosis ?
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In most cases, symptoms of NF1 are mild, and individuals live normal and productive lives. In some cases, however, NF1 can be severely debilitating and may cause cosmetic and psychological issues. The course of NF2 varies greatly among individuals. Loss of hearing in both ears develops in most individuals with NF2. In some cases of NF2, the damage to nearby vital structures, such as other cranial nerves and the brain stem, can be life-threatening. Most individuals with schwannomatosis have significant pain. In some extreme cases the pain will be severe and disabling.
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what research (or clinical trials) is being done for Neurofibromatosis ?
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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 researchers are working to identify signaling pathways in the nervous system, with the hope of eventually developing drugs and techniques to help diagnose and treat NF. Understanding the natural history of tumors in NF and determining possible factors that may regulate their growth patterns is another aim of NIH researchers Ongoing research continues to discover additional genes that appear to play a role in NF-related tumor suppression or growth Continuing research on these genes and their proteins is beginning to reveal how this novel family of growth regulators controls how and where tumors form and grow Researchers also hope to develop new and more effective treatments for neurofibromatosis. Several agents have been tested or are under investigation for NF2, including the monoclonal antibody, bevacizumab, which improves hearing in some individuals with NF2.Because schwannomas are particularly hard to treat tumors, NINDS researchers are developing a new treatment option, which uses a virus to kill tumor cells. Additional NINDS-funded researchers are testing novel radiation and chemotherapy regimens for NF1-related malignant tumors of the peripheral nerves.
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What is (are) Multiple System Atrophy ?
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Multiple system atrophy (MSA) is a progressive neurodegenerative disorder characterized by symptoms of autonomic nervous system failure such as fainting spells and bladder control problems, combined with motor control symptoms such as tremor, rigidity, and loss of muscle coordination. MSA affects both men and women primarily in their 50s. Although what causes MSA is unknown, the disorder's symptoms reflect the loss of nerve cells in several different areas in the brain and spinal cord that control the autonomic nervous system and coordinate muscle movements. The loss of nerve cells may be due to the buildup of a protein called alpha-synuclein in the cells that support nerve cells in the brain.
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What are the treatments for Multiple System Atrophy ?
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There is no cure for MSA. Currently, there are no treatments to delay the progress of neurodegeneration in the brain. But there are treatments available to help people cope with some of the more disabling symptoms of MSA. In some individuals, levodopa may improve motor function, but the benefit may not continue as the disease progresses.
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What is the outlook for Multiple System Atrophy ?
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The disease tends to advance rapidly over the course of 5 to 10 years, with progressive loss of motor skills, eventual confinement to bed, and death. There is no remission from the disease. There is currently no cure.
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what research (or clinical trials) is being done for Multiple System Atrophy ?
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The NINDS supports research about MSA through grants to major medical institutions across the country. Researchers hope to learn why alpha-synuclein buildup occurs in MSA and Parkinsons disease, and how to prevent it. Drugs that reduce the abnormal alpha-synuclein buildup may be promising treatments for MSA
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What is (are) Neurosarcoidosis ?
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Neurosarcoidosis is a manifestation of sarcoidosis in the nervous system. Sarcoidosis is a chronic inflammatory disorder that typically occurs in adults between 20 and 40 years of age and primarily affects the lungs, but can also impact almost every other organ and system in the body. Neurosarcoidosis is characterized by inflammation and abnormal cell deposits in any part of the nervous system the brain, spinal cord, or peripheral nerves. It most commonly occurs in the cranial and facial nerves, the hypothalamus (a specific area of the brain), and the pituitary gland. It is estimated to develop in 5 to 15 percent of those individuals who have sarcoidosis. Weakness of the facial muscles on one side of the face (Bells palsy) is a common symptom of neurosarcoidosis. The optic and auditory nerves can also become involved, causing vision and hearing impairments. It can cause headache, seizures, memory loss, hallucinations, irritability, agitation, and changes in mood and behavior. Neurosarcoidosis can appear in an acute, explosive fashion or start as a slow chronic illness. Because neurosarcoidosis manifests in many different ways, a diagnosis may be difficult and delayed.
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What are the treatments for Neurosarcoidosis ?
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There is no agreed upon standard of treatment for neurosarcoidosis. Doctors generally recommend corticosteroid therapy as first-line therapy for individuals with the condition. Additional treatment with immunomodulatory drugs such as hydroxychloroquine, pentoxyfilline, thalidomide, and infliximab, and immunosuppressive drugs such as methotrexate, azathioprine, cyclosporin, and cyclophosphamide, have benefited some individuals. While the use of corticosteroids and other immunosuppressive drugs is effective, these medications also have undesirable side effects. Side effects and experience with certain drugs may play a role in medication choices.
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What is the outlook for Neurosarcoidosis ?
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The prognosis for patients with neurosarcoidosis varies. Approximately two-thirds of those with the condition will recover completely; the remainder will have a chronically progressing or on-and-off course of illness. Complications resulting from immunosuppressive treatments, such as cryptococcal and tuberculous meningitis, progressive multifocal leukoencephalopathy, and inclusion body myositis, may be fatal for a small percentage of individuals.
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what research (or clinical trials) is being done for Neurosarcoidosis ?
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The National Institute of Neurological Disorders and Stroke (NINDS) has joined with other institutes of the National Institutes of Health (NIH) to form a trans-NIH working group to coordinate and fund research into the disease mechanisms of sarcoidosis, predisposing factors, genetic underpinnings, and the potential for clinical therapies. Grants are supporting research at major medical institutions across the country. The outcomes of this research will be better ways to diagnose, treat, and ultimately cure sarcoidosis and neurosarcardoisis.
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What is (are) Epilepsy ?
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The epilepsies are a spectrum of brain disorders ranging from severe, life-threatening and disabling, to ones that are much more benign. In epilepsy, the normal pattern of neuronal activity becomes disturbed, causing strange sensations, emotions, and behavior or sometimes convulsions, muscle spasms, and loss of consciousness. The epilepsies have many possible causes and there are several types of seizures. Anything that disturbs the normal pattern of neuron activityfrom illness to brain damage to abnormal brain developmentcan lead to seizures. Epilepsy may develop because of an abnormality in brain wiring, an imbalance of nerve signaling chemicals called neurotransmitters, changes in important features of brain cells called channels, or some combination of these and other factors. Having a single seizure as the result of a high fever (called febrile seizure) or head injury does not necessarily mean that a person has epilepsy. Only when a person has had two or more seizures is he or she considered to have epilepsy. A measurement of electrical activity in the brain and brain scans such as magnetic resonance imaging or computed tomography are common diagnostic tests for epilepsy.
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What are the treatments for Epilepsy ?
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Once epilepsy is diagnosed, it is important to begin treatment as soon as possible. For about 70 percent of those diagnosed with epilepsy, seizures can be controlled with modern medicines and surgical techniques. Some drugs are more effective for specific types of seizures. An individual with seizures, particularly those that are not easily controlled, may want to see a neurologist specifically trained to treat epilepsy. In some children, special diets may help to control seizures when medications are either not effective or cause serious side effects.
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What is the outlook for Epilepsy ?
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While epilepsy cannot be cured, for some people the seizures can be controlled with medication, diet, devices, and/or surgery. Most seizures do not cause brain damage, but ongoing uncontrolled seizures may cause brain damage. It is not uncommon for people with epilepsy, especially children, to develop behavioral and emotional problems in conjunction with seizures. Issues may also arise as a result of the stigma attached to having epilepsy, which can led to embarrassment and frustration or bullying, teasing, or avoidance in school and other social settings. For many people with epilepsy, the risk of seizures restricts their independence (some states refuse drivers licenses to people with epilepsy) and recreational activities.
Epilepsy can be a life-threatening condition. Some people with epilepsy are at special risk for abnormally prolonged seizures or sudden unexplained death in epilepsy.
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what research (or clinical trials) is being done for Epilepsy ?
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Scientists are studying the underlying causes of the epilepsies in children, adults, and the elderly, as well as seizures that occur following brain trauma, stroke, and brain tumors. Ongoing research is focused on developing new model systems that can be used to more quickly screen potential new treatments for the epilepsies. The identification of genes or other genetic information that may influence or cause the epilepsies may allow doctors to prevent the disorders or to predict which treatments will be most beneficial to individuals with specific types of epilepsy. Scientists also continue to study how neurotransmitters interact with brain cells to control nerve firing and how non-neuronal cells in the brain contribute to seizures. Researchers funded by the National Institutes of Health have developed a flexible brain implant that could one day be used to treat seizures. Scientists are continually improving MRI and other brain scans that may assist in diagnosing the epilepsies and identify the source, or focus, of the seizures in the brain. Other areas of study include prevention of seizures and the role of inflammation in epilepsy. Patients may enter trials of experimental drugs and surgical interventions.
More about epilepsy research
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What is (are) Cushing's Syndrome ?
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Cushing's syndrome, also called hypercortisolism, is a rare endocrine disorder caused by chronic exposure of the body's tissues to excess levels of cortisol - a hormone naturally produced by the adrenal gland. Exposure to too much cortisol can occur from long-term use of synthetic glucocorticoid hormones to treat inflammatory illnesses. Pituitary adenomas (benign tumors of the pituitary gland) that secrete increased amounts of ACTH (adrenocorticotropic hormone, a substance that controls the release of cortisol) can also spur overproduction of cortisol. Tumors of the adrenal gland and ectopic ACTH syndrome (a condition in which ACTH is produced by various types of potentially malignant tumors that occur in different parts of the body) can cause similar problems with cortisol balance. Common symptoms of Cushing's syndrome include upper body obesity, severe fatigue and muscle weakness, high blood pressure, backache, elevated blood sugar, easy bruising, and bluish-red stretch marks on the skin. In women, there may be increased growth of facial and body hair, and menstrual periods may become irregular or stop completely. Neurological symptoms include difficulties with memory and neuromuscular disorders.
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What are the treatments for Cushing's Syndrome ?
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Treatment of Cushing's syndrome depends on the cause of excess cortisol. If the cause is long-term use of a medication being used to treat another disorder, the physician may reduce the dosage until symptoms are under control. Surgery or radiotherapy may be used to treat pituitary adenomas. Surgery, radiotherapy, chemotherapy, immunotherapy, or a combination of these may be used to treat ectopic ACTH syndrome. The aim of surgical treatment is to cure hypercortisolism by removing the tumor while minimizing the chance of endocrine deficiency or long-term dependence on medications. The U.S. Food and Drug Administration has approved pasireotide diasparate, taken by injection, for individuals who cannot be helped through surgery.
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What is the outlook for Cushing's Syndrome ?
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The prognosis for those with Cushing's syndrome varies depending on the cause of the disease. Most cases of Cushing's syndrome can be cured. Many individuals with Cushing's syndrome show significant improvement with treatment, although some may find recovery complicated by various aspects of the causative illness. Some kinds of tumors may recur.
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what research (or clinical trials) is being done for Cushing's Syndrome ?
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NINDS supports research on Cushing's syndrome aimed at finding new ways to diagnose, treat, and cure the disorder.
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What is (are) Herpes Zoster Oticus ?
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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.
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What are the treatments for Herpes Zoster Oticus ?
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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
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What is the outlook for Herpes Zoster Oticus ?
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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.
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what research (or clinical trials) is being done for Herpes Zoster Oticus ?
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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.
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What is (are) Williams Syndrome ?
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Williams Syndrome (WS) is a rare genetic disorder characterized by mild to moderate delays in cognitive development or learning difficulties, a distinctive facial appearance, and a unique personality that combines over-friendliness and high levels of empathy with anxiety. The most significant medical problem associated with WS is cardiovascular disease caused by narrowed arteries. WS is also associated with elevated blood calcium levels in infancy. A random genetic mutation (deletion of a small piece of chromosome 7), rather than inheritance, most often causes the disorder. However, individuals who have WS have a 50 percent chance of passing it on if they decide to have children. The characteristic facial features of WS include puffiness around the eyes, a short nose with a broad nasal tip, wide mouth, full cheeks, full lips, and a small chin. People with WS are also likely to have a long neck, sloping shoulders, short stature, limited mobility in their joints, and curvature of the spine. Some individuals with WS have a star-like pattern in the iris of their eyes. Infants with WS are often irritable and colicky, with feeding problems that keep them from gaining weight. Chronic abdominal pain is common in adolescents and adults. By age 30, the majority of individuals with WS have diabetes or pre-diabetes and mild to moderate sensorineural hearing loss (a form of deafness due to disturbed function of the auditory nerve). For some people, hearing loss may begin as early as late childhood. WS also is associated with a characteristic cognitive profile of mental strengths and weaknesses composed of strengths in verbal short-term memory and language, combined with severe weakness in visuospatial construction (the skills used to copy patterns, draw, or write). Within language, the strongest skills are typically in concrete, practical vocabulary, which in many cases is in the low average to average range for the general population. Abstract or conceptual-relational vocabulary is much more limited. Most older children and adults with WS speak fluently and use good grammar. More than 50% of children with WS have attention deficit disorders (ADD or ADHD), and about 50% have specific phobias, such as a fear of loud noises. The majority of individuals with WS worry excessively.
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What are the treatments for Williams Syndrome ?
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There is no cure for Williams syndrome, nor is there a standard course of treatment. Because WS is an uncommon and complex disorder, multidisciplinary clinics have been established at several centers in the United States . Treatments are based on an individuals particular symptoms. People with WS require regular cardiovascular monitoring for potential medical problems, such as symptomatic narrowing of the blood vessels, high blood pressure, and heart failure
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What is the outlook for Williams Syndrome ?
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The prognosis for individuals with WS varies. Some degree of impaired intellect is found in most people with the disorder. Some adults are able to function independently, complete academic or vocational school, and live in supervised homes or on their own; most live with a caregiver. Parents can increase the likelihood that their child will be able to live semi-independently by teaching self-help skills early. Early intervention and individualized educational programs designed with the distinct cognitive and personality profiles of WS in mind also help individuals maximize their potential. Medical complications associated with the disorder may shorten the lifespans of some individuals with WS.
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what research (or clinical trials) is being done for Williams Syndrome ?
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The National Institutes of Health (NIH), and the National Institute of Neurological Disorders and Stroke (NINDS), have funded many of the research studies exploring the genetic and neurobiological origins of WS. In the early 1990s, researchers located and identified the genetic mutation responsible for the disorder: the deletion of a small section of chromosome 7 that contains approximately 25 genes. NINDS continues to support WS researchers including, for example, groups that are attempting to link specific genes with the corresponding facial, cognitive, personality, and neurological characteristics of WS.
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What is (are) Hypertonia ?
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Hypertonia is a condition in which there is too much muscle tone so that arms or legs, for example, are stiff and difficult to move. Muscle tone is regulated by signals that travel from the brain to the nerves and tell the muscle to contract. Hypertonia happens when the regions of the brain or spinal cord that control these signals are damaged. This can occur for many reasons, such as a blow to the head, stroke, brain tumors, toxins that affect the brain, neurodegenerative processes such as in multiple sclerosis or Parkinson's disease, or neurodevelopmental abnormalities such as in cerebral palsy.
Hypertonia often limits how easily the joints can move. If it affects the legs, walking can become stiff and people may fall because it is difficult for the body to react quickly enough to regain balance. If hypertonia is severe, it can cause a joint to become "frozen," which doctors call a joint contracture.
Spasticity is a term that is often used interchangeably with hypertonia. Spasticity, however, is a particular type of hypertonia in which the muscles' spasms are increased by movement. In this type, patients usually have exaggerated reflex responses.
Rigidity is another type of hypertonia in which the muscles have the same amount of stiffness independent of the degree of movement. Rigidity usually occurs in diseases such as Parkinson's disease, that involve the basal ganglia (a deep region of the brain). To distinguish these types of hypertonia, a doctor will as the patient to relax and then will move the arm or leg at different speeds and in a variety of directions.
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What are the treatments for Hypertonia ?
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Muscle relaxing drugs such as baclofen, diazepam, and dantrolene may be prescribed to reduce spasticity. All of these drugs can be taken by mouth, but baclofen may also be injected directly into the cerebrospinal fluid through an implanted pump. Botulinum toxin is often used to relieve hypertonia in a specific area of the body because its effects are local, not body-wide. People with hypertonia should try to preserve as much movement as possibly by exercising within their limits and using physical therapy.
Drugs that affect the dopamine system (dopamine is a chemical in the brain) such as levodopa/carbidopa, or entacapone, are often used to treat the rigidity associated with Parkinson's disease.
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What is the outlook for Hypertonia ?
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The prognosis depends upon the severity of the hypertonia and its cause. In some cases, such as cerebral palsy, the hypertonia may not change over the course of a lifetime. in other cases, the hypertonia may worsen along with the underlying disease If the hypertonia is mild, it has little or no effect on a person's health. If there is moderate hypertonia, falls or joint contractures may have an impact on a person's health and safety. If the hypertonia is so severe that is caused immobility, potential consequences include increased bone fragility and fracture, infection, bed sores, and pneumonia.
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what research (or clinical trials) is being done for Hypertonia ?
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NINDS supports research on brain and spinal cord disorders that can cause hypertonia. The goals of this research are to learn more about how the nervous system adapts after injury or disease and to find ways to prevent and treat these disorders.
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What is (are) Sjgren's Syndrome ?
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Sjgren's syndrome is an autoimmune disorder in which immune cells attack and destroy the glands that produce tears and saliva. Sjgren's syndrome is also associated with rheumatic disorders such as rheumatoid arthritis. The hallmark symptoms of the disorder are dry mouth and dry eyes. In addition, Sjogren's syndrome may cause skin, nose, and vaginal dryness, and may affect other organs of the body including the kidneys, blood vessels, lungs, liver, pancreas, and brain. Sjgren's syndrome affects 1-4 million people in the United States. Most people are more than 40 years old at the time of diagnosis. Women are 9 times more likely to have Sjgren's syndrome than men.
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What are the treatments for Sjgren's Syndrome ?
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There is no known cure for Sjgren's syndrome nor is there a specific treatment to restore gland secretion. Treatment is generally symptomatic and supportive. Moisture replacement therapies may ease the symptoms of dryness. Nonsteroidal anti-inflammatory drugs may be used to treat musculoskeletal symptoms. For individuals with severe complications, corticosteroids or immunosuppressive drugs may be prescribed.
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What is the outlook for Sjgren's Syndrome ?
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Sjgren's syndrome can damage vital organs of the body with symptoms that may remain stable, worsen, or go into remission. Some people may experience only the mild symptoms of dry eyes and mouth, while others go through cycles of good health followed by severe disease. Many patients are able to treat problems symptomatically. Others are forced to cope with blurred vision, constant eye discomfort, recurrent mouth infections, swollen parotid glands, hoarseness, and difficulty in swallowing and eating. Debilitating fatigue and joint pain can seriously impair quality of life.
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what research (or clinical trials) is being done for Sjgren's Syndrome ?
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The goals of research on disorders such as Sjgren's syndrome focus on increasing knowledge and understanding of the disorder, improving diagnostic techniques, testing interventions, and finding ways to treat, prevent, and cure the disease.
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