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What is (are) Tourette Syndrome ?
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Tourette syndrome (TS) is a neurological disorder characterized by repetitive, stereotyped, involuntary movements and vocalizations called tics. The first symptoms of TS are almost always noticed in childhood. Some of the more common tics include eye blinking and other vision irregularities, facial grimacing, shoulder shrugging, and head or shoulder jerking. Perhaps the most dramatic and disabling tics are those that result in self-harm such as punching oneself in the face, or vocal tics including coprolalia (uttering swear words) or echolalia (repeating the words or phrases of others). Many with TS experience additional neurobehavioral problems including inattention, hyperactivity and impulsivity, and obsessive-compulsive symptoms such as intrusive thoughts/worries and repetitive behaviors.
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What are the treatments for Tourette Syndrome ?
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Because tic symptoms do not often cause impairment, the majority of people with TS require no medication for tic suppression. However, effective medications are available for those whose symptoms interfere with functioning. There is no one medication that is helpful to all people with TS, nor does any medication completely eliminate symptoms. Effective medications are also available to treat some of the associated neurobehavioral disorders that can occur in patients with TS.
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What is the outlook for Tourette Syndrome ?
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Although TS can be a chronic condition with symptoms lasting a lifetime, most people with the condition experience their worst symptoms in their early teens, with improvement occurring in the late teens and continuing into adulthood. As a result, some individuals may actually become symptom free or no longer need medication for tic suppression.
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what research (or clinical trials) is being done for Tourette Syndrome ?
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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 in laboratories at the NIH and support additional research through grants to major medical institutions across the country. Knowledge about TS comes from studies across a number of medical and scientific disciplines, including genetics, neuroimaging, neuropathology, clinical trials, epidemiology, neurophysiology, neuroimmunology, and descriptive/diagnostic clinical science. Findings from these studies will provide clues for more effective therapies.
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What is (are) Klippel Feil Syndrome ?
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Klippel-Feil Syndrome is a rare disorder characterized by the congenital fusion of two or more cervical (neck) vertebrae. It is caused by a failure in the normal segmentation or division of the cervical vertebrae during the early weeks of fetal development. The most common signs of the disorder are short neck, low hairline at the back of the head, and restricted mobility of the upper spine. The fused vertebrae can cause nerve damage and pain in the head, neck, or back. Associated abnormalities may include scoliosis (curvature of the spine), spina bifida (a birth defect of the spine), cleft palate, respiratory problems, and heart malformations. Other features may include joint pain; anomalies of the head and face, skeleton, sex organs, muscles, brain and spinal cord, arms, legs, and fingers; and difficulties hearing. Most cases are sporadic (happen on their own) but mutations in the GDF6 (growth differentiation factor 6) or GDF3 (growth differentiation factor 3) genes can cause the disorder. These genes make proteins that are involved in bone development and segmentation of the vertebrae.
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What are the treatments for Klippel Feil Syndrome ?
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Treatment for Klippel-Feil Syndrome is symptomatic and may include surgery to relieve cervical or craniocervical instability and constriction of the spinal cord, and to correct scoliosis. Physical therapy may also be useful.
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What is the outlook for Klippel Feil Syndrome ?
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The prognosis for most individuals with Klippel-Feil Syndrome is good if the disorder is treated early and appropriately. Activities that can injure the neck should be avoided.
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what research (or clinical trials) is being done for Klippel Feil Syndrome ?
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The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge abuot the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. Research supported by the NINDS includes studies to understand how the brain and nervous system normally develop and function and how they are affected by disease and trauma. These studies contribute to a greater understanding of birth defects such as Klippel-Feil Syndrome and open promising new avenues for treatment.
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What is (are) Meralgia Paresthetica ?
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Meralgia paresthetica is a disorder characterized by tingling, numbness, and burning pain in the outer side of the thigh. The disorder is caused by compression of the lateral femoral cutaneous nerve, a sensory nerve to the skin, as it exits the pelvis. People with the disorder often notice a patch of skin that is sensitive to touch and sometimes painful. Meralgia paresthetica should not be associated with weakness or radiating pain from the back.
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What are the treatments for Meralgia Paresthetica ?
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Treatment for meralgia paresthetica is symptomatic and supportive. The majority of cases improve with conservative treatment by wearing looser clothing and losing weight. Medications used to treat neurogenic pain, such as anti-seizure or anti-depressant medications, may alleviate symptoms of pain. In a few cases, in which pain is persistent or severe, surgical intervention may be indicated.
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What is the outlook for Meralgia Paresthetica ?
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Meralgia paresthetica usually has a good prognosis. In most cases, meralgia paresthetica will improve with conservative treatment or may even spontaneously resolve. Surgical intervention is not always fully successful.
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what research (or clinical trials) is being done for Meralgia Paresthetica ?
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Within the NINDS research programs, meralgia paresthetica is addressed primarily through studies associated with pain research. NINDS vigorously pursues a research program seeking new treatments for pain and nerve damage with the ultimate goal of reversing these debilitating conditions.
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What is (are) Dyslexia ?
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Dyslexia is a brain-based type of learning disability that specifically impairs a person's ability to read. These individuals typically read at levels significantly lower than expected despite having normal intelligence. Although the disorder varies from person to person, common characteristics among people with dyslexia are difficulty with phonological processing (the manipulation of sounds), spelling, and/or rapid visual-verbal responding. In individuals with adult onset of dyslexia, it usually occurs as a result of brain injury or in the context of dementia; this contrasts with individuals with dyslexia who simply were never identified as children or adolescents. Dyslexia can be inherited in some families, and recent studies have identified a number of genes that may predispose an individual to developing dyslexia.
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What are the treatments for Dyslexia ?
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The main focus of treatment should be on the specific learning problems of affected individuals. The usual course is to modify teaching methods and the educational environment to meet the specific needs of the individual with dyslexia.
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What is the outlook for Dyslexia ?
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For those with dyslexia, the prognosis is mixed. The disability affects such a wide range of people and produces such different symptoms and varying degrees of severity that predictions are hard to make. The prognosis is generally good, however, for individuals whose dyslexia is identified early, who have supportive family and friends and a strong self-image, and who are involved in a proper remediation program.
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what research (or clinical trials) is being done for Dyslexia ?
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The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) support dyslexia research through grants to major research institutions across the country. Current research avenues focus on developing techniques to diagnose and treat dyslexia and other learning disabilities, increasing the understanding of the biological and possible genetic bases of learning disabilities, and exploring the relationship between neurophysiological processes and cognitive functions with regard to reading ability.
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What is (are) Hypersomnia ?
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Hypersomnia is characterized by recurrent episodes of excessive daytime sleepiness or prolonged nighttime sleep. Different from feeling tired due to lack of or interrupted sleep at night, persons with hypersomnia are compelled to nap repeatedly during the day, often at inappropriate times such as at work, during a meal, or in conversation. These daytime naps usually provide no relief from symptoms. Patients often have difficulty waking from a long sleep, and may feel disoriented. Other symptoms may include anxiety, increased irritation, decreased energy, restlessness, slow thinking, slow speech, loss of appetite, hallucinations, and memory difficulty. Some patients lose the ability to function in family, social, occupational, or other settings. Hypersomnia may be caused by another sleep disorder (such as narcolepsy or sleep apnea), dysfunction of the autonomic nervous system, or drug or alcohol abuse. In some cases it results from a physical problem, such as a tumor, head trauma, or injury to the central nervous system. Certain medications, or medicine withdrawal, may also cause hypersomnia. Medical conditions including multiple sclerosis, depression, encephalitis, epilepsy, or obesity may contribute to the disorder. Some people appear to have a genetic predisposition to hypersomnia; in others, there is no known cause. Typically, hypersomnia is first recognized in adolescence or young adulthood.
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What are the treatments for Hypersomnia ?
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Treatment is symptomatic in nature. Stimulants, such as amphetamine, methylphenidate, and modafinil, may be prescribed. Other drugs used to treat hypersomnia include clonidine, levodopa, bromocriptine, antidepressants, and monoamine oxidase inhibitors. Changes in behavior (for example avoiding night work and social activities that delay bed time) and diet may offer some relief. Patients should avoid alcohol and caffeine.
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What is the outlook for Hypersomnia ?
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The prognosis for persons with hypersomnia depends on the cause of the disorder. While the disorder itself is not life threatening, it can have serious consequences, such as automobile accidents caused by falling asleep while driving. The attacks usually continue indefinitely.
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what research (or clinical trials) is being done for Hypersomnia ?
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The NINDS supports and conducts research on sleep disorders such as hypersomnia. The goal of this research is to increase scientific understanding of the condition, find improved methods of diagnosing and treating it, and discover ways to prevent it.
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What is (are) Brown-Sequard Syndrome ?
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Brown-Sequard syndrome (BSS) is a rare neurological condition characterized by a lesion in the spinal cord which results in weakness or paralysis (hemiparaplegia) on one side of the body and a loss of sensation (hemianesthesia) on the opposite side. BSS may be caused by a spinal cord tumor, trauma (such as a puncture wound to the neck or back), ischemia (obstruction of a blood vessel), or infectious or inflammatory diseases such as tuberculosis, or multiple sclerosis.
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What are the treatments for Brown-Sequard Syndrome ?
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Generally treatment for individuals with BSS focuses on the underlying cause of the disorder. Early treatment with high-dose steroids may be beneficial in many cases. Other treatment is symptomatic and supportive.
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What is the outlook for Brown-Sequard Syndrome ?
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The prognosis for individuals with BSS varies depending on the cause of the disorder.
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what research (or clinical trials) is being done for Brown-Sequard Syndrome ?
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The NINDS supports and conducts a wide range of research on spinal cord disorders such as BSS. The goal of this research is to find ways to prevent, treat, and, ultimately, cure these disorders.
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What is (are) Infantile Spasms ?
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An infantile spasm (IS) is a specific type of seizure seen in an epilepsy syndrome of infancy and childhood known as West Syndrome. West Syndrome is characterized by infantile spasms, developmental regression, and a specific pattern on electroencephalography (EEG) testing called hypsarrhythmia (chaotic brain waves). The onset of infantile spasms is usually in the first year of life, typically between 4-8 months. The seizures primarily consist of a sudden bending forward of the body with stiffening of the arms and legs; some children arch their backs as they extend their arms and legs. Spasms tend to occur upon awakening or after feeding, and often occur in clusters of up to 100 spasms at a time. Infants may have dozens of clusters and several hundred spasms per day. Infantile spasms usually stop by age five, but may be replaced by other seizure types. Many underlying disorders, such as birth injury, metabolic disorders, and genetic disorders can give rise to spasms, making it important to identify the underlying cause. In some children, no cause can be found.
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What are the treatments for Infantile Spasms ?
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Treatment with corticosteroids such as prednisone is standard, although serious side effects can occur. Several newer antiepileptic medications, such as topiramate may ease some symptoms. Vigabatrin (Sabril) has been approved by the U.S. Food and Drug Administration to treat infantile spasms in children ages one month to two years. Some children have spasms as the result of brain lesions, and surgical removal of these lesions may result in improvement.
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What is the outlook for Infantile Spasms ?
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The prognosis for children with IS is dependent on the underlying causes of the seizures. The intellectual prognosis for children with IS is generally poor because many babies with IS have neurological impairment prior to the onset of spasms. Epileptic spasms usually reduce in number by mid-childhood, but more than half of the children with IS will develop other types of seizures. There appears to be a close relationship between IS and Lennox-Gastaut Syndrome, an epileptic disorder of later childhood.
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what research (or clinical trials) is being done for Infantile Spasms ?
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The NINDS supports broad and varied programs of research on epilepsy and other seizure disorders. This research is aimed at discovering new ways to prevent, diagnose, and treat these disorders and, ultimately, to find cures for them. Hopefully, more effective and safer treatments, such as neuroprotective agents, will be developed to treat IS and West Syndrome.
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What is (are) Dyssynergia Cerebellaris Myoclonica ?
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Dyssynergia Cerebellaris Myoclonica refers to a collection of rare, degenerative, neurological disorders characterized by epilepsy, cognitive impairment, myoclonus, and progressive ataxia. Symptoms include seizures, tremor, and reduced muscle coordination. Onset of the disorder generally occurs in early adulthood. Tremor may begin in one extremity and later spread to involve the entire voluntary muscular system. Arms are usually more affected than legs. Some of the cases are due to mitochondrial abnormalities.
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What are the treatments for Dyssynergia Cerebellaris Myoclonica ?
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Treatment of Dyssynergia Cerebellaris Myoclonica is symptomatic. Myoclonus and seizures may be treated with drugs like valproate.
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What is the outlook for Dyssynergia Cerebellaris Myoclonica ?
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The progression of the disorder is usually 10 years or longer.
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what research (or clinical trials) is being done for Dyssynergia Cerebellaris Myoclonica ?
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The NINDS supports a broad range of research on neurodegenerative disorders such as Dyssynergia Cerebellaris Myoclonica. The goals of this research are to find ways to prevent, treat, and cure these kinds of disorders.
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What is (are) Cerebral Atrophy ?
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Cerebral atrophy is a common feature of many of the diseases that affect the brain. Atrophy of any tissue means loss of cells. In brain tissue, atrophy describes a loss of neurons and the connections between them. Atrophy can be generalized, which means that all of the brain has shrunk; or it can be focal, affecting only a limited area of the brain and resulting in a decrease of the functions that area of the brain controls. If the cerebral hemispheres (the two lobes of the brain that form the cerebrum) are affected, conscious thought and voluntary processes may be impaired.
Associated Diseases/Disorders: The pattern and rate of progression of cerebral atrophy depends on the disease involved. Diseases that cause cerebral atrophy include:
- stroke and traumatic brain injury - Alzheimers disease, Picks disease, and fronto-temporal dementia - cerebral palsy, in which lesions (damaged areas) may impair motor coordination - Huntingtons disease, and other hereditary diseases that are associated with genetic mutations - leukodystrophies, such as Krabbe disease, which destroy the myelin sheath that protects axons - mitochondrial encephalomyopathies, such as Kearns-Sayre syndrome, which interfere with the basic functions of neurons - multiple sclerosis, which causes inflammation, myelin damage, and lesions in cerebral tissue - infectious diseases, such as encephalitis, neurosyphilis, and AIDS, in which an infectious agent or the inflammatory reaction to it destroys neurons and their axons
Symptoms of cerebral atrophy: Many diseases that cause cerebral atrophy are associated with dementia, seizures, and a group of language disorders called the aphasias.
- Dementia is characterized by a progressive impairment of memory and intellectual function that is severe enough to interfere with social and work skills. Memory, orientation, abstraction, ability to learn, visual-spatial perception, and higher executive functions such as planning, organizing, and sequencing may also be impaired. - Seizures can take different forms, appearing as disorientation, repetitive movements, loss of consciousness, or convulsions. - Aphasias are a group of disorders characterized by disturbances in speaking and understanding language. Receptive aphasia causes impaired comprehension. Expressive aphasia is reflected in odd choices of words, the use of partial phrases, disjointed clauses, and incomplete sentences.
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what research (or clinical trials) is being done for Cerebral Atrophy ?
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The NINDS funds research looking at many of the diseases and disorders that cause cerebral atrophy. Understanding the biological mechanisms that cause neurons to die in the brain will help researchers find ways to prevent, treat, and even cure the diseases that lead to cerebral atrophy.
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What is (are) Canavan Disease ?
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Canavan disease is a gene-linked neurological disorder in which the brain degenerates into spongy tissue riddled with microscopic fluid-filled spaces. Canavan disease has been classified as one of a group of genetic disorders known as the leukodystrophies. Recent research has indicated that the cells in the brain responsible for making myelin sheaths, known as oligodendrocytes, cannot properly complete this critical developmental task. Myelin sheaths are the fatty covering that act as insulators around nerve fibers in the brain, as well as providing nutritional support for nerve cells. In Canavan disease, many oligodendrocytes do not mature and instead die, leaving nerve cell projections known as axons vulnerable and unable to properly function. Canavan disease is caused by mutation in the gene for an enzyme called aspartoacylase, which acts to break down the concentrated brain chemical known as N-acetyl-aspartate.
Symptoms of Canavan disease usually appear in the first 3 to 6 months of life and progress rapidly. Symptoms include lack of motor development, feeding difficulties, abnormal muscle tone (weakness or stiffness), and an abnormally large, poorly controlled head. Paralysis, blindness, or hearing loss may also occur. Children are characteristically quiet and apathetic. Although Canavan disease may occur in any ethnic group, it is more frequent among Ashkenazi Jews from eastern Poland, Lithuania, and western Russia, and among Saudi Arabians. Canavan disease can be identified by a simple prenatal blood test that screens for the missing enzyme or for mutations in the gene that controls aspartoacylase. Both parents must be carriers of the defective gene in order to have an affected child. When both parents are found to carry the Canavan gene mutation, there is a one in four (25 percent) chance with each pregnancy that the child will be affected with Canavan disease.
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What are the treatments for Canavan Disease ?
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Canavan disease causes progressive brain atrophy. There is no cure, nor is there a standard course of treatment. Treatment is symptomatic and supportive.
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What is the outlook for Canavan Disease ?
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The prognosis for Canavan disease is poor. Death usually occurs before age 10, although some children may survive into their teens and twenties.
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what research (or clinical trials) is being done for Canavan Disease ?
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The gene for Canavan disease has been located. Many laboratories offer prenatal screening for this disorder to populations at risk. Scientists have developed animal models for this disease and are using the models to test potential therapeutic strategies. Three strategies are currently under investigation: gene transfer to the brain in order to replace the mutated gene for the enzyme; metabolic therapy to provide a crucial missing metabolite (acetate); and enzyme therapy where the enzyme aspartoacylase is engineered to be able to enter the brain and is injected in the the blood stream. Encouraging results have been obtained using these strategies.
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What is (are) Myotonia ?
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Myotonia is a medical term that refers to a neuromuscular condition in which the relaxation of a muscle is impaired. It can affect any muscle group. Repeated effort will be needed to relax the muscle, although the condition usually improves after the muscles have warmed-up. Individuals with myotonia may have trouble releasing their grip on objects or may have difficulty rising from a seated position. They may walk with a stiff, awkward gait. Myotonia is caused by an abnormality in the muscle membrane, and is often associated with inherited neurological disorders. Myotonia is commonly seen in individuals with myotonic muscular dystrophy, myotonia congenita, and in people who have one of a group of neurological disorders called the channelopathies, which are inherited diseases that are caused by mutations in the chloride sodium or potassium channels that regulate the muscle membrane. Myotonia may also be triggered by exposure to cold.
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What are the treatments for Myotonia ?
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Treatment for myotonia may include mexiletine, quinine, phenytoin, and other anticonvulsant drugs. Physical therapy and other rehabilitative measures may help muscle function.
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What is the outlook for Myotonia ?
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Myotonia is a chronic disorder. Symptoms may improve later in life.
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what research (or clinical trials) is being done for Myotonia ?
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The National Institute of Neurological Disorders and Stroke supports and conducts an extensive research program on neuromuscular disorders. The goals of this research are to learn more about these disorders and to find ways to treat, prevent, and cure them.
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What is (are) Lennox-Gastaut Syndrome ?
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Lennox-Gastaut syndrome is a severe form of epilepsy. Seizures usually begin before 4 years of age. Seizure types, which vary among patients, include tonic (stiffening of the body, upward deviation of the eyes, dilation of the pupils, and altered respiratory patterns), atonic (brief loss of muscle tone and consciousness, causing abrupt falls), atypical absence (staring spells), and myoclonic (sudden muscle jerks). There may be periods of frequent seizures mixed with brief, relatively seizure-free periods. Most children with Lennox-Gastaut syndrome experience some degree of impaired intellectual functioning or information processing, along with developmental delays, and behavioral disturbances. Lennox-Gastaut syndrome can be caused by brain malformations, perinatal asphyxia, severe head injury, central nervous system infection and inherited degenerative or metabolic conditions. In 30-35 percent of cases, no cause can be found.
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What are the treatments for Lennox-Gastaut Syndrome ?
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Treatment for Lennox-Gastaut syndrome includes clobazam and anti-epileptic medications such as valproate, lamotrigine, felbamate, or topiramate. There is usually no single antiepileptic medication that will control seizures. Children who improve initially may later show tolerance to a drug or have uncontrollable seizures.
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What is the outlook for Lennox-Gastaut Syndrome ?
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The prognosis for individuals with Lennox-Gastaut syndrome varies. There is no cure for the disorder. Complete recovery, including freedom from seizures and normal development, is very unusual.
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what research (or clinical trials) is being done for Lennox-Gastaut Syndrome ?
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The NINDS conducts and supports a broad program of basic and clinical research on epilepsy including Lennox-Gastaut syndrome. These studies are aimed at finding the causes of these disorders, improving the diagnosis, and developing new medications and other therapies.
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What is (are) Von Hippel-Lindau Disease (VHL) ?
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von Hippel-Lindau disease (VHL) is a rare, genetic multi-system disorder in which non-cancerous tumors grow in certain parts of the body. Slow-growing hemgioblastomas -- benign tumors with many blood vessels -- may develop in the brain, spinal cord, the retinas of the eyes, and near the inner ear. Cysts (fluid-filled sacs) may develop around the hemangioblastomas. Other types of tumors develop in the adrenal glands, the kidneys, or the pancreas. Symptoms of VHL vary among individuals and depend on the size and location of the tumors. Symptoms may include headaches, problems with balance and walking, dizziness, weakness of the limbs, vision problems, deafness in one ear, and high blood pressure. Individuals with VHL are also at a higher risk than normal for certain types of cancer, especially kidney cancer.
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What are the treatments for Von Hippel-Lindau Disease (VHL) ?
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Treatment for VHL varies according to the location and size of the tumor. In general, the objective of treatment is to treat the tumors before they grow to a size large enough to cause permanent problems by putting pressure on the brain or spinal cord. this pressure can block the flow of cerebrospinal fluid in the nervous system, impair vision, or create deafness. Treatment of most cases of VHL usually involves surgery to remove the tumors before they become harmful. Certain tumors can be treated with focused high-dose irradiation. Individuals with VHL need careful monitoring by a physician and/or medical team familiar with the disorder.
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What is the outlook for Von Hippel-Lindau Disease (VHL) ?
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The prognosis for individuals with VHL depends on then number, location, and complications of the tumors. Untreated, VHL may result in blindness and/or permanent brain damage. With early detection and treatment the prognosis is significantly improved. Death is usually caused by complications of brain tumors or kidney cancer.
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what research (or clinical trials) is being done for Von Hippel-Lindau Disease (VHL) ?
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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 pursues a vigorous program of research aimed at preventing and treating disorders that cause tumors in the brain and spinal cord such as VHL. A natural history study hopes to learn more about the growth of brain and spinal cord tumors, as well as cysts that develop in association with them in individuals with VHL. Researchers will examine how fast the tumors grow and try to determine which factors (such as puberty, pregnancy, menopause, or blood proteins) affect tumor growth. Based on laboratory findings, NINDS researchers are planning drug trials for individuals with VHL. For example, NNDS scientists hope to learn if a drug that fights other cancers might slow the growth of hemangioblastomas in some people with VHL. The NIH's National Cancer Institute conducts research aimed at treating kidney tumors in individuals with VHL, as well as studies to identify gene mutations in people who are at risk of developing the disease..
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What is (are) Frontotemporal Dementia ?
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Frontotemporal dementia (FTD) describes a clinical syndrome associated with shrinking of the frontal and temporal anterior lobes of the brain. Originally known as Picks disease, the name and classification of FTD has been a topic of discussion for over a century. The current designation of the syndrome groups together Picks disease, primary progressive aphasia, and semantic dementia as FTD. Some doctors propose adding corticobasal degeneration and progressive supranuclear palsy to FTD and calling the group Pick Complex. These designations will continue to be debated. As it is defined today, the symptoms of FTD fall into two clinical patterns that involve either (1) changes in behavior, or (2) problems with language. The first type features behavior that can be either impulsive (disinhibited) or bored and listless (apathetic) and includes inappropriate social behavior; lack of social tact; lack of empathy; distractability; loss of insight into the behaviors of oneself and others; an increased interest in sex; changes in food preferences; agitation or, conversely, blunted emotions; neglect of personal hygiene; repetitive or compulsive behavior, and decreased energy and motivation. The second type primarily features symptoms of language disturbance, including difficulty making or understanding speech, often in conjunction with the behavioral types symptoms. Spatial skills and memory remain intact. There is a strong genetic component to the disease; FTD often runs in families.
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What are the treatments for Frontotemporal Dementia ?
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No treatment has been shown to slow the progression of FTD. Behavior modification may help control unacceptable or dangerous behaviors. Aggressive, agitated, or dangerous behaviors could require medication. Anti-depressants have been shown to improve some symptoms.
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What is the outlook for Frontotemporal Dementia ?
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The outcome for people with FTD is poor. The disease progresses steadily and often rapidly, ranging from less than 2 years in some individuals to more than 10 years in others. Eventually some individuals with FTD will need 24-hour care and monitoring at home or in an institutionalized care setting.
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what research (or clinical trials) is being done for Frontotemporal Dementia ?
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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 FTD in laboratories at the NIH, and also support additional research through grants to major medical institutions across the country.
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What is (are) Huntington's Disease ?
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Huntington's disease (HD) is an inherited disorder that causes degeneration of brain cells, called neurons, in motor control regions of the brain, as well as other areas. Symptoms of the disease, which gets progressively worse, include uncontrolled movements (called chorea), abnormal body postures, and changes in behavior, emotion, judgment, and cognition. People with HD also develop impaired coordination, slurred speech, and difficulty feeding and swallowing. HD typically begins between ages 30 and 50. An earlier onset form called juvenile HD, occurs under age 20. Symptoms of juvenile HD differ somewhat from adult onset HD and include unsteadiness, rigidity, difficulty at school, and seizures. More than 30,000 Americans have HD. Huntingtons disease is caused by a mutation in the gene for a protein called huntingtin. The defect causes the cytosine, adenine, and guanine (CAG) building blocks of DNA to repeat many more times than is normal. Each child of a parent with HD has a 50-50 chance of inheriting the HD gene. If a child does not inherit the HD gene, he or she will not develop the disease and generally cannot pass it to subsequent generations. There is a small risk that someone who has a parent with the mutated gene but who did not inherit the HD gene may pass a possibly harmful genetic sequence to her/his children. A person who inherits the HD gene will eventually develop the disease. A genetic test, coupled with a complete medical history and neurological and laboratory tests, helps physicians diagnose HD.
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What are the treatments for Huntington's Disease ?
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There is no treatment that can stop or reverse the course of HD. Tetrabenazine is prescribed for treating Huntingtons-associated chorea. It is the only drug approved by the U.S. Food and Drug Administration specifically for use against HD. Antipsychotic drugs may help to alleviate chorea and may also be used to help control hallucinations, delusions, and violent outbursts. Drugs may be prescribed to treat depression and anxiety. Drugs used to treat the symptoms of HD may have side effects such as fatigue, sedation, decreased concentration, restlessness, or hyperexcitability, and should be only used when symptoms create problems for the individual.
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What is the outlook for Huntington's Disease ?
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Huntingtons disease causes disability that gets worse over time. People with this disease usually die within 15 to 20 years following diagnosis. At this time, no treatment is available to slow, stop or reverse the course of HD.
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what research (or clinical trials) is being done for Huntington's 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. A major focus of research on HD is to understand the toxicity of mutant huntingin protein to brain cells and to develop potential drugs for counteracting it. Animal models of the disorder allow scientists to study mechanisms of the disease and to move forward with strategies most likely to work and least likely to cause harm for individuals. The HD gene discovery is allowing scientists to recruit individuals who carry the HD gene into clinical studies early before they become ill. Researchers hope to understand how the defective gene affects various structures in the brain and the body's chemistry and metabolism. Since some of the clinical symptoms in neurodegenerative diseases may be caused by the ultimate malfunctioning of neuronal circuits rather than by the loss of individual cells, scientists are using cutting-edge methods such as optogenetics (where neurons are activated or silenced in the brains of living animals using light beams) to probe the cause and progression of such circuit defects in HD. Scientists are also using stem cells to study disease mechanisms and test potential therapeutic drugs.
The NINDS-funded PREDICT-HD study seeks to identify biomarkers (biological changes that can be used to predict, diagnose, or monitor a disease) for HD. One goal of PREDICT-HD is to determine if the progression of the disease correlates with changes in brain scans images, or with chemical changes in blood, urine, or cerebrospinal fluid. A large and related NINDS-supported study aims to identify additional genetic factors in people that influence the course of the disease. Since individuals with the same CAG expansions can differ widely in the age of disease onset and severity of symptoms, researchers are trying to identify variations in the genomes of individuals with HD that account for those differences in the hopes that they will point to new targets for disease intervention and therapy.
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What is (are) Chronic Pain ?
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While acute pain is a normal sensation triggered in the nervous system to alert you to possible injury and the need to take care of yourself, chronic pain is different. Chronic pain persists. Pain signals keep firing in the nervous system for weeks, months, even years. There may have been an initial mishap -- sprained back, serious infection, or there may be an ongoing cause of pain -- arthritis, cancer, ear infection, but some people suffer chronic pain in the absence of any past injury or evidence of body damage. Many chronic pain conditions affect older adults. Common chronic pain complaints include headache, low back pain, cancer pain, arthritis pain, neurogenic pain (pain resulting from damage to the peripheral nerves or to the central nervous system itself), psychogenic pain (pain not due to past disease or injury or any visible sign of damage inside or outside the nervous system). A person may have two or more co-existing chronic pain conditions. Such conditions can include chronic fatigue syndrome, endometriosis, fibromyalgia, inflammatory bowel disease, interstitial cystitis, temporomandibular joint dysfunction, and vulvodynia. It is not known whether these disorders share a common cause.
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What are the treatments for Chronic Pain ?
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Medications, acupuncture, local electrical stimulation, and brain stimulation, as well as surgery, are some treatments for chronic pain. Some physicians use placebos, which in some cases has resulted in a lessening or elimination of pain. Psychotherapy, relaxation and medication therapies, biofeedback, and behavior modification may also be employed to treat chronic pain.
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What is the outlook for Chronic Pain ?
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Many people with chronic pain can be helped if they understand all the causes of pain and the many and varied steps that can be taken to undo what chronic pain has done. Scientists believe that advances in neuroscience will lead to more and better treatments for chronic pain in the years to come.
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what research (or clinical trials) is being done for Chronic Pain ?
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Clinical investigators have tested chronic pain patients and found that they often have lower-than-normal levels of endorphins in their spinal fluid. Investigations of acupuncture include wiring the needles to stimulate nerve endings electrically (electroacupuncture), which some researchers believe activates endorphin systems. Other experiments with acupuncture have shown that there are higher levels of endorphins in cerebrospinal fluid following acupuncture. Investigators are studying the effect of stress on the experience of chronic pain. Chemists are synthesizing new analgesics and discovering painkilling virtues in drugs not normally prescribed for pain.
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What is (are) Normal Pressure Hydrocephalus ?
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Normal pressure hydrocephalus (NPH) is an abnormal buildup of cerebrospinal fluid (CSF) in the brain's ventricles, or cavities. It occurs if the normal flow of CSF throughout the brain and spinal cord is blocked in some way. This causes the ventricles to enlarge, putting pressure on the brain. Normal pressure hydrocephalus can occur in people of any age, but it is most common in the elderly. It may result from a subarachnoid hemorrhage, head trauma, infection, tumor, or complications of surgery. However, many people develop NPH even when none of these factors are present. In these cases the cause of the disorder is unknown.
Symptoms of NPH include progressive mental impairment and dementia, problems with walking, and impaired bladder control. The person also may have a general slowing of movements or may complain that his or her feet feel "stuck." Because these symptoms are similar to those of other disorders such as Alzheimer's disease, Parkinson's disease, and Creutzfeldt-Jakob disease, the disorder is often misdiagnosed. Many cases go unrecognized and are never properly treated. Doctors may use a variety of tests, including brain scans (CT and/or MRI), a spinal tap or lumbar catheter, intracranial pressure monitoring, and neuropsychological tests, to help them diagnose NPH and rule out other conditions.
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What are the treatments for Normal Pressure Hydrocephalus ?
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Treatment for NPH involves surgical placement of a shunt in the brain to drain excess CSF into the abdomen where it can be absorbed as part of the normal circulatory process. This allows the brain ventricles to return to their normal size. Regular follow-up care by a physician is important in order to identify subtle changes that might indicate problems with the shunt.
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What is the outlook for Normal Pressure Hydrocephalus ?
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The symptoms of NPH usually get worse over time if the condition is not treated, although some people may experience temporary improvements. While the success of treatment with shunts varies from person to person, some people recover almost completely after treatment and have a good quality of life. Early diagnosis and treatment improves the chance of a good recovery. Without treatment, symptoms may worsen and cause death.
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what research (or clinical trials) is being done for Normal Pressure Hydrocephalus ?
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The NINDS conducts and supports research on neurological disorders, including normal pressure hydrocephalus. Research on disorders such as normal pressure hydrocephalus focuses on increasing knowledge and understanding of the disorder, improving diagnostic techniques and neuroimaging, and finding improved treatments and preventions.
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What is (are) Cerebellar Hypoplasia ?
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Cerebellar hypoplasia is a neurological condition in which the cerebellum is smaller than usual or not completely developed. Cerebellar hypoplasia is a feature of a number of congenital (present at birth) malformation syndromes, such as Walker-Warburg syndrome (a form of muscular dystrophy. It is also associated with several inherited metabolic disorders, such as Williams syndrome, and some of the neurodegenerative disorders that begin in early childhood, such as ataxia telangiectasia. In an infant or young child, symptoms of a disorder that features cerebellar hypoplasia might include floppy muscle tone, developmental or speech delay, problems with walking and balance, seizures, intellectual disability, and involuntary side to side movements of the eyes. In an older child, symptoms might include headache, dizzy spells, clumsiness, and hearing impairment.
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What are the treatments for Cerebellar Hypoplasia ?
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There is no standard course of treatment for cerebellar hypoplasia. Treatment depends upon the underlying disorder and the severity of symptoms. Generally, treatment is symptomatic and supportive.
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What is the outlook for Cerebellar Hypoplasia ?
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The prognosis is dependent upon the underlying disorder. Some of the disorders that are associated with cerebellar hypoplasia are progressive, which means the condition will worsen over time, and will most likely have a poor prognosis. Other disorders that feature cerebellar hypoplasia are not progressive, such as those that are the result of abnormal brain formation during fetal development, and might have a better outcome.
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what research (or clinical trials) is being done for Cerebellar Hypoplasia ?
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The National Institute of Neurological Disorders and Stroke (NINDS) supports research related to cerebellar hypoplasia and its associated disorders 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 that feature cerebellar hypoplasia.
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What is (are) Menkes Disease ?
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Menkes disease is caused by a defective gene named ATPTA1 that regulates the metabolism of copper in the body. The disease primarily affects male infants. Copper accumulates at abnormally low levels in the liver and brain, but at higher than normal levels in the kidney and intestinal lining. Affected infants may be born prematurely, but appear healthy at birth and develop normally for 6 to 8 weeks. Then symptoms begin, including floppy muscle tone, seizures, and failure to thrive. Menkes disease is also characterized by subnormal body temperature and strikingly peculiar hair, which is kinky, colorless or steel-colored, and breaks easily. There is often extensive neurodegeneration in the gray matter of the brain. Arteries in the brain may be twisted with frayed and split inner walls. This can lead to rupture or blockage of the arteries. Weakened bones (osteoporosis) may result in fractures.
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What are the treatments for Menkes Disease ?
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Treatment with daily copper injections may improve the outcome in Menkes disease if it begins within days after birth. Other treatment is symptomatic and supportive.
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What is the outlook for Menkes Disease ?
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Since newborn screening for this disorder is not available, and early detection is infrequent because the clinical signs of Menkes disease are subtle in the beginning, the disease is rarely treated early enough to make a significant difference. The prognosis for babies with Menkes disease is poor. Most children with Menkes disease die within the first decade of life.
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what research (or clinical trials) is being done for Menkes Disease ?
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Recent research sponsored by the NINDS developed a blood test that could be given to newborns at risk for Menkes disease based on a positive family history for the disorder or other indications. The test measures 4 different chemicals in the blood and, depending upon their levels, can accurately diagnose the presence of Menkes disease before symptoms appear. Study results showed higher survival rates for children given the earliest copper injection treatment and improved, if not normal, 2. Additional research is being performed by the Eunice Kennedy Shriver National Institute of Child Health and Human Development, in collaboration with the NINDS, that applies gene therapy approaches to Menkes disease.3
1. Kaler, SG. The neurology of STPAT copper transporter disease: emerging concepts and future trends. Nature Reviews Neurology, 2001:7:15-19..
2. Kaler SG, et al.Neonatal Diagnosis and Treatment of Menkes Disease. N Engl J Med 2008;358:605-14.
3. Donsante, A. et. al. ATPTA gene addition to the choroid plexus results in long-term rescue of the lethal copper transport defect in a Menkes disease mouse model. Molecular Therapy (in press as of August 2011).
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What is (are) Tropical Spastic Paraparesis ?
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For several decades the term tropical spastic paraparesis (TSP) has been used to describe a chronic and progressive disease of the nervous system that affects adults living in equatorial areas of the world and causes progressive weakness, stiff muscles, muscle spasms, sensory disturbance, and sphincter dysfunction. The cause of TSP was obscure until the mid-1980s, when an important association was established between the human retrovirus human T-cell lymphotrophic virus type 1 (also known as HTLV-1) and TSP. TSP is now called HTLV-1 associated myelopathy/ tropical spastic paraparesis or HAM/TSP. The HTLV-1 retrovirus is thought to cause at least 80 percent of the cases of HAM/TSP by impairing the immune system. In addition to neurological symptoms of weakness and muscle stiffness or spasms, in rare cases individuals with HAM/TSP also exhibit uveitis (inflammation of the uveal tract of the eye), arthritis (inflammation of one or more joints), pulmonary lymphocytic alveolitis (inflammation of the lung), polymyositis (an inflammatory muscle disease), keratoconjunctivitis sicca (persistent dryness of the cornea and conjunctiva), and infectious dermatitis (inflammation of the skin). The other serious complication of HTLV-1 infection is the development of adult T-cell leukemia or lymphoma. Nervous system and blood-related complications occur only in a very small proportion of infected individuals, while most remain largely without symptoms throughout their lives.
The HTLV-1 virus is transmitted person-to-person via infected cells: breast-feeding by mothers who are seropositive (in other words, have high levels of virus antibodies in their blood), sharing infected needles during intravenous drug use, or having sexual relations with a seropositive partner. Less than 2 percent of HTLV-1 seropositive carriers will become HAM/TSP patients.
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What are the treatments for Tropical Spastic Paraparesis ?
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There is no established treatment program for HAM/TSP. Corticosteroids may relieve some symptoms, but arent likely to change the course of the disorder. Clinical studies suggest that interferon alpha provides benefits over short periods and some aspects of disease activity may be improved favorably using interferon beta. Stiff and spastic muscles may be treated with lioresal or tizanidine. Urinary dysfunction may be treated with oxybutynin.
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What is the outlook for Tropical Spastic Paraparesis ?
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HAM/TSP is a progressive disease, but it is rarely fatal. Most individuals live for several decades after the diagnosis. Their prognosis improves if they take steps to prevent urinary tract infection and skin sores, and if they participate in physical and occupational therapy programs.
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what research (or clinical trials) is being done for Tropical Spastic Paraparesis ?
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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 HAM/TSP in laboratories at the NIH, and 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 disorders such as HAM/TSP.
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What is (are) Stroke ?
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A stroke occurs when the blood supply to part of the brain is suddenly interrupted or when a blood vessel in the brain bursts, spilling blood into the spaces surrounding brain cells. Brain cells die when they no longer receive oxygen and nutrients from the blood or there is sudden bleeding into or around the brain. The symptoms of a stroke include sudden numbness or weakness, especially on one side of the body; sudden confusion or trouble speaking or understanding speech; sudden trouble seeing in one or both eyes; sudden trouble with walking, dizziness, or loss of balance or coordination; or sudden severe headache with no known cause. There are two forms of stroke: ischemic - blockage of a blood vessel supplying the brain, and hemorrhagic - bleeding into or around the brain.
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What are the treatments for Stroke ?
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Generally there are three treatment stages for stroke: prevention, therapy immediately after the stroke, and post-stroke rehabilitation. Therapies to prevent a first or recurrent stroke are based on treating an individual's underlying risk factors for stroke, such as hypertension, atrial fibrillation, and diabetes. Acute stroke therapies try to stop a stroke while it is happening by quickly dissolving the blood clot causing an ischemic stroke or by stopping the bleeding of a hemorrhagic stroke. Post-stroke rehabilitation helps individuals overcome disabilities that result from stroke damage. Medication or drug therapy is the most common treatment for stroke. The most popular classes of drugs used to prevent or treat stroke are antithrombotics (antiplatelet agents and anticoagulants) and thrombolytics.
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What is the outlook for Stroke ?
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Although stroke is a disease of the brain, it can affect the entire body. A common disability that results from stroke is complete paralysis on one side of the body, called hemiplegia. A related disability that is not as debilitating as paralysis is one-sided weakness or hemiparesis. Stroke may cause problems with thinking, awareness, attention, learning, judgment, and memory. Stroke survivors often have problems understanding or forming speech. A stroke can lead to emotional problems. Stroke patients may have difficulty controlling their emotions or may express inappropriate emotions. Many stroke patients experience depression. Stroke survivors may also have numbness or strange sensations. The pain is often worse in the hands and feet and is made worse by movement and temperature changes, especially cold temperatures.
Recurrent stroke is frequent; about 25 percent of people who recover from their first stroke will have another stroke within 5 years.
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what research (or clinical trials) is being done for Stroke ?
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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. Currently, NINDS researchers are studying the mechanisms of stroke risk factors and the process of brain damage that results from stroke. Basic research has also focused on the genetics of stroke and stroke risk factors. Scientists are working to develop new and better ways to help the brain repair itself to restore important functions. New advances in imaging and rehabilitation have shown that the brain can compensate for function lost as a result of stroke.
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What is (are) Hypotonia ?
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Hypotonia is a medical term used to describe decreased muscle tone. Normally, even when relaxed, muscles have a very small amount of contraction that gives them a springy feel and provides some resistance to passive movement. It is not the same as muscle weakness, although the two conditions can co-exist. Muscle tone is regulated by signals that travel from the brain to the nerves and tell the muscles to contract. Hypotonia can happen from damage to the brain, spinal cord, nerves, or muscles. The damage can be the result of trauma, environmental factors, or genetic, muscle, or central nervous system disorders. For example, it can be seen in Down syndrome, muscular dystrophy, cerebral palsy, Prader-Willi syndrome, myotonic dystrophy, and Tay-Sachs disease. Sometimes it may not be possible to find what causes the hypotonia. Infants with hypotonia have a floppy quality or rag doll appearance because their arms and legs hang by their sides and they have little or no head control. Other symptoms of hypotonia include problems with mobility and posture, breathing and speech difficulties, ligament and joint laxity, and poor reflexes. Hypotonia does not affect intellect. The opposite of hypotonia is hypertonia.
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What are the treatments for Hypotonia ?
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Treatment begins with a thorough diagnostic evaluation, usually performed by a neurologist, including an assessment of motor and sensory skills, balance and coordination, mental status, reflexes, and functioning of the nerves. Diagnostic tests that may be helpful include a CT or MRI scan of the brain, an EMG to evaluate nerve and muscle function, or an EEG to measure electrical activity in the brain. Once a diagnosis has been made, the underlying condition is treated first, followed by symptomatic and supportive therapy for the hypotonia. Physical therapy can improve motor control and overall body strength. Occupational therapy can help relearn ways to address activities of daily living. Speech-language therapy can help breathing, speech, and swallowing difficulties. Therapy for infants and young children may also include sensory stimulation programs.
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What is the outlook for Hypotonia ?
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Hypotonia can be a life-long condition. In some cases, however, muscle tone improves over time.
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what research (or clinical trials) is being done for Hypotonia ?
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The NINDS supports research on conditions that can result from neurological disorders, such as hypotonia. Much of this research is aimed at learning more about these conditions and finding ways to prevent and treat them.
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What is (are) Neuroaxonal dystrophy ?
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Infantile neuroaxonal dystrophy (INAD) is a rare inherited neurological disorder. It affects axons, the part of a nerve cell that carries messages from the brain to other parts of the body, and causes progressive loss of vision, muscular control, and mental skills. While the basic genetic and metabolic causes are unknown, INAD is the result of an abnormal build-up of toxic substances in nerves that communicate with muscles, skin, and the conjunctive tissue around the eyes. Symptoms usually begin within the first 2 years of life, with the loss of head control and the ability to sit, crawl, or walk, accompanied by deterioration in vision and speech. Some children may have seizures. Distinctive facial deformities may be present at birth, including a prominent forehead, crossed eyes, an unusually small nose or jaw, and large, low-set ears. INAD is an autosomal recessive disorder, which means that both parents must be carriers of the defective gene that causes INAD to pass it on to their child. Electrophysiology (nerve conduction velocities) may be helpful for diagnosis, although diagnosis is usually confirmed by tissue biopsy of skin, rectum, nerve or conjunctive tissue to confirm the presence of characteristic swellings (spheroid bodies) in the nerve axons.
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What are the treatments for Neuroaxonal dystrophy ?
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There is no cure for INAD and no treatment that can stop the progress of the disease. Treatment is symptomatic and supportive. Doctors can prescribe medications for pain relief and sedation. Physiotherapists and other physical therapists can teach parents and caregivers how to position and seat their child, and to exercise arms and legs to maintain comfort.
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What is the outlook for Neuroaxonal dystrophy ?
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INAD is a progressive disease. Once symptoms begin, they will worsen over time. Generally, a babys development starts to slow down between the ages of 6 months to 3 years. The first symptoms may be slowing of motor and mental development, followed by loss or regression of previously acquired skills. Rapid, wobbly eye movements and squints may be the first symptoms, followed by floppiness in the body and legs (more than in the arms). For the first few years, a baby with INAD will be alert and responsive, despite being increasingly physically impaired. Eventually, because of deterioration in vision, speech, and mental skills, the child will lose touch with its surroundings. Death usually occurs between the ages of 5 to 10 years.
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what research (or clinical trials) is being done for Neuroaxonal dystrophy ?
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Researchers continue to search for the defective gene that causes INAD in hopes of developing drugs that can stop the disease. The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to INAD 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 INAD.
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What is (are) Dravet Syndrome ?
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Dravet syndrome, also called severe myoclonic epilepsy of infancy (SMEI), is a severe form of epilepsy. It appears during the first year of life with frequent febrile seizures fever-related seizures that, by definition, are rare beyond age 5. Later, other types of seizures typically arise, including myoclonus (involuntary muscle spasms). Status epilepticus a state of continuous seizure requiring emergency medical care also may occur. Children with Dravet syndrome typically experience poor development of language and motor skills, hyperactivity, and difficulty relating to others.
In 30 to 80 percent of cases, Dravet syndrome is caused by defects in a gene required for the proper function of brain cells. Borderline SMEI (SMEB) and another type of infant-onset epilepsy called generalized epilepsy with febrile seizures plus (GEFS+) are caused by defects in the same gene. In GEFS+, febrile seizures may persist beyond age 5.
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What are the treatments for Dravet Syndrome ?
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Seizures in Dravet syndrome are difficult to control, but can be reduced by anticonvulsant drugs. A ketogenic diet, high in fats and low in carbohydrates, also may be beneficial.
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What is the outlook for Dravet Syndrome ?
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As children with Dravet syndrome get older, their decline in cognitive function stabilizes, and in many, it improves slightly. However, most teenagers with Dravet syndrome are dependent on caregivers. The degree of cognitive impairment appears to correlate with the frequency of seizures.
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what research (or clinical trials) is being done for Dravet Syndrome ?
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The NINDS conducts and supports a broad program of basic and clinical research on all types of epilepsy, including Dravet syndrome. Study of the genetic defects responsible for Dravet syndrome and related disorders is expected to lead to the development of effective drug therapies.
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What is (are) Complex Regional Pain Syndrome ?
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Complex regional pain syndrome (CRPS) is a chronic pain condition. The key symptom of CRPS is continuous, intense pain out of proportion to the severity of the injury, which gets worse rather than better over time. CRPS most often affects one of the arms, legs, hands, or feet. Often the pain spreads to include the entire arm or leg. Typical features include dramatic changes in the color and temperature of the skin over the affected limb or body part, accompanied by intense burning pain, skin sensitivity, sweating, and swelling. Doctors arent sure what causes CRPS. In some cases the sympathetic nervous system plays an important role in sustaining the pain. Another theory is that CRPS is caused by a triggering of the immune response, which leads to the characteristic inflammatory symptoms of redness, warmth, and swelling in the affected area.
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What are the treatments for Complex Regional Pain Syndrome ?
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Because there is no cure for CRPS, treatment is aimed at relieving painful symptoms. Doctors may prescribe topical analgesics, antidepressants, corticosteroids, and opioids to relieve pain. However, no single drug or combination of drugs has produced consistent long-lasting improvement in symptoms. Other treatments may include physical therapy, sympathetic nerve block, spinal cord stimulation, and intrathecal drug pumps to deliver opioids and local anesthetic agents via the spinal cord.
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What is the outlook for Complex Regional Pain Syndrome ?
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The prognosis for CRPS varies from person to person. Spontaneous remission from symptoms occurs in certain individuals. Others can have unremitting pain and crippling, irreversible changes in spite of treatment.
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what research (or clinical trials) is being done for Complex Regional Pain Syndrome ?
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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 CRPS and also support additional research through grants to major medical institutions across the country. NINDS-supported scientists are studying new approaches to treat CRPS and intervene more aggressively after traumatic injury to lower the chances of developing the disorder. Researchers hope to identify specific cellular and molecular changes in sensory neurons following peripheral nerve injury to better understand the processes that underlie neuroplasticity (the brains ability to reorganize or form new nerve connections and pathways following injury or death of nerve cells). Identifying these mechanisms could provide targets for new drug therapies that could improve recovery following regeneration. Other researchers hope to better understand how CRPS develops by studying immune system activation and peripheral nerve signaling using an animal model of the disorder.
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What is (are) Landau-Kleffner Syndrome ?
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Landau-Kleffner syndrome (LKS) is a rare, childhood neurological disorder characterized by the sudden or gradual development of aphasia (the inability to understand or express language) and an abnormal electro-encephalogram (EEG). LKS affects the parts of the brain that control comprehension and speech. The disorder usually occurs in children between the ages of 5 and 7 years. Typically, children with LKS develop normally but then lose their language skills for no apparent reason. While many of the affected individuals have seizures, some do not. The disorder is difficult to diagnose and may be misdiagnosed as autism, pervasive developmental disorder, hearing impairment, learning disability, auditory/verbal processing disorder, attention deficit disorder, childhood schizophrenia, or emotional/behavioral problems.
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What are the treatments for Landau-Kleffner Syndrome ?
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Treatment for LKS usually consists of medications, such as anticonvulsants and corticosteroids, and speech therapy, which should be started early. A controversial treatment option involves a surgical technique called multiple subpial transection in which the pathways of abnormal electrical brain activity are severed
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