qtype
stringclasses 16
values | instruction
stringlengths 16
191
| output
stringlengths 6
29k
|
|---|---|---|
outlook | What is the outlook for Todd's Paralysis ? | Todd's paralysis is an indication that an individual has had an epileptic seizure. The outcome depends on the effects of the seizure and the subsequent treatment of the epilepsy. |
research | what research (or clinical trials) is being done for Todd's Paralysis ? | The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to Todd's paralysis in its clinics and laboratories at The National Institutes of Health (NIH), and supports additional research through grants to major medical institutions across the country. Much of this research focuses on finding successful methods to prevent Todd's paralysis in individuals with epilepsy. |
information | What is (are) Syncope ? | Syncope is a medical term used to describe a temporary loss of consciousness due to the sudden decline of blood flow to the brain. Syncope is commonly called fainting or passing out. If an individual is about to faint, he or she will feel dizzy, lightheaded, or nauseous and their field of vision may white out or black out. The skin may be cold and clammy. The person drops to the floor as he or she loses consciousness. After fainting, an individual may be unconscious for a minute or two, but will revive and slowly return to normal. Syncope can occur in otherwise healthy people and affects all age groups, but occurs more often in the elderly.
Vasovagal
Carotid sinus
Situational |
treatment | What are the treatments for Syncope ? | The immediate treatment for an individual who has fainted involves checking first to see if their airway is open and they are breathing. The person should remain lying down for at least 10-15 minutes, preferably in a cool and quiet space. If this isnt possible, have the individual sit forward and lower their head below their shoulders and between their knees. Ice or cold water in a cup is refreshing. For individuals who have problems with chronic fainting spells, therapy should focus on recognizing the triggers and learning techniques to keep from fainting. At the appearance of warning signs such as lightheadedness, nausea, or cold and clammy skin, counter-pressure maneuvers that involve gripping fingers into a fist, tensing the arms, and crossing the legs or squeezing the thighs together can be used to ward off a fainting spell. If fainting spells occur often without a triggering event, syncope may be a sign of an underlying heart disease. |
outlook | What is the outlook for Syncope ? | Syncope is a dramatic event and can be life-threatening if not treated properly. Generally, however, people recover completely within minutes to hours. If syncope is symptomatic of an underlying condition, then the prognosis will reflect the course of the disorder. |
research | what research (or clinical trials) is being done for Syncope ? | The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to syncope 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 and treat syncope. |
information | What is (are) Cerebral Palsy ? | The term cerebral palsy refers to a group of neurological disorders that appear in infancy or early childhood and permanently affect body movement, muscle coordination, and balance.CP affects the part of the brain that controls muscle movements. The majority of children with cerebral palsy are born with it, although it may not be detected until months or years later.The early signs of cerebral palsy usually appear before a child reaches 3 years of age.The most common are a lack of muscle coordination when performing voluntary movements (ataxia); stiff or tight muscles and exaggerated reflexes (spasticity); walking with one foot or leg dragging; walking on the toes, a crouched gait, or a scissored gait; and muscle tone that is either too stiff or too floppy.Other neurological symptoms that commonly occur in individuals with CP include seizures, hearing loss and impaired vision, bladder and bowel control issues, and pain and abnormal sensations. A small number of children have CP as the result of brain damage in the first few months or years of life, brain infections such as bacterial meningitis or viral encephalitis, or head injury from a motor vehicle accident, a fall, or child abuse. The disorder isn't progressive, meaning that the brain damage typically doesn't get worse over time. Risk factors associated with CP do not cause the disorder but can increase a child's chance of being born with the disorder.CP is not hereditary. |
treatment | What are the treatments for Cerebral Palsy ? | Cerebral palsy cant be cured, but treatment will often improve a child's capabilities. In general, the earlier treatment begins the better chance children have of overcoming developmental disabilities or learning new ways to accomplish the tasks that challenge them.Early intervention, supportive treatments, medications, and surgery can help many individuals improve their muscle control. Treatment may include physical and occupational therapy, speech therapy, drugs to control seizures, relax muscle spasms, and alleviate pain; surgery to correct anatomical abnormalities or release tight muscles; braces and other orthotic devices; wheelchairs and rolling walkers; and communication aids such as computers with attached voice synthesizers. |
outlook | What is the outlook for Cerebral Palsy ? | Cerebral palsy doesnt always cause profound disabilities and for most people with CP the disorder does not affect life expectancy. Many children with CP have average to above average intelligence and attend the same schools as other children their age. Supportive treatments, medications, and surgery can help many individuals improve their motor skills and ability to communicate with the world..While one child with CP might not require special assistance, a child with severe CP might be unable to walk and need extensive, lifelong care. |
research | what research (or clinical trials) is being done for Cerebral Palsy ? | The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease.The NINDS is a component of the National Institutes of Health, the leading supporter of biomedical research in the world. Researchers supported by the NINDS are investigating the roles of mishaps early in brain development, including genetic defects, which are sometimes responsible for the brain malformations and abnormalities that result in cerebral palsy.Scientists are also looking at traumatic events in newborn babies brains, such as bleeding, epileptic seizures, and breathing and circulation problems, which can cause the abnormal release of chemicals that trigger the kind of damage that causes cerebral palsy. NINDS-supported researchers also hope to find ways to prevent white matter disease, the most common cause of cerebral palsy. To make sure children are getting the right kinds of therapies, studies are also being done that evaluate both experimental treatments and treatments already in use so that physicians and parents have valid information to help them choose the best therapy. |
information | What is (are) Tuberous Sclerosis ? | Tuberous sclerosis (TSC) is a rare genetic disease that causes benign tumors to grow in the brain and on other vital organs such as the kidneys, heart, eyes, lungs, and skin. It usually affects the central nervous system. In addition to the benign tumors that frequently occur in TSC, other common symptoms include seizures,impaired intellectual development, behavior problems, and skin abnormalities. TSC may be present at birth, but signs of the disorder can be subtle and full symptoms may take some time to develop. Three types of brain tumors are associated with TSC: cortical tubers, which generally form on the surface of the brain; subependymal nodules, which form in the walls of the ventricles (the fluid-filled cavities of the brain); and giant-cell astrocytomas, a type of tumor that can block the flow of fluids within the brain. |
treatment | What are the treatments for Tuberous Sclerosis ? | There is no cure for TSC, although treatment is available for a number of the symptoms. Rapamycin and related drugs are not yet approved by the U.S. Food and Drug Administration (FDA) for any purpose in individuals with TSC. The FDA has approved the drug everolimus (Afinitor) to treat subependymal giant cell astrocytomas (SEGA brain tumors) and angiomyolipoma kidney tumors. Antiepileptic drugs such as vigabatrin may be used to control seizures and medications may be prescribed for behavior problems. Intervention programs, including special schooling and occupational therapy, may benefit individuals with special needs and developmental issues. Surgery, including dermabrasion and laser treatment, may be useful for treatment of skin lesions. Because TSC is a lifelong condition, individuals need to be regularly monitored by a doctor. Due to the many varied symptoms of TSC, care by a clinician experienced with the disorder is recommended. |
outlook | What is the outlook for Tuberous Sclerosis ? | The prognosis for individuals with TSC depends on the severity of symptoms. Individuals with mild symptoms generally do well and live long productive lives, while individuals with the more severe form may have serious disabilities. In rare cases, seizures, infections, or tumors in vital organs such as the kidneys and brain can lead to severe complications and even death. However, with appropriate medical care, most individuals with the disorder can look forward to normal life expectancy. |
research | what research (or clinical trials) is being done for Tuberous Sclerosis ? | The National Institute of Neurological Disorders and Stroke (NINDS) conducts TSC research in its laboratories at the National Institutes of Health (NIH) and also supports TSC research through grants to major medical institutions across the country. Scientists in one study are learning more about the genes that can cause TSC and the function of the proteins those genes produce. Another study focuses on two major brain disorders --autism and epilepsy -- that occur in children with TSC. Other scientists are trying to determine what causes skin tumors to develop in individuals with TSC and to find the molecular basis of these tumors. Scientists hope knowledge gained from their current research will improve the genetic test for TSC and lead to new avenues of treatment, methods of prevention, and, ultimately, a cure. |
information | What is (are) Batten Disease ? | Batten disease is a fatal, inherited disorder of the nervous system that begins in childhood. In some cases, the early signs are subtle, taking the form of personality and behavior changes, slow learning, clumsiness, or stumbling. Symptoms of Batten disease are linked to a buildup of substances called lipopigments in the body's tissues. Lipopigments are made up of fats and proteins. Because vision loss is often an early sign, Batten disease may be first suspected during an eye exam. Often, an eye specialist or other physician may refer the child to a neurologist. Diagnostic tests for Batten disease include blood or urine tests, skin or tissue sampling, an electroencephalogram (EEG), electrical studies of the eyes, and brain scans. |
treatment | What are the treatments for Batten Disease ? | As yet, no specific treatment is known that can halt or reverse the symptoms of Batten disease. However, seizures can sometimes be reduced or controlled with anticonvulsant drugs, and other medical problems can be treated appropriately as they arise. Physical therapy and occupational therapy may help patients retain functioning as long as possible. |
outlook | What is the outlook for Batten Disease ? | Over time, affected children suffer cognitive impairment, worsening seizures, and progressive loss of sight and motor skills. Eventually, children with Batten disease become blind, bedridden, and demented. Batten disease is often fatal by the late teens or twenties. |
research | what research (or clinical trials) is being done for Batten Disease ? | The biochemical defects that underlie several NCLs have recently been discovered. An enzyme called palmitoyl-protein thioesterase has been shown to be insufficiently active in the infantile form of Batten disease (this condition is now referred to as CLN1). In the late infantile form (CLN2), a deficiency of an acid protease, an enzyme that hydrolyzes proteins, has been found as the cause of this condition. A mutated gene has been identified in juvenile Batten disease (CLN3), but the protein for which this gene codes has not been identified. In addition, research scientists are working with NCL animal models to improve understanding and treatment of these disorders. One research team, for example, is testing the usefulness of bone marrow transplantation in a sheep model, while other investigators are working to develop mouse models. Mouse models will make it easier for scientists to study the genetics of these diseases. |
information | What is (are) Holoprosencephaly ? | Holoprosencephaly is a disorder caused by the failure of the prosencephalon (the embryonic forebrain) to sufficiently divide into the double lobes of the cerebral hemispheres. The result is a single-lobed brain structure and severe skull and facial defects. In most cases of holoprosencephaly, the malformations are so severe that babies die before birth. In less severe cases, babies are born with normal or near-normal brain development and facial deformities that may affect the eyes, nose, and upper lip.
There are three classifications of holoprosencephaly. Alobar, in which the brain has not divided at all, is usually associated with severe facial deformities. Semilobar, in which the brain's hemispheres have somewhat divided, causes an intermediate form of the disorder. Lobar, in which there is considerable evidence of separate brain hemispheres, is the least severe form. In some cases of lobar holoprosencephaly the baby's brain may be nearly normal.
The least severe of the facial anomalies is the median cleft lip (premaxillary agenesis). The most severe is cyclopia, an abnormality characterized by a single eye located in the area normally occupied by the root of the nose, and a missing nose or a proboscis (a tubular-shaped nose) located above the eye. The least common facial anomaly is ethmocephaly, in which a proboscis separates closely-set eyes. Cebocephaly, another facial anomaly, is characterized by a small, flattened nose with a single nostril situated below incomplete or underdeveloped closely-set eyes. |
treatment | What are the treatments for Holoprosencephaly ? | There is no standard course of treatment for holoprosencephaly. Treatment is symptomatic and supportive. |
outlook | What is the outlook for Holoprosencephaly ? | The prognosis for individuals with the disorder depends on the severity of the brain and facial deformities. |
research | what research (or clinical trials) is being done for Holoprosencephaly ? | The NINDS supports and conducts a wide range of studies that focus on identifying and learning more about the factors involved in normal brain development. Recent research has identified specific genes that cause holoprosencephaly. The knowledge gained from these fundamental studies provides the foundation for understanding how to develop new ways to treat, and potentially prevent, this disorder. |
information | What is (are) Bell's Palsy ? | Bell's palsy is a form of temporary facial paralysis resulting from damage or trauma to the 7th cranial nerve, one of the facial nerves. It is the most common cause of facial paralysis. Generally, Bell's palsy affects only one side of the face, however, in rare cases, it can affect both sides. Symptoms usually begin suddenly and reach their peak within 72 hours, and can range in severity from mild weakness to total paralysis. Symptoms vary among individuals and include sudden weakness on one side of the face, drooping eyelid or corner of the mouth, drooling, dry eye or mouth, altered taste, and excessive tearing in the eye. Bells palsy can cause significant facial distortion. The exact cause of Bell's palsy isn't known, but many scientists believe that reactivation of a dormant viral infection can cause the facial nerve to swell and becomes inflamed. Several other conditions can cause facial paralysis that might be diagnosed as Bell's palsy.. |
treatment | What are the treatments for Bell's Palsy ? | Steroids such as prednisone -- used to reduce inflammation and swelling -- are an effective treatment for Bell's palsy. Antiviral drugs may have some benefit in shortening the course of the disease. Analgesics such as aspirin, acetaminophen, or ibuprofen may relieve pain. Because of possible drug interactions, individuals should always talk to their doctors before taking any over-the-counter medicines. Keeping the eye moist and protecting it from debris and injury, especially at night, is important. Lubricating eye drops can help. Other therapies such as physical therapy, facial massage or acupuncture may provide a potential small improvement in facial nerve function and pain.. |
outlook | What is the outlook for Bell's Palsy ? | The prognosis for individuals with Bell's palsy is generally very good. The extent of nerve damage determines the extent of recovery. With or without treatment, most individuals begin to get better within 2 weeks after the initial onset of symptoms and recover some or all facial function within 3 to 6 months. |
research | what research (or clinical trials) is being done for Bell's Palsy ? | The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS conducts and supports an extensive research program of basic science to increase understanding of how the nervous system works and circumstances that lead to nerve damage. Knowledge gained from this research may help scientists find the definitive cause of Bell's palsy, leading to the discovery of new effective treatments for the disorder. Other NINDS-supported research is aimed at developing methods to repair damaged nerves and restore full use and strength to injured areas, and finding ways to prevent nerve damage and injuries from occurring. |
information | What is (are) Multiple System Atrophy ? | 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. |
treatment | What are the treatments for Multiple System Atrophy ? | 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. |
outlook | What is the outlook for Multiple System Atrophy ? | 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. |
research | what research (or clinical trials) is being done for Multiple System Atrophy ? | 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 |
information | What is (are) Giant Axonal Neuropathy ? | Giant axonal neuropathy (GAN) is a rare inherited genetic disorder that affects both the central and peripheral nervous systems. The majority of children with GAN will begin to show symptoms of the disease sometime before five years of age. Signs of GAN usually begin in the peripheral nervous system, which controls movement and sensation in the arms, legs, and other parts of the body. The typical symptoms of GAN are clumsiness and muscle weakness that progresses from a waddling gait to a pronounced difficulty in walking. Additional symptoms include numbness or lack of feeling in the arms and legs, seizures, nystagmus (rapid back and forth movement of the eyes), and impaired cognitive development. A characteristic sign of the disease is dull, tightly curled hair that is markedly different from the parents in color and texture.
Researchers have discovered more than 20 different mutations associated with GAN in a gene, GAN1, which makes a protein called gigaxonin. These mutations disrupt the regulation or production of gigaxonin in the nervous system. As a result, axons, which are the long tails of neurons that allow them to communicate with other nerve cells, swell up with tangled filaments and become abnormally large. Eventually these axons deteriorate and cause problems with movement and sensation since neurons are no longer able to communicate with each other.
Doctors diagnose GAN by using several tests, including one that measures nerve conduction velocity, a brain MRI, and a peripheral nerve biopsy (in which a bit of tissue from a peripheral nerve is removed and examined to look for swollen axons). A definitive diagnosis using genetic testing is available on a research basis only.
GAN is inherited in an autosomal recessive pattern, which means that both parents of a child with GAN have to carry a copy of the mutated gene. Parents, typically, will show no signs of the disease. |
treatment | What are the treatments for Giant Axonal Neuropathy ? | Treatment is symptomatic. Children with GAN and their families usually work with a medical team that includes a pediatric neurologist, orthopedic surgeon, physiotherapist, psychologist, and speech and occupational therapists. The major goals of treatment are to maximize intellectual and physical development and minimize their deterioration as time passes. Many children with GAN begin with normal intellectual development and are able to attend a regular school program. Children should be monitored at least once a year to assess their intellectual abilities and to look for the presence of neurological deterioration. |
outlook | What is the outlook for Giant Axonal Neuropathy ? | GAN generally progresses slowly as neurons degenerate and die. Most children have problems with walking in the early stages of the disorder. Later they may lose sensation, coordination, strength, and reflexes in their arms and legs. As time goes on, the brain and spinal cord may become involved, causing a gradual decline in mental function, loss of control of body movement, and seizures. Most children become wheelchair dependent in the second decade of life. Some children may survive into early adulthood. |
research | what research (or clinical trials) is being done for Giant Axonal Neuropathy ? | The National Institute of Neurological Disorders and Stroke (NINDS) supports research related to GAN through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure inherited neurological disorders such as GAN. |
information | What is (are) Thoracic Outlet Syndrome ? | TOS is an umbrella term that encompasses three related syndromes that involve compression of the nerves, arteries, and veins in the lower neck and upper chest area and cause pain in the arm, shoulder, and neck. Most doctors agree that TOS is caused by compression of the brachial plexus or subclavian vessels as they pass through narrow passageways leading from the base of the neck to the armpit and arm, but there is considerable disagreement about its diagnosis and treatment. Making the diagnosis of TOS even more difficult is that a number of disorders feature symptoms similar to those of TOS, including rotator cuff injuries, cervical disc disorders, fibromyalgia, multiple sclerosis, complex regional pain syndrome, and tumors of the syrinx or spinal cord. The disorder can sometimes be diagnosed in a physical exam by tenderness in the supraclavicular area, weakness and/or a "pins and needles" feeling when elevating the hands, weakness in the fifth ("little") finger, and paleness in the palm of one or both hands when the individual raises them above the shoulders, with the fingers pointing to the ceiling. Symptoms of TOS vary depending on the type. Neurogenic TOS has a characteristic sign, called the Gilliatt-Sumner hand, in which there is severe wasting in the fleshy base of the thumb. Other symptoms include paresthesias (pins and needles sensation or numbness) in the fingers and hand, change in hand color, hand coldness, or dull aching pain in the neck, shoulder, and armpit. Venous TOS features pallor, a weak or absent pulse in the affected arm, which also may be cool to the touch and appear paler than the unaffected arm. Symptoms may include numbness, tingling, aching, swelling of the extremity and fingers, and weakness of the neck or arm.. Arterial TOS most prominently features change in color and cold sensitivity in the hands and fingers, swelling, heaviness, paresthesias and poor blood circulation in the arms, hands, and fingers..
There are many causes of TOS, including physical trauma, anatomical defects, tumors that press on nerves, poor posture that causes nerve compression, pregnancy, and repetitive arm and shoulder movements and activity, such as from playing certain sports. TOS is more common in women. The onset of symptoms usually occurs between 20 and 50 years of age. Doctors usually recommend nerve conduction studies, electromyography, or imaging studies to confirm or rule out a diagnosis of TOS. |
treatment | What are the treatments for Thoracic Outlet Syndrome ? | Treatment begins with exercise programs and physical therapy to strengthen chest muscles, restore normal posture, and relieve compression by increasing the space of the area the nerve passes through. Doctors will often prescribe non-steroidal anti-inflammatory drugs (such as naproxen or ibuprofen) for pain. Other medicines include thromobolytics to break up blood clots and anticoagulants to prevent clots. If this doesn't relieve pain, a doctor may recommend thoracic outlet decompression surgery to release or remove the structures causing compression of the nerve or artery. |
outlook | What is the outlook for Thoracic Outlet Syndrome ? | The outcome for individuals with TOS varies according to type. The majority of individuals with TOS will improve with exercise and physical therapy. Vascular TOS, and true neurogenic TOS often require surgery to relieve pressure on the affected vessel or nerve. |
research | what research (or clinical trials) is being done for Thoracic Outlet Syndrome ? | The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes at the National Institutes of Health support research in TOS through grants to major medical research institutions across the country. Much of this research focuses on finding better ways to diagnose and treat TOS. |
information | What is (are) Angelman Syndrome ? | Angelman syndrome is a genetic disorder that causes developmental delay and neurological problems. The physician Harry Angelman first delineated the syndrome in 1965, when he described several children in his practice as having "flat heads, jerky movements, protruding tongues, and bouts of laughter." Infants with Angelman syndrome appear normal at birth, but often have feeding problems in the first months of life and exhibit noticeable developmental delays by 6 to 12 months. Seizures often begin between 2 and 3 years of age. Speech impairment is pronounced, with little to no use of words. Individuals with this syndrome often display hyperactivity, small head size, sleep disorders, and movement and balance disorders that can cause severe functional deficits. Angelman syndrome results from absence of a functional copy of the UBE3A gene inherited from the mother. |
treatment | What are the treatments for Angelman Syndrome ? | There is no specific therapy for Angelman syndrome. Medical therapy for seizures is usually necessary. Physical and occupational therapies, communication therapy, and behavioral therapies are important in allowing individuals with Angelman syndrome to reach their maximum developmental potential. |
outlook | What is the outlook for Angelman Syndrome ? | Most individuals with Angelman syndrome will have severe developmental delays, speech limitations, and motor difficulties. However, individuals with Angelman syndrome can have normal life spans and generally do not show developmental regression as they age. Early diagnosis and tailored interventions and therapies help improve quality of life. |
research | what research (or clinical trials) is being done for Angelman Syndrome ? | The NINDS supports and conducts research on neurogenetic disorders such as Angelman syndrome, to develop techniques to diagnose, treat, prevent, and ultimately cure them. |
information | What is (are) Inclusion Body Myositis ? | Inclusion body myositis (IBM) is one of a group of muscle diseases known as the inflammatory myopathies, which are characterized by chronic, progressive muscle inflammation accompanied by muscle weakness. The onset of muscle weakness in IBM is generally gradual (over months or years) and affects both proximal (close to the trunk of the body) and distal (further away from the trunk) muscles. Muscle weakness may affect only one side of the body. Falling and tripping are usually the first noticeable symptoms of IBM. For some individuals, the disorder begins with weakness in the wrists and fingers that causes difficulty with pinching, buttoning, and gripping objects. There may be weakness of the wrist and finger muscles and atrophy (thinning or loss of muscle bulk) of the forearm muscles and quadricep muscles in the legs. Difficulty swallowing occurs in approximately half of IBM cases. Symptoms of the disease usually begin after the age of 50, although the disease can occur earlier. IBM occurs more frequently in men than in women. |
treatment | What are the treatments for Inclusion Body Myositis ? | There is no cure for IBM, nor is there a standard course of treatment. The disease is generally unresponsive to corticosteroids and immunosuppressive drugs. Some evidence suggests that intravenous immunoglobulin may have a slight, but short-lasting, beneficial effect in a small number of cases. Physical therapy may be helpful in maintaining mobility. Other therapy is symptomatic and supportive. |
outlook | What is the outlook for Inclusion Body Myositis ? | IBM is generally resistant to all therapies and its rate of progression appears to be unaffected by currently available treatments. |
research | what research (or clinical trials) is being done for Inclusion Body Myositis ? | The National Institute of Neurological Disorders and Stroke (NINDS), National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institute of Environmental Health Sciences (NIEHS) and other institutes of the National Institutes of Health (NIH) conduct research relating to IBM in laboratories at the NIH and support additional research through grants to major medical institutions across the country. Currently funded research is exploring patterns of gene expression among the inflammatory myopathies, the role of viral infection as a precursor to the disorders, and the safety and efficacy of various treatment regimens. |
information | What is (are) Subacute Sclerosing Panencephalitis ? | Subacute sclerosing panencephalitis (SSPE) is a progressive neurological disorder of children and young adults that affects the central nervous system (CNS). It is a slow, but persistent, viral infection caused by defective measles virus. SSPE has been reported from all parts of the world, but it is considered a rare disease in developed countries, with fewer than 10 cases per year reported in the United States. The incidence of SSPE declined by at least 90 percent in countries that have practiced widespread immunization with measles vaccine. The incidence of SSPE is still high in developing countries such as India and Eastern Europe. There is a higher incidence among males than females (male/female: 3/1). Most youngsters with SSPE have a history of measles infection at an early age, usually younger than 2 years, followed by a latent period of 6 to 8 years before neurological symptoms begin. Despite the long interval between the measles infection and the onset of SSPE, researchers think that the infection of the brain occurs soon after the primary bout with measles and progresses slowly. Why it persists and progresses still isn't clear. The initial symptoms of SSPE are subtle and include mild mental deterioration (such as memory loss) and changes in behavior (such as irritability) followed by disturbances in motor function, including uncontrollable involuntary jerking movements of the head, trunk or limbs called myoclonic jerks. Seizures may also occur. Some people may become blind. In advanced stages of the disease, individuals may lose the ability to walk, as their muscles stiffen or spasm. There is progressive deterioration to a comatose state, and then to a persistent vegetative state. Death is usually the result of fever, heart failure, or the brain's inability to continue controlling the autonomic nervous system. |
treatment | What are the treatments for Subacute Sclerosing Panencephalitis ? | Currently, there is no cure for SSPE. Clinical trials of antiviral (isoprinosine and ribavirin) and immunomodulatory (interferon alpha) drugs have suggested that these types of therapies given alone or in combination halt the progression of the disease and can prolong life, but their long-term effects on individuals, and eventual outcome, are unknown. Good nursing care is the most important aspect of treatment for SSPE, along with anticonvulsant and antispasmodic drugs when needed. |
outlook | What is the outlook for Subacute Sclerosing Panencephalitis ? | Most individuals with SSPE will die within 1 to 3 years of diagnosis. In a small percentage of people, the disease will progress rapidly, leading to death over a short course within three months of diagnosis. Another small group will have a chronic, slowly progressive form, some with relapses and remissions. A very small number (approximately 5 percent) may experience spontaneous long term improvement and regain lost function. Prevention, in the form of measles vaccination, is the only real "cure" for SSPE. |
research | what research (or clinical trials) is being done for Subacute Sclerosing Panencephalitis ? | The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes at the National Institutes of Health conduct research related to SSPE in their clinics and laboratories 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 SSPE. |
information | What is (are) Hemifacial Spasm ? | Hemifacial spasm is a neuromuscular disorder characterized by frequent involuntary contractions (spasms) of the muscles on one side (hemi-) of the face (facial). The disorder occurs in both men and women, although it more frequently affects middle-aged or elderly women. It is much more common in the Asian population. The first symptom is usually an intermittent twitching of the eyelid muscle that can lead to forced closure of the eye. The spasm may then gradually spread to involve the muscles of the lower face, which may cause the mouth to be pulled to one side. Eventually the spasms involve all of the muscles on one side of the face almost continuously. The condition may be caused by a facial nerve injury, or a tumor, or it may have no apparent cause. Rarely, doctors see individuals with spasm on both sides of the face. Most often hemifacial spasm is caused by a blood vessel pressing on the facial nerve at the place where it exits the brainstem. |
treatment | What are the treatments for Hemifacial Spasm ? | Surgical treatment in the form of microvascular decompression, which relieves pressure on the facial nerve, will relieve hemifacial spasm in many cases. This intervention has significant potential side-effects, so risks and benefits have to be carefully balanced. Other treatments include injections of botulinum toxin into the affected areas, which is the most effective therapy and the only one used in most cases. Drug therapy is generally not effective. |
outlook | What is the outlook for Hemifacial Spasm ? | The prognosis for an individual with hemifacial spasm depends on the treatment and their response. Some individuals will become relatively free from symptoms with injection therapy. Some may require surgery. In most cases, a balance can be achieved, with tolerable residual symptoms. |
research | what research (or clinical trials) is being done for Hemifacial Spasm ? | The National Institute of Neurological Disorders and Stroke (NINDS) conducts and supports research related to hemifacial spams through grants to major research institutions across the country. Much of this research focuses on better ways to prevent, treat, and ultimately cure neurological disorders, such as hemifacial spasm. |
information | What is (are) Olivopontocerebellar Atrophy ? | Olivopontocerebellar atrophy (OPCA) is a term that describes the degeneration of neurons in specific areas of the brain the cerebellum, pons, and inferior olives. OPCA is present in several neurodegenerative syndromes, including inherited and non-inherited forms of ataxia (such as the hereditary spinocerebellar ataxia known as Machado-Joseph disease) and multiple system atrophy (MSA), with which it is primarily associated. http://www.ninds.nih.gov/disorders/msa/msa.htm
OPCA may also be found in the brains of individuals with prion disorders and inherited metabolic diseases. The characteristic areas of brain damage that indicate OPCA can be seen by imaging the brain using CT scans or MRI studies. |
treatment | What are the treatments for Olivopontocerebellar Atrophy ? | There is no specific treatmentfor OPCA. Physicians may try different medications to treat the ataxia, tremor, and rigidity that are associated with the disorder. Other treatments are directed at specific symptoms. Stiffness, spasms, sleep disorders, depression, and tremor may be improved with medication. A physical therapist may be helpful in establishing a routine of exercise and stretching, and in obtaining devices or appliances to assist in walking and other daily activities. |
outlook | What is the outlook for Olivopontocerebellar Atrophy ? | There is no cure for OPCA. The disorder is slowly progressive with death usually occurring approximately 20 years after onset. |
research | what research (or clinical trials) is being done for Olivopontocerebellar Atrophy ? | The NINDS supports and conducts a broad range of basic and clinical research on cerebellar degeneration, including work aimed at finding the cause(s) of OPCA and ways to treat, cure, and, ultimately, prevent the disease. There has been great progress recently since the genes for several of the hereditary forms of OPCA have been found. |
information | What is (are) Multifocal Motor Neuropathy ? | Multifocal motor neuropathy is a progressive muscle disorder characterized by muscle weakness in the hands, with differences from one side of the body to the other in the specific muscles involved. It affects men much more than women. Symptoms also include muscle wasting, cramping, and involuntary contractions or twitching of the leg muscles. The disorder is sometimes mistaken for amyotrophic laterial sclerosis (ALS, or Lou Gehrig's disease) but unlike ALS, it is treatable. An early and accurate diagnosis allows patients to recover quickly. |
treatment | What are the treatments for Multifocal Motor Neuropathy ? | Treatment for multifocal motor neuropathy varies. Some individuals experience only mild, modest symptoms and require no treatment. For others, treatment generally consists of intravenous immunoglobulin (IVIg) or immunosuppressive therapy with cyclophosphamide. |
outlook | What is the outlook for Multifocal Motor Neuropathy ? | Improvement in muscle strength usually begins within 3 to 6 weeks after treatment is started. Most patients who receive treatment early experience little, if any, disability. However, there is evidence of slow progression over many years. |
research | what research (or clinical trials) is being done for Multifocal Motor Neuropathy ? | The NINDS supports a broad range of research on neuromuscular disorders with the goal of finding ways to prevent, treat, and, ultimately, cure them. |
information | What is (are) Occipital Neuralgia ? | 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. |
treatment | What are the treatments for Occipital Neuralgia ? | 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. |
outlook | What is the outlook for Occipital Neuralgia ? | 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. |
research | what research (or clinical trials) is being done for Occipital Neuralgia ? | 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. |
information | What is (are) Arachnoiditis ? | Arachnoiditis describes a pain disorder caused by the inflammation of the arachnoid, one of the membranes that surround and protect the nerves of the spinal cord. The arachnoid can become inflamed because of an irritation from chemicals, infection from bacteria or viruses, as the result of direct injury to the spine, chronic compression of spinal nerves, or complications from spinal surgery or other invasive spinal procedures. Inflammation can sometimes lead to the formation of scar tissue and adhesions, which cause the spinal nerves to stick together. If arachnoiditis begins to interfere with the function of one or more of these nerves, it can cause a number of symptoms, including numbness, tingling, and a characteristic stinging and burning pain in the lower back or legs. Some people with arachnoiditis will have debilitating muscle cramps, twitches, or spasms. It may also affect bladder, bowel, and sexual function. In severe cases, arachnoiditis may cause paralysis of the lower limbs. |
treatment | What are the treatments for Arachnoiditis ? | Arachnoiditis remains a difficult condition to treat, and long-term outcomes are unpredictable. Most treatments for arachnoiditis are focused on pain relief and the improvement of symptoms that impair daily function. A regimen of pain management, physiotheraphy, exercise, and psychotheraphy is often recommended. Surgical intervention is controversial since the outcomes are generally poor and provide only short-term relief. |
outlook | What is the outlook for Arachnoiditis ? | Arachnoiditis is adisorder that causes chronic pain and neurological deficits and does not improve significantly with treatment.Surgery may only provide temporary relief. The outlook for someone witharachnoiditis iscomplicated by the fact that the disorder has no predictable pattern or severity of symptoms. |
research | what research (or clinical trials) is being done for Arachnoiditis ? | Within the NINDS research programs, arachnoiditis 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 debilitating conditions such as arachnoiditis. |
information | What is (are) Craniosynostosis ? | Craniosynostosis is a birth defect of the skull characterized by the premature closure of one or more of the fibrous joints between the bones of the skull (called the cranial sutures) before brain growth is complete. Closure of a single suture is most common. Normally the skull expands uniformly to accommodate the growth of the brain; premature closure of a single suture restricts the growth in that part of the skull and promotes growth in other parts of the skull where sutures remain open. This results in a misshapen skull but does not prevent the brain from expanding to a normal volume. However, when many sutures close prematurely, the skull cannot expand to accommodate the growing brain, which leads to increased pressure within the skull and impaired development of the brain. Craniosynostosis can be gene-linked or caused by metabolic diseases (such as rickets )or an overactive thyroid. Some cases are associated with other disorders such as microcephaly (abnormally small head) and hydrocephalus (excessive accumulation of cerebrospinal fluid in the brain). The first sign of craniosynostosis is an abnormally shaped skull. Other features can include signs of increased intracranial pressure, developmental delays, or impaired cognitive development, which are caused by constriction of the growing brain. Seizures and blindness may also occur. |
treatment | What are the treatments for Craniosynostosis ? | Treatment for craniosynostosis generally consists of surgery to improve the symmetry and appearance of the head and to relieve pressure on the brain and the cranial nerves. For some children with less severe problems, cranial molds can reshape the skull to accommodate brain growth and improve the appearance of the head. |
outlook | What is the outlook for Craniosynostosis ? | The prognosis for craniosynostosis varies depending on whether single or multiple cranial sutures are involved or other abnormalities are present. The prognosis is better for those with single suture involvement and no associated abnormalities. |
research | what research (or clinical trials) is being done for Craniosynostosis ? | The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. The NINDS conducts and supports a wide range of studies that explore the complex mechanisms of brain development. The knowledge gained from these fundamental studies provides the foundation for understanding how this process can change and offers hope for new ways to treat and prevent birth defects that can prevent normal brain development, such as craniosynostosis. |
information | What is (are) Cavernous Malformation ? | Cerebral cavernous malformations (CCMs) are vascular lesions comprised of clusters of tightly packed, abnormally thin-walled small blood vessels (capillaries) that displace normal neurological tissue in the brain or spinal cord. The vessels are filled with slow-moving or stagnant blood that is usually clotted or in a state of decomposition. Cavernous malformations can occur in the brain, spinal cord, and some other body regions. In the brain and spinal cord these cavernous lesions are quite fragile and are prone to bleeding, causing hemorrhagic strokes (bleeding into the brain), seizures, and neurological deficits. CCMs can range in size from a few fractions of an inch to several inches in diameter, depending on the number of blood vessels involved. Some people develop multiple lesions while others never experience related medical problems. Hereditary forms of CCM are caused by mutations in one of three CCM disease genes: CCM1, CCM2, and CCM3. A large population with hereditary CCM disease is found in New Mexico and the Southwestern United States, in which the disease is caused by mutations in the gene CCM1 (or KRIT1). |
treatment | What are the treatments for Cavernous Malformation ? | The primary treatment option for a CCM is surgical removal. Radiation therapy has not been shown to be effective. The decision to operate is made based upon the risk of approaching the lesion. For example, symptomatic lesions close to the brain surface in non eloquent brain (areas for example, those areas not involved with motor function, speech, vision, hearing, memory, and learning) are very likely to be candidates for removal. On the other hand, lesions located in deep brain areas are associated with higher surgical risk and are often not candidates for surgery until the lesion has bled multiple times. Medications can often lessen general symptoms such as headache, back pain, and seizures. |
outlook | What is the outlook for Cavernous Malformation ? | Rebleeding from a cavernous angioma is common, it is not predictable, and individuals frequently have multiple CCMs found via magnetic resonance imaging. Individuals with CCM are faced with a diagnosis that imparts risk of multiple future hemorrhages that occur seemingly at random and without any preventative therapy except surgical removal. |
research | what research (or clinical trials) is being done for Cavernous Malformation ? | 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. Studies of cerebral cavernous malformations (CCMs) show that alterations in the function of structural proteins may also give rise to vascular malformations. Currently there is no therapy to prevent the development or progression of CCMs. NINDS-funded scientists have developed an animal model that studies two of the familial genes related to the development of CCMs. Research shows that the protein signaling pathway Rhoa/ROCK, which allows cells to communicate regarding the formation of cell structure, is involved in blood vessel activity/ and the flow of molecules and cells into and out of blood vessels. These scientists hypothesize that blocking ROCK activity will inhibit CCM development and hemorrhage, and possibly create a therapy for these malformations. |
information | What is (are) Locked-In Syndrome ? | Locked-in syndrome is a rare neurological disorder characterized by complete paralysis of voluntary muscles in all parts of the body except for those that control eye movement. It may result from traumatic brain injury, diseases of the circulatory system, diseases that destroy the myelin sheath surrounding nerve cells, or medication overdose. Individuals with locked-in syndrome are conscious and can think and reason, but are unable to speak or move. The disorder leaves individuals completely mute and paralyzed. Communication may be possible with blinking eye movements |
treatment | What are the treatments for Locked-In Syndrome ? | There is no cure for locked-in syndrome, nor is there a standard course of treatment. A therapy called functional neuromuscular stimulation, which uses electrodes to stimulate muscle reflexes, may help activate some paralyzed muscles. Several devices to help communication are available. Other treatment is symptomatic and supportive. |
outlook | What is the outlook for Locked-In Syndrome ? | While in rare cases some patients may regain certain functions, the chances for motor recovery are very limited. |
research | what research (or clinical trials) is being done for Locked-In Syndrome ? | The NINDS supports research on neurological disorders that can cause locked-in syndrome. The goals of this research are to find ways to prevent, treat, and cure these disorders. |
complications | What are the complications of Machado-Joseph Disease ? | Lyme disease is caused by a bacterial organism that is transmitted to humans via the bite of an infected tick. Most people with Lyme disease develop a characteristic skin rash around the area of the bite. The rash may feel hot to the touch, and vary in size, shape, and color, but it will often have a "bull's eye" appearance (a red ring with a clear center). However, there are those who will not develop the rash, which can make Lyme disease hard to diagnose because its symptoms and signs mimic those of many other diseases.
Anywhere from 7 to 14 days (or in some cases, 30 days) following an infected tick's bite, the first stage of Lyme disease may begin with flu-like symptoms such as fever, chills, swollen lymph nodes, headaches, fatigue, muscle aches, and joint pain.
Neurological complications most often occur in the second stage of Lyme disease, with numbness, pain, weakness, Bell's palsy (paralysis of the facial muscles), visual disturbances, and meningitis symptoms such as fever, stiff neck, and severe headache. Other problems, which may not appear until weeks, months, or years after a tick bite, include decreased concentration, irritability, memory and sleep disorders, and nerve damage in the arms and legs. |
treatment | What are the treatments for Machado-Joseph Disease ? | Lyme disease is treated with antibiotics under the supervision of a physician. |
outlook | What is the outlook for Machado-Joseph Disease ? | Most individuals with Lyme disease respond well to antibiotics and have full recovery. In a small percentage of individuals, symptoms may continue or recur, requiring additional antibiotic treatment. Varying degrees of permanent joint or nervous system damage may develop in individuals with late-stage Lyme disease. |
research | what research (or clinical trials) is being done for Machado-Joseph Disease ? | The NINDS supports research on Lyme disease. Current areas of interest include improving diagnostic tests and developing more effective treatments. The National Institute of Allergy and Infectious Diseases (NIAID), the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), and the National Center for Research Resources (NCRR), all parts of the National Institutes of Health (NIH), also support research on Lyme disease. |
information | What is (are) Acid Lipase Disease ? | Acid lipase disease or deficiency occurs when the enzyme needed to break down certain fats that are normally digested by the body is lacking or missing, resulting in the toxic buildup of these fats in the bodys cells and tissues. These fatty substances, called lipids, include fatty acids, oils, and cholesterol. Two rare lipid storage diseases are caused by the deficiency of the enzyme lysosomal acid lipase:
Wolmans disease (also known as acid lipase deficiency) is an autosomal recessive disorder marked by the buildup of cholesteryl esters (normally a tranport form of cholesterol that brings nutrients into the cells and carries out waste) and triglycerides (a chemical form in which fats exist in the body). Infants with the disorder appear normal at birth but quickly develop progressive mental deterioration, low muscle tone,enlarged liver and grossly enlarged spleen, gastrointestinal problems including an excessive amount of fats in the stools, jaundice, anemia, vomiting, and calcium deposits in the adrenal glands, which causes them to harden. Both male and female infants are affected by the disorder.
Cholesteryl ester storage disease (CESD) is an extremely rare disorder that results from storage of cholesteryl esters and triglycerides in cells in the blood and lymph and lymphoid tissue. Children develop an enlarged liver, leading to cirrhosis and chronic liver failure before adulthood. Children may also develop calcium deposits in the adrenal glands and jaundice. Onset varies, and the disorder may not be diagnosed until adulthood. |
treatment | What are the treatments for Acid Lipase Disease ? | Enzyme replacement therapy for both Wolman's and cholesteryl ester storage disease is currently under investigation. Certain drugs may be given to help with adrenal gland production, and children may need to be fed intravenously. Individuals with CESD may benefit from a low cholesterol diet. |
outlook | What is the outlook for Acid Lipase Disease ? | Wolmans disease is usually fatal by age 1. The onset and course of cholesteryl ester storage disease varies, and individuals may live into adulthood. |
research | what research (or clinical trials) is being done for Acid Lipase Disease ? | The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge abut the brain and nervous system, and to use that knowledge to reduce the burden of neurological diseaset. The NINDS conducts and supports research to understand lipid storage diseases such as acid lipase deficiency. Additional research studies hope to identify biomarkers (signs that may indicate risk of a disease and improve diagnosis) for thee lipid storage diseases that will speed the development of novel therapeutics for these disorders. Other investigators hope to establish an international disease registry designed to collect longitudinal data that would be used to improve the care and treatment of individuals with lysosomal acid lipase deficiency.
The National Library of Medicine (NLM), a part of the National Institutes of Health (NIH) within the U.S. Department of Health and Human Services, offers free searches of biomedical literature through an Internet service called PubMed. To search, go to: http://www.ncbi.nlm.nih.gov/PubMed . The NLM also offers extensive health information from NIH and other trusted sources. To research your condition, go to: http://www.medlineplus.gov . |
information | What is (are) Agenesis of the Corpus Callosum ? | Agenesis of the corpus callosum (ACC) is one of several disorders of the corpus callosum, the structure that connects the two hemispheres (left and right) of the brain. In ACC the corpus callosum is partially or completely absent. It is caused by a disruption of brain cell migration during fetal development. ACC can occur as an isolated condition or in combination with other cerebral abnormalities, including Arnold-Chiari malformation, Dandy-Walker syndrome, schizencephaly (clefts or deep divisions in brain tissue), and holoprosencephaly (failure of the forebrain to divide into lobes.) Girls may have a gender-specific condition called Aicardi syndrome, which causes severe cognitive impairment and developmental delays, seizures, abnormalities in the vertebra of the spine, and lesions on the retina of the eye. ACC can also be associated with malformations in other parts of the body, such as midline facial defects. The effects of the disorder range from subtle or mild to severe, depending on associated brain abnormalities. Children with the most severe brain malformations may have intellectual impairment, seizures, hydrocephalus, and spasticity. Other disorders of the corpus callosum include dysgenesis, in which the corpus callosum is developed in a malformed or incomplete way, and hypoplasia, in which the corpus callosum is thinner than usual. Individuals with these disorders have a higher risk of hearing deficits and cardiac abnormalities than individuals with the normal structure. It is estimated that at lease one in 4,000 individuals has a disorder of the corpus callosum. |
treatment | What are the treatments for Agenesis of the Corpus Callosum ? | There is no standard course of treatment for ACC. Treatment usually involves management of symptoms and seizures if they occur. Associated difficulties are much more manageable with early recognition and therapy, especially therapies focusing on left/right coordination. Early diagnosis and interventions are currently the best treatments to improve social and developmental outcomes. |
outlook | What is the outlook for Agenesis of the Corpus Callosum ? | Prognosis depends on the extent and severity of malformations. Intellectual impairment does not worsen. Individuals with a disorder of the corpus callosum typically have delays in attaining developmental milestones such as walking, talking, or reading; challenges with social interactions; clumsiness and poor motor coordination, particularly on skills that require coordination of left and right hands and feet (such as swimming, bicycle riding, and driving; and mental and social processing problems that become more apparent with age, with problems particularly evident from junior high school into adulthood. |
research | what research (or clinical trials) is being done for Agenesis of the Corpus Callosum ? | The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS conducts and supports a wide range of studies that explore the complex mechanisms of normal brain development. NINDS-funded research includes studies to understand the genetic causes of ACC, as well as to understand how magnetic resonance imaging findings may help predict outcome and response to therapy. |
information | What is (are) Trigeminal Neuralgia ? | Trigeminal neuralgia (TN), also called tic douloureux, is a chronic pain condition that causes extreme, sporadic, sudden burning or shock-like face pain. The painseldomlasts more than a few seconds or a minute or twoper episode. The intensity of pain can be physically and mentally incapacitating. TN pain is typically felt on one side of the jaw or cheek. Episodes can last for days, weeks, or months at a time and then disappear for months or years. In the days before an episode begins, some patients may experience a tingling or numbing sensation or a somewhat constant and aching pain. The attacks often worsen over time, with fewer and shorter pain-free periods before they recur. The intense flashes of pain can be triggered by vibration or contact with the cheek (such as when shaving, washing the face, or applying makeup), brushing teeth, eating, drinking, talking, or being exposed to the wind. TN occurs most often in people over age 50, but it can occur at any age, and is more common in women than in men. There is some evidence that the disorder runs in families, perhaps because of an inherited pattern of blood vessel formation. Although sometimes debilitating, the disorder is not life-threatening.
The presumed cause of TN is a blood vessel pressing on the trigeminal nerve in the head as it exits the brainstem. TN may be part of the normal aging process but in some cases it is the associated with another disorder, such as multiple sclerosis or other disorders characterized by damage to the myelin sheath that covers certain nerves. |
treatment | What are the treatments for Trigeminal Neuralgia ? | Because there are a large number of conditions that can cause facial pain, TN can be difficult to diagnose. But finding the cause of the pain is important as the treatments for different types of pain may differ. Treatment options include medicines such as anticonvulsants and tricyclic antidepressants, surgery, and complementary approaches. Typical analgesics and opioids are not usually helpful in treating the sharp, recurring pain caused by TN. If medication fails to relieve pain or produces intolerable side effects such as excess fatigue, surgical treatment may be recommended. Several neurosurgical procedures are available. Some are done on an outpatient basis, while others are more complex and require hospitalization. Some patients choose to manage TN using complementary techniques, usually in combination with drug treatment. These techniques include acupuncture, biofeedback, vitamin therapy, nutritional therapy, and electrical stimulation of the nerves. |
outlook | What is the outlook for Trigeminal Neuralgia ? | The disorder is characterized by recurrences and remissions, and successive recurrences may incapacitate the patient. Due to the intensity of the pain, even the fear of an impending attack may prevent activity. Trigeminal neuralgia is not fatal. |
research | what research (or clinical trials) is being done for Trigeminal Neuralgia ? | Within the NINDS research programs, trigeminal neuralgia 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 debilitating conditions such as trigeminal neuralgia. NINDS has notified research investigators that it is seeking grant applications both in basic and clinical pain research. |
information | What is (are) Neuronal Migration Disorders ? | Neuronal migration disorders (NMDs) are a group of birth defects caused by the abnormal migration of neurons in the developing brain and nervous system. In the developing brain, neurons must migrate from the areas where they are born to the areas where they will settle into their proper neural circuits. Neuronal migration, which occurs as early as the second month of gestation, is controlled by a complex assortment of chemical guides and signals. When these signals are absent or incorrect, neurons do not end up where they belong. This can result in structurally abnormal or missing areas of the brain in the cerebral hemispheres, cerebellum, brainstem, or hippocampus. The structural abnormalities found in NMDs include schizencephaly, porencephaly, lissencephaly, agyria, macrogyria, polymicrogyria, pachygyria, microgyria, micropolygyria, neuronal heterotopias (including band heterotopia), agenesis of the corpus callosum, and agenesis of the cranial nerves. Symptoms vary according to the abnormality, but often feature poor muscle tone and motor function, seizures, developmental delays, impaired cognitive development, failure to grow and thrive, difficulties with feeding, swelling in the extremities, and a smaller than normal head. Most infants with an NMD appear normal, but some disorders have characteristic facial or skull features that can be recognized by a neurologist. Several genetic abnormalities in children with NMDs have been identified. Defects in genes that are involved in neuronal migration have been associated with NMDs, but the role they play in the development of these disorders is not yet well-understood. More than 25 syndromes resulting from abnormal neuronal migration have been described. Among them are syndromes with several different patterns of inheritance; genetic counseling thus differs greatly between syndromes. |
treatment | What are the treatments for Neuronal Migration Disorders ? | Treatment is symptomatic, and may include anti-seizure medication and special or supplemental education consisting of physical, occupational, and speech therapies. |