Druvith/medqa huggingface dataset:
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
What are the treatments for Holoprosencephaly ? 

There is no standard course of treatment for holoprosencephaly. Treatment is symptomatic and supportive.
What is the outlook for Holoprosencephaly ? 

The prognosis for individuals with the disorder depends on the severity of the brain and facial deformities.
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.
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..
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..
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.
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.
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.
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.
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.
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
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.