Druvith/medqa1 huggingface dataset:
Question:  What are the treatments for Giant Axonal Neuropathy ?
Answer: 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.
Question:  What is the outlook for Giant Axonal Neuropathy ?
Answer: 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.
Question:  what research (or clinical trials) is being done for Giant Axonal Neuropathy ?
Answer: 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.
Question:  What is (are) Thoracic Outlet Syndrome ?
Answer: 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.
Question:  What are the treatments for Thoracic Outlet Syndrome ?
Answer: 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.
Question:  What is the outlook for Thoracic Outlet Syndrome ?
Answer: 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.
Question:  what research (or clinical trials) is being done for Thoracic Outlet Syndrome ?
Answer: 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.
Question:  What is (are) Angelman Syndrome ?
Answer: 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.
Question:  What are the treatments for Angelman Syndrome ?
Answer: 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.
Question:  What is the outlook for Angelman Syndrome ?
Answer: 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.
Question:  what research (or clinical trials) is being done for Angelman Syndrome ?
Answer: The NINDS supports and conducts research on neurogenetic disorders such as Angelman syndrome, to develop techniques to diagnose, treat, prevent, and ultimately cure them.
Question:  What is (are) Inclusion Body Myositis ?
Answer: 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.
Question:  What are the treatments for Inclusion Body Myositis ?
Answer: 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.
Question:  What is the outlook for Inclusion Body Myositis ?
Answer: IBM is generally resistant to all therapies and its rate of progression appears to be unaffected by currently available treatments.
Question:  what research (or clinical trials) is being done for Inclusion Body Myositis ?
Answer: 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.
Question:  What is (are) Subacute Sclerosing Panencephalitis ?
Answer: 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.
Question:  What are the treatments for Subacute Sclerosing Panencephalitis ?
Answer: 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.
Question:  What is the outlook for Subacute Sclerosing Panencephalitis ?
Answer: 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.
Question:  what research (or clinical trials) is being done for Subacute Sclerosing Panencephalitis ?
Answer: 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.
Question:  What is (are) Hemifacial Spasm ?
Answer: 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.
Question:  What are the treatments for Hemifacial Spasm ?
Answer: 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.
Question:  What is the outlook for Hemifacial Spasm ?
Answer: 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.
Question:  what research (or clinical trials) is being done for Hemifacial Spasm ?
Answer: 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.
Question:  What is (are) Olivopontocerebellar Atrophy ?
Answer: 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.
Question:  What are the treatments for Olivopontocerebellar Atrophy ?
Answer: 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.
Question:  What is the outlook for Olivopontocerebellar Atrophy ?
Answer: There is no cure for OPCA. The disorder is slowly progressive with death usually occurring approximately 20 years after onset.
Question:  what research (or clinical trials) is being done for Olivopontocerebellar Atrophy ?
Answer: 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.
Question:  What is (are) Multifocal Motor Neuropathy ?
Answer: 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.
Question:  What are the treatments for Multifocal Motor Neuropathy ?
Answer: 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.
Question:  What is the outlook for Multifocal Motor Neuropathy ?
Answer: 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.
Question:  what research (or clinical trials) is being done for Multifocal Motor Neuropathy ?
Answer: The NINDS supports a broad range of research on neuromuscular disorders with the goal of finding ways to prevent, treat, and, ultimately, cure them.
Question:  What is (are) Occipital Neuralgia ?
Answer: 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.
Question:  What are the treatments for Occipital Neuralgia ?
Answer: 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.
Question:  What is the outlook for Occipital Neuralgia ?
Answer: 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.
Question:  what research (or clinical trials) is being done for Occipital Neuralgia ?
Answer: 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.
Question:  What is (are) Arachnoiditis ?
Answer: 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.
Question:  What are the treatments for Arachnoiditis ?
Answer: 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.
Question:  What is the outlook for Arachnoiditis ?
Answer: 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.
Question:  what research (or clinical trials) is being done for Arachnoiditis ?
Answer: 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.