Ahmed062646/NLP_Medora_Datasets huggingface dataset:
Question: what research (or clinical trials) is being done for Neurological Complications of AIDS ?
Answer: Within the Federal government, the National Institute of Neurological Disorders and Stroke (NINDS), one part of the National Institutes of Health (NIH), supports research on the neurological consequences of AIDS. The NINDS works closely with its sister agency, the National Institute of Allergy and Infectious Diseases (NIAID), which has primary responsibility for research related to HIV and AIDS.
Question: What is (are) Familial Periodic Paralyses ?
Answer: Familial periodic paralyses are a group of inherited neurological disorders caused by mutations in genes that regulate sodium and calcium channels in nerve cells. They are characterized by episodes in which the affected muscles become slack, weak, and unable to contract. Between attacks, the affected muscles usually work as normal. The two most common types of periodic paralyses are: Hypokalemic periodic paralysis is characterized by a fall in potassium levels in the blood. In individuals with this mutation attacks often begin in adolescence and are triggered by strenuous exercise, high carbohydrate meals, or by injection of insulin, glucose, or epinephrine. Weakness may be mild and limited to certain muscle groups, or more severe and affect the arms and legs. Attacks may last for a few hours or persist for several days. Some patients may develop chronic muscle weakness later in life. Hyperkalemic periodic paralysis is characterized by a rise in potassium levels in the blood. Attacks often begin in infancy or early childhood and are precipitated by rest after exercise or by fasting. Attacks are usually shorter, more frequent, and less severe than the hypokalemic form. Muscle spasms are common.
Question: What are the treatments for Familial Periodic Paralyses ?
Answer: Treatment of the periodic paralyses focuses on preventing further attacks and relieving acute symptoms. Avoiding carbohydrate-rich meals and strenuous exercise, and taking acetazolamide daily may prevent hypokalemic attacks. Attacks can be managed by drinking a potassium chloride oral solution. Eating carbohydrate-rich, low-potassium foods, and avoiding strenuous exercise and fasting, can help prevent hyperkalemic attacks. Dichorphenamide may prevent attacks.
Question: What is the outlook for Familial Periodic Paralyses ?
Answer: The prognosis for the familial periodic paralyses varies. Chronic attacks may result in progressive weakness that persists between attacks. Some cases respond well to treatment, which can prevent or reverse progressive muscle weakness.
Question: what research (or clinical trials) is being done for Familial Periodic Paralyses ?
Answer: The NINDS conducts and supports research on neuromuscular disorders such as the familial periodic paralyses. These studies are aimed at increasing knowledge about these disorders and finding ways to prevent, treat, and cure them.
Question: What is (are) Central Pain Syndrome ?
Answer: Central pain syndrome is a neurological condition caused by damage to or dysfunction of the central nervous system (CNS), which includes the brain, brainstem, and spinal cord. This syndrome can be caused by stroke, multiple sclerosis, tumors, epilepsy, brain or spinal cord trauma, or Parkinson's disease. The character of the pain associated with this syndrome differs widely among individuals partly because of the variety of potential causes. Central pain syndrome may affect a large portion of the body or may be more restricted to specific areas, such as hands or feet. The extent of pain is usually related to the cause of the CNS injury or damage. Pain is typically constant, may be moderate to severe in intensity, and is often made worse by touch, movement, emotions, and temperature changes, usually cold temperatures. Individuals experience one or more types of pain sensations, the most prominent being burning. Mingled with the burning may be sensations of "pins and needles;" pressing, lacerating, or aching pain; and brief, intolerable bursts of sharp pain similar to the pain caused by a dental probe on an exposed nerve. Individuals may have numbness in the areas affected by the pain. The burning and loss of touch sensations are usually most severe on the distant parts of the body, such as the feet or hands. Central pain syndrome often begins shortly after the causative injury or damage, but may be delayed by months or even years, especially if it is related to post-stroke pain.
Question: What are the treatments for Central Pain Syndrome ?
Answer: Pain medications often provide some reduction of pain, but not complete relief of pain, for those affected by central pain syndrome. Tricyclic antidepressants such as nortriptyline or anticonvulsants such as neurontin (gabapentin) can be useful. Lowering stress levels appears to reduce pain.
Question: What is the outlook for Central Pain Syndrome ?
Answer: Central pain syndrome is not a fatal disorder, but the syndrome causes disabling chronic pain and suffering among the majority of individuals who have it.
Question: what research (or clinical trials) is being done for Central Pain Syndrome ?
Answer: The NINDS vigorously pursues a research program seeking new treatments for chronic pain and nervous system damage. The goals of this research are to develop ways to more effectively treat and potentially reverse debilitating conditions such as central pain syndrome.
Question: What is (are) Progressive Multifocal Leukoencephalopathy ?
Answer: Progressive multifocal leukoencephalopathy (PML) is a disease of the white matter of the brain, caused by a virus infection that targets cells that make myelin--the material that insulates nerve cells (neurons). Polyomavirus JC (often called JC virus) is carried by a majority of people and is harmless except among those with lowered immune defenses. The disease is rare and occurs in patients undergoing chronic corticosteroid or immunosuppressive therapy for organ transplant, or individuals with cancer (such as Hodgkins disease or lymphoma). Individuals with autoimmune conditions such as multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosis -- some of whom are treated with biological therapies that allow JC virus reactivation -- are at risk for PML as well. PML is most common among individuals with HIV-1 infection / acquired immune deficiency syndrome (AIDS). Studies estimate that prior to effective antiretroviral therapy, as many as 5 percent of persons infected with HIV-1 eventually develop PML that is an AIDS-defining illness. However, current HIV therapy using antiretroviral drugs (ART), which effectively restores immune system function, allows as many as half of all HIV-PML patients to survive, although they may sometimes have an inflammatory reaction in the regions of the brain affected by PML. The symptoms of PML are diverse, since they are related to the location and amount of damage in the brain, and may evolve over the course of several weeks to months The most prominent symptoms are clumsiness; progressive weakness; and visual, speech, and sometimes personality changes. The progression of deficits leads to life-threatening disability and (frequently) death. A diagnosis of PML can be made following brain biopsy or by combining observations of a progressive course of the disease, consistent white matter lesions visible on a magnetic resonance imaging (MRI) scan, and the detection of the JC virus in spinal fluid.
Question: What are the treatments for Progressive Multifocal Leukoencephalopathy ?
Answer: Currently, the best available therapy is reversal of the immune-deficient state, since there are no effective drugs that block virus infection without toxicity. Reversal may be achieved by using plasma exchange to accelerate the removal of the therapeutic agents that put patients at risk for PML. In the case of HIV-associated PML, immediately beginning anti-retroviral therapy will benefit most individuals. Several new drugs that laboratory tests found effective against infection are being used in PML patients with special permission of the U.S. Food and Drug Administration. Hexadecyloxypropyl-Cidofovir (CMX001) is currently being studied as a treatment option for JVC because of its ability to suppress JVC by inhibiting viral DNA replication.
Question: What is the outlook for Progressive Multifocal Leukoencephalopathy ?
Answer: In general, PML has a mortality rate of 30-50 percent in the first few months following diagnosis but depends on the severity of the underlying disease and treatment received. Those who survive PML can be left with severe neurological disabilities.
Question: what research (or clinical trials) is being done for Progressive Multifocal Leukoencephalopathy ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to PML in laboratories at the NIH, and support additional research through grants to majorresearch institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders such as PML.
Question: What is (are) Creutzfeldt-Jakob Disease ?
Answer: Creutzfeldt-Jakob disease (CJD) is a rare, degenerative,fatal brain disorder. Typically, onset of symptoms occurs at about age 60. There are three major categories of CJD: sporadic (the most common form, in which people do not have any risk factors for the disease); hereditary (in which the person has a family member with the disease and tests positive for a genetic mutation), and acquired (in which the disease is transmitted by exposure to brain and nervous system tissue, usually through certain medical procedures. A form called variant CJD can be acquired by eating meat from cattle affected by a disease similar to CJD, called bovine spongiform encephalopathy (commonly called mad cow disease). Symptoms of CJD include problems with muscular coordination, personality changes including progressive and severe mental impairment, impaired vision that may lead to blindness, and involuntary muscle jerks called myoclonus. People eventually lose the ability to move and speak and enter a coma. Tests that help in the diagnosis of CJD include electroencephalography (which measures brain waves), detection of certain proteins in the fluid that surrounds the brain and spinal cord, and magnetic resonance imaging.. The first concern is to rule out treatable forms of dementia such as encephalitis or chronic meningitis. The only way to confirm a diagnosis of CJD is by brain biopsy or autopsy. In a brain biopsy, a neurosurgeon removes a small piece of tissue from the person's brain so that it can be examined by a neurologist. Because a correct diagnosis of CJD does not help the individual, a brain biopsy is discouraged unless it is need to rule out a treatable disorder. .
Question: What are the treatments for Creutzfeldt-Jakob Disease ?
Answer: There is no treatment that can cure or control CJD, although studies of a variety of drugs are now in progress. Current treatment is aimed at alleviating symptoms and making the person as comfortable as possible. Opiate drugs can help relieve pain, and the drugs clonazepam and sodium valproate may help relieve involuntary muscle jerks.Intravenous fluids and artificial feeding may be needed in later stages of the disease.
Question: What is the outlook for Creutzfeldt-Jakob Disease ?
Answer: About 70 percent of individuals die within one year. In the early stages of disease, people may have failing memory, behavioral changes, lack of coordination and visual disturbances. As the illness progresses, mental deterioration becomes pronounced and involuntary movements, blindness, weakness of extremities, and coma may occur.
Question: what research (or clinical trials) is being done for Creutzfeldt-Jakob Disease ?
Answer: 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 leading scientific theory at this time maintains that CJD is caused by a type of protein called a prion. The harmless and the infectious forms of the prion protein are nearly identical, but the infectious form takes a different folded shape than the normal protein. Researchers are trying to discover factors that influence prion infectivity and how the disorder damages the brain. Using rodent models of the disease and brain tissue from autopsies, researchers are also trying to develop improved diagnostic tests for CJD and to learn what changes ultimately kill the neurons so that effective treatments can be developed.
Question: What is (are) Giant Axonal Neuropathy ?
Answer: 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.
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) SUNCT Headache ?
Answer: SUNCT-Short-lasting, Unilateral, Neuralgiform headache attacks with Conjunctival injection and Tearing-is a rare form of headache that is most common in men after age 50. The disorder is marked by bursts of moderate to severe burning, piercing, or throbbing pain, usually on one side of the head and around the eye or temple. The pain usually peaks within seconds of onset and may follow a pattern of increasing and decreasing intensity. Attacks typically occur in daytime hours and last from 5 seconds to 4 minutes per episode. Individuals generally have five to six attacks per hour. Autonomic nervous system responses include watery eyes, reddish or bloodshot eyes caused by dilation of blood vessels (conjunctival injection), nasal congestion, runny nose, sweaty forehead, swelling of the eyelids, and increased pressure within the eye on the affected side of head. Systolic blood pressure may rise during the attacks. Movement of the neck may trigger these headaches. SUNCT may be a form of trigeminal neuralgia and is considered one of the trigeminal autonomic cephalgias, or TACs.
Question: What are the treatments for SUNCT Headache ?
Answer: These headaches are generally non-responsive to usual treatment for other short-lasting headaches. Corticosteroids and the anti-epileptic drugs gabapentin, lamotrigine, and carbamazepine may help relieve some symptoms in some patients. Studies have shown that injections of glycerol to block nerve signaling along the trigeminal nerve may provide temporary relief in some severe cases, but the headaches recurred in about 40 percent of individuals studied.
Question: What is the outlook for SUNCT Headache ?
Answer: There is no cure for these headaches. The disorder is not fatal but can cause considerable discomfort.
Question: what research (or clinical trials) is being done for SUNCT Headache ?
Answer: The NINDS conducts a wide range of research on headache disorders. This research aims to discover ways to better diagnose, treat, and ultimately, prevent these disorders.
Question: What is (are) Neurotoxicity ?
Answer: Neurotoxicity occurs when the exposure to natural or manmade toxic substances (neurotoxicants) alters the normal activity of the nervous system. This can eventually disrupt or even kill neurons, key cells that transmit and process signals in the brain and other parts of the nervous system. Neurotoxicity can result from exposure to substances used in chemotherapy, radiation treatment, drug therapies, and organ transplants, as well as exposure to heavy metals such as lead and mercury, certain foods and food additives, pesticides, industrial and/or cleaning solvents, cosmetics, and some naturally occurring substances. Symptoms may appear immediately after exposure or be delayed. They may include limb weakness or numbness; loss of memory, vision, and/or intellect; headache; cognitive and behavioral problems; and sexual dysfunction. Individuals with certain disorders may be especially vulnerable to neurotoxicants.
Question: What are the treatments for Neurotoxicity ?
Answer: Treatment involves eliminating or reducing exposure to the toxic substance, followed by symptomatic and supportive therapy.
Question: What is the outlook for Neurotoxicity ?
Answer: The prognosis depends upon the length and degree of exposure and the severity of neurological injury. In some instances, exposure to neurotoxicants can be fatal. In others, patients may survive but not fully recover. In other situations, many individuals recover completely after treatment.
Question: what research (or clinical trials) is being done for Neurotoxicity ?
Answer: The NINDS supports research on disorders of the brain and nervous system such as neurotoxicity, aimed at learning more about these disorders and finding ways to prevent and treat them. Scientists are investigating the role occupational or environmental toxicants have on progressive neurodegenerative disorders such as Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis, and dementia. Also being studied are the mechanisms that trigger neuroimmune responses in the central nervous system and the possibility that some brain disorders in children may occur when environmental triggers interact with genes.
Question: What is (are) Spinal Cord Injury ?
Answer: A spinal cord injury usually begins with a sudden, traumatic blow to the spine that fractures or dislocates vertebrae. The damage begins at the moment of injury when displaced bone fragments, disc material, or ligaments bruise or tear into spinal cord tissue. Most injuries to the spinal cord don't completely sever it. Instead, an injury is more likely to cause fractures and compression of the vertebrae, which then crush and destroy axons -- extensions of nerve cells that carry signals up and down the spinal cord between the brain and the rest of the body. An injury to the spinal cord can damage a few, many, or almost all of these axons. Some injuries will allow almost complete recovery. Others will result in complete paralysis.
Question: What are the treatments for Spinal Cord Injury ?
Answer: Improved emergency care for people with spinal cord injuries and aggressive treatment and rehabilitation can minimize damage to the nervous system and even restore limited abilities. Respiratory complications are often an indication of the severity of spinal cord injury About one-third of those with injury to the neck area will need help with breathing and require respiratory support. The steroid drug methylprednisolone appears to reduce the damage to nerve cells if it is given within the first 8 hours after injury. Rehabilitation programs combine physical therapies with skill-building activities and counseling to provide social and emotional support.Electrical simulation of nerves by neural prosthetic devices may restore specific functions, including bladder, breathing, cough, and arm or leg movements, though eligibility for use of these devices depends on the level and type of the spinal cord injury.
Question: What is the outlook for Spinal Cord Injury ?
Answer: Spinal cord injuries are classified as either complete or incomplete. An incomplete injury means that the ability of the spinal cord to convey messages to or from the brain is not completely lost. People with incomplete injuries retain some motor or sensory function below the injury. A complete injury is indicated by a total lack of sensory and motor function below the level of injury. People who survive a spinal cord injury will most likely have medical complications such as chronic pain and bladder and bowel dysfunction, along with an increased susceptibility to respiratory and heart problems. Successful recovery depends upon how well these chronic conditions are handled day to day. Surgery to relieve compression of the spinal tissue by surrounding bones broken or dislocated by the injury is often necessary, through timing of such surgery may vary widely. A recent prospective multicenter trial called STASCIS is exploring whether performing decompression surgery early (less than 24 hours following injury) can improve outcomes for patients with bone fragments or other tissues pressing on the spinal cord.