Vanquish44/Healthcare_NLP huggingface dataset:
Question: what research (or clinical trials) is being done for Peripheral Neuropathy ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to peripheral neuropathies in laboratories at the NIH and also support additional research through grants to major medical institutions across the country. Current research projects funded by the NINDS involve investigations of genetic factors associated with hereditary neuropathies, studies of biological mechanisms involved in diabetes-associated neuropathies, and investigations exploring how the immune system contributes to peripheral nerve damage. Neuropathic pain is a primary target of NINDS-sponsored studies aimed at developing more effective therapies for symptoms of peripheral neuropathy. Some scientists hope to identify substances that will block the brain chemicals that generate pain signals, while others are investigating the pathways by which pain signals reach the brain.

Topic: Peripheral Neuropathy
Source: NINDS
Question: What is (are) Paroxysmal Hemicrania ?
Answer: Paroxysmal hemicrania is a rare form of headache that usually begins in adulthood. Patients experience severe throbbing, claw-like, or boring pain usually on one side of the face; in, around, or behind the eye; and occasionally reaching to the back of the neck. This pain may be accompanied by red and tearing eyes, a drooping or swollen eyelid on the affected side of the face, and nasal congestion. Patients may also feel dull pain, soreness, or tenderness between attacks. Attacks of paroxysmal hemicrania typically occur from 5 to 40 times per day and last 2 to 30 minutes. The disorder has two forms: chronic, in which patients experience attacks on a daily basis for a year or more, and episodic, in which the headaches may remit for months or years. Certain movements of the head or neck or external pressure to the neck may trigger these headaches in some patients. The disorder is more common in women than in men.

Topic: Paroxysmal Hemicrania
Source: NINDS
Question: What are the treatments for Paroxysmal Hemicrania ?
Answer: The nonsteroidal anti-inflammatory drug (NSAID) indomethacin often provides complete relief from symptoms. Other less effective NSAIDs, calcium-channel blocking drugs (such as verapamil), and corticosteroids may be used to treat the disorder. Patients with both paroxysmal hemicrania and trigeminal neuralgia (a condition of the 5th cranial nerve that causes sudden, severe pain typically felt on one side of the jaw or cheek) should receive treatment for each disorder.

Topic: Paroxysmal Hemicrania
Source: NINDS
Question: What is the outlook for Paroxysmal Hemicrania ?
Answer: Many patients experience complete to near-complete relief of symptoms following physician-supervised medical treatment. Paroxysmal hemicrania may last indefinitely but has been known to go into remission or stop spontaneously.

Topic: Paroxysmal Hemicrania
Source: NINDS
Question: what research (or clinical trials) is being done for Paroxysmal Hemicrania ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) support research related to paroxysmal hemicrania through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure headache disorders such as paroxysmal hemicrania.

Topic: Paroxysmal Hemicrania
Source: NINDS
Question: What is (are) Motor Neuron Diseases ?
Answer: The motor neuron diseases (MNDs) are a group of progressive neurological disorders that destroy cells that control essential muscle activity such as speaking, walking, breathing, and swallowing. Normally, messages from nerve cells in the brain (called upper motor neurons) are transmitted to nerve cells in the brain stem and spinal cord (called lower motor neurons) and from them to particular muscles. When there are disruptions in these signals, the result can be gradual muscle weakening, wasting away, and uncontrollable twitching (called fasciculations). Eventually, the ability to control voluntary movement can be lost. MNDs may be inherited or acquired, and they occur in all age groups. MNDs occur more commonly in men than in women, and symptoms may appear after age 40. In children, particularly in inherited or familial forms of the disease, symptoms can be present at birth or appear before the child learns to walk.
                
The causes of sporadic (noninherited) MNDs are not known, but environmental, toxic, viral, or genetic factors may be implicated. Common MNDs include amyotrophic lateral sclerosis (ALS), progressive bulbar palsy, primary lateral sclerosis, and progressive muscular atrophy. Other MNDs include the many inherited forms of spinal muscular atrophy and post-polio syndrome, a condition that can strike polio survivors decades after their recovery from poliomyelitis.

Topic: Motor Neuron Diseases
Source: NINDS
Question: What are the treatments for Motor Neuron Diseases ?
Answer: There is no cure or standard treatment for the MNDs. Symptomatic and supportive treatment can help patients be more comfortable while maintaining their quality of life. The drug riluzole (Rilutek), which as of this date is the only drug approved by the U.S. Food and Drug Administration to treat ALS, prolongs life by 2-3 months but does not relieve symptoms. Other medicines that may help reduce symptoms include muscle relaxants such as baclofen, tizanidine, and the benzodiazepines for spasticity; glycopyrrolate and atropine to treat excessive saliva; and anticonvulsants and nonsteroidal anti-inflammatory drugs to relieve pain. Panic attacks can be treated with benzodiazepines. Some patients may require stronger medicines such as morphine to cope with musculoskeletal abnormalities or pain in later stages of the disorders, and opiates are used to provide comfort care in terminal stages of the disease.
                
Physical and speech therapy, occupational therapy, and rehabilitation may help to improve posture, prevent joint immobility, slow muscle weakness and atrophy, and cope with swallowing difficulties. Applying heat may relieve muscle pain. Assistive devices such as supports or braces, orthotics, speech synthesizers, and wheelchairs help some patients retain independence. Proper nutrition and a balanced diet are essential to maintaining weight and strength.

Topic: Motor Neuron Diseases
Source: NINDS
Question: What is the outlook for Motor Neuron Diseases ?
Answer: Prognosis varies depending on the type of MND and the age of onset. Some MNDs, such as primary lateral sclerosis and Kennedy disease, are not fatal and progress slowly. Patients with spinal muscular atrophy may appear to be stable for long periods, but improvement should not be expected. Some MNDs, such as ALS and some forms of spinal muscular atrophy, are fatal.

Topic: Motor Neuron Diseases
Source: NINDS
Question: what research (or clinical trials) is being done for Motor Neuron Diseases ?
Answer: 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 (NIH), the leading supporter of biomedical research in the world. Researchers are testing whether different drugs, agents, or interventions are safe and effective in slowing the progression of motor neuron diseasess. NIH is also conducting clinical trials to study drugs to stimulate muscle growth in Kennedys disease and to suppress endogenous retroviruses in individuals with ALS. A large NIH-led collaborative study is investigating the genes and gene activity, proteins, and modifications of adult stem cell models from both healthy people and those with ALS,spinal muscular atrophy, and other neurodegenerative diseases to better understand the function of neurons and other support cells and identify candidate therapeutic compounds.
                

                
conducts research related to the MNDs in its laboratories at the National Institutes of Health (NIH), and also supports additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders such as the MNDs.

Topic: Motor Neuron Diseases
Source: NINDS
Question: What is (are) Lambert-Eaton Myasthenic Syndrome ?
Answer: Lambert-Eaton myasthenic syndrome (LEMS) is a disorder of the neuromuscular junction-the site where nerve cells meet muscle cells and help activate the muscles. It is caused by a disruption of electrical impulses between these nerve and muscle cells. LEMS is an autoimmune condition; in such disorders the immune system, which normally protects the body from foreign organisms, mistakenly attacks the body's own tissues. The disruption of electrical impulses is associated with antibodies produced as a consequence of this autoimmunity. Symptoms include muscle weakness, a tingling sensation in the affected areas, fatigue, and dry mouth. LEMS is closely associated with cancer, in particular small cell lung cancer. More than half the individuals diagnosed with LEMS also develop small cell lung cancer. LEMS may appear up to 3 years before cancer is diagnosed.

Topic: Lambert-Eaton Myasthenic Syndrome
Source: NINDS
Question: What are the treatments for Lambert-Eaton Myasthenic Syndrome ?
Answer: There is no cure for LEMS. Treatment is directed at decreasing the autoimmune response (through the use of steroids, plasmapheresis, or high-dose intravenous immunoglobulin) or improving the transmission of the disrupted electrical impulses by giving drugs such as di-amino pyridine or pyridostigmine bromide (Mestinon). For patients with small cell lung cancer, treatment of the cancer is the first priority.

Topic: Lambert-Eaton Myasthenic Syndrome
Source: NINDS
Question: What is the outlook for Lambert-Eaton Myasthenic Syndrome ?
Answer: The prognosis for individuals with LEMS varies. Those with LEMS not associated with malignancy have a benign overall prognosis. Generally the presence of cancer determines the prognosis.

Topic: Lambert-Eaton Myasthenic Syndrome
Source: NINDS
Question: what research (or clinical trials) is being done for Lambert-Eaton Myasthenic Syndrome ?
Answer: The NINDS supports research on neuromuscular disorders such as LEMS with the ultimate goal of finding ways to treat, prevent, and cure them.

Topic: Lambert-Eaton Myasthenic Syndrome
Source: NINDS
Question: What is (are) Cerebellar Hypoplasia ?
Answer: Cerebellar hypoplasia is a neurological condition in which the cerebellum is smaller than usual or not completely developed. Cerebellar hypoplasia is a feature of a number of congenital (present at birth) malformation syndromes, such as Walker-Warburg syndrome (a form of muscular dystrophy. It is also associated with several inherited metabolic disorders, such as Williams syndrome, and some of the neurodegenerative disorders that begin in early childhood, such as ataxia telangiectasia. In an infant or young child, symptoms of a disorder that features cerebellar hypoplasia might include floppy muscle tone, developmental or speech delay, problems with walking and balance, seizures, intellectual disability, and involuntary side to side movements of the eyes. In an older child, symptoms might include headache, dizzy spells, clumsiness, and hearing impairment.

Topic: Cerebellar Hypoplasia
Source: NINDS
Question: What are the treatments for Cerebellar Hypoplasia ?
Answer: There is no standard course of treatment for cerebellar hypoplasia. Treatment depends upon the underlying disorder and the severity of symptoms. Generally, treatment is symptomatic and supportive.

Topic: Cerebellar Hypoplasia
Source: NINDS
Question: What is the outlook for Cerebellar Hypoplasia ?
Answer: The prognosis is dependent upon the underlying disorder. Some of the disorders that are associated with cerebellar hypoplasia are progressive, which means the condition will worsen over time, and will most likely have a poor prognosis. Other disorders that feature cerebellar hypoplasia are not progressive, such as those that are the result of abnormal brain formation during fetal development, and might have a better outcome.

Topic: Cerebellar Hypoplasia
Source: NINDS
Question: what research (or clinical trials) is being done for Cerebellar Hypoplasia ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS) supports research related to cerebellar hypoplasia and its associated disorders through grants to major research institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders that feature cerebellar hypoplasia.

Topic: Cerebellar Hypoplasia
Source: NINDS
Question: What is (are) Cerebral Arteriosclerosis ?
Answer: Cerebral arteriosclerosis is the result of thickening and hardening of the walls of the arteries in the brain. Symptoms of cerebral arteriosclerosis include headache, facial pain, and impaired vision.
                
Cerebral arteriosclerosis can cause serious health problems. If the walls of an artery are too thick, or a blood clot becomes caught in the narrow passage, blood flow to the brain can become blocked and cause an ischemic stroke. When the thickening and hardening is uneven, arterial walls can develop bulges (called aneurysms). If a bulge ruptures, bleeding in the brain can cause a hemorrhagic stroke. Both types of stroke can be fatal.
                
Cerebral arteriosclerosis is also related to a condition known as vascular dementia, in which small, symptom-free strokes cause cumulative damage and death to neurons (nerve cells) in the brain. Personality changes in the elderly, such as apathy, weeping, transient befuddlement, or irritability, might indicate that cerebral arteriosclerosis is present in the brain. Computer tomography (CT) and magnetic resonance imaging (MRI) of the brain can help reveal the presence of cerebral arteriosclerosis before ischemic strokes, hemorrhagic strokes, or vascular dementia develop.

Topic: Cerebral Arteriosclerosis
Source: NINDS
Question: What are the treatments for Cerebral Arteriosclerosis ?
Answer: Treatment for cerebral arteriosclerosis can include medications or surgery. Physicians also may recommend treatments to help people control high blood pressure, quit cigarette smoking, and reduce cholesterol levels, all of which are risk factors for cerebral arteriosclerosis.

Topic: Cerebral Arteriosclerosis
Source: NINDS
Question: What is the outlook for Cerebral Arteriosclerosis ?
Answer: Cerebral arteriosclerosis can lead to life threatening health events such as ischemic or hemorrhagic strokes. People who survive stroke may have long-term neurological and motor impairments.

Topic: Cerebral Arteriosclerosis
Source: NINDS
Question: what research (or clinical trials) is being done for Cerebral Arteriosclerosis ?
Answer: The NINDS supports an extensive research program on stroke and conditions that can lead to stroke. Much of this research is aimed at finding ways to prevent and treat conditions such as cerebral arteriosclerosis.

Topic: Cerebral Arteriosclerosis
Source: NINDS
Question: What is (are) Metachromatic Leukodystrophy ?
Answer: Metachromatic leukodystrophy (MLD) is one of a group of genetic disorders called the leukodystrophies, which are characterized by the toxic buildup of lipids (fatty materials such as oils and waxes) and other storage materials in cells in the white matter of the central nervous system and peripheral nerves. The buildup of storage materials impairs the growth or development of the myelin sheath, the fatty covering that acts as an insulator around nerve fibers. (Myelin, which lends its color to the white matter of the brain, is a complex substance made up of a mixture of fats and proteins.) MLD is one of several lipid storage diseases, which result in the harmful buildup of lipids in brain cells and other cells and tissues in the body. People with lipid storage diseases either do not produce enough of one of the enzymes needed to break down (metabolize) lipids or they produce enzymes that do not work properly. Some leukodystrophies are caused by genetic defects of enzymes that regulate the metabolism of fats needed in myelin synthesis. MLD, which affects males and females, is cause by a deficiency of the enzyme arylsulfatase A. MLD has three characteristic forms: late infantile, juvenile, and adult. Late infantile MLD typically begins between 12 and 20 months following birth. Infants appear normal at first but develop difficulty walking after the first year of life and eventually lose the ability to walk. Other symptoms include muscle wasting and weakness,developmental delays, progressive loss of vision leading to blindness, impaired swallowing, and dementia before age 2. Most children with this form of MLD die by age 5. Symptoms of the juvenile form of MLD (which begins between 3-10 years of age) include impaired school performance, mental deterioration, an inability to control movements, seizures, and dementia. Symptoms continue to get worse, and death eventually occurs 10 to 20 years following disease onset.. The adult form commonly begins after age 16, with symptoms that include psychiatric disturbances, seizures, tremor, impaired concentration, depression, and dementia. Death generally occurs within 6 to 14 years after onset of symptoms.

Topic: Metachromatic Leukodystrophy
Source: NINDS
Question: What are the treatments for Metachromatic Leukodystrophy ?
Answer: There is no cure for MLD. Bone marrow transplantation may delay progression of the disease in some infantile-onset cases. Other treatment is symptomatic and supportive. Considerable progress has been made with regard to gene therapy in an animal model of MLD and in clinical trials.

Topic: Metachromatic Leukodystrophy
Source: NINDS
Question: What is the outlook for Metachromatic Leukodystrophy ?
Answer: The prognosis for MLD is poor. Most children within the infantile form die by age 5. Symptoms of the juvenile form progress with death occurring 10 to 20 years following onset. Those persons affected by the adult form typically die withing 6 to 14 years following onset of symptoms.

Topic: Metachromatic Leukodystrophy
Source: NINDS
Question: what research (or clinical trials) is being done for Metachromatic Leukodystrophy ?
Answer: 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 part of the National Institutes of Health (NIH), the leading supporter of biomedical research in the world. Research funded by the NINDS focuses on better understanding how neurological defects arise in lipid storage disorders and on the development of new treatments targeting disease mechanisms, including gene therapies, cell-based therapies, and pharmacological approaches. NINDS-funded preclinical research aims to study the effectiveness and safety of virus-based delivery of the normal ARSA gene to promote gene expression throughout the central nervous system and overcome the mutation-caused deficiency. If successful, the project could lead to trials in humans. Other research hopes to study the use of patient-specific induced pluripotent stem cells (cells that are capable of becoming other types of cells) in correcting the gene deficiency in metachromatic leukodystrophy.

Topic: Metachromatic Leukodystrophy
Source: NINDS
Question: What is (are) Neuroacanthocytosis ?
Answer: Neuroacanthocytosis refers to a group of genetic conditions that are characterized by movement disorders and acanthocytosis (abnormal, spiculated red blood cells). Four syndromes are classified as neuroacanthocytosis: Chorea-acanthocytosis, McLeod syndrome, Huntington's disease-like 2 (HDL2), and panthothenate kinase-associated neurodegeneration (PKAN). Acanthocytosis may not always be observed in HDL2 and PKAN. These disorders are caused by different genetic mutations, and the signs and symptoms vary, but usually include chorea (involuntary, dance-like movements), parkinsonism (slowness of movement), dystonia (abnormal body postures), and problems walking. There may also be muscle weakness, involuntary movements of the face and tongue, tongue/lip biting (which is mostly characteristic of Chorea-acanthocytosis), as well as difficulty with speech and eating, cognitive impairment, psychiatric symptoms, and seizures. Individuals with McLeod syndrome often have cardiac problems. Many features of these disorders are due to degeneration of the basal ganglia, a part of the brain that controls movement. Additional disorders that are also known have neurologic symptoms, acanthocytosis, and either lipoprotein disorders or systemic findings. The diagnosis of neuroacanthocytosis is typically based on the symptoms and clinical observation, a review of family history, and the evaluation of specific laboratory and imaging studies.

Topic: Neuroacanthocytosis
Source: NINDS
Question: What are the treatments for Neuroacanthocytosis ?
Answer: There are currently no treatments to prevent or slow the progression of neuroacanthocytosis and treatment is symptomatic and supportive. Medications that block dopamine, such as some of the antipsychotics, may decrease the involuntary movements. Botulinum toxin injections usually improve symptoms of dystonia. A feeding tube may be needed for individuals with feeding difficulties to maintain proper nutrition. Seizures may be treated with a variety of anticonvulsants, and antidepressants may also be appropriate for some individuals. Speech, occupational, and physical therapy may also be beneficial.

Topic: Neuroacanthocytosis
Source: NINDS
Question: What is the outlook for Neuroacanthocytosis ?
Answer: Neuroacanthocytosis is a progressive disease, and in some cases may be complicated by poor nutritional status, cardiac abnormalities, and pneumonia.

Topic: Neuroacanthocytosis
Source: NINDS
Question: what research (or clinical trials) is being done for Neuroacanthocytosis ?
Answer: The NINDS supports research on disorders such as neuroacanthocytosis, aimed at increasing scientific understanding of the disorders and finding ways to prevent and treat them. The genetic mutations responsible for some types of neuroacanthocytosis have recently been identified. Researchers are examining the role of the basal ganglia in neuroacanthocytosis and hope to correlate the specific genetic abnormalities with the clinical features of the disease. Other research is aimed at identifying possible causes of sudden death related to heart muscle abnormalities, which are observed in some individuals with neuroacanthocytosis.

Topic: Neuroacanthocytosis
Source: NINDS
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.

Topic: Arachnoiditis
Source: NINDS