Druvith/transformed_medDataset huggingface dataset:
What is (are) Myotonia ? 
 Myotonia is a medical term that refers to a neuromuscular condition in which the relaxation of a muscle is impaired. It can affect any muscle group. Repeated effort will be needed to relax the muscle, although the condition usually improves after the muscles have warmed-up. Individuals with myotonia may have trouble releasing their grip on objects or may have difficulty rising from a seated position. They may walk with a stiff, awkward gait. Myotonia is caused by an abnormality in the muscle membrane, and is often associated with inherited neurological disorders. Myotonia is commonly seen in individuals with myotonic muscular dystrophy, myotonia congenita, and in people who have one of a group of neurological disorders called the channelopathies, which are inherited diseases that are caused by mutations in the chloride sodium or potassium channels that regulate the muscle membrane. Myotonia may also be triggered by exposure to cold.
What are the treatments for Myotonia ? 
 Treatment for myotonia may include mexiletine, quinine, phenytoin, and other anticonvulsant drugs. Physical therapy and other rehabilitative measures may help muscle function.
What is the outlook for Myotonia ? 
 Myotonia is a chronic disorder. Symptoms may improve later in life.
what research (or clinical trials) is being done for Myotonia ? 
 The National Institute of Neurological Disorders and Stroke supports and conducts an extensive research program on neuromuscular disorders. The goals of this research are to learn more about these disorders and to find ways to treat, prevent, and cure them.
What is (are) Creutzfeldt-Jakob Disease ? 
 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. .
What are the treatments for Creutzfeldt-Jakob Disease ? 
 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.
What is the outlook for Creutzfeldt-Jakob Disease ? 
 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.
what research (or clinical trials) is being done for Creutzfeldt-Jakob Disease ? 
 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.
What is (are) Chorea ? 
 Chorea is an abnormal involuntary movement disorder, one of a group of neurological disorders called dyskinesias, which are caused by overactivity of the neurotransmitter dopamine in the areas of the brain that control movement. Chorea is characterized by brief, irregular contractions that are not repetitive or rhythmic, but appear to flow from one muscle to the next. Chorea often occurs with athetosis, which adds twisting and writhing movements. Chorea is a primary feature of Huntington's disease, a progressive, hereditary movement disorder that appears in adults, but it may also occur in a variety of other conditions. Syndenham's chorea occurs in a small percentage (20 percent) of children and adolescents as a complication of rheumatic fever. Chorea can also be induced by drugs (levodopa, anti-convulsants, and anti-psychotics) metabolic and endocrine disorders, and vascular incidents.
What are the treatments for Chorea ? 
 There is no standard course of treatment for chorea. Treatment depends on the type of chorea and the associated disease. Treatment for Huntington's disease is supportive, while treatment for Syndenham's chorea usually involves antibiotic drugs to treat the infection, followed by drug therapy to prevent recurrence. Adjusting medication dosages can treat drug-induced chorea. Metabolic and endocrine-related choreas are treated according to the cause(s) of symptoms.
What is the outlook for Chorea ? 
 The prognosis for individuals with chorea varies depending on the type of chorea and the associated disease. Huntington's disease is a progressive, and ultimately, fatal disease. Syndenham's chorea is treatable and curable.
what research (or clinical trials) is being done for Chorea ? 
 The NINDS supports research on movement disorders such as chorea. The goals of this research are to increase understanding of these disorders and to find ways to prevent and treat them.
What is (are) Ohtahara Syndrome ? 
 Ohtahara syndrome is a neurological disorder characterized by seizures. The disorder affects newborns, usually within the first three months of life (most often within the first 10 days) in the form of epileptic seizures. Infants have primarily tonic seizures, but may also experience partial seizures, and rarely, myoclonic seizures. Ohtahara syndrome is most commonly caused by metabolic disorders or structural damage in the brain, although the cause or causes for many cases cant be determined. Most infants with the disorder show significant underdevelopment of part or all of the cerebral hemispheres. The EEGs of infants with Ohtahara syndrome reveal a characteristic pattern of high voltage spike wave discharge followed by little activity. This pattern is known as burst suppression. Doctors have observed that boys are more often affected than girls.
What are the treatments for Ohtahara Syndrome ? 
 Antiepileptic drugs are used to control seizures, but are unfortunately not usually very effective for this disorder. Corticosteroids are occasionally helpful. In cases where there is a focal brain lesion (damage contained to one area of the brain) surgery may be beneficial. Other therapies are symptomatic and supportive.
What is the outlook for Ohtahara Syndrome ? 
 The course of Ohtahara syndrome is severely progressive. Seizures become more frequent, accompanied by delays in physical and cognitive development.Some children will die in infancy; others will survive but be profoundly handicapped. As they grow, some children will progress into other epileptic disorders such as West syndrome and Lennox-Gestaut syndrome.
what research (or clinical trials) is being done for Ohtahara Syndrome ? 
 The NINDS conducts and supports an extensive research program on seizures and seizure-related disorders. Much of this research is aimed at increasing scientific understanding of these disorders and finding ways to prevent, treat, and potentially cure them.
What is (are) Postural Tachycardia Syndrome ? 
 Postural orthostatic tachycardia syndrome (POTS) is one of a group of disorders that have orthostatic intolerance (OI) as their primary symptom. OI describes a condition in which an excessively reduced volume of blood returns to the heart after an individual stands up from a lying down position. The primary symptom of OI is lightheadedness or fainting. In POTS, the lightheadedness or fainting is also accompanied by a rapid increase in heartbeat of more than 30 beats per minute, or a heart rate that exceeds 120 beats per minute, within 10 minutes of rising. The faintness or lightheadedness of POTS are relieved by lying down again. Anyone at any age can develop POTS, but the majority of individuals affected (between 75 and 80 percent) are women between the ages of 15 to 50 years of age. Some women report an increase in episodes of POTS right before their menstrual periods. POTS often begins after a pregnancy, major surgery, trauma, or a viral illness. It may make individuals unable to exercise because the activity brings on fainting spells or dizziness.
                
Doctors aren't sure yet what causes the reduced return of blood to the heart that occurs in OI, or why the heart begins to beat so rapidly in POTS. Current thinking is that there are a number of mechanisms. Some individuals have peripheral denervation (neuropathic POTS); some have symptoms that are due to sustained or parosyxmal overactivity of the sympathetic nervous system (hyperadrenergic POTS); and many individuals with POTS have significant deconditioning.
What are the treatments for Postural Tachycardia Syndrome ? 
 Therapies for POTS are targeted at relieving low blood volume or regulating circulatory problems that could be causing the disorder. No single treatment has been found to be effect for all. A number of drugs seem to be effective in the short term. Whether they help in long term is uncertain. Simple interventions such as adding extra salt to the diet and attention to adequate fluid intake are often effective. The drugs fludrocortisone (for those on a high salt diet) and midodrine in low doses are often used to increase blood volume and narrow blood vessels. Drinking 16 ounces of water (2 glassfuls) before getting up can also help raise blood pressure. Some individuals are helped by beta receptor blocking agents. There is some evidence that an exercise program can gradually improve orthostatic tolerance.
What is the outlook for Postural Tachycardia Syndrome ? 
 POTS may follow a relapsing-remitting course, in which symptoms come and go, for years. In most cases (approximately 80 percent), an individual with POTS improves to some degree and becomes functional, although some residual symptoms are common.
what research (or clinical trials) is being done for Postural Tachycardia Syndrome ? 
 The National Institute of Neurological Disorders and Stroke (NINDS) and other Institutes of the National Institutes of Health (NIH) conduct research related to POTS and support additional research 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 such as POTS. NINDS-funded researchers are investigating if low levels of the hormone aldosterone contribute to low blood volume in individuals with POTS, and if high levels of angiotensin II, a peptide that helps regulate blood volume, leads to decreased adrenal sensitivity. Other NINDS-funded research is investigating the hypothesis that POTS is a syndrome of different subtypes, with different underlying mechanisms. Additionally, the NINDS funds the Autonomic Rare Diseases Consortium to further understand disorders such as orthostatic hypotension and hopefully alter the course of disease.
What is (are) Rasmussen's Encephalitis ? 
 Rasmussens encephalitis is a rare, chronic inflammatory neurological disease that usually affects only one hemisphere of the brain. It usually occurs in children under the age of 10 (more rarely in adolescents and adults), and is characterized by frequent and severe seizures, loss of motor skills and speech, paralysis on one side of the body (hemiparesis), inflammation of the brain (encephalitis), and mental deterioration. Most individuals with Rasmussens encephalitis will experience frequent seizures and progressive brain damage in the affected hemisphere of the brain over the course of the first 8 to 12 months, and then enter a phase of permanent, but stable, neurological deficits. Rasmussens encephalitis has features of an autoimmune disease in which immune system cells enter the brain and cause inflammation and damage.Research is ongoing into the causes of this rare disease.
What are the treatments for Rasmussen's Encephalitis ? 
 Anti-epileptic drugs are usually not effective in controlling seizures. Recent studies have shown some success with treatments that suppress or modulate the immune system, in particular those that use corticosteroids, intravenous immunoglobulin, or tacrolimus. Surgery to control seizures may be performed in later stages of the disease when neurological deficits stabilize. Surgical procedures, such as functional hemispherectomy and hemispherotomy, may reduce the frequency of seizures and also improve behavior and cognitive abilities.
What is the outlook for Rasmussen's Encephalitis ? 
 The prognosis for individuals with Rasmussens encephalitis varies. Despite the advances in medical treatment, none has yet been shown to halt the progress of the disease in the long term. The disorder may lead to severe neurological deficits or it may cause only milder impairments. For some children, surgery decreases seizures. However, most individuals with Rasmussens encephalitis are left with some paralysis, cognitive deficits, and problems with speech. In some cases, the disease can progress to involve the opposite brain hemisphere.
what research (or clinical trials) is being done for Rasmussen's Encephalitis ? 
 The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to Rasmussens encephalitis in its laboratories at the National Institutes of Health (NIH), and also supports additional research through grants to major research institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure progressive neurological disorders, such as Rasmussens encephalitis.
What is (are) Sydenham Chorea ? 
 Sydenham chorea (SD) is a neurological disorder of childhood resulting from infection via Group A beta-hemolytic streptococcus (GABHS), the bacterium that causes rheumatic fever. SD is characterized by rapid, irregular, and aimless involuntary movements of the arms and legs, trunk, and facial muscles. It affects girls more often than boys and typically occurs between 5 and 15 years of age. Some children will have a sore throat several weeks before the symptoms begin, but the disorder can also strike up to 6 months after the fever or infection has cleared. Symptoms can appear gradually or all at once, and also may include uncoordinated movements, muscular weakness, stumbling and falling, slurred speech, difficulty concentrating and writing, and emotional instability. The symptoms of SD can vary from a halting gait and slight grimacing to involuntary movements that are frequent and severe enough to be incapacitating. The random, writhing movements of chorea are caused by an auto-immune reaction to the bacterium that interferes with the normal function of a part of the brain (the basal ganglia) that controls motor movements. Due to better sanitary conditions and the use of antibiotics to treat streptococcal infections, rheumatic fever, and consequently SD, are rare in North America and Europe. The disease can still be found in developing nations.
What are the treatments for Sydenham Chorea ? 
 There is no specific treatment for SD. For people with the mildest form, bed rest during the period of active movements is sufficient. When the severity of movements interferes with rest, sedative drugs, such as barbiturates or benzodiazepines, may be needed. Antiepileptic medications, such as valproic acid, are often prescribed. Doctors also recommend that children who have had SD take penicillin over the course of the next 10 years to prevent additional manifestations of rheumatic fever.
What is the outlook for Sydenham Chorea ? 
 Most children recover completely from SD, although a small number will continue to have disabling, persistent chorea despite treatment. The duration of symptoms varies, generally from 3 to 6 weeks, but some children will have symptoms for several months. Cardiac complications may occur in a small minority of children, usually in the form of endocarditis. In a third of the children with the disease, SD will recur, typically 1  to 2  years after the initial attack. Researchers have noted an association between recurrent SD and the later development of the abrupt onset forms of obsessive-compulsive disorder, attention deficit/hyperactivity disorder, tic disorders, and autism, which they call PANDAS, for Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus infection. Further studies are needed to determine the nature of the association and the biological pathways that connect streptococcal infection, autoimmune response, and the later development of these specific behavioral disorders.
what research (or clinical trials) is being done for Sydenham Chorea ? 
 The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to SD in laboratories at the NIH, and support additional research through grants to major medical institutions across the country. Currently, researchers are studying how the interplay of genetic, developmental, and environmental factors could determine a childs vulnerability to SD after a GABHS infection. Other researchers are exploring whether children whose symptoms either begin or get worse following a GABHS infection share a common set of abnormal biomolecular pathways responsible for their similar clinical symptoms.
What is (are) Fahr's Syndrome ? 
 Fahr's Syndrome is a rare, genetically dominant, inherited neurological disorder characterized by abnormal deposits of calcium in areas of the brain that control movement, including the basal ganglia and the cerebral cortex. Symptoms of the disorder may include deterioration of motor function, dementia, seizures, headache, dysarthria (poorly articulated speech), spasticity (stiffness of the limbs) and spastic paralysis, eye impairments, and athetosis (involuntary, writhing movements). Fahr's Syndrome can also include symptoms characteristic of Parkinson's disease such as tremors, muscle rigidity, a mask-like facial appearance, shuffling gait, and a "pill-rolling" motion of the fingers. These symptoms generally occur later in the development of the disease. More common symptoms include dystonia (disordered muscle tone) and chorea (involuntary, rapid, jerky movements). Age of onset is typically in the 40s or 50s, although it can occur at any time in childhood or adolescence.
What are the treatments for Fahr's Syndrome ? 
 There is no cure for Fahr's Syndrome, nor is there a standard course of treatment. Treatment addresses symptoms on an individual basis.
What is the outlook for Fahr's Syndrome ? 
 The prognosis for any individual with Fahr's Syndrome is variable and hard to predict. There is no reliable correlation between age, extent of calcium deposits in the brain, and neurological deficit. Since the appearance of calcification is age-dependent, a CT scan could be negative in a gene carrier who is younger than the age of 55.
what research (or clinical trials) is being done for Fahr's Syndrome ? 
 The NINDS supports and conducts research on neurogenetic disorders such as Fahr's Syndrome. The goals of this research are to locate and understand the actions of the genes involved in this disorder. Finding these genes could lead to effective ways to treat and prevent Fahr's Syndrome.
What is (are) Lactose Intolerance ? 
 Lactose is a sugar found in milk and milk products. The small intestinethe organ where most food digestion and nutrient absorption take placeproduces an enzyme called lactase. Lactase breaks down lactose into two simpler forms of sugar: glucose and galactose. The body then absorbs these simpler sugars into the bloodstream.