Ahmed062646/NLP_Medora_Datasets huggingface dataset:
Question: What is the outlook for Transverse Myelitis ?
Answer: Most individuals will have only one episode of transverse myelitis. Recovery usually begins within 2 to 12 weeks of the onset of symptoms and may continue for up to 2 years and in some cases longer--requiring aggressive physical therapy and rehabilitation. However, if there is no improvement within the first 3 to 6 months, complete recovery is unlikely (although some recovery can occur). Historic data, shows that about one-third of people affected with transverse myelitis experience good or full recovery from their symptoms. Another one-third show only fair recovery and are left with significant deficits. The remaining one-third show no recovery at all, with marked dependence on others for basic functions of daily living. New, more aggressive treatment protocols may result in greater recovery statistics.
Question: what research (or clinical trials) is being done for Transverse Myelitis ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to transverse myelitis in its laboratories at the National Institutes of Health (NIH), and also supports additional transverse myelitis research through grants to major medical institutions across the country. Some studies focus on strategies to repair the spinal cord, including approaches using cell transplantation. The NINDS also funds researchers who are using animal models of spinal cord injury to study strategies for replacement or regeneration of spinal cord nerve cells. The knowledge gained from such research should lead to a greater knowledge of the mechanisms responsible for transverse myelitis and may ultimately provide a means to prevent and treat this disorder.
Question: What is (are) Encephalitis Lethargica ?
Answer: Encephalitis lethargica is a disease characterized by high fever, headache, double vision, delayed physical and mental response, and lethargy. In acute cases, patients may enter coma. Patients may also experience abnormal eye movements, upper body weakness, muscular pains, tremors, neck rigidity, and behavioral changes including psychosis. The cause of encephalitis lethargica is unknown. Between 1917 to 1928, an epidemic of encephalitis lethargica spread throughout the world, but no recurrence of the epidemic has since been reported. Postencephalitic Parkinson's disease may develop after a bout of encephalitis-sometimes as long as a year after the illness.
Question: What are the treatments for Encephalitis Lethargica ?
Answer: Treatment for encephalitis lethargica is symptomatic. Levodopa and other antiparkinson drugs often produce dramatic responses.
Question: What is the outlook for Encephalitis Lethargica ?
Answer: The course of encephalitis lethargica varies depending upon complications or accompanying disorders.
Question: what research (or clinical trials) is being done for Encephalitis Lethargica ?
Answer: The NINDS supports research on disorders that affect the brain, such as encephalitis lethargica, with the goal of finding ways to prevent and treat them. (The disease was the subject of the book and film, "Awakenings.")
Question: What is (are) Dystonias ?
Answer: The dystonias are movement disorders in which sustained muscle contractions cause twisting and repetitive movements or abnormal postures. The movements, which are involuntary and sometimes painful, may affect a single muscle; a group of muscles such as those in the arms, legs, or neck; or the entire body. Early symptoms may include deterioration in handwriting, foot cramps, or a dragging foot after running or walking some distance. Other possible symptoms are tremor and voice or speech difficulties. About half the cases of dystonia have no connection to disease or injury and are called primary or idiopathic dystonia. Of the primary dystonias, many cases appear to be inherited. Dystonias can also be symptoms of other diseases, some of which may be hereditary. Dystonia can occur at any age, but is often described as either early, or childhood, onset versus adult onset.
Question: What are the treatments for Dystonias ?
Answer: No one treatment has been found to be universally effective. Instead, doctors use a variety of therapies (medications, surgery, and other treatments such as physical therapy, splinting, stress management, and biofeedback) aimed at reducing or eliminating muscle spasms and pain. Since response to drugs varies among individuals and even in the same person over time, the most effective therapy is often individualized.
Question: What is the outlook for Dystonias ?
Answer: The initial symptoms can be very mild and may be noticeable only after prolonged exertion, stress, or fatigue. Dystonias often progress through various stages. Initially, dystonic movements are intermittent and appear only during voluntary movements or stress. Later, individuals may show dystonic postures and movements while walking and ultimately even while they are relaxed. Dystonic motions may lead to permanent physical deformities by causing tendons to shorten.
Question: what research (or clinical trials) is being done for Dystonias ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to dystonia in its laboratories at the National Institutes of Health (NIH) and also supports additional dystonia research through grants to major research institutions across the country. Scientists at other NIH Institutes (National institute on Deafness and Other Communications Disorders, National Eye Institute, and Eunice Kennnedy Shriver National Institute on Child Health and Human Development) also support research that may benefit individuals with dystonia. Investigators believe that the dystonias result from an abnormality in an area of the brain called the basal ganglia, where some of the messages that initiate muscle contractions are processed. Scientists at the NINDS laboratories have conducted detailed investigations of the pattern of muscle activity in persons with dystonias. Studies using EEG analysis and neuroimaging are probing brain activity. The search for the gene or genes responsible for some forms of dominantly inherited dystonias continues.
Question: What is (are) Dandy-Walker Syndrome ?
Answer: Dandy-Walker Syndrome is a congenital brain malformation involving the cerebellum (an area of the back of the brain that coordinates movement) and the fluid-filled spaces around it. The key features of this syndrome are an enlargement of the fourth ventricle (a small channel that allows fluid to flow freely between the upper and lower areas of the brain and spinal cord), a partial or complete absence of the area of the brain between the two cerebellar hemispheres (cerebellar vermis), and cyst formation near the lowest part of the skull. An increase in the size and pressure of the fluid spaces surrounding the brain (hydrocephalus) may also be present. The syndrome can appear dramatically or develop unnoticed. Symptoms, which often occur in early infancy, include slow motor development and progressive enlargement of the skull. In older children, symptoms of increased intracranial pressure (pressure within the skull) such as irritability and vomiting, and signs of cerebellar dysfunction such as unsteadiness, lack of muscle coordination, or jerky movements of the eyes may occur. Other symptoms include increased head circumference, bulging at the back of the skull, abnormal breathing problems, and problems with the nerves that control the eyes, face and neck. Dandy-Walker Syndrome is sometimes associated with disorders of other areas of the central nervous system, including absence of the area made up of nerve fibers connecting the two cerebral hemispheres (corpus callosum) and malformations of the heart, face, limbs, fingers and toes.
Question: What are the treatments for Dandy-Walker Syndrome ?
Answer: Treatment for individuals with Dandy-Walker Syndrome generally consists of treating the associated problems, if needed. A surgical procedure called a shunt may be required to drain off excess fluid within the brain, which will reduce pressure inside the skull and improve symptoms. Treatment may also include various forms of therapy (physicial, occupational) and specialized education.
Question: What is the outlook for Dandy-Walker Syndrome ?
Answer: The effect of Dandy-Walker Syndrome on intellectual development is variable, with some children having normal cognition and others never achieving normal intellectual development even when the excess fluid buildup is treated early and correctly. Longevity depends on the severity of the syndrome and associated malformations. The presence of multiple congenital defects may shorten life span.
Question: what research (or clinical trials) is being done for Dandy-Walker Syndrome ?
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 NINDS conducts and supports a wide range of studies that explore the complex mechanisms of normal brain development. Researchers are studying DNA samples from individuals with Dandy-Walker syndrome to identify genes involved with the syndrome, as well as to better understand its causes and improve diagnosis and treatment options. Other research indicates that mothers with diabetes and those with rubella (German measles) during pregnancy are more likely to have a child with Dandy-Walker syndrome.
Question: What is (are) Chiari Malformation ?
Answer: Chiari malformations (CMs) are structural defects in the cerebellum, the part of the brain that controls balance. When the indented bony space at the lower rear of the skull is smaller than normal, the cerebellum and brain stem can be pushed downward. The resulting pressure on the cerebellum can block the flow of cerebrospinal fluid (the liquid that surrounds and protects the brain and spinal cord) and can cause a range of symptoms including dizziness, muscle weakness, numbness, vision problems, headache, and problems with balance and coordination. Symptoms may change for some individuals depending on buildup of CNS and any resulting pressure on tissue and nerves. CMs are classified by the severity of the disorder and the parts of the brain that protrude into the spinal canal. The most common is Type I, which may not cause symptoms and is often found by accident during an examination for another condition. Type II (also called Arnold-Chiari malformation) is usually accompanied by a myelomeningocele-a form of spina bifida that occurs when the spinal canal and backbone do not close before birth, causing the spinal cord to protrude through an opening in the back. This can cause partial or complete paralysis below the spinal opening. Type III is the most serious form of CM, and causes severe neurological defects. Other conditions sometimes associated with CM include hydrocephalus, syringomyelia (a fluid-filled cyst in the spinal cord), and spinal curvature.
Question: What are the treatments for Chiari Malformation ?
Answer: Medications may ease certain symptoms, such as pain. Surgery is the only treatment available to correct functional disturbances or halt the progression of damage to the central nervous system. More than one surgery may be needed to treat the condition. Some CMs have no noticeable symptoms and do not interfere with the person's activities of daily living.
Question: What is the outlook for Chiari Malformation ?
Answer: Many people with Type I CM are asymptomatic and do not know they have the condition. Many individuals with the more severe types of CM and have surgery see a reduction in their symptoms and/or prolonged periods of relative stability, although paralysis is generally permanent.
Question: what research (or clinical trials) is being done for Chiari Malformation ?
Answer: The NINDS supports research on disorders of the brain and nervous system such as Chiari malformations. The goals of this research are to increase scientific understanding of these disorders and to find ways to prevent, treat, and, ultimately, cure them. Current NINDS-funded research includes studies to better understand the genetic factors responsible for the malformation, and factors that influence the development, progression, and relief of symptoms among people with syringomyelia, including those with Chiari I malformations.
Question: What is (are) Atrial Fibrillation and Stroke ?
Answer: Atrial fibrillation (AF) describes the rapid, irregular beating of the left atrium (upper chamber) of the heart. These rapid contractions of the heart are weaker than normal contractions, resulting in slow flow of blood in the atrium. The blood pools and becomes sluggish and can result in the formation of blood clots. If a clot leaves the heart and travels to the brain, it can cause a stroke by blocking the flow of blood through cerebral arteries. Some people with AF have no symptoms, but others may experience a fluttering feeling in the area of the chest above the heart, chest pain, lightheadness or fainting, shortness of breath, and fatigue. AF is diagnosed by an electrocardiogram (ECG), a device that records the hearts electrical activity. Other tests are often performed to rule out contributing causes, such as high blood pressure, an overactive thyroid gland, heart failure, faulty heart valves, lung disease, and stimulant or alcohol abuse. Some people will have no identifiable cause for their AF.
Question: What are the treatments for Atrial Fibrillation and Stroke ?
Answer: Within a few hours after onset of a stroke, treatment with drugs or devices that dissolve or break up the clot can restore blood flow to the brain and lead to a better recovery. To prevent strokes related to AF, doctors often prescribe medications to prevent formation of clots in the heart, which can travel to the brain and cause stroke. Immediately after a stroke, doctors may temporarily administer heparin by injection, while starting an oral medication for long-term protection from clots. The most commonly used drug has been warfarin. People taking warfarin must be closely monitored to make sure their blood is thin enough to prevent clots, but not so thin as to promote bleeding. Since some foods, vitamin supplements, and medications can affect warfarin action, keeping the blood just thin enough can be tricky. More recently, a number of new blood thinners, including dabigatran, rivaroxaban, and apixaban, have been shown to be as effective as warfarin in stroke prevention. These newer medications do not require regular blood test monitoring and may have less tendency to cause bleeding due to making the blood too thin. Some individuals with AF may have a lower risk of stroke and may be treated with aspirin, either alone or with another antiplatelet agency like clopidogrel. Other treatments for AF include medications such as beta blockers or calcium channel blockers to slow the heartbeat, and anti-arrhythmic drugs or electrical cardioversion (which delivers an electrical shock to the heart) to normalize the heartbeat.
Question: What is the outlook for Atrial Fibrillation and Stroke ?
Answer: AF, which affects as many as 2.2 million Americans, increases an individuals risk of stroke by 4 to 6 times on average. The risk increases with age. In people over 80 years old, AF is the direct cause of 1 in 4 strokes. Treating individuals with warfarin or new blood thinners reduces the rate of stroke for those who have AF by approximately one-half to two- thirds. People with AF can have multiple strokes, including silent strokes (strokes that don't show physical symptoms but show up on a brain scan) that, over time, can cause dementia, so prevention is important.
Question: what research (or clinical trials) is being done for Atrial Fibrillation and Stroke ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS) is the leading Federal agency directing and funding research relevant to AF and stroke prevention. The NINDS conducts basic and clinical research in its laboratories and clinics 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 disorders such as AF that can increase the risk of stroke.
Question: What is (are) X-linked congenital stationary night blindness ?
Answer: X-linked congenital stationary night blindness is a disorder of the retina, which is the specialized tissue at the back of the eye that detects light and color. People with this condition typically have difficulty seeing in low light (night blindness). They also have other vision problems, including loss of sharpness (reduced acuity), severe nearsightedness (high myopia), involuntary movements of the eyes (nystagmus), and eyes that do not look in the same direction (strabismus). Color vision is typically not affected by this disorder. The vision problems associated with this condition are congenital, which means they are present from birth. They tend to remain stable (stationary) over time. Researchers have identified two major types of X-linked congenital stationary night blindness: the complete form and the incomplete form. The types have very similar signs and symptoms. However, everyone with the complete form has night blindness, while not all people with the incomplete form have night blindness. The types are distinguished by their genetic cause and by the results of a test called an electroretinogram, which measures the function of the retina.
Question: How many people are affected by X-linked congenital stationary night blindness ?
Answer: The prevalence of this condition is unknown. It appears to be more common in people of Dutch-German Mennonite descent. However, this disorder has been reported in families with many different ethnic backgrounds. The incomplete form is more common than the complete form.
Question: What are the genetic changes related to X-linked congenital stationary night blindness ?
Answer: Mutations in the NYX and CACNA1F genes cause the complete and incomplete forms of X-linked congenital stationary night blindness, respectively. The proteins produced from these genes play critical roles in the retina. Within the retina, the NYX and CACNA1F proteins are located on the surface of light-detecting cells called photoreceptors. The retina contains two types of photoreceptor cells: rods and cones. Rods are needed for vision in low light. Cones are needed for vision in bright light, including color vision. The NYX and CACNA1F proteins ensure that visual signals are passed from rods and cones to other retinal cells called bipolar cells, which is an essential step in the transmission of visual information from the eyes to the brain. Mutations in the NYX or CACNA1F gene disrupt the transmission of visual signals between photoreceptors and retinal bipolar cells, which impairs vision. In people with the complete form of X-linked congenital stationary night blindness (resulting from NYX mutations), the function of rods is severely disrupted, while the function of cones is only mildly affected. In people with the incomplete form of the condition (resulting from CACNA1F mutations), rods and cones are both affected, although they retain some ability to detect light.
Question: Is X-linked congenital stationary night blindness inherited ?
Answer: This condition is inherited in an X-linked recessive pattern. The NYX and CACNA1F genes are located on the X chromosome, which is one of the two sex chromosomes. In males (who have only one X chromosome), one altered copy of the gene in each cell is sufficient to cause the condition. In females (who have two X chromosomes), a mutation would have to occur in both copies of the gene to cause the disorder. Because it is unlikely that females will have two altered copies of this gene, males are affected by X-linked recessive disorders much more frequently than females. A characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons. In X-linked recessive inheritance, a female with one altered copy of the gene in each cell is called a carrier. Carriers of an NYX or CACNA1F mutation can pass on the mutated gene, but most do not develop any of the vision problems associated with X-linked congenital stationary night blindness. However, carriers may have retinal changes that can be detected with an electroretinogram.
Question: What are the treatments for X-linked congenital stationary night blindness ?
Answer: These resources address the diagnosis or management of X-linked congenital stationary night blindness: - American Optometric Association: Infant Vision - Gene Review: Gene Review: X-Linked Congenital Stationary Night Blindness - Genetic Testing Registry: Congenital stationary night blindness - Genetic Testing Registry: Congenital stationary night blindness, type 1A - Genetic Testing Registry: Congenital stationary night blindness, type 2A - MedlinePlus Encyclopedia: Electroretinography - MedlinePlus Encyclopedia: Eye movements - Uncontrollable - MedlinePlus Encyclopedia: Nearsightedness - MedlinePlus Encyclopedia: Strabismus - MedlinePlus Encyclopedia: Vision - Night Blindness These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
Question: What is (are) Brugada syndrome ?
Answer: Brugada syndrome is a condition that causes a disruption of the heart's normal rhythm. Specifically, this disorder can lead to irregular heartbeats in the heart's lower chambers (ventricles), which is an abnormality called ventricular arrhythmia. If untreated, the irregular heartbeats can cause fainting (syncope), seizures, difficulty breathing, or sudden death. These complications typically occur when an affected person is resting or asleep. Brugada syndrome usually becomes apparent in adulthood, although it can develop any time throughout life. Signs and symptoms related to arrhythmias, including sudden death, can occur from early infancy to late adulthood. Sudden death typically occurs around age 40. This condition may explain some cases of sudden infant death syndrome (SIDS), which is a major cause of death in babies younger than 1 year. SIDS is characterized by sudden and unexplained death, usually during sleep. Sudden unexplained nocturnal death syndrome (SUNDS) is a condition characterized by unexpected cardiac arrest in young adults, usually at night during sleep. This condition was originally described in Southeast Asian populations, where it is a major cause of death. Researchers have determined that SUNDS and Brugada syndrome are the same disorder.
Question: How many people are affected by Brugada syndrome ?
Answer: The exact prevalence of Brugada syndrome is unknown, although it is estimated to affect 5 in 10,000 people worldwide. This condition occurs much more frequently in people of Asian ancestry, particularly in Japanese and Southeast Asian populations. Although Brugada syndrome affects both men and women, the condition appears to be 8 to 10 times more common in men. Researchers suspect that testosterone, a sex hormone present at much higher levels in men, may account for this difference.