Druvith/transformed_medDataset huggingface dataset:
What are the treatments for Myasthenia Gravis ? 
 Myasthenia gravis can be controlled. Some medications improve neuromuscular transmission and increase muscle strength, and some suppress the production of abnormal antibodies. These medications must be used with careful medical follow up because they may cause major side effects. Thymectomy, the surgical removal of the thymus gland (which often is abnormal in those with myasthenia gravis), improves symptoms in certain individuals Other therapies include plasmapheresis, a procedure in which abnormal antibodies are removed from the blood, and high-dose intravenous immune globulin, which temporarily modifies the immune system and provides the body with normal antibodies from donated blood.
What is the outlook for Myasthenia Gravis ? 
 With treatment, most individuals with myasthenia can significantly improve their muscle weakness. Some case of myasthenia gravis may go into remission temporarily, and muscle weakness may disappear so that medications can be discontinued. In a few cases, the severe weakness of myasthenia gravis may cause respiratory failure, which requires immediate emergency medical care.
what research (or clinical trials) is being done for Myasthenia Gravis ? 
 Scientists are evaluating new and improving current treatments for myasthenia gravis. Different drugs are being tested, either alone or in combination with existing drug therapies, to see if they are effective in treating the disorder. One study seeks to understand the molecular basis of synaptic transmission in the nervous system. Thymectomy is being studied in individuals who do not have thymoma, to assess long-term benefit the surgery may have over medical therapy alone. And investigators are examining the safety and efficacy of autologous hematopoietic stem cell transplantation to treat refractory and severe myasthenia gravis.
What is (are) Spinal Muscular Atrophy ? 
 Spinal Muscular Atrophy (SMA) Types I, II, and III belong to a group of hereditary diseases that cause weakness and wasting of the voluntary muscles in the arms and legs of infants and children. The disorders are caused by an abnormal or missing gene known as the survival motor neuron gene 1 (SMN1), which is responsible for the production of a protein essential to motor neurons. Without this protein, lower motor neurons in the spinal cord degenerate and die. The type of SMA (I, II, or III) is determined by the age of onset and the severity of symptoms. Type I (also known as Werdnig-Hoffman disease, or infantile-onset SMA) is evident at birth or within the first few months. Symptoms include floppy limbs and trunk, feeble movements of the arms and legs, swallowing and feeding difficulties, and impaired breathing. Type II (the intermediate form) usually begins 6 and 18 months of age. Legs tend to be more impaired than arms. Children with Type II may able to sit and some may be able to stand or walk with help. Symptoms of Type III (also called Kugelberg-Welander disease) appear between 2 and 17 years of age and include difficulty running, climbing steps, or rising from a chair. The lower extremities are most often affected. Complications include scoliosis and chronic shortening of muscles or tendons around joints.
What are the treatments for Spinal Muscular Atrophy ? 
 There is no cure for SMA. Treatment consists of managing the symptoms and preventing complications.
What is the outlook for Spinal Muscular Atrophy ? 
 The prognosis is poor for babies with SMA Type I. Most die within the first two years. For children with SMA Type II, the prognosis for life expectancy or for independent standing or walking roughly correlates with how old they are when they first begin to experience symptoms - older children tend to have less severe symptoms Life expectancy is reduced but some individuals live into adolescence or young adulthood. Individuals with SMA type III may be prone to respiratory infections but with care may have a normal lifespan.
what research (or clinical trials) is being done for Spinal Muscular Atrophy ? 
 Between 2003 and 2012, the NINDS piloted the Spinal Muscular Atrophy Project to expedite therapeutics development for this hereditary neurodegenerative disease. The Project was designed to accelerate the research process by identifying drugs that increase the level of SMN protein in cultured cells, so that they could be used as potential leads for further drug discovery and clinical testing. Read more about the history of this pioneering effort and how it led to collaboration with several pharmaceutical and biotechnology companies.
What is (are) Alzheimer's Disease ? 
 Alzheimer's disease (AD) is an age-related, non-reversible brain disorder that develops over a period of years. Initially, people experience memory loss and confusion, which may be mistaken for the kinds of memory changes that are sometimes associated with normal aging. However, the symptoms of AD gradually lead to behavior and personality changes, a decline in cognitive abilities such as decision-making and language skills, and problems recognizing family and friends. AD ultimately leads to a severe loss of mental function. These losses are related to the worsening breakdown of the connections between certain neurons in the brain and their eventual death. AD is one of a group of disorders called dementias that are characterized by cognitive and behavioral problems. It is the most common cause of dementia among people age 65 and older.
                
There are three major hallmarks in the brain that are associated with the disease processes of AD.
                
- Amyloid plaques, which are made up of fragments of a protein called beta-amyloid peptide mixed with a collection of additional proteins, remnants of neurons, and bits and pieces of other nerve cells. - Neurofibrillary tangles (NFTs), found inside neurons, are abnormal collections of a protein called tau. Normal tau is required for healthy neurons. However, in AD, tau clumps together. As a result, neurons fail to function normally and eventually die. - Loss of connections between neurons responsible for memory and learning. Neurons can't survive when they lose their connections to other neurons. As neurons die throughout the brain, the affected regions begin to atrophy, or shrink. By the final stage of AD, damage is widespread and brain tissue has shrunk significantly.
What are the treatments for Alzheimer's Disease ? 
 Currently there are no medicines that can slow the progression of AD. However, four FDA-approved medications are used to treat AD symptoms. These drugs help individuals carry out the activities of daily living by maintaining thinking, memory, or speaking skills. They can also help with some of the behavioral and personality changes associated with AD. However, they will not stop or reverse AD and appear to help individuals for only a few months to a few years. Donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne) are prescribed to treat mild to moderate AD symptoms. Donepezil was recently approved to treat severe AD as well. The newest AD medication is memantine (Namenda), which is prescribed to treat moderate to severe AD symptoms.
What is the outlook for Alzheimer's Disease ? 
 In very few families, people develop AD in their 30s, 40s, and 50s. This is known as "early onset" AD. These individuals have a mutation in one of three different inherited genes that causes the disease to begin at an earlier age. More than 90 percent of AD develops in people older than 65. This form of AD is called "late-onset" AD, and its development and pattern of damage in the brain is similar to that of early-onset AD. The course of this disease varies from person to person, as does the rate of decline. In most people with AD, symptoms first appear after age 65.
                
We don't yet completely understand the causes of late-onset AD, but they probably include genetic, environmental, and lifestyle factors. Although the risk of developing AD increases with age, AD and dementia symptoms are not a part of normal aging. There are also some forms of dementia that aren't related to brain diseases such as AD, but are caused by systemic abnormalities such as metabolic syndrome, in which the combination of high blood pressure, high cholesterol, and diabetes causes confusion and memory loss.
what research (or clinical trials) is being done for Alzheimer's Disease ? 
 The National Institute of Neurological Disorders and Stroke (NINDS) supports basic and translational research related to AD through grants to major medical institutions across the country. Current studies are investigating how the development of beta amyloid plaques damages neurons, and how abnormalities in tau proteins create the characteristic neurofibrillary tangles of AD. Other research is exploring the impact of risk factors associated with the development of AD, such as pre-existing problems with blood flow in the blood vessels of the brain. Most importantly, the NINDS supports a number of studies that are developing and testing new and novel therapies that can relieve the symptoms of AD and potentially lead to a cure.
                
On May 15, 2012 the Obama Administration announced the release of the National Alzheimers Plan. U.S. Secretary of Health and Human Services Kathleen Sebelius reaffirmed our nations commitment to conquering Alzheimers disease and related dementias, with a specific goal of finding effective ways to prevent and treat the disease by 2025.
What is (are) Incontinentia Pigmenti ? 
 Incontinentia pigmenti (IP) is an inherited disorder of skin pigmentation that is also associated with abnormalities of the teeth, skeletal system, eyes, and central nervous system. It is one of a group of gene-linked diseases known as neurocutaneous disorders. In most cases, IP is caused by mutations in a gene called NEMO (NF-kappaB essential modulator). Males are more severely affected than females. Discolored skin is caused by excessive deposits of melanin (normal skin pigment). Most newborns with IP will develop discolored skin within the first two weeks. The pigmentation involves the trunk and extremities, is slate-grey, blue or brown, and is distributed in irregular marbled or wavy lines. The discoloration fades with age. Neurological problems include loss of brain tissue (known as cerebral atrophy), the formation of small cavities in the central white matter of the brain, and the loss of neurons in the cerebellar cortex. About 20% of children with IP will have slow motor development, muscle weakness in one or both sides of the body, impaired cognitive development, and seizures. They are also likely to have visual problems, including crossed eyes, cataracts, and severe visual loss. Dental problems are also common, including missing or peg-shaped teeth. A related disorder, incontinentia pigmenti achromians, features skin patterns of light, unpigmented swirls and streaks that are the reverse of IP. Associated neurological problems are similar.
What are the treatments for Incontinentia Pigmenti ? 
 The skin abnormalities of IP usually disappear by adolescence or adulthood without treatment. Diminished vision may be treated with corrective lenses, medication, or, in severe cases, surgery. A specialist may treat dental problems. Neurological symptoms such as seizures, muscle spasms, or mild paralysis may be controlled with medication and/or medical devices and with the advice of a neurologist.
What is the outlook for Incontinentia Pigmenti ? 
 Although the skin abnormalities usually regress, and sometimes disappear completely, there may be residual neurological difficulties.
what research (or clinical trials) is being done for Incontinentia Pigmenti ? 
 Researchers have begun to use genetic linkage studies to map the location of genes associated with the neurocutaneous disorders. Research supported by the NINDS includes studies to understand how the brain and nervous system normally develop and function and how they are affected by genetic mutations. These studies contribute to a greater understanding of gene-linked disorders such as IP, and have the potential to open promising new avenues of treatment.
What is (are) Whipple's Disease ? 
 Whipple's disease is a multi-system infectious bacterial disease that interferes with the body's ability to metabolize fats. Caused by the bacterium Tropheryma whipplei, the disorder can affect any system in the body, including the brain, eyes, heart, joints, and lungs, but usually occurs in the gastrointestinal system. Neurological symptoms occur in up to 40 percent of individuals and may include dementia, abnormalities of eye and facial muscle movements, headaches, seizures, loss of muscle control, memory loss, weakness, and vision problems. Gastrointestinal symptoms may include diarrhea, weight loss, fatigue, weakness, and abdominal bleeding and pain. Fever, cough, anemia, heart and lung damage, darkening of the skin, and joint soreness may also be present. The disease is more common in men and neurological symptoms are more common in individuals who have severe abdominal disease, Rarely, neurological symptoms may appear without gastrointestinal symptoms and can mimic symptoms of almost any neurologic disease..
What are the treatments for Whipple's Disease ? 
 The standard treatment for Whipple's disease is a prolonged course of antibiotics (up to two years), including penicillin and cefriaxone or doxycycline with hydroxychloroquine. Sulfa drugs (sulfonamides) such as sulfadizine or solfamethoxazole can treat neurological symptoms. Relapsing neurologic Whipple's disease. (marked by bouts of worsening of symptoms) is sometimes treated with a combination of antibiotics and weekly injections of interfron gamma, a substance made by the body that activates the immune system.
What is the outlook for Whipple's Disease ? 
 Generally, long-term antibiotic treatment to destroy the bacteria can relieve symptoms and cure the disease. If left untreated, the disease is progressive and fatal. Individuals with involvement of the central nervous system generally have a worse prognosis and may be left with permanent neurologic disability. Deficits may persist and relapses may still occur in individuals who receive appropriate treatment in a timely fashion. Prognosis may improve with earlier recognition, diagnosis, and treatment of the disorder.
what research (or clinical trials) is being done for Whipple's Disease ? 
 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 supportsa broad range of research on disorders that affect the central nervous system. The National Institute of Diabetes and Digestive and Kidney Diseases also supports research on disorders such as Whipple's disease. Much of this research is aimed at learning more about these disorders and finding ways to prevent, treat, and, ultimately, cure them.
What is (are) Landau-Kleffner Syndrome ? 
 Landau-Kleffner syndrome (LKS) is a rare, childhood neurological disorder characterized by the sudden or gradual development of aphasia (the inability to understand or express language) and an abnormal electro-encephalogram (EEG). LKS affects the parts of the brain that control comprehension and speech. The disorder usually occurs in children between the ages of 5 and 7 years. Typically, children with LKS develop normally but then lose their language skills for no apparent reason. While many of the affected individuals have seizures, some do not. The disorder is difficult to diagnose and may be misdiagnosed as autism, pervasive developmental disorder, hearing impairment, learning disability, auditory/verbal processing disorder, attention deficit disorder, childhood schizophrenia, or emotional/behavioral problems.
What are the treatments for Landau-Kleffner Syndrome ? 
 Treatment for LKS usually consists of medications, such as anticonvulsants and corticosteroids, and speech therapy, which should be started early. A controversial treatment option involves a surgical technique called multiple subpial transection in which the pathways of abnormal electrical brain activity are severed
What is the outlook for Landau-Kleffner Syndrome ? 
 The prognosis for children with LKS varies. Some affected children may have a permanent severe language disorder, while others may regain much of their language abilities (although it may take months or years). In some cases, remission and relapse may occur. The prognosis is improved when the onset of the disorder is after age 6 and when speech therapy is started early. Seizures generally disappear by adulthood.
what research (or clinical trials) is being done for Landau-Kleffner Syndrome ? 
 The NINDS supports broad and varied programs of research on epilepsy and developmental disorders. This research is aimed at discovering new ways to prevent, diagnose, and treat epilepsy and developmental disorders and, ultimately, to find cures for them.
What is (are) Central Pain Syndrome ? 
 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.
What are the treatments for Central Pain Syndrome ? 
 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.
What is the outlook for Central Pain Syndrome ? 
 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.
what research (or clinical trials) is being done for Central Pain Syndrome ? 
 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.
What is (are) Complex Regional Pain Syndrome ? 
 Complex regional pain syndrome (CRPS) is a chronic pain condition. The key symptom of CRPS is continuous, intense pain out of proportion to the severity of the injury, which gets worse rather than better over time. CRPS most often affects one of the arms, legs, hands, or feet. Often the pain spreads to include the entire arm or leg. Typical features include dramatic changes in the color and temperature of the skin over the affected limb or body part, accompanied by intense burning pain, skin sensitivity, sweating, and swelling. Doctors arent sure what causes CRPS. In some cases the sympathetic nervous system plays an important role in sustaining the pain. Another theory is that CRPS is caused by a triggering of the immune response, which leads to the characteristic inflammatory symptoms of redness, warmth, and swelling in the affected area.
What are the treatments for Complex Regional Pain Syndrome ? 
 Because there is no cure for CRPS, treatment is aimed at relieving painful symptoms. Doctors may prescribe topical analgesics, antidepressants, corticosteroids, and opioids to relieve pain. However, no single drug or combination of drugs has produced consistent long-lasting improvement in symptoms. Other treatments may include physical therapy, sympathetic nerve block, spinal cord stimulation, and intrathecal drug pumps to deliver opioids and local anesthetic agents via the spinal cord.
What is the outlook for Complex Regional Pain Syndrome ? 
 The prognosis for CRPS varies from person to person. Spontaneous remission from symptoms occurs in certain individuals. Others can have unremitting pain and crippling, irreversible changes in spite of treatment.
what research (or clinical trials) is being done for Complex Regional Pain Syndrome ? 
 The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research relating to CRPS and also support additional research through grants to major medical institutions across the country. NINDS-supported scientists are studying new approaches to treat CRPS and intervene more aggressively after traumatic injury to lower the chances of developing the disorder. Researchers hope to identify specific cellular and molecular changes in sensory neurons following peripheral nerve injury to better understand the processes that underlie neuroplasticity (the brains ability to reorganize or form new nerve connections and pathways following injury or death of nerve cells). Identifying these mechanisms could provide targets for new drug therapies that could improve recovery following regeneration. Other researchers hope to better understand how CRPS develops by studying immune system activation and peripheral nerve signaling using an animal model of the disorder.
What is (are) Arteriovenous Malformation ? 
 Arteriovenous malformations (AVMs) are abnormal, snarled tangles of blood vessels that cause multiple irregular connections between the arteries and veins. These malformations most often occur in the spinal cord and in any part of the brain or on its surface, but can develop elsewhere in the body. AVMs can damage the brain and spinal cord by reducing the amount of oxygen reaching neurological tissues, bleeding into surrounding tissue (hemorrhage) that can cause stroke or brain damage, and by compressing or displacing parts of the brain or spinal cord. Many people with an AVM experience few, if any, significant symptoms, which can include headache, weakness, seizures, pain, and problems with speech, vision, or movement. Most often AVMs are congenital, but they can appear sporadically. In some cases the AVM may be inherited, but it is more likely that other inherited conditions increase the risk of having an AVM. The malformations tend to be discovered only incidentally, usually during treatment for an unrelated disorder or at autopsy.
What are the treatments for Arteriovenous Malformation ? 
 Treatment options depend on the type of AVM, its location, noticeable symptoms, and the general health condition of the individual. Medication can often alleviate general symptoms such as headache, back pain, and seizures caused by AVMs and other vascular lesions. The definitive treatment for AVMs is either surgery to either remove the AVM or to create an artificial blood clot to close the lesion or focused irradiation treatment that is designed to damage the blood vessel walls and close the lesion. The decision to treat an AVM requires a careful consideration of possible benefits versus risks.