Druvith/medqa1 huggingface dataset:
Question:  What is the outlook for Diabetic Neuropathy ?
Answer: The prognosis for diabetic neuropathy depends largely on how well the underlying condition of diabetes is handled. Treating diabetes may halt progression and improve symptoms of the neuropathy, but recovery is slow. The painful sensations of diabetic neuropathy may become severe enough to cause depression in some patients.
Question:  what research (or clinical trials) is being done for Diabetic Neuropathy ?
Answer: The NINDS conducts and supports research on diabetic neuropathy to increase understanding of the disorder and find ways to prevent and cure it. New medications are currently being examined to assess improvement or stabilization of neuropathic symptoms.
Question:  What is (are) Wernicke-Korsakoff Syndrome ?
Answer: Wernicke's encephalopathy is a degenerative brain disorder caused by the lack of thiamine (vitamin B1). It may result from alcohol abuse, dietary deficiencies, prolonged vomiting, eating disorders, or the effects of chemotherapy. B1 deficiency causes damage to the brain's thalamus and hypothalamus. Symptoms include mental confusion, vision problems, coma, hypothermia, low blood pressure, and lack of muscle coordination (ataxia). Korsakoff syndrome (also called Korsakoff's amnesic syndrome) is a memory disorder that results from vitamin B1 deficiency and is associated with alcoholism. Korsakoff's syndrome damages nerve cells and supporting cells in the brain and spinal cord, as well as the part of the brain involved with memory. Symptoms include amnesia, tremor, coma, disorientation, and vision problems, The disorder's main features are problems in acquiring new information or establishing new memories, and in retrieving previous memories. Although Wernicke's and Korsakoff's are related disorders, some scientists believe them to be different stages of the same disorder, which is called Wernicke-Korsakoff syndrome. Wernicke's encephalopathy represents the "acute" phase of the disorder and Korsakoff's amnesic syndrome represents the disorder progressing to a "chronic" or long-lasting stage.
Question:  What are the treatments for Wernicke-Korsakoff Syndrome ?
Answer: Treatment involves replacement of thiamine and providing proper nutrition and hydration. In some cases, drug therapy is also recommended.Stopping alcohol use may prevent further nerve and brain damage. In individuals with Wernicke's encephalopathy, it is very important to start thiamine replacement before beginning nutritional replenishment.
Question:  What is the outlook for Wernicke-Korsakoff Syndrome ?
Answer: Most symptoms of Wernicke's encephalopathy can be reversed if detected and treated promptly and completely. Stopping alcohol use may prevent further nerve and brain damage. However, improvement in memory function is slow and, usually, incomplete. Without treatment, these disorders can be disabling and life-threatening.
Question:  what research (or clinical trials) is being done for Wernicke-Korsakoff 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 supports research on neurological disorders such as Wernicke's encephalopathy, Korsakoff's amnesic syndrome, and Wernicke-Korsakoff syndrome, to expand our understanding of the functional changes of the diseases and ways to treat them..One areas of research is studying how exercise can improve cognitive functioning based on modulation of certain nerve cells in a rodent model of amnesia produced by by thiamine deficiency. The National Institute of Alcohol Abuse and Alcoholism also supports research on these disorders.
Question:  What is (are) Cerebellar Degeneration ?
Answer: Cerebellar degeneration is a process in which neurons in the cerebellum - the area of the brain that controls coordination and balance - deteriorate and die. Diseases that cause cerebellar degeneration can also involve other areas of the central nervous system,including the spinal cord, medulla oblongata, cerebral cortex, and brain stem. Cerebellar degeneration may be the result of inherited genetic mutations that alter the normal production of specific proteins that are necessary for the survival of neurons.
                
Associated diseases: Diseases that are specific to the brain, as well as diseases that occur in other parts of the body, can cause neurons to die in the cerebellum. Neurological diseases that feature cerebellar degeneration include:
                
- ischemic or hemorrhagic stroke, when there is lack of blood flow or oxygen to the cerebellum - cerebellar cortical atrophy, multisystem atrophy, and olivopontocerebellar degeneration, progressive degenerative disorders in which cerebellar degeneration is a key feature - Friedreichs ataxia, and other spinocerebellar ataxias, which are caused by inherited genetic mutations that result in ongoing loss of neurons in the cerebellum, brain stem, and spinal cord - transmissible spongiform encephalopathies (such as Creutzfeldt-Jakob disease) in which abnormal proteins cause inflammation in the brain, including the cerebellum - multiple sclerosis, in which damage to the insulating membrane (myelin) that wraps around and protects nerve cells can involve the cerebellum  Other diseases that can cause cerebellar degeneration include: - chronic alcohol abuse that leads to temporary or permanent cerebellar damage - paraneoplastic disorders, in which a malignancy (cancer) in other parts of the body produces substances that cause immune system cells to attack neurons in the cerebellum  Symptoms of cerebellar degeneration: The most characteristic symptom of cerebellar degeneration is a wide-based, unsteady, lurching walk, often accompanied by a back and forth tremor in the trunk of the body. Other symptoms may include slow, unsteady and jerky movement of the arms or legs, slowed and slurred speech, and nystagmus -- rapid, small movements of the eyes.
Question:  what research (or clinical trials) is being done for Cerebellar Degeneration ?
Answer: The NINDS funds research to find the genes involved in diseases that cause cerebellar degeneration. Discovering these genes, identifying their mutations, and understanding how the abnormal proteins they produce cause cerebellar degeneration may eventually help scientists find ways to prevent, treat, and even cure the diseases that involve cerebellar degeneration.
Question:  What is (are) Parry-Romberg ?
Answer: Parry-Romberg syndrome is a rare disorder characterized by slowly progressive deterioration (atrophy) of the skin and soft tissues of half of the face (hemifacial atrophy), usually the left side. It is more common in females than in males. Initial facial changes usually involve the tissues above the upper jaw (maxilla) or between the nose and the upper corner of the lip (nasolabial fold) and subsequently progress to the angle of the mouth, areas around the eye, the brow, the ear, and the neck. The deterioration may also affect the tongue, the soft and fleshy part of the roof of the mouth, and the gums. The eye and cheek of the affected side may become sunken and facial hair may turn white and fall out (alopecia). In addition, the skin overlying affected areas may become darkly pigmented (hyperpigmentation) with, in some cases, areas of hyperpigmentation and patches of unpigmented skin (vitiligo). Parry-Romberg syndrome is also accompanied by neurological abnormalities including seizures and episodes of severe facial pain (trigeminal neuralgia). The onset of the disease usually begins between the ages of 5 and 15 years. The progression of the atrophy often lasts from 2 to 10 years, and then the process seems to enter a stable phase. Muscles in the face may atrophy and there may be bone loss in the facial bones. Problems with the retina and optic nerve may occur when the disease surrounds the eye.
Question:  What are the treatments for Parry-Romberg ?
Answer: There is no cure and there are no treatments that can stop the progression of Parry-Romberg syndrome. Reconstructive or microvascular surgery may be needed to repair wasted tissue. The timing of surgical intervention is generally agreed to be the best following exhaustion of the disease course and completion of facial growth. Most surgeons will recommend a waiting period of one or two years before proceeding with reconstruction. Muscle or bone grafts may also be helpful. Other treatment is symptomatic and supportive.
Question:  What is the outlook for Parry-Romberg ?
Answer: The prognosis for individuals with Parry-Romberg syndrome varies. In some cases, the atrophy ends before the entire face is affected. In mild cases, the disorder usually causes no disability other than cosmetic effects.
Question:  what research (or clinical trials) is being done for Parry-Romberg ?
Answer: The NINDS supports research on neurological disorders such as Parry-Romberg syndrome with the goal of finding ways to prevent, treat, and cure them.
Question:  What is (are) Myotonia Congenita ?
Answer: Myotonia congenita is an inherited neuromuscular disorder characterized by the inability of muscles to quickly relax after a voluntary contraction. The condition is present from early childhood, but symptoms can be mild. Most children will be 2 or 3 years old when parents first notice their muscle stiffness, particularly in the legs, often provoked by sudden activity after rest. The disease doesnt cause muscle wasting; in fact, it may cause muscle enlargement. Muscle strength is increased. There are two forms of the disorder: Becker-type, which is the most common form; and Thomsens disease, which is a rare and milder form. The disorder is cause by mutations in a gene responsible for shutting off electrical excitation in the muscles.
Question:  What are the treatments for Myotonia Congenita ?
Answer: Most people with myotonia congenita dont require special treatments. Stiff muscles usually resolve with exercise, or light movement, especially after resting. For individuals whose symptoms are more limiting, doctors have had some success with medications such as quinine, or anticonvulsant drugs such as phenytoin. Physical therapy and other rehabilitative therapies are also sometimes used to improve muscle function.
Question:  What is the outlook for Myotonia Congenita ?
Answer: Most individuals with myotonia congenita lead long, productive lives. Although muscle stiffness may interfere with walking, grasping, chewing, and swallowing, it is usually relieved with exercise.
Question:  what research (or clinical trials) is being done for Myotonia Congenita ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to myotonia congenita and also supports additional research through grants to major research institutions across the country. Current research is exploring how, at the molecular level, the defective gene in myotonia congenita causes the specific symptoms of the disorder. Additional research is focused on developing animal models of the disorder to test potential treatments and therapies.
Question:  What is (are) Congenital Myopathy ?
Answer: A myopathy is a disorder of the muscles that usually results in weakness. Congenital myopathy refers to a group of muscle disorders that appear at birth or in infancy. Typically, an infant with a congenital myopathy will be "floppy," have difficulty breathing or feeding, and will lag behind other babies in meeting normal developmental milestones such as turning over or sitting up.
                
Muscle weakness can occur for many reasons, including a problem with the muscle, a problem with the nerve that stimulates the muscle, or a problem with the brain. Therefore, to diagnose a congenital myopathy, a neurologist will perform a detailed physical exam as well as tests to determine the cause of weakness. If a myopathy is suspected, possible tests include a blood test for a muscle enzyme called creatine kinase, an electromyogram (EMG) to evaluate the electrical activity of the muscle, a muscle biopsy, and genetic testing.
                
There are currently seven distinct types of congenital myopathy, with some variation in symptoms, complications, treatment options, and outlook.
                
Nemaline myopathy is the most common congenital myopathy. Infants usually have problems with breathing and feeding. Later, some skeletal problems may arise, such as scoliosis (curvature of the spine). In general, the weakness does not worsen during life.
                
Myotubular myopathy is rare and only affects boys. Weakness and floppiness are so severe that a mother may notice reduced movements of the baby in her womb during pregnancy. There are usually significant breathing and swallowing difficulties; many children do not survive infancy. Osteopenia (weakening of the bones) is also associated with this disorder.
                
Centronuclear myopathy is rare and begins in infancy or early childhood with weakness of the arms and legs, droopy eyelids, and problems with eye movements. Weakness often gets worse with time.
                
Central core disease varies among children with regard to the severity of problems and the degree of worsening over time. Usually, there is mild floppiness in infancy, delayed milestones, and moderate limb weakness, which do not worsen much over time. Children with central core disease may have life-threatening reactions to general anesthesia. Treatment with the drug salbutamol has been shown to reduce weakness significantly, although it does not cure the disorder.
                
Multi-minicore disease has several different subtypes. Common to most is severe weakness of the limbs and scoliosis. Often breathing difficulties occur as well. Some children have weakened eye movements.
                
Congenital fiber-type disproportion myopathy is a rare disorder that begins with floppiness, limb and facial weakness, and breathing problems.
                
Hyaline body myopathy is a disorder characterized by the specific appearance under the microscope of a sample of muscle tissue. It probably includes several different causes. Because of this, the symptoms are quite variable.
Question:  What are the treatments for Congenital Myopathy ?
Answer: Currently, only central core disease has an effective treatment (see above). There are no known cures for any of these disorders. Supportive treatment may involve orthopedic treatments, as well as physical, occupational or speech therapy.
Question:  What is the outlook for Congenital Myopathy ?
Answer: When breathing difficulties are severe, and particularly if there is also a problem with feeding and swallowing, infants may die of respiratory failure or complications such as pneumonia. Sometimes muscle weakness can lead to skeletal problems, such as scoliosis, reduced mobility of joints, or hip problems. The heart muscle is rarely involved.
Question:  what research (or clinical trials) is being done for Congenital Myopathy ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research related to congenital myopathies in their laboratories at the NIH and also support 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 the disorders that make up the congenital myopathies.
Question:  What is (are) Ataxia ?
Answer: Ataxia often occurs when parts of the nervous system that control movement are damaged. People with ataxia experience a failure of muscle control in their arms and legs, resulting in a lack of balance and coordination or a disturbance of gait. While the term ataxia is primarily used to describe this set of symptoms, it is sometimes also used to refer to a family of disorders. It is not, however, a specific diagnosis.
                
Most disorders that result in ataxia cause cells in the part of the brain called the cerebellum to degenerate, or atrophy. Sometimes the spine is also affected. The phrases cerebellar degeneration and spinocerebellar degeneration are used to describe changes that have taken place in a persons nervous system; neither term constitutes a specific diagnosis. Cerebellar and spinocerebellar degeneration have many different causes. The age of onset of the resulting ataxia varies depending on the underlying cause of the degeneration.
                
Many ataxias are hereditary and are classified by chromosomal location and pattern of inheritance: autosomal dominant, in which the affected person inherits a normal gene from one parent and a faulty gene from the other parent; and autosomal recessive, in which both parents pass on a copy of the faulty gene. Among the more common inherited ataxias are Friedreichs ataxia and Machado-Joseph disease. Sporadic ataxias can also occur in families with no prior history.
                
Ataxia can also be acquired. Conditions that can cause acquired ataxia include stroke, multiple sclerosis, tumors, alcoholism, peripheral neuropathy, metabolic disorders, and vitamin deficiencies.
Question:  What are the treatments for Ataxia ?
Answer: There is no cure for the hereditary ataxias. If the ataxia is caused by another condition, that underlying condition is treated first. For example, ataxia caused by a metabolic disorder may be treated with medications and a controlled diet. Vitamin deficiency is treated with vitamin therapy. A variety of drugs may be used to either effectively prevent symptoms or reduce the frequency with which they occur. Physical therapy can strengthen muscles, while special devices or appliances can assist in walking and other activities of daily life.
Question:  What is the outlook for Ataxia ?
Answer: The prognosis for individuals with ataxia and cerebellar/spinocerebellar degeneration varies depending on its underlying cause.
Question:  what research (or clinical trials) is being done for Ataxia ?
Answer: The NINDS supports and conducts a broad range of basic and clinical research on cerebellar and spinocerebellar degeneration, including work aimed at finding the cause(s) of ataxias and ways to treat, cure, and, ultimately, prevent them. Scientists are optimistic that understanding the genetics of these disorders may lead to breakthroughs in treatment.
Question:  What is (are) Septo-Optic Dysplasia ?
Answer: Septo-optic dysplasia (SOD) is a rare disorder characterized by abnormal development of the optic disk, pituitary deficiencies, and often agenesis (absence) of the septum pellucidum (the part of the brain that separates the anterior horns or the lateral ventricles of the brain). Symptoms may include blindness in one or both eyes, pupil dilation in response to light, nystagmus (a rapid, involuntary to-and-fro movement of the eyes), inward and outward deviation of the eyes, hypotonia (low muscle tone), and hormonal problems. Seizures may also occur. In a few cases, jaundice (prolonged yellow skin discoloration) may occur at birth. Intellectual problems vary in severity among individuals. While some children with SOD have normal intelligence, others have learning disabilities. Most, however, are developmentally delayed due to vision impairment or neurological problems.
Question:  What are the treatments for Septo-Optic Dysplasia ?
Answer: Treatment for SOD is symptomatic. Hormone deficiencies may be treated with hormone replacement therapy. The optical problems associated with SOD are generally not treatable. Vision, physical, and occupational therapies may be required.
Question:  What is the outlook for Septo-Optic Dysplasia ?
Answer: The prognosis for individuals with SOD varies according to the presence and severity of symptoms.
Question:  what research (or clinical trials) is being done for Septo-Optic Dysplasia ?
Answer: The NINDS supports and conducts neurogenetic research which focuses on identifying and studying the genes involved in normal brain development. The knowledge gained from these fundamental studies provides the foundation for understanding how this process can go awry and, thus, may eventually give clues to understanding disorders such as SOD.
Question:  What is (are) Coffin Lowry Syndrome ?
Answer: Coffin-Lowry syndrome is a rare genetic disorder characterized by craniofacial (head and facial) and skeletal abnormalities, delayed intellectual development, short stature, and hypotonia. Characteristic facial features may include an underdeveloped upper jaw bone (maxillary hypoplasia), a broad nose, protruding nostrils (nares), an abnormally prominent brow, down-slanting eyelid folds (palpebral fissures), widely spaced eyes (hypertelorism), large low-set ears, and unusually thick eyebrows. Skeletal abnormalities may include abnormal front-to-back and side-to-side curvature of the spine (kyphoscoliosis), unusual prominence of the breastbone (pigeon chest, or pectus carinatum), dental abnormalities, and short, hyperextensible, tapered fingers. Other features may include feeding and respiratory problems, developmental delay, hearing impairment, awkward gait, stimulus-induced drop episodes, and heart and kidney involvement. The disorder affects males and females in equal numbers, but symptoms are usually more severe in males. The disorder is caused by a defective gene, RSK2, which is found in 1996 on the X chromosome (Xp22.2-p22.1). Thus, the syndrome is typically more severe in males because males have only one X chromosome, while females have two. It is unclear how changes (mutations) in the DNA structure of the gene lead to the clinical findings.
Question:  What are the treatments for Coffin Lowry Syndrome ?
Answer: There is no cure and no standard course of treatment for Coffin-Lowry syndrome. Treatment is symptomatic and supportive, and may include physical and speech therapy and educational services.
Question:  What is the outlook for Coffin Lowry Syndrome ?
Answer: The prognosis for individuals with Coffin-Lowry syndrome varies depending on the severity of symptoms. Early intervention may improve the outlook for patients. Life span is reduced in some individuals with Coffin-Lowry syndrome.
Question:  what research (or clinical trials) is being done for Coffin Lowry Syndrome ?
Answer: The NINDS supports and conducts research on genetic disorders, such as Coffin-Lowry syndrome, in an effort to find ways to prevent, treat, and ultimately cure these disorders.
Question:  What is (are) Lipoid Proteinosis ?
Answer: Lipoid proteinosis (LP) is a rare disease that affects the skin and the brain. Three distinctive features characterize the disease: a hoarse voice, unusual growths on the skin and mucus membranes, and damage to the temporal lobes or hippocampus of the brain. The symptoms of LP may begin as early as infancy with hoarseness or a weak cry, due to growths on the vocal cords. Skin lesions appear sometime in the next 3 years, leaving acne- or pox-like scars on the face, hands, and mucous membranes. The most characteristic symptom of LP is waxy, yellow, bead-like bumps along the upper and lower edges of the eyelids. Brain damage develops over time and is associated with the development of cognitive abilities and epileptic seizures. Damage to the amygdala, a part of the brain that regulates emotions and perceptions, leads to difficulties in discriminating facial expressions and in making realistic judgments about the trustworthiness of other people. LP is a hereditary disease that equally affects males and females. Nearly a quarter of all reported cases have been in the Afrikaner population of South Africa, but the disease is increasingly being reported from other parts of the world including India. The gene responsible for LP has recently been identified. It performs an unknown function in the skin related to the production of collagen.