fenil210/Med-Lamma huggingface dataset:
What is (are) Kleine-Levin Syndrome ?
Kleine-Levin syndrome is a rare disorder that primarily affects adolescent males (approximately 70 percent of those with Kleine-Levin syndrome are male). It is characterized by recurring but reversible periods of excessive sleep (up to 20 hours per day). Symptoms occur as "episodes," typically lasting a few days to a few weeks. Episode onset is often abrupt, and may be associated with flu-like symptoms. Excessive food intake, irritability, childishness, disorientation, hallucinations, and an abnormally uninhibited sex drive may be observed during episodes. Mood can be depressed as a consequence, but not a cause, of the disorder. Affected individuals are completely normal between episodes, although they may not be able to remember afterwards everything that happened during the episode. It may be weeks or more before symptoms reappear. Symptoms may be related to malfunction of the hypothalamus and thalamus, parts of the brain that govern appetite and sleep. + NINDS + Kleine-Levin Syndrome
What are the treatments for Kleine-Levin Syndrome ?
There is no definitive treatment for Kleine-Levin syndrome and watchful waiting at home, rather than pharmacotherapy, is most often advised. Stimulant pills, including amphetamines, methylphenidate, and modafinil, are used to treat sleepiness but may increase irritability and will not improve cognitive abnormalities. Because of similarities between Kleine-Levin syndrome and certain mood disorders, lithium and carbamazepine may be prescribed and, in some cases, have been shown to prevent further episodes. This disorder should be differentiated from cyclic re-occurrence of sleepiness during the premenstrual period in teen-aged girls, which may be controlled with birth control pills. It also should be differentiated from encephalopathy, recurrent depression, or psychosis. + NINDS + Kleine-Levin Syndrome
What is the outlook for Kleine-Levin Syndrome ?
Episodes eventually decrease in frequency and intensity over the course of eight to 12 years. + NINDS + Kleine-Levin Syndrome
what research (or clinical trials) is being done for Kleine-Levin Syndrome ?
NINDS supports a broad range of clinical and basic research on diseases causing sleep disorders in an effort to clarify the mechanisms of these conditions and to develop better treatments for them. + NINDS + Kleine-Levin Syndrome
What is (are) Hypersomnia ?
Hypersomnia is characterized by recurrent episodes of excessive daytime sleepiness or prolonged nighttime sleep. Different from feeling tired due to lack of or interrupted sleep at night, persons with hypersomnia are compelled to nap repeatedly during the day, often at inappropriate times such as at work, during a meal, or in conversation. These daytime naps usually provide no relief from symptoms. Patients often have difficulty waking from a long sleep, and may feel disoriented. Other symptoms may include anxiety, increased irritation, decreased energy, restlessness, slow thinking, slow speech, loss of appetite, hallucinations, and memory difficulty. Some patients lose the ability to function in family, social, occupational, or other settings. Hypersomnia may be caused by another sleep disorder (such as narcolepsy or sleep apnea), dysfunction of the autonomic nervous system, or drug or alcohol abuse. In some cases it results from a physical problem, such as a tumor, head trauma, or injury to the central nervous system. Certain medications, or medicine withdrawal, may also cause hypersomnia. Medical conditions including multiple sclerosis, depression, encephalitis, epilepsy, or obesity may contribute to the disorder. Some people appear to have a genetic predisposition to hypersomnia; in others, there is no known cause. Typically, hypersomnia is first recognized in adolescence or young adulthood. + NINDS + Hypersomnia
What are the treatments for Hypersomnia ?
Treatment is symptomatic in nature. Stimulants, such as amphetamine, methylphenidate, and modafinil, may be prescribed. Other drugs used to treat hypersomnia include clonidine, levodopa, bromocriptine, antidepressants, and monoamine oxidase inhibitors. Changes in behavior (for example avoiding night work and social activities that delay bed time) and diet may offer some relief. Patients should avoid alcohol and caffeine. + NINDS + Hypersomnia
What is the outlook for Hypersomnia ?
The prognosis for persons with hypersomnia depends on the cause of the disorder. While the disorder itself is not life threatening, it can have serious consequences, such as automobile accidents caused by falling asleep while driving. The attacks usually continue indefinitely. + NINDS + Hypersomnia
what research (or clinical trials) is being done for Hypersomnia ?
The NINDS supports and conducts research on sleep disorders such as hypersomnia. The goal of this research is to increase scientific understanding of the condition, find improved methods of diagnosing and treating it, and discover ways to prevent it. + NINDS + Hypersomnia
What is (are) Corticobasal Degeneration ?
Corticobasal degeneration is a progressive neurological disorder characterized by nerve cell loss and atrophy (shrinkage) of multiple areas of the brain including the cerebral cortex and the basal ganglia. Corticobasal degeneration progresses gradually. Initial symptoms, which typically begin at or around age 60, may first appear on one side of the body (unilateral), but eventually affect both sides as the disease progresses. Symptoms are similar to those found in Parkinson disease, such as poor coordination, akinesia (an absence of movements), rigidity (a resistance to imposed movement), disequilibrium (impaired balance); and limb dystonia (abnormal muscle postures). Other symptoms such as cognitive and visual-spatial impairments, apraxia (loss of the ability to make familiar, purposeful movements), hesitant and halting speech, myoclonus (muscular jerks), and dysphagia (difficulty swallowing) may also occur. An individual with corticobasal degeneration eventually becomes unable to walk. + NINDS + Corticobasal Degeneration
What are the treatments for Corticobasal Degeneration ?
There is no treatment available to slow the course of corticobasal degeneration, and the symptoms of the disease are generally resistant to therapy. Drugs used to treat Parkinson disease-type symptoms do not produce any significant or sustained improvement. Clonazepam may help the myoclonus. Occupational, physical, and speech therapy can help in managing disability. + NINDS + Corticobasal Degeneration
What is the outlook for Corticobasal Degeneration ?
Corticobasal degeneration usually progresses slowly over the course of 6 to 8 years. Death is generally caused by pneumonia or other complications of severe debility such as sepsis or pulmonary embolism. + NINDS + Corticobasal Degeneration
what research (or clinical trials) is being done for Corticobasal Degeneration ?
The NINDS supports and conducts research studies on degenerative disorders such as corticobasal degeneration. The goals of these studies are to increase scientific understanding of these disorders and to find ways to prevent, treat, and cure them. + NINDS + Corticobasal Degeneration
What is (are) Dysautonomia ?
Dysautonomia refers to a disorder of autonomic nervous system (ANS) function that generally involves failure of the sympathetic or parasympathetic components of the ANS, but dysautonomia involving excessive or overactive ANS actions also can occur. Dysautonomia can be local, as in reflex sympathetic dystrophy, or generalized, as in pure autonomic failure. It can be acute and reversible, as in Guillain-Barre syndrome, or chronic and progressive. Several common conditions such as diabetes and alcoholism can include dysautonomia. Dysautonomia also can occur as a primary condition or in association with degenerative neurological diseases such as Parkinson's disease. Other diseases with generalized, primary dysautonomia include multiple system atrophy and familial dysautonomia. Hallmarks of generalized dysautonomia due to sympathetic failure are impotence (in men) and a fall in blood pressure during standing (orthostatic hypotension). Excessive sympathetic activity can present as hypertension or a rapid pulse rate. + NINDS + Dysautonomia
What are the treatments for Dysautonomia ?
There is usually no cure for dysautonomia. Secondary forms may improve with treatment of the underlying disease. In many cases treatment of primary dysautonomia is symptomatic and supportive. Measures to combat orthostatic hypotension include elevation of the head of the bed, water bolus (rapid infusion of water given intravenously), a high-salt diet, and drugs such as fludrocortisone and midodrine. + NINDS + Dysautonomia
What is the outlook for Dysautonomia ?
The outlook for individuals with dysautonomia depends on the particular diagnostic category. People with chronic, progressive, generalized dysautonomia in the setting of central nervous system degeneration have a generally poor long-term prognosis. Death can occur from pneumonia, acute respiratory failure, or sudden cardiopulmonary arrest. + NINDS + Dysautonomia
what research (or clinical trials) is being done for Dysautonomia ?
The NINDS supports and conducts research on dysautonomia. This research aims to discover ways to diagnose, treat, and, ultimately, prevent these disorders. + NINDS + Dysautonomia
What is (are) Dyssynergia Cerebellaris Myoclonica ?
Dyssynergia Cerebellaris Myoclonica refers to a collection of rare, degenerative, neurological disorders characterized by epilepsy, cognitive impairment, myoclonus, and progressive ataxia. Symptoms include seizures, tremor, and reduced muscle coordination. Onset of the disorder generally occurs in early adulthood. Tremor may begin in one extremity and later spread to involve the entire voluntary muscular system. Arms are usually more affected than legs. Some of the cases are due to mitochondrial abnormalities. + NINDS + Dyssynergia Cerebellaris Myoclonica
What are the treatments for Dyssynergia Cerebellaris Myoclonica ?
Treatment of Dyssynergia Cerebellaris Myoclonica is symptomatic. Myoclonus and seizures may be treated with drugs like valproate. + NINDS + Dyssynergia Cerebellaris Myoclonica
What is the outlook for Dyssynergia Cerebellaris Myoclonica ?
The progression of the disorder is usually 10 years or longer. + NINDS + Dyssynergia Cerebellaris Myoclonica
what research (or clinical trials) is being done for Dyssynergia Cerebellaris Myoclonica ?
The NINDS supports a broad range of research on neurodegenerative disorders such as Dyssynergia Cerebellaris Myoclonica. The goals of this research are to find ways to prevent, treat, and cure these kinds of disorders. + NINDS + Dyssynergia Cerebellaris Myoclonica
What are the treatments for Transmissible Spongiform Encephalopathies ?
TSEs tend to progress rapidly and usually culminate in death over the course of a few months to a few years. + NINDS + Transmissible Spongiform Encephalopathies
What is the outlook for Transmissible Spongiform Encephalopathies ?
There is currently no treatment that can halt progression of any of the TSEs. Treatment is aimed at alleviating symptoms and making the patient as comfortable as possible. A clinical trial of a potential therapy for CJD is expected to begin soon at the University of California at San Francisco. + NINDS + Transmissible Spongiform Encephalopathies
what research (or clinical trials) is being done for Transmissible Spongiform Encephalopathies ?
The NINDS conducts and supports research on TSEs. This research is aimed at determining how abnormal prion proteins lead to disease, at finding better tests for diagnosing CJD and other disorders, and ultimately at finding ways to treat TSEs. + NINDS + Transmissible Spongiform Encephalopathies
What is (are) Orthostatic Hypotension ?
Orthostatic hypotension is a sudden fall in blood pressure that occurs when a person assumes a standing position. It is due to a lesion of the baroreflex loop, which senses a change in blood pressure and adjusts heart rate and activates sympathetic nerve system fibers to cause the blood vessels to narrow and correct blood pressure. It may also be caused by hypovolemia (a decreased amount of blood in the body), resulting from the excessive use of diuretics, vasodilators, or other types of drugs, dehydration, or prolonged bed rest. The disorder may be associated with Addison's disease, diabetes, and certain neurological disorders including Multiple System Atrophy with Orthostatic Hypotension (formerly known as Shy-Drager syndrome), autonomic system neuropathies, and other dysautonomias. Symptoms, which generally occur after sudden standing, include dizziness, lightheadedness, blurred vision, and syncope (temporary loss of consciousness). + NINDS + Orthostatic Hypotension
What are the treatments for Orthostatic Hypotension ?
When orthostatic hypotension is caused by hypovolemia due to medications, the disorder may be reversed by adjusting the dosage or by discontinuing the medication. When the condition is caused by prolonged bed rest, improvement may occur by sitting up with increasing frequency each day. In some cases, physical counterpressure such as elastic hose or whole-body inflatable suits may be required. Dehydration is treated with salt and fluids. More severe cases can be treated with drugs, such as midodrine, to raise blood pressure. + NINDS + Orthostatic Hypotension
What is the outlook for Orthostatic Hypotension ?
The prognosis for individuals with orthostatic hypotension depends on the underlying cause of the condition. + NINDS + Orthostatic Hypotension
what research (or clinical trials) is being done for Orthostatic Hypotension ?
The NINDS supports research on conditions such as neurogenic orthostatic hypotension aimed at increasing scientific understanding of the condition and finding ways to treat and prevent it. + NINDS + Orthostatic Hypotension
What is (are) Sotos Syndrome ?
Sotos syndrome (cerebral gigantism) is a rare genetic disorder caused by mutation in the NSD1 gene on chromosome 5. It is characterized by excessive physical growth during the first few years of life. Children with Sotos syndrome tend to be large at birth and are often taller, heavier, and have larger heads (macrocrania) than is normal for their age. Symptoms of the disorder, which vary among individuals, include a disproportionately large and long head with a slightly protrusive forehead and pointed chin, large hands and feet, hypertelorism (an abnormally increased distance between the eyes), and down-slanting eyes. The disorder is often accompanied by mild cognitive impairment; delayed motor, cognitive, and social development; hypotonia (low muscle tone), and speech impairments. Clumsiness, an awkward gait, and unusual aggressiveness or irritability may also occur. Although most cases of Sotos syndrome occur sporadically (meaning they are not known to be inherited), familial cases have also been reported. + NINDS + Sotos Syndrome
What are the treatments for Sotos Syndrome ?
There is no standard course of treatment for Sotos syndrome. Treatment is symptomatic. + NINDS + Sotos Syndrome
What is the outlook for Sotos Syndrome ?
Sotos syndrome is not a life-threatening disorder and patients may have a normal life expectancy. The initial abnormalities of Sotos syndrome usually resolve as the growth rate becomes normal after the first few years of life. Developmental delays may improve in the school-age years, and adults with Sotos syndrome are likely to be within the normal range for intellect and height. However, coordination problems may persist into adulthood. + NINDS + Sotos Syndrome
what research (or clinical trials) is being done for Sotos Syndrome ?
The NINDS supports and conducts a wide range of studies which focus on identifying and learning more about 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 Sotos syndrome. + NINDS + Sotos Syndrome
What is (are) Spinal Cord Infarction ?
Spinal cord infarction is a stroke either within the spinal cord or the arteries that supply it. It is caused by arteriosclerosis or a thickening or closing of the major arteries to the spinal cord. Frequently spinal cord infarction is caused by a specific form of arteriosclerosis called atheromatosis, in which a deposit or accumulation of lipid-containing matter forms within the arteries. Symptoms, which generally appear within minutes or a few hours of the infarction, may include intermittent sharp or burning back pain, aching pain down through the legs, weakness in the legs, paralysis, loss of deep tendon reflexes, loss of pain and temperature sensation, and incontinence. + NINDS + Spinal Cord Infarction
What are the treatments for Spinal Cord Infarction ?
Treatment is symptomatic. Physical and occupational therapy may help individuals recover from weakness or paralysis. A catheter may be necessary for patients with urinary incontinence. + NINDS + Spinal Cord Infarction
What is the outlook for Spinal Cord Infarction ?
Recovery depends upon how quickly treatment is received and how severely the body is compromised. Paralysis may persist for many weeks or be permanent. Most individuals have a good chance of recovery. + NINDS + Spinal Cord Infarction
what research (or clinical trials) is being done for Spinal Cord Infarction ?
NINDS conducts and supports research on disorders of the spinal cord such as spinal cord infarction, aimed at learning more about these disorders and finding ways to prevent and treat them. + NINDS + Spinal Cord Infarction
What is (are) Acid Lipase Disease ?
Acid lipase disease or deficiency occurs when the enzyme needed to break down certain fats that are normally digested by the body is lacking or missing, resulting in the toxic buildup of these fats in the bodys cells and tissues. These fatty substances, called lipids, include fatty acids, oils, and cholesterol. Two rare lipid storage diseases are caused by the deficiency of the enzyme lysosomal acid lipase:
                
Wolmans disease (also known as acid lipase deficiency) is an autosomal recessive disorder marked by the buildup of cholesteryl esters (normally a tranport form of cholesterol that brings nutrients into the cells and carries out waste) and triglycerides (a chemical form in which fats exist in the body). Infants with the disorder appear normal at birth but quickly develop progressive mental deterioration, low muscle tone,enlarged liver and grossly enlarged spleen, gastrointestinal problems including an excessive amount of fats in the stools, jaundice, anemia, vomiting, and calcium deposits in the adrenal glands, which causes them to harden. Both male and female infants are affected by the disorder.
                
Cholesteryl ester storage disease (CESD) is an extremely rare disorder that results from storage of cholesteryl esters and triglycerides in cells in the blood and lymph and lymphoid tissue. Children develop an enlarged liver, leading to cirrhosis and chronic liver failure before adulthood. Children may also develop calcium deposits in the adrenal glands and jaundice. Onset varies, and the disorder may not be diagnosed until adulthood. + NINDS + Acid Lipase Disease
What are the treatments for Acid Lipase Disease ?
Enzyme replacement therapy for both Wolman's and cholesteryl ester storage disease is currently under investigation. Certain drugs may be given to help with adrenal gland production, and children may need to be fed intravenously. Individuals with CESD may benefit from a low cholesterol diet. + NINDS + Acid Lipase Disease
What is the outlook for Acid Lipase Disease ?
Wolmans disease is usually fatal by age 1. The onset and course of cholesteryl ester storage disease varies, and individuals may live into adulthood. + NINDS + Acid Lipase Disease
what research (or clinical trials) is being done for Acid Lipase Disease ?
The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge abut the brain and nervous system, and to use that knowledge to reduce the burden of neurological diseaset. The NINDS conducts and supports research to understand lipid storage diseases such as acid lipase deficiency. Additional research studies hope to identify biomarkers (signs that may indicate risk of a disease and improve diagnosis) for thee lipid storage diseases that will speed the development of novel therapeutics for these disorders. Other investigators hope to establish an international disease registry designed to collect longitudinal data that would be used to improve the care and treatment of individuals with lysosomal acid lipase deficiency.
                
The National Library of Medicine (NLM), a part of the National Institutes of Health (NIH) within the U.S. Department of Health and Human Services, offers free searches of biomedical literature through an Internet service called PubMed. To search, go to: http://www.ncbi.nlm.nih.gov/PubMed . The NLM also offers extensive health information from NIH and other trusted sources. To research your condition, go to: http://www.medlineplus.gov . + NINDS + Acid Lipase Disease
What is (are) Erb-Duchenne and Dejerine-Klumpke Palsies ?
The brachial plexus is a network of nerves that conducts signals from the spine to the shoulder, arm, and hand. Brachial plexus injuries are caused by damage to those nerves. Erb-Duchenne (Erb's) palsy refers to paralysis of the upper brachial plexus. Dejerine-Klumpke (Klumpke's) palsy refers to paralysis of the lower brachial plexus. Although injuries can occur at any time, many brachial plexus injuries happen when a baby's shoulders become impacted during delivery and the brachial plexus nerves stretch or tear. There are four types of brachial plexus injuries: avulsion, the most severe type, in which the nerve is torn from the spine; rupture, in which the nerve is torn but not at the spinal attachment; neuroma, in which the nerve has torn and healed but scar tissue puts pressure on the injured nerve and prevents it from conducting signals to the muscles; and neuropraxia or stretch, in which the nerve has been damaged but not torn. Neuropraxia is the most common type of brachial plexus injury. Symptoms of brachial plexus injury may include a limp or paralyzed arm; lack of muscle control in the arm, hand, or wrist; and lack of feeling or sensation in the arm or hand. + NINDS + Erb-Duchenne and Dejerine-Klumpke Palsies
What are the treatments for Erb-Duchenne and Dejerine-Klumpke Palsies ?
Some brachial plexus injuries may heal without treatment. Many children who are injured during birth improve or recover by 3 to 4 months of age. Treatment for brachial plexus injuries includes physical therapy and, in some cases, surgery. + NINDS + Erb-Duchenne and Dejerine-Klumpke Palsies
What is the outlook for Erb-Duchenne and Dejerine-Klumpke Palsies ?
The site and type of brachial plexus injury determines the prognosis. For avulsion and rupture injuries, there is no potential for recovery unless surgical reconnection is made in a timely manner. The potential for recovery varies for neuroma and neuropraxia injuries. Most individuals with neuropraxia injuries recover spontaneously with a 90-100 percent return of function. + NINDS + Erb-Duchenne and Dejerine-Klumpke Palsies
what research (or clinical trials) is being done for Erb-Duchenne and Dejerine-Klumpke Palsies ?
The NINDS conducts and supports research on injuries to the nervous system such as brachial plexus injuries. Much of this research is aimed at finding ways to prevent and treat these disorders. + NINDS + Erb-Duchenne and Dejerine-Klumpke Palsies