Druvith/transformed_medDataset huggingface dataset:
What is the outlook for Angelman Syndrome ? 
 Most individuals with Angelman syndrome will have severe developmental delays, speech limitations, and motor difficulties. However, individuals with Angelman syndrome can have normal life spans and generally do not show developmental regression as they age. Early diagnosis and tailored interventions and therapies help improve quality of life.
what research (or clinical trials) is being done for Angelman Syndrome ? 
 The NINDS supports and conducts research on neurogenetic disorders such as Angelman syndrome, to develop techniques to diagnose, treat, prevent, and ultimately cure them.
What is (are) Inclusion Body Myositis ? 
 Inclusion body myositis (IBM) is one of a group of muscle diseases known as the inflammatory myopathies, which are characterized by chronic, progressive muscle inflammation accompanied by muscle weakness. The onset of muscle weakness in IBM is generally gradual (over months or years) and affects both proximal (close to the trunk of the body) and distal (further away from the trunk) muscles. Muscle weakness may affect only one side of the body. Falling and tripping are usually the first noticeable symptoms of IBM. For some individuals, the disorder begins with weakness in the wrists and fingers that causes difficulty with pinching, buttoning, and gripping objects. There may be weakness of the wrist and finger muscles and atrophy (thinning or loss of muscle bulk) of the forearm muscles and quadricep muscles in the legs. Difficulty swallowing occurs in approximately half of IBM cases. Symptoms of the disease usually begin after the age of 50, although the disease can occur earlier. IBM occurs more frequently in men than in women.
What are the treatments for Inclusion Body Myositis ? 
 There is no cure for IBM, nor is there a standard course of treatment. The disease is generally unresponsive to corticosteroids and immunosuppressive drugs. Some evidence suggests that intravenous immunoglobulin may have a slight, but short-lasting, beneficial effect in a small number of cases. Physical therapy may be helpful in maintaining mobility. Other therapy is symptomatic and supportive.
What is the outlook for Inclusion Body Myositis ? 
 IBM is generally resistant to all therapies and its rate of progression appears to be unaffected by currently available treatments.
what research (or clinical trials) is being done for Inclusion Body Myositis ? 
 The National Institute of Neurological Disorders and Stroke (NINDS), National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institute of Environmental Health Sciences (NIEHS) and other institutes of the National Institutes of Health (NIH) conduct research relating to IBM in laboratories at the NIH and support additional research through grants to major medical institutions across the country. Currently funded research is exploring patterns of gene expression among the inflammatory myopathies, the role of viral infection as a precursor to the disorders, and the safety and efficacy of various treatment regimens.
What is (are) Subacute Sclerosing Panencephalitis ? 
 Subacute sclerosing panencephalitis (SSPE) is a progressive neurological disorder of children and young adults that affects the central nervous system (CNS). It is a slow, but persistent, viral infection caused by defective measles virus. SSPE has been reported from all parts of the world, but it is considered a rare disease in developed countries, with fewer than 10 cases per year reported in the United States. The incidence of SSPE declined by at least 90 percent in countries that have practiced widespread immunization with measles vaccine. The incidence of SSPE is still high in developing countries such as India and Eastern Europe. There is a higher incidence among males than females (male/female: 3/1). Most youngsters with SSPE have a history of measles infection at an early age, usually younger than 2 years, followed by a latent period of 6 to 8 years before neurological symptoms begin. Despite the long interval between the measles infection and the onset of SSPE, researchers think that the infection of the brain occurs soon after the primary bout with measles and progresses slowly. Why it persists and progresses still isn't clear. The initial symptoms of SSPE are subtle and include mild mental deterioration (such as memory loss) and changes in behavior (such as irritability) followed by disturbances in motor function, including uncontrollable involuntary jerking movements of the head, trunk or limbs called myoclonic jerks. Seizures may also occur. Some people may become blind. In advanced stages of the disease, individuals may lose the ability to walk, as their muscles stiffen or spasm. There is progressive deterioration to a comatose state, and then to a persistent vegetative state. Death is usually the result of fever, heart failure, or the brain's inability to continue controlling the autonomic nervous system.
What are the treatments for Subacute Sclerosing Panencephalitis ? 
 Currently, there is no cure for SSPE. Clinical trials of antiviral (isoprinosine and ribavirin) and immunomodulatory (interferon alpha) drugs have suggested that these types of therapies given alone or in combination halt the progression of the disease and can prolong life, but their long-term effects on individuals, and eventual outcome, are unknown. Good nursing care is the most important aspect of treatment for SSPE, along with anticonvulsant and antispasmodic drugs when needed.
What is the outlook for Subacute Sclerosing Panencephalitis ? 
 Most individuals with SSPE will die within 1 to 3 years of diagnosis. In a small percentage of people, the disease will progress rapidly, leading to death over a short course within three months of diagnosis. Another small group will have a chronic, slowly progressive form, some with relapses and remissions. A very small number (approximately 5 percent) may experience spontaneous long term improvement and regain lost function. Prevention, in the form of measles vaccination, is the only real "cure" for SSPE.
what research (or clinical trials) is being done for Subacute Sclerosing Panencephalitis ? 
 The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes at the National Institutes of Health conduct research related to SSPE in their clinics and laboratories and 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 SSPE.
What is (are) Hemifacial Spasm ? 
 Hemifacial spasm is a neuromuscular disorder characterized by frequent involuntary contractions (spasms) of the muscles on one side (hemi-) of the face (facial). The disorder occurs in both men and women, although it more frequently affects middle-aged or elderly women. It is much more common in the Asian population. The first symptom is usually an intermittent twitching of the eyelid muscle that can lead to forced closure of the eye. The spasm may then gradually spread to involve the muscles of the lower face, which may cause the mouth to be pulled to one side. Eventually the spasms involve all of the muscles on one side of the face almost continuously. The condition may be caused by a facial nerve injury, or a tumor, or it may have no apparent cause. Rarely, doctors see individuals with spasm on both sides of the face. Most often hemifacial spasm is caused by a blood vessel pressing on the facial nerve at the place where it exits the brainstem.
What are the treatments for Hemifacial Spasm ? 
 Surgical treatment in the form of microvascular decompression, which relieves pressure on the facial nerve, will relieve hemifacial spasm in many cases. This intervention has significant potential side-effects, so risks and benefits have to be carefully balanced. Other treatments include injections of botulinum toxin into the affected areas, which is the most effective therapy and the only one used in most cases. Drug therapy is generally not effective.
What is the outlook for Hemifacial Spasm ? 
 The prognosis for an individual with hemifacial spasm depends on the treatment and their response. Some individuals will become relatively free from symptoms with injection therapy. Some may require surgery. In most cases, a balance can be achieved, with tolerable residual symptoms.
what research (or clinical trials) is being done for Hemifacial Spasm ? 
 The National Institute of Neurological Disorders and Stroke (NINDS) conducts and supports research related to hemifacial spams through grants to major research institutions across the country. Much of this research focuses on better ways to prevent, treat, and ultimately cure neurological disorders, such as hemifacial spasm.
What is (are) Olivopontocerebellar Atrophy ? 
 Olivopontocerebellar atrophy (OPCA) is a term that describes the degeneration of neurons in specific areas of the brain  the cerebellum, pons, and inferior olives. OPCA is present in several neurodegenerative syndromes, including inherited and non-inherited forms of ataxia (such as the hereditary spinocerebellar ataxia known as Machado-Joseph disease) and multiple system atrophy (MSA), with which it is primarily associated. http://www.ninds.nih.gov/disorders/msa/msa.htm
                
OPCA may also be found in the brains of individuals with prion disorders and inherited metabolic diseases. The characteristic areas of brain damage that indicate OPCA can be seen by imaging the brain using CT scans or MRI studies.
What are the treatments for Olivopontocerebellar Atrophy ? 
 There is no specific treatmentfor OPCA. Physicians may try different medications to treat the ataxia, tremor, and rigidity that are associated with the disorder. Other treatments are directed at specific symptoms. Stiffness, spasms, sleep disorders, depression, and tremor may be improved with medication. A physical therapist may be helpful in establishing a routine of exercise and stretching, and in obtaining devices or appliances to assist in walking and other daily activities.
What is the outlook for Olivopontocerebellar Atrophy ? 
 There is no cure for OPCA. The disorder is slowly progressive with death usually occurring approximately 20 years after onset.
what research (or clinical trials) is being done for Olivopontocerebellar Atrophy ? 
 The NINDS supports and conducts a broad range of basic and clinical research on cerebellar degeneration, including work aimed at finding the cause(s) of OPCA and ways to treat, cure, and, ultimately, prevent the disease. There has been great progress recently since the genes for several of the hereditary forms of OPCA have been found.
What is (are) Multifocal Motor Neuropathy ? 
 Multifocal motor neuropathy is a progressive muscle disorder characterized by muscle weakness in the hands, with differences from one side of the body to the other in the specific muscles involved. It affects men much more than women. Symptoms also include muscle wasting, cramping, and involuntary contractions or twitching of the leg muscles. The disorder is sometimes mistaken for amyotrophic laterial sclerosis (ALS, or Lou Gehrig's disease) but unlike ALS, it is treatable. An early and accurate diagnosis allows patients to recover quickly.
What are the treatments for Multifocal Motor Neuropathy ? 
 Treatment for multifocal motor neuropathy varies. Some individuals experience only mild, modest symptoms and require no treatment. For others, treatment generally consists of intravenous immunoglobulin (IVIg) or immunosuppressive therapy with cyclophosphamide.
What is the outlook for Multifocal Motor Neuropathy ? 
 Improvement in muscle strength usually begins within 3 to 6 weeks after treatment is started. Most patients who receive treatment early experience little, if any, disability. However, there is evidence of slow progression over many years.
what research (or clinical trials) is being done for Multifocal Motor Neuropathy ? 
 The NINDS supports a broad range of research on neuromuscular disorders with the goal of finding ways to prevent, treat, and, ultimately, cure them.
What is (are) Occipital Neuralgia ? 
 Occipital neuralgia is a distinct type of headache characterized by piercing, throbbing, or electric-shock-like chronic pain in the upper neck, back of the head, and behind the ears, usually on one side of the head. Typically, the pain of occipital neuralgia begins in the neck and then spreads upwards. Some individuals will also experience pain in the scalp, forehead, and behind the eyes. Their scalp may also be tender to the touch, and their eyes especially sensitive to light. The location of pain is related to the areas supplied by the greater and lesser occipital nerves, which run from the area where the spinal column meets the neck, up to the scalp at the back of the head. The pain is caused by irritation or injury to the nerves, which can be the result of trauma to the back of the head, pinching of the nerves by overly tight neck muscles, compression of the nerve as it leaves the spine due to osteoarthritis, or tumors or other types of lesions in the neck. Localized inflammation or infection, gout, diabetes, blood vessel inflammation (vasculitis), and frequent lengthy periods of keeping the head in a downward and forward position are also associated with occipital neuralgia. In many cases, however, no cause can be found. A positive response (relief from pain) after an anesthetic nerve block will confirm the diagnosis.
What are the treatments for Occipital Neuralgia ? 
 Treatment is generally symptomatic and includes massage and rest. In some cases, antidepressants may be used when the pain is particularly severe. Other treatments may include local nerve blocks and injections of steroids directly into the affected area.
What is the outlook for Occipital Neuralgia ? 
 Occipital neuralgia is not a life-threatening condition. Many individuals will improve with therapy involving heat, rest, anti-inflammatory medications, and muscle relaxants. Recovery is usually complete after the bout of pain has ended and the nerve damage repaired or lessened.
what research (or clinical trials) is being done for Occipital Neuralgia ? 
 The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes at the National Institutes of Health conduct research related to pain and occipital neuralgia in their clinics and laboratories and support additional research through grants to major medical institutions across the country. Much of this research focuses on understanding the basic mechanisms of pain and testing treatments in order to find better ways to treat occipital neuralgia.
What is (are) Arachnoiditis ? 
 Arachnoiditis describes a pain disorder caused by the inflammation of the arachnoid, one of the membranes that surround and protect the nerves of the spinal cord. The arachnoid can become inflamed because of an irritation from chemicals, infection from bacteria or viruses, as the result of direct injury to the spine, chronic compression of spinal nerves, or complications from spinal surgery or other invasive spinal procedures. Inflammation can sometimes lead to the formation of scar tissue and adhesions, which cause the spinal nerves to stick together. If arachnoiditis begins to interfere with the function of one or more of these nerves, it can cause a number of symptoms, including numbness, tingling, and a characteristic stinging and burning pain in the lower back or legs. Some people with arachnoiditis will have debilitating muscle cramps, twitches, or spasms. It may also affect bladder, bowel, and sexual function. In severe cases, arachnoiditis may cause paralysis of the lower limbs.
What are the treatments for Arachnoiditis ? 
 Arachnoiditis remains a difficult condition to treat, and long-term outcomes are unpredictable. Most treatments for arachnoiditis are focused on pain relief and the improvement of symptoms that impair daily function. A regimen of pain management, physiotheraphy, exercise, and psychotheraphy is often recommended. Surgical intervention is controversial since the outcomes are generally poor and provide only short-term relief.
What is the outlook for Arachnoiditis ? 
 Arachnoiditis is adisorder that causes chronic pain and neurological deficits and does not improve significantly with treatment.Surgery may only provide temporary relief. The outlook for someone witharachnoiditis iscomplicated by the fact that the disorder has no predictable pattern or severity of symptoms.
what research (or clinical trials) is being done for Arachnoiditis ? 
 Within the NINDS research programs, arachnoiditis is addressed primarily through studies associated with pain research. NINDS vigorously pursues a research program seeking new treatments for pain and nerve damage with the ultimate goal of reversing debilitating conditions such as arachnoiditis.
What is (are) Craniosynostosis ? 
 Craniosynostosis is a birth defect of the skull characterized by the premature closure of one or more of the fibrous joints between the bones of the skull (called the cranial sutures) before brain growth is complete. Closure of a single suture is most common. Normally the skull expands uniformly to accommodate the growth of the brain; premature closure of a single suture restricts the growth in that part of the skull and promotes growth in other parts of the skull where sutures remain open. This results in a misshapen skull but does not prevent the brain from expanding to a normal volume. However, when many sutures close prematurely, the skull cannot expand to accommodate the growing brain, which leads to increased pressure within the skull and impaired development of the brain. Craniosynostosis can be gene-linked or caused by metabolic diseases (such as rickets )or an overactive thyroid. Some cases are associated with other disorders such as microcephaly (abnormally small head) and hydrocephalus (excessive accumulation of cerebrospinal fluid in the brain). The first sign of craniosynostosis is an abnormally shaped skull. Other features can include signs of increased intracranial pressure, developmental delays, or impaired cognitive development, which are caused by constriction of the growing brain. Seizures and blindness may also occur.
What are the treatments for Craniosynostosis ? 
 Treatment for craniosynostosis generally consists of surgery to improve the symmetry and appearance of the head and to relieve pressure on the brain and the cranial nerves. For some children with less severe problems, cranial molds can reshape the skull to accommodate brain growth and improve the appearance of the head.
What is the outlook for Craniosynostosis ? 
 The prognosis for craniosynostosis varies depending on whether single or multiple cranial sutures are involved or other abnormalities are present. The prognosis is better for those with single suture involvement and no associated abnormalities.
what research (or clinical trials) is being done for Craniosynostosis ? 
 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 brain development. The knowledge gained from these fundamental studies provides the foundation for understanding how this process can change and offers hope for new ways to treat and prevent birth defects that can prevent normal brain development, such as craniosynostosis.
What is (are) Cavernous Malformation ? 
 Cerebral cavernous malformations (CCMs) are vascular lesions comprised of clusters of tightly packed, abnormally thin-walled small blood vessels (capillaries) that displace normal neurological tissue in the brain or spinal cord. The vessels are filled with slow-moving or stagnant blood that is usually clotted or in a state of decomposition. Cavernous malformations can occur in the brain, spinal cord, and some other body regions. In the brain and spinal cord these cavernous lesions are quite fragile and are prone to bleeding, causing hemorrhagic strokes (bleeding into the brain), seizures, and neurological deficits. CCMs can range in size from a few fractions of an inch to several inches in diameter, depending on the number of blood vessels involved. Some people develop multiple lesions while others never experience related medical problems. Hereditary forms of CCM are caused by mutations in one of three CCM disease genes: CCM1, CCM2, and CCM3. A large population with hereditary CCM disease is found in New Mexico and the Southwestern United States, in which the disease is caused by mutations in the gene CCM1 (or KRIT1).
What are the treatments for Cavernous Malformation ? 
 The primary treatment option for a CCM is surgical removal. Radiation therapy has not been shown to be effective. The decision to operate is made based upon the risk of approaching the lesion. For example, symptomatic lesions close to the brain surface in non eloquent brain (areas for example, those areas not involved with motor function, speech, vision, hearing, memory, and learning) are very likely to be candidates for removal. On the other hand, lesions located in deep brain areas are associated with higher surgical risk and are often not candidates for surgery until the lesion has bled multiple times. Medications can often lessen general symptoms such as headache, back pain, and seizures.
What is the outlook for Cavernous Malformation ? 
 Rebleeding from a cavernous angioma is common, it is not predictable, and individuals frequently have multiple CCMs found via magnetic resonance imaging. Individuals with CCM are faced with a diagnosis that imparts risk of multiple future hemorrhages that occur seemingly at random and without any preventative therapy except surgical removal.
what research (or clinical trials) is being done for Cavernous Malformation ? 
 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. Studies of cerebral cavernous malformations (CCMs) show that alterations in the function of structural proteins may also give rise to vascular malformations. Currently there is no therapy to prevent the development or progression of CCMs. NINDS-funded scientists have developed an animal model that studies two of the familial genes related to the development of CCMs. Research shows that the protein signaling pathway Rhoa/ROCK, which allows cells to communicate regarding the formation of cell structure, is involved in blood vessel activity/ and the flow of molecules and cells into and out of blood vessels. These scientists hypothesize that blocking ROCK activity will inhibit CCM development and hemorrhage, and possibly create a therapy for these malformations.
What is (are) Locked-In Syndrome ? 
 Locked-in syndrome is a rare neurological disorder characterized by complete paralysis of voluntary muscles in all parts of the body except for those that control eye movement. It may result from traumatic brain injury, diseases of the circulatory system, diseases that destroy the myelin sheath surrounding nerve cells, or medication overdose. Individuals with locked-in syndrome are conscious and can think and reason, but are unable to speak or move. The disorder leaves individuals completely mute and paralyzed. Communication may be possible with blinking eye movements
What are the treatments for Locked-In Syndrome ? 
 There is no cure for locked-in syndrome, nor is there a standard course of treatment. A therapy called functional neuromuscular stimulation, which uses electrodes to stimulate muscle reflexes, may help activate some paralyzed muscles. Several devices to help communication are available. Other treatment is symptomatic and supportive.
What is the outlook for Locked-In Syndrome ? 
 While in rare cases some patients may regain certain functions, the chances for motor recovery are very limited.