fenil210/Med-Lamma huggingface dataset:
what research (or clinical trials) is being done for Arteriovenous 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. The NINDS has established an Arteriovenous Study Group to learn more about the natural causes of AVMs and to improve surgical treatment of these lesions. An NINDS study at Columbia University, A Randomized Trial of Unruptured Brain AVMs (ARUBA), showed that medical management alone is superior to medical management and interventional therapy (conventional surgery, endovascular procedures, and radiosurgery) for improving the long-term outcome of individuals with unruptured brain arteriovenous malformations. Data from a recently closed observational phase will show if the disparities continued over the additional five years of follow-up.
                
Among other NINDS-funded research, scientists are testing a class of drugs called beta-blockers to see if they may lead to the development of new treatments for people with vascular malformations. Other NINDS-funded investigators hope to develop biomarkers (signs that may indicate risk of a disease) for AVM that may improve risk assessment and aid in the choice of therapy that may provide maximize benefit with minimal risk to the individual. Additional NINDS-funded research hopes to determine molecular pathways fundamental to the formation of brain AVMs. + NINDS + Arteriovenous Malformation
What is (are) Myotonia ?
Myotonia is a medical term that refers to a neuromuscular condition in which the relaxation of a muscle is impaired. It can affect any muscle group. Repeated effort will be needed to relax the muscle, although the condition usually improves after the muscles have warmed-up. Individuals with myotonia may have trouble releasing their grip on objects or may have difficulty rising from a seated position. They may walk with a stiff, awkward gait. Myotonia is caused by an abnormality in the muscle membrane, and is often associated with inherited neurological disorders. Myotonia is commonly seen in individuals with myotonic muscular dystrophy, myotonia congenita, and in people who have one of a group of neurological disorders called the channelopathies, which are inherited diseases that are caused by mutations in the chloride sodium or potassium channels that regulate the muscle membrane. Myotonia may also be triggered by exposure to cold. + NINDS + Myotonia
What are the treatments for Myotonia ?
Treatment for myotonia may include mexiletine, quinine, phenytoin, and other anticonvulsant drugs. Physical therapy and other rehabilitative measures may help muscle function. + NINDS + Myotonia
What is the outlook for Myotonia ?
Myotonia is a chronic disorder. Symptoms may improve later in life. + NINDS + Myotonia
what research (or clinical trials) is being done for Myotonia ?
The National Institute of Neurological Disorders and Stroke supports and conducts an extensive research program on neuromuscular disorders. The goals of this research are to learn more about these disorders and to find ways to treat, prevent, and cure them. + NINDS + Myotonia
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 + NINDS + Locked-In Syndrome
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. + NINDS + Locked-In Syndrome
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. + NINDS + Locked-In Syndrome
what research (or clinical trials) is being done for Locked-In Syndrome ?
The NINDS supports research on neurological disorders that can cause locked-in syndrome. The goals of this research are to find ways to prevent, treat, and cure these disorders. + NINDS + Locked-In Syndrome
What is (are) Arachnoid Cysts ?
Arachnoid cysts are cerebrospinal fluid-filled sacs that are located between the brain or spinal cord and the arachnoid membrane, one of the three membranes that cover the brain and spinal cord. Primary arachnoid cysts are present at birth and are the result of developmental abnormalities in the brain and spinal cord that arise during the early weeks of gestation. Secondary arachnoid cysts are not as common as primary cysts and develop as a result of head injury, meningitis, or tumors, or as a complication of brain surgery. The majority of arachnoid cysts form outside the temporal lobe of the brain in an area of the skull known as the middle cranial fossa. Arachnoid cysts involving the spinal cord are rarer. The location and size of the cyst determine the symptoms and when those symptoms begin. Most individuals with arachnoid cysts develop symptoms before the age of 20, and especially during the first year of life, but some people with arachnoid cysts never have symptoms. Males are four times more likely to have arachnoid cysts than females.
                
Typical symptoms of an arachnoid cyst around the brain include headache, nausea and vomiting, seizures, hearing and visual disturbances, vertigo, and difficulties with balance and walking. Arachnoid cysts around the spinal cord compress the spinal cord or nerve roots and cause symptoms such as progressive back and leg pain and tingling or numbness in the legs or arms. Diagnosis usually involves a brain scan or spine scan using diffusion-weighted MRI (magnetic resonance imaging) which helps distinguish fluid-filled arachnoid cysts from other types of cysts. + NINDS + Arachnoid Cysts
What are the treatments for Arachnoid Cysts ?
There has been active debate about how to treat arachnoid cysts. The need for treatment depends mostly upon the location and size of the cyst. If the cyst is small, not disturbing surrounding tissue, and not causing symptoms, some doctors will refrain from treatment. In the past, doctors placed shunts in the cyst to drain its fluid. Now with microneurosurgical techniques and endoscopic tools that allow for minimally invasive surgery, more doctors are opting to surgically remove the membranes of the cyst or open the cyst so its fluid can drain into the cerebrospinal fluid and be absorbed. + NINDS + Arachnoid Cysts
What is the outlook for Arachnoid Cysts ?
Untreated, arachnoid cysts may cause permanent severe neurological damage when progressive expansion of the cyst(s) or bleeding into the cyst injures the brain or spinal cord. Symptoms usually resolve or improve with treatment. + NINDS + Arachnoid Cysts
what research (or clinical trials) is being done for Arachnoid Cysts ?
The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to brain abnormalities and disorders of the nervous system such as arachnoid cysts in laboratories at the National Institutes of Health (NIH), and supports 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 neurological disorders such as arachnoid cysts. + NINDS + Arachnoid Cysts
What is (are) Congenital Myasthenia ?
All forms of myasthenia are due to problems in the communication between nerve cells and muscles. Most involve the activities of neurotransmitters. Neurotransmitters are chemicals that allow neurons to relay information from one cell to the next. For neurotransmitters to be effective, the nerve cell must release the neurotransmitter properly, and the muscle cell must be able to detect the neurotransmitter and respond to its signal properly.
                
The most common type of myasthenia, myasthenia gravis, is caused by an abnormal immune response in which antibodies block the ability of the muscle to detect the neurotransmitter. Congenital myasthenia, however, differs from myasthenia gravis because the disrupted communication isn't caused by antibodies, but by genetic defects.
                
There are several different subtypes of congenital myasthenia, each the result of a specific genetic mutation. Since all types of myasthenia are due to the inability of nerves to trigger muscle activity, they all involve weakness, although there is some variability in the specific muscles affected.
                
Symptoms of congenital myasthenia usually appear in the first few years of childhood, but may not be noticeable until much later, occasionally remaining unrecognized until adulthood. If the symptoms begin in infancy, they usually appear as "floppiness" and a failure to meet developmental milestones, such as rolling over or sitting up. Some infants may also have episodes of choking or pauses in breathing. If the symptoms begin in toddlers or preschool children, they appear as weakness during physical activities or an inability to perform age-appropriate actions, such as running or climbing. In addition, if eye muscles are involved, children may have droopy eyelids, "lazy eye," or double vision. If mouth or throat muscles are involved, children may have difficulty speaking or swallowing. An important characteristic of myasthenia is that the weakness worsens during continuous activity, with strength returning, at least partially, after resting.
                
Congenital myasthenia is an inherited (genetic) disorder. All but one known subtype are recessive disorders, which means that a child will have to have two copies of the abnormal gene (one from each parent) in order to develop the disease. To diagnose congenital myasthenia, a neurologist will test various muscles to determine if they grow weaker with repeated activity. The doctor will also test the electrical activity of nerves and muscles using electromyography (EMG) and nerve conduction tests (NCS). Blood tests are often used to determine if antibodies could be causing the symptoms. Genetic tests may be ordered. + NINDS + Congenital Myasthenia
What are the treatments for Congenital Myasthenia ?
The possibilities for treatment depend on the specific subtype of congenital myasthenia. Most treatments attempt to improve the signaling between nerve cell and muscle. These drugs include pyridostigmine, fluoxetine, ephedrine, and 3,4-diaminopyridine. Treatments to alter the immune system are not used for this form of myasthenia. There are no treatments to cure the underlying genetic abnormality. + NINDS + Congenital Myasthenia
What is the outlook for Congenital Myasthenia ?
The prognosis depends on the specific subtype of congenital myasthenia, the muscles involved, and the age at onset of symptoms. If a child has difficulty breathing, feeding, or swallowing, they may be vulnerable to pneumonia or respiratory failure. In other cases, weakness is stable and does not worsen over time. In one subtype, weakness improves with time. Life-span is normal in most cases in which respiratory function is not compromised. + NINDS + Congenital Myasthenia
what research (or clinical trials) is being done for Congenital Myasthenia ?
The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) support research related to congenital myasthenia through grants to major research institutions across the country. Much of this research focuses on finding better ways to prevent, treat and ultimately cure disorders such as congenital myasthenia. + NINDS + Congenital Myasthenia
What is (are) Neuromyelitis Optica ?
Neuromyelitis optica (NMO) is an autoimmune disease of the central nervous system (CNS) that predominantly affects the optic nerves and spinal cord. It is sometimes also referred to as NMO spectrum disorder.In NMO, the body's immune system mistakenly attacks healthy cells and proteins in the body, must often those in the spinal cord and eyes. Individuals with NMO develop optic neuritis, which caused pain in the eye and vision loss. Individuals also develop transverse myelitis, which causes weakness or paralysis of arms and legs,and numbness, along with loss of bladder and bowel control Magnetic resonance imaging of the spine often shows an abnormality that extends over long segments of the spinal cord. Individuals may also develop episodes of severe nausea and vomiting, with hiccups from involvement of a part of the brain that ocntrols vomiting The disease is caused by abnormal autoantibodies that bind to a protein called aquaporin-4. Binding of the aquaporin-4 antibody activates other components of the immune system, causing inflammation and damage to these cells. This also results in the brain and spinal cord the loss of myelin, the fatty substance that acts as insulation around nerve fibers and helps nerve signals move from cell to cell.
                
NMO is different from multiple sclerosis (MS). Attacks are usually more severe in NMO than in MS, and NMO is treated differently than MS. Most individuals with NMO experience clusters of attacks days to months or years apart, followed by partial recovery during periods of remission. Women are more often affected by NMO than men. African Americans are at greater risk of the disease than are Caucasians. The onset of NMO varies from childhood to adulthood, with two peaks, one in childhood and the other in adults in their 40s. + NINDS + Neuromyelitis Optica
What are the treatments for Neuromyelitis Optica ?
There is no cure for NMO and no FDA-approved therapies, but there are therapies to treat an attack while it is happening, to reduce symptoms, and to prevent relapses.NMO relapses and attacks are often treated with corticosteroid drugs and plasma exchange (also called plasmapheresis, a process used to remove harmful antibodies from the bloodstream). Immunosuppressvie drugs used to prevent attacks include mycophenolate mofetil, rituximab, and azathioprine. Pain, stiffness, muscle spasms, and bladder and bowel control problems can be managed with medicaitons and therapies. Individuals with major disability will require the combined efforts to physical and occupational therapists, along with social services professionals to address complex rehabilitation needs. + NINDS + Neuromyelitis Optica
What is the outlook for Neuromyelitis Optica ?
Most individuals with NMO have an unpredictable, relapsing course of disease with attacks occurring months or years apart. Disability is cumulative, the result of each attack damaging new areas of the central nervous system. Some individuals are severely affected by NMO and can lose vision in both eyes and the use of their arms and legs. Most individuals experience some degree of permanent limb weakness or vision loss from NMO. However, reducing the number of attacks with immunosuppressive medications may help prevent with accumulation of disability. Rarely, muscle weakness can be severe enough to cause breathing difficulties and may require the use of artificial ventilation. + NINDS + Neuromyelitis Optica
what research (or clinical trials) is being done for Neuromyelitis Optica ?
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 is a component of the National Institutes of Health, the leading supporter of biomedical research in the world. NINDS researchers are working to better understand the process by which the immune system destroys or attacks the nerve insulating substance called myelin in autoijmune diseases or disorders. Other work focuses on strategies to repair demyelinated spinal cords, including approaches using cell transplantation. this research may lead to a grater understanding of the mechanisms responsible for damaging myelin and may ultimately provide a means to prevent and treat transverse myelitis An NINDS-funded study comparing clinical MRI and lumbar puncture of healthy individuals to those with symptoms of immune-related central nervous system damage hopes to identify processes or mechanisms to inhibit or minimize spinal tissue damage and enhance recovery mechanisms. Multiple studies are looking at ways to target different components of the immune system known to be involved in NMO spectrum disorders to allow more directly targeted treatment of this disease. + NINDS + Neuromyelitis Optica
What is (are) Cerebral Hypoxia ?
Cerebral hypoxia refers to a condition in which there is a decrease of oxygen supply to the brain even though there is adequate blood flow. Drowning, strangling, choking, suffocation, cardiac arrest, head trauma, carbon monoxide poisoning, and complications of general anesthesia can create conditions that can lead to cerebral hypoxia. Symptoms of mild cerebral hypoxia include inattentiveness, poor judgment, memory loss, and a decrease in motor coordination. Brain cells are extremely sensitive to oxygen deprivation and can begin to die within five minutes after oxygen supply has been cut off. When hypoxia lasts for longer periods of time, it can cause coma, seizures, and even brain death. In brain death, there is no measurable activity in the brain, although cardiovascular function is preserved. Life support is required for respiration. + NINDS + Cerebral Hypoxia
What are the treatments for Cerebral Hypoxia ?
Treatment depends on the underlying cause of the hypoxia, but basic life-support systems have to be put in place: mechanical ventilation to secure the airway; fluids, blood products, or medications to support blood pressure and heart rate; and medications to suppress seizures. + NINDS + Cerebral Hypoxia
What is the outlook for Cerebral Hypoxia ?
Recovery depends on how long the brain has been deprived of oxygen and how much brain damage has occurred, although carbon monoxide poisoning can cause brain damage days to weeks after the event. Most people who make a full recovery have only been briefly unconscious. The longer someone is unconscious, the higher the chances of death or brain death and the lower the chances of a meaningful recovery. During recovery, psychological and neurological abnormalities such as amnesia, personality regression, hallucinations, memory loss, and muscle spasms and twitches may appear, persist, and then resolve. + NINDS + Cerebral Hypoxia
what research (or clinical trials) is being done for Cerebral Hypoxia ?
The NINDS supports and conducts studies aimed at understanding neurological conditions that can damage the brain, such as cerebral hypoxia. The goals of these studies are to find ways to prevent and treat these conditions. + NINDS + Cerebral Hypoxia
What is (are) Essential Tremor ?
Tremor is an unintentional, somewhat rhythmic, muscle movement involving to-and-fro movements (oscillations) of one or more parts of the body. Essential tremor (previously called benign essential tremor) is the most common form of abnormal tremor. (In some people, tremor is a symptom of a neurological disorder or appears as a side effect of certain drugs.) Although it may be mild and nonprogressive in some people, in others the tremor is slowly progressive, starting on one side of the body but eventually affecting both sides. Hand tremor is most common but the head, arms, voice, tongue, legs, and trunk may also be involved. Hand tremor may cause problems with purposeful movements such as eating, writing, sewing, or shaving. Head tremor may be seen as a "yes-yes" or "no-no" motion. Essential tremor may be accompanied by mild gait disturbance. Heightened emotion, stress, fever, physical exhaustion, or low blood sugar may trigger tremors or increase their severity. There may be mild degeneration in the certain parts of the cerebellum in persons with essential tremor. Onset is most common after age 40, although symptoms can appear at any age. Children of a parent who has essential tremor have up to a 50 percent chance of inheriting the condition. Essential tremor is not associated with any known pathology. + NINDS + Essential Tremor
What are the treatments for Essential Tremor ?
There is no definitive cure for essential tremor. Symptomatic drug therapy may include propranolol or other beta blockers and primidone, an anticonvulsant drug. Eliminating tremor "triggers" such as caffeine and other stimulants from the diet is often recommended. Physical and occupational therapy may help to reduce tremor and improve coordination and muscle control for some individuals. Deep brain stimulation uses a surgically implanted, battery-operated medical device called a neurostimulator to delivery electrical stimulation to targeted areas of the brain that control movement, temporarily blocking the nerve signals that cause tremor. Other surgical intervention is effective but may have side effects. + NINDS + Essential Tremor
What is the outlook for Essential Tremor ?
Although essential tremor is not life-threatening, it can make it harder to perform daily tasks and is embarrassing to some people. Tremor frequency may decrease as the person ages, but the severity may increase, affecting the person's ability to perform certain tasks or activities of daily living. In many people the tremor may be mild throughout life. + NINDS + Essential Tremor
what research (or clinical trials) is being done for Essential Tremor ?
The National Institute of Neurological Disorders and Stroke, a unit of the National Institutes of Health (NIH) within the U.S. Department of Health and Human Services, is the nation's leading federal funder of research on disorders of the brain and nervous system. The NINDS sponsors research on tremor both at its facilities at the NIH and through grants to medical centers.
                
Scientists at the NINDS are evaluating the effectiveness of 1-octanol, a substance similar to alcohol but less intoxicating, for treating essential tremor. Results of two previous NIH studies have shown this agent to be promising as a potential new treatment.
                
Scientists are also studying the effectiveness of botulinum toxin as a treatment for a variety of involuntary movement disorders, including essential tremor of the hand. + NINDS + Essential Tremor