Ahmed062646/NLP_Medora_Datasets huggingface dataset:
Question: What is (are) Central Cord Syndrome ?
Answer: Central cord syndrome is the most common form of incomplete spinal cord injury characterized by impairment in the arms and hands and to a lesser extent in the legs. The brain's ability to send and receive signals to and from parts of the body below the site of injury is reduced but not entirely blocked. This syndrome is associated with damage to the large nerve fibers that carry information directly from the cerebral cortex to the spinal cord. These nerves are particularly important for hand and arm function. Symptoms may include paralysis or loss of fine control of movements in the arms and hands, with relatively less impairment of leg movements. Sensory loss below the site of the injury and loss of bladder control may also occur, as well as painful sensations such as tinging, burning, or dull ache. The overall amount and type of functional loss is dependent upon the severity of nerve damage. Central cord syndrome is usually the result of trauma that causes damage to the vertebrae in the neck or herniation of the vertebral discs. It also may develop in persons over the age of 50 due to gradual weakening of the vertebrae and discs, which narrows the spinal column and may contribute to compression of the spinal cord when the neck is hyper-extended.
Question: What are the treatments for Central Cord Syndrome ?
Answer: There is no cure for central cord syndrome although some people recover near-normal function. There is no standard course of treatment, although drug therapy, surgery, and rest are often part of the program. Magnetic resonance imaging (MRI) is used to indicate the degree of spinal cord compression and vertebral instability. Vertebral instability due to acute traumatic injury or cervical disc herniation is often treated by surgery to prevent further damage to the spinal cord. Recent reports indicate that earlier surgery may improve chances for recovery. Numerous recent studies suggest that surgery also can be beneficial in individuals with persistent compression of the spinal cord and ongoing neurological deterioration.
Question: What is the outlook for Central Cord Syndrome ?
Answer: The prognosis for central cord syndrome varies, but most people whose syndrome is caused by trauma have some recovery of neurological function. Evaluation of abnormal signals on MRI images can help predict he likelihood that neurological recovery may occur naturally. Those who receive medical intervention soon after their injury often have good outcomes. Many people with the disorder recover substantial function after their initial injury, and the ability to walk is recovered in most cases, although some impairment may remain. Improvement occurs first in the legs, then the bladder, and may be seen in the arms. Hand function recovers last, if at all. Recovery is generally better in younger patients, compared to those over the age of 50.
Question: what research (or clinical trials) is being done for Central Cord Syndrome ?
Answer: Our understanding of central cord syndrome has increased greatly in recent decades as a result of research funded conducted by the National Institute of Neurological Disorders and Stroke (NINDS). Much of this research focuses on finding better ways to prevent, treat, and ultimately cure neurological disorders such as central cord syndrome.
Question: What is (are) Fibromuscular Dysplasia ?
Answer: Fibromuscular dysplasia (FMD) is the abnormal development or growth of cells in the walls of arteries that can cause the vessels to narrow or bulge. The carotid arteries, which pass through the neck and supply blood to the brain, are commonly affected. Arteries within the brain and kidneys can also be affected. A characteristic string of beads pattern caused by the alternating narrowing and enlarging of the artery can block or reduce blood flow to the brain, causing a stroke or mini-stroke. Some patients experience no symptoms of the disease while others may have high blood pressure, dizziness or vertigo, chronic headache, intracranial aneurysm, ringing in the ears, weakness or numbness in the face, neck pain, or changes in vision. FMD is most often seen in persons age 25 to 50 years and affects women more often than men. More than one family member may be affected by the disease. The cause of FMD is unknown. An angiogram can detect the degree of narrowing or obstruction of the artery and identify changes such as a tear (dissection) or weak area (aneurysm) in the vessel wall. FMD can also be diagnosed using computed tomography, magnetic resonance imaging, or ultrasound.
Question: What are the treatments for Fibromuscular Dysplasia ?
Answer: There is no standard protocol to treat FMD. Any treatment to improve blood flow is based on the arteries affected and the progression and severity of the disease. The carotid arteries should be tested if FMD is found elsewhere in the body since carotid involvement is linked to an increased risk of stroke. Patients with minimal narrowing may take a daily antiplatelet such as an aspirin or an anticoagulant to thin the blood and reduce the chances that a clot might form. Medications such as aspirin can also be taken for headache and neck pain, symptoms that can come from FMD. Patients with arterial disease who smoke should be encouraged to quit as smoking worsens the disease. Further treatment may include angioplasty, in which a small balloon is inserted through a catheter and inflated to open the artery. Small tubes called stents may be inserted to keep arteries open. Surgery may be needed to treat aneurysms that have the potential to rupture and cause bleeding within the brain.
Question: What is the outlook for Fibromuscular Dysplasia ?
Answer: Currently there is no cure for FMD. Medicines and angioplasty can reduce the risk of initial or recurrent stroke. In rare cases, FMD-related aneurysms can burst and bleed into the brain, causing stroke, permanent nerve damage, or death.
Question: what research (or clinical trials) is being done for Fibromuscular Dysplasia ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS), a component of the National Institutes of Health (NIH) within the U.S. Department of Health and Human Services, is the nations primary funding source for research on the brain and nervous system. The NINDS conducts research on stroke and vascular lesions of the nervous system and supports studies through grants to medical institutions across the country.
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) Periventricular Leukomalacia ?
Answer: Periventricular leukomalacia (PVL) is characterized by the death of the white matter of the brain due to softening of the brain tissue. It can affect fetuses or newborns; premature babies are at the greatest risk of the disorder. PVL is caused by a lack of oxygen or blood flow to the periventricular area of the brain, which results in the death or loss of brain tissue. The periventricular area-the area around the spaces in the brain called ventricles-contains nerve fibers that carry messages from the brain to the body's muscles. Although babies with PVL generally have no outward signs or symptoms of the disorder, they are at risk for motor disorders, delayed mental development, coordination problems, and vision and hearing impairments. PVL may be accompanied by a hemorrhage or bleeding in the periventricular-intraventricular area (the area around and inside the ventricles), and can lead to cerebral palsy. The disorder is diagnosed by ultrasound of the head.
Question: What are the treatments for Periventricular Leukomalacia ?
Answer: There is no specific treatment for PVL. Treatment is symptomatic and supportive. Children with PVL should receive regular medical screenings to determine appropriate interventions.
Question: What is the outlook for Periventricular Leukomalacia ?
Answer: The prognosis for individuals with PVL depends upon the severity of the brain damage. Some children exhibit fairly mild symptoms, while others have significant deficits and disabilities.
Question: what research (or clinical trials) is being done for Periventricular Leukomalacia ?
Answer: The NINDS supports and conducts research on brain injuries such as PVL. Much of this research is aimed at finding ways to prevent and treat these disorders.
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) Zellweger Syndrome ?
Answer: Zellweger syndrome is one of a group of four related diseases called peroxisome biogenesis disorders (PBD). The diseases are caused by defects in any one of 13 genes, termed PEX genes, required for the normal formation and function of peroxisomes. The PBDs are divided into two groups: Zellweger spectrum disorders and Rhizomelic Chondrodysplasia Punctua spectrum. The Zellweger spectrum is comprised of three disorders that have considerable overlap of features. These include Zellweger syndrome (ZS, the most severe form), neonatal adrenoleukodystrophy (NALD), and Infantile Refsum disease (IRD, the least severe form). Peroxisomes are cell structures that break down toxic substances and synthesize lipids (fatty acids. oils, and waxes) that are necessary for cell function. Peroxisomes are required for normal brain development and function and the formation of myelin, the whitish substance that coats nerve fibers. They are also required for normal eye, liver, kidney, and bone functions. Zellweger spectrum disorders result from dysfunctional lipid metabolism, including the over-accumulation of very long-chain fatty acids and phytanic acid, and defects of bile acids and plasmalogens--specialized lipids found in cell membranes and myelin sheaths of nerve fibers. Symptoms of these disorders include an enlarged liver; characteristic facial features such as a high forehead, underdeveloped eyebrow ridges, and wide-set eyes; and neurological abnormalities such as cognitive impairment and seizures. Infants will Zellweger syndrome also lack muscle tone, sometimes to the point of being unable to move, and may not be able to suck or swallow. Some babies will be born with glaucoma, retinal degeneration, and impaired hearing. Jaundice and gastrointestinal bleeding also may occur.
Question: What are the treatments for Zellweger Syndrome ?
Answer: There is no cure for Zellweger syndrome, nor is there a standard course of treatment. Since the metabolic and neurological abnormalities that cause the symptoms of Zellweger syndrome are caused during fetal development, treatments to correct these abnormalities after birth are limited. Most treatments are symptomatic and supportive.
Question: what research (or clinical trials) is being done for Zellweger Syndrome ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS), and other institutes of the National Institutes of Health (NIH), conduct research exploring the molecular and genetic basis of Zellweger syndrome and the other PBDs, and also support additional research 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 Zellweger syndrome.
Question: What are the treatments for Parkinson's Disease ?
Answer: At present, there is no cure for PD, but a variety of medications provide dramatic relief from the symptoms. Usually, affected individuals are given levodopa combined with carbidopa. Carbidopa delays the conversion of levodopa into dopamine until it reaches the brain. Nerve cells can use levodopa to make dopamine and replenish the brain's dwindling supply. Although levodopa helps at least three-quarters of parkinsonian cases, not all symptoms respond equally to the drug. Bradykinesia and rigidity respond best, while tremor may be only marginally reduced. Problems with balance and other symptoms may not be alleviated at all. Anticholinergics may help control tremor and rigidity. Other drugs, such as bromocriptine, pramipexole, and ropinirole, mimic the role of dopamine in the brain, causing the neurons to react as they would to dopamine. An antiviral drug, amantadine, also appears to reduce symptoms. In May 2006, the FDA approved rasagiline to be used along with levodopa for patients with advanced PD or as a single-drug treatment for early PD. In some cases, surgery may be appropriate if the disease doesn't respond to drugs. A therapy called deep brain stimulation (DBS) has now been approved by the U.S. Food and Drug Administration. In DBS, electrodes are implanted into the brain and connected to a small electrical device called a pulse generator that can be externally programmed. DBS can reduce the need for levodopa and related drugs, which in turn decreases the involuntary movements called dyskinesias that are a common side effect of levodopa. It also helps to alleviate fluctuations of symptoms and to reduce tremors, slowness of movements, and gait problems. DBS requires careful programming of the stimulator device in order to work correctly.
Question: What is the outlook for Parkinson's Disease ?
Answer: PD is both chronic, meaning it persists over a long period of time, and progressive, meaning its symptoms grow worse over time. Although some people become severely disabled, others experience only minor motor disruptions. Tremor is the major symptom for some individuals, while for others tremor is only a minor complaint and other symptoms are more troublesome. It is currently not possible to predict which symptoms will affect an individual, and the intensity of the symptoms also varies from person to person.
Question: what research (or clinical trials) is being done for Parkinson's Disease ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS) conducts PD research in laboratories at the National Institutes of Health (NIH) and also supports additional research through grants to major medical institutions across the country. Current research programs funded by the NINDS are using animal models to study how the disease progresses and to develop new drug therapies. Scientists looking for the cause of PD continue to search for possible environmental factors, such as toxins, that may trigger the disorder, and study genetic factors to determine how defective genes play a role. Other scientists are working to develop new protective drugs that can delay, prevent, or reverse the disease. http://www.ninds.nih.gov/research/parkinsonsweb/index.htm
Question: What is (are) Bell's Palsy ?
Answer: Bell's palsy is a form of temporary facial paralysis resulting from damage or trauma to the 7th cranial nerve, one of the facial nerves. It is the most common cause of facial paralysis. Generally, Bell's palsy affects only one side of the face, however, in rare cases, it can affect both sides. Symptoms usually begin suddenly and reach their peak within 72 hours, and can range in severity from mild weakness to total paralysis. Symptoms vary among individuals and include sudden weakness on one side of the face, drooping eyelid or corner of the mouth, drooling, dry eye or mouth, altered taste, and excessive tearing in the eye. Bells palsy can cause significant facial distortion. The exact cause of Bell's palsy isn't known, but many scientists believe that reactivation of a dormant viral infection can cause the facial nerve to swell and becomes inflamed. Several other conditions can cause facial paralysis that might be diagnosed as Bell's palsy..
Question: What are the treatments for Bell's Palsy ?
Answer: Steroids such as prednisone -- used to reduce inflammation and swelling -- are an effective treatment for Bell's palsy. Antiviral drugs may have some benefit in shortening the course of the disease. Analgesics such as aspirin, acetaminophen, or ibuprofen may relieve pain. Because of possible drug interactions, individuals should always talk to their doctors before taking any over-the-counter medicines. Keeping the eye moist and protecting it from debris and injury, especially at night, is important. Lubricating eye drops can help. Other therapies such as physical therapy, facial massage or acupuncture may provide a potential small improvement in facial nerve function and pain..
Question: What is the outlook for Bell's Palsy ?
Answer: The prognosis for individuals with Bell's palsy is generally very good. The extent of nerve damage determines the extent of recovery. With or without treatment, most individuals begin to get better within 2 weeks after the initial onset of symptoms and recover some or all facial function within 3 to 6 months.