Druvith/medqa1 huggingface dataset:
Question:  What is the outlook for Foot Drop ?
Answer: The prognosis for foot drop depends on the cause. Foot drop caused by trauma or nerve damage usually shows partial or even complete recovery. For progressive neurological disorders, foot drop will be a symptom that is likely to continue as a lifelong disability, but it will not shorten life expectancy.
Question:  what research (or clinical trials) is being done for Foot Drop ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to the neurological conditions that cause foot drop in its laboratories at the National Institutes of Health (NIH), and also 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 the kinds of neurological disorders that cause foot drop.
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) Anencephaly ?
Answer: Anencephaly is a defect in the closure of the neural tube during fetal development. The neural tube is a narrow channel that folds and closes between the 3rd and 4th weeks of pregnancy to form the brain and spinal cord of the embryo. Anencephaly occurs when the "cephalic" or head end of the neural tube fails to close, resulting in the absence of a major portion of the brain, skull, and scalp. Infants with this disorder are born without a forebrain (the front part of the brain) and a cerebrum (the thinking and coordinating part of the brain). The remaining brain tissue is often exposed--not covered by bone or skin. A baby born with anencephaly is usually blind, deaf, unconscious, and unable to feel pain. Although some individuals with anencephaly may be born with a rudimentary brain stem, the lack of a functioning cerebrum permanently rules out the possibility of ever gaining consciousness. Reflex actions such as breathing and responses to sound or touch may occur.
                
The cause of anencephaly is unknown. Although it is thought that a mother's diet and vitamin intake may play a role, scientists believe that many other factors are also involved.
                
Recent studies have shown that the addition of folic acid (vitamin B9) to the diet of women of childbearing age may significantly reduce the incidence of neural tube defects. Therefore it is recommended that all women of childbearing age consume 0.4 mg of folic acid daily.
Question:  What are the treatments for Anencephaly ?
Answer: There is no cure or standard treatment for anencephaly. Treatment is supportive.
Question:  What is the outlook for Anencephaly ?
Answer: The prognosis for babies born with anencephaly is extremely poor. If the infant is not stillborn, then he or she will usually die within a few hours or days after birth.
Question:  what research (or clinical trials) is being done for Anencephaly ?
Answer: Research supported by the NINDS includes studies to understand how the brain and nervous system normally develop. These studies contribute to a greater understanding of neural tube disorders, such as anencephaly, and open promising new avenues to treat and prevent neurological birth defects.
Question:  What is (are) Neurological Consequences of Cytomegalovirus Infection ?
Answer: Cytomegalovirus (CMV) is a virus found throughout the world that infects between 50 to 80 percent of all adults in the United States by the age of 40. CMV is in the same family of viruses that causes cold sores (herpes simplex virus), infectious mononucleosis (Epstein-Barr virus), and chickenpox/shingles (varicella zoster virus).  Most people who acquire CVM as children or adults display no signs of illness or have mild symptoms such as fever, fatigue, or tender lymph nodes. People with a compromised immune system may have more severe forms of infection involving the nervous system.
                
A hallmark of CMV infection is that the virus cycles through periods of dormancy and active infection during the life of the individual Infected persons of any age periodically shed the virus in their body fluids, such as saliva, urine, blood, tears, semen, or breast milk. CMV is most commonly transmitted when infected body fluids come in contact with the mucous membranes of an uninfected person, but the virus can also pass from mother to fetus during pregnancy.
Question:  What are the treatments for Neurological Consequences of Cytomegalovirus Infection ?
Answer: Since the virus remains in the person for life, there is no treatment to eliminate CMV infection. However, minimizing contact with infected body fluids can decrease the risk of viral transmission between individuals or from mother to fetus. Contact can be minimized by using gloves or other protective barriers when handling body fluids or contaminated materials (such as diapers or tissues), avoiding shared dishes, utensils, and other personal items, and consistent and thorough hand-washing. 
                
Antiviral drugs (ganciclovir and others)can be used to prevent or control the symptoms of CMV infection in immunocompromised individuals or some infants with congenital infection. CMV immunoglobulin may also be used in some patients. Vaccines are in the development and human clinical trial stages, which shows that vaccines may help prevent initial CMV infection or decrease the severity of symptoms.
Question:  What is the outlook for Neurological Consequences of Cytomegalovirus Infection ?
Answer: For most people CMV infection is not a problem. However, two groups of people are at high risk of neurological or other severe symptoms that may lead to long-term effects:
                
- Unborn infants whose mothers have CMV infection. CMVis the most common congenital infection in the U.S. Most infants will have no permanent health consequences, but a small number will have at birth or will develop long-term neurological conditions, such as hearing loss, visual impairment, seizures, or disabilities f mental or physical function. The highest risk of these severe effects on the fetus is for women who acquire CMV infection for the first time during pregnancy. The risk is much lower for women who have had CMV infection in the past before pregnancy. - Immunocompromised individuals. CMV infection may be severe in solid organ or blood cell transplant recipients, people with untreated or end-stage HIV-AIDS, or others with altered immune function. Infection may affect the brain (encephalitis), spinal cord (myelitis), eye (retinitis), or other organs such as the lungs (pneumonia) or intestinal gract (gastritis, enteritis, or colitis). In addition, transplant recipients may develop organ rejection or graft-versus-host disease associated with CMV infection.
Question:  what research (or clinical trials) is being done for Neurological Consequences of Cytomegalovirus Infection ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS), and other institutes of the National Institutes of Health (NIH), conduct research related to CMV infection in laboratories at the NIH, and support additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent and treat CMV infection in people at risk of severe neurological consequences, especially a safe and effective CMV vaccine.
Question:  What is (are) Muscular Dystrophy ?
Answer: The muscular dystrophies (MD) are a group of more than 30 genetic diseases characterized by progressive weakness and degeneration of the skeletal muscles that control movement. Some forms of MD are seen in infancy or childhood, while others may not appear until middle age or later. The disorders differ in terms of the distribution and extent of muscle weakness (some forms of MD also affect cardiac muscle), age of onset, rate of progression, and pattern of inheritance. Duchenne MD is the most common form of MD and primarily affects boys. It is caused by the absence of dystrophin, a protein involved in maintaining the integrity of muscle. Onset is between 3 and 5 years and the disorder progresses rapidly. Most boys are unable to walk by age 12, and later need a respirator to breathe. Girls in these families have a 50 percent chance of inheriting and passing the defective gene to their children. Boys with Becker MD (very similar to but less severe than Duchenne MD) have faulty or not enough dystrophin. Facioscapulohumeral MD usually begins in the teenage years. It causes progressive weakness in muscles of the face, arms, legs, and around the shoulders and chest. It progresses slowly and can vary in symptoms from mild to disabling. Myotonic MD is the disorder's most common adult form and is typified by prolonged muscle spasms, cataracts, cardiac abnormalities, and endocrine disturbances. Individuals with myotonic MD have long, thin faces, drooping eyelids, and a swan-like neck.
Question:  What are the treatments for Muscular Dystrophy ?
Answer: There is no specific treatment to stop or reverse any form of MD. Treatment may include physical therapy, respiratory therapy, speech therapy, orthopedic appliances used for support, and corrective orthopedic surgery. Drug therapy includes corticosteroids to slow muscle degeneration, anticonvulsants to control seizures and some muscle activity, immunosuppressants to delay some damage to dying muscle cells, and antibiotics to fight respiratory infections. Some individuals may benefit from occupational therapy and assistive technology. Some patients may need assisted ventilation to treat respiratory muscle weakness and a pacemaker for cardiac abnormalities.
Question:  What is the outlook for Muscular Dystrophy ?
Answer: The prognosis for people with MD varies according to the type and progression of the disorder. Some cases may be mild and progress very slowly over a normal lifespan, while others produce severe muscle weakness, functional disability, and loss of the ability to walk. Some children with MD die in infancy while others live into adulthood with only moderate disability.
Question:  what research (or clinical trials) is being done for Muscular Dystrophy ?
Answer: The NINDS supports a broad program of research studies on MD. The goals of these studies are to understand MD and to develop techniques to diagnose, treat, prevent, and ultimately cure the disorder.
                
The NINDS is a member of the Muscular Dystrophy Coordinating Committee (MDCC). For additional information, please visit: http://www.ninds.nih.gov/about_ninds/groups/mdcc/
Question:  What is (are) Tourette Syndrome ?
Answer: Tourette syndrome (TS) is a neurological disorder characterized by repetitive, stereotyped, involuntary movements and vocalizations called tics. The first symptoms of TS are almost always noticed in childhood. Some of the more common tics include eye blinking and other vision irregularities, facial grimacing, shoulder shrugging, and head or shoulder jerking. Perhaps the most dramatic and disabling tics are those that result in self-harm such as punching oneself in the face, or vocal tics including coprolalia (uttering swear words) or echolalia (repeating the words or phrases of others). Many with TS experience additional neurobehavioral problems including inattention, hyperactivity and impulsivity, and obsessive-compulsive symptoms such as intrusive thoughts/worries and repetitive behaviors.
Question:  What are the treatments for Tourette Syndrome ?
Answer: Because tic symptoms do not often cause impairment, the majority of people with TS require no medication for tic suppression. However, effective medications are available for those whose symptoms interfere with functioning. There is no one medication that is helpful to all people with TS, nor does any medication completely eliminate symptoms. Effective medications are also available to treat some of the associated neurobehavioral disorders that can occur in patients with TS.
Question:  What is the outlook for Tourette Syndrome ?
Answer: Although TS can be a chronic condition with symptoms lasting a lifetime, most people with the condition experience their worst symptoms in their early teens, with improvement occurring in the late teens and continuing into adulthood. As a result, some individuals may actually become symptom free or no longer need medication for tic suppression.
Question:  what research (or clinical trials) is being done for Tourette Syndrome ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research in laboratories at the NIH and support additional research through grants to major medical institutions across the country. Knowledge about TS comes from studies across a number of medical and scientific disciplines, including genetics, neuroimaging, neuropathology, clinical trials, epidemiology, neurophysiology, neuroimmunology, and descriptive/diagnostic clinical science. Findings from these studies will provide clues for more effective therapies.
Question:  What is (are) Hypertonia ?
Answer: Hypertonia is a condition in which there is too much muscle tone so that arms or legs, for example, are stiff and difficult to move. Muscle tone is regulated by signals that travel from the brain to the nerves and tell the muscle to contract. Hypertonia happens when the regions of the brain or spinal cord that control these signals are damaged. This can occur for many reasons, such as a blow to the head, stroke, brain tumors, toxins that affect the brain, neurodegenerative processes such as in multiple sclerosis or Parkinson's disease, or neurodevelopmental abnormalities such as in cerebral palsy.
                
Hypertonia often limits how easily the joints can move. If it affects the legs, walking can become stiff and people may fall because it is difficult for the body to react quickly enough to regain balance. If hypertonia is severe, it can cause a joint to become "frozen," which doctors call a joint contracture.
                
Spasticity is a term that is often used interchangeably with hypertonia. Spasticity, however, is a particular type of hypertonia in which the muscles' spasms are increased by movement. In this type, patients usually have exaggerated reflex responses.
                
Rigidity is another type of hypertonia in which the muscles have the same amount of stiffness independent of the degree of movement. Rigidity usually occurs in diseases such as Parkinson's disease, that involve the basal ganglia (a deep region of the brain). To distinguish these types of hypertonia, a doctor will as the patient to relax and then will move the arm or leg at different speeds and in a variety of directions.
Question:  What are the treatments for Hypertonia ?
Answer: Muscle relaxing drugs such as baclofen, diazepam, and dantrolene may be prescribed to reduce spasticity. All of these drugs can be taken by mouth, but baclofen may also be injected directly into the cerebrospinal fluid through an implanted pump. Botulinum toxin is often used to relieve hypertonia in a specific area of the body because its effects are local, not body-wide. People with hypertonia should try to preserve as much movement as possibly by exercising within their limits and using physical therapy.
                
Drugs that affect the dopamine system (dopamine is a chemical in the brain) such as levodopa/carbidopa, or entacapone, are often used to treat the rigidity associated with Parkinson's disease.
Question:  What is the outlook for Hypertonia ?
Answer: The prognosis depends upon the severity of the hypertonia and its cause. In some cases, such as cerebral palsy, the hypertonia may not change over the course of a lifetime. in other cases, the hypertonia may worsen along with the underlying disease If the hypertonia is mild, it has little or no effect on a person's health. If there is moderate hypertonia, falls or joint contractures may have an impact on a person's health and safety. If the hypertonia is so severe that is caused immobility, potential consequences include increased bone fragility and fracture, infection, bed sores, and pneumonia.
Question:  what research (or clinical trials) is being done for Hypertonia ?
Answer: NINDS supports research on brain and spinal cord disorders that can cause hypertonia. The goals of this research are to learn more about how the nervous system adapts after injury or disease and to find ways to prevent and treat these disorders.
Question:  What is (are) Friedreich's Ataxia ?
Answer: Friedreich's ataxia is a rare inherited disease that causes progressive damage to the nervous system and movement problems. Neurological symptoms include awkward, unsteady movements, impaired sensory function, speech problems, and vision and hearing loss. Thinking and reasoning abilities are not affected.Impaired muscle coordination (ataxia) results from the degeneration of nerve tissue in the spinal cord and of nerves that control muscle movement in the arms and legs. Symptoms usually begin between the ages of 5 and 15 but can appear in adulthood or later. The first symptom is usually difficulty in walking. The ataxia gradually worsens and slowly spreads to the arms and then the trunk. People lave loss of sensation in the arms and legs, which may spread to other parts of the body. Many people with Friedreich's ataxia develop scoliosis (a curving of the spine to one side), which, if severe, may impair breathing. Other symptoms include chest pain, shortness of breath, and heart problems. Some individuals may develop diabetes. Doctors diagnose Friedreich's ataxia by performing a careful clinical examination, which includes a medical history and a thorough physical examination. Several tests may be performed, including electromyogram (EMG, which measures the electrical activity of cells) and genetic testing.
Question:  What are the treatments for Friedreich's Ataxia ?
Answer: There is currently no effective cure or treatment for Friedreich's ataxia. However, many of the symptoms and accompanying complications can be treated to help individuals maintain optimal functioning as long as possible. Diabetes and heart problems can be treated with medications. Orthopedic problems such as foot deformities and scoliosis can be treated with braces or surgery. Physical therapy may prolong use of the arms and legs.
Question:  What is the outlook for Friedreich's Ataxia ?
Answer: Generally, within 15 to 20 years after the appearance of the first symptoms, the person is confined to a wheelchair, and in later stages of the disease, individuals may become completely incapacitated. Friedreich's ataxia can shorten life expectancy; heart disease is the most common cause of death. Many individuals with Friedreich's ataxia die in early adulthood, but some people with less severe symptoms live into their 60s, 70s, or longer.
Question:  what research (or clinical trials) is being done for Friedreich's Ataxia ?
Answer: Friedreich's ataxia is caused by a mutation in the protein frataxin, which is involved in the function of mitochondriathe energy producing power plants of the cell. Frataxin controls important steps in mitochondrial iron metabolism and overall cell iron stability.NINDS-funded researchers are studying the metabolic functions of mitochondria in individuals with Friedreichs ataxia. Ongoing research is aimed at understanding the molecular basis for and mechanisms involved in the inactivation of the gene that provides instructions for frataxin, which could lead to potential ways to reverse the silencing and restore normal gene function.And researchers are using next-generation sequencing (which can quickly identify the structure of millions of small fragments of DNA at the same time) to identify novel genes in Friedreich's ataxia.