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Parkinson's disease

 

<!--<h1>Parkinson's disease </h1>--> Parkinson's disease (PD) is a degenerative disorder of the central nervous system. It was first described in 1817 by James Parkinson, a British physician who published a paper on what he called "the shaking palsy." In this paper, he set forth the major symptoms of the disease that would later bear his name.<br><br> <strong>What is Parkinson's Disease? </strong><br><br> Parkinson's disease belongs to a group of conditions called movement disorders. The four main symptoms are tremor, or trembling in hands, arms, legs, jaw, or head; rigidity, or stiffness of the limbs and trunk; bradykinesia, or slowness of movement; and postural instability, or impaired balance. These symptoms usually begin gradually and worsen with time. As they become more pronounced, patients may have difficulty walking, talking, or completing other simple tasks. Not everyone with one or more of these symptoms has PD, as the symptoms sometimes appear in other diseases as well. <br> PD is both chronic, meaning it persists over a long period of time, and progressive, meaning its symptoms grow worse over time. It is not contagious. Although some PD cases appear to be hereditary, and a few can be traced to specific genetic mutations, most cases are sporadic  that is, the disease does not seem to run in families. Many researchers now believe that PD results from a combination of genetic susceptibility and exposure to one or more environmental factors that trigger the disease. <br> PD is the most common form of parkinsonism, the name for a group of disorders with similar features and symptoms. PD is also called primary parkinsonism or idiopathic PD. The term idiopathic means a disorder for which no cause has yet been found. While most forms of parkinsonism are idiopathic, there are some cases where the cause is known or suspected or where the symptoms result from another disorder. For example, parkinsonism may result from changes in the brain's blood vessels. <br><br> <strong>Causes</strong><br><br> Parkinson's disease occurs when nerve cells, or neurons, in an area of the brain known as the substantia nigra die or become impaired. Normally, these neurons produce an important brain chemical known as dopamine. Dopamine is a chemical messenger responsible for transmitting signals between the substantia nigra and the next "relay station" of the brain, the corpus striatum, to produce smooth, purposeful movement. Loss of dopamine results in abnormal nerve firing patterns within the brain that cause impaired movement. Studies have shown that most Parkinson's patients have lost 60 to 80 percent or more of the dopamine-producing cells in the substantia nigra by the time symptoms appear. Recent studies have shown that people with PD also have loss of the nerve endings that produce the neurotransmitter norepinephrine. Norepinephrine, which is closely related to dopamine, is the main chemical messenger of the sympathetic nervous system, the part of the nervous system that controls many automatic functions of the body, such as pulse and blood pressure. <br><br> Many brain cells of people with PD contain Lewy bodies  unusual deposits or clumps of the protein alpha-synuclein, along with other proteins. Researchers do not yet know why Lewy bodies form or what role they play in development of the disease. The clumps may prevent the cell from functioning normally, or they may actually be helpful, perhaps by keeping harmful proteins "locked up" so that the cells can function. <br> Scientists have identified several genetic mutations associated with PD, and many more genes have been tentatively linked to the disorder. Studying the genes responsible for inherited cases of PD can help researchers understand both inherited and sporadic cases. The same genes and proteins that are altered in inherited cases may also be altered in sporadic cases by environmental toxins or other factors. Researchers also hope that discovering genes will help identify new ways of treating PD. <br> Although the importance of genetics in PD is increasingly recognized, most researchers believe environmental exposures increase a person's risk of developing the disease. Even in familial cases, exposure to toxins or other environmental factors may influence when symptoms of the disease appear or how the disease progresses. There are a number of toxins, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, or MPTP (found in some kinds of synthetic heroin), that can cause parkinsonian symptoms in humans. Other, still-unidentified environmental factors also may cause PD in genetically susceptible individuals. <br> Viruses are another possible environmental trigger for PD. Several lines of research suggest that mitochondria may play a role in the development of PD. Mitochondria are the energy-producing components of the cell and are major sources of free radicals  molecules that damage membranes, proteins, DNA, and other parts of the cell. This damage is often referred to as oxidative stress. Oxidative stress-related changes, including free radical damage to DNA, proteins, and fats, have been detected in brains of PD patients. <br><br> Other research suggests that the cell's protein disposal system may fail in people with PD, causing proteins to build up to harmful levels and trigger cell death. Additional studies have found evidence that clumps of protein that develop inside brain cells of people with PD may contribute to the death of neurons, and that inflammation or overstimulation of cells (because of toxins or other factors) may play a role in the disease. However, the precise role of the protein deposits remains unknown. Some researchers even speculate that the protein buildup is part of an unsuccessful attempt to protect the cell. While mitochondrial dysfunction, oxidative stress, inflammation, and many other cellular processes may contribute to PD, the actual cause of the dopamine cell death is still undetermined.<br><br> <strong>Genes that are Linked to Parkinson's Disease</strong><br><br> Several genes have now been definitively linked to PD. The first to be identified was alpha-synuclein. After that it was found a second alpha-synuclein mutation. These findings prompted studies of the role of alpha-synuclein in PD, which led to the discovery that Lewy bodies from people with the sporadic form of PD contained clumps of alpha-synuclein protein. This discovery revealed a potential link between hereditary and sporadic forms of the disease.<br> Researchers studying inherited PD discovered that the disease in one large family was caused by a triplication of the normal alpha-synuclein gene on one copy of chromosome 4. This triplication caused people in the affected family to produce too much of the normal alpha-synuclein. <br> Other genes linked to PD include parkin, DJ-1, PINK1, and LRRK2. Parkin, DJ-1, and PINK-1 cause rare, early-onset forms of PD. The parkin gene is translated into a protein that normally helps cells break down and recycle proteins. DJ-1 normally helps regulate gene activity and protect cells from oxidative stress. PINK1 codes for a protein active in mitochondria. Mutations in this gene appear to increase susceptibility to cellular stress. <br> LRRK2, which is translated into a protein called dardarin, was originally identified and causes a late-onset form of PD. Researchers are continuing to investigate the normal functions and interactions of these genes in order to find clues about how PD develops. They also have identified a number of other genes and chromosome regions that may play a role in PD, but the nature of these links is not yet clear. <br><br> <strong>Who Gets Parkinson's Disease?</strong><br><br> PD strikes about 50 percent more men than women, but the reasons for this discrepancy are unclear. While it occurs in people throughout the world, a number of studies have found a higher incidence in developed countries, possibly because of increased exposure to pesticides or other toxins in those countries. Other studies have found an increased risk in people who live in rural areas and in those who work in certain professions, although the studies to date are not conclusive and the reasons for the apparent risks are not clear. <br> One clear risk factor for PD is age. The average age of onset is 60 years, and the incidence rises significantly with increasing age. However, about 5 to 10 percent of people with PD have "early-onset" disease that begins before the age of 50. Early-onset forms of the disease are often inherited, though not always, and some have been linked to specific gene mutations. People with one or more close relatives who have PD have an increased risk of developing the disease themselves, but the total risk is still just 2 to 5 percent unless the family has a known gene mutation for the disease. <br> In very rare cases, parkinsonian symptoms may appear in people before the age of 20. This condition is called juvenile parkinsonism. It is most commonly seen in Japan but has been found in other countries as well. It usually begins with dystonia and bradykinesia, and the symptoms often improve with levodopa medication. Juvenile parkinsonism often runs in families and is sometimes linked to a mutated parkin gene. <br><br> <strong>Symptoms </strong><br><br> Early symptoms of PD are subtle and occur gradually. Affected people may feel mild tremors or have difficulty getting out of a chair. They may notice that they speak too softly or that their handwriting is slow and looks cramped or small. They may lose track of a word or thought, or they may feel tired, irritable, or depressed for no apparent reason. This very early period may last a long time before the more classic and obvious symptoms appear. <br> Friends or family members may be the first to notice changes in someone with early PD. They may see that the person's face lacks expression and animation (known as "masked face") or that the person does not move an arm or leg normally. They also may notice that the person seems stiff, unsteady, or unusually slow. <br> As the disease progresses, the shaking or tremor that affects the majority of Parkinson's patients may begin to interfere with daily activities. Patients may not be able to hold utensils steady or they may find that the shaking makes reading a newspaper difficult. Tremor is usually the symptom that causes people to seek medical help. <br> People with PD often develop a so-called parkinsonian gait that includes a tendency to lean forward, small quick steps as if hurrying forward (called festination), and reduced swinging of the arms. They also may have trouble initiating movement (start hesitation), and they may stop suddenly as they walk (freezing). <br> PD does not affect everyone the same way, and the rate of progression differs among patients. Tremor is the major symptom for some patients, while for others, tremor is nonexistent or very minor. <br> PD symptoms often begin on one side of the body. However, as it progresses, the disease eventually affects both sides. Even after the disease involves both sides of the body, the symptoms are often less severe on one side than on the other. <br><br> <strong>The four primary symptoms of PD are: </strong><br><br> <strong>Tremor. </strong>The tremor associated with PD has a characteristic appearance. Typically, the tremor takes the form of a rhythmic back-and-forth motion at a rate of 4-6 beats per second. It may involve the thumb and forefinger and appear as a "pill rolling" tremor. Tremor often begins in a hand, although sometimes a foot or the jaw is affected first. It is most obvious when the hand is at rest or when a person is under stress. For example, the shaking may become more pronounced a few seconds after the hands are rested on a table. Tremor usually disappears during sleep or improves with intentional movement. <br> <strong>Rigidity.</strong> Rigidity, or a resistance to movement, affects most people with PD. A major principle of body movement is that all muscles have an opposing muscle. Movement is possible not just because one muscle becomes more active, but because the opposing muscle relaxes. In PD, rigidity comes about when, in response to signals from the brain, the delicate balance of opposing muscles is disturbed. The muscles remain constantly tensed and contracted so that the person aches or feels stiff or weak. The rigidity becomes obvious when another person tries to move the patient's arm, which will move only in ratchet-like or short, jerky movements known as "cogwheel" rigidity. <br> <strong>Bradykinesia.</strong> Bradykinesia, or the slowing down and loss of spontaneous and automatic movement, is particularly frustrating because it may make simple tasks somewhat difficult. The person cannot rapidly perform routine movements. Activities once performed quickly and easily  such as washing or dressing  may take several hours. <br> <strong>Postural instability. </strong>Postural instability, or impaired balance, causes patients to fall easily. Affected people also may develop a stooped posture in which the head is bowed and the shoulders are drooped. <br> A number of other symptoms may accompany PD. Some are minor; others are not. Many can be treated with medication or physical therapy. No one can predict which symptoms will affect an individual patient, and the intensity of the symptoms varies from person to person. <br> <strong>Depression.</strong> This is a common problem and may appear early in the course of the disease, even before other symptoms are noticed. Fortunately, depression usually can be successfully treated with antidepressant medications. <br> <strong>Emotional changes.</strong> Some people with PD become fearful and insecure. Perhaps they fear they cannot cope with new situations. They may not want to travel, go to parties, or socialize with friends. Some lose their motivation and become dependent on family members. Others may become irritable or uncharacteristically pessimistic. <br> <strong>Difficulty with swallowing and chewing.</strong> Muscles used in swallowing may work less efficiently in later stages of the disease. In these cases, food and saliva may collect in the mouth and back of the throat, which can result in choking or drooling. These problems also may make it difficult to get adequate nutrition. Speech-language therapists, occupational therapists, and dieticians can often help with these problems. <br> <strong>Speech changes. </strong>About half of all PD patients have problems with speech. They may speak too softly or in a monotone, hesitate before speaking, slur or repeat their words, or speak too fast. A speech therapist may be able to help patients reduce some of these problems. <br> <strong>Urinary problems or constipation.</strong> In some patients, bladder and bowel problems can occur due to the improper functioning of the autonomic nervous system, which is responsible for regulating smooth muscle activity. Some people may become incontinent, while others have trouble urinating. In others, constipation may occur because the intestinal tract operates more slowly. Constipation can also be caused by inactivity, eating a poor diet, or drinking too little fluid. The medications used to treat PD also can contribute to constipation. It can be a persistent problem and, in rare cases, can be serious enough to require hospitalization. <br> <strong>Skin problems. </strong>In PD, it is common for the skin on the face to become very oily, particularly on the forehead and at the sides of the nose. The scalp may become oily too, resulting in dandruff. In other cases, the skin can become very dry. These problems are also the result of an improperly functioning autonomic nervous system. Standard treatments for skin problems can help. Excessive sweating, another common symptom, is usually controllable with medications used for PD. <br> <strong>Sleep problems. </strong>Sleep problems common in PD include difficulty staying asleep at night, restless sleep, nightmares and emotional dreams, and drowsiness or sudden sleep onset during the day. Patients with PD should never take over-the-counter sleep aids without consulting their physicians. <br> <strong>Dementia or other cognitive problems.</strong> Some, but not all, people with PD may develop memory problems and slow thinking. In some of these cases, cognitive problems become more severe, leading to a condition called Parkinson's dementia late in the course of the disease. This dementia may affect memory, social judgment, language, reasoning, or other mental skills. There is currently no way to halt PD dementia, but studies have shown that a drug called rivastigmine may slightly reduce the symptoms. The drug donepezil also can reduce behavioral symptoms in some people with PD-related dementia. <br> <strong>Orthostatic hypotension. </strong> Orthostatic hypotension is a sudden drop in blood pressure when a person stands up from a lying-down position. This may cause dizziness, lightheadedness, and, in extreme cases, loss of balance or fainting. Studies have suggested that, in PD, this problem results from a loss of nerve endings in the sympathetic nervous system that controls heart rate, blood pressure, and other automatic functions in the body. The medications used to treat PD also may contribute to this symptom. <br> <strong>Muscle cramps and dystonia. </strong> The rigidity and lack of normal movement associated with PD often causes muscle cramps, especially in the legs and toes. Massage, stretching, and applying heat may help with these cramps. PD also can be associated with dystonia  sustained muscle contractions that cause forced or twisted positions. Dystonia in PD is often caused by fluctuations in the body's level of dopamine. It can usually be relieved or reduced by adjusting the person's medications. <br> <strong>Pain.</strong> Many people with PD develop aching muscles and joints because of the rigidity and abnormal postures often associated with the disease. Treatment with levodopa and other dopaminergic drugs often alleviates these pains to some extent. Certain exercises also may help. People with PD also may develop pain due to compression of nerve roots or dystonia-related muscle spasms. In rare cases, people with PD may develop unexplained burning, stabbing sensations. This type of pain, called "central pain," originates in the brain. Dopaminergic drugs, opiates, antidepressants, and other types of drugs may all be used to treat this type of pain. <br> <strong>Fatigue and loss of energy.</strong> The unusual demands of living with PD often lead to problems with fatigue, especially late in the day. Fatigue may be associated with depression or sleep disorders, but it also may result from muscle stress or from overdoing activity when the person feels well. Fatigue also may result from akinesia  trouble initiating or carrying out movement. Exercise, good sleep habits, staying mentally active, and not forcing too many activities in a short time may help to alleviate fatigue. <br> <strong>Sexual dysfunction.</strong> PD often causes erectile dysfunction because of its effects on nerve signals from the brain or because of poor blood circulation. PD-related depression or use of antidepressant medication also may cause decreased sex drive and other problems. These problems are often treatable. <br><br> <strong>Diagnosis</strong><br><br> There are currently no blood or laboratory tests that have been proven to help in diagnosing sporadic PD. Therefore the diagnosis is based on medical history and a neurological examination. The disease can be difficult to diagnose accurately. Early signs and symptoms of PD may sometimes be dismissed as the effects of normal aging. The physician may need to observe the person for some time until it is apparent that the symptoms are consistently present. Doctors may sometimes request brain scans or laboratory tests in order to rule out other diseases. However, CT and MRI brain scans of people with PD usually appear normal. Since many other diseases have similar features but require different treatments, making a precise diagnosis as soon as possible is essential so that patients can receive the proper treatment. <br><br> <strong>Prognosis</strong><br><br> PD is not by itself a fatal disease, but it does get worse with time. The average life expectancy of a PD patient is generally the same as for people who do not have the disease. However, in the late stages of the disease, PD may cause complications such as choking, pneumonia, and falls that can lead to death. Fortunately, there are many treatment options available for people with PD. <br> The progression of symptoms in PD may take 20 years or more. In some people, however, the disease progresses more quickly. There is no way to predict what course the disease will take for an individual person. One commonly used system for describing how the symptoms of PD progress is called the Hoehn and Yahr scale. <br> Hoehn and Yahr Staging of Parkinson's Disease <ul> <li>Stage one: Symptoms on one side of the body only.</li> <li>Stage two: Symptoms on both sides of the body. No impairment of balance.</li> <li>Stage three: Balance impairment. Mild to moderate disease. Physically independent.</li> <li>Stage four: Severe disability, but still able to walk or stand unassisted.</li> <li>Stage five: Wheelchair-bound or bedridden unless assisted.</li> </ul> Another commonly used scale is the Unified Parkinson's Disease Rating Scale (UPDRS). This much more complicated scale has multiple ratings that measure mental functioning, behavior, and mood; activities of daily living; and motor function. Both the Hoehn and Yahr scale and the UPDRS are used to measure how individuals are faring and how much treatments are helping them. <br> With appropriate treatment, most people with PD can live productive lives for many years after diagnosis. <br><br> <strong>Treatment</strong><br><br> At present, there is no cure for PD. But medications or surgery can sometimes provide dramatic relief from the symptoms.<br><br> <strong>Drug Treatments</strong><br><br> Medications for PD fall into three categories. The first category includes drugs that work directly or indirectly to increase the level of dopamine in the brain. The most common drugs for PD are dopamine precursors  substances such as levodopa that cross the blood-brain barrier and are then changed into dopamine. Other drugs mimic dopamine or prevent or slow its breakdown. <br> The second category of PD drugs affects other neurotransmitters in the body in order to ease some of the symptoms of the disease. For example, anticholinergic drugs interfere with production or uptake of the neurotransmitter acetylcholine. These drugs help to reduce tremors and muscle stiffness, which can result from having more acetylcholine than dopamine. <br> The third category of drugs prescribed for PD includes medications that help control the non-motor symptoms of the disease, that is, the symptoms that don't affect movement. For example, people with PD-related depression may be prescribed antidepressants. <br><br> <strong>Surgery</strong><br><br> Treating PD with surgery was once a common practice. But after the discovery of levodopa, surgery was restricted to only a few cases. Studies in the past few decades have led to great improvements in surgical techniques, and surgery is again being used in people with advanced PD for whom drug therapy is no longer sufficient. <br> Pallidotomy and Thalamotomy. The earliest types of surgery for PD involved selectively destroying specific parts of the brain that contribute to the symptoms of the disease. Investigators have now greatly refined the use of these procedures. The most common of these procedures is called pallidotomy. In this procedure, a surgeon selectively destroys a portion of the brain called the globus pallidus. Pallidotomy can improve symptoms of tremor, rigidity, and bradykinesia, possibly by interrupting the connections between the globus pallidus and the striatum or thalamus. Some studies have also found that pallidotomy can improve gait and balance and reduce the amount of levodopa patients require, thus reducing drug-induced dyskinesias and dystonia. A related procedure, called thalamotomy, involves surgically destroying part of the brain's thalamus. Thalamotomy is useful primarily to reduce tremor. <br><br> Because these procedures cause permanent destruction of brain tissue, they have largely been replaced by deep brain stimulation for treatment of PD. Deep Brain Stimulation. Deep brain stimulation, or DBS, uses an electrode surgically implanted into part of the brain. The electrodes are connected by a wire under the skin to a small electrical device called a pulse generator that is implanted in the chest beneath the collarbone. <br><br> DBS can be used on one or both sides of the brain. If it is used on just one side, it will affect symptoms on the opposite side of the body. DBS is primarily used to stimulate one of three brain regions: the subthalamic nucleus, the globus pallidus, or the thalamus. However, the subthalamic nucleus, a tiny area located beneath the thalamus, is the most common target. Stimulation of either the globus pallidus or the subthalamic nucleus can reduce tremor, bradykinesia, and rigidity. Stimulation of the thalamus is useful primarily for reducing tremor. <br> DBS usually reduces the need for levodopa and related drugs, which in turn decreases dyskinesias. It also helps to relieve on-off fluctuation of symptoms. People who initially responded well to treatment with levodopa tend to respond well to DBS. While the benefits of DBS can be substantial, it usually does not help with speech problems, "freezing," posture, balance, anxiety, depression, or dementia. <br><br> One advantage of DBS compared to pallidotomy and thalamotomy is that the electrical current can be turned off using a handheld device. The pulse generator also can be externally programmed. <br> Patients must return to the medical center frequently for several months after DBS surgery in order to have the stimulation adjusted by trained doctors or other medical professionals. The pulse generator must be programmed very carefully to give the best results. Doctors also must supervise reductions in patients' medications. After a few months, the number of medical visits usually decreases significantly, though patients may occasionally need to return to the center to have their stimulator checked. Also, the battery for the pulse generator must be surgically replaced every three to five years, though externally rechargeable batteries may eventually become available. Long-term results of DBS are still being determined. DBS does not stop PD from progressing, and some problems may gradually return. However, studies up to several years after surgery have shown that many people's symptoms remain significantly better than they were before DBS. <br><br> DBS is not a good solution for everyone. It is generally used only in people with advanced, levodopa-responsive PD who have developed dyskinesias or other disabling "off" symptoms despite drug therapy. It is not normally used in people with memory problems, hallucinations, a poor response to levodopa, severe depression, or poor health. DBS generally does not help people with "atypical" parkinsonian syndromes such as multiple system atrophy, progressive supranuclear palsy, or post-traumatic parkinsonism. Younger people generally do better than older people after DBS, but healthy older people can undergo DBS and they may benefit a great deal. <br><br> As with any brain surgery, DBS has potential complications, including stroke or brain hemorrhage. These complications are rare, however. There is also a risk of infection, which may require antibiotics or even replacement of parts of the DBS system. The stimulator may sometimes cause speech problems, balance problems, or even dyskinesias. However, those problems are often reversible if the stimulation is modified. <br><br> Researchers are continuing to study DBS and to develop ways of improving it. They are conducting clinical studies to determine the best part of the brain to receive stimulation and to determine the long-term effects of this therapy. They also are working to improve the technology used in DBS. <br><br> <strong>Complementary and Supportive Therapies</strong><br><br> A wide variety of complementary and supportive therapies may be used for PD. Among these therapies are standard physical, occupational, and speech therapy techniques, which can help with such problems as gait and voice disorders, tremors and rigidity, and cognitive decline. Other types of supportive therapies include the following: <br><br> <strong>Diet.</strong> At this time there are no specific vitamins, minerals, or other nutrients that have any proven therapeutic value in PD. Some early reports have suggested that dietary supplements might be protective in PD. In addition, a phase II clinical trial of a supplement called coenzyme Q10 suggested that large doses of this substance might slow disease progression in patients with early-stage PD. The NINDS and other components of the National Institutes of Health are funding research to determine if caffeine, antioxidants, and other dietary factors may be beneficial for preventing or treating PD. While there is currently no proof that any specific dietary factor is beneficial, a normal, healthy diet can promote overall well-being for PD patients just as it would for anyone else. Eating a fiber-rich diet and drinking plenty of fluids also can help alleviate constipation. A high protein diet, however, may limit levodopa's effectiveness. <br><br> <strong>Exercise.</strong> Exercise can help people with PD improve their mobility and flexibility. Some doctors prescribe physical therapy or muscle-strengthening exercises to tone muscles and to put underused and rigid muscles through a full range of motion. Exercises will not stop disease progression, but they may improve body strength so that the person is less disabled. Exercises also improve balance, helping people minimize gait problems, and can strengthen certain muscles so that people can speak and swallow better. Exercise can also improve the emotional well-being of people with PD, and it may improve the brain's dopamine synthesis or increase levels of beneficial compounds called neurotrophic factors in the brain. Although structured exercise programs help many patients, more general physical activity, such as walking, gardening, swimming, calisthenics, and using exercise machines, also is beneficial. People with PD should always check with their doctors before beginning a new exercise program. <br><br> Other complementary therapies that are used by some individuals with PD include massage therapy, yoga, tai chi, hypnosis, acupuncture, and the Alexander technique, which optimizes posture and muscle activity. There have been limited studies suggesting mild benefits with some of these therapies, but they do not slow PD and there is no convincing evidence that they are beneficial. <br><br> <strong>Self care</strong><br><br> While PD usually progresses slowly, eventually the most basic daily routines may be affected  from socializing with friends and enjoying normal relationships with family members to earning a living and taking care of a home. These changes can be difficult to accept. Support groups can help people cope with the disease emotionally. These groups can also provide valuable information, advice, and experience to help people with PD, their families, and their caregivers deal with a wide range of issues, including locating doctors familiar with the disease and coping with physical limitations. A list of national organizations that can help patients locate support groups in their communities appears at the end of this brochure. Individual or family counseling also may help people find ways to cope with PD. <br><br> People with PD also can benefit from being proactive and finding out as much as possible about the disease in order to alleviate fear of the unknown and to take a positive role in maintaining their health. Many people with PD continue to work either full- or part-time, although eventually they may need to adjust their schedule and working environment to cope with the disease. <br><br> <strong>Can Scientists Predict or Prevent Parkinson's Disease?</strong><br><br> In most cases, there is no way to predict or prevent sporadic PD. However, researchers are looking for a biomarker  a biochemical abnormality that all patients with PD might share  that could be picked up by screening techniques or by a simple chemical test given to people who do not have any parkinsonian symptoms. This could help doctors identify people at risk of the disease. It also might allow them to find treatments that will stop the disease process in the early stages.<br> Positron emission tomography (PET) scanning may lead to important advances in our knowledge about PD. PET scans of the brain produce pictures of chemical changes as they occur. Using PET, research scientists can study the brain's dopamine receptors (the sites on nerve cells that bind with dopamine) to determine if the loss of dopamine activity follows or precedes degeneration of the neurons that make this chemical. This information could help scientists better understand the disease process and may potentially lead to improved treatments. <br> In rare cases, where people have a clearly inherited form of PD, researchers can test for known gene mutations as a way of determining an individual's risk of the disease. However, this genetic testing can have far-reaching implications and people should carefully consider whether they want to know the results of such tests. Genetic testing is currently available only as a part of research studies.

 


 
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