Understanding Stem Cells
Stem Cell Primer
1) Educating Yourself on Parkinson's Disease - What is it, how it's treated, how to cope, and much more. - click here
2) Living with Parkinson's Disease - click here
3) Stages of Parkinson's Disease - click here
4) Differences between Young Onset Parkinson's Disease (YOPD) and Parkinson's Disease. - click here


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Educating Yourself on Parkinson's Deisease - Introduction
What is Parkinson's Disease?
What Causes the Disease?
What Genes are Linked to Parkinson's Disease?
Who Gets Parkinson's Disease?
What are the Symptoms of the Disease?
What Other Diseases Resemble Parkinson's?
How is Parkinson's Disease Diagnosed?
What is the Prognosis?
How is the Disease Treated?
Drug Treatments
Complementary and Supportive Therapies
How Can People Cope with Parkinson's Disease?
Can Scientists Predict or Prevent Parkinson's Disease?
What Can I Do to Help?

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.
Researchers believe that at least 500,000 people in the United States currently have PD, although some estimates are much higher. Society pays an enormous price for PD. The total cost to the nation is estimated to exceed $6 billion annually.  The risk of PD increases with age, so analysts expect the financial and public health impact of this disease to increase as the population gets older.

What is Parkinson's Disease?
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.
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.
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.

What Causes the Disease?
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. The loss of norepinephrine might help explain several of the non-motor features seen in PD, including fatigue and abnormalities of blood pressure regulation.

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.

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.

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.

Viruses are another possible environmental trigger for PD. People who developed encephalopathy after a 1918 influenza epidemic were later stricken with severe, progressive Parkinson's-like symptoms. A group of Taiwanese women developed similar symptoms after contracting herpes virus infections. In these women, the symptoms, which later disappeared, were linked to a temporary inflammation of the substantia nigra.

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.

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.

What Genes are Linked to Parkinson's Disease?
Several genes have now been definitively linked to PD. The first to be identified was alpha-synuclein. In the 1990s, researchers at NIH and other institutions studied the genetic profiles of a large Italian family and three Greek families with familial PD and found that their disease was related to a mutation in this gene. They found a second alpha-synuclein mutation in a German family with PD. 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.

In 2003, 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.  This study showed that an excess of the normal form of the protein could result in PD, just as the abnormal form does.

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.

LRRK2, which is translated into a protein called dardarin, was originally identified in several English and Basque families and causes a late-onset form of PD.  Subsequent studies have identified this gene in other families with PD as well as in a small percentage of people with apparently sporadic 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.

Who Gets Parkinson's Disease?
About 50,000 Americans are diagnosed with PD each year, but getting an accurate count of the number of cases may be impossible because many people in the early stages of the disease assume their symptoms are the result of normal aging and do not seek help from a physician. Also, diagnosis is sometimes difficult and uncertain because other conditions may produce symptoms of PD and there is no definitive test for the disease. People with PD may sometimes be told by their doctors that they have other disorders, and people with PD-like diseases may be incorrectly diagnosed as having PD.

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.

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.  An estimated 15 to 25 percent of people with PD have a known relative with the disease.

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.

What are the Symptoms of the Disease?
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.

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.

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.

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). 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. 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.  The four primary symptoms of PD are:

  • Tremor . 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.
  • Rigidity . 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.
  • Bradykinesia . 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.
  • Postural instability . 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.

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.

  • Depression . 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.
  • Emotional changes. 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.

  • Difficulty with swallowing and chewing . 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.

  • Speech changes . 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.

  • Urinary problems or constipation . 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.
  • Skin problems . 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.

  • Sleep problems. 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.

  • Dementia or other cognitive problems. 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.
  • Orthostatic hypotension. 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.

  • Muscle cramps and dystonia. 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.
  • Pain. 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.
  • Fatigue and loss of energy. 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.

  • Sexual dysfunction. 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.

    What Other Diseases Resemble Parkinson's?
    A number of disorders can cause symptoms similar to those of PD.  People with symptoms that resemble PD but that result from other causes are sometimes said to have parkinsonism .  Some of these disorders are listed below.
  • Postencephalitic parkinsonism . Just after the first World War, a viral disease, encephalitis lethargica, attacked almost 5 million people throughout the world, and then suddenly disappeared in the 1920s. Known as sleeping sickness in the United States , this disease killed one third of its victims and led to post-encephalitic parkinsonism in many others.  This resulted in a particularly severe form of movement disorder that appeared sometimes years after the initial illness. (In 1973, neurologist Oliver Sacks published Awakenings , an account of his work in the late 1960s with surviving post-encephalitic patients in a New York hospital. Using the then-experimental drug levodopa, Dr. Sacks was able to temporarily "awaken" these patients from their statue-like state). In rare cases, other viral infections, including western equine encephalomyelitis, eastern equine encephalomyelitis, and Japanese B encephalitis, have caused parkinsonian symptoms.
  • Drug-induced parkinsonism . A reversible form of parkinsonism sometimes results from use of certain drugs, such as chlorpromazine and haloperidol, which are prescribed for patients with psychiatric disorders. Some drugs used for stomach disorders (metoclopramide), high blood pressure (reserpine), and epilepsy (valproate) may also produce parkinsonian symptoms. Stopping the medication or lowering the dosage of these medications usually causes the symptoms to go away.
  • Toxin-induced parkinsonism . Some toxins — such as manganese dust, carbon disulfide, and carbon monoxide — can cause parkinsonism. The chemical MPTP also causes a permanent form of parkinsonism that closely resembles PD. Investigators discovered this reaction in the 1980s when heroin addicts in California who had taken an illicit street drug contaminated with MPTP began to develop severe parkinsonism. This discovery, which showed that a toxic substance could damage the brain and produce parkinsonian symptoms, caused a dramatic breakthrough in Parkinson's research: for the first time, scientists were able to simulate PD in animals and conduct studies to increase understanding of the disease.

  • Arteriosclerotic parkinsonism . Sometimes known as pseudoparkinsonism, vascular parkinsonism, or atherosclerotic parkinsonism, arteriosclerotic parkinsonism involves damage to the brain due to multiple small strokes.  Tremor is rare in this type of parkinsonism, while dementia — the loss of mental skills and abilities — is common. Antiparkinsonian drugs are of little help to patients with this form of parkinsonism.

  • Parkinsonism-dementia complex of Guam. This disease occurs among the Chamorro populations of Guam and the Mariana Islands and may be accompanied by a motor neuron disease resembling amyotrophic lateral sclerosis (Lou Gehrig's disease). The course of the disease is rapid, with death typically occurring within 5 years.

  • Post-traumatic parkinsonism. Also known as post-traumatic encephalopathy or "punch-drunk syndrome," parkinsonian symptoms can sometimes develop after a severe head injury or frequent head trauma that results from boxing or other activities.  This type of trauma also can cause a form of dementia called dementia pugilistica.

  • Essential tremor. Essential tremor, sometimes called benign essential tremor or familial tremor, is a common condition that tends to run in families and progresses slowly over time. The tremor is usually equal in both hands and increases when the hands are moving. The tremor may involve the head but usually spares the legs. Patients with essential tremor have no other parkinsonian features. Essential tremor is not the same as PD, and usually does not lead to it, although in some cases the two conditions may overlap in one person.  Essential tremor does not respond to levodopa or most other PD drugs, but it can be treated with other medications.

  • Normal pressure hydrocephalus .  Normal pressure hydrocephalus (NPH) is an abnormal increase of cerebrospinal fluid (CSF) in the brain's ventricles, or cavities. It occurs if the normal flow of CSF throughout the brain and spinal cord is blocked in some way. This causes the ventricles to enlarge, putting pressure on the brain.  Symptoms include problems with walking, impaired bladder control leading to urinary frequency or incontinence, and progressive mental impairment and dementia. The person also may have a general slowing of movements or may complain that his or her feet feel "stuck."  These symptoms may sometimes be mistaken for PD.  Brain scans, intracranial pressure monitoring, and other tests can help to distinguish NPH from PD and other disorders.  NPH can sometimes be treated by surgically implanting a CSF shunt that drains excess cerebrospinal fluid into the abdomen, where it is absorbed.

  • Progressive supranuclear palsy. Progressive supranuclear palsy (PSP), sometimes called Steele-Richardson-Olszewski syndrome, is a rare, progressive brain disorder that causes problems with control of gait and balance.  People often tend to fall early in the course of PSP.  One of the most obvious signs of the disease is an inability to move the eyes properly.  Some patients describe this effect as a blurring. PSP patients often show alterations of mood and behavior, including depression and apathy as well as mild dementia.  The symptoms of PSP are caused by a gradual deterioration of brain cells in the brainstem. It is often misdiagnosed because some of its symptoms are very much like those of PD, Alzheimer's disease, and other brain disorders. PSP symptoms usually do not respond to medication.

  • Corticobasal degeneration. Corticobasal degeneration results from atrophy of multiple areas of the brain, including the cerebral cortex and the basal ganglia. Initial symptoms may first appear on one side of the body, but eventually affect both sides. Symptoms are similar to those found in PD, including rigidity, impaired balance and coordination, and dystonia.  Other symptoms may include cognitive and visual-spatial impairments, apraxia (loss of the ability to make familiar, purposeful movements), hesitant and halting speech, myoclonus (muscular jerks), and dysphagia (difficulty swallowing).  Unlike PD, corticobasal degeneration usually does not respond to medication.

  • Multiple system atrophy .  Multiple system atrophy (MSA) refers to a set of slowly progressive disorders that affect the central and autonomic nervous systems. MSA may have symptoms that resemble PD.  It also may take a form that primarily produces poor coordination and slurred speech, or it may have a mixture of these symptoms.  Other symptoms may include breathing and swallowing difficulties, male impotence, constipation, and urinary difficulties.  The disorder previously called Shy-Drager syndrome refers to MSA with prominent orthostatic hypotension — a fall in blood pressure every time the person stands up.  MSA with parkinsonian symptoms is sometimes referred to as striatonigral degeneration, while MSA with poor coordination and slurred speech is sometimes called olivopontocerebellar atrophy.

  • Dementia with Lewy bodies. Dementia with Lewy bodies is a neurodegenerative disorder associated with abnormal protein deposits (Lewy bodies) found in certain areas of the brain.  Symptoms can range from traditional parkinsonian symptoms, such as bradykinesia, rigidity, tremor, and shuffling gait, to symptoms similar to those of Alzheimer's disease. These symptoms may fluctuate, or wax and wane dramatically. Visual hallucinations may be one of the first symptoms, and patients may suffer from other psychiatric disturbances such as delusions and depression.  Cognitive problems also occur early in the course of the disease. Levodopa and other antiparkinsonian medications can help with the motor symptoms of dementia with Lewy bodies, but they may make hallucinations and delusions worse.

  • Parkinsonism accompanying other conditions . Parkinsonian symptoms may also appear in patients with other, clearly distinct neurological disorders such as Wilson's disease, Huntington's disease, Alzheimer's disease, spinocerebellar ataxias, and Creutzfeldt-Jakob disease.  Each of these disorders has specific features that help to distinguish them from PD.

MSA, corticobasal degeneration, and progressive supranuclear palsy are sometimes referred to as "Parkinson's-plus" diseases because they have the symptoms of PD plus additional features.

How is Parkinson's Disease Diagnosed?
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.

What is the Prognosis?
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.
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.

Hoehn and Yahr Staging of Parkinson's Disease

Stage one
Symptoms on one side of the body only.
Stage two
Symptoms on both sides of the body.  No impairment of balance.
Stage three
Balance impairment.  Mild to moderate disease.  Physically independent.
Stage four
Severe disability, but still able to walk or stand unassisted.
Stage five
Wheelchair-bound or bedridden unless assisted.

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.
With appropriate treatment, most people with PD can live productive lives for many years after diagnosis.

How is the Disease Treated?
At present, there is no cure for PD. But medications or surgery can sometimes provide dramatic relief from the symptoms.

Drug Treatments
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.
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.
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.

  • Levodopa. The cornerstone of therapy for PD is the drug levodopa (also called L-dopa). Levodopa (from the full name L-3,4-dihydroxyphenylalanine) is a simple chemical found naturally in plants and animals. Levodopa is the generic name used for this chemical when it is formulated for drug use in patients. Nerve cells can use levodopa to make dopamine and replenish the brain's dwindling supply. People cannot simply take dopamine pills because dopamine does not easily pass through the blood-brain barrier, a lining of cells inside blood vessels that regulates the transport of oxygen, glucose, and other substances into the brain.  Usually, patients are given levodopa combined with another substance called carbidopa. When added to levodopa, carbidopa delays the conversion of levodopa into dopamine until it reaches the brain, preventing or diminishing some of the side effects that often accompany levodopa therapy. Carbidopa also reduces the amount of levodopa needed.

Levodopa is very successful at reducing the tremors and other symptoms of PD during the early stages of the disease.  It allows the majority of people with PD to extend the period of time in which they can lead relatively normal, productive lives.
Although levodopa helps most people with PD, not all symptoms respond equally to the drug. Levodopa usually helps most with bradykinesia and rigidity. Problems with balance and other non-motor symptoms may not be alleviated at all.
People who have taken other medications before starting levodopa therapy may have to cut back or eliminate these drugs in order to feel the full benefit of levodopa. People often see dramatic improvement in their symptoms after starting levodopa therapy.  However, they may need to increase the dose gradually for maximum benefit. A high-protein diet can interfere with the absorption of levodopa, so some physicians recommend that patients taking the drug restrict their protein consumption during the early parts of the day or avoid taking their medications with protein-rich meals.

Levodopa is often so effective that some people may temporarily forget they have PD during the early stages of the disease. But levodopa is not a cure. Although it can reduce the symptoms of PD, it does not replace lost nerve cells and it does not stop the progression of the disease.

Levodopa can have a variety of side effects. The most common initial side effects include nausea, vomiting, low blood pressure, and restlessness. The drug also can cause drowsiness or sudden sleep onset, which can make driving and other activities dangerous.  Long-term use of levodopa sometimes causes hallucinations and psychosis.  The nausea and vomiting caused by levodopa are greatly reduced by combining levodopa and carbidopa, which enhances the effectiveness of a lower dose.
Dyskinesias , or involuntary movements such as twitching, twisting, and writhing, commonly develop in people who take large doses of levodopa over an extended period. These movements may be either mild or severe and either very rapid or very slow. The dose of levodopa is often reduced in order to lessen these drug-induced movements.  However, the PD symptoms often reappear even with lower doses of medication. Doctors and patients must work together closely to find a tolerable balance between the drug's benefits and side effects. If dyskinesias are severe, surgical treatment may be considered. Because dyskinesias tend to occur with long-term use of levodopa, doctors often start younger PD patients on other dopamine-increasing drugs and switch to levodopa only when those drugs become ineffective.

Other troubling and distressing problems may occur with long-term levodopa use. Patients may begin to notice more pronounced symptoms before their first dose of medication in the morning, and they may develop muscle spasms or other problems when each dose begins to wear off. The period of effectiveness after each dose may begin to shorten, called the wearing-off effect . Another potential problem is referred to as the on-off effect — sudden, unpredictable changes in movement, from normal to parkinsonian movement and back again. These effects probably indicate that the patient's response to the drug is changing or that the disease is progressing.

One approach to alleviating these side effects is to take levodopa more often and in smaller amounts.  People with PD should never stop taking levodopa without their physician's knowledge or consent because rapidly withdrawing the drug can have potentially serious side effects, such as immobility or difficulty breathing.
Fortunately, physicians have other treatment choices for some symptoms and stages of PD. These therapies include the following:

  • Dopamine agonists. These drugs, which include bromocriptine, apomorphine, pramipexole, and ropinirole, mimic the role of dopamine in the brain. They can be given alone or in conjunction with levodopa. They may be used in the early stages of the disease, or later on in order to lengthen the duration of response to levodopa in patients who experience wearing off or on-off effects.  They are generally less effective than levodopa in controlling rigidity and bradykinesia.  Many of the potential side effects are similar to those associated with the use of levodopa, including drowsiness, sudden sleep onset, hallucinations, confusion, dyskinesias, edema (swelling due to excess fluid in body tissues), nightmares, and vomiting.  In rare cases, they can cause compulsive behavior, such as an uncontrollable desire to gamble, hypersexuality, or compulsive shopping.  Bromocriptine can also cause fibrosis, or a buildup of fibrous tissue, in the heart valves or the chest cavity.  Fibrosis usually goes away once the drugs are stopped.
  • MAO-B inhibitors . These drugs inhibit the enzyme monoamine oxidase B, or MAO-B, which breaks down dopamine in the brain.  MAO-B inhibitors cause dopamine to accumulate in surviving nerve cells and reduce the symptoms of PD.  Selegiline, also called deprenyl, is an MAO-B inhibitor that is commonly used to treat PD. Studies supported by the NINDS have shown that selegiline can delay the need for levodopa therapy by up to a year or more. When selegiline is given with levodopa, it appears to enhance and prolong the response to levodopa and thus may reduce wearing-off fluctuations.  Selegiline is usually well-tolerated, although side effects may include nausea, orthostatic hypotension, or insomnia.  It should not be taken with the antidepressant fluoxetine or the sedative mepiridine, because combining seligiline with these drugs can be harmful.  An NINDS-sponsored study of seligiline in the late 1980s suggested that it might help to slow the loss of nerve cells in PD.  However, follow-up studies cast doubt on this finding. Another MAO-B inhibitor, rasagiline, was approved by the FDA in May 2006 for use in treating PD.
  • COMT inhibitors .  COMT stands for catechol-O-methyltransferase, another enzyme that helps to break down dopamine.  Two COMT inhibitors are approved to treat PD in the United States:  entacapone and tolcapone.  These drugs prolong the effects of levodopa by preventing the breakdown of dopamine. COMT inhibitors can decrease the duration of "off" periods, and they usually make it possible to reduce the person's dose of levodopa.  The most common side effect is diarrhea.  The drugs may also cause nausea, sleep disturbances, dizziness, urine discoloration, abdominal pain, low blood pressure, or hallucinations.  In a few rare cases, tolcapone has caused severe liver disease.  Because of this, patients taking tolcapone need regular monitoring of their liver function.
  • Amantadine . An antiviral drug, amantadine, can help reduce symptoms of PD and levodopa-induced dyskinesia.  It is often used alone in the early stages of the disease.  It also may be used with an anticholinergic drug or levodopa.  After several months, amantadine's effectiveness wears off in up to half of the patients taking it. Amantadine's side effects may include insomnia, mottled skin, edema, agitation, or hallucinations. Researchers are not certain how amantadine works in PD, but it may increase the effects of dopamine.

  • Anticholinergics . These drugs, which include trihexyphenidyl, benztropine, and ethopropazine, decrease the activity of the neurotransmitter acetylcholine and help to reduce tremors and muscle rigidity.  Only about half the patients who receive anticholinergics are helped by it, usually for a brief period and with only a 30 percent improvement.  Side effects may include dry mouth, constipation, urinary retention, hallucinations, memory loss, blurred vision, and confusion.

When recommending a course of treatment, a doctor will assess how much the symptoms disrupt the patient's life and then tailor therapy to the person's particular condition. Since no two patients will react the same way to a given drug, it may take time and patience to get the dose just right. Even then, symptoms may not be completely alleviated.
Medications to Treat the Motor Symptoms of Parkinson's Disease

Drugs that increase brain levels of dopamine
Drugs that mimic dopamine (dopamine agonists)
Drugs that inhibit dopamine breakdown (MAO-B inhibitors)
Selegiline (deprenyl)
Drugs that inhibit dopamine breakdown (COMT inhibitors)
Drugs that decrease the action of acetylcholine anticholinergics)
Drugs with an unknown mechanism of action for PD

Medications for Non-Motor Symptoms. Doctors may prescribe a variety of medications to treat the non-motor symptoms of PD, such as depression and anxiety.  For example, depression can be treated with standard anti-depressant drugs such as amitriptyline or fluoxetine (however, as stated earlier, fluoxetine should not be combined with MAO-B inhibitors).  Anxiety can sometimes be treated with drugs called benzodiazepines.  Orthostatic hypotension may be helped by increasing salt intake, reducing antihypertension drugs, or prescribing medications such as fludrocortisone.
Hallucinations, delusions, and other psychotic symptoms are often caused by the drugs prescribed for PD.  Therefore reducing or stopping PD medications may alleviate psychosis.  If such measures are not effective, doctors sometimes prescribe drugs called atypical antipsychotics, which include clozapine and quetiapine.  Clozapine also may help to control dyskinesias.  However, clozapine also can cause a serious blood disorder called agranulocytosis, so people who take it must have their blood monitored frequently.

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.

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.
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.  The pulse generator and electrodes painlessly stimulate the brain in a way that helps to stop many of the symptoms of PD.  DBS has now been approved by the U.S. Food and Drug Administration, and it is widely used as a treatment for PD. 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.

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. 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.

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.

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. 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.

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.

Complementary and Supportive Therapies
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:
Diet. 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.

Exercise. 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.
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.

How Can People Cope with Parkinson's Disease?
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.

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.

Can Scientists Predict or Prevent Parkinson's Disease?
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.
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.
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.

What Can I Do to Help?

American Parkinson Disease Association
135 Parkinson Avenue
Staten Island, NY   10305-1425
[email protected]
Tel: 718-981-8001 800-223-2732 Calif:  800-908-2732
Fax: 718-981-4399
Dedicated to funding Parkinson's disease research. Offers comprehensive medical information and extensive public/professional education and support services.

National Parkinson Foundation
1501 N.W. 9th Avenue
Bob Hope Road
Miami, FL   33136-1494
[email protected]
Tel: 305-243-6666 800-327-4545
Fax: 305-243-5595
Provides research, patient services, clinical studies, public and professional education, and physician referrals at over 60 locations and through a nationwide network of chapters and support groups.

Parkinson Alliance
P.O. Box 308
Kingston, NJ   08528-0308
[email protected]
Tel: 609-688-0870 800-579-8440
Fax: 609-688-0875
Raises and distributes money for the most promising research leading to a cure for Parkinson's disease. Partners with the Tuchman Foundation to ensure that every dollar donated by individuals and all net proceeds of events go directly to research. The Alliance is also devoted to improving quality of life within the DBS-STN community through an affiliated resource, www.DBS-STN.org.

Michael J. Fox Foundation for Parkinson's Research
Grand Central Station
P.O. Box 4777
New York, NY   10163
Tel:  212-509-0995
Dedicated to advancing a cure for Parkinson’s disease by identifying promising research and raising funds for research support.

Parkinson's Action Network (PAN)
1025 Vermont Ave., NW
Suite 1120
Washington, DC   20005
[email protected]
Tel: 800-850-4726 202-638-4101
Fax: 202-638-7257
Non-profit education and advocacy organization that serves as a voice for the Parkinson's community by fighting for promising research that will produce effective treatments and a cure.

Parkinson's Disease Foundation (PDF)
1359 Broadway
Suite 1509
New York, NY   10018

Tel: 212-923-4700 800-457-6676
Fax: 212-923-4778
National nonprofit organization that supports Parkinson's disease research, education, and public advocacy programs.

Parkinson's Institute
1170 Morse Avenue
Sunnyvale, CA   94089-1605
Tel: 408-734-2800 800-786-2958
Fax: 408-734-8522
Non-profit organization conducting patient care and research activities in the neurological specialty area of movement disorders.

Parkinson's Resource Organization
74-090 El Paseo Drive
Suite 102
Palm Desert, CA   92260-4135

Tel: 760-773-5628 310-476-7030 877-775-4111
Fax: 760-773-9803
Helps families affected by Parkinson’s by offering emotional and educational support programs, publishing a monthly newsletter about quality of life and family issues, providing information and referral services, promoting advocacy and public awareness, and providing respite for family caregivers.

WE MOVE (Worldwide Education & Awareness for Movement Disorders)
204 West 84th Street
New York, NY   10024

Tel:  212-875-8312
Fax: 212-875-8389
WE MOVE provides movement disorder information and educational materials to physicians, patients, the media, and the public.

Bachmann-Strauss Dystonia & Parkinson Foundation
Mt. Sinai Medical Center One Gustave L. Levy Place
P.O. Box 1490
New York, NY   10029
[email protected]
Tel:  212-682-9900
Fax: 212-987-0662
Non-profit foundation that supports patients, family members, researchers, clinicians, and volunteers working in partnership to find better medical treatments and a cure for dystonia and Parkinson's disease.



  • Ablation
    Surgical destruction or removal of any part of the body.
  • Acetylcholine
    A chemical messenger released by cholinergic nerves. Normally found in many parts of the body, including the brain, and necessary to normal body functioning. Medications that block the action of acetylcholine can help with the symptoms of Parkinson’s disease. There appears to be a reciprocal seesaw relationship between acetylcholine and dopamine and their respective nerve cell systems.
  • Action tremor
    Rhythmic, involuntary movement of a limb when movement is initiated, e.g., when writing or lifting a cup. Not usually seen in the earlier stages of Parkinson's.
  • Adjunctive
    Another treatment used together with the primary treatment. Its purpose is to assist the primary treatment.
  • Adrenaline (epinephrine)
    The neurotransmitter of the adrenal gland that is secreted in moments of crisis. It stimulates the heart to beat faster and work harder, increases the flow of blood to the muscles, causes an increased alertness of mind, and produces other changes to prepare the body to meet an emergency. It is also a chemical messenger in the brain.
  • Agonist
    A chemical or drug that mimics neurotransmitter activity. For example, a dopamine agonist used in the treatment of Parkinson’s disease "fools" the brain into thinking that it is dopamine and the brain responses with improvement in symptoms.
  • Akinesia
    Absence or difficulty in producing of body movements.
  • Alpha-tocopherol
    Chemical name for biologically active form of Vitamin E.
  • Amantadine
    A drug that stimulates the release of available dopamine in the brain thereby improving symptoms. Also, amantidine can act on NMDA glutamate receptors in the brain that may help to reduce the involuntary movements (dyskinesia) sometimes associated with Parkinson’s disease treatments.
  • Anticholinergic
    Adjective applied to a substance (medication) that reduces the action of acetylcholine.
  • Anticholinergic drugs (Artane, Cogentin)
    The group of drugs that decreases the action of acetylcholine. The specified drugs may help reduce rigidity, tremor and drooling in Parkinson's.
  • Anticoagulant
    A substance that prevents blood clotting.
  • Antihistamines
    Drugs that oppose the actions of histamine; commonly used to treat allergies. Used in the past for Parkinson's as they sometimes had beneficial effects on symptoms due to their anticholinergic properties.
  • Apomorphine
    A derivative of morphine and a dopamine agonist. Currently experimentally used as injectable treatment for severe Parkinson's.
  • Ataxia
    Loss of balance.
  • Athetosis
    Dyskinesias in which there are slow, repetitive, sinuous involuntary movements.
  • Atypical
    Unusual; not conforming to type.
  • Autonomic nervous system
    The branch of the nervous system that controls internal organs in the body, i.e., heart, lungs.
  • Basal ganglia or nuclei
    Deep structures in the brain, concerned with normal movement and walking. The caudate nucleus, putamen, subthalamic nucleus and Substantia Nigra are basal ganglia affected in Parkinson's.
  • Benign essential tremor
    A condition characterized by tremor of the hands, head, voice and sometimes other parts of the body. Essential tremor often runs in families and is sometimes called familial tremor. It is sometimes mistaken for a symptom of Parkinson’s. However, this is an action tremor and there is no rigidity or bradykinesia.
  • Beta-blockers (ß-blockers)
    Drugs that block the action of epinephrine at certain sites. Usually used to treat hypertension and heart disease, they may be effective in the treatment of benign essential tremor.
  • Bilateral
    Occurring on both sides of the body.
  • Bioavailability
    Effectiveness; The degree to which a substance is absorbed and circulated in the body.
  • Blepharospasm
    Spasmodic blinking or involuntary closing of the eyelids; a type of dystonia.
  • Bradykinesia
    The slowing down and gradual loss of spontaneous movement. It is a major symptom of Parkinson's.
  • Bromocriptine (Parlodel)
    A dopamine agonist useful in treating all of the primary symptoms of Parkinson's. It may be used alone or with other anti-Parkinson medications. This is an older-generation dopamine agonist that is less effective and has higher risks of side effects compared to newer dopamine agonists.
  • Carbidopa (Lodosyn)
    The ingredient in Sinemet that prevents the breakdown of the levodopa in the body before it can reach the brain. Carbidopa helps levodopa to be more effective and can be used to reduce the side effects of levodopa and dopamine agonists.
  • Central nervous system (CNS)
    The brain and spinal cord.
  • Cerebellum
    The part of the brain that is involved in coordination.
  • Cerebral cortex
    The largest part of the brain; responsible for thought, reasoning, memory, sensation and voluntary movement.
  • Chorea
    A type of dyskinesia (abnormal movement), characterized by continuing, rapid, dance-like movements. May result from high doses of levodopa and/or long-term levodopa therapy.
  • Choreoathetosis
    A dyskinesia characterized by choreic and athetoid movements.
  • Cognitive function
    A person’s ability to perceive, reason and understand.
  • Cogwheel rigidity
    Stiffness in the muscles, with a jerky quality when arm and leg joints are repeatedly moved.
  • COMT inhibitors
    Drugs that block catechol-O-methyltransferase, an enzyme that breaks down dopamine.
  • Constipation
    Diminished ability of intestinal muscles to move stool, often resulting in difficulty voiding or in very hard stool.
  • Deep brain stimulation (DBS)
    A new surgical procedure that has proven to be very effective in treating Parkinson’s disease. The surgery includes the implantation of permanent electrodes in various parts of the brain through which continuous pulses of electricity are given. Further, the stimulation is adjustable. This surgery has largely replaced older types of surgery where specific areas of the brain were purposefully destroyed. DBS is safer and more effective than older, destructive surgeries. Targets for DBS include the subthalamic nucleus and globus pallidus. The thalamus also can be targeted but thalamic DBS is less effective.
  • Dementia
    The loss of some intellectual abilities; characterized by loss of awareness, reality and confusion.
  • Deprenyl (Eldepryl, Selegiline, Jumex)
  • A drug that slows the breakdown of chemicals like dopamine by inhibiting the action of certain enzymes. It increases effects of dopamine in the brain. There is some data that this medication can help slow the progression of Parkinson’s disease early in the course of the illness, though this research is controversial.
  • Dopamine
    A chemical produced by the brain; it assists in the effective transmission of messages from one nerve cell to the next. It is deficient in the basal ganglia and substantia nigra of a person with Parkinson's. It coordinates the actions of movement, balance and walking.
  • Dopamine Agonists
    Drugs that mimic the effects of dopamine and stimulate the dopamine receptors.
  • Dopaminergic
    An adjective used to describe a chemical, a drug or a drug effect related to dopamine.
  • Drug-induced Parkinsonism
    Parkinson's symptoms brought on by drugs used to treat other conditions, e.g., neuroleptic drugs; metoclopramide, which is used to treat stomach problems; certain antidepressants such as amoxiapine and the SSRIs; and reserpine, used to be used to treat hypertension.
  • Dysarthria
    Speech difficulties caused by the disturbance of the muscles associated with speech.
  • Dyskinesia
    Abnormal movement of voluntary muscles. May appear as a side effect of long-term drug treatment in Parkinson's and may worsen in response to stress. (also see levodopa-induced dyskinesia)
  • Dysphasia
    Difficulty in swallowing.
  • Dystonia
    A movement disorder that commonly involves the head, neck and tongue. It can result in involuntary writing movements and unusual postures.
  • Electrocautery
    A surgical treatment in which electric current is used to remove growths.
  • Encephalitis
    Inflammation of the brain usually caused by a viral infection.
  • Essential tremor (ET)
    A neurological disorder characterized by tremors. Areas affected most often include the hands, arms, head and sometimes the voice.
  • Ethopropazine (Parsidol/Parsitan)
    A drug sometimes used in the past for Parkinson's due to its anticholinergic effects.
  • Extrapyramidal nervous system
    Refers to the caudate, putamen, subthalamic nucleus and Substantia Nigra. It is affected in Parkinson's.
  • Festination
    Walking in rapid, short, shuffling steps.
  • Flexion
    A bent, curved posture.
  • Glaucoma
    A sustained increase of pressure within the eyeball that can injure the optic nerve and cause impaired vision or blindness. Although rare, treatment with anticholinergics may exacerbate glaucoma.
  • Globus pallidus
    The inner part of the basal ganglia.
  • Hydrolysis
    The process of adding water to split a chemical compound.
  • Hypokinesia
    Abnormally diminished motor activity.
  • Hypomania
    A milder form of mania, which is a state often characterized by extreme excitement, elation, irritability and/or hyperactivity.
  • Idiopathic
    An adjective meaning "of unknown cause." The usual form of Parkinson's is idiopathic Parkinson's.
  • Intention tremor
    Tremor occurring when the person attempts voluntary movement.
  • Lenticular nucleus
    This group of cells along with the caudate nucleus form the Striatum or Corpus Striatum.
  • Levodopa
    The international generic name for the medicinal formulation of L-Dopa. It is contained in Sinemet and Prolopa.
  • Levodopa-induced dyskinesias
    A side effect of medication that may occur with prolonged use. Reducing the amount of medication may alleviate these abnormal, involuntary movements. Modern approaches to medical therapy try to avoid or minimize the use of levodopa in order to reduce the risks of levodopa-induced dyskinesia.
  • Livido reticularis
    A purplish or bluish coloration of the skin seen usually below the knee and on the forearm in persons treated with amantadine (Symmetrel). This is usually a benign condition.
  • Lodosyn (carbidopa)
    The ingredient in Sinemet that prevents the breakdown of the levodopa in the body before it can reach the brain. Carbidopa helps levodopa to be more effective and can be used to reduce the side effects of levodopa and dopamine agonists.
  • Mirapex (pramipexole)
    A new-generation dopamine agonist that is better tolerated and more effective.
  • Micrographia
    The tendency to have very small handwriting due to difficulty with fine motor movements in Parkinson's.
  • MPTP
    A toxic chemical, exposure to which may lead to Parkinsonism in intravenous drug abusers. It is now used to produce Parkinsonism in laboratory animals in order to study the disease.
  • Multiple sclerosis (MS)
    A disease in which the body’s immune system mistakenly attacks normal tissues of the body. In MS, these attacks are aimed at the myelin in the central nervous system.
  • Myoclonus
    Jerking, involuntary movement of arms and legs, usually occurring during sleep.
  • Neostriatum
    Vital part of the brain comprised of two basal ganglia (caudate and putamen). These are part of the basal ganglia.
  • Neuroleptic drugs (Also called major tranquilizers)
    A class of drugs that act as dopamine antagonists (by blocking some dopamine receptors). These medications are used in the treatment of serious psychiatric disorders. They can produce or aggravate symptoms of Parkinsonism. This class includes Haloperidol (Haldol) and the phenothiazines, e.g., Compazine, Stelazine, Chlorpromazine, etc.
  • Neuron
    A nerve cell.
  • Neurotransmitter
    A specialized chemical produced in nerve cells that permits the transmission of information between nerve cells .
  • Nigrostriatal degeneration
    Degeneration of the nerve pathways from substantia nigra to the striatum.
  • Norepinephrine
    Chemical transmitter found mainly in two areas of the brain involved in governing the involuntary autonomic nervous system.
  • On-off effect
    Fluctuations that occur in response to levodopa therapy in which the person’s mobility changes suddenly and unpredictably from a good response (on) to a poor response (off).
  • Orthostatic hypotension
    A drop in blood pressure during rapid changes in body position (e.g., from sitting to standing). This can produce dizziness or light-headedness.
  • Palilalia
    A symptom of Parkinsonism, especially the postencephalitic form, in which a word or syllable is repeated and the flow of speech is interrupted.
  • Pallidectomy
    Surgical procedure where the globus pallidus is separated to improve tremors, rigidity and bradykinesia. This type of surgery is rarely indicated and has been replaced by deep brain stimulation (DBS).
  • Pallidotomy
    Surgery that permanently destroys the overactive globus pallidus to improve the symptoms of Parkinson's disease.
  • Paraesthesia
    Sensations, usually unpleasant, arising spontaneously in a limb or other part of the body, experienced as "pins and needles" or a fluctuations of warmth or coldness (thermal paresthesias).
  • Parkinson's facies
    A stoic, mask-like facial expression, with infrequent blinking that is characteristic of Parkinson's disease.
  • Parkinsonism
    The term referring to the group of conditions characterized by the most typical symptoms: tremor, rigidity, bradykinesia, stooped posture and shuffling gait. The more common causes of Parkinsonism are Parkinson's disease, striatonigral degeneration and a reversible syndrome that is induced by certain drugs.
  • Paralysis agitans
    The Latin form of the older, popular term "shaking palsy," which was used to designate early Parkinson's diagnosis.
  • Parlodel (bromocriptine)
    A dopamine agonist useful in treating all of the primary symptoms of Parkinson's. It may be used alone or with other anti-Parkinson medications.
  • Pergolide (Permax)
    A dopamine agonist. This is an older-generation dopamine agonist that is less effective and has higher risks of side effects compared to newer dopamine agonists.
  • Postural instability
    Difficulty with balance.
  • Postural tremor
    Tremor that increases when hands are stretched out in front.
  • Precursor
    Something that precedes, e.g., Levodopa is a precursor to dopamine in that levodopa is converted to dopamine in the brain.
  • Progressive supranuclear palsy (PSP)
    A degenerative brain disorder sometimes difficult to distinguish from Parkinson's especially in the early stages. PSP symptoms are rigidity and akinesia, difficulty looking up and down, speech and balance problems. Those with PSP often have poor response to antiparkinson medications.
  • Prolopa
    Trade name for the anti-Parkinson drug composed of levodopa and benserazide. This drug combination contains a ratio of 4 mg. of levodopa to 1 mg. of benserazide (Prolopa 50-12.5, 100-25, 200-50).
  • Propulsive gait
    Disturbance of gait typical of Parkinsonism in which, during walking, steps become faster and faster with progressively shorter steps that passes from a walking to a running pace and may precipitate falling forward.
  • Pseudobulbar palsy
    A disorder that occurs in patients with arteriosclerosis that is often mistaken for Parkinson’s disease.
  • Range of motion
    The extent that a joint will move from being fully straightened to completely bent.
  • Resting tremor
    Shaking that occurs in a relaxed and supported limb.
  • Retropulsive gait
    Walking that is propelled backwards.
  • Rigidity
    Muscular stiffness that is common in people with Parkinson's disease. It is characterized by a resistance to movement in the limbs.
  • Requip (ropinirole )
    A new generation dopamine agonist that is better tolerated and more effective.
  • Seborrhea
    Increased oily discharge from the sebaceous glands of the skin in those with Parkinson’s.
  • Seborrheic dermatitis
    Inflammation of the skin sometimes associated with seborrhea.
  • Shaking palsy
    An older, popular term that was used to designate early Parkinson's diagnosis.
  • Shy-Drager Syndrome
    A rare condition in which the symptoms are the result of abnormalities in motor function and problems in the autonomic nervous system. A person with Shy-Drager Syndrome has Parkinsonism, extremely low blood pressure that worsens upon standing, bladder problems, severe constipation and decreased sweating.
  • Sialorrhea
  • Sinemet
    Trade name for the anti-Parkinson drug that is a mixture of levodopa and carbidopa. This drug combination contains a ratio of levodopa 4 mg. or 10 mg. to carbidopa 1 mg. (Sinemet 100/25, Sinemet 250/25).
  • Sinemet CR
    Controlled-release Sinemet. A combination of levodopa and carbidopa in a capsule tablet contained in a matrix (outer layer) that releases the drug more slowly in the body.
  • These capsules are not to be taken all at once, but rather in separate doses over the course of a day.
  • Stereotactic headframe
    A metallic frame bolted to a patient's head to prevent any movement during brain surgery that utilizes stereotactic methods.
  • Stereotactic surgery
    Surgical technique that involves placing a small electrode in an area of the brain to destroy a tiny amount of brain tissue (see Deep Brain Stimulation).
  • Striatonigral degeneration
    A degenerative disorder similar to idiopathic Parkinson’s disease in which there is a degeneration of the nerve pathways traveling from the striatum to the substantia nigra. People with this degeneration also appear to have Parkinsonism but respond differently to drug therapy.
  • Striatum
    Area of brain basal ganglia that controls movement, balance and walking.
  • Subthalamic nucleus (STN)
    A nerve center deep within the brain that controls many aspects of normal motor function. It may be targeted for deep brain stimulation to reduce symptoms of Parkinson's disease.
  • Sustention or postural tremor
    Tremor that increases when hands are stretched out in front.
  • Supranuclear gaze palsy
    A cerebral degenerative disorder in which patients develop paralysis of their eye movements.
  • Symmetrel (amantadine)
    A drug that releases dopamine and is useful in PS.
  • Tardive dyskinesia
    A movement disorder associated with long-term use of certain medications, such as the neuroleptic drugs Chlorpromazine, Haloperidol, Loxapine, etc. Movements of a person with tardive dyskinesia are similar in appearance to those of a person with levodopa-induced dyskinesias, but the causes of the two conditions are different.

Operation in which a small region of the thalamus is destroyed. Tremor and rigidity in Parkinsonism and other conditions may be relieved by thalamotomy. This surgery is rarely indicated and has been replaced by deep brain stimulation.
A mass of gray matter centrally placed deep in the brain near its base and serving as a major relay station for impulses traveling from the spinal cord and cerebellum to the cerebral cortex.
A poisonous substance.
Rhythmic shaking and involuntary movement of part(s) of the body as a result of muscle contractions.
Occurring on one side of the body. Parkinson's symptoms usually begin unilaterally.
Wearing-off effect
The tendency, following long-term levodopa treatment, for each dose of the drug to be effective for shorter periods of time.


Living With Parkinson's Disease

Denial. Helplessness. Anger. Withdrawal from social circles. These are all forms of  coping with Parkinson's Disease that may manifest themselves on diagnoses. It's not uncommon for patient's to begin avoiding doctor's appointments, or refusing to take their medication. All in the very human hope that the diagnosis is somehow not true. Ultimately it is important to confront the diagnosis as timely treatment and making changes to one's lifestyle can make a huge difference in living with Parkinson's Disease.
Going from being a strong, independent and healthy individual to being progressively, and chronically ill can be hard to come to terms with. It is not hard to understand why Parkinson's Disease patients would deny having the disease, or ask why this affliction has been cast upon them. It is all the more devastating when as patients realize that as things stand now they will never be free of it, for there is no cure. Ultimately the only course of action available is to learn to live with the disease.

Parkinson's Disease patients will often try to hide their symptoms in the early stages. It is not uncommon for them not to tell friends and family of their diagnosis. Most people fear that people will look at them differently. Fears range from, bosses not thinking they can be a productive member of the company, their children may not see them as the strong parent they need, or their spouse may become scared themselves. Obviously people react differently, and the particular fears depend on where they are in life. The key here is that having Parkinson's Disease is not a sign of weakness. Reaching out for help when needed however, is a sign of strength and courage.

Living with Parkinson's Disease can be made easier with the use of psychological services when necessary. Many patients experience high levels of anxiety, anger and depression. There is a difference in the severity of depression in patients living with Parkinson's disease. Risk factors for the onset of depression in this situation include psychosis, right-sided hemiparkinsonism, and the extent of disability. Some research has found that the prevalence of depression among those living with Parkinson's Disease is increased in females and those patients who have taken Levodopa. Seeking professional psychological help is important in these circumstances. In addition, reaching out to support groups and psychological services within your community can help you to cope with this aspect of the disease.
Stress dampens our body's ability to cope with disease. All Parkinson's disease symptoms are amplified in the presence of stress. Some patients end up overdosing on their medication just so they can get through stressful days (ironically, they end up prematurely disabled). It's important to identify the cause of your stress, and eliminate or reduce its impact on your life. Even if this means making adjustments to your lifestyle. Consider the following changes:


  • What are your work arrangements?
  • Are you finding it hard to cope with the workload from a fulltime job?
  • Are you struggling to perform at your optimum level?

Not everyone can stop work completely as there are financial implications. Consider switching to home based or part time work if these options are viable. You could also ask your employer to reduce your workload.
If you are qualified for a job, you are as legally entitled to be considered for a job as anyone else. The Americans with Disabilities ACT means that an employer cannot discriminate against you because of any disabilities you have.

Visit Your Doctor Regularly

Take this as the chance to understand your condition. Ask the doctor as many questions as you need to. If your doctor seems too busy to answer your questions, then find one who will! It is important to understand your conditions and any medications you are taking. This will allow you to manage day to day living more effectively.

Support Groups

It is highly likely that there are Parkinson's Disease support groups in your area. It's amazing how much inspiration you can get from surrounding yourself with people trying to overcome the same problem. It would not be surprising if you meet role models who are managing well and are very happy with their life.
If nothing else, you will be surrounded by people who know exactly how you feel. It is also a great chance to be educated on the disease and maybe even help others where you can.

Love and Sex

Even when living with Parkinson's Disease, it is important to maintain a loving relationship. Couples can still express their love through touch, caressing, and lovemaking. A few difficulties could be faced:

  • Tiredness in both partners. One may now be a full time caregiver, and the patient's symptoms, make it hard to perform sexually. The autonomic nervous system can be affected by parkinsonism, and it is this system that controls a man's erection. Changes to medication can help with this problem.
  • People with Parkinson's Disease can become embarrassed by their tremors and drooling.

Your Spouse

It is important to include your spouse when dealing with this disease. Make sure that they too understand it, and are aware about how you feel about it. Share your fears and concerns, and allow them to help you where they can.
It is important to discuss:

  • What role you played before the disease.
  • The limitations that exist now.
  • What role your spouse needs to take now.
  • What role your spouse can cope with or is willing to take.

Your Children

Even the thought that our children could think less of us is painful. We fear that our children will no longer see us as a strong protector or a role model. This is the fear that Parkinson's Disease patients often face. With honesty and communication hopefully instead of seeing a weakened parent, they will come to see someone who is persevering and coping in a hard situation. This will give them inspiration to deal with ordeals in their life.
Living with Parkinson's disease is no easy task, but making a few lifestyle changes can make a huge difference. These changes will allow you to live your life to the fullest, and still be involved in both your work and social life.



Parkinson's disease affects everyone differently. Symptoms range from mild to severe. The disease progresses slowly in some, rapidly in others. The following stages of Parkinson's disease were described by Hoehn and Yahr. This is the most commonly used scale in the evaluation of the progression of Parkinson’s disease.

1. Stage One
• Signs and symptoms on one side only
• Symptoms mild
• Symptoms inconvenient but not disabling
• Usually presents with tremor of one limb
• Friends have noticed changes in posture, movement and facial expression

2. Stage Two
• Symptoms on both sides of body
• Minimal disability
• Posture and gait affected

3. Stage Three
• Significant slowing of body movements
• Early impairment of equilibrium on walking or standing

4. Stage Four
• Severe symptoms
• Can still walk to a limited extent
• Muscle Stiffness and Slowness of Movement
• No longer able to live alone
• Tremor may be less pronounced than in earlier stages

5. Stage Five
• Cachectic stage (severe loss of weight and muscle mass)
• Invalidism complete
• Cannot stand or walk
• Requires constant nursing care
• Generalized dysfunction that is moderately severe

The information contained on this page is for general purposes only. Focus on a Cure Foundation for Parkinson's strongly recommends that any drug or treatment decisions be made by a physician or other qualified medical professional.


Young Onset Parkinson's Disease (YOPD)

When Dr. James Parkinson first described "a pronounced trembling and an increasing sense of weakness" in his 1817 essay on the Shaking Palsy, he was diagnosing what would become known ever after as Parkinson's disease. The incidence of Parkinson's disease is greatest in people over the age of 60 and for many years was considered an `old person's disease'. Increasingly, however, symptoms are being observed in patients in their thirties or younger.

Young Onset Parkinson's disease affects approximately 10,000 of the 1.5 million people in the United States who suffer from Parkinson's disease. Young people who exhibit early symptoms may not consider that they are experiencing Parkinson's disease until years later when a diagnosis is finally made.

The diagnosis of Parkinson's disease is never welcome but can be particularly difficult when one is young and looking ahead to the future. We hope that the following information will help you deal with the challenges Young Onset Parkinson's disease presents.

Differences between PD and YOPD

Although of the same nature, there are some significant differences between Parkinson's disease and Young Onset Parkinson's disease. Some of these differences are:

  • PD affects 1 in every 100 people in the United States over the age of 60. YOPD statistics are more difficult to establish as many patients go undiagnosed for years. However, it is estimated that there are 10,000 YOPD sufferers in the United States
  • The most common early symptom of PD is a slight tremor of the hand YOPD often presents as a stiffening or `drawing up' of the muscles in the foot or leg, much like a `charley horse' which will not release. This `drawing up' is called Dystonia.
  • Levadopa is the most effective medication in use for PD. In cases of YOPD Levadopa can sometimes increase dystonia and tremors. Dopamine receptor agonists, anticholinergics and amantadine are more commonly used.

Treatment for YOPD- Diet and Exercise

YOPD patients often respond more positively to changes in diet and exercise than older PD patients. The following principles should be kept in mind when considering an exercise program.

The Five Principles of Fitness:

  1. You will derive greater benefits from more frequent exercise. It is not necessary to engage in long duration or high intensity workouts. You will be more likely to stick with an exercise program that you are comfortable with.
  2. Low-intensity, moderate-duration exercise programs are best for maintaining a state of fitness. One major benefit of frequent exercise is that it resets the body's metabolic rate. As a result the body burns more calories even when you are not exercising, making it easier to maintain a healthy body weight.
  3. Choose an exercise that is enjoyable to you. The old saying "no pain, no gain" does not apply here. You should not think of exercise as a chore or stressful. You should, instead, look forward to your daily routine. You will engage in exercises you enjoy more frequently.
  4. Exercise at 50% of your maximum capacity. If you can run a mile in six minutes, pace yourself back to running that mile in twelve minutes. Your maximum capacity will rise and you will become stronger as you continue to work out.
  5. Never over-exercise. Over-exercise can lead to injury and may slow your metabolism. Further, over-exercise can lead to "burn-out", a feeling of fatigue after exercising. You will be less inclined to exercise regularly if your sessions leave you exhausted.

With the Five Principles of Fitness in mind, consider carefully what you feel capable of doing. Consult with your physician before embarking on a regular exercise program. The following suggestions will help you enjoy the greatest benefits from your daily regimen:

  • Choose a time to exercise when you feel well- rested and alert
  • Wear loose, comfortable clothing and footwear that provides solid support
  • Make sure to take time to rest during your routine
  • Pace yourself and move slowly at first; avoid "bouncing" motions
  • Breathe normally throughout your routine
  • Stop if something feels wrong and consult with your physician

Work and Family and YOPD

People with YOPD may have young children in the home. It is important to take into consideration how this illness might affect a child. The flat affect, or reduced facial movement, seen in Young Onset Parkinson's disease patients may be interpreted by a child as a look of continual displeasure, pain, anger or sorrow. Children should be reassured that:

  • Their parent's disease is not their fault
  • The disease is not contagious
  • Their mother or father is ill, not angry or sad
  • Their parent's symptoms can improve and be controlled
  • The family is still a family

Employment considerations are more important for YOPD patients. It is important to consider ones job requirements and how ones symptoms might impact job performance. Fortunately with proper medication, diet, and exercise most YOPD patients can continue to work for years.

You and YOPD

Attitude and one's ability to adapt both play major roles in dealing successfully with YOPD. You may no longer be able to play baseball but you can coach. Finding alternatives instead of lamenting the loss of abilities will enhance one's quality of life.


© 2008 Focus on a Cure Foundation for Parkinson's.  All Rights Reserved.