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Parkinson's Disease

Parkinson's disease


Parkinson's disease (PD) is a neurodegenerative disorder that causes slowed movements, tremor, rigidity, and a wide variety of other symptoms. "Neurodegenerative" refers to the degeneration, or death, of neurons, the type of cell in the brain that is the basis for all brain activity.


Parkinson's disease occurs when neurons (nerve cells) in a part of the brain called the substantia nigra degenerate, or die off. The loss of these cells disrupts the brain's normal control of movement, causing the person to experience slowed movements, stiffness or rigidity, and tremor.


PD is one of the most common neurodegenerative diseases, second only to Alzheimer's disease in the number of people affected. Estimates suggest that approximately 750,000 Americans have PD. It affects older people much more than younger, and indeed, old age is the single greatest risk factor for PD. The average age at diagnosis is 62. Onset before age 40 is extremely rare. Men are slightly more likely to be affected than women.

Causes and symptoms

In the vast majority of cases, the cause of PD is un-known. Besides old age, there are several well-recognized risk factors. These include exposure to pesticides or herbicides, rural living, and drinking well water. Because of this, it is assumed that some type of environmental pollutant, either a pesticide or something associated with its use, is involved in causing PD. Other known risk factors include welding and exposure to manganese, further strengthening the case for an environmental toxin.

There is also evidence that genes play an important role in determining the risk of PD. PD can run in families, affecting members of the family at a much higher rate than expected by chance alone. Among identical twins, the situation is complex: if one twin develops the disease early, the other is more likely to as well; but if one twin has typical late-onset PD, the other is no more likely to develop the disease than would be expected by chance.

Several genes have been identified that cause PD in some people, but the number of people affected by these genes is quite small. Therefore, the interest of these genes is more in what they can reveal about the disease process than in providing the solution to the mystery of what causes PD in most people. Two of the genetic mutations identified involve a protein called alpha-synuclein, whose normal function is unknown. It is believed that the mutations prevent the normal breakdown of alpha-synuclein, leading it to accumulate in the neuron, where it then goes on to damage the cell. Another gene mutation that causes PD affects a protein called parkin, which normally helps break down proteins. It is believed that the loss of parkin causes build-up of proteins (though not of alpha-synuclein), again leading to damage. Researchers believe that environmental toxins may also cause similar problems, and it now seems likely that problems in protein breakdown are a significant step leading to PD, whether of genetic or environmental causation. Finally, a combination of genetic and environmental factors is likely to be important in most cases. For instance, a person with a genetically weaker ability to dispose of proteins, who was also exposed to pesticides, might develop PD, whereas a person with different genes but the same exposure might not.

Whatever the ultimate cause, people with PD share the same pathology, or disease process, in their brains. The symptoms of PD arise when cells in the substantia nigra (SN) degenerate. The SN is located at the base of the brain, near the top of the spinal column. Neurons of the SN receive messages from, and send messages to, several other portions of the brain, all of which are involved in the control of movement. By interacting with these other regions, the SN helps to ensure that movements will be smooth, fluid, and controlled.

SN cells communicate with other cells by releasing the chemical dopamine. Dopamine released by SN cells stimulates cells in other brain regions to act. As SN cells die, they release less dopamine, and the receiving cells are not stimulated as much. This leads to the disordered movement of PD. The SN is also involved in regulating numerous other types of brain behaviors, and late-stage PD is marked by a wide variety of symptoms that probably reflect loss of this regulation.

The earliest symptoms of PD, and the most widely recognized, are tremor, slowed movements (bradykinesia), and stiffness or rigidity. Symptoms often begin on one side of the body, and progress over time to involve both sides. The tremor of PD is a rest tremorthe shaking occurs when the patient is not trying to use the limb, and diminishes when the limb is in use. Bradykinesia and stiffness, along with loss of some balance reflexes, can combine to cause postural instability, and increase the likelihood of falling down.

Other symptoms of PD include:

  • orthostatic hypotension , or loss of blood pressure upon standing, which can cause dizziness and fainting
  • painful foot cramps
  • micrographia, or reduced size of handwriting
  • reduced voice volume
  • reduced facial expression
  • excessive sweating
  • constipation
  • decreased ability to smell
  • male impotence
  • drooling
  • sleep disturbance
  • depression
  • anxiety
  • panic attacks
  • late-stage dementia


Parkinson's disease is diagnosed by a careful neurological examination, testing movements, coordination, reflexes, and other aspects of function. If the physician suspects PD, the patient will usually be referred to a neurologist for definitive diagnosis. Unilateral (one-sided) tremor, slowed movements, and muscle stiffness are generally enough to confirm the diagnosis; two of the three are usually considered definitive. Several specialized tests may be used, including imaging of the brain with magnetic resonance imaging (MRI) or positron emission tomography (PET) . These are not essential to diagnosis in most cases, but may help to confirm the diagnosis in difficult cases and to distinguish PD from similar diseases such as progressive supranuclear palsy , corticobasal degeneration , or multiple system atrophy . Clues that the disease is one of these, rather than PD, include early or rapidly progressing dementia, loss of coordination, or early and prominent orthostatic hypotension (lightheadedness upon standing).

Certain medications can cause a PD-like syndrome, and it is important to rule these out. These drugs include certain antipsychotic medications (haloperidol) and antivomiting drugs (metoclopramide).

Treatment team

Treatment of PD is headed by a neurologist, who may be either a general neurologist or a movement disorders specialist. The movement disorders specialist is most likely to be aware of the most current trends in treatment. Since PD therapy continues to undergo rapid advances, it may be an advantage to see a specialist when possible. Other team members may include a speech/language pathologist for addressing voice and swallowing disorders , a geriatric medicine specialist to coordinate other medical and social issues, a neuropsychologist for expertise on cognitive aspects of PD and its treatment, and a neurosurgeon.


There are no treatments that have been proven to slow the course of PD, although research published in 2003 suggested that coenzyme Q10 may offer a slight benefit in this regard. The study has not been replicated, and its authors noted it would be premature to recommend treatment with this very expensive supplement. Additional claims have been made that two medications used to treat PD symptomsselegiline and dopamine agonistsmay have

some disease-slowing effects. These claims are not widely accepted.

The treatment of the symptoms of PD is complex for several reasons. First, PD is a progressive disease, getting worse over time, so that the medications and doses that work well early in the disease are insufficient later on. Second, the most effective drugs have long-term side effects that are troubling and difficult to control. Third, there are a lot of different treatment options, and finding the right combination can be time consuming. Fourth, the PD patient is likely being treated for other conditions associated with advancing age, and these conditions or their treatment may interfere with treatment of PD. Finally, a major treatment option for late-stage PD is surgery, but the risks of surgery are significant, and determining when and what kind of surgery to perform is a complicated decision.

Once the diagnosis of PD has been made, a central question is when to begin treatment. Treatment is typically not started right away (unless the patient elects to use coenzyme Q10), but instead is delayed until symptoms begin to interfere with his or her ability to work or engage in activities of daily living. This may be a year or even more after diagnosis.

Drug treatment

The next question is what drug to begin with. The most powerful treatment for the symptoms of PD is levodopa, which is taken into the brain and substitutes for the dopamine no longer being made by the substantia nigra. Similar in effect are the dopamine agonists, which mimic the effect of dopamine on the cells that normally receive dopamine from the SN. Three other medications also commonly used in PD, whose effects are not nearly as strong as either levodopa or the dopamine agonists, are anti-cholinergics , selegiline, and amantadine . These are often prescribed early on, when symptoms are not severe, saving the more powerful medications for later on.

Anticholinergics include benztropine and trihexyphenidyl. The loss of SN activity means that another brain system that controls movement, the cholinergic system, is relatively overactive. Anticholinergics dampen the activity of this system, restoring some balance to the control of movement. Anticholinergics are usually well tolerated in younger patients, but their side effects can be a significant barrier to their use in the elderly. Side effects include sedation, confusion, hallucinations, delirium , dry mouth, constipation, and urinary retention.

Selegiline inhibits the action of monoamine oxidase B, an enzyme in the brain that breaks down dopamine. Thus, selegiline prolongs the activity of dopamine in the brain. It can cause insomnia and hallucinations, as well as orthostatic hypotension. It may also interact with certain types of antidepressants, and for this reason, selegiline may be discontinued when beginning treatment for depression. In the early 1990s, selegiline was examined for its potential for neuroprotection, or disease slowing. The results of that trial were inconclusive; selegiline had such a significant and long-lasting symptomatic benefit that it was difficult to examine its disease-slowing effects independently.

Amantadine improves PD symptoms through an un-known mechanism. It is beneficial for each of the major movement symptoms of PD, although its effects are not strong. It also can lessen dyskinesias, which are unwanted movements that develop late in PD due to treatment. Amantadine can cause orthostatic hypotension and confusion.

Most drugs have side effects, and drugs for PD are no exception. The most effective drugs for PD, levodopa and the dopamine agonists, cause a set of side effects called "dopaminergic" side effects, indicating they derive from mimicking the action of dopamine. Dopaminergic side effects include nausea and vomiting, orthostatic hypotension, excessive sleepiness, hallucinations, and dyskinesias (in more advanced patients). Nausea, vomiting, and orthostatic hypotension tend to lessen with use, and do not pose long-term problems for most patients. Excessive sleepiness is a problem for many patients. Dyskinesias are an unavoidable effect of dopaminergic treatments, although dopamine agonists tend to cause less of it than levodopa. Dyskinesias tend to appear after three or more years of successful treatment, and become worse over time. Episodes of dyskinesias can be lessened by reducing the dose of the dopaminergic drug, but may lose symptomatic benefit. Adjusting drugs to minimize dyskinesias while maintaining good symptom control is a central challenge of managing PD.

Levodopa is the most effective treatment for PD symptoms, and is the drug used most often at the beginning of disease in elderly patients, because it is less likely to cause hallucinations than dopamine agonists. It is given in a pill that also contains another medication, called carbidopa, which inhibits an enzyme that would act on dopamine in the bloodstream, thus allowing more of it to reach the brain. In order for levodopa to be taken up by the gut and to pass from the bloodstream to the brain, a carrier that also moves amino acids from food must transport the drug. For this reason, doctors typically suggest that patients avoid taking levodopa with or right after a proteinrich meal. Levodopa may also be given with another medication, called a COMT inhibitor, which further prevents its breakdown in the bloodstream. A new pill combines levodopa, carbidopa, and a COMT inhibitor.

Dopamine agonists are almost as effective as levodopa for combating PD symptoms, and have the advantage that their use does not lead to dyskinesias as frequently as levodopa does. For this reason, many movement disorder specialists begin their patients on a dopamine agonist rather than levodopa. This is especially true for younger patients, who can anticipate more years of dopaminergic therapy, and a higher likelihood of developing dyskinesias as a result. There are four major dopamine agonists available in the United States: pergolide, pramipexole, bromocriptine, and ropinirole. Each is taken as a pill, and can be taken alone or in combination with levodopa or other medications. Some patients respond better to one than another, and inadequate relief from one does not mean the same should be expected from another. The U.S. Food and Drug Administration was expected to approve a fifth dopamine agonist, called apo-morphine, by mid-2004. Unlike the others, it is injected, and provides very rapid, short-term symptomatic relief when a dose of levodopa wears off.

Excessive sleepiness is a potentially dangerous side effect for all the dopaminergic drugs (levodopa and the dopamine agonists). This can take the form of predictable, peak-dose sleepiness, or general increase in sleepiness during the day, or a sudden, unpredictable "attack" of sleepiness and falling asleep. The latter can be dangerous if it occurs while driving or performing another activity requiring full awareness. Patients are cautioned to be aware of changes in sleepiness especially after changing a medication, and to avoid driving whenever possible if excessive sleepiness does become a side effect issue.

Complications of advanced disease

After several years of successful treatment, most patients begin to develop one or more motor complications. These often begin with "wearing off," a reduction in the duration of effect of a given dose of levodopa, which initially can be countered by dosing more frequently. Another complication is "on-off," in which the symptomatic benefit of a given dose suddenly switches off and the patient becomes rigid, with tremor and slowed movements emerging. When this occurs at home, the patient will typically just take another dose of medication, and wait for it to begin to work. It is more of a problem when it occurs while the patient is out and about, and frequent on-off episodes may make the patient reluctant to leave the home. Apomorphine injection may be useful in this situation, since it works very rapidly (approximately seven minutes), and can therefore be used as a "rescue" for sudden off periods. Dyskinesias are a third motor complication. Dyskinesias are uncontrolled writhing movements that typically occur at the peak of effect of a levodopa dose. In some cases for some patients, dyskinesias are mild enough that they are not problematic. In other cases, they interfere with function, and attempting to reduce them becomes an important treatment issue. While drug adjustments can have some effect, as the disease progresses it becomes more and more difficult to maintain adequate symptom control while avoiding dyskinesias. At this stage, the patient may consider surgery for treatment of PD symptoms.

Other complications arise in advanced PD, especially in "non-motor" symptoms, those that do not affect movement. Low voice volume may be amenable to speech therapy treatment, with one of the most effective programs being Lee Silverman voice treatment , which focuses on conscious attempts to increase volume. Orthostatic hypotension may be treatable with increased salt intake, compression stockings, and medication. Drooling may become an issue in later-stage disease; there are both drug treatments and non-drug therapies available to reduce this problem. Constipation is a significant problem for many advanced PD patients, and can be treated with standard measures such as increasing the fiber in the diet and bulking laxatives.

Panic attacks and anxiety are common in PD. These can be addressed both through helping the patient understand that this is a feature of the disease, and through antianxiety medication. Depression affects many PD patients, and can worsen other aspects of the disease. It usually responds well to antidepressant medications. Dementia (loss of memory and impairment of other thinking functions) occurs more frequently in PD patients than in the population at large. Treatment is similar to that in non-PD patients, although some medications cannot be used because they have undesirable side effects for PD patients. Psychosis-hallucinations, paranoia, nightmares, and delusions may be a response to dopaminergic medications. If these side effects cannot be controlled through modification of treatments, an antipsychotic drug may be useful.


Brain surgery is a treatment option in late-stage PD. The best candidate is the individual who continues to respond to levodopa, but whose treatment is complicated by unacceptable dyskinesias even after medication adjustment. Dementia or other significant health-related conditions may make the patient unsuitable for the rigors of surgery. The patient is usually evaluated by the neurologist, a neuropsychologist, and a neurosurgeon before deciding whether surgery is the right option.

There are two types of surgery for PD. An "ablative" lesion destroys a small portion of the brain, and in so doing, restores the balance of neural activity within the movement control circuits of the brain; ablation means to destroy or remove. The second option is deep brain stimulation (DBS), which accomplishes the same thing by implanting an electrode in the target brain region; electrical pulses shut the region down. Ablative lesions are simpler and less prone to long-term complications, but they are not adjustable after the lesion has been made. DBS is more complex, expensive, and time consuming, and carries a significant risk for infection or equipment malfunction, but it can be adjusted to more precisely target the brain region, thereby enhancing the surgical effect.

Three brain regions are targeted in PD surgery. Ablation of the thalamus (thalamotomy) is primarily effective in controlling tremor, and is not widely performed any-more since other, more effective targets are available. The globus pallidus internus (GPi) can either be ablated (pallidotomy ) or stimulated (GPi DBS), which is effective for all the major motor symptoms of PD (tremor, bradykinesia, rigidity), and can improve them by 2560%. It is also effective for reducing dyskinesias by up to 90%. The subthalamic nucleus can be stimulated in STN DBS, and is highly effective for all the major motor symptoms and dyskinesias, to a somewhat greater extent than GPi DBS. An additional advantage of STN DBS is that it is safer to do on both sides of the brain (left and right, termed bilateral) than GPi DBS. Therefore, if the patient is affected by disabling symptoms on both sides, as is often the case in advanced PD, bilateral STN DBS may be a better choice.

Clinical trials

Parkinson's disease is the subject of intense research, and there are usually several large and important clinical trials going on at any time. Trials may focus on slowing the disease, determining the best drug treatment, or refining surgical methods and targets.

Two experimental forms of surgery have been the subject of recent clinical trials. The first is the implantation of cells into the substantia nigra to replace the lost dopamine-producing cells. The implanted cells come from fetal tissue. Fetal-tissue transplants have led to success, but also to uncontrolled dyskinesias in some patients. For this reason, such trials on are on hold until a better understanding of this problem is discovered and methods are developed to avoid it.

The second form of surgery delivers a growth factor to the substantia nigra via an implanted pump and tube. The growth factor, called GDNF, has been shown to slow cell death in experimental systems. A small group of patients undergoing this surgery has improved, although these results are quite preliminary.


PD is a progressive disease, and the loss of brain tissue in the SN is inevitable. PD patients tend to live almost as long as age-matched individuals without PD, although with an increasing level of disability. Loss of motor control can lead to an increased risk for falls, and swallowing difficulty can cause choking or aspiration (inhaling) of food. Aspiration pneumonia is a common cause of death in late-stage PD patients.



Cram, David L. Understanding Parkinson's Disease: A Self-Help Guide. Milford, CT: LPC, 1999.

Hauser, Robert, and Theresa Zesiewicz. Parkinson's Disease: Questions and Answers, 2nd edition. Coral Springs, FL: Merit Publishing International, 1997.

Jahanshahi, Marjan, and C. David Marsden. Parkinson's Disease: A Self-Help Guide. San Diego: Demos Medical Publishing, 2000.


WE MOVE. <> (April 27, 2004).

Parkinson's Disease Foundation. <> (April 27, 2004).

Richard Robinson

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Parkinson's Disease

Parkinson's disease


Parkinson's disease (PD) is a motor system disorder caused by the chronic, progressive degeneration of neurons (nerve cells) in regions of the brain that control movement. PD causes a decline in the initiation, speed, and smoothness of movement. Over time it may come to affect many bodily functions.


Parkinson's Disease (PD) was first described in 1817 by James Parkinson. It affects more than one million people in the United States, including some 500,000 people who have yet to be diagnosed. About 50,000 new cases are diagnosed each year. The average age of PD onset is 60. Symptoms of PD are seen in as many as 15% of those between the ages 65 and 74 and almost 30% of those between the ages of 75 and 84. Only 5 to 10% of PD cases occur before the age of 50. Young-onset PD occurs in those under age 40. A parent or sibling with PD increases one's risk of developing the disease.

PD results from the degeneration and death of neurons in the substantia nigra, movement control centers on each side of the brain. These cells secrete dopamine, a neurotransmitter that attaches to receptors on cell surfaces in another part of the brainthe corpus striatumthat controls muscle action. When dopamine levels fall, the neurons of the corpus striatum begin to misfire. It is estimated that dopamine-producing cells begin dying about 13 years before PD symptoms become evident. The symptoms of PD begin when about 60% of the dopamine-producing cells have died.

Causes & symptoms


Although the cause of Parkinson's Disease (PD) is unknown, it appears to result from a combination of environmental and hereditary factors as well as oxidative damage and aging . Factors for PD may include:

  • herbicide and pesticide exposure
  • an as-yet-unidentified toxin or virus
  • cellular damage from oxidation by free-radicals (atoms or molecules with an unpaired electron)
  • loss of dopamine-secreting cells with age, particularly with accelerated aging
  • fewer dopamine-secreting cells at birth


Early symptoms of PD often are quite subtle, developing on one or both sides of the body. The primary symptoms of PD are:

  • tremors (shaking) while at rest. (The classic PD tremor is the rubbing of the thumb and forefinger at a frequency of about three rubs per second. Tremors may spread to the hands, arms, legs, feet, jaw, and face. The tremors increase with stress . However, many people with PD do not experience tremors)
  • slow movement (bradykinesia) or freezing during movement (akinesia)
  • stiffness or rigidity of the limbs and trunk
  • poor balance leading to frequent falls

Other early symptoms of PD:

  • short, shuffling steps
  • stooped posture
  • masking (reduction) of facial expression and infrequent blinking
  • slow or rapid, soft, monotonic (without inflection) speech
  • other speech changes
  • insomnia, restlessness, and nightmares
  • depression
  • emotional changes, including fear, irritability, and insecurity
  • incontinence
  • constipation
  • small, illegible handwriting
  • frequent, dramatic swings in mobility and moods

Later-stage PD symptoms may include:

  • frozen muscles that prevent the initiation of movement
  • oily or very dry skin
  • sweating
  • digestive tract shutdown causing difficulties in swallowing, digesting, and elimination
  • auditory and/or visual hallucinations
  • progressive deterioration of intellectual function
  • (dementia ), affecting 30 to 40% of those with late-stage PD
  • loss of contact with reality (psychosis)

Medications for PD can also cause some of these symptoms.


There is no definitive test for PD. Diagnosis is based on a careful medical history and complete neurological examination.

In addition to PD, anything that damages the substantia nigra can cause Parkinson's-like symptoms, called parkinsonism. Possible causes of parkinsonism:

  • infection
  • nausea
  • trauma
  • stroke
  • exposure to manganese or other toxins
  • medications for psychiatric disorders, such as haloperidol (Haldol) or chlorpromazine (thorazine)
  • a chemical called MPTP, found as an impurity in some illegal drugs
  • epilepsy
  • alzheimer's disease
  • other neurodegenerative diseases that sometimes are referred to as Parkinson's plus or parkinsonism plus syndromes

Brain scans, blood tests, lumbar puncture, or x rays may be used to rule out causes of parkinsonism other than PD.


There is no cure for Parkinson's disease, nor is there a treatment that slows its progression.

Many factors can help relieve PD symptoms, at least temporarily:

  • maintaining general health
  • regular, moderate, muscle-building exercise
  • erequent rest
  • smaller, more frequent, meals to accomodate gastrointestinal slowdowns
  • physical, occupational, and/or speech therapies
  • encouragement and emotional support

Fatigue, anxiety , and depression can aggravate PD symptoms significantly.

Therapies that may relieve muscle tightness in PD:

  • acupuncture
  • massage
  • yoga
  • feldenkrais
  • t'ai chi
  • qigong
  • meditation .

A physical therapist can design an appropriate exercise program and suggest strategies and techniques for improving balance and stimulating movement during slowdowns or freezing.

Supplementation therapies for PD:

  • amino acids
  • essential fatty acids including omega-3 and omega-6 fatty acids, fish oil, and flax oil
  • antioxidants including carotenoids (dark green and orange fruits and vegetables) and other bioflavenoids (antioxidants derived from foods)
  • vitamins A, B, C, and E
  • selenium and zinc
  • calcium and magnesium
  • coenzyme Q10 (CoQ10)

For more than 4,000 years, practitioners of Ayurvedatraditional Indian medicinehave prescribed mucuna seeds (Mucuna pruriens ) to treat Parkinson's disease. Mucuna contains a natural form of levodopa.

Allopathic treatment


The pharmacological treatment of Parkinson's disease is very complex. Although many drugs may relieve at least some symptoms of PD, their effectiveness varies with the patient and the progression of the disease. Side effects may preclude the use of the most effective dose or require another drug to counteract them.

LEVODOPA. Levodopa (L-dopa, L-3,4-dihydroxyphenylalanine) has been the standard treatment for PD since the 1960s and remains one of the best drugs for treating symptoms, particularly tremors and movement problems. Levodopa (Laradopa) is a naturally occurring derivative of dopamine that is converted into dopamine in the brain. However, unlike dopamine, levodopa can reach the brain from the bloodstream. Levodopa treatment may begin at the onset of PD symptoms or when the symptoms begin to interfere with daily life. At least 75% of patients are helped to some degree by levodopa and the drug enables many people with PD to live relatively normal lives for a number of years. Levodopa normally is prescribed only in combination with other drugs.

Side effects of levodopa:

  • nausea and vomiting
  • low blood pressure, particularly when standing up, resulting in dizziness and fainting
  • dyskinesias (abnormal movements including twisting and tics) in at least 50% of patients
  • agitation
  • hallucinations

These effects usually lessen after several weeks on levodopa.

After five or more years on levodopa, many patients develop:

  • motor fluctuations, including "peak-dose" dyskinesias when the drug is at its highest level in the brain
  • on-off phenomenasignificant changes in response as the drug levels fluctuate
  • unpredictable responses to the drug

The levodopa dosage is usually increased when these changes occur. However, dyskinesias may increase with increasing dosages.

Levodopa is an amino acid that is absorbed from the digestive system by the same transporters that carry amino acids from dietary proteins. Therefore some healthcare practitioners may limit or redistribute protein intake to improve levodopa adsorption into the bloodstream.

ENZYME INHIBITORS. Since levodopa and dopamine are amino acids, they can be broken down by the same enzyme systems that break down other amino acids. Therefore the two most-commonly prescribed forms of levodopa include an amino-acid-decarboxylase (AADC) inhibitor: carbidopa (in Sinemet) or benzaseride (in Madopar). These drugs enable more levodopa to enter the brain and may reduce some side effects. Controlled-release formulations (Sinemet CR) can prolong the interval between doses. Carbidopa also prevents vitamin B6 (pyridoxin) from interfering with levodopa.

Catechol-O-methyltransferase (COMT) also breaks down levodopa. The COMT inhibitor entacapone (Comtan) prolongs the effects of levodopa and may moderate its fluctuations. Stalevo contains levodopa, carbidopa, and entacapone. Although the COMT inhibitor tolcapone (Tasmar) reduces the average required dosage of levodopa by 25%, it is no longer commonly used because of severe side effects and possible liver damage and failure.

Selegiline (deprenyl) inhibits monoamine oxidase B (MAO-B), which metabolizes dopamine in the brain. Selegiline can delay levodopa treatment for an average of nine months and also is used in combination with levodopa (Eldepryl) in early-stage PD. Common side effects include dyskinesias, dry mouth , and mood swings.

DOPAMINE AGONISTS. Dopamine agonists (DAs) are drugs that activate dopamine receptors, mimicking the effects of dopamine. In younger adults with early-stage PD, DAs appear to be more effective than levodopa. More often, DAs are used in conjunction with Sinemet to prolong the action of levodopa and reduce levodopa-induced dyskinesias. Although they are expensive, DAs may postpone or prevent the need for expensive neurosurgery at later stages of PD.

DAs include:

  • Bromocriptine (Parlodel
  • Pergolide (Permax)
  • Pramipexole (Mirapex)
  • Ropinirole (Requip)

Side effects of DAs are similar to those of levodopa, including drowsiness and confusion. DAs may cause dyskinesias in at least 50% of patients. Pergolide has been associated with a type of heart disease .

ANTICHOLINERGIC DRUGS. The neurotransmitters dopamine and acetylcholine balance each other's effects in the brain. Anticholinergics help maintain this balance when dopamine levels fall. Although they may control tremors in early-stage PD, their side effectsincluding dry mouth, urine retention, severe constipation, blurred vision, confusion, memory loss , and hallucinationsare usually too severe for older patients or those with dementia. Anticholinergics rarely work for very long. Trihexyphenidyl (Artane) and benztropine (Cogentin) are the most common anticholinergics for PD.

OTHER DRUGS. Other common PD medications:

  • Diphenhydramine (Benadryl), an antihistamine, and antidepressants such as amitryptiline (Elavil), have similar effects as anticholinergics and may be appropriate for older patients.
  • Amantadine (Symmetrel) is an antiviral drug used in later-stage PD, particularly to treat tremors and levodopa-induced dyskinesias. Its effects include increased dopamine release and blocking of glutamate, an amino acid that destroys neurons. Side effects include swollen ankles and purple mottling of the skin.
  • Clozapine (Clozaril) is particularly effective for psychiatric symptoms of late-stage PD, including psychosis and hallucinations.

Although drug therapies can relieve most symptoms of early-stage PD, as the disease advances, drug responses begin to fluctuate and their overall effectiveness decreases.


Surgery may be used to help manage severe or debilitating PD symptoms when drug treatments fail.

Pallidotomy uses an electrical current to destroy a small amount of brain tissue in the globus pallidus, which is over-stimulated by the corpus striatum in PD. Pallidotomy may relieve tremors and slow, rigid movements, and decrease dyskenisias caused by drug therapy, by interfering with the neural pathway between the globus pallidus and the thalamus (a major transmission center in the brain). The benefits often do not last and the surgery may cause slurred speech, disabling weakness, and vision problems, particularly with a double pallidotomy (surgery on both sides of the brain).

Thalamotomy reduces hand and arm tremors by destroying small amounts of tissue in the thalamus. Because a double thalamotomy leaves patients extremely weak and with slurred speech, it usually is performed on only one side of the brain, relieving tremors on the opposite side of the body.

With deep brain stimulation (DBS), a device similar to a heart pacemaker sends signals to fine electrodes implanted in the subthalamic nuclei or the globus pallidus (Activa Therapy). The electrical pulses appear to interrupt signals from the thalamus that are involved in tremors. DBS restores a balance between excitatory (tending to excite) and inhibitory (interfering or retarding) signals in brain signal transmission centers, thereby decreasing or abolishing dyskinesias without slowing normal movement. Patients use a magnetic device to adjust stimulation in one or both halves of the brain, as the response dictates. DBS usually results in a significant improvement in some motor symptoms, including tremors and peak-dose dyskinesias, and improves motor function and mobility. It also enables patients to take higher doses of levodopa.

The implantation of fetal cells to replace the dopamine-producing cells of the substantia nigra appears to benefit only patients under age 60. It can have serious side effects and about 15% of patients later develop severe dykinesia due to dopamine-overproduction.

The use of stem cells derived from embryos discarded by infertility clinics is a potentially useful treatment for PD. However, it remains morally and ethically controversial.


There is no way to predict the course of PD. Many people live active, productive lives for 12 to 15 years. However, in others the disease progresses rapidly. Regardless of treatment, PD symptoms worsen with time and become less responsive to drug therapy. Most people with PD experience some additional problem every year. A small number of patients eventually become completely incapacitated. Although PD is not fatal, its effects can lead to fatal accidents or illnesses.


There are no clear risk factors or preventions for PD. Central body obesity may increase the risk. Some studies have found that coffee drinking or hormone replacement therapy (HRT) in postmenopausal women may decrease the risk of PD. However, heavy coffee drinking in combination with HRT appears to increase the risk of Parkinson's disease.



Federoff, Howard J., et al., editors. Parkinson's Disease: The Life Cycle of the Dopamine Neuron. New York: New York Academy of Sciences, 2003.

Foltynie Thomas, et al. Parkinson's Disease: Your Questions Answered. New York: Churchill Livingstone, 2003.

Kondracke, Morton. Saving Milly: Love, Politics, and Parkinson's Disease. New York: Public Affairs, 2001.

Mittel, Charles S., editor. Parkinson's Disease: Overview and Current Abstracts. New York: Nova Science, 2003.

Mosley, Anthony D., and Deborah S. Romaine. The Encyclopedia of Parkinson's Disease. New York: Facts on File, 2004.

Pahwa, Rajesh, et al., editors. Handbook of Parkinson's Disease. 3rd ed. New York: Marcel Dekker, 2004.

Weiner, William J., et al. Parkinson's Disease: A Complete Guide for Patients and Families. Baltimore: Johns Hopkins University Press, 2001.


Ascherio, A., et al. "Caffeine, Postmenopausal Estrogen, and Risk of Parkinson's Disease." Neurology 60, no. 5 (March 11, 2003): 79095.

Powers, K. M., et al. "Parkinson's Disease Risks Associated with Dietary Iron, Manganese, and Other Nutrient Intakes." Neurology 60 (June 2003): 176166.

Van Camp, Guy, et al. "Treatment of Parkinson's Disease with Pergolide and Relation to Restrictive Valvular Heart Disease." Lancet 363, no. 9416 (April 10, 2004): 117983.


American Parkinson Disease Association, Inc. 1250 Hylan Blvd., Suite 4B, Staten Island, NY 10305. 800-223-2732. <>.

Michael J. Fox Foundation for Parkinson's Research. Grand Central Station, P. O. Box 4777, New York, NY 10163. 8007087644. <>.

National Parkinson Foundation, Inc. 1501 NW Ninth Ave./Bob Hope Road, Miami, FL 331361494. 8003274545. <>.

Parkinson Alliance. P.O. Box 308, Kingston, NJ 08528-0308. 8005798440. <>.

Parkinson's Action Network. 1000 Vermont Ave. NW, Washington, DC 20005. 8008504725. 2028424101. info@ <>.

Parkinson's Disease Foundation. 710 West 168th Street, New York, NY 10032-9982. 8004576676. 2129234778. <>.


NINDS Parkinson's Disease Information Page. National Institute of Neurological Disorders and Stroke. August 17, 2001 [cited May 12, 2004]. <>.

Talampanel in Parkinson Disease: Why the Excitement? National Parkinson Foundation, Inc. [Cited May 12, 2004]. <>.

Paula Ford-Martin

Margaret Alic, PhD

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Parkinson's disease

Parkinson's disease or Parkinsonism, degenerative brain disorder first described by the English surgeon James Parkinson in 1817. When there is no known cause, the disease usually appears after age 40 and is referred to as Parkinson's disease; a number of genes have been found to be associated with the disease. Parkinsonism usually refers to similar symptoms resulting from head injury, encephalitis, syphilis, carbon monoxide poisoning, cerebral arteriosclerosis, or use of MPTP (a synthetic narcotic). The disorder is also termed paralysis agitans, or shaking palsy.

Parkinson's disease is a debilitating and progressive disorder in which the chemicals that facilitate electrical transmission between nerve cells are depleted. It was the first disease to be treated by drugs that replace deficient neurotransmitters. Symptoms usually begin in middle to later life with trembling of the lips and hands, loss of facial expression, and muscular rigidity. As it progresses it may bring on body tremors, particularly in muscles at rest. Movements become slow and difficult; walking degrades to a shuffle. After many years physical incapacity may occur. Dementia occurs in at least 50% of the patients; depression is also common.

When drugs such as levodopa (L-Dopa) are taken orally, many of the worst symptoms are lessened. New drugs such as pramipexole (Mirapex) and ropinirole (Requip) can delay the need for levodopa. Apomorphine (Apokyn) is used treat episodes of reduced mobility in patients with advanced Parkinson's that responds less effectively to levodopa. Future approaches to treatment include a focus on early detection and slowing progression of the disease. Encouraging results have been reported from surgical insertion of a pacemakerlike device deep in the brain to suppress uncontrolled movements, but surgical transplantation of fetal dopamine-producing cells failed to show significant benefits in a controlled study. Traditional surgery can alleviate some tremors, and physical therapy may help mobility.

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Parkinson's Disease

Parkinson's disease

A relatively common degenerative disorder of the central nervous system.

Parkinson's disease is a degenerative disorder of the central nervous system named for James Parkinson (1755-1824), the physician who first described it in 1817. This disorder is also called paralysis agitans, shaking palsy, or parkinsonism.

Typically, the symptoms of Parkinson's disease begin to appear in late middle life, and the course of the disease is slowly progressive over 20 years or more. In its advanced stages, Parkinson's disease is characterized by poorly articulated speech, difficulty in chewing and swallowing, loss of motor coordination, a general tendency toward exhaustion, and especially by stooped posture, positioning the arms in front of the body when walking, caution and slowness of movement, rigidity of facial expression, and tremor of the hands. Mental ability and the senses are not directly affected by this disease. Parkinson's disease is believed to be caused by a deficiency of dopamine in the basal ganglia of the brain .

Further Reading

McGoon, Dwight. The Parkinson's Handbook. New York: Norton, 1990.

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Parkinson's Disease



Parkinson's disease (PD) is a chronic, progressive disorder of the nervous system. A chronic disorder continues for long periods of time, usually many years. Parkinson's disease affects a person's muscular coordination. Symptoms of PD include tremor (shaking), rigidity in some muscles, slow movements, and problems with maintaining normal posture. The disease is caused by the death of cells in one of the movement control centers of the brain. These nerve cells control body movement.


Parkinson's disease affects about five hundred thousand people in the United States. It occurs with equal frequency in men and women. About fifty thousand new cases appear each year. The disease usually develops when a person is in his or her late fifties or early sixties. It develops gradually over a matter of months and years. A PD patient slowly loses control over the muscles that control movement. About 15 percent of people between the ages of sixty-five and seventy-four show some signs of PD. The rate among those in the age group between seventy-five and eighty-four is about 30 percent.


The immediate cause of Parkinson's disease is the destruction of brain cells in a part of the brain known as the substantia nigra (SN). The substantia nigra controls many types of muscular movement by releasing a neurotransmitter called dopamine. A neurotransmitter is a chemical that transports electrical signals between brain cells. Dopamine is needed to carry nerve messages from one brain cell to another.

Parkinson's Disease: Words to Know

Recurring frequently or lasting a long time.
A neurotransmitter that helps send signals that control movement.
A chemical that helps transmit electrical signals from one brain cell to another.
Substantia nigra:
A region of the brain that controls movement.

When brain cells die in the substantia nigra it doesn't release enough dopamine. Without dopamine, signals cannot travel from SN brain cells to cells in other parts of the brain. The "instructions" that brain cells need to move muscles do not reach their targets. Eventually, walking, writing, reaching for objects, and other basic movements do not occur correctly. Muscular movement becomes weaker and more erratic.

Researchers have not yet discovered the basic cause of Parkinson's disease. They do not know why SN brain cells lose the ability to produce dopamine. Some scientists think that the disease is hereditary. They believe that PD can be passed down from generation to generation. Other researchers think that environmental factors may be to blame. They suspect that certain chemicals in the world around us get into the human body and damage SN brain cells.

So far, a few chemicals have been found that cause the symptoms of PD. One chemical known to cause symptoms of PD is called MPTP. MPTP is sometimes found as an impurity in illegal drugs. A person who accidentally ingests (eats) MPTP begins to show signs of PD within hours. These symptoms become permanent.


"Shaking palsy" was a disease well known to physicians for hundreds of years. Patients with the disorder gradually became worse over a period of years. They slowly lost control over their limbs, and eventually lost the ability to dress and care for themselves.

The first scientific description of this disease was written in 1817 by Dr. James Parkinson (17551824). Parkinson was a man of many interests. Not only did he describe the nature of "shaking palsy," but he also provided the first explanation of appendicitis. Parkinson was also interested in the study of geology and paleontology (fossils), and was a social reformer. He fought for reform of the English parliamentary system and for better treatment of mental patients.

Parkinson also went one step beyond describing "shaking palsy." He conducted an autopsy on a patient who died of the condition. He found a swelling of the medulla, a part of the brain, which he said might be the cause of the disorder. For his research on this disease, "shaky palsy" was eventually renamed Parkinson's disease in his honor.


The symptoms by which PD can be identified include:

  • Tremor (shaking), usually beginning in the hands. The classic tremor associated with PD is called "pill-rolling tremor." The movement is like rolling a pill between the thumb and forefinger. The movement occurs about three times per second.
  • Slowing down of movements. A person may slow down or even stop in the middle of familiar movements, such as walking, eating, or shaving.
  • Muscle rigidity (stiffness). A PD patient's movements may be jerky rather than smooth.
  • Problems with posture and balance. A person may change the way he or she walks to keep from falling over.
  • "Masked face." This condition gets its name from the fact that the patient seems to have no facial expression. He or she may even have a greatly reduced rate of eye blinking.

Parkinson's disease may also be accompanied by one or more other symptoms, including:

  • Depression
  • Changes in the way a person speaks
  • Sleep problems, including restlessness and nightmares
  • Emotional changes, including increased fear, irritability, and feelings of insecurity
  • Incontinence (loss of bladder control)
  • Constipation
  • Changes in handwriting
  • Dementia (increased problems with mental functions)


There are no laboratory tests for the diagnosis of Parkinson's disease. The condition is fairly easy to diagnose based on the presence of the characteristic symptoms listed above. A person suspected of having PD will have a complete neurological (nervous system) examination. Tests may be conducted to rule out other conditions with similar symptoms. PD can also be diagnosed after a person has died. Characteristic structures in the brain are taken as proof of the disease.


There is no cure for Parkinson's disease. One drug, selegiline (trade name Eldepryl) may slow the destruction of SN brain cells. However, there are a number of treatments for the symptoms of PD.

Exercise, Nutrition, and Physical Therapy

Regular, moderate exercise can improve motor (muscular) control. It improves a person's circulation and appetite and frees up stiff muscles. A physical therapist can help a patient design an exercise program for his or her special needs.

Good nutrition is also important. PD patients often lose interest in food. They may simply lose their appetite, or they may have nausea from drugs they are taking for treatment. Also, as their bodies begin to move more slowly, they may become irritated by how long it takes to eat. Food may digest slowly as well, causing the person to feel full much of the day.

These problems can be partially solved by including more fiber in a person's diet. Soft foods also go down more easily and are digested more quickly. Certain types of drugs can also increase the movement of food through the digestive system.

There is currently no evidence that vitamins, minerals, or other nutritional supplements have any effect on the symptoms of PD.


Researchers have discovered a number of drugs that can help relieve the symptoms of Parkinson's disease. The effectiveness of the drugs depends on many factors. These factors include the patient's body chemistry, the rate at which the disease is progressing, and the length of time the drug has been used. Each PD drug also has side effects. In some cases, those side effects may limit the use of a drug by some patients.

There are presently five classes of drugs used to treat Parkinson's disease.

DRUGS THAT REPLACE DOPAMINE. The symptoms of the disease develop because SN brain cells do not produce enough dopamine. One solution, then, would be to give dopamine to the brain.

The problem with this solution is that the body's blood-brain barrier (BBB) gets in the way. It stops certain toxins and chemicals from entering the brain. In most places in the body substances can pass easily in and out of the blood vessels. This is how the cells of the body get the things they need to function properly. In the BBB, the walls of the blood vessels are much less permeable (open to penetration). The blood-brain barrier is very important because it protects the brain from harmful chemicals and helps maintain a safe, stable environment for sensitive brain tissues. But sometimes helpful chemicals are also kept from entering the brain.

The BBB doesn't allow neurotransmitters or hormones from elsewhere in the body to enter the brain. Dopamine, the chemical needed by Parkinson's patients, is a neurotransmitter. This is a problem for doctors. A person cannot be treated for Parkinson's by being given a pill or an injection of dopamine. The chemical in the pill or injection cannot get through the blood-brain barrier into the brain.

One solution is to "fool" the blood-brain barrier. A patient can be given a drug that looks to the blood-brain barrier like a material it should let through. Researchers have had some success attaching medicines to elements that can pass through the BBB.

In the case of Parkinson's doctors found that they could inject the body with levodopa or L-dopa, a substance that the BBB lets pass into the brain and then turns into dopamine. L-dopa treatments often work for five years or longer. Then the drug begins to lose its effectiveness. It may also begin to produce side effects that are as bad as the symptoms of PD itself.

ENZYME INHIBITORS. Dopamine does not stay in the brain forever. Instead, it is attacked by other chemicals that break it down into other substances. These chemicals are known as enzymes.

Another way to relieve the symptoms of PD, then, is to prevent enzymes from acting on dopaminethat is, to inhibit them from breaking it down. If the enzymes are inhibited, more dopamine will remain in the brain. The drugs given to PD patients often contain L-dopa and one or more enzyme inhibitors.

DOPAMINE AGONISTS. A dopamine agonist is a drug that acts in the brain in much the same way that dopamine does. Patients with Parkinson's disease can take dopamine agonists to make up for missing dopamine. Like other drugs used to treat PD, dopamine agonists can have serious side effects, including confusion and hallucinations at higher doses.

ANTICHOLINERGIC DRUGS. Dopamine is only one of many neurotransmitters in the brain. Brain function depends on a balance of all neurotransmitters. This balance changes as the amount of dopamine decreases. One way to restore this balance is with anticholinergic drugs. These drugs reduce the

amount of other neurotransmitters in the brain. They help maintain the correct balance of all neurotransmitters.

DRUGS WHOSE MODE OF ACTION IS UNCERTAIN. Sometimes drugs will work with PD patients, but researchers don't know why. The drug known as amantadine (pronounced uh-MANT-uh-deen, trade name Symmetrel) is an example. Amantadine is used to treat the symptoms of a variety of mental disorders. No one knows exactly how the drug relieves these symptoms, but it does, at least to a modest degree.


Some symptoms of Parkinson's disease occur because one part of the brain receives too much stimulation or another part receives too little. These problems can sometimes be helped by surgery. In one surgical procedure, a long thin needle is inserted into a certain part of the brain. The cells in that part of the brain are then killed with heat or electricity. This procedure prevents that region of the brain from becoming overactive.

A similar procedure can be used to make another part of the brain more active. A needle is inserted into the correct region of the brain. A mild electric current is then sent into the brain through the needle. The electric current may cause that region of the brain to become more active.

Surgery is used when patients do not respond to drugs or when drugs no longer work. Surgical procedures are often effective in helping people recover some of their normal muscular movement.

A third surgical procedure involves transplanting SN cells from the brain of a fetus. The brain cells in a fetus are in an early stage of development. When implanted into the brain of a PD patient, they sometimes take over the job of making dopamine. They begin to function in place of the patient's own SN cells that have lost the ability to produce dopamine. This procedure is still in an experimental stage.

Alternative Treatment

Alternative treatments have limited promise for treating Parkinson's disease. Acupuncture, massage, and yoga may help relieve some symptoms of the disease by loosening tight muscles. Some alternative practitioners recommend the use of herbs and nutritional supplements, such as vitamins A, B, C, E, and the minerals calcium, selenium, and zinc. These supplements can sometimes have harmful side effects when used with drugs, however.


There is no cure for Parkinson's disease. Drugs may help relieve symptoms for a few or many years. Those symptoms eventually get worse, however. Drug therapy becomes less successful. During the late stages of the disease, psychiatric symptoms become most troubling. These symptoms include problems with sleeping, increasing dementia, hallucinations, and loss of contact with reality.


There is no known way to prevent Parkinson's disease.



Atwood, Glenna Wotton. Living Well With Parkinson's. New York: John Wiley & Sons, 1991.

Biziere, Kathleen, and Matthias Kurth. Living with Parkinson's Disease. New York: Demos Vermande, 1997.

Hauser, Robert, and Theresa Zesiewica. Parkinson's Disease : Questions and Answers, 2nd edition. Chicago: Merit Publishing International, 1998.

Williams, Frank L. Parkinson's Disease : The Complete Guide for Patients and Caregivers. New York: Fireside, 1993.


National Parkinson Foundation. 1501 NW Ninth Ave., Bob Hope Road, Miami, FL 33136.

Parkinson's Disease Foundation. 710 West 168th St., New York, NY 10032. (800) 4576676.

Worldwide Education and Awareness for movement Disorders. Mt. Sinai Medical Center, 1 Gustave Levy Place, New York, NY 10029. (800) 437MOV2.

Web sites

About Parkinson's Disease. [Online] (accessed on October 27, 1999).

"Ask NOAH About: Parkinson's Disease." NOAH: New York Online Access to Health. [Online] (accessed on October 27, 1999).

AWAKENINGS. [Online] (accessed on October 27, 1999).

"Parkinson's Disease." [Online] (accessed on October 27, 1999).

The Parkinson's Web. [Online] (accessed on October 28, 1999).

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Parkinsons disease

Par·kin·son's dis·ease / ˈpärkinsənz/ • n. a progressive disease of the nervous system marked by tremor, muscular rigidity, and slow, imprecise movement, chiefly affecting middle-aged and elderly people. It is associated with degeneration of the basal ganglia of the brain and a deficiency of the neurotransmitter dopamine.

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Parkinsons disease

Parkinson's disease Degenerative brain disorder characterized by tremor, muscular rigidity and poverty of movement and facial expression. It arises from a lack of the neurotransmitter, dopamine. Slightly more common in men, it is rare before the age of 50. Foremost among the drugs used to control the disease is L-dopa.

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