Causes and Symptoms (Magill’s Medical Guide, Sixth Edition)
In 1817, James Parkinson, a British physician, wrote a description of six patients suffering from a slowly progressing disease characterized by “involuntary tremulous motion, with lessened muscular power in parts not in action even when supported, with a propensity to bend their trunks forward from a walking to a running pace.” Throughout the modern world, this disease—which Parkinson named shaking palsy—is called Parkinson’s disease in his honor.
Parkinson’s disease, also called paralysis agitans, is now defined as a medical condition characterized by a combination of symptoms including involuntary shaking (tremor) of the limbs at rest, stiffness of the muscles (rigidity), slowed or reduced ability to move the limbs and facial muscles (bradykinesia), and general muscular weakness. Worldwide, its occurrence is estimated at between 1.5 and 3 people per 1,000. In people over the age of fifty, this number increases to nearly 1 per 100, with the first appearance of symptoms usually occurring after the age of forty. The disease occurs in similar proportions in populations that eat such widely different diets that no particular food has been implicated as causative.
The most-often-used clinical scale that describes the extent of severity of Parkinson’s disease is that of Melvin Yahr and his associates, which is divided into five stages. In stage 1, mild tremor or rigidity is seen on one side of the body....
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Treatment and Therapy (Magill’s Medical Guide, Sixth Edition)
Parkinson’s disease is most often identified by physical evidence (such as tremor and bradykinesia), coupled with a careful study of the medical history of the patient being evaluated. In all but a few cases, no information can be obtained via the three powerful tools useful in many other neurologic exams: The complex X-ray method, computed tomography (CT) scanning, is informative only when stroke or tumor is involved; magnetic resonance imaging (MRI) gives no more information than do CT scans; and electroencephalograms (EEGs) do not show abnormal electrical discharge such as that observed in brains of epileptics. In practice, however, many physicians carry out CT scans, MRI, and EEGs and count their negative results into a diagnostic positive for Parkinson’s disease.
Once Parkinson’s disease is diagnosed, three main methods exist for handling it: chemotherapy, surgery, and physical therapy. All these methods—alone or in combination—are intended for symptom reversal because there is no cure for the disease. It is usually recommended that none of these methods be started until the disease interferes seriously with a patient’s work or daily life. Chemotherapy is the preponderant treatment mode in most cases. Many different medications are used, such as anticholinergics, L-dopa (levodopa), dopamine agonists, and antidepressants.
The anticholinergics were the first drugs used for Parkinson’s disease,...
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Perspective and Prospects (Magill’s Medical Guide, Sixth Edition)
Treatment of Parkinson’s disease has evolved tremendously, particularly since the late 1960’s, when wide use of L-dopa began. At that time, most physicians were astounded to observe that its use converted many bedridden and wheelchair-bound stage 5 patients to much more functional, mobile states. A temporary setback occurred when severe L-dopa side effects were observed at high doses.
The discovery of carbidopa and related inhibitors of nonbrain dopamine decarboxylase ended this problem and produced a new generation of chemotherapy. Patients could take L-dopa at lower concentrations, which minimized its side effects, because diminished nonbrain L-dopa conversion to dopamine left more L-dopa available to enter the brain. In addition, carbidopa was the forerunner of a group of dopamine agonists that became candidates for independent use or use in mixed therapy. Perhaps stimulated by this type of discovery, wide examination of the entire arsenal of potentially valuable pharmaceuticals led to the discovery that many other types of drugs (for example, tranquilizers, inhibitors of the bodily destruction of dopamine, or hypertension drugs), and even vitamins and diet, could be utilized in the fight to control symptoms. In addition, new drugs were discovered.
Researchers at the turn of the twenty-first century closely examined the genetic links in familial forms of Parkinson’s disease. One gene, a-synuclein, is...
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For Further Information: (Magill’s Medical Guide, Sixth Edition)
Beers, Mark H., et al., eds. The Merck Manual of Diagnosis and Therapy. 18th ed. Whitehouse Station, N.J.: Merck Research Laboratories, 2006. Offers a brief but valuable exposition of the characteristics, etiology, diagnosis, and treatment of Parkinson’s disease. Information on related topics is also included.
Carroll, David L. Living with Parkinson’s: A Guide for the Patient and Caregiver. New York: HarperCollins, 1992. This book is based on methods used by the Brookdale Center on Aging. The main topic issues include an explanation and identification of Parkinson’s disease, the medications and surgery used to treat it, the value of exercise, and advice on everyday living with the disease.
Gordin, Ariel, Seppo Kaakkola, and Heikki Teräväinenet, eds. Parkinson’s Disease. Philadelphia: Lippincott Williams & Wilkins, 2003. Collects research presented at a 2001 international conference and covers the history and future of the disease, epidemiology and genetics, imaging, medical treatment, surgical treatment, comorbid conditions, and related disorders.
Krause, J. K., and Joseph Jankovic. “Surgical Treatment of Parkinson’s Disease.” American Family Physician 54, no. 5 (1996): 1621-1629. An excellent article that succinctly explains recent pathophysiological mechanisms in neurosurgery, neuroradiology, and neurophysiology, particularly the use of...
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Introduction (Psychology and Mental Health)
Parkinson’s disease is one of the most common neurological disorders, affecting one person in every thousand. James Parkinson, in 1817, aptly described some of the classic symptoms in his book An Essay on the Shaking Palsy. Parkinson reported the patients as having a chronic and progressive disorder of the nervous system that had a late-age onset with the first mild symptoms not appearing until middle age. He also noted a tremor or shaking which typically appeared in the hand on one side and later spread to the other side. The disease progressed for a variable number of years, eventually leading to invalidism and death. A significant contribution was his ability to recognize the disorder as a disease distinct from previously described diseases.
Although Parkinson’s disease is thought of as a disease with its onset in middle age, there is a considerable variation in the age of onset, and there are other forms of the disease in addition to the classical form. The average age of onset is somewhere in the sixties. About 15 percent of patients develop symptoms between the ages of twenty-one and forty years. An extremely rare form of the disease, juvenile Parkinsonism, begins before the age of twenty-one. In addition to the severe neuromuscular symptoms, dementia may occur in some patients. In addition to tremors, other major symptoms are muscle stiffness or rigidity and bradykinesia or slow movement and even a...
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Clinical Features (Psychology and Mental Health)
The disease that subsequently became known as Parkinson’s disease was called “shaking palsy” by Parkinson. The shaking refers to the tremor which, although it is thought by many people to be invariably associated with Parkinson’s disease, may be completely absent or present to a minor degree in some patients. Four symptoms which are present in many patients are a progressive tremor, bradykinesia and even akinesia, muscular rigidity, and loss of postural reflexes. There still is no specific test that can be used to diagnose Parkinson’s disease. No biochemical, electrophysiologic, or radiologic test has been found to be completely reliable. As a result, misdiagnosis and underdiagnosis have been common with the disease. The situation is complicated further as a number of other diseases and conditions share some of the same symptoms, including Wilson’s disease, familial Alzheimer’s disease, Huntington’s disease, and encephalitis, as well as responses to certain drugs. Symptoms of Parkinson’s disease may also develop consequent to trauma to the brain.
A slight tremor in the hands may indicate the first symptoms of Parkinson’s disease, and the tremor may or may not also be found in the legs, jaws, and neck. An interesting symptom that may appear in later stages of the disease is seborrhea or acne. Intellectual functioning usually remains normal, but approximately 20 percent of the patients may experience...
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Causes (Psychology and Mental Health)
The most striking pathological change noted in Parkinson’s disease is a loss of nerve cells in a region of the brain known as the substantia nigra, a layer of deeply pigmented gray matter located in the midbrain. The region contains nerve cells that produce dopamine, a neurotransmitter associated with the control of movement. The levels of dopamine are normally in balance with another neurotransmitter, acetylcholine. In Parkinson’s disease, the loss of dopamine-producing cells causes a decrease in the levels of dopamine, with a consequent imbalance with acetylcholine. This leads to the symptoms of Parkinson’s disease.
The factors that lead to an upset of the dopaminergic system in the disease are complex. The disease is found throughout the world and occurs in nearly equal frequency in males and females, with slightly more males being affected than females. Parkinson’s disease is found in all ethnic groups, although there are some striking ethnic differences. The disease is relatively high among whites and relatively low among African blacks and Asians. Ethnic differences may reflect genetic and environmental differences. It is of interest to note that American blacks have a higher incidence than African blacks, indicating a likely role of local environmental factors.
The role of genetics in Parkinson’s disease has been difficult to establish. A family history of Parkinson’s disease appears to be a strong...
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Treatment (Psychology and Mental Health)
Once it became known that dopamine was depleted in patients with Parkinson’s disease, a rationale opened for a potential treatment. Levodopa was the first drug to be used to treat Parkinson’s disease successfully and is still the most effective treatment available. Dopamine can pass from the blood into the brain, and the drug increases the synthesis of dopamine. The drug does not cure the disease, but it is used in the attempt to control the symptoms. Although the effectiveness of levodopa may diminish somewhat after several years, most patients continue to benefit from its use. It is necessary to monitor patients closely to maintain proper dose levels as well as to register the appearance of new symptoms, side effects, and other complications.
A number of other drugs, alone or in combination, are being used or being tested. Drugs that enhance the action of dopamine are dopaminergic medications. Such drugs may increase dopamine release or may inhibit the breakdown of dopamine. Other drugs are known as anticholinergic medications, and these drugs inhibit the action of acetylcholine.
Surgery has also been used to treat symptoms of Parkinson’s disease, but results have been somewhat mixed. Surgical techniques include thalamotomy, a procedure producing a lesion in the thalamus gland for relief of severe unilateral tremor, and pallidotomy, the removal of part of the globus palledus region of the brain, which is used to...
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Sources for Further Study (Psychology and Mental Health)
Cram, David L. Understanding Parkinson’s Disease: A Self-Help Guide. Omaha, Nebr.: Addicus Books, 1999. A physician himself, Cram provides a well-written account of the symptoms and progression of the disease from his personal perspective and also discusses present and future treatments.
Garie, Gretchen, and Michael J. Church. Living Well with Parkinson’s Disease: What Your Doctor Doesn’t Tell You . . . That You Need to Know. New York: Collins, 2007. The authors both suffer from Parkinson’s, so this resource offers practical tips for living with the disease. It covers such topics as treatment options, emotional challenges, and dealing with relationships.
Jahanshahi, Marian, and C. David Marsden. Parkinson’s Disease: A Self-Help Guide. New York: Demos Medical Publishing, 2000. This book is an excellent self-help guide. In addition to chapters on the basic medical facts about Parkinson’s disease, there are chapters dealing with living and coping with the disease from the personal and family point of view.
Kondrack, Morton. Saving Milly: Love, Politics, and Parkinson’s Disease. New York: Public Affairs, 2002. The author provides a moving memoir of his life with his wife, Milly, and the development and impact of Parkinson’s disease.
Lanad, Anthony E., and Andres M. Lozano. “Parkinson’s Disease: The First of Two Parts.” The New England...
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Parkinson's Disease (Encyclopedia of Medicine)
Parkinson's disease (PD) is a progressive movement disorder marked by tremors, rigidity, slow movements (bradykinesia), and posture instability. It occurs when cells in one of the movement-control centers of the brain begin to die for unknown reasons. PD was first noted by British physician James Parkinson in the early 1800s.
Usually beginning in a person's late fifties or early sixties, Parkinson disease causes a progressive decline in movement control, affecting the ability to control initiation, speed, and smoothness of motion. Symptoms of PD are seen in up to 15% of those ages 654, and almost 30% of those ages 754.
Most cases of PD are sporadic. This means that there is a spontaneous and permanent change in nucleotide sequences (the building blocks of genes). Sporadic mutations also involve unknown environmental factors in combination with genetic defects. The abnormal gene (mutated gene) will form an altered end-product or protein. This will cause abnormalities in specific areas in the body where the protein is used. Some evidence suggests that the disease is transmitted by autosomal dominant inheritance. This implies that an affected parent has a 50% chance of transmitting the disease to any child. This type of inheritance is not commonly observed. The most recent evidence is...
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Parkinson's Disease (Encyclopedia of Neurological Disorders)
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,...
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Parkinson's Disease (Encyclopedia of Psychology)
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.
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Parkinson's Disease (Encyclopedia of Alternative Medicine)
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 brainhe corpus striatumhat controls muscle action. When dopamine levels fall, the neurons of the corpus striatum begin to misfire. It is estimated that dopamine-producing cells...
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Parkinson's Disease (Encyclopedia of Nursing & Allied Health)
Parkinson's disease (PD) is a progressive movement disorder marked by tremors, rigidity, slow movements (bradykinesia), and postural instability. It occurs when, for unknown reasons, cells in one of the movement-control centers of the brain begin to die.
Usually beginning in a person's late 50s or early 60s, PD causes a progressive decline in movement control, affecting the ability to control initiation, speed, and smoothness of motion. Symptoms of PD are seen in up to 15% of those between the ages 654, and almost 30% of those between the ages 754.
Most cases of PD are sporadic. This means that there is a spontaneous and permanent change in nucleotide sequences (the building blocks of genes). Sporadic mutations also involve unknown environmental factors in combination with genetic defects. The abnormal gene (mutated gene) will form an altered end-product or protein. This will cause abnormalities in specific areas of the body where the protein is used. Some evidence suggests that the disease is transmitted by autosomal dominant inheritance. This implies that an affected parent has a 50% chance of transmitting the disease to any child. This type of inheritance is not commonly observed. The most recent evidence links PD with a gene that codes for a protein called alpha-synuclein. Further research is attempting to fully understand the relationship with this protein and nerve cell degeneration.
PD affects approximately 500,000 people in the United States, both men and women, with as many as 50,000 new cases being diagnosed each year.
Causes and symptoms
The immediate cause of PD is degeneration of brain cells in the area known as the substantia nigra, one of the movement control centers of the brain. Damage to this area leads to the cluster of symptoms known as parkinsonism. In PD, degenerating brain cells contain Lewy bodies, which help identify the disease. The cell death leading to parkinsonism may be caused by a number of conditions, including infection, trauma, and poisoning. Some drugs given for psychosis, such as haloperidol (Haldol) or chlorpromazine (Thorazine), may cause parkinsonism. When no cause for nigral cell degeneration can be found, the disorder is called idiopathic parkinsonism, or Parkinson's disease. Parkinsonism may be seen in other degenerative conditions, known as the parkinsonism plus syndromes, such as progressive supranuclear palsy.
The substantia nigra, or black substance, is one of the principal movement control centers in the brain. By releasing the neurotransmitter known as dopamine, it helps to refine movement patterns throughout the body. The dopamine released by nerve cells of the substantia nigra stimulates another brain region, the corpus striatum. Without enough dopamine, the corpus striatum cannot control its target muscles. Ultimately, the movement patterns of walking, writing, reaching for objects, and other basic programs cannot operate properly, and the symptoms of parkinsonism are the result.
There are some known toxins that can cause parkinsonism, most notoriously a chemical called MPTP, found as an impurity in some illegal drugs. Parkinsonian symptoms appear within hours of ingestion and are permanent. MPTP may exert its effects through generation of toxic molecular fragments called free radicals. Reducing free radicals has been a target of several experimental treatments for PD using antioxidants.
It is possible that early exposure to some as-yetunidentified environmental toxin or virus leads to undetected nigral cell death, and that PD then becomes manifest as normal age-related decline brings the number of functioning nigral cells below the threshold needed for normal movement. It is also possible that, for genetic reasons, some people are simply born with fewer cells in their substantia nigra than others, and develop PD again as a consequence of normal decline.
The identifying symptoms of PD include:
- Tremors, usually beginning in the hands, often occurring on one side before the other. The classic tremor of PD is called a pill-rolling tremor, because the movement resembles rolling a pill between the thumb and forefinger. This tremor occurs at a frequency of about three per second.
- Slow movements (bradykinesia) occur, which may involve slowing down or stopping in the middle of familiar tasks such as walking, eating, or shaving. This may include freezing in place during movements (akinesia).
- Muscle rigidity or stiffness, occurring with jerky movements replacing smooth motion.
- Postural instability or balance difficulty occurs. This may lead to a rapid, shuffling gait (festination) to prevent falling.
- In most cases, there is a typical facial expression called masked face, characterized by little facial expression and decreased eye-blinking.
In addition, a wide range of other symptoms may often be seen, some beginning earlier than others:
- speech changes, including rapid speech without inflection changes
- problems with sleep, including restlessness and nightmares
- emotional changes, including fear, irritability, and insecurity
- handwriting changes, with letters becoming smaller across the page (micrographia)
- progressive problems with intellectual function (dementia)
The diagnosis of Parkinson disease involves a careful medical history and a neurological exam to look for characteristic symptoms. There are no definitive tests for PD, although a variety of lab tests may be done to rule out other causes of symptoms, especially if only some of the identifying symptoms are present. Tests for other causes of parkinsonism may include brain scans, blood tests, lumbar puncture, and x rays.
There is no cure for Parkinson disease. Most drugs treat only the symptoms of the disease, although one drug, selegiline (Eldepryl), may slow degeneration of the substantia nigra.
Exercise, nutrition, and physical therapy
Regular, moderate exercise has been shown to improve motor function without an increase in medication for a person with PD. Exercise helps maintain range of motion in stiff muscles, improve circulation, and stimulate appetite. An exercise program designed by a physical therapist has the best chance of meeting the specific needs of a person with PD. A physical therapist may also suggest strategies for balance compensation and techniques to stimulate movement during slowdowns or freezes.
Good nutrition is important to maintenance of general health. A person with PD may lose some interest in food, especially if depressed, and may have nausea from the disease or from medications, especially those known as dopamine agonists. Slow movements may make it difficult to eat quickly, and delayed gastric emptying may lead to a feeling of fullness without having eaten much. Increasing fiber in the diet can improve constipation, soft foods can reduce the amount of needed chewing, and a prokinetic drug such as cisapride (Propulsid) can increase the movement of food through the digestive system.
People with PD may need to limit the amount of protein in their diets. The main drug used to treat PD, L-dopa, is an amino acid, and is absorbed by the digestive system by the same transporters that pick up other amino acids broken down from proteins in the diet. Limiting protein, under the direction of a physician or nutritionist, can improve the absorption of L-dopa.
No evidence indicates that vitamin or mineral supplements can have any effect on the disease other than in their improvement of general health. No antioxidants used to date have shown promise as a treatment except for selegiline, an MAO-B inhibitor. A large, carefully controlled study of vitamin E demonstrated that it could not halt disease progression.
The pharmacological treatment of Parkinson disease is complex. While there are a large number of drugs that can be effective, their effectiveness varies among individuals, disease progression, and the length of time the drug has been used. Dose-related side effects may preclude the use of the most effective dose, or require the introduction of a new drug to counteract them. There are five classes of drugs currently used to treat PD.
DRUGS THAT REPLACE DOPAMINE. One drug that helps replace dopamine, levodopa (L-dopa), is the single most effective treatment for the symptoms of PD. L-dopa is a derivative of dopamine, and is converted into dopamine by the brain. It may be started when symptoms begin, or when they become serious enough to interfere with work or daily living.
L-dopa therapy usually remains effective for five years or longer. Following this, many persons develop motor fluctuations, including peak-dose dyskinesias (abnormal movements such as tics, twisting, or restlessness); rapid loss of response after dosing (known as the on-off phenomenon); and unpredictable drug response. Higher doses are usually tried, but may lead to an increase in dyskinesias. In addition, side effects of L-dopa include nausea and vomiting, and low blood pressure upon standing (orthostatic hypotension), which can cause dizziness. These effects usually lessen after several weeks of therapy.
ENZYME INHIBITORS. Dopamine is broken down by several enzyme systems in the brain and elsewhere in the body, and blocking these enzymes is a key strategy to prolonging the effect of a dose of dopamine. The two most commonly prescribed forms of L-dopa contain a drug to inhibit the amino acid decarboxylase (an AADC inhibitor), one type of enzyme that breaks down dopamine. These combination drugs are Sinemet (L-dopa plus carbidopa) and Madopar (L-dopa plus benzaseride). Controlled-release formulations also aid in prolonging the effective interval of an L-dopa dose.
The enzyme monoamine oxidase B (MAO-B) inhibitor selegiline may be given as add-on therapy for L-dopa. Research indicates selegiline may have a neuroprotective effect, sparing nigral cells from damage by free radicals. Because of this, and the fact that it has few side
AADC inhibitorsrugs that block the amino acid decarboxylase; one type of enzyme that breaks down dopamine. Also called DC inhibitors, they include carbidopa and benserazide.
Akinesia loss of the ability to move; freezing in place.
Bradykinesiaxtremely slow movement.
COMT inhibitorsrugs that block catechol-O-methyltransferase, an enzyme that breaks down dopamine. COMT inhibitors include entacapone and tolcapone.
Dopamine chemical in the brain (neurotransmitter) that helps send signals that control movement.
Dyskinesian abnormal involuntary movement. Dyskinesias are common late in PD as L-dopa therapy becomes less effective.
MAO-B inhibitorsnhibitors of the enzyme monoamine oxidase B. MAO-B helps break down dopamine; inhibiting it prolongs the action of dopamine in the brain. Selegiline is an MAO-B inhibitor.
Orthostatic hypotension sudden decrease in blood pressure upon sitting up or standing. May be a side effect of several types of drugs.
Substantia nigrane of the movement control centers of the brain.
effects, it is also frequently prescribed early in the disease before L-dopa is begun. Entacapone (Comtan) and tolcapone (Tasmar), two inhibitors of another enzyme system called catechol-O-methyltransferase (COMT), have recently been approved for use and marketed. They effectively treat PD symptoms with fewer motor fluctuations and decreased daily L-dopa requirements.
DOPAMINE AGONISTS. Dopamine works by stimulating receptors on the surface of corpus striatum cells. Drugs that also stimulate these cells are called dopamine agonists, or DAs. DAs may be used before L-dopa therapy, or added on to avoid requirements for higher L-dopa doses late in the disease. DAs available in the United States as of 2001, include bromocriptine (Permax, Parlodel), pergolide (Permax), pramipexole (Mirapex), cabergoline (Dostinex), and ropinirole (Requip). Other dopamine agonists in use elsewhere include lisuride (Dopergine) and apomorphine. Side effects of all the DAs are similar to those of dopamine, plus confusion and hallucinations at higher doses.
ANTICHOLINERGIC DRUGS. Anticholinergics maintain dopamine balance as levels decrease. However, the side effects of anticholinergics (dry mouth, constipation, confusion, and blurred vision) are usually too severe in older individuals or in persons with dementia. In addition, anticholinergics rarely work for very long. They are often prescribed for younger people who have predominant shaking. Trihexyphenidyl (Artane) is the most commonly prescribed drug.
DRUGS WHOSE MODE OF ACTION IS UNCERTAIN. Amantadine (Symmetrel) is sometimes used as an early therapy before L-dopa is begun, and as an add-on later in the disease. Its anti-parkinsonian effects are mild, and are not seen in many persons. Clozapine (Clozaril) is effective, especially against psychiatric symptoms of late PD, including psychosis and hallucinations.
Two surgical procedures are used for treatment of PD that cannot be controlled adequately with drug therapy. In PD, a brain structure called the globus pallidus (GPi) receives excess stimulation from the corpus striatum. In a pallidotomy, the GPi is destroyed by heat that is delivered by long thin needles inserted under anesthesia. Electrical stimulation of the GPi is another way to reduce its action. In this procedure, fine electrodes are inserted to deliver the stimulation, which may be adjusted or turned off as the response dictates. Other regions of the brain may also be stimulated by electrodes inserted elsewhere. In most persons, these procedures lead to significant improvement for some motor symptoms, including peak-dose dyskinesias. This allows a person to receive more L-dopa, since these dyskinesias are usually responsible for any upper limit on the L-dopa dose.
A third procedure, transplant of fetal nigral cells, is still highly experimental. Its benefits to date have been modest, although improvements in technique and surgical candidate selection are likely to increase successful outcomes.
Currently, the best treatments for PD involve the use of conventional drugs such as levodopa. Alternative therapies, including acupuncture, massage, and yoga, can help relieve some symptoms of the disease and loosen tight muscles. Alternative practitioners have also applied herbal and dietary therapies, including amino acid supplementation, antioxidant (vitamins A, C, E, selenium, and zinc) therapy, B vitamin supplementation, and calcium and magnesium supplementation to the treatment of PD. Persons using these therapies in conjunction with conventional drugs should check with their doctor to avoid the possibility of adverse interactions. For example, vitamin B6 (either as a supplement or from foods such as whole grains, bananas, beef, fish, liver, and potatoes) can interfere with the action of L-dopa when the drug is taken without carbidopa.
Despite medical treatment, the symptoms of Parkinson's disease worsen over time, and become less responsive to drug therapy. Late-stage psychiatric symptoms are disease often the most troubling. These include difficulty sleeping, nightmares, intellectual impairment (dementia), hallucinations, and loss of contact with reality (psychosis).
Health care team roles
A physician usually makes an initial diagnosis of Parkinson's disease. Treatment is often managed by a family physician or internist. Neurologists may be asked for consultations. Occasionally, neurosurgeons perform surgery in the treatment of parkinsonism. Clinical nutritionists and physical therapists may assist in managing persons with PD. Nurses provide bedside care in the hospital, and administer the frequent patient neurologic evaluations. They also provide patient and family education about the diagnosis and home management.
There is no known way to prevent Parkinson's disease.
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American Academy of Neurology. 1080 Montreal Avenue, St. Paul, MN 55116. (651) 695-1940. <<a href="http://www.aan.com">http://www.aan.com>.
American College of Physicians. 190 N. Independence Mall West, Philadelphia, PA 19106-1572. (800) 523-1546. <<a href="http://www.acponline.org">http://www.acponline.org>.
American Parkinson Disease Association. Inc., 1250 Hylan Boulevard, Suite 4B, Staten Island, NY 10305-1946. (800) 223-2732. <<a href="http://www.apdaparkinson.com">http://www.apdaparkinson.com>.
Parkinson's Disease Foundation. 710 West 168th Street, New York, NY 10032-9982. (800) 457-6676. <<a href="http://www.pdf.org">http://www.pdf.org>.
Parkinson's Disease Society (UK). 215 Vauxhall Bridge Road, London SW1V 1EJ. (020) 7931-8080. <<a href="http://www.parkinsons.org.uk">http://www.parkinsons.org.uk>.
American Academy of Family Physicians. <<a href="http://www.aafp.org/afp/990415ap/2155.html">http://www.aafp.org/afp/990415ap/2155.html>.
Bowman Gray University School of Medicine. <<a href="http://www.bgsm.edu/bgsm/surg-sci/ns/pd.html">http://www.bgsm.edu/bgsm/surg-sci/ns/pd.html>.
National Institute of Health. <<a href="http://www.nhgri.nih.gov/DIR/LGDR/PARK/about_parks.html">http://www.nhgri.nih.gov/DIR/LGDR/PARK/about_parks.html>.
National Institute of Neurological Diseases and Stroke. <<a href="http://www.ninds.nih.gov">http://www.ninds.nih.gov>.
National Library of Medicine. <<a href="http://www.nlm.nih.gov/medlineplus/parkinsonsdisease.html">http://www.nlm.nih.gov/medlineplus/parkinsonsdisease.html>.
National Parkinson Foundation. <<a href="http://www.parkinson.org/sources.htm">http://www.parkinson.org/sources.htm>.
Parkinson's Disease Web Ring. <<a href="http://www.pdring.com">http://www.pdring.com>.
United States Food and Drug Administration. <<a href="http://www.fda.gov/fdac/features/1998/498_pd.html">http://www.fda.gov/fdac/features/1998/498_pd.html>.
World Parkinson Disease Association. <<a href="http://www.wpda.org">http://www.wpda.org>.
L. Fleming Fallon, Jr., MD, DrPH