Parkinson Disease

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Parkinson Disease



Parkinson 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 65-74, and almost 30% of those ages 75-84.
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 linking 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 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 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 substantia nigra stimulates another brain region, the corpus striatum. Without enough dopamine, the corpus striatum cannot control its targets, and so on down the line. 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, and reducing free radicals has been a target of several experimental treatments for PD using antioxidants.
It is possible that early exposure to some as-yet-unidentified environmental toxin or virus leads to undetected nigral cell death, and PD then manifests 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 they develop PD as a consequence of normal decline.


The identifying symptoms of PD include:
  • Tremors, usually beginning in the hands, often occuring 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, occuring 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 "masked face," with little facial expression and decreased eye-blinking.
In addition, a wide range of other symptoms may often be seen, some beginning earlier than others:
  • depression
  • speech changes, including rapid speech without inflection changes
  • problems with sleep, including restlessness and nightmares
  • emotional changes, including fear, irritability, and insecurity
  • incontinence
  • constipation
  • 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 the symptoms of the disease only, 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 the 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 the physician or a 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 the improvement of the patient's general health. No antioxidants used to date have shown promise as a treatment except for selegiline, an MAO-B inhibitor which is discussed in the Drugs section. 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 with the patient, disease progression, and the length of time the drug has been used. Dose-related side effects may preclude using 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 patients 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 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 (Ldopa 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 effects, it is also frequently prescribed early in the disease before L-dopa is begun. Entacapone and tolcapone, two inhibitors of another enzyme system called catechol-o-methyl transferase (COMT), may soon reach the market as early studies suggest that 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 early 1998, include bromocriptine (Permax, Parlodel), pergolide (Permax), and pramipexole (Mirapex). Two more, cabergoline (Dostinex) and ropinirole (Requip), are expected to be approved soon. 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 patients or in patients with dementia. In addition, anticholinergics rarely work for very long. They are often prescribed for younger patients who have predominant shaking. Trihexyphenidyl (Artane) is the drug most commonly prescribed.
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 patients. 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, 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 patients, these procedures lead to significant improvement for some motor symptoms, including peak-dose dyskinesias. This allows the patient to receive more L-dopa, since these dyskinesias are usually what causes an 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 patient selection are likely to change that.

Alternative treatment

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. Anyone 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 disease worsen over time, and become less responsive to drug therapy. Late-stage psychiatric symptoms are often the most troubling, including difficulty sleeping, nightmares, intellectual impairment (dementia), hallucinations, and loss of contact with reality (psychosis).


There is no known way to prevent Parkinson disease.



National Parkinson Foundation. 1501 NW Ninth Ave., Bob Hope Road, Miami, FL 33136.
Parkinson Disease Foundation. 710 West 168th St., New York, NY 10032. (800) 457-6676. 〈〉.
Worldwide Education and Awareness for Movement Disorders. One Gustave Levy Place, New York, NY 10029. (800) 437-MOV2.



Key terms

AADC inhibitors — Drugs that block the amino acid decarboxylase; one type of enzyme that breaks down dopamine. Also called DC inhibitors, they include carbidopa and benserazide.
Akinesia — A loss of the ability to move; freezing in place.
Bradykinesia — Extremely slow movement.
COMT inhibitors — Drugs that block catechol-o-methyl transferase, an enzyme that breaks down dopamine. COMT inhibitors include entacapone and tolcapone.
Dopamine — A neurochemical made in the brain that is involved in many brain activities, including movement and emotion.
Dyskinesia — Impaired ability to make voluntary movements.
MAO-B inhibitors — Inhibitors 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 — A sudden decrease in blood pressure upon sitting up or standing. May be a side effect of several types of drugs.
Substantia nigra — One of the movement control centers of the brain.
Gale Encyclopedia of Medicine. Copyright 2008 The Gale Group, Inc. All rights reserved.


1. A neurologic syndrome usually resulting from deficiency of the neurotransmitter dopamine as the consequence of degenerative, vascular, or inflammatory changes in the basal ganglia; characterized by rhythmic muscular tremors, rigidity of movement, festination, droopy posture, and masklike facies. Synonym(s): Parkinson disease, shaking palsy, trembling palsy
2. A syndrome similar to parkinsonism. Some features seen with Parkinson disease that occur with other disorders (for example, progressive supranuclear palsy) or as a side effect of certain medications (for example, antipsychotic drugs).
[J. Parkinson]
Farlex Partner Medical Dictionary © Farlex 2012


1. A neurologic syndrome usually resulting from deficiency of the neurotransmitter dopamine as the consequence of degenerative, vascular, or inflammatory changes in the basal ganglia; characterized by rhythmic muscular tremors, rigidity of movement, festination, droopy posture, and masklike facies.
Synonym(s): Parkinson disease.
2. A syndrome similar to parkinsonism appearing as an adverse effect of some antipsychotic drugs.
[J. Parkinson]
Medical Dictionary for the Health Professions and Nursing © Farlex 2012

Parkinson Disease

DRG Category:57
Mean LOS:4.8 days
Description:MEDICAL: Degenerative Nervous System Disorders Without Major CC

Parkinson disease (PD) is a neurological disorders that affects 1% of older adults beyond the seventh decade of life. It is a common clinical condition characterized by gradual slowing of voluntary movement (bradykinesia); muscular rigidity; stooped posture; distinctive gait with short, accelerating steps; diminished facial expression; and resting tremor. The disease occurs with progressive parkinsonism in the absence of a toxic or known etiology and is a progressively degenerative disease of the substantia nigra and basal ganglia. PD is also called paralysis agitans.

PD is caused by a degeneration of the substantia nigra in the basal ganglia of the midbrain, which leads to depletion of the neurotransmitter dopamine (DA). DA is normally produced and stored in this location and promotes smooth, purposeful movements and modulation of motor function. Depletion of DA leads to impairment of the extrapyramidal tracts and consequent loss of movement coordination. Almost 80% of DA neurons are lost before the patient begins to have the motor signs of PD.

Complications include injuries from falls, skin breakdown from immobility, and urinary tract infections. Death is usually caused by aspiration pneumonia or other infection.


The majority of all cases of classic PD are primary, or idiopathic, Parkinson disease (IPD). The cause is unknown; a few cases suggest a hereditary pattern. Secondary, or iatrogenic, PD is drug or chemical related. Dopamine-depleting drugs such as reserpine, phenothiazine, metoclopramide, tetrabenazine, and the butyrophenones (droperidol and haloperidol) can lead to secondary PD.

Genetic considerations

Recent advances in genetics have demonstrated that PD has strong genetic influences. Genetic loci identified as PARK 1–9 are associated with either autosomal dominant or recessive forms of the disease. Mutations of additional genes (HTRA2, LRRK2, NR4A2, NDUFV2, ADH3, FGF20, GBA, and MAPT) appear to increase susceptibility.

Gender, ethnic/racial, and life span considerations

PD occurs in 1% of the population over age 60. Juvenile parkinsonism, however, is associated in people younger than age 40 who have Wilson’s disease, progressive lenticular degeneration, or Huntington’s disease. PD affects men slightly more often than it does women. Approximately 15% of people with IPD develop dementia as they age. People with Hispanic/Latino and white/European ancestry have a higher incidence of PD than other groups.

Global health considerations

The global incidence of PD is 10 to 20 cases per 100,000 individuals per year. Environmental factors in different global regions most likely explain the variation in incidence by location.



Obtain a family, medication, and occupational history. PD progresses through the following stages: (1) mild unilateral dysfunction; (2) mild bilateral dysfunction, as evidenced by expressionless face and gait changes; (3) increasing dysfunction, with difficulties in walking, initiating movements, and maintaining equilibrium; (4) severe disability, including difficulties in walking and maintaining balance and steady propulsion, rigidity, and slowed movement; and (5) invalidism, which requires total care. Note the timing of progression of all symptoms.

The three cardinal signs of PD are involuntary tremors, akinesia, and progressive muscle rigidity. The first symptom of PD is a coarse, rest tremor of the fingers and thumb (pill-rolling movement) of one hand. It occurs during rest and intensifies with stress, fatigue, cold, or excitation. This tremor disappears during sleep or purposeful movement. The tremor can occur in the tongue, lip, jaw, chin, and closed eyelids. Eventually, the tremor can spread to the foot on the same side and then to the limbs on the other side of the body.

Physical examination

The diagnosis of PD is made on the basis of two out of the four important symptoms: resting tremor, bradykinesia (slowing down or loss of voluntary muscle movement), cogwheel rigidity (rigidity of a muscle that gives way in a series of little jerks when passive stretching occurs), and postural instability; one of the two symptoms must be resting tremor or bradykinesia. Generally, the onset of symptoms are asymmetric and may begin with a resting tremor in one arm.

Assess the patient for signs of bradykinesia. Perform a passive range-of-motion examination, assessing for rigidity. Rigidity of the antagonistic muscles, which causes resistance to both extension and flexion, is a cardinal sign of PD. Flexion contractures develop in the neck, trunk, elbows, knees, and hips. Note alterations in the respiratory status because rigidity of the intercostal muscles may decrease breath sounds or cause labored respirations. Observe the patient’s posture, noting if he or she is stooped, and assess gait dysfunction. Note involuntary movements, slowed movements, decreased movements, loss of muscle movement, repetitive muscle spasms, an inability to sit down, and difficulty in swallowing.

Observe the patient’s face, noting an expressionless, masklike appearance, drooling, and decreased tearing ability; note eyeballs fixed in an upward direction or eyelids completely closed, which are rare complications of PD. Assess for defective speech, a high-pitched monotone voice, and parroting the speech of others. Autonomic disorders that are manifested in PD include hypothalamic dysfunction, so assess for decreased or Parkinson’s perspiration, heat intolerance, seborrhea, and excess oil production. Observe the patient for orthostatic hypotension, which manifests in fainting or dizziness. Note constipation or bladder dysfunction (urgency, frequency, retention).


PD does not usually affect intellectual ability, but 20% of patients with PD develop dementia similar to that of Alzheimer’s disease. The PD patient commonly develops depression later in the disease process, and this is characterized by withdrawal, sadness, loss of appetite, and sleep disturbance. Patients may also demonstrate problems with social isolation, ineffective coping, potential for injury, and sleep pattern disturbance.

Diagnostic highlights

The diagnosis of PD is usually made through clinical findings rather than diagnostic tests because there is no specific biological marker that exists for PD. The key to diagnosis is the patient’s response to levodopa (see Pharmacologic Highlights).

TestNormal ResultAbnormality With ConditionExplanation
Positron emission tomography and single photon emission computed tomographyNormal dopamine uptake in basal gangliaDecreased dopamine uptake in the basal gangliaDegeneration of substantia nigra in the basal ganglia of midbrain leads to depletion of dopamine

Other Tests: Magnetic resonance imaging and computed tomography scan are usually normal in people with PD.

Primary nursing diagnosis


Self-care deficit related to rigidity and tremors


Self-care: Activities of daily living—Bathing, Hygiene, Dressing, Grooming, Eating; Anxiety control; Endurance; Comfort level; Mood equilibrium; Energy conservation; Muscle function; Mobility level


Exercise therapy: Ambulation, Balance, Joint mobility, Muscle control; Environmental management, Self-care assistance; Exercise promotion; Energy management; Body image enhancement

Planning and implementation


To control tremor and rigidity, pharmacologic management is the treatment of choice. Generally, people have good control of their symptoms for about 5 years. After that time, their disability progresses with long-term motor complications; difficulty with their balance; and, for some, dementia. Long-term levodopa therapy can result in drug tolerance or drug toxicity. Symptoms of drug toxicity are confusion, hallucinations, and decreased drug effectiveness. Treatment for drug tolerance and toxicity is either a change in drug dosage or a drug holiday. Autologous transplantation of small portions of the adrenal gland into the brain’s caudate nucleus of PD patients is offered on an experimental basis in some medical centers as a palliative treatment. In addition, if medications are ineffective, a thalamotomy or stereotaxic neurosurgery may be done to treat intractable tremor.

Physical and occupational therapy consultation is helpful to plan a program to reduce flexion contractures and to maximize functions for the activities of daily living. To prevent impaired physical mobility, perform passive and active range-of-motion exercises and muscle-stretching exercises. In addition, include exercises for muscles of the face and tongue to facilitate speech and swallowing. Use of a cane or walker promotes ambulation and prevents falls.

Pharmacologic highlights

Medication or Drug ClassDosageDescriptionRationale
AntiparkinsonVaries with drugLevodopa (L-dopa); carbidopa levodopa (Sinemet)Controls tremor and rigidity; converted to dopamine in the basal ganglia; dopamine replacement therapy
Amantadine hydrochloride (Symmetrel)100 mg bid POAntiviralControls tremor and rigidity by increasing the release of dopamine to the basal ganglia
Synthetic anticholinergicsVaries with drugTrihexyphenidyl (Artane); benztropine mesylate (Cogentin)Block acetylcholine-stimulated nerves that lead to tremors

Other Drugs: Antihistamines are sometimes prescribed with the anticholinergics to inhibit dopamine uptake; bromocriptine mesylate, a dopamine antagonist, is ordered to stimulate dopaminergic receptors. Selegiline may have a neuroprotective effect if started at the time of diagnosis.


Promote independence in the patient. Encourage maximum participation in self-care activities. Allow sufficient time to perform activities and schedule outings in late morning or in the afternoon to avoid rushing the patient. Reinforce occupational and physical therapy recommendations. Use adaptive devices as needed. If painful muscle cramps threaten to limit the patient’s mobility, consider warm baths or muscle massage.

To facilitate communication, encourage the PD patient to speak slowly and to pause for a breath at appropriate intervals in each sentence. Teach deep-breathing exercises to promote chest expansion and adequate air exchange. Be alert to nonverbal clues and supplement interactions with a communication board, mechanical voice synthesizer, computer, or electric typewriter.

To maintain nutritional status, monitor the patient’s ability to chew and swallow. Monitor weight, intake, and output. Position the patient in the upright position for eating to facilitate swallowing. Offer small, frequent meals; soft foods; and thick, cold fluids. Supplemental puddings or nutritional shakes may be given throughout the day to maintain weight.

Help the patient maintain a positive self-image by emphasizing her or his abilities and by reinforcing success. Encourage the patient to verbalize feelings and to write in a journal. Help the patient maintain a clean, attractive appearance. Caregivers may need a great deal of emotional support. Explore strategies for long-term care with the patient and significant others.

Evidence-Based Practice and Health Policy

Tickle-Degnen, L., Ellis, T., Saint-Hilaire, M.H., Thomas, C.A., & Wagenaar, R.C. (2010). Self-management rehabilitation and health-related quality of life in Parkinson disease: A randomized controlled trial. Movement Disorders, 25(2), 194–204.

  • Investigators randomized 116 patients with Parkinson disease to either a rehabilitation intervention group or a control group that received no rehabilitation to determine the intervention’s effects on the patients’ health-related quality of life (HRQOL).
  • The intervention included up to 27 hours of rehabilitation training over a 2- to 3-week period, which was conducted by a team of physical, occupational, and speech therapists who worked with patients to observe their own behaviors, identify issues and strengths related to mobility, communicate effectively, participate in activities of daily living, set realistic goals to manage problems, and implement plans of action.
  • Immediately postintervention, 54% of patients who received rehabilitation training reported improved HRQOL compared to 18% of patients who received no rehabilitation training. The difference in HRQOL between the two groups decreased from 36% immediately postintervention (95% CI, 20% to 53%; p < 0.001) to 28% at 6 months (95% CI, 14% to 43%; p < 0.001). There were no significant differences in HRQOL between the two groups at baseline.

Documentation guidelines

  • Ability to ambulate, perform the activities of daily living, progress in an exercise program
  • Use of verbal and nonverbal communication
  • Statements about body image and self-esteem
  • Discomfort during activity

Discharge and home healthcare guidelines

Be sure the patient or caregiver understands all medications, including the dosage, route, action, and adverse reactions. Avoid the use of alcohol, reserpine, pyridoxine, and phenothiazine while taking levodopa. In general, recommend massage and relaxation techniques and reinforce exercises recommended by the physical therapist. Several techniques facilitate mobility and enhance safety in PD patients. Instruct the patient to try the following strategies: (1) To assist in maintaining balance, concentrate on taking larger steps with feet apart, keeping back straight and swinging the arms; (2) to overcome akinesia, tape the “frozen” leg to initiate movement; (3) to reduce tremors, hold objects (coins, keys, or purse) in the hand; (4) to obtain partial control of tremors when seated, grasp chair arms; (5) to reduce rigidity before exercise, take a warm bath; (6) to initiate movement, rock back and forth; (7) to prevent spine flexion, periodically lie prone and avoid using a neck pillow; and (8) teach the patient to eliminate loose carpeting, install grab bars, and elevate the toilet seat. Use of chair lifts can also be beneficial.

Explore coping strategies with the patient and family. Support groups for the PD patient and family are available in most cities. Contact the American Parkinson Disease Association and Referral Center (APDA) at or 116 John Street, New York, NY (1-800-223-2732). Encourage the patient to be independent in the activities of daily living. Use devices and assistance as necessary. Provide ample time to complete self-care.

Diseases and Disorders, © 2011 Farlex and Partners


James, English physician, 1755-1824.
Parkinson disease - a neurological disorder usually resulting from deficiency of dopamine as the consequence of degenerative, vascular, or inflammatory changes in the basal ganglia. Synonym(s): parkinsonism (1)
Parkinson facies - the expressionless or masklike facies characteristic of parkinsonism. Synonym(s): masklike face; Parkinson sign
Parkinson sign - Synonym(s): Parkinson facies
Parkinson triangle
parkinsonism (1) - Synonym(s): Parkinson disease - (2) syndrome similar to Parkinson disease appearing as a side effect of certain drugs.
Medical Eponyms © Farlex 2012


Neurologic syndrome usually resulting from deficiency of neurotransmitter dopamine as consequence of degenerative, vascular, or inflammatory changes in basal ganglia; characterized by rhythmic muscular tremors, rigidity of movement, festination, droopy posture, and masklike facies.
Synonym(s): Parkinson disease.
[J. Parkinson]
Medical Dictionary for the Dental Professions © Farlex 2012

Patient discussion about Parkinson Disease

Q. What to expect from a Parkinson's patient? My 70 year old father has been diagnosed with Parkinson's. What will he be like from now on, what to expect?

A. Some of the symptoms of Parkinson's disease are:
• Trembling of hands, arms, legs, jaw and face
• Stiffness of the arms, legs and trunk
• Slowness of movement
• Poor balance and coordination
The symptoms usually get worse with time and then people with the disease may have trouble walking, talking or doing simple tasks.

Q. what is the latest on parkinson?

A. the "National Institute of Neurological Disorders and Stroke" keeps an article on "what's new in Parkinson research" and they update it every now and then. i have to say that the last one is from 2005, but it has some interesting things you might wanna know...:

and the "National Parkinson Foundation" also keeps their readers updated and have a jornal you may find useful things in:

Q. How do you tell between temporal shaky hands and parkinson disease? My dear granpa's hands are being a bit shaky lately. I was wondering if I should worry about Parkinson's disease or is it most likely to be something else? How to tell? are there other symptoms for Parkinson's?? Any help...

A. The tremor (shaking body parts) of Parkinson disease appears during rest of the limb and disappears or weakens during active movement. Additionally, Parkinson's disease cause walking problems and slow movements.

You may read more here:

More discussions about Parkinson Disease
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References in periodicals archive ?
The aim of this study is to describe the severe morbidity and mortality of Parkinson disease by age, gender, race, and parish-level in the Louisiana population.
Mortality data was collected from Louisiana death certificates for the years 1999-2012 with Parkinson Disease as primary or underlying death cause which yielded a sample size of n=5,291.
Fifty-two persons who had Parkinson disease, who were members of the Wisconsin Parkinson Association, completed a semantic differential task (Osgood, Suci, & Tannenbaum, 1957).
We decided to use this semantic differential because it included a depressed/happy scale, and since it contained so many scales, participants would be unlikely to infer the purpose of our study (i.e., to determine whether the majority of persons with Parkinson disease are depressed) from examining it.
Evidence for the Environmental Origins of Parkinson Disease
Update on Parkinson Disease. Ann Intern Med 138:651-658.
Parkinson disease is unique from AD in that it is characterized by abnormalities of motor control, as opposed to intellectual and personality changes.
Pesticides and Parkinson disease. Environ Health Perspect 112:A548.
The study, conducted at the Parkinson Institute in Milan, Italy, included 188 patients with Parkinson disease who also reported significant past exposure to hydrocarbon solvents, found in many common products such as paints, glues, and petroleum derivatives.
According to Feldman, there are insufficient data to indicate whether Parkinson disease was a direct toxic effect or an induced condition in genetically susceptible people.
An earlier NIEHS-led neurodegenerative disease program announcement issued in partnership with the National Institute of Neurological Disorders and Stroke (NINDS), the National Institute on Aging (NIA), and the National Institute of Mental Health (NIMH) titled Xenobiotics and Cell Death/Injury in Neurodegenerative Disease (PAS-99-054) continues to solicit new research projects, primarily in the area of Parkinson disease. An NIEHS-led partnership with the NINDS recently issued a targeted solicitation for research investigating the role of the environment in Parkinson disease.
In addition, the NIEHS convened national experts in population-based research on Parkinson disease to discuss ways of accelerating and advancing progress on population-based research aimed at elucidating the environmental risk factors for this disease.