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Causes and symptoms
- 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.
- 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)
Exercise, nutrition, and physical therapy
Synonym(s): Parkinson disease.
|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.
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.
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.
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).
|Test||Normal Result||Abnormality With Condition||Explanation|
|Positron emission tomography and single photon emission computed tomography||Normal dopamine uptake in basal ganglia||Decreased dopamine uptake in the basal ganglia||Degeneration 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
DiagnosisSelf-care deficit related to rigidity and tremors
OutcomesSelf-care: Activities of daily living—Bathing, Hygiene, Dressing, Grooming, Eating; Anxiety control; Endurance; Comfort level; Mood equilibrium; Energy conservation; Muscle function; Mobility level
InterventionsExercise 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.
|Medication or Drug Class||Dosage||Description||Rationale|
|Antiparkinson||Varies with drug||Levodopa (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 PO||Antiviral||Controls tremor and rigidity by increasing the release of dopamine to the basal ganglia|
|Synthetic anticholinergics||Varies with drug||Trihexyphenidyl (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.
- 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 http://www.apdaparkinson.org 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.
Parkinson,James, English physician, 1755-1824.
Synonym(s): Parkinson disease.
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?
• 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?
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...
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