PARKINSONS DISEASE

Parkinson's disease is the second most common neurodegenerative disorder and the most common movement disorder. It is characterized by progressive loss of muscle control, which leads to trembling of the limbs and head while at rest, stiffness, slowness, and impaired balance. As symptoms worsen, it may become difficult to walk, talk, and complete simple tasks. The progression of Parkinson's disease and the degree of impairment vary from individual to individual. Many people with Parkinson's disease live long productive lives, whereas others become disabled much more quickly. Premature death is usually due to complications such as falling-related injuries or pneumonia. In the United States, about 1 million people are affected by Parkinson's disease and worldwide about 5 million. Most individuals who develop Parkinson's disease are 60 years of age or older. Parkinson's disease occurs in approximately 1% of individuals aged 60 years and in about 4% of those aged 80 years. Since overall life expectancy is rising, the number of individuals with Parkinson's disease will increase in the future. Adult-onset Parkinson's disease is most common, but early-onset Parkinson's disease (onset between 21-40 years), and juvenile-onset Parkinson's disease (onset before age 21) also exist. Descriptions of Parkinson's disease date back as far as 5000 BC. Around that time, an ancient Indian civilization called the disorder Kampavata and treated it with the seeds of a plant containing therapeutic levels of what is today known as levodopa. Parkinson's disease was named after the British doctor James Parkinson, who in 1817 first described the disorder in great detail as "shaking palsy." The three cardinal signs of Parkinsons disease are involuntary tremors, akinesia, and progressive muscle rigidity. The first symptom of Parkinsons disease 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. Pathophysiology A substance called dopamine acts as a messenger between two brain areas - the substantia nigra and the corpus striatum - to produce smooth, controlled movements. Most of the movementrelated symptoms of Parkinson's disease are caused by a lack of dopamine due to the loss of dopamineproducing cells in the substantia nigra. When the amount of dopamine is too low, communication between the substantia nigra and corpus striatum becomes ineffective, and movement becomes impaired; the greater the loss of dopamine, the worse the movement-related symptoms. Other cells in the brain also degenerate to some degree and may contribute to non-movement related symptoms of Parkinson's disease. Although it is well known that lack of dopamine causes the motor symptoms of Parkinson's disease, it is not clear why the dopamine-producing brain cells deteriorate. Genetic and pathological studies have revealed that various dysfunctional cellular processes, inflammation, and stress can all contribute to cell damage. In addition, abnormal clumps called Lewy bodies, which contain the protein alpha-synuclein, are found in many brain cells of individuals with Parkinson's disease. The function of

these clumps in regards to Parkinson's disease is not understood. In general, scientists suspect that dopamine loss is due to a combination of genetic and environmental factors. The majority of all cases of classic Parkinsons disease are primary, or idiopathic, Parkinsons disease (IPD). The cause is unknown; a few cases suggest a hereditary pattern. Secondary, or iatrogenic, Parkinsons disease is drug- or chemical-related. Dopamine-depleting drugs such as reserpine, phenothiazine, metoclopramide, tetrabenazine, and the butyrophenones (droperidol and haloperidol) can lead to secondary Parkinsons disease.

Diagnostic Evaluation 1. Diagnosis is based on observation of clinical symptoms and consideration of patients age and history, confirmed by favorable response to levodopa therapy. a) The diagnosis of Parkinsons disease 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. 2. CT scanning and MRI may be performed to rule out other disorder. Pharmacologic Interventions 1. Various drugs can be used, often in combination to prolong effectiveness because tolerance develops. o Anticholinergics to reduce activation of cholinergic pathways, which are thought to be overactive in dopamine deficiency. o Amantadine, which may improve dopamine release in the brain. o Levodopa, a dopamine precursor, combined with carbidopa, a decarboxylase inhibitor, to inhibit destruction of L-dopa in the bloodstream, making more available to the brain. o Bromocriptine, a dopaminergic agonist that activates dopamine receptors in the brain. o Monoamine oxidase inhibitors as adjunct to levodopa therapy. o Catecholamine-O-methyltransferase (COMT) inhibitors, as adjunct therapy in combination with levodopa therapy; COMT is an enzyme that eliminates dopamine from the brain. Surgical Interventions 1. Medical pallidotomy to improve dyskinesia, rigidity, and tremor. 2. Chronic deep brain stimulation through electrodes implanted into the thalamus or globus pallidus to decrease tremor. 3. Brain tissue transplants through the use of stem cells and genetically engineered animal cells are a promising area of research.

Nursing assessment and physical examination

1. Obtain a family, medication, and occupational history. Parkinsons disease progresses through the following stages: a. Mild unilateral dysfunction b. Mild bilateral dysfunction, as evidenced by expressionless face and gait changes c. Increasing dysfunction, with difficulties in walking, initiating movements, and maintaining equilibrium d. Severe disability, including difficulties in walking and maintaining balance and steady propulsion, rigidity, and slowed movement e. Invalidism, which requires total care. Note the timing of progression of all symptoms 2. Characteristic resting tremor of the extremities (may be worse on one side), and possibly affecting the head and neck. 3. Bradykinesia (slowness of movement). 4. Muscle rigidity in performing all movements, as well as rest. 5. Verbal fluency may be impaired. 6. Signs of autonomic dysfunction (sleeplessness, salivation, sweating, orthostatic hypotension). 7. Depression, dementia. 8. Masklike faces. 9. Poor balance, gait disturbances, speech problems

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 Parkinsons disease. 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 patients 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 patients 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 Parkinsons disease. Assess for defective speech, a highpitched monotone voice, and parroting the speech of others. Autonomic disorders that are manifested in Parkinsons disease include hypothalamic dysfunction, so assess for decreased or Parkinsons 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). Parkinsons disease does not usually affect intellectual ability, but 20% of patients with Parkinsons disease develop dementia similar to that of Alzheimers disease. The Parkinsons disease 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. Nursing intervention To control tremor and rigidity, pharmacologic management is the treatment of choice. Longterm 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 brains caudate nucleus of Parkinsons disease 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-motionexercises 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. 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 andphysical therapy recommendations. Use adaptive devices as needed. If painful muscle cramps threaten to limit the patients mobility, consider warm baths or muscle massage. To facilitate communication, encourage the Parkinsons disease 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 patients 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. Nursing home care 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 Parkinsons disease patients. Instruct the patient to try the following strategies: a. To assist in maintaining balance, concentrate on taking larger steps with feet apart, keeping back straight and swinging the arms; b. to overcome akinesia, tape the frozen leg to initiate movement; c. to reduce tremors, hold objects (coins, keys, or purse) in the hand; d. to obtain partial control of tremors when seated, grasp chair arms; e. to reduce rigidity before exercise, take a warm bath; f. to initiate movement, rock back and forth; g. to prevent spine flexion, periodically lie prone and avoid using a neck pillow; and h. Teach the patient to eliminate loose carpeting, install grab bars, and elevate the toilet seat. Use of chair lifts can also be beneficial.