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Park in Son Ism

Park in Son Ism

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Published by: Recca Guirigay on Oct 20, 2011
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04/28/2012

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PARKINSON’S DISEASE

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

a) The diagnosis of Parkinson’s disease is made on the basis of two out of the four important symptoms: resting tremor. making more available to the brain. COMT is an enzyme that eliminates dopamine from the brain. or idiopathic. and tremor. Various drugs can be used. Brain tissue transplants through the use of stem cells and genetically engineered animal cells are a promising area of research. Parkinson’s disease (IPD). Diagnosis is based on observation of clinical symptoms and consideration of patient’s age and history. Nursing assessment and physical examination . The majority of all cases of classic Parkinson’s disease are primary. scientists suspect that dopamine loss is due to a combination of genetic and environmental factors. as adjunct therapy in combination with levodopa therapy. metoclopramide. rigidity. which are thought to be overactive in dopamine deficiency.these clumps in regards to Parkinson's disease is not understood. Dopamine-depleting drugs such as reserpine. 3. 2. tetrabenazine. which may improve dopamine release in the brain. o Bromocriptine. to inhibit destruction of L-dopa in the bloodstream. a few cases suggest a hereditary pattern. phenothiazine. and postural instability. o Amantadine. or iatrogenic. o Levodopa. cogwheel rigidity (rigidity of a muscle that gives way in a series of little jerks when passive stretching occurs). In general. combined with carbidopa. Diagnostic Evaluation 1. Chronic deep brain stimulation through electrodes implanted into the thalamus or globus pallidus to decrease tremor.or chemical-related. Pharmacologic Interventions 1. o Catecholamine-O-methyltransferase (COMT) inhibitors. Secondary. o Anticholinergics to reduce activation of cholinergic pathways. Surgical Interventions 1. a dopaminergic agonist that activates dopamine receptors in the brain. confirmed by favorable response to levodopa therapy. o Monoamine oxidase inhibitors as adjunct to levodopa therapy. one of the two symptoms must be resting tremor or bradykinesia. Parkinson’s disease is drug. Medical pallidotomy to improve dyskinesia. a dopamine precursor. 2. CT scanning and MRI may be performed to rule out other disorder. often in combination to prolong effectiveness because tolerance develops. a decarboxylase inhibitor. The cause is unknown. and the butyrophenones (droperidol and haloperidol) can lead to secondary Parkinson’s disease. bradykinesia (slowing down or loss of voluntary muscle movement).

6. orthostatic hypotension). heat intolerance. Note the timing of progression of all symptoms 2. sadness. elbows. Signs of autonomic dysfunction (sleeplessness. a highpitched monotone voice.1. and decreased tearing ability. frequency. hallucinations. but 20% of patients with Parkinson’s disease develop dementia similar to that of Alzheimer’s disease. 9. and possibly affecting the head and neck. Parkinson’s disease does not usually affect intellectual ability. and difficulty in swallowing. Autologous transplantation of small portions of the adrenal . Observe the patient’s posture. noting an expressionless. gait disturbances. noting if he or she is stooped. with difficulties in walking. trunk. loss of appetite. and occupational history. Observe the patient’s face. Nursing intervention To control tremor and rigidity. Characteristic resting tremor of the extremities (may be worse on one side). Symptoms of drug toxicity are confusion. Note alterations in the respiratory status because rigidity of the intercostal muscles may decrease breath sounds or cause labored respirations. Flexion contractures develop in the neck. loss of muscle movement. and maintaining equilibrium d. and slowed movement e. and sleep disturbance. retention). initiating movements. medication. and this is characterized by withdrawal. Depression. seborrhea. note eyeballs fixed in an upward direction or eyelids completely closed. Treatment for drug tolerance and toxicity is either a change in drug dosage or a drug holiday. salivation. is a cardinal sign of Parkinson’s disease. as evidenced by expressionless face and gait changes c. dementia. which are rare complications of Parkinson’s disease. decreased movements. pharmacologic management is the treatment of choice. and excess oil production. rigidity. Mild bilateral dysfunction. Masklike faces. and hips. which requires total care. 3. Obtain a family. assessing for rigidity. 8. Invalidism. drooling. 4. knees. Muscle rigidity in performing all movements. and assess gait dysfunction. ineffective coping. Longterm levodopa therapy can result in drug tolerance or drug toxicity. 5. 7. which causes resistance to both extension and flexion. Increasing dysfunction. sweating. slowed movements. potential for injury. Observe the patient for orthostatic hypotension. so assess for decreased or Parkinson’s perspiration. Bradykinesia (slowness of movement). and decreased drug effectiveness. Autonomic disorders that are manifested in Parkinson’s disease include hypothalamic dysfunction. Patients may also demonstrate problems with social isolation. masklike appearance. Assess for defective speech. The Parkinson’s disease patient commonly develops depression later in the disease process. Poor balance. speech problems Assess the patient for signs of bradykinesia. Perform a passive range-of-motion examination. Parkinson’s disease progresses through the following stages: a. Note constipation or bladder dysfunction (urgency. and parroting the speech of others. Verbal fluency may be impaired. which manifests in fainting or dizziness. and sleep pattern disturbance. including difficulties in walking and maintaining balance and steady propulsion. repetitive muscle spasms. Rigidity of the antagonistic muscles. an inability to sit down. Note involuntary movements. Severe disability. as well as rest. Mild unilateral dysfunction b.

Offer small. and schedule outings in late morning or in the afternoon to avoid rushing the patient. periodically lie prone and avoid using a neck pillow. In addition. grasp chair arms. To prevent impaired physical mobility. Reinforce occupational andphysical therapy recommendations. and supplement interactions with a communication board. route. recommend massage and relaxation techniques. d. Teach the patient to eliminate loose carpeting. take a warm bath. perform passive and active range-of-motionexercises and muscle-stretching exercises. . 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. a thalamotomy or stereotaxic neurosurgery may be done to treat intractable tremor. g. Use of a cane or walker promotes ambulation and prevents falls. If painful muscle cramps threaten to limit the patient’s mobility. to reduce tremors. Use of chair lifts can also be beneficial. include exercises for muscles of the face and tongue to facilitate speech and swallowing. hold objects (coins. In addition. Help the patient maintain a clean. mechanical voice synthesizer. reserpine. Promote independence in the patient. install grab bars. To facilitate communication. and reinforce exercises recommended by the physical therapist. Caregivers may need a great deal of emotional support. Nursing home care guidelines Be sure the patient or caregiver understands all medications. Encourage maximum participation in self-care activities. pyridoxine. to reduce rigidity before exercise. and output. rock back and forth. Several techniques facilitate mobility and enhance safety in Parkinson’s disease patients. Use adaptive devices as needed. attractive appearance. In general. Teach deep-breathing exercises to promote chest expansion and adequate air exchange. or purse) in the hand. and h. to prevent spine flexion. Allow sufficient time to perform activities. and phenothiazine while taking levodopa. to overcome akinesia. soft foods. Position the patient in the upright position for eating to facilitate swallowing. Be alert to nonverbal clues. computer. and adverse reactions. To assist in maintaining balance. tape the “frozen” leg to initiate movement. b. consider warm baths or muscle massage. Monitor weight. e. to initiate movement. frequent meals. concentrate on taking larger steps with feet apart. c. Explore strategies for long-term care with the patient and significant others. if medications are ineffective. and thick. keeping back straight and swinging the arms. encourage the Parkinson’s disease patient to speak slowly and to pause for a breath at appropriate intervals in each sentence. cold fluids. to obtain partial control of tremors when seated. action. intake. Help the patient maintain a positive self-image by emphasizing her or his abilities and by reinforcing success. or electric typewriter. Avoid the use of alcohol. Supplemental puddings or nutritional shakes may be given throughout the day to maintain weight. keys. Encourage the patient to verbalize feelings and to write in a journal. and elevate the toilet seat.gland into the brain’s caudate nucleus of Parkinson’s disease patients is offered on an experimental basis in some medical centers as a palliative treatment. Instruct the patient to try the following strategies: a. monitor the patient’s ability to chew and swallow. To maintain nutritional status. including the dosage. f.

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