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Pathophysiology and management of idiopathic Parkinson's disease.

Introduction

Parkinson's disease is a progressive degenerative disease of the nervous system which eventually leads to disability. Idiopathic parkinsonism refers to the presence of a characteristic constellation of symptoms, tremor, rigidity, bradykinesia and impairment of righting reflexes,[6] and pathologic changes, including the loss of pigmented neurons and the presence of Lewy bodies in the substantia nigra[9] with no identifiable cause. The same features may be referred to as secondary parkinsonism when there is a known cause of injury to the basal ganglia by cerebrovascular disease, drugs, infections, trauma or toxins. Parkinsonian syndromes include neurodegenerative disorders such as Huntington's disease, and other acquired degenerative diseases such as progressive supranuclear palsy.[9] This article explores the various treatment options for idiopathic parkinsonism (IP), after a brief review of the epidemiology, manifestations, pathophysiology and theories of causation of the disease.

Epidemiology

IP makes up the largest subgroup of parkinsonian syndromes, accounting for 78% of affected patients,[43] or about 1% of the US population over 60 years of age. Males and females are equally affected.[45] IP is more prevalent in North America and Europe than in Asia or Africa.[46]

Manifestations

Although initial presentation is variable, a slow, unilateral, resting tremor is present in 70% of patients at initial diagnosis.[38] Muscular rigidity is manifested as stiffness throughout the range of passive movement of a limb segment. Involvement of the facial muscles leads to the characteristic masked facies. Bradykinesia, or slowness of movement, is one aspect of "akinetic phenomena" which occur in IP;[10] other aspects include difficulty reaching a target with a single continuous movement, rapid fatigue with repetitive movement and difficulty with sequential and simultaneous actions because of motor planning deficits. "Freezing," a state of complete immobility, is most evident at the onset of movement, and is generally thought to be an extreme form of bradykinesia. These cardinal features all contribute to disability through slowness, decreased range of motion and difficulty initiating and stopping purposeful movement; they are all exacerbated by emotional stress, which itself may be worsened by the visibility of the symptoms.[10]

Postural instability refers to the loss of balance or lack of recovery of balance in response to perturbation, and is probably related to bradykinesia secondary to dopamine deficiency.[9] Gait disturbances may include retropulsion, leading to backward falls, or a rapid, festinating gait, leading to forward falls.

Tremor, rigidity, bradykinesia and postural instability, the direct effects of IP, may lead to indirect musculoskeletal effects, including stooped posture, kyphosis, head flexion, shoulder protraction and knee or elbow contractures which further impair physical performance in tasks such as getting in and out of bed, dressing, bathing and walking.[40] It is generally agreed that dementia is more common in older IP patients than in non-IP patients; prevalence is approximately 25%.[49] The pattern of impairment is similar to that observed in equally demented patients with probable Alzheimer's disease. Some suggest that similar pathological processes may result in IP, Alzheimer's disease and amyotrophic lateral sclerosis because of epidemiological, clinical, chemical and histological similarities among the three conditions.[49] Patients with IP who are not demented may have impairment of visuospatial function, executive function and memory, language disorders and bradyphrenia (slowing of thought processes).[30]

A variety of other symptoms illustrate further involvement of motor and nonmotor systems. Swallowing and speech deficits, seborrhea, pedal edema, fatigability and weight loss are typical.[19] Autonomic involvement is manifested by orthostatic hypotension, paroxysmal flushing, diaphoresis, thermal dysregulation, constipation and bladder, sphincter and sexual disturbances.[19]

Pathophysiology

Pathologic findings in IP include the loss of neurons in the substantia nigra compacta and other pigmented nuclei, gliosis in these same regions and greater than normal numbers of Lewy bodies in the degenerating neurons.[49] The Lewy body is an eosinophilic inclusion body with a characteristic halo.[3] Loss of cells from the substantia nigra results in profound dopamine depletion in the striatum, which regulates control of motor function from the cerebral cortex.[47] Other neurotransmitters such as serotonin and norepinephrine are affected in IP;[10] however, loss of dopamine input is thought to be primarily responsible for the motor disorders associated with IP, through its opposite effects on two striatal efferent pathways.[44,51] Briefly, the direct pathway for facilitating or sustaining movement becomes underactive because of loss of excitatory dopaminergic input, resulting in bradykinesia. The indirect pathway for suppressing movement becomes overactive because of loss of inhibitory dopaminergic input, resulting in excessive suppression of unwanted movements, and difficulty generating new movements. This mechanism may be responsible for akinesia and rigidity. Two sources provide more detailed discussion of the mechanisms of the direct and indirect path

Theories of Causation

The pathogenesis of IP is thought to be multifactorial, resulting from some combination of environmental factors and genetic predisposition. There is conflicting evidence for the role of inheritance in IP. A positive family history is reported in about 15% of index cases;[15] however, a higher prevalence of familial parkinsonism is found whenever an informative history is available. The prevalence of essential tremor in relatives of IP patients has been estimated to be 20%[26] and clear transmission of the disease is clinically evident in some families.[27] On the other hand, although the same prevalence rates have been reported for US whites and blacks,[49] US blacks have nearly five times the prevalence of IP as Nigerian blacks,[41] suggesting the effect of an environmental factor. There is agreement that twin surveys lack the power to confirm or dismiss a genetic etiology for IP.[20]

The role of normal aging has also been debated. Several areas of the brain lose neurons with aging, including the nigrostriatal pathway.[49] There is progressive (normal) loss of over 60% of dopaminergic neurons in the substantia nigra beginning at approximately 30 years of age. With aging, there is also a decline in the concentration of striatal dopamine, increased striatal dopamine turnover, and a loss of striatal D2 receptors. Compensatory mechanisms (an increased rate of dopamine synthesis and increased postsynaptic receptor sensitivity) are thought to be responsible for the absence of parkinsonism prior to an 80% decrease in striatal dopamine.[7] It is suggested that some initial insult causes additional loss of cells eventually resulting in IP.[49]

There are several theories on the role of environmental factors in the development of IP, including the suggestion of increased vulnerability of "old" neurons to environmental toxins.[47] One-methyl-4-phenyl-1,2,3,6-tetrahydrophridine (MPTP), a contaminant of illegally synthesized heroin, acts to induce a Parkinsonian syndrome in humans. Since MPTP does not occur naturally in the environment it is unlikely to be the cause of IP;[49] however this model suggests a role for an environmental insult. Several other environmental factors have been considered. In North America and Europe, rural living has been found to be more common in patients with early onset IP;[24] however, specific causes within the rural environment have not been identified. In China, the disease is concentrated in urban regions.[3] Infection has been considered because of transient parkinsonian states following several viral encephalitic infections. However, there is no evidence of a higher incidence of obvious viral exposure in IP to support this theory.[49] Various metals including manganese, iron, and aluminum have also been suspected as causing cell damage in IP through oxidative stress.[32]

The free radical-oxidative stress hypothesis has been a focus of attention in the etiology of several degenerative diseases including IP. Free radicals such as the hydroxyl and superoxide radicals are produced in the normal oxidative degradation of dopamine. This process is referred to as oxidative stress because the free radicals formed in the oxidation process are potentially cytotoxic.[49] One report indicates that there is evidence of increased oxidative stress in IP which includes increased iron levels, decreased glutathione, decreased superoxide dismutase activity and increased lipid peroxidation in the substantia nigra.[4] Others believe that this hypothesis is not yet adequate to explain the pathogenesis of IP.[49] Excitatory neurotoxicity may also be involved in the pathogenesis of IP.[49] Glutamate and aspartate are cytotoxic in excess amounts. Various processes may contribute to elevated levels of these substances; they may also be ingested in food additives. This theory also requires more investigation.

Several studies have revealed a reduced incidence of IP in cigarette smokers. Some consider this "protective effect" of cigarette smoking an important etiologic clue which merits further investigation.[31]

Pharmacological Treatment

The treatment for IP has traditionally been primarily pharmacological. Physical, occupational and speech therapies are important adjuncts to pharmacological treatment, but will not be addressed in this paper. Various medical comorbidities which may complicate the treatment of IP must be considered. One example is diabetes mellitus. All Parkinsonian patients should be routinely screened and treated for glucose intolerance. Hyperglycemia may exacerbate symptoms as well as diminishing the effects of dopamine agonists; it may also be a risk factor for levodopa-induced dyskinesias.[39]

A brief explanation of the mechanisms of action and adverse reactions for the various drugs will be followed by discussion of overall treatment approaches.

The goals of treatment of IP are to relieve symptoms and restore striatal dopaminergic activity as much as possible. The various drugs and even the nondrug treatments act to restore the balance between dopaminergic and cholinergic activities, by increasing the availability of dopamine or reducing the activity of acetylcholine.

The anticholinergic drugs are the oldest (and, at one time, the only) treatment for IP, and are most effective for reduction of tremor.[37] Benztropine (Cogentin) and trihexyphenidyl (Artane) are most often used in the United States (US).[2] The adverse effects of anticholinergics can be significant, and are poorly tolerated, especially by the elderly.[2] They include memory impairment, tachycardia, urinary retention, dry mouth and blurred vision. Amantadine (Symmetrel) blocks the reuptake of dopamine into presynaptic neurons and causes direct stimulation of postsynaptic receptors.[2] It is somewhat effective for tremor, rigidity and bradykinesia,[5] but most patients develop tolerance within a few months. Adverse effects occur in fewer than 10% of patients;[2] they include some anticholinergic effects, ankle edema and livedo reticularis (purplish mottling of the skin, which resolves on discontinuation of the drug). Dose adjustment is necessary in patients with renal dysfunction because of renal excretion.

Dopamine agonists stimulate dopamine receptors in the substantia nigra. Bromocriptine (Parlodel) and pergolide (Permax) are available in the US. They are most effective on rigidity and bradykinesia.[9] When these drugs are used as monotherapy, symptoms improve but recur after one or two years; adverse effects of gastrointestinal intolerance, central nervous system (CNS) effects (especially in the elderly) and orthostatic hypotension are significant.

Selegiline (Deprenyl) is a selective inhibitor of monoamine oxidase type B (MAO-B), which inactivates dopamine in the brain.[9] Some believe that selegiline has a neuroprotective effect because it was found to prevent development of parkinsonian symptoms induced by MPTP.[9] It is theorized that selegiline may prevent the death of nigral cells which results from the generation of free radicals via MAO-B. Metabolic byproducts include me/amphetamine which can aggravate peptic ulcer disease and cause insomnia. Other side effects (confusion, hallucinations and orthostatic hypotension) occur in fewer than 10% of patients.[2]

Levodopa (L-dopa), the precursor of dopamine, is the mainstay of treatment, because of its high level of efficacy.[3] Although, unlike dopamine, levodopa does cross the blood brain barrier, most of the ingested levodopa is metabolized peripherally to dopamine, by dope decarboxylase with a cofactor of vitamin B6. The large doses of levodopa required for effective CNS dosing can cause nausea and vomiting and orthostasis,[9] and preclude ingestion of vitamin B6. Thus, levodopa is usually given in combination with a peripheral decarboxylase inhibitor (Carbidopa) to prevent peripheral conversion to dopamine. Sinemet is composed of carbidopa and levodopa in a 1:10 or 1:4 ratio.

Levodopa is particularly efficacious in reducing bradykinesia and rigidity.[3] Initial adverse effects include nausea or vomiting, to which patients may accommodate, and orthostasis. The most troublesome adverse effects are dyskinesias and clinical fluctuations, one or both of which 50% of patients will develop within the first five years of levodopa therapy.[36] Psychiatric disturbances may also occur.

Clinical fluctuations include the "wearing off" or deterioration that occurs as the effective period of levodopa grows shorter over time, and the "on-off" syndrome, or oscillations in response to drug therapy. Abrupt loss of drug effectiveness resulting in akinesia ("off") may be followed by sudden return of effectiveness which can include dyskinesias ("on"). "Off" periods are associated with paresthesias, pain, autonomic symptoms such as tachycardia, sweating and constipation and psychological alterations including panic, depression, paranoia and hallucinations.[35] Although the pathophysiology underlying these fluctuations is not well understood, it appears to involve both central mechanisms, eg pharmacodynamic receptor changes, and peripheral mechanisms such as levodopa pharmacokinetics, gastric emptying and intestinal transport.[35] Because administration with protein decreases levodopa absorption, low protein diets have been suggested for patients with "on-off" fluctuations. New evidence indicates that continuous delivery (via enteral infusion) of levodopa may be most efficacious for this phenomenon.[35]

Dyskinesias (abnormal involuntary movements) may be caused by a differential response of the dopamine D1 and D2 receptors; another theory involves hyperactivity of a GABA pathway.[35] Dyskinesias may occur in differing patterns. Treatment, which has not been satisfactory, involves adjustment of drug combinations and timing.

Drug-related psychiatric disturbances in IP include visual hallucinations occurring on a background of a clear sensorium (occurring in 30% of treated patients), and less commonly, hallucinations or paranoid delusions accompanied by confusion or frank delirium.[14] Abnormal dreams and sleep disruption may also occur. Causative mechanisms have been thought to include dopamine receptor hypersensitivity, accumulation of toxic metabolites of dopamine and dysfunction of central serotonergic pathways.[14] Hallucinations occurring with a clear sensorium may not require treatment if they are nonthreatening and the patient has preserved insight; careful monitoring is needed because escalation of these symptoms can occur without provocation.[14] Psychotic symptoms which have a sudden onset may be triggered by a metabolic, infectious or vascular event; investigation and treatment is indicated.

Drug-related psychoses are managed initially by dosage reduction. When drug therapy for the psychosis is needed, standard neuroleptics are avoided because of their exacerbation of other symptoms (caused by their high affinity for D2 receptors and potential for causing tardive dyskinesia, especially in the elderly).[13] Clozapine, an atypical neuroleptic, has received much attention in treating psychosis in IP because it does not induce the D2 receptor hypersensitivity that is associated with increased involuntary movements.[34] Clozapine has been found to be efficacious and safe for long term management of psychosis in Parkinson's patients.[13] Adverse effects, which include sialorrhea, sedation, confusion and agranulcytosis, are mild with low dosages, but mandate very close monitoring. Depression occurs in nearly half of IP patients,[30] but is considered a symptom of the disease, rather than a drug effect.[14]

The question of when to start therapy requires consideration of individual factors, eg is employment threatened because of mild but noticeable motor symptoms? There is controversy over how soon levodopa should be started because of the previously described problems which are known to occur with long-term therapy, and the idea (not scientifically supported) that it could actually accelerate the disease process. Several approaches are used to delay starting levodopa.

Selegiline was initially thought to have a neuroprotective effect because it prevents MPTP induced parkinsonism in animals.[48] Although this effect has not been proven, one large trial[33] showed that selegiline does delay the need for levodopa therapy for about nine months. It is not clear whether its effect is neuroprotective or partially or wholly symptomatic. One author does recommend starting therapy particularly in young patients (less than 50 years) with selegiline to delay the need for levodopa, because they develop fluctuations and dyskinesias sooner and more severely than older patients, they will require drug therapy for decades, they can better tolerate multiple drugs and dementia is uncommon.[37] Selegiline is also used to enhance the effect of levodopa in patients who have developed tolerance to it.[2]

Symptomatic therapy is often begun with anticholinergics, particularly in patients whose only problem is tremor.[3,37] Amantadine is another option for initial treatment. A dopamine agonist is often the next choice and may be used as monotherapy, or it may be added to levodopa when response to levodopa is insufficient.[2] Dopamine agonists can be very effective in treatment of motor fluctuations caused by levodopa.[28] However, a different approach is recommended in elderly (greater than 70 years) patients, who comprise over 50% of all persons diagnosed with IP.[45] They develop motor complications to a milder degree and later after levodopa, they may die of other diseases before developing them, they are less tolerant of multiple drugs and they may be more likely to develop cognitive impairment especially with anticholinergic drugs.[37] Therefore, it is suggested that levodopa be started as soon as treatment of symptoms is needed, anticholinergics be avoided, and amantadine and dopamine agonists be used with caution. The age group 50-70 years can be the most challenging since they may overlap the criteria for the other age groups; flexibility is encouraged in treating this group.[37]

Levodopa dosage and timing is individualized based on the patient's symptoms and schedule. It is rapidly absorbed and peaks at 1-3 hours when taken on an empty stomach[2] thus several daily doses are needed. Immediate release levodopa produces abrupt changes in plasma concentration within a two-three hour period. Sustained release (SR) carbidopa/levodopa (Sinemet) is used to reduce the number of daily doses and to treat the "wearing off" and "on-off" phenomena. The SR formula is delayed in reaching its peak so it is sometimes combined with immediate release levodopa.[37] Patients with advanced IP become increasingly sensitive to small changes in plasma levodopa concentrations. Gastro-intestinal absorption becomes a critical factor in maintaining the optimal clinical effect.[28] Even with the SR preparation, inconsistent gastric emptying interferes with the drug reaching sites of absorption in the small intestine. A new method to improve absorption of levodopa is enteral infusion. One author describes gastric jejunal infusion, in which a small bore feeding tube, inserted endoscopically, is used for delivery of levodopa directly to its primary absorption sites in the duodenum and jejunum, by means of a pump system.[28] A titration process can be used to achieve the optimal effect; rapid drug absorption is illustrated by the clinical effect of a change in infusion rate being experienced by the patient within five minutes. "Wearing off" is eliminated; there is improved control of dyskinesia. The tube can also be used for administration of food/fluids when necessitated by dysphagia.

Several nontraditional drug therapies have been reported. Alpha-tocopherol has been investigated as a treatment for IP because of its antioxidant effects. However, in the DATATOP study, it did not affect the probability that the patient would need levodopa.[28] Apomorphine, an injectable dopamine agonist, is under investigation as a treatment for late levodopa failure. Subcutaneous injection provides prompt reversal of "off" periods. Rectal suppository and enema' sublingual and intranasal formulations have potential for extended action and prevention of "off" periods.[8] Domperidone, a peripheral D2 dopaminergic receptor antagonist, is administered prior to apomorphine for prevention of nausea, vomiting, drowsiness and orthostasis.

Catechol-O-methyl-transferase (COMT) inhibitors are under investigation because they reduce the degradation of levodopa in the GI tract, kidney and liver.[2,28] COMT inhibitors may be helpful in addressing the wearing off phenomenon.

Glutamate antagonists are being seriously considered as adjuvants to levodopa. Glutamate is active at N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors, among others.[44] It is hypothesized that dopamine loss in IP leads to hyperactivity of various excitatory glutamatergic pathways of the basal ganglia, thus contributing to the evolution of parkinsonian symptoms. Another hypothesis is that the neurotoxic action of L-glutamate contributes to the selective degeneration of the substantia nigra.[23] The NMDA antagonist memantadine (licensed in Germany) has been shown to significantly reduce the frequency of "off" periods. Some believe that although the antiparkinsonian potential of glutamate antagonists in animal models has been overstated, there is hope for the development of new NMDA and non-NMDA antagonists.[44] Neurotrophic factors (brain-derived, BDNF, and glial cell line derived, GDNF, among others) show promise in the treatment of IP because of their ability to promote survival and differentiation of neurons. Their ability to act in vivo has yet to be demonstrated, and because they must be administered locally, they are considered unsuitable in this form for therapeutic use in humans.[23]

Surgical Treatment

Surgical attempts to control IP have received considerable attention for over forty years. Between 1950 and 1968, stereotactic ablative surgery played a major role in the treatment of IP. Posteroventral pallidotomy (PVP), was effective in decreasing the cardinal symptoms of IP,[25] although both efficacy and adverse effects varied due to problems with stereotactic localization. PVP was later abandoned in favor of surgical lesions of the ventrolateral thalamus which had a dramatic effect on tremor. With the introduction of levodopa in 1968, surgical treatment declined substantially.[16] However, the limitations of levodopa therapy and improvements in stereotactic surgery have stimulated renewed interest in surgical treatment.

Direct lesioning of the subthalamic nucleus (STN) is based on the hypothesis that excessive subthalamopallidal drive is the major factor producing parkinsonian signs. The cardinal signs are abolished by such lesions but there is a significant risk of inducing severe and persistent dyskinesias.[42] The literature reveals considerable attention to stereotactic ventral[11] or posteroventral[25] pallidotomy (VP), using computed tomography (CT) or magnetic resonance imaging (MRI) to define the target. In most cases, there is bilateral improvement following a unilateral lesion, although contralateral improvement is greater.[25,11,18] Homonymous hemianopsia is the most emphasized complication,[25] because of the close proximity of the pallidal lesions to the optic tract, but its incidence has been reduced by improved stereotactic techniques.[18] Optimum candidates for VP are those with akinesia partially responsive to medication, bradykinesia with freezing during repetition, asymmetrical severe rigidity, or frequent disabling dyskinesia.[11,18]

Cerebral transplantation continues to be studied as another means of replacing dopaminergic nigrostriatal neurons. The transplantation of autologous adrenal medullary tissue as a source of dopamine initially held great promise because it eliminated the need for immunosuppressive therapy and dramatic response was reported.[12] However, the degree of success of these results was never replicated, and even lesser improvements were short-lived.[1] Subsequent autopsy studies revealed absent or minimal surviving adrenal medullary tissue at the graft site. Fetal mesencephalon transplantation has shown varied results in overall degree of improvement and in the specific symptoms affected. Technical factors, including immunosuppression, postabortion delay, volume of fetal tissue and graft placement vary considerably in the various studies. It has been suggested that neurotrophic factors may be the key to reversing IP by means of grafting and would allow a wider array of tissue to be used for grafting.[1] Transplantation of genetically-engineered cell lines could be a source of neurotrophic factors, and would not be limited by the unpredictable availability of abortion materials. Finally, electroconvulsive therapy (ECT) is reported to have a significant antiparkinsonian effect, which is not simply a result of treatment of depression.[21] Various theories regarding the mechanism of action of ECT in IP include increased D1 receptor binding in the substantia nigra, interactions between dopamine and gamma aminobutyric acid (GABA) and greater brain concentrations of circulating levodopa as a result of temporary changes in the permeability of the blood brain barrier.

Nursing Issues

A comprehensive discussion of nursing care of the IP patient is beyond the scope of this paper. Relevant nursing diagnoses describing likely patient responses to the disease and its therapy are listed in Table 1.[22] Several important aspects of the nursing role can be identified. Assessment of the IP patient includes the use of specific tools, eg the Unified Rating Scale for Parkinsonism to monitor the existence and severity of symptoms and their effect on overall function.[29] Nursing involvement in administering these tools is appropriate since the management of symptoms and functional deficits is often a nursing role. Patient and family education are most important in optimal management of IP, and should be included in the plan for any of the problems described in the nursing diagnosis list. With regard to pharmacotherapy, the patient and/or caregiver should be knowledgeable on the following topics:[17]

* disease process and mechanism of action of drugs

* timing of drugs with regard to symptoms and meals

* the potential for interaction of Parkinson's drugs with other medical conditions or drugs to treat them

* adverse effects which should be reported

* monitoring drug effectiveness in symptom control
Table 1. Nursing Diagnoses in
Idiopathic Parkinsonism[22]

 * Activity intolerance related to (R/T) bradykinesia perceived as
weakness
 * Ineffective breathing patter to R/T bradykinesia and rigidity,
and/or levodopa induced dyskinesia of throat and thorax muscles
and diaphragm
 * Body image disturbance R/T bradykinesia, tremor, masked facies,
blepharospasm, sialorrhea and stooped posture
 * Caregiver role strain R/T patient's increasing dependence,
altered communication patterns and loss of facial animation
 * Impaired verbal communication R/T weak voice (hypophonia),
absence of normal pitch and rhythm of speech (aprosody) and
difficult articulation (dysarthria).
 * Constipation R/T slowed intestinal peristalsis and/or
(cholinergic) drug effect
 * Fatigue R/T increased energy expenditure caused by rigidity and
bradykinesia, and sleep disturbances
 * High risk for ineffective individual and/or family coping R/T
disease process causing role changes
 * High risk for disuse syndrome R/T muscle rigidity and weakness,
and self imposed mobility restriction (eg fear of falling)
 * Altered health maintenance R/T alteration in written and verbal
communication skills and gross and/or fine motor skills
 * Functional incontinence R/T mobility deficits
 * High risk for injury R/T muscle rigidity/weakness, postural
instability and gait disturbance
 * Knowledge deficit regarding disease process and management
 * Impaired memory R/T effects of disease process
 * Impaired physical mobility R/T bradykinesia, rigidity, akinesia
 * Nutrition, altered: less than body requirements R/T dysphagia,
drug related nausea, and increased energy expenditure associated
with tremors and dyskinesia
 * Pain R/T dyskinesias
 * Powerlessness R/T progressive physical deterioration and lack of
control of body movement
 * Self-care deficit R/T bradykinesia, akinesia, tremor and fatigue
 * Sexual dysfunction R/T impotence caused by disease process,
fatigue and depression
 * Sleep pattern disturbance R/T dyskinesias, rigidity, medication
effect and/or depression
 * Impaired social interaction R/T voice and speech changes and
impaired mobility
 * Altered thought processes R/T disease process and/or drug
effects (hallucination)
 * Altered urinary elimination R/T impaired mobility, rigidity and
bradykinesia of bladder and/or anticholinergic drug effects

R/T=related to




The nursing role may also include initiating and coordinating therapies by other disciplines such as physical, occupational and speech therapies, to maintain function or adapt to functional decline. Emotional support of the patient and caregiver will also be an area for nursing intervention. Although results were not statistically significant, one author reported that contact with a nurse practitioner (NP) was rated as very useful by her sample of forty Parkinson's patients.[50] In this group, 92% indicated that the opportunity to talk to someone about the illness and associated problems was the most important aspect of their contact with the NP. Finally, referral to the national Parkinson's groups is important for the further provision of information and emotional support for patients and caregivers.

Summary

There is much more to be learned about IP. Clarification of genetic and environmental factors may eventually contribute to understanding of disease prevention and more effective treatment. Refinement of surgical techniques and the use of neurotrophic factors offer hope.

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Questions or comments about this article may be directed to: Stephanie A. Lusis, RN, MSN, CS, William Beaumont Hospital, Medical Nursing Division, 3601 West Thirteen Mile Road, Royal Oak, Michigan 48073. She is a gerontology clinical nurse specialist.
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Author:Lusis, Stephanie A.
Publication:Journal of Neuroscience Nursing
Date:Feb 1, 1997
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