-------------------------------------------------------------- Parkinson's Disease Quality of Life Issues Barbara Fitzsimmons, RN, MS Lisette K. Bunting, RN, MScN -------------------------------------------------------------- Individuals who develop Parkinson's disease (PD) are confronted not only with the physical manifestations of the disorder but with the psychosocial issues that impact on quality of life. Psychosocial aspects of PD may present as subtle changes with progression of the disease. Many patients with PD are reluctant to discuss these concerns with health care providers, however. Unfortunately, these unvoiced concerns have a negative effect on acceptance of the disease state, corn- phance with treatment, and response to therapy, and they can significantly affect quality of life. Current nursing literature has focused on management of mobility in PD, and little attention has been devoted to psychosocial issues. This paucity of literature is attributed to the belief that if motor symptoms are treated, psychosocial aspects of the disease will spontaneously improve. Quality of life has been reported to be the primary concern of patients with PD and their famidy members.(12) Medicine is learning to recognize and accept quality of life as a major criterion in evaluation of health interventions. "The concept of quality of life then goes beyond the dimen- sions of health functioning to performance of social roles, mental acuity, emotional states, subjective well-being, and interrelationships."(5) Life satisfaction, self-esteem, and physical health have also been identified as key elements of quality of fife. This article briefly reviews salient points regarding PD as a degenerative neurologic process and focuses primarily on the motor and nonmotor features that impact on quality of life. In addition, nursing care is presented and reviewed to assist the reader in facilitating the development of goals with the patient and family that are congruent with achieving maximum quality of life (Table 1). HISTORY OF PARKINSON'S DISEASE James Parkinson, a London general practitioner, first described Parkinson's disease in a monograph entitled "An Essay on the Shaking Palsy" in 1817. It was -------------------------------------------------------------------------------------- Table 1. NURSING PLAN OF CARE ----------------------------------------------------------------------------------------------------------- Nursing Diagnosis Expected Outcomes Nursing Interventions Impaired physical mobility Patient will demonstrate Consult with physical related to rigidity, maximal independence therapy for exercises and bradykinesia, and/or with performing activities assistive devices to postural instability of daily living. maximize independence with self-care activities. Plan for patient to participate in care when medications are at peak level. Provide for safety in environment. Impaired verbal Patient will communicate Facilitate consultation with communication related to effectively with others. speech therapy. softening of voice Provide opportunities for patient to practice speech exercises. Encourage patient not to hurry to complete speech. Refrain from completing sentences for patient. Altered self-esteem related Patient will actively Incorporate patient into to dependency on participate in decisions decision-making process spouse/significant other related to care prior to about taking medication, discharge, participating in diversional activities, and so on. Offer suggestions for patient to have opportunities to socialize in the community. Altered thought processes Patient will state that Provide reality orientation to related to hallucinations hallucinations are not real patient as needed. and confusion prior to discharge. Be calm and offer reassurance if patient becomes fearful. Umit environmental stimuli. Promote restful sleep-wake cycle. ----------------------------------------------------------------------------------------------------------- here that Dr. Parkinson described the classic parkinsonian symptoms of resting tremor, propulsion, and stooped posture. Parkinson wrote that he found that 11 senses and intellect" were "uninjured;" however, he went on to describe patients as "unhappy," "dejected," and "melancholic."(2) PD is a chronic, progressive disease of the central nervous system. The classi(- triad of symptoms is resting tremor, rigidity, and bradykinesia. PD has been de- scribed as a collection of symptoms rather than one distinct clinical picture. Thus, diagnosis can be difficult in the early stages of the disease. Typically tremor or rigidity are noted on one side of the body, although they may progress to bilateral involvement. (13) Physicians often refer to PD as the "waiting room diagnosis." This refers to the classic signs of pill-rolling tremor, stooped posture, bradykinesia, and masked face that are easily observed in the clinical setting. Patients typically seek consultation with a neurologist to confirm or rule out a diagnosis of PD. Frequently patients will request testing to substantiate the diagnosis. No such test exists, however. PD is a diagnosis made by history and physical. In today's technologic health care environ- ment, patients are often frustrated with the fact that PD is a clinical diagnoSis.13 EPIDEMIOLOGY Approximately 1 million Americans are currently diagnosed with PD. Men have a slightly higher incidence of the disease, and whites are disproportionately affected when compared with other races. PD is typically considered to be a disease of the aged. The mean age of onset is 60 years of age, although cases have been identified in individuals as early as 30 years of age. With increased incidence of PD in young patients, that is, in those diagnosed before the age of 50, a new set of quality-of-life issues has emerged.(6,8) For example, an older patient, a more "traditional Parkinson's patient," has probably planned for retirement. Facing a degenerative disease in what had been hoped to be the "golden years," elderly couples are often confronted with not being able to travel and thus change their focus to planning for long-term care. On the other hand, the concerns of the younger patient with PD focus on raising children, managing a career, and maintaining a home. These two age groups have distinct differences in issues affecting their quality of life. CAUSE The cause of PD is unknown. However, the following theories are the focus of current research: genetic, viral, and environmental toxins. Genetic research is fo- cusing on mitochondrial defects and family linage.'-' Twin studies have failed to demonstrate any clear inherited trait, however. The viral theory was first suggested with the outbreak of encephalitis lethargica, which occurred worldwide from 1918 to 1926. This viral epidemic resulted in postencephalitic parkinsonism killing more than 2000 Americans. The mortality rate approached 40%, and only 15% of patients fully recovered. As survivors of this viral epidemic die, fewer individuals with this form of PD are seen. Environmental toxin theories have continued to be a focus of epidemiologic studies. (13) PATHOLOGY The hallmark pathologic feature of PD is the degeneration of the dopaminergic nigrostriatal pathway. It has been shown that 80% of the dopan-dne-producing cells must be lost before manifestations of the disease can be seen. The severity of PD is associated with the degree of neuronal loss in the midbrain at the level of the substantia nigra.11 Dopamine, a neurotransn-titter, is the primary neurocheniical responsible for the signs and symptoms of PD. The balance of dopamine and acetylcholine are responsible for normal motor function. The development of symptoms is explained by an imbalance of dopaminergic (inhibitory) and chohnergic (excitatory) activity in the caudate and putamen of the basal ganglia. When degeneration of the dopamin- ergic nigrostriatal pathway occurs, there is depletion of dopan-dne and relative excess of cholinergic activity in the feedback circuit involving the cerebral cortex, basal ganglia, and thalamus. This change in neuronal activity is responsible for the classic manifestations seen in PD.(9) MOTOR FEATURES The Motor features of PD include the classic triad of tremor, rigidity, and bradykinesia. In addition, there is postural instability and disordered gait as well as disorders in fine motor movement. A brief description of each motor feature follows. Tremor Resting tremor is the most classic and visible sign of PD. Seventy percent of patients present with resting tremor as their chief complaint for seeking diagnosis and treatment. Parkinsonian tremor has been described as having a pfll-rolling quality and can affect all four limbs and the head.(13) Many patients express feelings of embarrassment related to their tremor. Tremor is the most difficult symptom to treat but the least disabling. It subsides with action and is thus described as a resting tremor. The resting quality of the Parkinson tremor allows patients to maintain activities of daily living within some lin-titations. Unfortunately, patients will restrict social activities due to fear of social stigma and being labeled as ill. In addition, stress can intensify tremor, which further restricts the patient's willingness to participate in social life, Rigidity Rigidity is often described as a plastic resistance to passive movement. Patients often describe this characteristic as stiffness. On examination, rigidity can be de- tected as a coglike release of muscle resistance in the wrist, elbows, neck, and knees as the limb is moved through passive range of motion.(13) Rigidity can cause the face of the patient with PD to take on a masklike quality. The face appears fixed and rigid, and previously recognizable nonverbal messages are misinterpreted or lost in communication. Fanifly members find this change to be most disturbing because the patient no longer has a change of facial expression. Bradykinesis Bradykinesia refers to difficulty with initiating and continuing movement. Movements are slowed and are performed with conscious effort. Patients have described bradykinesia as feeling as if "My brain is sending the message to the body, but the body won't listen."(7) Postural Instability and Gait Disorders As PD progresses, patients may demonstrate difficulty maintaining erect pos- ture. Typically, there is forward flexion of the neck, hips, knees, and elbows. Postural abnormalities greatly reduce the patients' ability to be ambulatory and places them at high risk for injury.(7) This may also lead to reliance on assistive devices. Because of rigidity and postural changes, patients also develop a shuffling quality to their gait and use small steps. Another abnormal gait characteristic is propulsion, a disturbance in which the patient goes from a slow walking pace to runnin with an inability to stop. Patients are only able to stop themselves by grabbing stationary objects such as a door frame. It is important to note that patients who develop an unsteady festinating gait may appear to be under the influence of drugs or alcohol. The inability to be freely ambulatory restricts the independence of the patient with PD. The use of a cane, walker, or wheelchair gives the patient a message that the disease is progressing. Resistance to the use of assistive devices is often an attempt to maintain self-esteem as the patient is dealing with declining health. Limitations of mobility further restrict social fife, and many patients express an inability to maintain pace with friends or family members. Often patients will express embarrassment due to their gait disturbance and verbalize a realistic fear that others will assume they have a substance abuse problem. On-Off Phenomenon As the disease advances, patients enter a narrow therapeutic window. Re- sponse to treatment is less predictable, resulting in what is termed the "on-off" phenomenon. This phenomenon refers to a syndrome in which patients are freely ambulatory one n-tinute and then find they are "frozen" and unable to move the next. Patients also describe "off" periods as if someone has turned off the switch and their feet have sprouted roots. The cause of the on-off phenomenon is un- known but may be associated with years of therapy compounded with continued loss of dopan-tine-producing cells.(13) Because the on-off phenomenon is unpredictable, it can play a major role in family dynan-dcs. The concept of a person exhibiting a behavior that is severely disabling, sudden in onset, and resolving without intervention is a difficult concept for patients and health professionals to grasp. Understanding that on-off phenom- enon behavior is not intentional and is not psychogenic in origin is essential. Patients and farnfly members need education about this feature of the disease process to assist the patient with PD to maintain a sense of control. Swallowing and Speech Defects Dysphagia is a common disorder that affects patients with PD and was first recognized by James Parkinson. He described patients as having significant weight loss with complaints of difficulty swallowing solid foods as compared to liquids. As the disease progresses, patients report difficulty with chewing or moving food to the back of the mouth. This may lead to choking episodes and places the patient at high risk for aspiration. Management of dysphagia in PD may be difficult. Consul- tation with a dietitian and swallowing therapist may be beneficial in providing optimal nutrition. In addition, meals should be eaten when levodopa dosages are reaching maximum effectiveness. (10,16) The motor disturbances responsible for swallowing deficits can also lead to disorders of speech in the patient with PD. Dysarthria, a form of speech distur- bance, is characterized by deviations in phonation, prosidic disturbances in which speech may be slow or extremely fast, and an articulatory disorder in which vocal sounds are distorted. Dysarthria is a common problem for patients with PD and can have a dramatic and devastating effect in a patient's interpersonal communication and self-image. Management of dysarthria involves the use of medication and speech therapy. Levodopa has been shown to improve speech intelligibility, and speech therapy can assist the patient in using techniques to enhance projection. To gain maximum benefit from speech therapy, the patient must be invested in practicing the exercises assigned by the speech therapist. (10) Handwriting Difficulty with handwriting can be an early sign of PD. Patients with PD typically will initiate handwriting with normal-sized penmanship and trail off words and sentences with smaller illegible handwriting. This small writing is referred to as "n-dcrographia." Patients with micrographia can have difficulty sign- ing checks, and banks frequently request patients to sign a new bank card because of the dramatic change in signature. The inability of patients to spontaneously write can also inhibit communication. (14) NONMOTOR FEATURES Depression Depression in PD has been the focus of numerous studies. Research indicates that 20% to 90% of patients with PD will experience a major depressive episode as compared to 7% of the general population. Depression accounts for the majority of psychiatric referrals in patients with PD and can be the initial feature of PD. It has been hypothesized that the shared neurochemistry of these two disorders accounts for the high incidence of depression in PD.(2) Depression can be viewed in two ways. Some patients may become demora- lized with the diagnosis of PD and experience a "reactive depression." Reactive depressions are linked to external events and are short in duration. Typically the patient experiencing a reactive depression is able to resolve the issue and accept the diagnosis. Individuals experiencing a reactive depression may benefit from sup- portive psychotherapy, however.(2) The most typical depression experienced by the patient with PD is endogenous depression. Endogenous depression is caused by a biochemical imbalance in the brain and can be life-threatening if not treated. The difficulty in diagnosing depres- sion in patients with PD lies in the shared clinical features of the two disorders (Table 2). Dementia Dementia is also a common feature of PD. It is estimated that 20% of patients with PD will become demented.(11,14) Dementia can be defined as an acquired, ------------------------------------------------------------------------------------------------------------- Table 2. COMPARISON OF CLINICAL FEATURES ASSOCIATED WITH PARKINSON'S DISEASE AND DEPRESSION Features Parkinson's Disease Depression Motor manifestations Stooped posture, bradykinesia, Slumped posture, psychomotor masked face retardation, diminished facial affect Sleep disturbances Insomnia, sleep fragmentation Insomnia, early morning awakening Gastrointestinal Constipation, weight loss Constipation, weight loss Concentration Bradyphrenia Poor concentration Hallucinations Visual, usually nonthreatening Visual, auditory, olfactory and tactile Adapted from Bunting LB, Fitzsimmons, B: Depression in Parkinson's disease. J Neurosci Nurs 23(3):160, 1991; wwith permission. ------------------------------------------------------------------------------------------------------------- persistent impairment of intellectual function with compron-dse in at least three of the following areas of mental activity: language, memory, visuospatial skills, emo- tionality and personality and cognition in the presence of clear consciousnesS.3,4 The retention of long-term memory permits the patient to maintain aspects of normal social behavior early in the disease. The severe loss of ability to learn new material and the limitations of short-term memory result in episodes of frustration that can escalate into agitation, however. In addition, individuals with dementing illnesses may have enough insight to experience a clear sense of loss, thus leaving patients and families demoralized and dispirited.(4) Nursing management of demen- tia care should encompass the principles of preservation of dignity and provision of safety. Sleep Disturbances Sleep disorders are a frequent complaint in patients with PD. Disorders of sleep initiation, sleep fragmentation, early morning awakening, excessive daytime somnolence, and parasomnias represent the disorders of sleep seen in PD. A detailed history of the sleep complaint, validated by a bedpartner, is the best method of establishing the cause of sleep disturbances.(11) Patients may complain of initiation insomnia as, "I can't get to sleep." C)nce asleep they are able to sleep soundly through the night, however. Researchers have concluded that sleep initiation insomnia in PD is related to anxiety, agitated de- pression, or levodopa therapy. The more typical sleep disorders seen in PD are sleep fragmentation and early morning awakening." Sleep fragmentation can be related to the inability to turn over in bed. Rigidity compounded by the wearing off of medication reduces pa- tients' ability to reposition themselves in bed. Patients state that they must wake up to change sleeping positions and then are unable to return to sleep. One solution to this problem is the use of satin sheets to decrease friction and facilitate turning. Early morning awakening typically represents onset of a depressive episode, and the nurse should evaluate the patient for other vegetative symptoms such as decreased appetite, psychomotor retardation, and constipation. Early morning awakening may be related to focal dystonic cramping in the calf and feet, however. Focal dystonia is related to diminished levels of levodopa.(11) Excessive daytime somnolence is the most frequent sleep complaint made by family members of PD patients. In some individuals, daytime somnolence is related to a disturbance in the circadian control of sleep. These patients are up at night and take multiple naps throughout the day. Families report that daytime sonuiolence is disruptive to normal family life. Families should discourage day time napping in an attempt to correct the circadian clock. Patients who are described as sleeping all day, however, should be screened for metabolic abnormalities that may cause disturbances in the sleep-wake cycle. Parasomnias are the most debilitating and difficult of the sleep disorders to manage. Sleep talking, sleep walking, vivid dreams, and nightmares are the most frequently reported parasomnias experienced by patients with PD. Most typically, these occur as a side effect of levodopa therapy. Unfortunately, treatment for parasomnias is limited.(11) Sexual Dysfunction Sexual functioning in patients with PD has received inadequate attention. The paucity of literature can be attributed to the assumption that patients with PD are elderly and therefore have a diminished interest in sex. Research indicates that frequency of sexual intercourse decreases with age; however, sexuality continues to play a role in the lives of the elderly. Sexual dysfunction has a significant impact on patients who are diagnosed with PD in their midadult years when an active sex life is the norm.(1) Dysfunction of the autonomic nervous system, depression, medications, and interpersonal issues all play a role in sexual dysfunction in PD. Autonomic dys- function in the urogenital system resulting in impotence is the primary reason for sexual dysfunction in male patients with PD. Secondary issues affecting sexual function include motor fluctuations, fatigue, medications, sleep disorders, depres- sion, and interpersonal issues.(1) The motor fluctuations and fatigue can be related to antiparkinsonian drugs, primarily levodopa. Patients with PD find that they are better able to function in the morning, after their initial dose of medication, and become more fatigued with greater motor fluctuations as the day progresses. Numerous reports document hypersexuality with the use of levodopa. This may result in a problem when one partner has heightened sexual interest that is not shared by the other partner. To adapt to these changes in their sexual life, couples may need to change their daily routine to accommodate morning sexual activity and take advantage of optimum energy levels and motor functioning. Unfortunately, sleep disorders experienced in patients with PD may result in bedpartners sleeping in separate beds, which diminishes opportunity for spontaneous sexual activity.(1) Depression can also have a significant impact on sexual activity in patients with PD. As discussed earlier, depression is common in patients with PD and can produce a markedly decreased libido. Sexual partners may also experience depres- sion and fatigue as they struggle with the caregiving role in the relationship; thus, they also may not have the energy or interest to engage in sexual activity. In addition, autonon-dc dysfunctions that result in droohn& diaphoresis, and excessive facial oiliness may interfere with perceived attractiveness of the patient by the sexual partner.(1) The issues surrounding sexuality in PD are complex. Patients should be rou- tinely questioned regarding satisfaction of their sexual life. A referral to a urologist or sex therapist can assist in identifying issues affecting sexuality. Open conununi- cafion regarding sexual issues can be limited by the patient's reduced facial expres- sion and altered speech pattern. The ability of the couple to communicate their sexual needs within the liniitafions of the disease state can have a significant impact on the couple's marriage and sexual life.(1) Driving Performance When a patient is seen for the management of PD, no discussion would be complete without addressing driving. Motor manifestations of the disease as well as a decline in cognition may impair the pafient's ability to function safely behind the wheel. Some patients may willingly retire their driver's license, whereas others may view this as giving up valued independence. Evaluation of driving skills by a professional driving instructor may provide a nonthreatening avenue to assess auto safety. Family members should be involved in the evaluation of driving to arrange alternate transportation if the patient's driving is found to be unsafe. Employment PD can be a disability and liability in the work place. Many patients ask, "Should I tell my boss?" There is no clear answer to this question because each situation is different. Patients should be encouraged to have a frank and open discussion with their health professionals regarding the limitations imposed by their symptoms and the effect of these lin-dtations on their job responsibilities. This discussion should include the benefits and potential disadvantages of revealing this information to their supervisor. Frequently, coworkers have suspected that a prob- lem exists. By sharing the diagnosis, an empathefic supervisor may facilitate a pafient's medical appointments and make environmental adjustments to expedite an optimum working relationship. Unfortunately, the risk of sharing the diagnosis of PD can have a negative impact on job security. It has been the experience of these authors that patients have been reassigned to other job responsibilities or pressured into early retirement. Physicians and nurses should strive to provide strategies and guidance for handling this difficult situation. DRUG THERAPY Drug therapy is the mainstay of management of PD. The primary medications used in PD are classified as anticholinergics, antihistamines, dopaminergics, and dopamine agonists (Table 3). (17) Unfortunately, all drugs used in the treatment of PD have potential for side effects that impact on quality of life. Indication for medica- tion is determined when the patient develops deficits in activities of daily living or is expressing embarrassment from tremor or gait disturbances. The approach to drug therapy is to maintain the patient on conservative levels of medication while maintaining mobility. As the disease progresses, patients become less responsive to medications and experience end of dose failure, peak dose dyskinesias, and painful dystonic cramps. They are also more prone to developing de@um and hal- ludnations.(13,14) Levodopo Therapy Levodopa is the drug of choice for treatment of PD. It is marketed as a combination drug called Sinemet and is composed of carbidopa and levodopa. The ------------------------------------------------------------------------------------------------------------------- Table 3. SUMMARY OF MEDICATIONS USED IN PARKINSON'S DISEASE ------------------------------------------------------------------------------------------------------------------- Type Drug Name Indications Side Effects ------------------------------------------------------------------------------------------------------------- Anticholinergics Tdhexyphenidyl Tremor, rigidity, Dry mouth, (Artane), drooling constipaflon, benztropine blurred vision, (Cogentin) confusion, visual hallucinations Antihistamine Diphenhydramine Tremor, rigidity, Dry mouth, lethargy, (Benadryl) insomnia confusion Dopaminergics Amantadine Rigidity, Leg edema, livedo (Symmetrel), bradykinesia, reticularls, carbidopa/ tremor hallucinations, levodopa orthostatic (sinemet) hypotension, nausea, confusion Dopamine agonists Bromocriptine Motor fluctuations in Hallucinations, (Parb"), Parkinson's mental cloudiness pergolide (Permax) disease orthostatic hypotension, confusion ------------------------------------------------------------------------------------------------------------- action of carbidopa is to block the breakdown of levodopa in the peripheral organs and allows more levodopa to cross the blood-brain barrier. Levodopa is converted to dopamine. in the brain through a series of enzymatic reactions.(13) Levodopa therapy is responsible for promoting quality of life for the vast majority of patients with PD. Levodopa therapy has lin-dtations, however. Early in treatment, patients are maintained on low doses of levodopa to preserve the therapeutic window for the future. Typically patients respond well to levodopa and only experience mild side effects such as nausea and orthostatic hypotension. As the illness progresses, patients require higher levels of levodopa, a@d'response to therapy is less predictable.(13) Levodopa has a relatively short half-life. It has a rapid onset of actions and patients report getting a surge of energy with each dose. Similarly, patients com- plain of "wearing off" symptoms as levodopa is metabolized and PD features return. When levodopa is at therapeutic levels, the patient's functioning may appear quite normal. As the medication "wears off," however, patients may be- come akinetic and rigid. Like the on-off phenomenon, wearing off can be frustrat- ing for the patient and family. In contrast to the on-off phenomenon, however, the wearing-off symptoms are predictable and are associated with declining levodopa levels. When levodopa alone is not maintaining symptomatic control, the physician may add a dopamine agonist such as bromocriptine (Parlodel) or pergofide (Per- max). There agents act to smooth out levodopa levels and help to control the rapid rise and fall of levodopa levels.(13,14) With progression of symptoms, patients with PD may experience peak-dose dyskinesias. The term "dyskinesia" describes the development of extra movements of the head, neck, trunk, and extremities as levodopa doses rise and peak rapidly. Most patients find that these extraneous movements limit social activities. Al- though dyskinesias can be devastating, patients can function within the limitation of the movement disorders.(13) Compliance Compliance in taking prescribed drugs is essential to successful management of PD. Patients with PD often verbalize feelings of being chained to the clock because they require levodopa to maintain mobility. Levodopa dosage schedules can be prescribed as frequently as every 2 hours during the waking day. The need for levodopa can overshadow all other aspects of the patients life because he or she is unable to function without it. If medications are late or missed, the patient can experience dystonic pain, increased tremor, rigidity, and personality changes. Com- pliance can also be an issue when patients with PD take extra doses of levodopa to boost their levels of energy and function. This behavior should be discouraged, and any change in treatment plan should be discussed with the physician. Alarm clocks or pill boxes with alarms can assist the patient with remembering to take the medication on time. Cost of medication can also affect compliance. It is not uncommon for patients to spend approximately $300 per month on medications for PD. The financial impact of medications can preclude physicians from ordering additional therapy. Nurses can assist in deterring the cost of therapy by investigating drug-cost- sharing programs sponsored by drug companies or pricing mafl-order pharmacies to find lower Cost medications. Side Effects of Delirium and Hallucinations Medications used in the management of PD often need to be titrated. Usually, the higher the dose of drug, the more frequently side effects are encountered. (13) The side effect of delirium is a constant danger with all medications usld in PD. The probability of delirium is determined by each patient's tolerance to the medication and predisposing factors such as age and general health. Living with a drug- induced delirium is a difficult issue for many patients and families. Families are often asked to make a choice between clear mentation and motor functioning. It may be easier for a family to care for a mobile patient with PD who is cognitively impaired. The occurrence of hallucinations is well documented in the management of patients with PD. Amantadine, a dopaminergic medication, is notorious for causing visual hallucinations. Other medications in which hallucinations have been docu- mented as a side effect include anficholinergic medications such as trihexyphenidyl (Artane) and benztropine (Cogentin), levodopa in the form of carbidopa/levodopa, and dopan-dne agonists such as bromoctiptine and pergolide. All of these drugs act to increase the levels of dopamine in the brain through different mechanisms of action. (13) Patients frequently are able to tolerate continued use of medications knowing that hallucinations are a side effect of therapy. Typical treatment-induced halluci- nations in PD are visual and may consist of seeing small children or animals. These hallucinations are seldom threatening. If hallucinations become auditory or threat- ening in content, patients should be evaluated for depression or dementia by a qualified psychiatrist. SUMMARY PD affects many dimensions of quality of life. This article has identified motor and nonmotor features of PD that are directly related to a patient's quality of life. Medication therapy can help to ameliorate some of the symptoms, yet side effects can be as disabling as the symptoms of PD. Nursing care should include assess- ment, intervention, and evaluation of both physical and psychosocial aspects of care for patients with PD to assist them in achieving maximum functioning, References 1. Brown RG, Jahanshahi M, Quinn N, et al: Sexual function in patients with Parkinson's disease and their partners. J Neurol Neurosurg Psychiatry 53:480-486, 1990 2. Bunting LK, Fitzsimmons B: Depression in Parkinson's disease. J Neurosci Nurs 23(3): 158-164, 1991 3. Cummings JL, Benson DF: Dementia: Definition, prevalence, classification, and approach to diagnosis. In Dementia: A Clinical Approach. Massachusetts, Butterworth, 1992, p 1 4. Folstein MF, Ross C: Cognitive impairment in the elderly. In Kelly WN led); Textbook of Internal Medicine. JB Lippincott, 1992, p 2408 5. Gentile KM: A review of the literature on interventions and quality of fife in the frad elderly. In Birren JE, Lubben JE, Rowe JC, et a] (eds): The Concept and Measurement of Quality of Life in the Frafl Elderly. San Diego, Academia Press, 1991, p 74 6. Giovannini P, Piccolo 1, et al: Early onset Parkinson's disease. Movement Disorders 6(l):36-42, 1991 7. Hickey J: Nervous system degenerative diseases. In The Clinical Practice of Neurological and NeUTOSurgical Nursing. Philadelphia, JB Lippincott, 1992, p 651 8. Marttila Rj: Epidemiology. In Koller WC led): Handbook of Parkinson's Disease. New York, Marcel Dekker, 1987, p 35 9. McCance KL, Huether, SE: Alterations in neurologic function. In Pathophysiology: The biologic basis for disease in adults and children. St. Louis, CV Mosby, 1990, p 509 10. Micoch AG: Diagnosis and treatment of patkinsonian dysarthria. In Koller WC (ed): Handbook of Parkinson's Disease. New York, Marcel Decker, 1987, p 181