Thursday, March 13, 2008

Quality of Life

--------------------------------------------------------------
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

http://parkinsons.dirtybutter.com/blog/

No comments: