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PARKINSON’S DISEASE
INTRODUCTION
Parkinson’s disease is a very common chronic, degenerative disease of the nervous
system. It is chronic, progressive, and causes serious, debilitating motor and psychiatric
signs and symptoms. Most cases of Parkinson’s disease are idiopathic, but there are
genetic and (possibly) environmental causes that have been identified. There is no cure
for Parkinson’s disease, and people with Parkinson’s disease have significant morbidity
and a higher mortality rates than the population without the disease. Medications can
alleviate the signs and symptoms and help restore function, but do not alter the course or
progression of the disease.
OBJECTIVES
When the student has finished this module, he/she will be able to:
1. Identify a definition of Parkinson’s disease.
2. Identify the basic pathophysiologic cause of Parkinson’s disease.
3. Identify an important fact about the development/progression of Parkinson’s disease.
4. Identify the pathologic process most likely to cause the neurological damage of
Parkinson’s disease.
5. Identify the three causes of Parkinson’s disease.
6. Identify the three motor abnormalities strongly associated with Parkinson’s disease.
7. Identify three other signs/symptoms of Parkinson’s disease.
8. Identify three neuropsychiatric disorders commonly associated with Parkinson’s
disease.
9. Identify the drug most commonly use to treat Parkinson’s disease.
10. Identify three other drugs commonly used to treat Parkinson’s disease.
11. Identify the common side effects of the dopaminergic drugs used to treat Parkinson’s
disease
12. Identify a surgical technique used to treat Parkinson’s disease.
13. Identify two advantages offered by this surgical technique.
14. Identify two other surgical techniques used to treat Parkinson’s disease.
15. Identify the first treatment step used for treating psychosis associated with
Parkinson’s disease.
EPIDEMIOLOGY
Parkinson’s disease is relatively common; it is the second most common
neurodegenerative disease worldwide (Alzheimer’s is first). The incidence of the disease
is approximately 120 cases per 100,000 population, and it affects approximately 1 to 1.5
million people in the United States.1,2 The disease gets progressively more common with
advancing age, and it is most common in people over the age of 60. It affects
approximately 20 per 100,000 population in their 50s and approximately 90 per 100,000
population in their 70s.3 Parkinson’s disease is unusual in young people. Early onset
Parkinson’s disease (between the ages of 20 and 40) accounts for approximately 4% 10% of all cases.4 People with Parkinson’s disease have a mortality rate two to five times
as high as the general population.5
Parkinson’s disease is approximately 1.5 times more common in men than in women,
and women are generally older when they develop the disease.6 However, women with
Parkinson’s are more likely to develop certain complications such as depression and
dyskinesia.7
PATHOPHYSIOLOGY
The basic pathologic process of Parkinson’s disease is understood. The disease is
caused by destruction of pigmented, dopamine producing neurons in the substantia nigra
pars compacta in the basal ganglia section of the brain, and the presence of Lewy
bodies.8,9
Learning Break: Lewy bodies are proteins – ubiquitin and α-synuclein – that are found
in the many parts of the brain and the central nervous system in patients with Parkinson’s
disease. The exact contribution of Lewy bodies to the pathophysiology of Parkinson’s has
not been outlined.
The basal ganglia is the area of the brain that controls and modifies the brain output
from the cerebral cortex that controls normal motor movements. Signals for
movement from the cerebral cortex move through the basal ganglia (with dopamine being
the major neurotransmitter) and then processed through an inhibitory pathway and a
direct pathway. The destruction of the dopamine producing neurons inhibits the
inhibitory pathway and movement is suppressed.10
Learning Break: Dopamine is one of the primary neurotransmitters. Neurotransmitters
are chemicals that are released from nerve endings into a synapse. The neurotransmitter
binds to post-synaptic dopamine receptors located on the cell membrane of the target cell.
This binding affects ion flux across the cell membrane; the ion flux excites or inhibits the
action of the cell (i.e., producing or inhibiting cell depolarization) and produces a
particular effect. Once the post-synaptic cell has been affected, the dopamine is released
back into the synapse and enzymes (e.g., monoamine oxidase) break it down and remove
it. Dopamine is a catecholamine (like epinephrine and norepinephrine). Dopaminergic
neurons are highly concentrated in certain areas of the brain, e.g., the limbic system and
the basal ganglia. Drugs can affect the dopaminergic system by acting as direct stimulants
of dopamine receptors (agonists), by inhibiting the breakdown of dopamine, or acting a a
direct source of dopamine.
The development of Parkinson’s disease appears to be a relatively slow and
progressive process. The destruction of dopamine producing neurons probably starts
three to six years (and perhaps much longer) before there is clinical evidence of the
disease,11 and approximately 60% to 80% of the dopamine producing neurons are lost
before the clinical signs and symptoms of the disease are seen.12
Although it is clear that the destruction of the dopamine producing neurons is the cause
of the signs and symptoms of Parkinson’s disease, it is not clear why this happens.
Multiple processes may be responsible:13
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Mitochondrial dysfunction
Oxidative damage
Proteasome dysfunction
Lysosome dysfunction
Protein aggregation
Glutamate toxicity
Calcium toxicity
Cytotoxic cytokines
Loss of trophic factors
Inflammation
It is currently thought that mitochondrial dysfunction, caused by oxidative stress, is the
pathologic process most likely responsible for the neurological damage of Parkinson’s
disease, but the exact nature and role of these processes in cell death of the dopaminergic
neurons is not clear. However, these processes are thought to be caused/initiated by
environmental factors, genetics, or a combination of genetic susceptibility and an
environmental trigger – the idiopathic cases.
CAUSES OF PARKINSON’S DISEASE
Environmental
Researchers have been looking for environmental causes of Parkinson’s disease for
many years. Exposure to pesticides and herbicides, consumption of well water, residence
in a rural environment, and living near factories have all been investigated as being
possible environmental causes of Parkinson’s.
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Well water: Several studies have provided evidence that drinking well water
contaminated with pesticides or chemicals increases the risk of developing
Parkinson’s disease.14,15
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Pesticides and herbicides: There is a seemingly strong association between
pesticide exposure and an increased risk of developing Parkinson’s disease.16,17
Some of the pesticides are neurotoxic, they can cause oxidative stress, and animal
studies have shown that they damage the dopaminergic system in the brain.
Genetic polymorphisms in the enzymes that break down pesticides may increase
an individual’s risk.18
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Rural environment: There is evidence for and against a rural environment
increasing the risk of developing Parkinson’s disease.19,20
Learning Break: Although there is a lot of evidence for environmental/toxin causes for
Parkinson’s disease, this evidence is not yet conclusive.
Genetic
Cases of Parkinson’s disease that can be unequivocally attributed to a single genetic
mutation account for approximately 5% - 10% of the incidence of the disease.21 More
commonly, genetic variations affect an individual’s susceptibility to the disease, affect
the age at which the disease is contracted, or influence the severity and progression of the
disease.22 For example, mutations in the leucine-rich repeat kinase 2 (LRRK-2) gene (a
gene that encodes a large, complex mitochondrial protein) could affect dopamine
synthesis and transmission and the structural integrity of dopaminergic neurons.23 Some
researchers feel that these gene mutations cause mitochondrial dysfunction and increased
oxidative stress (the two are closely related) and an increased production of reactive
oxygen species (aka free radicals), and this could be the cause of the dopaminergic cell
death in Parkinson’s disease.24,25
Most cases of Parkinson’s disease (approximately 85% to 90%) are classified as
idiopathic; there is no clear genetic or environmental cause for the disease. There are
also cases of Parkinson’s disease that are classified as secondary Parkinson’s.
Secondary Parkinson’s is caused by neurological disorders such as stroke, meningitis,
and encephalitis. Medications – haloperidol, amlodipine, calcium channel blockers,
sertraline, trazodone, valproic acid, cyclosporine, metoclopramide, some phenothiazines,
surgical anesthestics – and toxins such as copper, manganese, cyanide, and carbon
monoxide can also cause secondary Parkinson’s disease. If the Parkinson’s is caused by a
drug, it is usually reversible. If it is caused by an infection, a neurological disorder, or a
toxin, it is usually will not improve or disappear.
DIAGNOSING PARKINSON’S DISEASE
Diagnosing Parkinson’s disease can be difficult. There are no confirmatory laboratory
studies. Magnetic resonance imaging (MRI) and computed tomography (CT) cannot
confirm the diagnosis. A positron emission tomography (PET) scan, however, can be
used to detect and confirm the presence of Parkinson’s.26 Parkinson’s disease is,
essentially, a clinical diagnosis; the physician will look for the very characteristic signs,
symptoms, and clinical course of the disease
SIGNS AND SYMPTOMS OF PARKINSON’S DISEASE
Motor Signs of Parkinson’s Disease
The three cardinal signs of Parkinson’s disease are resting tremor, rigidity, and
bradykinesia, and two of these must be present in order for a diagnosis of Parkinson’s
disease to be confirmed.27 Postural instability is also characteristic of Parkinson’s disease,
but this sign occurs late in the course of the illness.
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Tremor: Tremor usually begins in one extremity, and it usually remains
asymmetric in presentation. The hand and arm are most often affected, but the
chin, jaw, lips, and lower extremities can be affected, as well. Tremor is made
worse by stress and is alleviated by rest. Tremor is assessed while the extremities
are at rest and while the extremities are held in various positions of extension
(resting and active tremor).28
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Rigidity: Rigidity in Parkinson’s disease refers to resistance of an extremity to
passive movement. The rigidity can be smooth/continuous (a.k.a. lead pipe
rigidity), or intermittent/oscillating (a.k.a. cog wheel rigidity). Rigidity is checked
in the neck and all four extremities. The joint is supported and the extremity is
moved through a full range of motion. Rigidity of the head is checked by placing
one hand on the forehead and the other on the occipital area. The head is flexed
and extended and the degree of rigidity is assessed.29
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Bradykinesia: Bradykinesia refers to movements that are very slow, but it can also
refer to a relative lack of movements, and decreased amplitude of movements.
The presence of bradykinesia is ascertained using a variety of tests, e.g., the
patient is asked to open and close his/her hand as rapidly as possible. If the patient
can only open and close his/her hand seven to ten times in five seconds, a
moderate degree of bradykinesia is considered to be present.30
Patients with Parkinson’s disease can also be seen to have postural instability (lack of
balance, the inability to right oneself when out of balance), a shuffling gait with small,
hesitant steps, soft and indistinct speech, and an inability to make spontaneous facial
expressions – the so-called Parkinson’s “mask.”31,32
Neuropsychiatric and Other Signs and Symptoms of Parkinson’s Disease
Parkinson’s disease is characterized by physical disabilities, but it also causes many
neuropsychiatric signs and symptoms.
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Depression: Depression affects approximately 40% to 50% of all patients with
Parkinson’s disease.33 Depression in and of itself is serious, but people with
Parkinson’s disease who are depressed have worse long-term outcome, a poorer
quality of life, an increased level of disability, more symptoms, worse symptoms,
a faster progression of the disease, and decreased cognitive skills.34,35
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Anxiety: Anxiety is also very common in patients with Parkinson’s disease.
Estimates vary for the incidence of anxiety in this patient population, and range
from 29% to 40%.36 Panic attacks are also very common: approximately 13% to
30% of all patients with Parkinson’s disease experience panic attacks.37,38 Much
like depression, anxiety and panic attacks decrease the quality of life and increase
the incidence and severity of motor signs and symptoms.39,40
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Psychosis: The psychosis that can occur in patients with Parkinson’s disease is
characterized by visual hallucinations (very common), delusions, illusions, and
disorganized thinking.41 These episodes can last from minutes to hours, the
psychosis usually begins in the end stages of the disease, and it worsens over
time. Approximately 20% to 40% of all patients with Parkinson’s disease will
suffer from psychosis.42 No one is certain why the psychosis occurs – many
patients never develop it – but it is most likely due to a combination of
neurological damage and adverse effects of the medications used to treat
Parkinson’s. As with depression, anxiety, and panic attacks, psychosis in patients
with Parkinson’s disease is associated with a decrease in the quality of life and an
increase in the frequency and intensity of other signs and symptoms.
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Dementia: The presence of Parkinson’s disease will cause a six-fold increase in an
individual’s chances of developing dementia.43 Patient’s with Parkinson’s disease
dementia (PDD) have significant impairment of attention, memory, executive and
visuo-spatial function, and they often experience mood changes, apathy, and
hallucinations/delusions.44 Advanced age, male gender, a comparatively worse
case of the disease, and other psychiatric conditions (psychosis, depression)
appear to be risk factors that increase an individual’s chances of developing PDD.
PDD increases the rates of morbidity and mortality of patients with Parkinson’s
disease.45 The exact incidence of PDD is not known, but estimates vary from 28%
to 44%, and it definitely increases with advancing age.46,47. Damage to the
dopaminergic, serotonergic, noradrenergic, and cholinergic systems is thought to
be the cause of PDD.48
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Fatigue: People with Parkinson’s disease often feel both physically and mentally
tired.49
Other signs and symptoms of Parkinson’s disease include dysphagia, dysarthria,
constipation, urinary incontinence or dysuria, dry or oily skin, and sleep
disturbances.
EARLY DIAGNOSIS OF PARKINSON’S DISEASE
Parkinson’s disease is well advanced when the clinical signs and symptoms become
evident. Some clinicians have noted that there are signs and symptoms that are seen
before the development of the definitive motor and neuropyschiatric signs of Parkinson’s.
Changes in olfaction, diarrhea or constipation, sleep disturbances, and changes in
cognitive and motor behavior may be predictive of Parkinson’s disease, and one author
has coined the term Parkinson’s associated risk syndrome (PARS).50 Unfortunately at this
point, reliable tests and markers have not been develop and predicting the development of
Parkinson’s disease is still a challenge.
PHARMACOLOGICAL TREATMENT OF PARKINSON’S DISEASE
Parkinson’s disease can be treated, but the disease is progressive and there is no cure.
Patients who have developed Parkinson’s disease eventually progress to a rigid, akinetic
state. The patient will become bedridden, cannot care for himself/herself, and most often
succumbs to infection or a cardiovascular event. Patients with Parkinson’s disease can
live for 20 years or more with the disease, but the presence of Parkinson’s definitely can
mean an earlier death.
Treatment is designed to alleviate the signs and symptoms and to improve the quality
of life. There is no evidence that starting treatment before the signs and symptoms are
strongly evident has a protective effect; most clinicians begin treatment when the disease
interferes with the activities of daily living.51 Currently, medications are the mainstay of
treatment, but surgical options have been used and continue to be developed.
Drugs that are use to treat Parkinson’s disease can be divided into three categories:
drugs that affect dopamine and/or the dopaminergic system, anticholinergic drugs, and
drugs that may have neuroprotective effect.
Drugs that affect Dopamine or the Dopaminergic System
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Levodopa: Levodopa is a naturally occurring amino acid which is used by the
body to synthesize dopamine. It is the most effective drug for the treatment of
Parkinson’s disease.52,53 Levodopa is converted in the brain to dopamine
(dopamine itself cannot be given because it does not cross the blood-brain
barrier), and the drug often produces a significant improvement in the signs and
symptoms; within 15 minutes of a dose, the patient’ speech, gait, and dexterity are
improved, and the tremor, bradykinesia, and rigidity may almost disappear54
Tremor and balance problems are not improved with levodopa.
The drug is often given in conjunction with carbidopa. Carbidopa inhibits an
enzyme in the gut that breaks down levodopa; without carbidopa, only a small
fraction of levodopa would reach the brain and be converted to dopamine.
Sinemet® is a commonly prescribed form of levodopa and carbidopa. The usual
dose is one tablet, three times a day.
Common side effects of levodopa include nausea, postural hypotension,
hallucinations, and confusion.
Learning Break: There are several significant problems with levodopa therapy.
Rigidity and bradykinesia are improved, but only for several hours; this is called the
“wearing off” effect. Increasing the dose and the frequency of the doses can solve this
issue, but doing so can cause dyskinesias that are as troubling as the rigidity and
bradykinesia.55 The second problem is that after several years of levodopa therapy, the
patient’s response to any single dose begins to fluctuate and becomes unpredictable.56
Because of these issues, levodopa is usually given when the patient has functional
disabilities, and is not given early in the course of the disease.
Learning Break: Stalevo® is a relatively new drug that combines levodopa, carbidopa
and entacapone. Entacapone is a catechol-O-methyltransferase (COMT) inhibitor. This
enzyme metabolizes catecholamines (e.g., dopamine) and when it is combined with
levodopa and carbidopa, the availability of levodopa in the plasma is increased, so more
levodopa reaches the brain. The combination of the three drugs has been shown to
provide greater symptomatic relief and cause fewer complications than
levodopa/carbidopa.57
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Dopamine receptor agonists; Drugs such as bromocriptine, apomorphine,
ropinirole (Requip®), rotigotine (Neupro®) and pramipexole (Mirapex®) are
direct agonists of dopamine receptors. Bromocriptine, ropinirole, and
bromocriptine are oral medications, apomorphine is an injection, and rotigotine is
available as a transdermal patch. Because of the dyskinesias, motor fluctuations,
and unpredictable response associated with levodopa, the dopamine agonists are
often used in younger patients and they can be very effective at controlling the
signs and symptoms of Parkinson’s disease. When they are used in combination
with levodopa, the incidence of dyskinesias and motor fluctuations is reduced.58
Unfortunately, after a few years of monotherapy with dopamine agonists, they
become less effective than levodopa. The side effects of the dopamine agonists
are similar to those of levodopa. There is some evidence that dopamine agonists
may slow the progression of Parkinson’s, but this is not conclusive.59
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Monoamine oxidase inhibitors: The isoenzyme monoamine oxidase B (MAO-B)
carries out most of the oxidative metabolism of dopamine in the brain. MAO-B
inhibitors – selegiline (e.g., Eldepryl®) and rasagiline (Azilect®) – have been
used successfully to (selegiline less so) to treat the signs and symptoms of
Parkinson’s disease.60 The side effect profile of these drugs when used for
patients with Parkinson’s disease is similar to that of levodopa: orthostatic
hypotension, hallucinations, and dykinesias. Rasagiline has attracted attention
because it may have a disease-modifying effect; the evidence for this is strong,
but not conclusive.61,62
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COMT inhibitors: When levodopa is taken orally, almost 99% of a dose is
catabolized by MAO-B and COMT. The COMT inhibitors – entacapone and
tolcapone – have both been used to help alleviate the “wearing off” effect caused
by levodopa, and they increase the amount of levodopa that reaches the brain and
is converted to dopamine.63 These drugs can cause nausea, hallucinations,
confusion, and orthostatic hypotension.
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Amantadine: Amantadine (Symmetrel®) is an antiviral drug that is used to treat
influenza A. It affects dopamine release, it has anticholinergic actions, and it also
acts as an antagonist at N-methyl-D-aspartate (NDMA) glutamate receptors. It can
be helpful as adjunct therapy as it reduces the incidence of levodopa-induced
dyskinesias.64
Learning Break: The medications used to treat Parkinson’s disease that affect the
dopaminergic system all cause nausea, confusion, orthostatic hypotension, and
hallucinations.
Learning Break: These drugs either, a) provide a source of dopamine, b) inhibit the
breakdown of dopamine, or c) actively stimulate dopamine receptors.
Anticholinergic Drugs
Acetylcholine is one of the primary neurotransmitters of the autonomic nervous
system. The nerve endings that release and receive acetylcholine are called cholinergic.
Drugs that block the effects of acetylcholine on cholinergic receptors are acetylcholine
antagonists and are said to have anticholinergic effects.
Anticholinergic drugs such as trihexyphenidyl (Artane®), benztropine mesylate
(Cogentin®), and diphenhydramine (Benadryl®) have been used to treat Parkinson’s
disease. These drugs are not usually stand alone therapy for the disease. They are used as
an adjunct to dopaminergic drugs, and they can relieve tremor but not decrease rigidity or
bradykinesia.65 It is not clear why these drugs are helpful. Side effects include dry mouth,
urinary retention, constipation, sedation, and confusion.66
Neuroprotective Drugs
Rasagiline, Coenzyme Q10, other MAO inhibitors, dopamine agonists, and levodopa
have all been used to try and modify and/or slow the progression of Parkinson’s disease.
As mentioned previously, there has been some encouraging (but inconclusive) research
using rasagiline in this area. Shults et al used Coenzyme Q10 (Coenzyme Q10 is a
cofactor in mitochondrial processes) in a small study and found that it could slow the
progression of the signs and symptoms of Parkinson’s, but the authors felt that their
findings needed to be confirmed with more and larger studies.67 None of the other drugs
mentioned above were able to affect disease progression or offer a neuroprotective
effect.68 Creatine and minocycline produced small improvements in the Unified
Parkinson’s Disease Rating Scale (UPDRS: an evaluation scale of the motor and mental
abilities), but the studies were small and more research is needed.69
SURGICAL TREATMENT OF PARKINSON’S DISEASE
Surgery can be used to treat Parkinson’s disease. Stimulation therapies, lesion surgery,
and transplantation (experimental) have all been explored.
Stimulation Therapy
Stimulation therapy is the surgical technique that is most often used to treat
Parkinson’s diseases. Deep brain stimulation (e.g., thalamic stimulation, pallidal
stimulation, and subthalmic stimulation) have been used.
Deep brain stimulation (DBS) has approval from the Food and Drug Administration
(FDA) and is the procedure of choice.70 Criteria for patient selection include: a diagnosis
of idiopathic Parkinson’s disease; a positive response to levodopa; advanced disease that
has not responded to dopaminergic medications; no atypical disease features; normal
cognition; absence of psychiatric disease; good social support and access to programming
of the pulse generator.71 In this procedure, a lead is implanted into a particular brain
structure, and the lead is attached to an implanted pulse generator. The amplitude,
frequency, and pulse width of the electrical stimulation are adjusted to control the signs
and symptoms. It is not clear how DBS, but it is clear that is can be very effective; it can
be more effective than medical therapy.72 Other advantages of DBS are adjustability,
reversibility, and no need for destruction of brain tissue. Complications of DBS include,
a) surgical complications (e.g., hemorrhage, infection, etc.), b) device-related
complications such as displacement of the lead, malfunction of the pulse generator, c)
side effects of the stimulation itself such as muscle spasms, pain, mood changes, and
paresthesia, and d) cost. The pulse generator costs approximately $10,000, and the battery
must be changed every few years at a cost of $8000.
Learning Break: One recent study found that combination of DBS and best medical
therapy was superior to best medical therapy alone when treating Parkinson’s disease.73
Lesion Therapy
Lesion therapy involves destruction of a specific part of the brain, e.g., the thalamus (a
thalamotomy) or the globus pallidus pars interna (a pallidotomy). Lesion therapy can be
effective, and in some countries where cost and access to programming of a pulse
generator is limited, lesion therapy is still used. However, because of the effectiveness,
reversibility, and adjustability of DBS, these techniques are infrequently used in the
United States.
Transplantation
Researchers have transplanted human fetal cells, adrenal medullary cells, retinal
epithelial pigment cells, stem and genetically engineered cells, but at this point, these
techniques are either experiemental or have not been successful.74,75
TREATMENT OF NEUROPSYCHIATRIC COMPLICATIONS OF
PARKINSON’S DISEASE
Because the physical signs and symptoms of Parkinson’s disease are easily seen and
can be so dramatic, it can be easy to overlook the less observable complications of the
disease – depression, anxiety, psychosis, PDD, and fatigue – that are very common and
are very are serious and debilitating.
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PDD: Cholinesterase inhibitors, specifically rivastigmine (Exelon®) and
donepezil (Aricept®) have been shown to effective in increasing cognition and
improving the ability to perform activities of daily living (ADL) in patient’s with
PDD.76 These drugs increase the concentration of acetylcholine at cholinergic
receptors. It is thought that at least part of the pathological changes associated
with PDD are due to damage to cholinergic nerve pathways, and this may be why
the cholinesterase inhibitors can be useful for patients with PDD.
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Psychosis: The first step to take when treating psychosis associated with
Parkinson’s disease is to reduce the medications. It is recommended that he
medications be withdrawn starting with the anticholinergic agents, then selegiline,
amantadine, dopamine receptor agonists, COMT inhibitors and finally,
levodopa.77 If the doses are reduced up to the point where the amount given is
significantly less, the patient doesn’t suffer exacerbation of motor
signs/symptoms, but the psychosis persists, an antipsychotic drugs should be
given. Atypical antipsychotics such as olanzapine (Zyprexa®) are preferred and
can be helpful. There is also evidence that the cholinesterase inhibitor
rivastigmine can be effective in these situations.78
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Depression: Patients with Parkinson’s disease who have depression can benefit
from treatment with traditional antidepressants such as nortriptyline or a
serontonin reuptake inhibitor.79 However, there is not enough data on the safety
and effectiveness of any of the antidepressants to be confident that they will be
useful and not cause significant adverse effects.80
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Fatigue: Levodopa, modafinil, and methyphenidate can all be used to treat fatigue
associated with Parkinson’s disease.81
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Anxiety: A short-acting benzodiazepine (e.g., alprazolam, oxazepam) or
buspirone can be used to treat anxiety associated with Parkinson’s disease.82
These drugs must be used carefully in this patient population because
oversedation could increase the risk of falling. Cognitive behavioral therapy has
also been used successfully.83
SUMMARY
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Parkinson’s disease is a chronic, progressive neurological disease.
Parkinson’s disease is the second-most common neurodegenerative disease.
Parkinson’s disease is progressively more common as people age; most cases
occur in people over the age of 60.
The disease is more common in men than in women.
Parkinson’s disease is caused by destruction of dopaminergic neurons.
Most cases of Parkinson’s disease are idiopathic in nature.
Some cases of Parkinson’s disease are caused by genetic or environmental factors.
Parkinson’s disease causes a significant increase in morbidity and mortality; it is
very disabling and debilitating.
Bradykinesia, tremor, and muscular rigidity are the characteristic motor signs of
Parkinson’s disease.
Depression, psychosis, dementia, and anxiety commonly occur in the patient
population with Parkinson’s disease. These increase the intensity and frequency
of the motor signs and are prognostic for an earlier death.
There is no cure for Parkinson’s disease.
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The clinical course of Parkinson’s disease cannot – at this time – be significantly
altered. Over time, the patient’s condition worsens.
Most medications used for Parkinson’s disease supply a source of dopamine,
decrease the breakdown of dopamine, or act as dopamine agonists.
Levodopa/carbidopa is the most commonly used medication used for treating
Parkinson’s disease.
Anticholinergic medications and medications that inhibit the breakdown of
acetylcholine can also be used.
There is some evidence that certain medications may slow the pathological
process of Parkinson’s disease, but this evidence is inconclusive.
Surgery using deep brain stimulation has been shown to be effective in certain
patients who have Parkinson’s disease.
Lesion therapy is seldom used and transplant therapy at this point has not been
effective or is still experimental.
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