Parkinson’s Disease

Named for the English physician who first accurately described the disease in 1817,
Parkinson’s disease characteristically produces progressive muscle rigidity, akinesia,
and involuntary tremors. Deterioration commonly progresses, culminating in death,
which usually results from aspiration pneumonia or some other infection.
Also called parkinsonism, paralysis agitans , or shaking palsy, Parkinson’s disease is one
of the most common crippling diseases in the United States. It affects males more
commonly than females and usually occurs in middle age or later. Due to
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advances in treatment of complications, increased patient longevity is more common.

Causes
The cause of Parkinson’s disease is unknown in most cases. However, studies of the
extrapyramidal brain nuclei (corpus striatum, globus pallidus, substantia nigra) have
established that in this disease a dopamine deficiency prevents affected brain cells from
performing their normal inhibitory function within the central nervous system.
Some cases of Parkinson’s disease are caused by exposure to toxins (such as
manganese dust and carbon monoxide), which destroy cells in the substantia nigra.
Complications
Common complications associated with Parkinson’s disease include injury from falls,
food aspiration because of impaired voluntary movements, urinary tract infections, and
skin breakdown as the patient becomes less mobile.
Assessment
The patient history notes the cardinal symptoms of Parkinson’s disease, which include
muscle rigidity, akinesia, and an insidious tremor known as unilateral pill-roll tremor,
which begins in the fingers. Although the patient often can’t pinpoint exactly when
tremors began, he typically reports that they increase during stress or anxiety and
decrease with purposeful movement and sleep. He may also report dysphagia.
The patient may complain that he becomes fatigued when he tries to perform activities
of daily living and that he experiences muscle cramps of the legs, neck, and trunk. He
may also mention oily skin, increased perspiration, insomnia, and mood changes. You
may note dysarthria and find that the patient speaks in a high-pitched monotone.
Inspection may reveal drooling, a masklike facial expression, and difficulty walking. The
patient’s gait commonly lacks normal parallel motion and may be retropulsive or
propulsive. In addition, the patient may demonstrate a loss of posture control when he
walks. Typically, the patient who loses posture control walks with the body bent
forward. These signs result from akinesia.
You may note other results of akinesia, such as oculogyric crisis (eyes fixed upward,
with involuntary tonic movements) or blepharospasm (eyelids closed). You may also
discover that the patient takes a long time to initiate movement to perform a purposeful
action.
In addition to gait changes, musculoskeletal and neurologic assessment may point to
muscle rigidity that results in resistance to passive muscle stretching. Such rigidity may
be uniform (lead-pipe rigidity) or jerky (cogwheel rigidity). The patient may also pivot
with difficulty and lose his balance easily.
As you assess this patient, keep in mind that Parkinson’s disease itself doesn’t impair
the intellect but that a coexisting disorder, such as arteriosclerosis, may.
Diagnostic tests
Diagnosis is based primarily on history and physical examination. Diagnosis is confirmed
when the patient’s symptoms decrease after anti-parkinsonism drugs are initiated.
Although urinalysis may reveal decreased dopamine levels, laboratory test results
usually have little value in identifying Parkinson’s disease.
Computed tomography scan or magnetic resonance imaging  may be performed to rule
out other disorders such as intracranial tumors. A conclusive diagnosis is possible only
after ruling out other causes of tremor, such as involutional depression, cerebral
arteriosclerosis and, in patients younger than age 30, intracranial tumors, Wilson’s
disease, or phenothiazine or other drug toxicity.
Treatment
Because no cure exists for Parkinson’s disease, treatment aims to relieve symptoms and
keep the patient functional as long as possible. Treatment consists of drugs, physical
therapy and, in severe disease unresponsive to drugs, stereotaxic neurosurgery.
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Some experimental procedures show promise as treatments for Parkinson’s disease.

Drug therapy usually includes levodopa, a dopamine replacement that’s most effective
for the first few years after it’s initiated. The drug is given in increasing doses until
signs and symptoms are relieved or adverse reactions appear. Because adverse
reactions can be serious, levodopa is commonly given in combination with carbidopa (a
dopadecarboxylase inhibitor) to halt peripheral dopamine synthesis. The patient may
receive bromocriptine as an additive to reduce the levodopa dose. Drug dosage, type,
and frequency may be changed, or a 10–day drug hold (especially for levodopa) may be
prescribed if tolerance or toxicity occurs.
When levodopa proves ineffective or too toxic, alternative drug therapy includes
anticholinergics (such as trihexyphenidyl or benztropine) and antihistamines (such as
diphenhydramine).
Antihistamines may help decrease tremors because of their central anticho-linergic and
sedative effects. Anticholinergics may be used to control tremors and rigidity. They may
also be used in combination with levodopa.
Amantadine, an antiviral agent, is used early in treatment to reduce rigidity, tremors,
and akinesia. Selegiline, an enzyme-inhibiting agent, allows conservation of dopamine
and enhances the therapeutic effect of levodopa. Monoamine oxidase inhibitors are
given to reduce the metabolic breakdown of dopamine. Catechol O-methyltransferase
inhibitors are given to slow the breakdown of levodopa. Research in oxidative stress
therapy has caused a controversy in drug therapy for Parkinson’s disease. Although
levodopa and carbidopa have traditionally been first-line drug treatment, they may
accelerate the disease process. Selegiline following levodopa and carbidopa treatment
may be more effective.
Pramipexole dihydrochloride (Mirapex), a dopamine agonist, delays the onset of motor
complications in patients with Parkinson’s disease. The adverse effects usually
experienced with the long-term use of levodopa are reduced with the use of this agent.
Tricyclic antidepressants may be given to decrease the depression that commonly
accompanies the disease.
When drug therapy fails, stereotaxic neurosurgery sometimes offers an effective
alternative. In this procedure, electrical coagulation, freezing, radioactivity, or
ultrasound destroys the ventrolateral nucleus of the thalamus to prevent involuntary
movement. Such neurosurgery is most effective in comparatively young, otherwise
healthy people with unilateral tremor or muscle rigidity. Like drug therapy,
neurosurgery is a palliative measure that can only relieve symptoms.
Deep brain stimulation is another procedure that may be performed to relieve
symptoms. It involves implanting an electrode in the affected area of the brain to
deliver electrical impulses that provide relief from tremors, rigidity, slowness of
movement, and stiffness. Deep brain stimulation may also help balance problems
associated with Parkinson’s disease. The electrode is powered by a battery pack
implanted under the skin in the chest.
Physical therapy complements drug treatment and neurosurgery to maintain the
patient’s normal muscle tone and function. Appropriate physical therapy includes both
active and passive range-of-motion exercises, routine daily activities, walking, and
baths and massage to help relax muscles.