1434 SECTION 11 Problems Related to Movement and Coordination
rest and is aggravated by emotional stress or increased concen-
tration. The hand tremor is described as “pill rolling” because
the thumb and forefinger appear to move in a rotary fashion as
if rolling a pill, coin, or other small object. Tremor can also
involve the diaphragm, tongue, lips, and jaw but rarely causes
shaking of the head.
Unfortunately, in many people a benign essential tremor is
mistakenly diagnosed as PD. Essential tremor occurs during
voluntary movement, has a more rapid frequency than parkin-
sonian tremor, and is often familial.
Rigidity. Rigidity, the second sign of the triad, is the increased
resistance to passive motion when the limbs are moved through
their range of motion. Parkinsonian rigidity is typified by cog-
wheel rigidity, or a jerky quality, as if there were intermittent
catches in the movement of a cogwheel, when the joint is moved
passively. Sustained muscle contraction causes the rigidity and
consequently elicits complaints of muscle soreness; feeling tired
and achy; or pain in the head, the upper body, the spine, or the
legs. Another consequence of rigidity is slowness of movement
because it inhibits the alternating of contraction and relaxation
in opposing muscle groups (e.g., biceps and triceps).
Bradykinesia. Bradykinesia is particularly evident in the
loss of automatic movements, which is secondary to the physi-
cal and chemical alteration of the basal ganglia and related
structures in the extrapyramidal portion of the CNS. In the
unaffected patient, automatic movements are involuntary and
occur subconsciously. They include blinking of the eyelids,
swinging of the arms while walking, swallowing of saliva, self-
expression with facial and hand movements, and minor move-
ment of postural adjustment.
The patient with PD does not execute these movements and
lacks spontaneous activity. This accounts for the stooped pos-
ture, masked face (deadpan expression), drooling of saliva, and
shuffling gait ( festination) that are characteristic of a person
with this disease. The posture is that of a slowed “old man”
image, with the head and trunk bent forward and the legs con-
stantly flexed (Fig. 59-9).
Postural instability is common. Patients may complain of
being unable to stop themselves from going forward (propul-
Blank facial Forward tilt
to posture
expression
Slow, monotonous,
slurred speech
Tremor
Short, shuffling gait
FIG. 59-9 Characteristic appearance of a patient with Parkinson’s disease.
sion) or backward (retropulsion). Assessment of postural insta-
bility includes the “pull test,” in which the examiner stands
behind the patient and gives a tug backward on the shoulder,
causing the patient to lose his or her balance and fall backward.
In addition to the motor signs of PD, many nonmotor symp-
toms are common. They include depression, anxiety, apathy,
fatigue, pain, constipation, impotence, and short-term memory
impairment. Sleep problems are common in patients with PD
and include difficulty staying asleep at night, restless sleep,
nightmares, and drowsiness or sudden sleep onset during
the day.18
Complications
As the disease progresses, complications increase. These include
motor symptoms (e.g., dyskinesias [spontaneous, involuntary
movements], weakness, akinesia [total immobility]), neurologic
problems (e.g., dementia), and neuropsychiatric problems (e.g.,
depression, hallucinations, psychosis). As PD progresses, it
often results in a severe dementia, which is associated with an
increase in mortality.
As swallowing becomes more difficult (dysphagia), malnu-
trition or aspiration may result. General debilitation may lead
to pneumonia, urinary tract infections, and skin breakdown.
Orthostatic hypotension may occur in some patients and,
along with loss of postural reflexes, may result in falls or other
injury.22
Diagnostic Studies
Because there is no specific diagnostic test for PD, the diagnosis
is based on the history and the clinical features. A firm diagnosis
can be made only when at least two of the three signs of the
classic triad are present: tremor, rigidity, and bradykinesia. The
ultimate confirmation of PD is a positive response to antipar-
kinsonian drugs. Research is ongoing regarding the role of
genetic testing and MRI in diagnosing patients with PD.23
Collaborative Care
Because PD has no cure, collaborative care focuses on relieving
the symptoms (Table 59-17).
Drug Therapy. Drug therapy for PD is aimed at correcting
the imbalance of neurotransmitters within the CNS. Antipar-
kinsonian drugs either enhance the release or the supply of DA
(dopaminergic) or antagonize or block the effects of the overac-
tive cholinergic neurons in the striatum (anticholinergic) (see
Fig. 59-7). Levodopa with carbidopa (Sinemet) is often the first
drug used. Levodopa is a chemical precursor of DA and can
TABLE 59-17 COLLABORATIVE CARE
Parkinson’s Disease
Diagnostic
• History and physical examination
• Tremor, rigidity, and bradykinesia
• Positive response to antiparkinsonian drugs
• MRI
• Rule out side effects of phenothiazines, reserpine,
benzodiazepines, haloperidol
Collaborative Therapy
• Antiparkinsonian drugs (see Table 59-18)
• Deep brain stimulation
• Ablation surgery