There is a gradual degeneration of the midbrain area known as the substantia nigra.
The neurons use the neurotransmitter dopamine to send their signals from cell to
cell. The loss of neurons within the substantia nigra continues and results in dimin-
ished voluntary fine motor skills due to dopamine loss. There is also development
of sympathetic noradrenergic lesions, causing norepinephrine loss within the sym-
pathetic nervous system. There is excess effect of the excitatory neurotransmitter
acetylcholine on the neurons; this causes increased muscle tone, leading to rigid-
ity and tremors. There seems to be a genetic tendency towards development of
Parkinson’s disease. Environmental factors such as exposure to airborne contami-
nants, occupational chemicals, toxins, or a virus have been implicated in the devel-
opment of the disease. Typical age of onset is after the fifth decade of life.
PROGNOSIS
Parkinson’s disease is a progressive disorder and does not have a cure. The symp-
toms can be managed with medications, but will return as the medications wear off.
The dosages will need to be adjusted periodically, and additional medications may
be needed to address the side effects of the medications used. Some patients
develop mental status changes or dementia in conjunction with Parkinson’s disease.
SIGNS AND SYMPTOMS
• Mask-like facial expressions
• Slow, shuffling gait
• Pill-rolling movements of hands
• Stooping posture
• Tremor at rest
• Change in handwriting—gets progressively smaller over time
• Bradykinesia (slow movement)
• Trouble chewing or swallowing
• Drooling
• Inability to control voluntary movement (dyskinesia) and fine-skilled move-
ment, or to initiate movement—due to loss of dopamine which has an
inhibitory effect and helps refine movements while acetylcholine retains the
excitatory effect on the neurons
• Rigidity of limbs:
• Cogwheeling—there is a rhythmic stopping or interruption of the move-
ment of the extremity
• Lead pipe—no bending; resists movement completely
• Orthostatic hypotension due to lack of norepinephrine within the sympa-
thetic nervous system, affecting the cardiovascular system
TREATMENT
• Administer antiparkinsonian agents which are able to cross the blood-brain
barrier. These drugs absorb better on an empty stomach:
• levodopa
• carbidopa-levodopa
• Administer dopamine receptor agonists to act directly on the dopamine
receptor sites:
• pergolide
• bromocriptine
• pramipexole
• ropinirole
• Administer selegiline, a selective monoamine oxidase B inhibitor that slows
the breakdown of dopamine and allows lower doses of levodopa to be used
because it prolongs its effect.
• Administer catechol O-methyltransferase (COMT) inhibitors which help block
the breakdown of levodopa:
• entacapone
• tolcapone
• Administer acetylcholine blocking drugs to decrease tremor and rigidity in
patients:
• biperiden
• benztropine mesylate
• procyclidine
• orphenadrine
• trihexyphenidyl
• Diet high in protein and calories.
• Soft food diet.
• Physical therapy.
NURSING DIAGNOSES
• Activity intolerance
• Impaired mobility
• Risk for injury
NURSING INTERVENTION
• Monitor neurological status for changes.
• Monitor respiratory status for changes.
• Encourage self-care, allow patient extra time.
• Encourage exercise; assist with passive ROM if necessary.
• Weigh patient.
• Record food intake.
• Explain to the patient:
• Importance of following medication time schedule as well as effects of
medication wearing off.
• Reduce risk of falls at home.
