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Upon completion of the chapter, the reader will be able to:
Describe the pathophysiology of Parkinson disease (PD) related to neurotransmitter involvement and targets for drug therapy.
Recognize the cardinal motor symptoms of PD and determine a patient’s clinical status and disease progression based on the Movement Disorder Society Unified Parkinson Disease Rating Scale (MDS UPDRS).
For a patient initiating therapy for PD, recommend appropriate drug therapy and construct patient-specific treatment goals.
Recognize and recommend appropriate treatment for nonmotor symptoms.
Formulate a plan to minimize patient “off-time” and maximize “on-time” including timing, dosage, and frequency of medications.
Recognize and treat various motor complications in PD.
Construct appropriate patient counseling regarding medications and lifestyle modifications for PD.
Develop a monitoring plan to assess effectiveness and adverse effects of treatment.
Parkinson disease (PD) is a slow, progressive neurodegenerative disease of the extrapyramidal motor system. Dopamine neurons in the substantia nigra are primarily affected, and degeneration of these neurons causes a disruption in smooth motor control. Cardinal features of PD include tremor at rest, rigidity, akinesia/bradykinesia, and postural instability. There is no cure, and treatment aims at controlling symptoms and maintaining quality of life (QOL) or functioning.
EPIDEMIOLOGY AND ETIOLOGY
PD affects approximately 1 million Americans, and a lifetime risk of developing the disease is 1.5%. Median age of the onset is 60 years, but about 10% of people with PD are younger than 45 years. The average time span from diagnosis to death is about 15 years. Approximately 15% of patients with PD have a first-degree relative with the disease.1,2
The etiology of neuron degeneration in PD remains unknown, but aging is a primary risk factor. Thus, as the fraction of the population that is elderly continues to increase, this disease may see a subsequent increase in prevalence. Cell death may be caused by oxidative stress, mitochondrial dysfunction, increased excitotoxic amino acids and inflammatory cytokines, immune system disorders, signal-mediated apoptosis, and environmental toxins. Oxidative stress may result from increased monoamine oxidase-B (MAO-B) metabolism or decreased glutathione clearance of free radicals.2–5
Genetic mutations such as those in LRRK2 have been linked to PD, and particular mutations may predict early versus late onset of the disease.2,3 Most likely, a combination of inducers of cell death and genetic mutations are involved in PD.2 Pigmented cells in the substantia nigra that make and store dopamine are lost. At the time of diagnosis, 50% to 60% of dopamine neurons located here may be dysfunctional. Neurons have lost about 80% of their activity in the striatum at the onset of PD. Cortical Lewy bodies along with Lewy neurites in the central nervous system (CNS) ...