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Upon completion of the chapter, the reader will be able to:

  1. Describe the pathophysiology of Parkinson disease (PD) related to neurotransmitter involvement and targets for drug therapy in the brain.

  2. 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).

  3. For a patient initiating therapy for PD, recommend appropriate drug therapy and construct patient-specific treatment goals.

  4. Recognize and recommend appropriate treatment for nonmotor symptoms.

  5. Formulate a plan to minimize patient “off-time” and maximize “on-time” including timing, dosage, and frequency of medications.

  6. Recognize and treat various motor complications that develop as PD progresses.

  7. Construct appropriate patient counseling regarding medications and lifestyle modifications for a patient with PD.

  8. Develop a monitoring plan to assess effectiveness and adverse effects of treatment.


KEY CONCEPT 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 the ability to generate body movements. Cardinal features of PD include tremor at rest, rigidity, akinesia/bradykinesia, and postural instability. There is no cure, and treatment is aimed at controlling symptoms and slowing disease progression.


PD affects approximately 1 million Americans, and a lifetime risk of developing the disease is 1.5%. Median age of onset is 60 years, but about 10% of people with PD are younger than 45 years. The average duration of time 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 has been implicated as a primary risk factor. Other explanations for the cell death may include oxidative stress, mitochondrial dysfunction, increased concentrations of excitotoxic amino acids and inflammatory cytokines, immune system disorders, trophic factor deficiency, signal-mediated apoptosis, and environmental toxins. Conditions that may promote oxidative stress include increased monoamine oxidase-B (MAO-B) metabolism or decreased glutathione clearance of free radicals.2,3,4,5

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 A combination of inducers of cell death and genetic mutations may be at play in the development of PD.2 In PD pigmented cells in the substantia nigra that make and store dopamine are lost. When patients are diagnosed, they have lost 50% to 60% of their dopamine neurons located here, and the remaining neurons elsewhere in the central nervous system (CNS) may be dysfunctional. Neurons have lost about 80% ...

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