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LEARNING OBJECTIVES
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 clinical signs, symptoms, and assessment tools.
When 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 as well as the use of adjunctive medications.
Recognize and treat 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.
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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; however, nonmotor symptoms are also common and may present earlier than these motor symptoms. There is no cure, and treatment aims at controlling symptoms and maintaining quality of life (QOL) or functioning.1-3
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EPIDEMIOLOGY AND ETIOLOGY
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PD is the second most common neurodegenerative illness occurring in 1% to 2% of people older than 60 years.2 While it is typically diagnosed in older patients, juvenile onset is possible but rare, and an early onset before age 50 can also occur. Genetics play a role in this disorder with about 10% to 15% of patients having an affected relative.2,4
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The etiology of neuron degeneration in PD remains unknown, but aging is a primary risk factor.4 Pigmented cells in the substantia nigra that make and store dopamine are lost.3 Neurons have lost about 30% to 70% of their activity in the striatum at the onset of PD.2 Cortical Lewy bodies along with Lewy neurites in the central nervous system (CNS) and the gastrointestinal (GI) system may explain some of the nonmotor symptoms (e.g., psychiatric, autonomic) of PD.1,5
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The cause of cell death and PD symptoms is likely multifactorial, with both endogenous and exogenous factors such as genetic susceptibility and environmental toxin exposure (eg, pesticides and solvents).6 Numerous genetic mutations are linked to PD, and particular mutations may predict early versus late onset of the disease, possibly explaining why the presentation and course of illness varies substantially. Genome-wide association studies have linked at least 26 single-nucleotide polymorphisms (SNPs) to PD.6 In contrast, protective factors have also been documented and include a history of smoking and coffee consumption.6
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