The Neuropsychology of Parkinson’s Disease

Abstract

Parkinson’s disease (PD) is among the most common neurological disorders among the elderly and estimates of its prevalence in the United States are approximately 0.5% to 1% among individuals 65 to 69 years of age, rising to 1% to 3% among individuals older than 80 years of age. 1 Although idiopathic PD is most often first diagnosed in the sixth decade of life, there are many conditions which can mimic its presentation throughout the lifespan. This so-called parkinsonism may stem from long-term use of neuroleptics, other neurodegenerative diseases, such as supranuclear palsy, or even substance abuse. Nonetheless, the diagnosis of idiopathic PD is made via clinical symptoms, particularly the key motor symptoms of tremor, bradykinesia or hypokinesia, muscular rigidity, and postural instability. These symptoms are a direct result of the neuropathology which is characterized by loss of cells in the substantia nigra and other brain-stem nuclei that cause a significant diminishment of dopamine throughout the basal ganglia and other brain regions. Given the intimate connections of circuits between the basal ganglia and frontal lobe and the role such circuits play in cognition, it is not surprising that cognitive deficits are also observed in PD. Whereas typically mild at the beginning of the disease, these may later progress to full-blown dementia in some patients. This article is a brief overview of the cognitive or neuropsychological deficits associated with PD, as well as the effect newer neurosurgical interventions for PD have on cognition. The neuropsychological measures described below and more detailed information on PD are reviewed more fully in Lezak’s seminal text Neuropsychological Assessment, 2 as well as the more convenient Clinical Neuropsychol