Profile of cognitive impairment in Parkinson's disease

Abstract

Cognitive impairment (CI) is a common nonmotor complication of Parkinson's disease (PD), and is associated with significant disability for patients and burden for caregivers. Similar to motor symptoms, the characteristics of CI in PD can be quite variable, both in terms of what cognitive domains are impaired, and the timing of onset and rate of progression. This review will examine the profile of cognitive domain impairments observed in PD, with a focus on early CI (without dementia). We will also discuss possible relationships between specific cognitive domain impairments in PD and pathological processes such as Lewy-related pathology and Alzheimer's disease. It is our hypothesis that the specific characteristics of CI observed in individual PD patients provide clues to the underlying pathological processes, and that understanding the biological basis of this clinical phenomenon will assist in directing disease-specific treatments. Given the high lifetime risk for CI in PD, it is imperative that we improve our understanding and treatments for this common and disabling problem in PD.

Figure 1

A simple schema for understanding declarative memory. Information to be remembered (black box on the left) must be attended to and filtered through perceptual processes (e.g. language or visuoperceptual functions) before it can enter short‐term or working memory (active information). A limited amount of active information can be held in short‐term memory where it is available for mental operations or behavioral responses. The hippocampus is essential for encoding, but not for storing or retrieving, declarative memories from the long‐term store of information. As it is needed, information is retrieved from long‐term memory (store of information) and transferred to short‐term memory where it is once again available for use. Impaired attention and frontal‐executive functions, which are common in Parkinson's disease (PD), are most likely to influence gathering of information into short‐term memory and retrieval of information from long‐term storage. Therefore, memory output should be improved when attentional demands are reduced and retrieval strategies are provided. In contrast, Alzheimer's disease reduces the amount of information encoded; improving attention and providing retrieval strategies should be less likely to help the person with Alzheimer's disease than the person with PD. A finding that immediate memory was intact and that delayed memory was impaired in a group of PD patients with cognitive impairment without dementia (CIND) would suggest an amnestic CIND subtype distinct from the expected “so‐called subcortical” picture characterized by impaired attention and executive skills.