Functional correlates of strategy formation and verbal suppression in Parkinson's disease

• Type of Material: Article
• Authors: Megan L. Isaacs, University of Queensland; Katie L. McMahon, University of Queensland; Anthony J. Angwin, University of Queensland; Bruce Crosson, Emory University; David A. Copland, University of Queensland
• Language: English
• Date: 2019-01-01
• Publisher: Elsevier: Creative Commons
• Publication Version: Final Published Version
• Copyright Statement: © 2019 The Authors
• License: Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1016/j.nicl.2019.101683
• Title of Journal or Parent Work: NeuroImage: Clinical
• ISSN: 2213-1582
• Volume: 22
• Start Page: 101683
• End Page: 101683
• Grant/Funding Information: D. Copland was supported by the University of Queensland Vice Chancellor's Fellowship and ARC Future Fellowship.; This work is supported by the Australian Research Council [grant number DP120104420].; M. Isaacs was supported by an Australian Government Research Training Program Scholarship and the Asia-Pacific Centre for Neuromodulation.
• Keywords: fMRI; Parkinson's disease; Prefrontal cortex; Inhibition; Lexical-semantics
• Research Categories: Health Sciences, Radiology; Biology, Neuroscience; Psychology, Cognitive

Abstract

Individuals with Parkinson's disease (PD) have shown impaired performance on the verbal suppression component of the Haylings Sentence Completion Test (HSCT). The present study aimed to determine whether this performance related to (i) the inability to suppress a pre-potent response or (ii) difficulty in the generation of a strategy to facilitate task execution. The study adopted a novel variation of the HSCT that isolated each process and employed fMRI to examine the associated neural correlates in a comparison of individuals with PD and matched healthy controls. No significant behavioral differences were detected between these two groups. However, fMRI results revealed atypical underlying neural activity in the PD group. Controls exhibited increased activation in the left dorsolateral prefrontal cortex and striatum when generating a response independently, relative to generation when a supporting strategy was provided. The PD group demonstrated the opposite pattern of activation, in addition to greater recruitment of right hemisphere regions. This pattern of activation was postulated to be evidence of compensatory mechanisms, acting to bolster the output of frontostriatal circuits compromised by disease pathology.