Lexical-semantic inhibitory mechanisms in Parkinson's disease as a function of subthalamic stimulation

Joanna E. Castner, David A. Copland, Peter A. Silburn, Terry J. Coyne, Felicity Sinclair, Helen J. Chenery*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

40 Citations (Scopus)


Inhibitory control may be affected by Parkinson's disease (PD) due to impairment within the non-motor basal ganglia-thalamocortical circuits. The present study aimed to identify the effects of chronic stimulation of the subthalamic nucleus (STN) on lexical-semantic inhibitory control. Eighteen participants with PD who had undergone surgery for deep brain stimulation (DBS) of the STN, completed a picture-word interference (PWI) task and the Hayling test in on and off stimulation conditions. The results of PD participants were compared with 21 non-neurologically impaired control participants. PD participants performed no differently from controls on the PWI task, and no significant differences between on and off stimulation conditions were revealed, therefore suggesting that PD participants are not impaired in lexical-semantic interference control. In contrast, in the off stimulation condition, PD participants had significantly delayed reaction times and increased errors on the inhibition section of the Hayling test compared with the STN stimulation condition and control participants. These results suggest that PD patients are impaired in aspects of inhibitory control that are dependent on behavioural inhibition (such as the suppression of prepotent responses) and selection from competing alternatives without the presence of external cues. Furthermore, STN stimulation acts to restore these behavioural inhibitory processes. (C) 2007 Elsevier Ltd. All rights reserved.

Original languageEnglish
Pages (from-to)3167-3177
Number of pages11
Issue number14
Publication statusPublished - 2007
Externally publishedYes


Dive into the research topics of 'Lexical-semantic inhibitory mechanisms in Parkinson's disease as a function of subthalamic stimulation'. Together they form a unique fingerprint.

Cite this