Neural correlates of impaired response inhibition in the antisaccade task in Parkinson’s disease

• Published in: Behavioural brain research 2022-03, Vol.422, p.113763-113763, Article 113763
• Main Authors: Waldthaler, Josefine, Vinding, Mikkel C., Eriksson, Allison, Svenningsson, Per, Lundqvist, Daniel
• Format: Article
• Language: English
• Subjects: Antisaccade; Executive function; Eye-tracking; Impulsivity; Inhibition control; Parkinson’s disease
• ISSN: 0166-4328; 1872-7549
• DOI: 10.1016/j.bbr.2022.113763

Deficits in response inhibition are a central feature of the highly prevalent dysexecutive syndrome found in Parkinson’s disease (PD). Such deficits are related to a range of common clinically relevant symptoms including cognitive impairment as well as impulsive and compulsive behaviors. In this study, we explored the cortical dynamics underlying response inhibition during the mental preparation for the antisaccade task by recording magnetoencephalography (MEG) and eye-movements in 21 non-demented patients with early to mid-stage Parkinson’s disease and 21 age-matched healthy control participants (HC). During the pre-stimulus preparatory period for antisaccades we observed: •a preparation-related increase in beta band activity in the right dorsolateral prefrontal cortex (DLPFC) of HC (n = 15) for antisaccades compared with prosaccades that was not detectable in the PD group (n = 17);•a significant attenuation of the preparation-related increase in alpha band power in bilateral FEF and reduced alpha band connectivity between the right DLPFC and right FEF in the PD group compared with HC, suggesting reduced top-down control to inhibit pre-potent activation of FEF in PD; and•a positive correlation between the magnitude of pre-stimulus beta desynchronization in FEF and subsequent antisaccade latency in PD and HC, indicating a relationship between preparatory beta band modulation and effectiveness of subsequent antisaccade execution. Taken together, the results indicate that alterations in pre-stimulus prefrontal alpha and beta activity hinder proactive response inhibition and in turn result in higher error rates and prolonged response latencies in PD.