ePoster

LIMITED CORTICAL INVOLVEMENT IN ASSOCIATIVE LEARNING DEFICITS IN TOURETTE SYNDROME

Kálmán Tótand 5 co-authors

Albert Szent-Györgyi Medical School, University of Szeged

FENS Forum 2026 (2026)
Barcelona, Spain
Board PS07-10AM-337

Presentation

Date TBA

Board: PS07-10AM-337

Poster preview

LIMITED CORTICAL INVOLVEMENT IN ASSOCIATIVE LEARNING DEFICITS IN TOURETTE SYNDROME poster preview

Event Information

Poster Board

PS07-10AM-337

Abstract

Previous studies demonstrated that children with Tourette syndrome show impaired performance during the learning phase of visually guided associative learning tasks, while performance during the test phase shows no alteration compared to that of healthy controls. The aim of the present study was to determine whether this learning deficit is associated with alterations in cortical electrical activity and functional connectivity.
Sixty-four channel EEG was recorded during a visually guided associative learning task, which includes acquisition and test phases. Following preprocessing, data were epoched time-locked to button press, which shows the decision of the participant. Group-level differences in cortical oscillatory power were assessed using cluster-based permutation statistics across multiple frequency bands. In addition, phase-based functional connectivity (wPLI) was examined.
Cluster-based permutation analysis revealed no significant group differences in cortical oscillatory power during either the learning or test phases across frequency bands. Connectivity analysis, however, identified a focal alteration in low-beta (13–20 Hz) phase synchronization between the right anterior frontal and centroparietal regions during the learning phase in children with Tourette syndrome. No connectivity differences were observed during the test phase.
The absence of cortical oscillatory differences, together with a highly focal connectivity alteration, suggests that learning-related deficits in Tourette syndrome originate primarily from non-cortical dysfunction. Instead, these findings are consistent with a predominantly subcortical mechanism, likely involving basal ganglia–related learning circuits, with limited or secondary cortical involvement. This interpretation aligns with established models of Tourette syndrome pathophysiology and highlights the importance of subcortical systems in associative learning impairments.

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