Hyperfunctioning and -binding of procedural memory processes in Tourette syndrome: the role of neurophysiological and structure-related neurobiochemical processes

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Tourette syndrome (TS) is a multifaceted neurodevelopmental disorder characterized by at least one vocal tic and multiple motor tics, which are not explained by medications or another medical condition. Recent studies presented enhanced procedural memory functions in TS. Both atypical cognition and tics in TS are thought to be related to the alterations of corticostriatal loops. However, a mechanistic link between procedural hyperfunctioning in TS, tics and structural alterations is missing. The goal of this project is to examine the neurophysiological and structure-related neurobiochemical processes underlying a hyperfunctioning of procedural memory in TS. For that, I propose two work packages to examine the role of cortico-striatal networks in learning probabilistic information in TS, by testing the link amongst procedural learning performance, its neurophysiological correlates (ERPs, and task-related EEG functional connectivity). EEG connectivity during procedural learning will be examined for the first time in TS along with ERPs to understand the dynamic interplay between brain networks during learning, memory reactivation, and memory interference. Moreover, EEG beamforming methods will be applied. Guided by a theoretical approach of procedural hyperfunctioning in TS, the project will provide novel fundamental insight into procedural processing and tic formation in TS at multiple levels. Namely, Hommel’s Theory of Event Coding will be used as a framework to analyze the binding of information during learning and changing the acquired information in a new environment. This approach will be used as a cognitive model of how tics develop, and how can they be modified. In sum, I propose a series of multilevel, neuroscientific experiments to dovetail the theory of tic formation and cognition in TS.