Objective: Given the GABAergic nature of TMS-evoked EEG activity, we tested whether GABAergic deficits in Huntington’s disease (HD) patients produce any significant change in TMS-EEG measures, compared to healthy volunteers (HV).

Background: HD is an autosomal dominant neurodegenerative disorder characterized by cortical and striatal pathology. One of the first HD-related alterations is the progressive degeneration of cannabinoid type 1 receptors in basal ganglia, which are highly expressed in GABAergic neurons of the striatum.

Methods: We stimulated the primary motor cortex (M1) and premotor area (PM) with single-pulse TMS (90% of RMT) while recording EEG in 16 HD patients and 16 HV. TMS-evoked activity was analyzed in time, space and oscillatory domain.

Results: Time-domain analysis revealed a strong reduction of later M1-TMS-evoked activity (150-250 ms after TMS) in HD patients, compared to HV. The effect was prominent over the site of stimulation. Oscillatory-domain analysis revealed that this effect was due to a strong desynchronization of TMS-evoked responses of HD patients in the theta and alpha range.

Conclusions: The observed decrease of GABAb-mediated TEPs may be a consequence of lower GABAergic inhibition that causes excitotoxicity in HD patients. This interpretation is corroborated by the weak synchronization in slow (theta and alpha) and late (150-250 ms) post-synaptic potentials evoked by TMS, that are thought to be of GABAb origin.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/tms-eeg-markers-of-inhibitory-deficits-in-huntingtons-disease/