• George M Opie, Ngee Foo, Maggie Killington, Michael C Ridding, and John G Semmler.
• Discipline of Physiology, Adelaide Medical School, The University of Adelaide, Adelaide, Australia.
• J. Neurotrauma. 2019 Oct 1; 36 (19): 2774-2784.

AbstractWhile the potential long-term side effects of mild traumatic brain injury (mTBI) are becoming increasingly recognized, the associated neurophysiological mechanisms remain poorly understood. However, changes in cortical inhibitory function and neuroplasticity have been suggested as possible contributing factors. The current study applied transcranial magnetic stimulation (TMS) in conjunction with electroencephalography (combined TMS-EEG) to investigate further the effects of mTBI on these processes. In 17 patients with a history of mTBI and 15 healthy control subjects with no mTBI history, paired-pulse TMS-EEG measures of short- (SICI) and long-interval intracortical inhibition (LICI) were used to assess intracortical inhibitory function. Single-pulse TMS-EEG was used to assess neuroplastic changes in cortical excitability after application of continuous theta burst stimulation (cTBS, a plasticity inducing TMS paradigm). Inhibition of the TMS-evoked EEG potential after application of SICI and LICI was not different between groups. In contrast, the inhibitory effects of cTBS on both P30 (p < 0.05) and N45 (p = 0.04) TEP components was significantly increased in patients, with the modulation of N45 in patients significantly related to the time since injury (p = 0.04). While these results provide further evidence that inhibitory circuits involving γ-aminobutyric acid (GABA) are modified after mTBI, they place greater emphasis on the plasticity of inhibitory networks involving the GABAA receptor subtype.

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