The Effects of Galvanic Vestibular Stimulation on Motor Cortical Excitability

Galvanic vestibular stimulation (GVS) can reduce the symptoms of numerous neurological conditions including episodic migraine, parkinsonism, acquired prosopagnosia and hemi-spatial neglect. Despite these preliminary findings, the mechanism underlying these therapeutic effects are still poorly understood. Functional imaging conducted during GVS indicates a potential change in cortical activation across widespread regions of the brain. However, these imaging studies are limited because they lack a functional correlate and rely on a relatively crude and poorly localised measure of excitability. The current study aimed to investigate the effects of GVS on cortical excitability via the more precise markers of TMS-induced motor-evoked potentials (MEPs) and movement-related cortical potentials (MRCPs), surrogate markers of long-term potentiation (LTP) and long-term depression (LTD) which are often compromised in neurological patients. Experiment 1 (N = 40) examined the effects of 25 minutes 1mA noisy, bipolar GVS on MEPs in the minutes and subsequent day after stimulation. Relative to sham, GVS reduced MEP amplitude 24 hours following stimulation for all participants who showed high cortical excitability at baseline. Experiment 2 (N = 24) followed a similar pre-post design to Experiment 1, however, the effects of GVS on the MRCP were measured via the Bereitschaftspotential (BP) while participants performed voluntary finger movements. Most likely owing to methodological shortcomings, Experiment 2 failed to obtain a BP response at baseline so did not enable the study hypothesis to be assessed. Experiment 3 was designed to both address these potential shortcomings and increase clinical relevance, recruiting a single individual with right hemisphere chronic stroke. A BP at baseline was observed but there was no evidence of GVS modulation. In sum, whilst Experiments 2 and 3 yielded few novel insights, the results of Experiment 1 indicate that GVS inhibits cortical excitability, potentially reflecting LTD-like effects. This observation may help explain its reported therapeutic benefits and also suggests that is should be applied to other disorders that involve cortical hyper-excitability