Peripheral vestibular stimulation elicits brainstem reflex responses manifesting as a vestibular-ocular reflex nystagmus (‘VOR’) and evokes a perception of self-motion or ‘vertigo’. While VOR responses are objectively measured via eye movements, no such objective measure exists for assessing the cortical vestibular processing of self-motion. Understanding how the brain encodes vestibular-mediated self-motion could provide electrophysiological markers for clinical syndromes where reflex and perception are uncoupled, e.g. in vestibular agnosia. Hence, here we investigated the brain’s encoding of bottom-up vestibular signals, using passive yaw-plane chair rotations performed in complete darkness with simultaneous EEG. Healthy controls (n = 8) were compared to patients with bilateral vestibulopathy (BVP), either with residual function (BVP-residual; n=6) or complete loss (BVP-complete; n=1), at five acceleration levels (range: 30-150º /s2). Comparing healthy controls with BVP-residual, we found: 1) no differences in time-frequency analyses; and 2) differences in vestibular evoked potentials magnitude ( P < 0.01). Chair acceleration changes were consistently accompanied by phase-locked and induced (non-phase locked) theta-increases as well as alpha reduction in both, healthy and patients. Importantly, while the induced theta component was present in BVP-residual, it was absent in BVP-complete. Overall, findings indicate potential utility of: 1) vestibular evoked EEG responses for identifying attenuated vestibular signalling; and 2) theta activity as a cortical signature of preserved bottom-up vestibular signalling. These preliminary findings would require further investigation to confirm their functional role
Hadi et al. (Sun,) studied this question.