Seemungal, B. M. | Search bioRxiv

bioRxiv2024

Vestibular prepulse inhibition of the human blink reflex

ObjectiveAuditory and somatosensory prepulses are commonly used to assess prepulse inhibition (PPI). The effect of a vestibular prepulse upon blink reflex (BR) excitability has not been hitherto assessed. MethodsTwenty-two healthy subjects and two patients with bilateral peripheral vestibular failure took part in the study. Whole body yaw rotation in the dark provided a vestibular inertial prepulse. BR was electrically evoked after the end of the rotation. The area-under-the-curve (area) of the BR responses (R1, R2, and R2c) was recorded and analysed. ResultsA vestibular prepulse inhibited the R2 (p < 0.001) and R2c area (p < 0.05). Increasing the angular acceleration did not increase the R2/R2c inhibition (p>0.05). Voluntary suppression of the vestibular-ocular reflex did not affect the magnitude of inhibition (p>0.05). Patients with peripheral vestibular failure did not show any inhibition. ConclusionsOur data support a vestibular-gating mechanism in humans. SignificanceThe main brainstem nucleus mediating PPI - the pedunculopontine nucleus (PPN) - is heavily vestibular responsive, which is consistent with our findings of a vestibular-mediated PPI. Our technique may be used to interrogate the fidelity of brain circuits mediating vestibular-related PPN functions. Given the PPNs importance in human postural control, our technique may also provide a neurophysiological biomarker of balance. HighlightsO_LIThis is the first report of a vestibular prepulse inhibition of the blink reflex. C_LIO_LIA vestibular prepulse inhibits the R2/R2c area in healthy subjects but not in patients with bilateral peripheral vestibular failure. C_LIO_LIVestibular PPI is a potential neurophysiological marker of vestibular-motor integration at the brainstem level. C_LI

neuroscience↗

bioRxiv2021

Vestibular Agnosia is linked to abnormal functional brain networks

Vestibular Agnosia - where peripheral vestibular activation triggers the usual reflex nystagmus response but with attenuated or no self-motion perception - is found in brain disease with disrupted cortical network functioning, e.g. traumatic brain injury (TBI) or neurodegeneration (Parkinsons Disease). Patients with acute focal hemispheric lesions (e.g. stroke) do not manifest vestibular agnosia. Thus brain network mapping techniques, e.g. resting state functional MRI (rsfMRI), are needed to interrogate functional brain networks mediating vestibular agnosia. Whole-brain rsfMRI was acquired from 39 prospectively recruited acute TBI patients with preserved peripheral vestibular function, along with self-motion perceptual thresholds during passive yaw rotations in the dark. Following quality-control checks, 25 patient scans were analyzed. TBI patients were classified as having vestibular agnosia (n = 11) or not (n = 14) via laboratory testing of self-motion perception. Using independent component analysis, we found altered functional connectivity in the right superior longitudinal fasciculus and left rostral prefrontal cortex in vestibular agnosia. Moreover, regions of interest analyses showed both inter-hemispheric and intra-hemispheric network disruption in vestibular agnosia. In conclusion, our results show that vestibular agnosia is mediated by bilateral anterior and posterior network dysfunction and reveal the distributed brain mechanisms mediating vestibular self-motion perception.

neuroscience↗