| Summary: | Following repeated exposure to vestibular stimulation, the vestibular response as measured by the vestibular-ocular reflex and perception of self-motion is reduced. Similarly, prolonged viewing of a visual motion stimulus results in a reduced sensitivity to the adapting motion stimulus. These phenomena of visual-vestibular desensitisation are utilised as part of treatment of patients with peripheral or central vestibular disorders. Patients typically receive vestibular rehabilitation therapy, which involves exposure to repeated visual and/or vestibular stimulation. Whilst the effects of vestibular rehabilitation at the behavioural level have been widely studied, the neural mechanism of how it works is unclear. In this thesis, asymptomatic subjects were recruited to investigate the neural mechanisms underlying visual and vestibular desensitisation. In the first study, the effect of long term vestibular training was investigated on the vestibular psychophysical measures and on the structure of the brain. To this aim, a group of high level dancers and a group of non-dancers were recruited with both groups undergoing a battery of vestibular tests and neuroimaging brain scans. Compared to controls, dancers showed a significant reduction in both vestibular ocularmotor response and perception of self-motion. Moreover, in controls a significant correlation was found between ocularmotor and perceptual measures, which was absent in dancers. This uncoupling of the vestibular measures was also seen at the neuroanatomical level in the locus of the vestibular-cerebellum, as revealed by voxel based morphometry (VBM) analysis of the dancers' brain grey matter. Using diffusion tensor imaging (DTI), a widespread cortical white matter (WM) network was found to correlate with vestibular perception in the control group only. The findings suggest that in dancers, a cerebellar gating of perceptual signals to cortical regions takes place that may mediate the training-related resistance to vertigo. The second study of the thesis looked at the effect of a single prolonged exposure to unilateral visual motion stimulus in healthy untrained subjects. This involved using transcranial magnetic stimulation (TMS) induced phosphenes to assess early visual cortical excitability. Following visual motion adaptation, excitability of visual cortex (V1) was significantly reduced when viewing motion in the adapted direction and significantly increased when viewing motion in the non-adapted direction. This suggests that reciprocal inhibition takes place between oppositely tuned directionally selective neurones in V1 to facilitate motion perception. The visual cortical excitability returned to its prior-adaptation state after five minutes suggesting that a single exposure to visual motion stimulus is not sufficient to cause a long-term adaptive effect. The final study of the thesis investigated potential neural mechanisms involved in suppressing visual symptom of oscillopsia (perception of the world oscillating/moving), a potentially distressing condition that occurs in some vestibular and ocularmotor disorders. The study recruited participants with nystagmus and they were divided into two groups according to their experience of oscillopsia: symptomatic (with oscillopsia) and asymptomatic (no oscillopsia). TMS induced phosphenes were used to assess (1) whether visual cortical spatial updating takes place according to the eye position and (2) whether modulation of visual cortical excitability takes place during nystagmus. In the asymptomatic group only, evidence for both visual cortical updating and modulation of visual cortical excitability was found, which was absent in the symptomatic group. The findings suggest that spatial updating of eye position and changes in visual cortical excitability are implicated in the suppression of oscillopsia. In particular, the work presented in the thesis provides neuroanatomical imaging basis for vestibular adaptation and provides evidence for a direct cortical involvement in visual motion adaptation. Both of these mechanisms are likely to be involved in the clinical recovery process of patients with vestibular and ocularmotor disorders. Greater understanding of the neural mechanisms involved in long lasting visual-vestibular desensitisation will bring us closer to developing personalised treatments that are more effective in improving symptoms of patients with visuo-vestibular disorders.
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