Cortical and subcortical contributions to balance in health and disease

The role of the brainstem and cerebellum in dizziness and balance have been studied extensively however subcortical and cortical contributions to dizziness and balance have largely been neglected. Accordingly, this thesis has studied the mechanisms of vestibular cortical modulation using non-invasive stimulation, structural and functional changes occurring in the cerebral cortex following vestibular disorders and lastly the association of unexplained dizziness with cerebral small vessel disease. In the first study, bihemispheric tDCS was used to non-invasively stimulate critical temporo-parietal areas with simultaneous eye movement recordings to analyse whether it acted indirectly through pursuit and VOR suppression mechanisms or direct modulation of the VOR. This observed modulation was likely due to top-down cortical control of the VOR as a result of disruption to parietal interhemispheric balance and not mediated via brainstem pathways. In the second study, cortical adaptation mechanisms in patients who have bilateral deficit of the VOR (bilateral vestibular failure) were investigated. Initial manifestation of severe oscillopsia diminishes gradually in these patients, however the underlying adaptive mechanisms remain unclear. Hence, primary visual cortex (V1) excitability was directly assessed using single pulse transcranial magnetic stimulation to induce phosphene percepts (an indirect measure of cortical excitability). Patients exhibited raised phosphene thresholds implying reduced V1 excitability and were inversely correlated with oscillopsia scores, suggesting reduced visual cortical excitability is associated with improved functional status. A significant decrease in the probability of phosphene perception was observed in patients when viewing visual motion compared to controls. A subset of patients exhibited markedly reduced V1 excitability, with strong or complete suppression of phosphenes during visual motion; a novel “disappearing phosphene” phenomenon. This study provided the first neurophysiological evidence that cortical adaptation mechanisms play a critical role in recovery from vestibular failure. Dizzy patients referred to two neuro-otology centres were divided into 'explained' and 'unexplained' causes of dizziness based on a retrospective casenote analysis and a blinded review of white matter hyperintensities on T2 and FLAIR sequences in 3T MRI using validated visual Fazekas scale was conducted. Increased severity of white matter hyperintensity in cases of unexplained dizziness suggests that such abnormalities are likely contributory to the development of dizziness. White matter lesions may induce dizziness either because patients perceive a degree of objective unsteadiness or by a disconnection syndrome involving vestibular or locomotor areas of the brain.Open Acces