The mechanisms and loci of human vestibular perception
This thesis' primary aims were to characterise the what, where and how of vestibular cortical processing. A secondary aim was to assess the effects of early visual deprivation on vestibular perception, in particular the what and where.;The What: Using an angular vestibular navigation paradigm with physiological range stimuli, we quantitatively demonstrated that healthy subjects were able to actively reproduce spatial and kinetic parameters of a passively travelled trajectory (displacement, time, velocity and acceleration). Early blind subjects showed no deficit in the perception of raw vestibular signals but were relatively impaired in more complex spatial vestibular navigation tasks. Congenitally blind subjects did not show the normal prolongation of the vestibular signal coming from the labyrinth (i.e. velocity storage mechanism) at perceptual level and two blind subjects who had superior navigational ability also had ultra-short vestibular time constants. Based upon a questionnaire assessment of these subjects, we concluded that frequent exposure to specific activities (e.g. down-hill skiing for one subject!) may be protective in allowing a normal navigational capacity in these subjects. The mechanism for the ultra-short time constants and their role in superior navigational performance remains unclear.;The Where: Using repetitive transcranial stimulation (rTMS) to the right posterior parietal cortex we disrupted the perceptual encoding of vestibular signals during a passive yaw-plane rotation. We found no effect of rTMS on vestibular encoding with occipital cortical stimulation in sighted or blind subjects.;The How: We hypothesised that vestibular signals may be encoded via an internal model at perceptual level. Using a novel paradigm, we found that by perturbing the internal estimate of displacement of a previously travelled trajectory (yaw plane rotation), we could alter the perception of motion duration but not velocity, of the rotation, a finding consistent with our hypothesis. The last experiment in this thesis was developed in an attempt to bridge the gap between brainstem and perceptual vestibular function. We quantitatively show that brainstem thresholds to angular acceleration are lower than for cortical (perceptual) thresholds. The hypothesis that we aim to test in the future is that patients who show a large dichotomy between brainstem and cortical thresholds to angular acceleration may be either objectively compromised by worse balance function or subjectively worse as defined by their symptoms of dizziness and disorientation.