Activation of the peripheral vestibular apparatus simultaneously elicits a reflex vestibular nystagmus and the vestibular perception of self-motion (vestibular-motion perception) or vertigo. In a newly characterised condition called Vestibular Agnosia found in conditions with disrupted brain network connectivity, e.g. traumatic brain injury (TBI) or neurodegeneration (Parkinson's Disease), the link between vestibular reflex and perception is uncoupled, such that, peripheral vestibular activation elicits a vestibular ocular reflex nystagmus but without vertigo. Using structural brain imaging in acute traumatic brain injury, we recently linked vestibular agnosia to postural imbalance via disrupted right temporal white-matter circuits (inferior longitudinal fasciculus), however no white-matter tracts were specifically linked to vestibular agnosia. Given the relative difficulty in localizing the neuroanatomical correlates of vestibular-motion perception, and compatible with current theories of human consciousness (viz. the Global Neuronal Workspace Theory), we postulate that vestibular-motion perception (vertigo) is mediated by the coordinated interplay between fronto-parietal circuits linked to whole-brain broadcasting of the vestibular signal of self-motion. We thus used resting state functional MRI (rsfMRI) to map functional brain networks and hence test our postulate of an anterior-posterior cortical network mediating vestibular agnosia. Whole-brain rsfMRI was acquired from 39 prospectively recruited acute TBI patients (and 37 matched controls) with preserved peripheral and reflex vestibular function, along with self-motion perceptual thresholds during passive yaw rotations in the dark, and posturography. Following quality control of the brain imaging, 25 TBI patients' images were analyzed. We classified 11 TBI patients with vestibular agnosia and 14 without vestibular agnosia based on laboratory testing of self-motion perception. Using independent component analysis, we found altered functional connectivity within posterior (right superior longitudinal fasciculus) and anterior networks (left rostral prefrontal cortex) in vestibular agnosia. Regions of interest analyses showed both inter-hemispheric and intra-hemispheric (left anterior-posterior) network disruption in vestibular agnosia. Assessing the brain regions linked via right inferior longitudinal fasciculus, a tract linked to vestibular agnosia in unbalanced patients (but now controlled for postural imbalance), seed-based analyses showed altered connectivity between higher order visual cortices involved in motion perception and mid-temporal regions. In conclusion, vestibular agnosia in our patient group is mediated by multiple brain network dysfunction, involving primarily left frontal and bilateral posterior networks. Understanding the brain mechanisms of vestibular agnosia provide both an insight into the physiological mechanisms of vestibular perception as well as an opportunity to diagnose and monitor vestibular cognitive deficits in brain disease such as TBI and neurodegeneration linked to imbalance and spatial disorientation.
People with Parkinsons disease (PD) experience postural imbalance, leading to considerably increased risk of falls. Galvanic Vestibular Stimulation (GVS) is postulated to modulate postural balance in humans and improve it in PD. This systematic review and meta-analysis investigate the effects of GVS on postural balance in PD. Six separate databases and research registers were searched for cross-over design trials that evaluated the effects of GVS on postural balance in PD. We used standardized mean difference (Hedges g) as a measure of effect size in all studies. We screened 223 studies, evaluated 14, of which five qualified for the meta-analysis. Among n = 40 patients in five studies (range n= 5 to 13), using a fixed effects model we found an effect size estimate of g = 0.43 (p < 0.001, 95% CI [0.29,0.57]). However, the test for residual heterogeneity was significant (p < 0.001), thus we used a random effects model and found a pooled effect size estimate of 0.62 (p > 0.05, 95% CI [− 0.17, 1.41], I2 = 96.21%). Eggers test was not significant and thus trim and funnel plot indicated no bias. To reduce heterogeneity, we performed sensitivity analysis and by removing one outlier study (n = 7 patients), we found an effect size estimate of 0.16 (p < 0.05, 95% CI [0.01, 0.31], I2 = 0%). Our meta-analysis found GVS has a favourable effect on postural balance in PD patients, but due to limited literature and inconsistent methodologies, this favourable effect must be interpreted with caution.
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