Barry M. Seemungal

Noisy galvanic vestibular stimulation (nGVS) has previously been shown to reduce postural sway during quiet standing. But whether nGVS can modify balance during destabilizing perturbations is unknown. We demonstrate that nGVS reduces the initial backward trunk angular velocity in response to discrete perturbations. These effects occurred without changes in perturbation-evoked muscle responses, but with increased preperturbation ankle muscle activity. These findings suggest that nGVS alters preperturbation tonic vestibulospinal output, as evidenced by elevated preperturbation ankle EMG, rather than reactive feedback gain.

Peripheral vestibular stimulation elicits brainstem reflex responses manifesting as a vestibular-ocular reflex nystagmus (‘VOR’) and evokes a perception of self-motion or ‘vertigo’. While VOR responses are objectively measured via eye movements, no such objective measure exists for assessing the cortical vestibular processing of self-motion. Understanding how the brain encodes vestibular-mediated self-motion could provide electrophysiological markers for clinical syndromes where reflex and perception are uncoupled, e.g. in vestibular agnosia. Hence, here we investigated the brain’s encoding of bottom-up vestibular signals, using passive yaw-plane chair rotations performed in complete darkness with simultaneous EEG. Healthy controls (n = 8) were compared to patients with bilateral vestibulopathy (BVP), either with residual function (BVP-residual; n=6) or complete loss (BVP-complete; n=1), at five acceleration levels (range: 30-150º /s2). Comparing healthy controls with BVP-residual, we found: 1) no differences in time-frequency analyses; and 2) differences in vestibular evoked potentials magnitude ( P < 0.01). Chair acceleration changes were consistently accompanied by phase-locked and induced (non-phase locked) theta-increases as well as alpha reduction in both, healthy and patients. Importantly, while the induced theta component was present in BVP-residual, it was absent in BVP-complete. Overall, findings indicate potential utility of: 1) vestibular evoked EEG responses for identifying attenuated vestibular signalling; and 2) theta activity as a cortical signature of preserved bottom-up vestibular signalling. These preliminary findings would require further investigation to confirm their functional role

An unexpected loud sound typically elicits a reflexive eye-blink. This response is attenuated when preceded by a weaker non-startling stimulus, a phenomenon known as prepulse inhibition (PPI), which reflects sensory gating. PPI has been reported to differ between sitting and standing, suggesting a relationship with postural control. Sensory gating may dynamically suppress irrelevant inputs while preserving responsiveness to salient cues, a process likely supporting postural stability in complex environments. In this study, we investigated how PPI is modulated by postural demands and whether these changes relate to postural sway. Forty-five healthy participants underwent PPI testing while supine, standing on a hard surface, soft surface, and in tandem stance. We examined both auditory and somatosensory PPI, with and without visual input. Consistent with the hypothesis of dynamic gating, PPI was strongest during quiet standing on a firm surface, but weakened during more challenging postural conditions. While both somatosensory and auditory PPI were modulated, no significant modality-specific differences emerged. Removing visual input slightly reduced PPI but did not alter the overall pattern. These findings suggest that PPI reflects a flexible inhibitory mechanism tuned to postural context. While no causal relationship can be inferred, the results indicate a potential functional link between sensory gating and postural control, supporting future investigations into whether PPI could serve as a physiological marker of balance regulation.

Background: Postural imbalance with falls affects 80% of patients with Parkinson’s disease (PD) at 10 years. Standard PD therapies (e.g., levodopa and/or deep brain stimulation—DBS) are poor at improving postural imbalance. Additionally, the mechanistic complexity of interpreting postural control is a major barrier to improving our understanding of treatment effects. In this paper, we review the effects of DBS on balance as measured using posturography. We also critically appraise the quantitative measures and analyses used in these studies. Methods: A literature search was performed independently by 2 researchers using the PUBMED database. Thirty-eight studies are included in this review, with DBS at the subthalamic nucleus (STN-) (n = 25), globus pallidus internus (GPi-) (n = 6), ventral intermediate nucleus (VIM)/thalamus (n = 2), and pedunculopontine nucleus (PPN) (n = 5). Results: STN- and GPi-DBS reduce static sway in PD and mitigate the increased sway from levodopa. STN-DBS impairs automatic responses to perturbations, whilst GPi-DBS has a more neutral effect. STN-DBS may promote protective strategies following external perturbations but does not improve adaptation. The evidence regarding the effects on gait initiation is less clear. Insufficient evidence exists to make conclusions regarding VIM- and PPN-DBS. Conclusions: STN- and GPi-DBS have differing effects on posturography, which suggests site-specific and possibly non-dopaminergic mechanisms. Posturography tests should be utilised to answer specific questions regarding the mechanisms of and effects on postural control following DBS. We recommend standardising posturography measures and test conditions by expert consensus and greater long-term data collection, utilising ongoing DBS registries.

Background : Postural imbalance with falls affects 80% of patients with Parkinson’s Disease (PD) at 10 years. Standard PD therapies (e.g. levodopa and/or deep brain stimulation - DBS) are poor at improving postural imbalance. Additionally, the mechanistic complexity of interpreting postural control is a major barrier to improving our understanding of treatment effects. In this paper, we review the effects of DBS on balance as measured using posturography. We also critically appraise the quantitative measures and analyses used in these studies. Methods: A literature search was performed independently by 2 researchers using PUBMED database. 38 studies are included in this review, with DBS at subthalamic nucleus (STN-) alone (n=25), globus pallidus internus (GPi-) (n=6), ventral intermediate nucleus (VIM)/thalamus (n=2) and pedunculopontine nucleus (PPN) (n=5). Results : STN- and GPi-DBS reduce static sway in PD and mitigate the increased sway from levodopa. STN-DBS impairs automatic responses to perturbations, whilst GPi-DBS has a more neutral effect. STN-DBS may promote protective strategies following external perturbations but does not improve adaptation. The evidence regarding the effects on gait initiation are less clear. Insufficient evidence exists to make conclusions regarding VIM- and PPN-DBS. Conclusions: STN- and GPi-DBS have differing effects on posturography which suggest site-specific and possibly non-dopaminergic mechanisms. Posturography tests should be utilised to answer specific questions regarding the mechanisms of and effects on postural control following DBS. We recommend standardising posturography measures and test conditions by expert consensus and greater long-term data collection, utilising ongoing DBS registries.

Background: Vestibular dysfunction causing imbalance affects c. 80% of acute hospitalized traumatic brain injury (TBI) cases. Poor balance recovery is linked to worse return-to-work rates and reduced longevity. We previously showed that white matter network disruption, particularly of right inferior longitudinal fasciculus, mediates the overlap between imbalance and impaired vestibular perception of self-motion (i.e., vestibular agnosia) in acute hospitalized TBI. However, there are no prior reports tracking the acute-longitudinal trajectory of objectively measured vestibular function for hospitalized TBI patients. We hypothesized that recovery of vestibular agnosia and imbalance is linked and mediated by overlapping brain networks. Methods: We screened 918 acute major trauma in-patients, assessed 146, recruited 39 acutely, and retested 34 at 6 months. Inclusion criteria were 18–65-year-old adults hospitalized for TBI with laboratory-confirmed preserved peripheral vestibular function. Benign paroxysmal positional vertigo and migraine were treated prior to testing. Vestibular agnosia was quantified by participants’ ability to perceive whole-body yaw plane rotations via an automated rotating-chair algorithm. Subjective symptoms of imbalance (via questionnaires) and objective imbalance (via posturography) were also assessed. Results: Acute vestibular agnosia predicted poor balance recovery at 6 months. Recovery of vestibular agnosia and linked imbalance was mediated by bihemispheric fronto-posterior cortical circuits. Recovery of subjective symptoms of imbalance and objective imbalance were not correlated. Conclusion: Vestibular agnosia mediates balance recovery post-TBI. The link between subjective dizziness and brain injury recovery, although important, is unclear. Therapeutic trials of vestibular recovery post-TBI should target enhancing bi-hemispheric connectivity and linked objective clinical measures (e.g., posturography).

In 2007, the Bárány Society embarked on a project to establish definitions of vestibular syndromes and disorders based on best available evidence, referred to as the International Classification of Vestibular Disorders (ICVD). Since then, numerous publications providing consensus-driven diagnostic criteria for vestibular symptoms, syndromes, and disorders have been published. Here, we reflect on the rationale for developing the ICVD as well as its subsequent achievements, challenges, and outlook. In this summary of the work of the ICVD to date, the authors will focus on practical aspects to help improve the utility and applicability of these diagnostic criteria moving forward.