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Featured Application: This study protocol will promote efficient sensory reweighting and the integration of postural control, and will modify vestibular and motor responses. The training will be used as a rehabilitation protocol for neurological populations who have sensory integration issues, including those with mild traumatic brain injuries, strokes, and multiple sclerosis. Postural instability is a common symptom of vestibular dysfunction due to an insult to the vestibular system. Vestibular rehabilitation is effective in decreasing dizziness and visual symptoms, and improving postural control through several mechanisms, including sensory reweighting. As part of the sensory reweighting mechanisms, vestibular activation training with headshake activities influences vestibular reflexes. However, combining challenging vestibular and postural tasks to facilitate more effective rehabilitation outcomes is underutilized. Our research goal is to develop a virtual reality vestibular rehabilitation method for vestibular-postural control in neurological populations with vestibular and/or sensorimotor control impairment. The NeuroCom® SMART Balance Master (Natus Medical Inc., Pleasanton, CA, USA), which was used in a prior study, is expensive and bulky. Hence, a novel study protocol is established in this paper with the detailed objectives and pre-/post-intervention data analysis pipeline (ANOVA, t-test, post hoc analysis, etc.) involving modern off-the-shelf sensors and custom instrumentation (electromyography, electrooculography, video head impulse testing, force plates, and virtual reality headsets). It is expected that the training will significantly decrease vestibuloocular reflex gains and eye movement variability, as well as reweight the somatosensory ratio, finetune postural muscle activation, and consequently improve postural flexibility and produce a faster automatic postural response. The findings may have implications for the future development of vestibular rehabilitation protocols. [ABSTRACT FROM AUTHOR]

Spinocerebellar Ataxia Type 6 (SCA6) is a mid-life onset neurodegenerative disease characterized by progressive ataxia, dysarthria, and eye movement impairment. This autosomal dominant disease is caused by the expansion of a CAG repeat tract in the CACNA1A gene that encodes the α1A subunit of the P/Q type voltage-gated Ca2+ channel. Mouse models of SCA6 demonstrate impaired locomotive function and reduced firing precision of cerebellar Purkinje in the anterior vermis. Here, to further assess deficits in other cerebellar-dependent behaviors, we characterized the oculomotor phenotype of a knock-in mouse model with hyper-expanded polyQ repeats (SCA684Q). We found a reduction in the efficacy of the vestibulo-ocular reflex (VOR) and optokinetic reflex (OKR) in SCA6 mutant mice, without a change in phase, compared to their litter-matched controls. Additionally, VOR motor learning was significantly impaired in SCA684Q mice. Given that the floccular lobe of the cerebellum plays a vital role in the generation of OKR and VOR calibration and motor learning, we investigated the firing behavior and morphology of floccular cerebellar Purkinje cells. Overall, we found a reduction in the firing precision of floccular lobe Purkinje cells but no morphological difference between SCA684Q and wild-type mice. Taken together, our findings establish that gaze stabilization and motor learning are impaired in SCA684Q mice and suggest that altered cerebellar output contributes to these deficits. [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate gain and refixation saccades (covert and overt) using a video head impulse test (vHIT) in the horizontal and vertical planes in patients after the onset of unilateral acute vestibular neuritis (AVN). Thirty-five patients were examined in the acute stage of AVN and at follow-up (range, 6–30 months); a control group of 32 healthy subjects also participated. At onset, the mean gain was significantly lower on the affected side in all of the semi-circular canal planes, mainly in the horizontal canal plane, and saccades (covert and overt) were more prevalent in the horizontal compared to the vertical canal planes. Multi-canal affection occurred more frequently (80% for gain, 71% for saccades) than isolated canal affection. At follow-up, which ranged from 6 to 30 months, the gain was recovered in all of the canals (anterior in 50%, horizontal in 42.8%, and posterior canal in 41.1% of cases), while covert and overt saccades were reduced in the horizontal and vertical planes. However, covert saccades were still recorded in a greater proportion (69%) than overt saccades (57%) in the horizontal plane and at a lower rate in the vertical planes. The compensatory mechanisms after AVN mainly involve the horizontal canal, as the refixation saccades—especially covert ones—were more frequently recorded in the horizontal than vertical canals. [ABSTRACT FROM AUTHOR]