Abstract
Objective:To identify in an observational study the neurophysiologic mechanisms that mediate adaptation to oscillopsia in patients with bilateral vestibular failure (BVF).Methods:We directly probe the hypothesis that adaptive changes that mediate oscillopsia suppression implicate the early visual-cortex (V1/V2). Accordingly, we investigated V1/V2 excitability using transcranial magnetic stimulation (TMS) in 12 avestibular patients and 12 healthy controls. Specifically, we assessed TMS-induced phosphene thresholds at baseline and cortical excitability changes while performing a visual motion adaptation paradigm during the following conditions: baseline measures (i.e., static), during visual motion (i.e., motion before adaptation), and during visual motion after 5 minutes of unidirectional visual motion adaptation (i.e., motion adapted).Results:Patients had significantly higher baseline phosphene thresholds, reflecting an underlying adaptive mechanism. Individual thresholds were correlated with oscillopsia symptom load. During the visual motion adaptation condition, no differences in excitability at baseline were observed, but during both the motion before adaptation and motion adapted conditions, we observed significantly attenuated cortical excitability in patients. Again, this attenuation in excitability was stronger in less symptomatic patients.Conclusions:Our findings provide neurophysiologic evidence that cortically mediated adaptive mechanisms in V1/V2 play a critical role in suppressing oscillopsia in patients with BVF.
Highlights
Our findings provide neurophysiologic evidence that cortically mediated adaptive mechanisms in V1/V2 play a critical role in suppressing oscillopsia in patients with bilateral vestibular failure (BVF)
Previous work has suggested that this compensatory process involves in part the generation of plastic oculomotor changes to improve gaze stability during head movements[3,6,8,9] and perceptually mediated compensatory mechanisms such that avestibular patients become desensitized to visual motion.[5]
During establishment of baseline phosphene thresholds, we observed that patients with BVF required a higher level of maximum stimulator output to reach threshold compared to healthy controls
Summary
We directly probe the hypothesis that adaptive changes that mediate oscillopsia suppression implicate the early visual-cortex (V1/V2). We investigated V1/V2 excitability using transcranial magnetic stimulation (TMS) in 12 avestibular patients and 12 healthy controls. We assessed TMS-induced phosphene thresholds at baseline and cortical excitability changes while performing a visual motion adaptation paradigm during the following conditions: baseline measures (i.e., static), during visual motion (i.e., motion before adaptation), and during visual motion after 5 minutes of unidirectional visual motion adaptation (i.e., motion adapted). Twelve right-handed[21] patients with BVF were recruited from a tertiary referral clinic (Charing Cross Hospital) between November 2013 and December 2015 (7 men, age range 29–65 years; mean age 54.5 years, SD 11.9 years; table). Twelve right-handed matched healthy controls (7 men, age range 28–66 years, mean age 55 years, SD 5 11.1 years) with no neurologic or audiovestibular disease were recruited. All participants and healthy controls had normal or corrected normal visual acuity.
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