Differential effect of visual motion adaption upon visual cortical excitability

Abstract

The objectives of this study were ) to probe the effects of visual motion adaptation on early visual and V5/MT cortical excitability and) to investigate whether changes in cortical excitability following visual motion adaptation are related to the degree of visual dependency, i.e., an overreliance on visual cues compared with vestibular or proprioceptive cues. Participants were exposed to a roll motion visual stimulus before, during, and after visual motion adaptation. At these stages, 20 transcranial magnetic stimulation (TMS) pulses at phosphene threshold values were applied over early visual and V5/MT cortical areas from which the probability of eliciting a phosphene was calculated. Before and after adaptation, participants aligned the subjective visual vertical in front of the roll motion stimulus as a marker of visual dependency. During adaptation, early visual cortex excitability decreased whereas V5/MT excitability increased. After adaptation, both early visual and V5/MT excitability were increased. The roll motion-induced tilt of the subjective visual vertical (visual dependence) was not influenced by visual motion adaptation and did not correlate with phosphene threshold or visual cortex excitability. We conclude that early visual and V5/MT cortical excitability is differentially affected by visual motion adaptation. Furthermore, excitability in the early or late visual cortex is not associated with an increase in visual reliance during spatial orientation. Our findings complement earlier studies that have probed visual cortical excitability following motion adaptation and highlight the differential role of the early visual cortex and V5/MT in visual motion processing. We examined the influence of visual motion adaptation on visual cortex excitability and found a differential effect in V1/V2 compared with V5/MT. Changes in visual excitability following motion adaptation were not related to the degree of an individual's visual dependency.

Downregulation of early visual cortex excitability mediates oscillopsia suppression

“…That is, less symptomatic (i.e., better adapted) patients had a less excitable visual cortex compared to more functionally impaired patients (i.e., poorly adapted, higher cortical excitability). This initial finding suggests that everyday exposure to excessive retinal slip initiates a cortically mediated compensatory process, resulting in downregulation of V1/V2 excitability, similar to that observed in healthy controls after prolonged visual motion adaptation 19 , 20 and during involuntary eye oscillations. 30 Given that such downregulation of excitability correlates with the oscillopsia questionnaire scores, the findings indicate that background visuo-cortical excitability levels may partly mediate clinical recovery.…”

“…This finding in healthy controls is in agreement with our previous findings that we attributable to a nonspecific effect (i.e., generalized arousal or attention) in response to visual motion. 19 , 20 Further group differences in cortical excitability between patients and healthy controls were found after adaptation. In healthy controls, cortical excitability was reduced, which again is in line with our previous reports in young healthy controls, 20 whereas in patients we observed no differences in cortical excitability when comparing the preadaptation and motion adapted conditions.…”

“…Hence, our results illustrate a dissociation in behavior when comparing participants with and without vestibular function. We postulate that the dissociations observed may be attributable to the 2 following non–mutually exclusive explanations: there is a preexisting cortical adaptation induced by the constant retinal image slippage and oscillopsia in patients, 19 , 20 and avestibular patients are desensitized to the influence of further visual motion, 5 , 13 i.e., a ceiling effect.…”

“… 25 , 26 Initially, we placed the coil centrally over the inion with the coil handle turned laterally, and if required, we moved the coil dorsally in 1-cm incremental steps until a bright, stationary, midline phosphene was perceived by the participant. 19 , 20 , 27 , 28 All participants were naive to the hypothesis but were told that the purpose of the experiment was to investigate changes in the visual part of the brain after the complete loss of inner ear balance function. All participants underwent a short standardized training session in darkness to familiarize them with phosphene detection.…”

“…Given that avestibular patients have an absent VOR and thus are continuously exposed to retinal image slip, we predict on the basis of previous findings in normal individuals 19 , 20 that (1) patients may have a more adapted (i.e., less excitable) visual cortex 19 , 20 at rest (i.e., baseline threshold) compared to controls; (2) given that patients are less susceptible (i.e., already desensitized) to visual motion, 5 implementation of a visual motion adaptation paradigm 20 would have a less potent modulatory effect on cortical excitability in patients compared to healthy controls; and (3) if such findings are relevant to the central changes mediating oscillopsia adaptation, then they should relate to oscillopsia symptom load as measured with clinical questionnaires.…”