Downregulation of early visual cortex excitability mediates oscillopsia
File(s)
Published version
Accepted version
Author(s)
Type
Journal Article
Abstract
Objective; Identifying the neurophysiological mechanisms that mediate adaptation to oscillopsia in patients with bilateral-vestibular failure (BVF); an observational study.
Methods; We directly probe the hypothesis that adaptive changes which 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 whilst performing a visual-motion adaptation paradigm during the following conditions: (i) BASELINE measures (i.e. static), (ii) during visual-motion (i.e. MOTION PRE ADAPTATION) and, (iii) during visual-motion following 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 MOTION PRE ADAPTATION and MOTION ADAPTED conditions, we observed significantly attenuated cortical excitability in patients. Again this attenuation in excitability was stronger in less symptomatic patients.
Conclusion; Our findings provide neurophysiological evidence that cortically-mediated adaptive mechanisms in V1/V2 play a critical role in suppressing oscillopsia in patients with bilateral vestibular failure.
Methods; We directly probe the hypothesis that adaptive changes which 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 whilst performing a visual-motion adaptation paradigm during the following conditions: (i) BASELINE measures (i.e. static), (ii) during visual-motion (i.e. MOTION PRE ADAPTATION) and, (iii) during visual-motion following 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 MOTION PRE ADAPTATION and MOTION ADAPTED conditions, we observed significantly attenuated cortical excitability in patients. Again this attenuation in excitability was stronger in less symptomatic patients.
Conclusion; Our findings provide neurophysiological evidence that cortically-mediated adaptive mechanisms in V1/V2 play a critical role in suppressing oscillopsia in patients with bilateral vestibular failure.
Date Issued
2017-08-16
Date Acceptance
2017-06-06
Citation
Neurology, 2017, 89 (11), pp.1179-1185
ISSN
0028-3878
Publisher
American Academy of Neurology (AAN)
Start Page
1179
End Page
1185
Journal / Book Title
Neurology
Volume
89
Issue
11
License URL
Sponsor
Medical Research Council (MRC)
Grant Number
MR/J004685/1
Subjects
Science & Technology
Life Sciences & Biomedicine
Clinical Neurology
Neurosciences & Neurology
BILATERAL VESTIBULAR FAILURE
TRANSCRANIAL MAGNETIC STIMULATION
EYE-HEAD COORDINATION
FUNCTIONAL CONNECTIVITY
VESTIBULOOCULAR REFLEX
CORTICAL EXCITABILITY
MOTION
MECHANISMS
ADAPTATION
ACTIVATION
1103 Clinical Sciences
1109 Neurosciences
1702 Cognitive Science
Neurology & Neurosurgery
Publication Status
Published