Imperial College London
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DrBarrySeemungal

Faculty of Medicine, Department of Brain Sciences

Honorary Clinical Senior Lecturer
 
 
 
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Contact

 

+44 (0)20 3311 7042b.seemungal Website

 
 
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Assistant

 

Miss Lorna Stevenson +44 (0)20 3313 5525

 
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Location

 

10L16Lab BlockCharing Cross Campus

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Summary

 

Publications

Citation

BibTex format

@article{Ahmad:2017:10.​1212/​WNL.​0000000000004360,
author = {Ahmad, H and Roberts, E and Patel, M and Lobo, R and Seemungal, B and Arshad, Q and Bronstein, A},
doi = {10.1212/WNL.0000000000004360},
journal = {Neurology},
pages = {1179--1185},
title = {Downregulation of early visual cortex excitability mediates oscillopsia},
url = {http://hdl.handle.net/10044/1/49006},
volume = {89},
year = {2017}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - 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.
AU  - Ahmad,H
AU  - Roberts,E
AU  - Patel,M
AU  - Lobo,R
AU  - Seemungal,B
AU  - Arshad,Q
AU  - Bronstein,A
DO  - 10.1212/WNL.0000000000004360
EP  - 1185
PY  - 2017///
SN  - 0028-3878
SP  - 1179
TI  - Downregulation of early visual cortex excitability mediates oscillopsia
T2  - Neurology
UR  - http://hdl.handle.net/10044/1/49006
VL  - 89
ER  -
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