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PLoS One. 2011 Apr 11;6(4):e18211. doi: 10.1371/journal.pone.0018211.

Migraine increases centre-surround suppression for drifting visual stimuli.

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Department of Optometry & Vision Sciences, The University of Melbourne, Parkville, Australia.



The pathophysiology of migraine is incompletely understood, but evidence points to hyper-responsivity of cortical neurons being a key feature. The basis of hyper-responsiveness is not clear, with an excitability imbalance potentially arising from either reduced inhibition or increased excitation. In this study, we measure centre-surround contrast suppression in people with migraine as a perceptual analogue of the interplay between inhibition and excitation in cortical areas responsible for vision. We predicted that reduced inhibitory function in migraine would reduce perceptual surround suppression. Recent models of neuronal surround suppression incorporate excitatory feedback that drives surround inhibition. Consequently, an increase in excitation predicts an increase in perceptual surround suppression.


Twenty-six people with migraine and twenty approximately age- and gender-matched non-headache controls participated. The perceived contrast of a central sinusoidal grating patch (4 c/deg stationary grating, or 2 c/deg drifting at 2 deg/sec, 40% contrast) was measured in the presence and absence of a 95% contrast annular grating (same orientation, spatial frequency, and drift rate). For the static grating, similar surround suppression strength was present in control and migraine groups with the presence of the surround resulting in the central patch appearing to be 72% and 65% of its true contrast for control and migraine groups respectively (t(44) = 0.81, p = 0.42). For the drifting stimulus, the migraine group showed significantly increased surround suppression (t(44) = 2.86, p<0.01), with perceived contrast being on average 53% of actual contrast for the migraine group and 68% for non-headache controls.


In between migraines, when asymptomatic, visual surround suppression for drifting stimuli is greater in individuals with migraine than in controls. The data provides evidence for a behaviourally measurable imbalance in inhibitory and excitatory visual processes in migraine and is incompatible with a simple model of reduced cortical inhibitory function within the visual system.

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