Department of Optometry & Vision Sciences, The University of Melbourne, Parkville, Australia.
PLoS One. 2011 Apr 11;6(4):e18211. doi: 10.1371/journal.pone.0018211.
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.
偏头痛的病理生理学尚未完全阐明，但有证据表明皮质神经元的高反应性是其关键特征。高反应性的基础尚不清楚，兴奋性失衡可能源于抑制作用减弱或兴奋作用增强。在这项研究中，我们测量偏头痛患者的中心-周围对比抑制，作为负责视觉的皮质区域内抑制和兴奋相互作用的知觉类似物。我们预测偏头痛患者的抑制功能减弱会降低知觉周围抑制。最近的神经元周围抑制模型纳入了驱动周围抑制的兴奋性反馈。因此，兴奋的增加预测知觉周围抑制的增加。
26 名偏头痛患者和 20 名年龄和性别大致匹配的非头痛对照组参加了研究。在中央正弦光栅（4 c/deg 静止光栅，或 2 c/deg 以 2 deg/sec 的速度漂移，对比度为 40%）的存在和不存在情况下，测量中央正弦光栅的感知对比度（同一方向、空间频率和漂移率的 95%对比度环形光栅）。对于静止光栅，在控制组和偏头痛组中均存在相似的周围抑制强度，存在周围光栅会使中央光栅看起来分别为其真实对比度的 72%和 65%（t(44) = 0.81，p = 0.42）。对于漂移刺激，偏头痛组的周围抑制明显增加（t(44) = 2.86，p<0.01），偏头痛组的感知对比度平均为实际对比度的 53%，而非头痛对照组为 68%。
在偏头痛发作之间，无症状时，偏头痛患者对漂移刺激的视觉周围抑制大于对照组。该数据为偏头痛中存在可测量的抑制和兴奋性视觉过程失衡提供了证据，与视觉系统内皮质抑制功能减弱的简单模型不一致。
