Abstract
Visual allodynia is a key symptom of migraine occurring during and in-between migraine attacks. Visual stimulation can trigger migraines suggesting a link with migraine pathophysiology. Visual allodynia is commonly associated with hyper-excitability in visual cortex. However, abnormal activity in retinal receptors has recently been identified in migraine. We examined cortical and retinal responses to visual stimulation to identify which measures expressed hyper-excitability in migraine. We measured electroencephalography (EEG) and electroretinography activity in 5 migraine and 6 headache-free individuals. EEG over visual cortex was used to measure cortical responses to 28.3Hz flickering light. To assess rod activity, dark-adapted participants were presented with low luminance light. To assess cone activity, bright flicker at 28.3Hz and 1.96Hz were presented. To assess retinal ganglion activity, red and blue flashes were used to identify the photopic negative response (PhNR). Stimuli intensities were modulated by measuring participant pupil diameter to maintain consistent retinal stimulation. Individuals with migraine exhibited greater EEG responses to visual flicker than headache-free individuals (d=0.94), consistent with cortical hyper-excitability. At the level of the retina, our migraine group expressed greater b-wave amplitudes (d=0.47) from rod-driven ganglion cells than our headache-free group. However, headache-free individuals expressed greater cone-driven a-wave amplitudes to 1.96Hz flicker (d=0.55) and greater activity at 28.3Hz than migraine (d=0.60). The PhNR from retinal ganglion cells was larger in migraine compared to the headache-free group (d=0.09). This is one of the first studies to examine visual allodynia at multiple levels of the visual pathway in the same individuals. We found individuals with migraine exhibited greater activity over visual cortex compared to headache-free individuals. Retinal receptors showed smaller and inconsistent effects of migraine. These findings indicate the origin of visual allodynia is likely in the cortex.