Localizing Visual Allodynia in Migraine

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Authors

Smith, Carson

Issue Date

2025

Type

Thesis

Language

en_US

Keywords

Allodynia , Hyperexcitability , Migraine , Retina

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Abstract

A hallmark symptom of migraine is photophobia, a sensitivity and aversion to light that can occur during and in between migraine attacks. Visual stimulation can reportedly trigger migraines suggesting a link between visual processing and migraine pathophysiology. This study examined the neural correlates of visual processing in migraine. Previous studies have found that visual allodynia, pain, and discomfort in response to innocuous stimuli in migraine is associated with hyperexcitability in the visual cortex. Recently, abnormal activity in retinal receptors has been identified in migraine, at the level of the cones, rods, and retinal ganglion cells. This challenges the cortical hyperexcitability hypothesis of photophobia. We examined the cortical and retinal responses to visual stimulation in individuals with migraine to identify where along the visual pathway hyperexcitability is first expressed. We measured electroencephalography (EEG) and electroretinography (ERG) activity in 26 migraine and 16 headache-free individuals. EEG over visual cortex was used to measure cortical responses to flickering light (28.3Hz). To assess the activity from the retina, we used ISCEV standard methods for assessing cone, rod, and retinal ganglion activity. Specifically, to assess rod activity, participants were dark adapted and presented light at low luminance 0.28 Td and 85 Td. To assess cone activity, 28.3Hz and 1.96Hz bright flicker were presented to maximize cone driven responses. To assess retinal ganglion activity, we used red-blue light at 3.4Hz to identify the photopic negative response (PhNR). Stimuli intensities were modulated by measuring participant pupillary response to maintain consistent retinal stimulation. We found that individuals with migraine exhibited moderately greater cortical responses to visual flicker than headache-free individuals, consistent with the cortical hyperexcitability hypothesis. At the level of the retina, we found that individuals with migraine displayed abnormal retinal ganglion cell activity to visual flicker, implicating retinal cells in migraine-associated photophobia. This is one of the first studies to comprehensively examine visual allodynia at multiple levels of the visual pathway in the same individuals. Our results may have implications for targeted treatment for visual allodynia and migraine.

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