Linking trigeminal and visual sensitivity in migraine

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Project Summary Hypersensitivity is a canonical feature of migraine, with pain from light (photophobia) and touch (facial allodynia) present during the ictal headache phase, and sometimes the inter-ictal period as well. Headache and facial allodynia appear to reflect potentiation of trigeminal signals in migraine. This same mechanism may account for photophobia as well. A subset of retinal ganglion cells express the photopigment melanopsin, rendering them intrinsically photosensitive (the “ipRGCs”). Rodent studies show that these cells project to thalamic and brainstem sites that also receive somatosensory input from the trigeminal nerve, providing a point of neural interaction of somatic and visual signals. Can this promising biological model—derived in animal studies—account for the properties of sensory symptoms in human migraine? To explore this question, we require a quantitative hypothesis testing framework, and a reproducible, objective measure of trigeminal sensitivity to supra-threshold stimuli. We propose to create this experimental platform and test key elements of the trigeminal hypersensitivity model. We have modified a commercial “blink reflexometer” to measure parameters of the corneal blink reflex to graded air-puff stimulation. We will test (Aim 1) if people with migraine and inter-ictal photophobia, as compared to headache-free controls, have a systematic, group difference in the slope of this reflexive sensitivity function or in a report of discomfort. Further, we will determine (Aim 2) if graded variation in a simultaneous light stimulus interacts with air-puff intensity in the production of these explicit and reflexive responses, thereby testing for anatomical convergence of visual and trigeminal somatic signals.