Cephalalgia : an international journal of headache · 2020
Melanopsin hypersensitivity dominates interictal photophobia in migraine.
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Zele Andrew J, Dey Ashim, Adhikari Prakash, Feigl Beatrix
Аннотация
PURPOSE: To define the melanopsin and cone luminance retinogeniculate pathway contributions to photophobia in healthy controls and migraineurs.
METHODS: Healthy controls and migraineurs were categorized according to the International Classification of Headache Disorders criteria. Photophobia was measured under full-field illumination using electromyography in response to narrowband lights spanning the melanopsin and cone luminance action spectra. Migraineurs were tested during their interictal headache-free period. Melanopsin-mediated post-illumination pupil responses quantified intrinsically photosensitive Retinal Ganglion Cell (ipRGC) function.
RESULTS: A model combining the melanopsin and cone luminance action spectra best described photophobia thresholds in controls and migraineurs; melanopsin contributions were ∼1.5× greater than cone luminance. In the illumination range causing photophobia, migraineurs had lower photophobia thresholds (∼0.55 log units; p < 0.001) and higher post-illumination pupil response amplitudes (p = 0.03) than controls.
CONCLUSION: Photophobia is driven by melanopsin and cone luminance inputs to the cortex via the retino-thalamocortical pathway. In migraineurs, lower photophobia thresholds reflect hypersensitivity of ipRGC and cone luminance pathways, with the larger and prolonged post-illumination pupil response amplitude indicative of a supranormal melanopsin response. Our findings inform artificial lighting strategies incorporating luminaires with low melanopsin excitation and photopic luminance to limit the lighting conditions leading to photophobia.
METHODS: Healthy controls and migraineurs were categorized according to the International Classification of Headache Disorders criteria. Photophobia was measured under full-field illumination using electromyography in response to narrowband lights spanning the melanopsin and cone luminance action spectra. Migraineurs were tested during their interictal headache-free period. Melanopsin-mediated post-illumination pupil responses quantified intrinsically photosensitive Retinal Ganglion Cell (ipRGC) function.
RESULTS: A model combining the melanopsin and cone luminance action spectra best described photophobia thresholds in controls and migraineurs; melanopsin contributions were ∼1.5× greater than cone luminance. In the illumination range causing photophobia, migraineurs had lower photophobia thresholds (∼0.55 log units; p < 0.001) and higher post-illumination pupil response amplitudes (p = 0.03) than controls.
CONCLUSION: Photophobia is driven by melanopsin and cone luminance inputs to the cortex via the retino-thalamocortical pathway. In migraineurs, lower photophobia thresholds reflect hypersensitivity of ipRGC and cone luminance pathways, with the larger and prolonged post-illumination pupil response amplitude indicative of a supranormal melanopsin response. Our findings inform artificial lighting strategies incorporating luminaires with low melanopsin excitation and photopic luminance to limit the lighting conditions leading to photophobia.