Abstract

In the past few years, researchers have detected subtle macular vision abnormalities using different psychophysical experimental tasks in patients with migraine. Recording of visual evoked potential (VEP) after photostress (PS) represents an objective way to verify the integrity of the dynamic properties of macular performance after exposure to intense light. VEPs were recorded before and after PS in 51 patients with migraine (19 with aura (MA) and 22 without aura (MO) between attacks, and 10 recorded during an attack (MI)) and 14 healthy volunteers. All study participants were exposed to 30 s of PS through the use of a 200-watt bulb lamp. The P100 implicit time and N75-P100 amplitude of the baseline VEP were compared with those collected every 20 s up to 200 s after PS. VEP parameters recorded at baseline did not differ between groups. In all groups, the VEP recordings exhibited a significant increase in implicit times and a reduction in amplitude at 20 s after the PS. In migraine, the percentage decrease in amplitudes observed at 20 s after photostress was significantly lower than in healthy volunteers, in both MO and MA patients, but not in MI patients. When data for MO and MA patients were combined, the percentage of amplitude change at 20 s was negatively correlated with the number of days that had elapsed since the last migraine attack, and positive correlated with attack frequency. We showed dynamic changes of recovery of VEP after PS depending on the migraine cycle. This finding, in conjunction with those previously attained with other neuromodulatory interventions using VEPs, leads us to argue that migraine-disease-related dysrhythmic thalamocortical activity precludes amplitude suppression by PS.

Highlights

  • The visual system is deeply involved in the pathophysiology of migraine

  • The most interesting result of our study was that the level of suppression of visual evoked potential (VEP)

  • The most interesting result our study was that the level of suppression of VEP

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Summary

Introduction

The visual system is deeply involved in the pathophysiology of migraine. Dysfunctions have been described from the outermost layers of the retina [1] to the visual cortex [2,3]and its associative areas [4,5], passing through its thalamic station [6,7]. The visual system is deeply involved in the pathophysiology of migraine. By applying different technical approaches, a specific involvement of macula cells and an alteration of color vision in the outer retinal layers by cone photoreceptors for the blue–yellow axis has been proposed for migraine patients [8,9]. Other authors have described abnormalities in color perception, such as for red and blue, in addition to cortical involvement [10,11,12,13]. There is evidence in favor of an involvement in migraine of a specific macular pathway mediated by a population of photosensitive retinal ganglion cells, which are in direct connection with the thalamus, the trigeminal system, and several associated brain areas [14,15]

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