Habituation in migraineurs has been extensively studied with visual evoked potentials. Despite discrepant results, possibly related to the use of different stimulus conditions, lack of habituation in the period between attacks is presently considered to be a neurophysiological hallmark of migraine. Midoccipital
monocular visual evoked potentials were recorded and analyzed in 27 interictal migraineurs and 34 healthy controls using a blinded study design. Small 8′ checks and large 65′ checks were applied in random order, both with 3 reversals per second. Six consecutive blocks of 100 responses were recorded for each check size. N70-P100 and P100-N145 peak-to-peak amplitudes were measured. Regression slopes across the 6 blocks, supplemented by last block/first block ratio and repeated measures analysis of variance with amplitude as the dependent variable, were used to test for habituation. N70-P100 Stem Cell Compound Library supplier habituation to small and large checks
was observed in controls (mean slope −0.30 and −0.11 μV/block) and interictal migraineurs (−0.32 and −0.26 μV/block). P100-N145 habituation to small checks in controls (mean slope −0.39 μV/block) and to small and large checks in interictal migraineurs (−0.38 and −0.17 μV/block) was also observed. None of the habituation MI-503 molecular weight measures were significantly different between healthy controls and migraineurs (F < 1.6, P > .18). The check-size effect was similar in the 2 groups (F < 2.3, P > .14). Reversal rate and check-size differences do not seem to explain the discrepant visual evoked potential habituation results selleck kinase inhibitor in the migraine literature. Furthermore, no differences in first block amplitudes or N70, P100, and N145 latencies between healthy controls and migraineurs were found. We recommend blinded evaluation designs in future habituation studies in migraine. “
“Migraine has been linked with an increased risk
of stroke and an increased prevalence of clinically silent brain lesions and white-matter hyperintensities. As it is known that stroke and structural brain lesions are associated with an increased risk of cognitive decline, it has been hypothesized that migraine may be a progressive brain disorder and associated with an increased risk of cognitive impairment. Given the prevalence of migraine in the population, especially among women, and the aging of the population, an association between migraine and cognitive impairment would have substantial public health implications. In this review, we will summarize the existing evidence evaluating the association between migraine and cognitive function. Additionally, we will discuss methodological issues in migraine and cognitive function assessment and elaborate on study design strategies to address this important question.