Photic driving in migraine

In this issue of Cepkalalgia, the study by Puca et al. on steady state visual evoked potentials provides additional data confirming that hyperexcitability to light is a hallmark of the cerebral cortex in migraineurs between attacks. Since the seminal observation by Golla & Winter (1) of an increased photic drive of the EEG in migraineurs, cortical hyperreactivity to visual stimuli has been demonstrated with various methods, e.g. epidemiological surveys (2) functional tests (3, 4), steady state (5) , flash (6) or pattern reversal (7, 8) evoked potentials. It is not clear whether the cortical hyperexcitability is due to lack of inhibition by intrinsic GABAergic neurons (4) or to an abnormal modulation of the cortex by subcortical (monoaminergic) pathways (9). It was hypothesized that the former, which postulates a loss of cortical interneurons, might be an acquired consequence of repeated insults (hypoxia/spreading depression) to the visual cortex, while the latter could be a genetic abnormality. One major interest of Puca et al.’s study is that they find a positive correlation between visual reactivity and family history of migraine or autonomic symptoms during the attack, which favors the hypothesis of an inherited, subcortical dysfunction. Unfortunately, the reliability of information concerning severity of attack-associated symptoms and affected family members can be questioned in the absence of diary card data and of family interviews. Because of their importance for migraine pathogenesis, the correlations found here need to be confirmed using these more stringent methods.