Local and global motion after-effects are both enhanced in migraine, and the underlying mechanisms differ across cortical areas.
Visual after-effects are illusions that occur after prolonged viewing of visual displays (pattern adaptation). The motion after-effect (MAE), for example, is an illusory impression of motion that is seen after viewing moving displays. After-effects have been used extensively in basic vision research as well as in clinical settings, and have been reported to be enhanced in migraine. Pattern adaptation is a cortical phenomenon that reflects both cellular mechanisms acting within individual neurons and specific interactions between groups of neurons activated by the adapting display. A remarkable feature of the MAE is that its duration is only slightly reduced if a delay is inserted between the end of the adaptation and the test display ('storage'). The reduction is consistent with recovery of the cellular component, and the residual with network changes that are maintained during the delay. This study aimed (i) to assess explanations for prolonged MAEs in migraine by teasing apart the proposed cellular and network components of adaptation using storage; (ii) to determine the extent of cortical abnormality in migraine using local and global MAEs, which reflect adaptation at different stages of the visual system. Fifty migraine (22 with, 28 without aura) and 50 control participants adapted to motion before viewing a stationary or dynamic (random motion) test, which consequently appeared to move in the opposite direction (local and global MAEs, respectively). Half of the trials included a delay between the adapting and test displays. The results extend those reported previously, as both local and global MAEs lasted longer in migraine compared with the control group. Global MAEs survived delays almost completely for both groups, whereas local MAEs were reduced to a greater extent in migraine. There were no significant differences between migraine subgroups classified according to the presence or absence of visual aura. These results suggest that cellular recovery is slowed in migraine for early but not later visual cortical areas. Sustained network changes following adaptation are implicated across cortical areas. Differences between people with and without migraine on various measures of visual perception have been attributed to abnormal cortical processing in migraine, variously described by hyperexcitability, heightened responsiveness and/or a lack of intra-cortical inhibition. The results are not consistent with hyperexcitability resulting from a lack of inhibition in migraine, but are consistent with extended suppression of intra-cortical excitation. The implications of these results for alternative models of hyperexcitability are discussed.
Shepherd
A J
AJ
School of Psychology, Birkbeck College, University of London, London, UK. a.shepherd@bbk.ac.uk