Topographic and dipolar analysis of laser-evoked potentials during migraine attack

Objective.-The aim of this study was to perform further evaluation of laser-evoked potentials (LEPs) during migraine attacks using multichannel recording and topographic analysis. Specifically, this study aimed to confirm the pattern previously observed in acute migraine, while also defining the components of LEPs that are mainly modified during headache, as well as the correlation between features of LEPs and clinical variables. In addition, we aimed to conduct a dipolar source analysis of the main LEP waves in migraine patients to check the variability in the source location of LEPs during acute migraine. Background.-An amplitude enhancement of LEPs was previously detected during migraine attack using a single scalp derivation on the vertex; hyperalgesia to heat stimuli was also detected for both the face and hand. Methods.-Eighteen patients suffering from migraine without aura were analyzed. The supraorbital zones and the dorsum of the hand were stimulated on both the symptomatic and nonsymptomatic sides in all patients. The LEPs were recorded via 25 scalp electrodes. Dipolar source analysis of the P2 components was performed using a spherical model in all patients and using a realistic Magnetic Resonance model in four patients. Results.-During attacks, the later waves, and particularly the P2 component, were significantly enhanced; the amplitude of the P2 component obtained during the attack by stimulation of the supraorbital zone on the side of the headache was significantly correlated with the intensity of pain and the frequency of headache. In our patients, the P2 wave was generated in the anterior cingulate cortex, with a shift toward its rostrocaudal portion, and was mainly devoted to elaboration of the emotive compound of pain during migraine attack. Conclusions.-Cortical activation by laser stimuli during migraine attack was confirmed. This effect was more pronounced in patients with a higher frequency of migraine attacks. This may be due to a lack of inhibitory control over the transmission of pain to the cortex. The increased activation of cortical areas devoted to attention and emotion may be linked to headache.