Pathophysiological changes in incentive processing in episodic migraine

Abstract

Abstract Background Multiple lines of research suggests that dysregulation in the dopaminergic system may contribute to migraine pain. However, it is only in recent years that researchers have begun to investigate this by exploring how the system is dysregulated during incentive processing in migraineurs. Still little is known about the pathophysiological changes in incentive processing along the temporal scale in migraineurs. Therefore, the present study examined migraine-related changes in neural processing implicated in incentive anticipation and its delivery.Methods A total of 19 episodic migraine (EM) patients (mean age = 31.95 ± 1.42, 17 females) and 19 healthy controls (HCs) (mean age = 30.16 ± 0.98, 16 females) underwent a monetary incentive delay (MID) task, while event-related potentials (ERPs) were recorded in their brains.Results Electrophysiologically, during the incentive anticipation phase, both Cue-N2 and Cue-P3 amplitudes were of higher magnitude for the reward-anticipation and punishment-anticipation cues compared to the control cue across both groups. This indicates no significant differences in neural activity supporting incentive/no incentive cue evaluation between groups. During the outcome phase, the amplitude of the FRN, an ERP component related to performance evaluation, was significantly larger for punishing feedback than rewarding feedback across both groups. However, the Feedback-P3 amplitude, an ERP component related to attentional processing of motivational value of outcome feedback, was significantly larger for rewarding feedback than punishing feedback in HCs, but not in EM patients. Moreover, a negative correlation was observed between the Feedback-P3 amplitude difference for rewarding minus punishing feedback and subjective pain intensity measured by the VAS in EM patients. Finally, the amplitude of the Feedback-LPP, an ERP component related to attentional processing of the affective value of outcome feedback, was significantly larger for punishing feedback than rewarding feedback only in HCs, but not in EM patients.Conclusions Our findings suggest that pathophysiological changes in incentive processing may act as a core mechanism underlying migraine pathophysiology. This study may also provide sensitive and reliable biomarkers for evaluating the efficacy of migraine therapeutics.