Abstract

BackgroundMigraine is characterized by a hypersensitivity to environmental stimulation which climaxes during headache attacks but persists during attack-free period. Despite ongoing debates about the nature of the mechanisms giving rise to this abnormality, the presence of deficient inhibitory cortical processes has been proposed to be one possible mechanism underlying its pathogenesis. Empirical evidence supporting this claim is mainly based on previous accounts showing functional cortical disexcitability in the sensory domain. Considering that a general inhibitory control process can play an important role across early to later stage of information processing, this may indicate the important role other dimensions of inhibitory control can play in migraine disability. The present study examined the pathophysiological features of inhibitory control that takes place during suppression of prepotent responses in migraineurs.MethodsTwenty-two patients with migraine without aura (mean age = 30.86 ± 5.69 years; 19 females) during the interictal period and 25 healthy controls (mean age = 30.24 ± 3.52 years; 18 females) were recruited. We used a stop signal task in combination with event-related potentials (ERPs) to examine participants’ neural activity supporting response inhibition.ResultsBehaviorally, migraineurs exhibited prolonged stop signal reaction times relative to healthy controls. At the neural level, the amplitude of the stop-N2 over fronto-central, central and centro-parietal scalp regions, a component of the ERPs related to conflict monitoring during early, non-motoric stages of inhibition, was significantly increased in migraineurs. Meanwhile, the amplitude of the stop-P3 over central and centro-parietal scalp regions, a component of the ERPs reflecting late-stage inhibition of the motor system and cognitive evaluation of motor inhibition, was also significantly increased in migraineurs. Ultimately, our time-frequency analysis further revealed increased delta activity in migraineurs.ConclusionsConsistent with the theory that alterations in cognitive cortical processes are a key signature of migraine, our findings revealed an abnormal state of suppressing prepotent responses in migraineurs, which can be attributed to cortical disexcitability of the pre-frontal executive network and centro-parietal sensorimotor network. These novel findings extend to show the existence of dysfunctional inhibition control that occurs during suppression of prepotent responses in migraneurs.

Highlights

  • Migraine is a common episodic neurological disorder mainly characterized by recurrent headache attacks, which has a detrimental influence on quality of life [1, 2]

  • Consistent with the theory that alterations in cognitive cortical processes are a key signature of migraine, our findings revealed an abnormal state of suppressing prepotent responses in migraineurs, which can be attributed to cortical disexcitability of the pre-frontal executive network and centro-parietal sensorimotor network

  • Electrophysiological results N2 (200–250 ms) A mixed ANOVA performed on the mean amplitude of N2 revealed a significant main effect of trial type (F (1, 45) = 383.95, p < 0.001), with the N2 amplitude being larger on Stop trials than on Go trials (p < 0.001)

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Summary

Introduction

Migraine is a common episodic neurological disorder mainly characterized by recurrent headache attacks, which has a detrimental influence on quality of life [1, 2]. Despite ongoing debates about the nature of the mechanisms giving rise to these abnormalities [8, 16], the presence of deficient inhibitory cortical processes has been argued to be one possible mechanism underlying the pathogenesis of these conditions [16,17,18,19,20] Available evidence supporting this claim is mainly based on previous studies on the cortical response to external sensory stimuli in migraineurs [10, 14, 21, 22]. Despite ongoing debates about the nature of the mechanisms giving rise to this abnormality, the presence of deficient inhibitory cortical processes has been proposed to be one possible mechanism underlying its pathogenesis Empirical evidence supporting this claim is mainly based on previous accounts showing functional cortical disexcitability in the sensory domain. The present study examined the pathophysiological features of inhibitory control that takes place during suppression of prepotent responses in migraineurs

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