Response inhibition alterations in migraine: An event-related potential study

Abstract

Background Migraine 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 notion is mainly based on previous findings showing functional cortical hyperexcitability 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 in turn indicate the important role other dimensions of inhibitory control can play in migraine disability. To this end, the present study was designed to examine the pathophysiological basis of inhibitiory control that takes place during suppression of prepotent responses. Methods Twenty-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 employed a stop signal task in combination with event-related potentials (ERPs) to examine participants’ neural activity supporting response inhibition. Results Behaviorally, migraineurs exhibited prolonged reaction times to the stop signal relative to healthy controls. At the neural level, the amplitude of the stop-N2, 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, a component of the ERPs reflecting late-stage inhibition of the motor system itself and cognitive evaluation of motor inhibition, was also significantly increased in migraineurs. Moreover, our time-frequency analysis has further revealed increased delta activity in the time window used to extract the mean amplitude of the stop-P3 in migraineurs relative to healthy controls. Conclusions Consistent with the theory that cortical hyperexcitability is a key signature of migraine, these findings revealed a decrease in suppressing prepotent responses in migraineurs, which can be attributable to cortical hyperexcitability. These novel findings imply the existence of dysfunctional inhibitory control at later stage of information processing.