Conflict of Interest: None
Enhanced Pain Expectation in Migraine: EEG-Based Evidence for Impaired Prefrontal Function
Article first published online: 6 DEC 2012
© 2012 American Headache Society
Headache: The Journal of Head and Face Pain
Volume 53, Issue 7, pages 1054–1070, July/August 2013
How to Cite
Lev, R., Granovsky, Y. and Yarnitsky, D. (2013), Enhanced Pain Expectation in Migraine: EEG-Based Evidence for Impaired Prefrontal Function. Headache: The Journal of Head and Face Pain, 53: 1054–1070. doi: 10.1111/j.1526-4610.2012.02297.x
Disclosure: The authors report no disclosures.
- Issue published online: 18 JUL 2013
- Article first published online: 6 DEC 2012
- Manuscript Accepted: 26 SEP 2012
- cortical generator;
- pain-evoked potential;
Dysexcitability characterizes the interictal migraineous brain. The main central expressions of this dysexcitability are decreased habituation and enhanced anticipation and attention to pain and other external sensory stimuli.
This study evaluates the effects of anticipation on pain modulation and their neural correlates in migraine.
In 39 migraineurs (20 migraine with aura [MWA] and 19 migraine without aura [MOA]) and 22 healthy controls, cortical responses to 2 successive trains of noxious contact-heat stimuli, presented in either predicted or unpredicted manner, were analyzed using standardized low-resolution electromagnetic tomography key.
A lack of habituation to repeated predicted pain was associated with significantly increased pain-evoked potential amplitudes in MWAs (increase of 3.9 μV) and unchanged ones in MOAs (1.1 μV) but not in controls (decrease of 5 μV). Repeated unpredicted pain resulted in enhanced pain-evoked potential amplitudes in both MWA and MOA groups (increase of 5.5 μV and 4.4 μV, respectively) compared with controls (decrease of 0.2 μV). Source localization revealed reduced activations in the anterior-medial prefrontal cortices and subsequent increased somatosensory activity in migraineurs (P < .05). The prefrontal-somatosensory dysfunction positively correlated with lifetime headache duration (P < .05) and concern of upcoming migraine attacks (P < .05) in MWAs, and with frequency of migraine attacks in MOAs (P < .05).
Our findings of impaired modulation of anticipated pain in migraine suggest a heightened state of anticipatory readiness combined with ineffective recruitment of prefrontal inhibitory pathways during experience of pain; the latter might account for the former, at least partially. In line, less efficient inhibitory capability is a plausible mechanistic explanation for patients' high concern about their upcoming migraine attacks.