What initiates a migraine attack? Conclusions from four longitudinal studies of quantitative EEG and steady-state visual-evoked potentials in migraineurs
Article first published online: 28 JUN 2011
© 2011 John Wiley & Sons A/S
Acta Neurologica Scandinavica
Special Issue: Selected Articles from the Annual Meeting of the Norwegian Neurological Association, Oslo, November 2010
Volume 124, Issue Supplement s191, pages 56–63, August 2011
How to Cite
Bjørk, M., Stovner, L. J., Hagen, K. and Sand, T. (2011), What initiates a migraine attack? Conclusions from four longitudinal studies of quantitative EEG and steady-state visual-evoked potentials in migraineurs. Acta Neurologica Scandinavica, 124: 56–63. doi: 10.1111/j.1600-0404.2011.01545.x
- Issue published online: 28 JUN 2011
- Article first published online: 28 JUN 2011
- Accepted for publication April 10, 2011.
- cortical excitability;
Bjørk M, Stovner LJ, Hagen K, Sand T. What initiates a migraine attack? Conclusions from four longitudinal studies of quantitative EEG and steady-state visual-evoked potentials in migraineurs. Acta Neurol Scand: 2011: 124 (Suppl. 191): 56–63. © 2011 John Wiley & Sons A/S.
Objectives – Quantitative electroencephalograpic (QEEG) frequency spectra and steady-state visual-evoked potentials (SSVEP) are indicators of corticothalamic excitability (e.g., arousal). Increased interictal excitability is suggested to be an important element in the migraine pathophysiology. In this paper, we summarize our results from four studies of QEEG and SSVEP recordings in migraineurs interictally and in the days before an attack with the intention to shed light on attack-initiating mechanisms.
Material and methods – Thirty-two healthy controls, 33 migraineurs without and eight with aura each had three EEGs with photic stimulation on different days. Using the patient headache diaries, we classified the recordings as interictal, preictal, ictal, or post-ictal retrospectively. Interictal recordings were compared pairwise with attack-related EEGs from the same patient as well as with control EEGs. We also correlated clinical variables with the QEEG and SSVEP data.
Results – Between attacks, we found increased relative theta activity and attenuated medium-frequency photic responses in migraineurs without aura compared with those in controls. Within 36 h before the attack, slow and asymmetric EEG activity developed. Increased trigger sensitivity and photophobia correlated with higher theta power and depressed photic responses. Attack duration, migraine history duration, and pain intensity were associated with EEG slowing.
Conclusions – A general tendency toward EEG slowing and depression of photic responses characterized the migraine group. This pattern was also related to increased severity of symptoms. A change in cortical activity occurred within 36 h before attacks. Our results indicate that thalamocortical hypoexcitability is associated with attack initiation and sensory hypersensitivity in migraine.