| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3047608 | Clinical Neurophysiology | 2008 | 11 Pages |
ObjectiveReduced habituation and increased intensity-dependence of cortical auditory-evoked potentials have been reported in migraine, but it is not known if brainstem mechanisms are chiefly or partly responsible for this hypersensitivity, if brainstem excitability or habituation changes across the migraine cycle, or how excitability relates to symptoms and serotonin metabolism.MethodsBrainstem auditory-evoked potentials (BAEPs) to 40, 55, and 70 dB binaural rarefaction clicks were recorded in four blocks of 750 stimuli in a blinded longitudinal study in 41 migraine patients. Serotonin was measured in a blood sample from the cubital vein. The test day was classified as baseline, attack, pre-attack or post-attack.ResultsPre-attack BAEP changes were not found. Wave I, V and interpeak III–V latency increased after the attack. III–V latency correlated with headache history duration and usual headache attack duration. Habituation in wave IV–V dispersion to 40 dB was found in controls but not in migraine (p = 0.04). Serotonin correlated with BAEP amplitude in controls. Low serotonin correlated with more autonomic symptoms. BAEP intensity-dependence was normal in migraine.ConclusionsBAEP latencies, but not amplitude, increase temporarily after a migraine attack. Abnormal habituation of brainstem wave IV–V dispersion in migraine may suggest increased excitation in colliculus inferior at low sound intensities, but no relation to the migraine cycle was found for wave IV–V amplitude, dispersion or habituation. The correlation between BAEP amplitude and serotonin was deranged in migraine patients, but reappeared temporarily within 72 h after an attack.SignificanceNo evidence for pre-attack brainstem auditory sensitization was found in migraine. Intensity-dependence of AEP in migraine is probably not a passive reflection of brainstem dysfunction. BAEP changes seem to reflect a slight impact of migraine on serotonergic brainstem pathways.
