Sand Trond, Zhitniy Nikita, White Linda R, Stovner Lars Jacob
Department of Neuroscience, Norwegian University of Science and Technology, Norway.
Clin Neurophysiol. 2008 May;119(5):1190-200. doi: 10.1016/j.clinph.2008.01.007. Epub 2008 Mar 7.
Reduced 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.
Brainstem auditory-evoked potentials (BAEPs) to 40, 55, and 70dB 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.
Pre-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 40dB 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.
BAEP 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 72h after an attack.
No 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.
已有报道称偏头痛患者存在皮质听觉诱发电位的习惯化降低和强度依赖性增加，但尚不清楚脑干机制是主要还是部分导致了这种超敏反应，脑干兴奋性或习惯化是否在偏头痛周期中发生变化，以及兴奋性与症状和血清素代谢之间的关系。
在一项针对41名偏头痛患者的双盲纵向研究中，记录了对40、55和70分贝双耳疏波短声的脑干听觉诱发电位（BAEP），共四个750次刺激的组块。采集肘静脉血样测量血清素。将测试日分为基线期、发作期、发作前期或发作后期。
未发现发作前期BAEP有变化。发作后波I、V及峰间III-V潜伏期增加。III-V潜伏期与头痛病史时长及通常的头痛发作时长相关。在对照组中发现波IV-V离散度对40分贝刺激有习惯化现象，而偏头痛患者中未发现（p=0.04）。血清素与对照组的BAEP波幅相关。血清素水平低与更多自主神经症状相关。偏头痛患者的BAEP强度依赖性正常。
偏头痛发作后BAEP潜伏期会暂时增加，但波幅不会。偏头痛患者脑干波IV-V离散度的习惯化异常可能表明在低声强时下丘兴奋性增加，但未发现波IV-V波幅、离散度或习惯化与偏头痛周期有关。偏头痛患者中BAEP波幅与血清素之间的相关性紊乱，但在发作后72小时内暂时重现。
在偏头痛中未发现发作前脑干听觉致敏的证据。偏头痛中AEP的强度依赖性可能不是脑干功能障碍的被动反映。BAEP变化似乎反映了偏头痛对血清素能脑干通路的轻微影响。
