Lauritzen M
Laboratory of Clinical Neurophysiology, Rigshospitalet, Copenhagen, Denmark.
Brain. 1994 Feb;117 ( Pt 1):199-210. doi: 10.1093/brain/117.1.199.
The characteristic form and development of sensory disturbances during migraine auras suggests that the underlying mechanism is a disturbance of the cerebral cortex, probably the cortical spreading depression (CSD) of Leão. The demonstration of unique changes of brain blood flow during attacks of migraine with aura, which have been replicated in animal experiments during CSD, constitutes another important line of support for the 'spreading depression' theory, which may be a key to an understanding of the migraine attack. Cortical spreading depression is a short-lasting depolarization wave that moves across the cortex at a rate of 3-5 mm/min. A brief phase of excitation heralds the reaction which is immediately followed by prolonged nerve cell depression synchronously with a dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells and enhanced energy metabolism. Recent experimental work has shown that CSD in the neocortex of a variety of species including man is dependent on activation of a single receptor, the N-methyl-D-aspartate receptor, one of the three subtypes of glutamate receptors. The combined experimental and clinical studies point to fruitful areas in which to look for migraine treatments of the future and provide a framework within which important aspects of the migraine attack can be modelled.
偏头痛先兆期间感觉障碍的特征性形式及发展表明,其潜在机制是大脑皮层紊乱,可能是莱昂的皮层扩散性抑制(CSD)。有先兆偏头痛发作期间脑血流独特变化的证明,在CSD动物实验中也得到了重现,这构成了对“扩散性抑制”理论的另一重要支持依据,该理论可能是理解偏头痛发作的关键。皮层扩散性抑制是一种短暂的去极化波,以3 - 5毫米/分钟的速度在皮层移动。短暂的兴奋期预示着该反应,随后紧接着是长时间的神经细胞抑制,同时伴有脑离子稳态的显著破坏、神经细胞中兴奋性氨基酸外流以及能量代谢增强。最近的实验研究表明,包括人类在内的多种物种新皮层中的CSD依赖于单一受体即N - 甲基 - D - 天冬氨酸受体的激活,它是谷氨酸受体三种亚型之一。综合的实验和临床研究指出了未来寻找偏头痛治疗方法的有效领域,并提供了一个可对偏头痛发作重要方面进行建模的框架。