Lauritzen M
Department of General Physiology and Biophysics, University of Copenhagen, Panum Institute, Denmark.
Pathol Biol (Paris). 1992 Apr;40(4):332-7.
Cortical spreading depression (CSD) is a slowly-moving suppression of electrical activity that travels across the cortex at a rate of 2-5 min-1. CSD is transient, and accompanied by a severe disruption of ion homeostasis, depolarization of nerve cells and enhanced energy metabolism. The slow march of migraine prodromes has many features in common with CSD. On this background it has been suggested that CSD is a mechanism of migraine. Recently, the notion has gained renewed credibility with the demonstration of unique abnormalities of brain blood flow, energy metabolism and magnetoencephalography during migraine attacks which have been replicated point-by-point in the animal model during CSD. Simultaneously, a series of experiments have indicated that CSD is closely linked to activity of the N-methyl-D-aspartate (NMDA)-subtype of the glutamate-receptor. It is suggested, that N-methyl-D-aspartate-antagonism could be the next bid of a rational migraine therapy.
皮层扩散性抑制(CSD)是一种缓慢移动的电活动抑制,以每分钟2 - 5毫米的速度穿过皮层。CSD是短暂的,伴有离子稳态的严重破坏、神经细胞的去极化和能量代谢增强。偏头痛前驱症状的缓慢进展与CSD有许多共同特征。在此背景下,有人提出CSD是偏头痛的一种机制。最近,随着偏头痛发作期间脑血流、能量代谢和脑磁图独特异常的证实,这一观点重新获得了可信度,这些异常在CSD动物模型中已被逐一复制。同时,一系列实验表明CSD与谷氨酸受体的N - 甲基 - D - 天冬氨酸(NMDA)亚型的活性密切相关。有人认为,N - 甲基 - D - 天冬氨酸拮抗剂可能是合理偏头痛治疗的下一个方向。