Richter F, Lehmenkühler A
Institut für Physiologie I/Neurophysiologie, Friedrich-Schiller-Universität Jena, Teichgraben 8, 07740 Jena, Deutschland.
Schmerz. 2008 Oct;22(5):544-6, 548-50. doi: 10.1007/s00482-008-0653-9.
Cortical spreading depression (CSD) is a transient (60-120 s) and at 3-5 mm/min propagating depolarization wave of cortical neurons and glial cells and is characterized by a DC shift of 20-35 mV. It is accompanied by massive redistribution of ions between extracellular and intracellular compartments and by a water influx into the cells. Extracellular potassium ion concentration increases up to 60 mM/l. Potassium ions and the excitatory neurotransmitter glutamate essentially contribute to the initiation and propagation of CSD. Both depolarization and disturbance of brain ion homeostasis regenerate within a few minutes while enhancing energy metabolism, but do not cause damage to normally perfused brain tissue. The similar propagation velocity of CSD and visual scotoma during migraine aura led to the assumption that CSD could be the underlying mechanism of migraine aura. The observation of CSD waves in migraine aura patients with the magnet encephalogram (MEG) technique confirmed this theory. Although many data support the relationship between CSD and aura phase in migraine, the role of CSD in migraine headache is still disputed.
皮层扩散性抑制(CSD)是一种短暂的(60 - 120秒)、以3 - 5毫米/分钟速度传播的皮层神经元和神经胶质细胞去极化波,其特征为出现20 - 35毫伏的直流偏移。它伴随着细胞外和细胞内区室之间离子的大量重新分布以及水流入细胞内。细胞外钾离子浓度增加至60毫摩尔/升。钾离子和兴奋性神经递质谷氨酸在CSD的起始和传播中起重要作用。去极化和脑离子稳态的紊乱在几分钟内会再生,同时增强能量代谢,但不会对正常灌注的脑组织造成损害。CSD与偏头痛先兆期间视觉暗点的相似传播速度导致人们推测CSD可能是偏头痛先兆的潜在机制。用脑磁图(MEG)技术在偏头痛先兆患者中观察到CSD波证实了这一理论。尽管许多数据支持CSD与偏头痛先兆期之间的关系,但CSD在偏头痛头痛中的作用仍存在争议。