Migraine is a complex brain disorder and initiating events for acute attacks still remain unclear. It seems difficult to explain the development of migraine headache with one mechanism and/or a single anatomical location. Cortical spreading depression (CSD) is recognized as the biological substrate of migraine aura and experimental animal studies have provided mechanisms that possibly link CSD to the activation of trigeminal neurons mediating lateralized head pain. However, some CSD features do not match the clinical features of migraine headache and there are gaps in translating CSD to migraine with aura. Clinical features of migraine headache and results from research are critically evaluated; and consistent and inconsistent findings are discussed according to the known basic features of canonical CSD: typical SD limited to the cerebral cortex as it was originally defined. Alternatively, arguments related to the emergence of SD in other brain structures in addition to the cerebral cortex or CSD initiated dysfunction in the thalamocortical network are proposed. Accordingly, including thalamus, particularly reticular nucleus and higher order thalamic nuclei, which functions as a hub connecting the visual, somatosensory, language and motor cortical areas and subjects to modulation by brain stem projections into the CSD theory, would greatly improve our current understanding of migraine.

中文翻译：

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先兆和头痛：转化模型中的关系和差距

偏头痛是一种复杂的脑部疾病，急性发作的起始事件仍不清楚。似乎很难用一种机制和/或单一解剖位置来解释偏头痛的发生。皮质扩散抑制 (CSD) 被认为是偏头痛先兆的生物学基础，实验动物研究提供了可能将 CSD 与介导偏头痛的三叉神经元激活联系起来的机制。然而，某些 CSD 特征与偏头痛的临床特征并不相符，将 CSD 转化为先兆偏头痛也存在差距。对偏头痛的临床特征和研究结果进行严格评估；根据典型 CSD 的已知基本特征讨论一致和不一致的发现：典型的 SD 仅限于最初定义的大脑皮层。或者，提出了与除了大脑皮层之外的其他大脑结构中出现 SD 或 CSD 引发丘脑皮质网络功能障碍有关的论点。因此，将丘脑，特别是网状核和高阶丘脑核纳入 CSD 理论中，它们作为连接视觉、体感、语言和运动皮质区域的枢纽，并受到脑干投射的调节，将极大地提高我们目前对偏头痛。