1 Department of Systems Neuroscience, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
2 Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado, Aurora, CO, USA.
J Cereb Blood Flow Metab. 2019 Apr;39(4):573-594. doi: 10.1177/0271678X17733655. Epub 2017 Sep 26.
Vascular theories of migraine and cluster headache have dominated for many years the pathobiological concept of these disorders. This view is supported by observations that trigeminal activation induces a vascular response and that several vasodilating molecules trigger acute attacks of migraine and cluster headache in susceptible individuals. Over the past 30 years, this rationale has been questioned as it became clear that the actions of some of these molecules, in particular, calcitonin gene-related peptide and pituitary adenylate cyclase-activating peptide, extend far beyond the vasoactive effects, as they possess the ability to modulate nociceptive neuronal activity in several key regions of the trigeminovascular system. These findings have shifted our understanding of these disorders to a primarily neuronal origin with the vascular manifestations being the consequence rather than the origin of trigeminal activation. Nevertheless, the neurovascular component, or coupling, seems to be far more complex than initially thought, being involved in several accompanying features. The review will discuss in detail the anatomical basis and the functional role of the neurovascular mechanisms relevant to migraine and cluster headache.
多年来，偏头痛和丛集性头痛的血管学说一直主导着这些疾病的病理生物学概念。这一观点得到了以下观察结果的支持：三叉神经激活会引起血管反应，并且几种血管扩张分子会在易感个体中引发偏头痛和丛集性头痛的急性发作。在过去的 30 年中，随着一些分子（特别是降钙素基因相关肽和垂体腺苷酸环化酶激活肽）的作用远远超出了血管活性作用变得明显，这种推理受到了质疑，因为它们具有调节三叉神经系统中几个关键区域的伤害性神经元活动的能力。这些发现使我们对这些疾病的认识从主要是神经元起源转变，血管表现是三叉神经激活的结果而不是起源。然而，神经血管成分（或耦合）似乎比最初想象的要复杂得多，涉及到几个伴随的特征。这篇综述将详细讨论与偏头痛和丛集性头痛相关的神经血管机制的解剖学基础和功能作用。
