Glinskii Olga V, Huxley Virginia H, Glinsky Vladislav V
Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO, United States.
Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO, United States.
Front Neurol. 2017 Oct 18;8:549. doi: 10.3389/fneur.2017.00549. eCollection 2017.
The pathogenesis of headaches is a matter of ongoing discussion of two major theories describing it either as a vascular phenomenon resulting from vasodilation or primarily as a neurogenic process accompanied by secondary vasodilation associated with sterile neurogenic inflammation. While summarizing current views on neurogenic and vascular origins of headache, this mini review adds new insights regarding how smooth muscle-free microvascular networks, discovered within dura mater connective tissue stroma (previously thought to be "avascular"), may become a site of initial insult generating the background for the development of headache. Deficiencies in estrogen-dependent control of microvascular integrity leading to plasma protein extravasation, potential activation of perivascular and connective tissue stroma nociceptive neurons, and triggering of inflammatory responses are described. Finally, possible avenues for controlling and preventing these pathophysiological changes are discussed.
头痛的发病机制是一个持续讨论的问题，有两种主要理论，一种将其描述为血管扩张导致的血管现象，另一种主要将其描述为伴有与无菌性神经源性炎症相关的继发性血管扩张的神经源性过程。在总结当前关于头痛的神经源性和血管源性起源的观点时，本综述补充了新的见解，即硬脑膜结缔组织基质（以前认为是“无血管的”）中发现的无平滑肌微血管网络如何可能成为初始损伤的部位，从而为头痛的发展产生背景。文中描述了雌激素依赖性微血管完整性控制不足导致血浆蛋白外渗、血管周围和结缔组织基质伤害感受神经元的潜在激活以及炎症反应的触发。最后，讨论了控制和预防这些病理生理变化的可能途径。
