May A, Goadsby P J
University Department of Clinical Neurology, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, London, UK.
J Cereb Blood Flow Metab. 1999 Feb;19(2):115-27. doi: 10.1097/00004647-199902000-00001.
Primary headache syndromes, such as cluster headache and migraine, are widely described as vascular headaches, although considerable clinical evidence suggests that both are primarily driven from the brain. The shared anatomical and physiologic substrate for both of these clinical problems is the neural innervation of the cranial circulation. Functional imaging with positron emission tomography has shed light on the genesis of both syndromes, documenting activation in the midbrain and pons in migraine and in the hypothalamic gray in cluster headache. These areas are involved in the pain process in a permissive or triggering manner rather than as a response to first-division nociceptive pain impulses. In a positron emission tomography study in cluster headache, however, activation in the region of the major basal arteries was observed. This is likely to result from vasodilation of these vessels during the acute pain attack as opposed to the rest state in cluster headache, and represents the first convincing activation of neural vasodilator mechanisms in humans. The observation of vasodilation was also made in an experimental trigeminal pain study, which concluded that the observed dilation of these vessels in trigeminal pain is not inherent to a specific headache syndrome, but rather is a feature of the trigeminal neural innervation of the cranial circulation. Clinical and animal data suggest that the observed vasodilation is, in part, an effect of a trigeminoparasympathetic reflex. The data presented here review these developments in the physiology of the trigeminovascular system, which demand renewed consideration of the neural influences at work in many primary headaches and, thus, further consideration of the physiology of the neural innervation of the cranial circulation. We take the view that the known physiologic and pathophysiologic mechanisms of the systems involved dictate that these disorders should be collectively regarded as neurovascular headaches to emphasize the interaction between nerves and vessels, which is the underlying characteristic of these syndromes. Moreover, the syndromes can be understood only by a detailed study of the cerebrovascular physiologic mechanisms that underpin their expression.
原发性头痛综合征，如丛集性头痛和偏头痛，尽管有大量临床证据表明两者主要由脑部驱动，但仍被广泛描述为血管性头痛。这两种临床问题共同的解剖和生理基础是颅循环的神经支配。正电子发射断层扫描功能成像揭示了这两种综合征的发病机制，记录了偏头痛时中脑和脑桥以及丛集性头痛时下丘脑灰质的激活。这些区域以允许或触发的方式参与疼痛过程，而不是作为对第一分支伤害性疼痛冲动的反应。然而，在一项丛集性头痛的正电子发射断层扫描研究中，观察到主要基底动脉区域的激活。这可能是由于这些血管在急性疼痛发作期间与丛集性头痛的静息状态相比发生了血管舒张，代表了人类神经血管舒张机制的首次令人信服的激活。在一项实验性三叉神经痛研究中也观察到了血管舒张，该研究得出结论，三叉神经痛中观察到的这些血管舒张并非特定头痛综合征所固有，而是颅循环三叉神经支配的一个特征。临床和动物数据表明，观察到的血管舒张部分是三叉神经 - 副交感神经反射的作用。本文所呈现的数据回顾了三叉神经血管系统生理学的这些进展，这些进展需要重新考虑许多原发性头痛中起作用的神经影响，从而进一步考虑颅循环神经支配的生理学。我们认为，所涉及系统的已知生理和病理生理机制表明，这些疾病应被统称为神经血管性头痛，以强调神经与血管之间的相互作用，这是这些综合征的潜在特征。此外，只有通过对支撑其表现的脑血管生理机制进行详细研究，才能理解这些综合征。
