May A, Bahra A, Büchel C, Frackowiak R S, Goadsby P J
University Department of Clinical Neurology, Institute of Neurology, National Hospital for Neurology and Neurosurgery, London, UK.
Neurology. 2000 Nov 14;55(9):1328-35. doi: 10.1212/wnl.55.9.1328.
Cluster headache (CH), like migraine, is still regarded as a vascular headache although in both conditions a CNS cause has been suggested.
To examine neurovascular mechanisms in CH.
The authors used functional imaging with PET to investigate 18 CH patients (25 to 62 years old). Ten were in the active period (nine patients with induced attacks and one with spontaneous attack) and eight were out of their bout. In addition, the authors studied spontaneous CH and experimental pain in volunteers using MR angiography.
When an acute CH attack was triggered with nitroglycerin (NTG), activation occurred in the ipsilateral posterior inferior hypothalamic gray, the contralateral ventroposterior thalamus, the anterior cingulate cortex, the ipsilateral basal ganglia, the right anterior frontal lobe, and both insulae. In patients out of the bout who experienced only a mild NTG headache, activation was seen bilaterally in the insulae and frontal cortices, the anterior cingulate cortex, the right thalamus, and the left basal ganglia, but not in the hypothalamic gray area. In addition, the authors found a significant activation (vasodilatation) in the region of the major basal arteries that was caused in part by NTG but was also observed in the spontaneous case and could be induced by capsaicin injection into the forehead. Therefore, the vasodilatation is likely to be mediated by neural mechanisms involved in the acute CH attacks that are present in every human being.
Dilatation of cranial vessels is not specific to any particular headache syndrome but generic to cranial neurovascular activation, probably mediated by the trigeminoparasympathetic reflex. These data confirm that CH is a CNS disorder best considered as a form of neurovascular headache.
丛集性头痛（CH）与偏头痛一样，尽管在这两种情况下都有人提出中枢神经系统病因，但仍被视为血管性头痛。
研究丛集性头痛中的神经血管机制。
作者使用正电子发射断层扫描（PET）功能成像技术对18例丛集性头痛患者（年龄在25至62岁之间）进行研究。其中10例处于发作期（9例为诱发发作，1例为自发发作），8例处于发作间歇期。此外，作者还使用磁共振血管造影术研究了志愿者的自发性丛集性头痛和实验性疼痛。
用硝酸甘油（NTG）诱发急性丛集性头痛发作时，同侧下丘脑后下部灰质、对侧腹后丘脑、前扣带回皮质、同侧基底神经节、右前额叶和双侧脑岛均出现激活。在发作间歇期仅经历轻度NTG头痛的患者中，双侧脑岛和额叶皮质、前扣带回皮质、右丘脑和左基底神经节出现激活，但下丘脑灰质区域未出现激活。此外，作者发现主要基底动脉区域有显著激活（血管扩张），这部分是由NTG引起的，但在自发病例中也观察到，并且可以通过在前额注射辣椒素诱发。因此，这种血管扩张可能由参与急性丛集性头痛发作的神经机制介导，而这种机制存在于每个人体内。
颅内血管扩张并非任何特定头痛综合征所特有，而是颅内神经血管激活的共性，可能由三叉神经副交感神经反射介导。这些数据证实丛集性头痛是一种中枢神经系统疾病，最好被视为神经血管性头痛的一种形式。
