Jensen K
University of Copenhagen, Department of Neurology, Gentofte Hospital, Hellerup, Denmark.
Acta Neurol Scand Suppl. 1993;147:1-27.
Migraine pain has traditionally been ascribed to dilatation of primarily extracranial arteries. Such dilatation has, however, not been demonstrated so far. Studies of microcirculation reveal no major hyperperfusion or ischemia in the temporal muscle or the subcutaneous tissue in the temporal region during attacks of migraine. However, a reduction in the orthostatic reactivity of the subcutaneous arterioles was observed on the side of the headache. Increased tenderness of the pericranial myofascial tissues is observed during migraine attacks, particularly on the side of the headache. Increased tension of pericranial muscles on the other hand is not a constant finding and migraine attacks are not induced by experimentally increased tension of the temporal and masseter muscles. Extracranial pain and tenderness may, however, be induced experimentally by intramuscular injections of hypertonic saline and potassium chloride as well as of endogenous substances like bradykinin with 5-hydroxytryptamine and bradykinin with substance P. The extracranial arteries and myofascial structures are both supplied by unmyelinated trigeminal sensory nerve fibers containing a variety of neuropeptides which are released during migraine attacks. Axonal reflexes between extracranial arteries and neighbouring myofascial tissues as well as referred pain mechanisms may account for the observed tenderness during migraine attacks.
传统上，偏头痛疼痛被归因于主要是颅外动脉的扩张。然而，迄今为止尚未证实这种扩张。微循环研究表明，在偏头痛发作期间，颞肌或颞区皮下组织没有明显的高灌注或缺血。然而，在头痛一侧观察到皮下小动脉的直立反应性降低。在偏头痛发作期间，观察到颅周肌筋膜组织的压痛增加，尤其是在头痛一侧。另一方面，颅周肌肉张力增加并非持续存在的现象，并且实验性增加颞肌和咬肌的张力并不会诱发偏头痛发作。然而，通过肌肉注射高渗盐水、氯化钾以及内源性物质如缓激肽与5-羟色胺和缓激肽与P物质，可实验性诱发颅外疼痛和压痛。颅外动脉和肌筋膜结构均由含有多种神经肽的无髓三叉神经感觉神经纤维供应，这些神经肽在偏头痛发作期间释放。颅外动脉与相邻肌筋膜组织之间的轴突反射以及牵涉痛机制可能解释了偏头痛发作期间观察到的压痛。
