Thomsen L L, Olesen J
Department of Neurology, Glostrup Hospital, University of Copenhagen, Denmark.
Clin Auton Res. 1995 Oct;5(5):243-50. doi: 10.1007/BF01818887.
Abnormal regulation of the large cranial arteries seems to play a significant role in the mechanisms of migraine pain. Thus, vasodilatation of extra- and intracranial conductance arteries has been described both during spontaneous migraine attacks and during experimentally provoked vascular headaches. The regulation of the diameter of these arteries is complex and involves autonomic, trigeminovascular, endothelial and humoral mechanisms. Studies concerned with the function of the autonomic nervous system in migraine suggest that a mild parasympathetic dysfunction may be present. Cerebral arteries in migraineurs are hypersensitive to nitric oxide, which may induce migraine attacks. As the enzyme responsible for nitric oxide synthesis is present in parasympathetic nerve endings around cerebral arteries, this supports a role for the parasympathetic nervous system in migraine. In addition, vasoactive transmitters released from perivascular trigeminal nerve endings may be implicated. Several of these aspects are closely linked to the presumed mechanisms of action of modern migraine therapeutics.
大脑主要动脉的异常调节似乎在偏头痛疼痛机制中起重要作用。因此,在自发性偏头痛发作期间以及实验诱发的血管性头痛期间,均已观察到颅外和颅内传导动脉的血管扩张。这些动脉直径的调节很复杂,涉及自主神经、三叉神经血管、内皮和体液机制。有关自主神经系统在偏头痛中作用的研究表明,可能存在轻度副交感神经功能障碍。偏头痛患者的脑动脉对一氧化氮高度敏感,一氧化氮可能诱发偏头痛发作。由于负责一氧化氮合成的酶存在于脑动脉周围的副交感神经末梢中,这支持了副交感神经系统在偏头痛中的作用。此外,血管周围三叉神经末梢释放的血管活性递质可能也与之有关。其中几个方面与现代偏头痛治疗药物的假定作用机制密切相关。