Johnson E S
Postgrad Med J. 1978 Apr;54(630):231-43. doi: 10.1136/pgmj.54.630.231.
The concept that migraine results from an initial vasoconstriction due to increased release of noradrenaline from the sympathetic nerves to cranial blood vessels has been reappraised in the light of recently acquired knowledge of the mechanisms of action of drugs used in the treatment of migraine, physiological and pharmacological evidence implicating noradrenaline, and the observations by others that several migraine variants may be associated with some degree of sympathetic overactivity. If the theory is correct, it suggests that both prophylaxis and management of the acute condition should be possible by means of selective alpha-adrenoceptor antagonism. The use of drugs with potentially dangerous vasoconstrictor properties appears to be unnecessary. The suggestion is made that the increased adrenergic activity might result from changes within the hypothalamus.
偏头痛是由于交感神经向颅脑血管释放去甲肾上腺素增加,导致初始血管收缩所致,鉴于最近在偏头痛治疗药物作用机制、涉及去甲肾上腺素的生理和药理学证据以及其他人的观察结果(即几种偏头痛变体可能与某种程度的交感神经过度活动有关)方面获得的知识,这一概念已被重新评估。如果该理论正确,这表明通过选择性α-肾上腺素能受体拮抗作用,应该能够对急性病症进行预防和治疗。使用具有潜在危险血管收缩特性的药物似乎没有必要。有人提出,肾上腺素能活性增加可能是由下丘脑内的变化引起的。