Leone M, Patruno G, Vescovi A, Bussone G
Istituto Neurologico C. Besta, Milano, Italy.
Cephalalgia. 1990 Oct;10(5):235-9. doi: 10.1046/j.1468-2982.1990.1005235.x.
Current views on cluster headache pathogenesis indicate a primary central nervous system dysfunction, in particular a hypothalamic involvement. To confirm the hypothalamic involvement in cluster headache we evaluated the hypothalamic-pituitary axis responsiveness with the thyrotrophin releasing hormone (TRH) test. A dose of 200 micrograms of TRH was administered i.v. to nine healthy controls, 32 patients with cluster headache during cluster period and 16 in remission period. Delta maximum thyrotrophin (TSH) was significantly lower in patients with cluster headache during cluster period (p less than 0.05 versus healthy controls and cluster headache patients in remission). No difference was observed between healthy controls and cluster headache patients in remission. A monoaminergic dysfunction at the hypothalamic level is hypothesized.
目前关于丛集性头痛发病机制的观点表明存在原发性中枢神经系统功能障碍,尤其是下丘脑受累。为了证实下丘脑与丛集性头痛有关,我们通过促甲状腺激素释放激素(TRH)试验评估了下丘脑 - 垂体轴的反应性。向9名健康对照者、32名处于丛集期的丛集性头痛患者和16名缓解期患者静脉注射200微克TRH。处于丛集期的丛集性头痛患者的促甲状腺激素(TSH)最大变化值显著更低(与健康对照者及缓解期丛集性头痛患者相比,p < 0.05)。健康对照者与缓解期丛集性头痛患者之间未观察到差异。推测在下丘脑水平存在单胺能功能障碍。