Srikiatkhachorn A, Maneesri S, Govitrapong P, Kasantikul V
Department of Physiology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Headache. 1998 Jan;38(1):43-9. doi: 10.1046/j.1526-4610.1998.3801043.x.
Accumulating evidence indicates that serotonin (5-HT) may be involved in the process of analgesic-induced headache transformation. In order to clarify this hypothesis, we investigated the 5-HT system in migraine patients with analgesic abuse headache by using platelets as a neuronal model. Our results revealed a significant decrease in platelet 5-HT content in these patients compared to migraine patients and nonheadache controls (179.24 +/- 10.18, 451.22 +/- 14.35, and 480.22 +/- 13.98 ng/10(9) platelets, respectively; P < 0.001). This biochemical result was well correlated with a significant decrease (P < 0.001) in platelet dense body number observed in these patients (5.9 +/- 0.4 and 9.2 +/- 0.6 granules/10 platelets. For migraine patients with and without analgesic abuse headache, respectively). Beside the 5-HT depletion, the presence of numerous large intracytoplasmic vacuoles formed from the surface-connecting canaliculi system was found in this condition. Such a finding has not been previously described. The total area occupied by these vacuoles was significantly greater (P < 0.01) in migraine patients with analgesic overuse than in migraine patients and nonheadache controls (249.2 +/- 19.5, 164.1 +/- 19.5, and 183.1 +/- 20.3 nm2/cells, respectively). As this canaliculi system plays a significant role in the platelet secretory response, such dilatation may imply an excessive release of substances from this system. Based on this platelet model, we suggest that excessive use of analgesics alters the central 5-HT system by depleting 5-HT from its storage sites and results in the hyposerotonergic state. This analgesic-induced 5-HT alteration may be a possible mechanism of headache transformation observed in this condition.
越来越多的证据表明，血清素（5-羟色胺）可能参与了止痛药物诱发的头痛转化过程。为了阐明这一假说，我们以血小板作为神经元模型，对患有止痛药物滥用性头痛的偏头痛患者的5-羟色胺系统进行了研究。我们的结果显示，与偏头痛患者和非头痛对照组相比，这些患者的血小板5-羟色胺含量显著降低（分别为179.24±10.18、451.22±14.35和480.22±13.98 ng/10⁹个血小板；P<0.001）。这一生化结果与在这些患者中观察到的血小板致密体数量显著减少（P<0.001）密切相关（分别为5.9±0.4和9.2±0.6个颗粒/10个血小板，分别对应有和无止痛药物滥用性头痛的偏头痛患者）。除了5-羟色胺耗竭外，在这种情况下还发现存在许多由表面连接小管系统形成的大的胞浆内空泡。这样的发现以前尚未有过描述。这些空泡占据的总面积在止痛药物过度使用的偏头痛患者中显著大于偏头痛患者和非头痛对照组（分别为249.2±19.5、164.1±19.5和183.1±20.3 nm²/细胞）。由于这个小管系统在血小板分泌反应中起重要作用，这种扩张可能意味着该系统物质的过度释放。基于这个血小板模型，我们认为止痛药物的过度使用通过从其储存部位消耗5-羟色胺来改变中枢5-羟色胺系统，并导致5-羟色胺能低下状态。这种止痛药物诱发的5-羟色胺改变可能是在这种情况下观察到的头痛转化的一种可能机制。
