Cortical hyperexcitability and mechanism of medication-overuse headache
Cortical hyperexcitability and mechanism of medication-overuse headache
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DOI：
10.1177/0333102409355600
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发表时间：
2010-09-01
期刊：
影响因子：
4.9
通讯作者：
Srikiatkhachorn, Anan
中科院分区：
文献类型：
--
作者：
Supornsilpchai, Weera;le Grand, Supang Maneesri;Srikiatkhachorn, Anan
本研究旨在确定急性（1 h）和慢性（每日剂量，持续30天）给予对乙酰氨基酚对皮质扩散性抑制（CSD）、CSD诱发的皮质充血和CSD诱导的大脑皮质和三叉神经尾侧核（TNC）Fos表达的影响。对Wistar大鼠给予对乙酰氨基酚（200 mg/ kg体重，腹膜内）。CSD由局部应用固体KCl引起。记录皮层脑电图和皮层血流量。结果显示，急性对乙酰氨基酚给药显著降低了顶叶皮质和TNC中Fos免疫反应细胞的数量，而不会引起CSD频率的变化。另一方面，对乙酰氨基酚长期给药导致CSD频率增加以及CSD诱发的顶叶皮层和TNC中Fos表达增加，表明皮层兴奋性增加和三叉神经伤害感受易化。皮质兴奋性的改变导致CSD发展的易感性增加可能是药物过度使用性头痛的潜在机制。
The present study was conducted to determine the effect of acute (1 h) and chronic (daily dose for 30 days) paracetamol administration on the development of cortical spreading depression (CSD), CSD-evoked cortical hyperaemia and CSD-induced Fos expression in cerebral cortex and trigeminal nucleus caudalis (TNC). Paracetamol (200 mg/ kg body weight, intraperitonealy) was administered to Wistar rats. CSD was elicited by topical application of solid KCl. Electrocorticogram and cortical blood flow were recorded. Results revealed that acute paracetamol administration substantially decreased the number of Fos-immunoreactive cells in the parietal cortex and TNC without causing change in CSD frequency. On the other hand, chronic paracetamol administration led to an increase in CSD frequency as well as CSD-evoked Fos expression in parietal cortex and TNC, indicating an increase in cortical excitability and facilitation of trigeminal nociception. Alteration of cortical excitability which leads to an increased susceptibility of CSD development can be a possible mechanism underlying medication-overuse headache.