Pathophysiology of Medication-overuse Headache: Implications from Animal Studies

被引：21

作者：

Bongsebandhu-Phubhakdi, Saknan ^{[1
]}

Srikiatkhachorn, Anan ^{[1
]}

机构：

[1] Chulalongkorn Univ, Neurosci Unit, Dept Physiol, Fac Med, Bangkok 10330, Thailand

来源：

CURRENT PAIN AND HEADACHE REPORTS | 2012年 / 16卷 / 01期

关键词：

Analgesics; Calcitonin gene-related peptide; Cortical spreading depression; Ergot; Headache; Medication overuse headache; Migraine; Nitric oxide; Nociception; Serotonin; Substance P; Tension-type headache; Trigeminal system; Triptans; CORTICAL SPREADING DEPRESSION; GENE-RELATED PEPTIDE; SEROTONIN DEPLETION; POSSIBLE MECHANISM; 5-HT2A RECEPTOR; SUBSTANCE-P; MIGRAINE; INCREASES; EXPOSURE; HYPEREXCITABILITY;

D O I：

10.1007/s11916-011-0234-y

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Recent animal experiments have shown that chronic medication exposure profoundly affects the function of several areas in the nervous system related to headache pathogenesis. These changes include upregulation of calcitonin gene-related peptide, substance P, and nitric oxide synthase in trigeminal ganglia; expansion of receptive field and decreased nociceptive threshold of central trigeminal neurons; decrease in diffuse noxious inhibitory control; and increased susceptibility to develop cortical spreading depression (CSD). These changes indicate an increase in excitability of cortical and trigeminal neurons. The neuronal hyperexcitability may be the result of derangement of a central, possibly serotonin (5-HT)-dependent, modulating control system. Experiments with animals with low 5-HT showed that the processes of CSD and trigeminal nociception are enhanced in this condition. Derangement in the central 5-HT-dependent modulating system as a result of chronic medication use may underlie the chronification of headache as observed in patients with medication-overuse headache.

引用

页码：110 / 115

页数：6

共 29 条

[1] Suppression of cortical spreading depression in migraine prophylaxis [J].