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药物过度使用性头痛的病理生理学:来自临床前研究的见解和假说。

Pathophysiology of medication overuse headache: insights and hypotheses from preclinical studies.

机构信息

University of New England, USA.

出版信息

Cephalalgia. 2011 May;31(7):851-60. doi: 10.1177/0333102411402367. Epub 2011 Mar 28.

Abstract

INTRODUCTION

Medication overuse headache (MOH) is a clinical concern in the management of migraine headache. MOH arises from the frequent use of medications used for the treatment of a primary headache. Medications that can cause MOH include opioid analgesics as well as formulations designed for the treatment of migraine, such as triptans, ergot alkaloids, or drug combinations that include caffeine and barbiturates.

LITERATURE REVIEW

Gathering evidence indicates that migraine patients are more susceptible to development of MOH, and that prolonged use of these medications increases the prognosis for development of chronic migraine, leading to the suggestion that similar underlying mechanisms may drive both migraine headache and MOH. In this review, we examine the link between several mechanisms that have been linked to migraine headache and a potential role in MOH. For example, cortical spreading depression (CSD), associated with migraine development, is increased in frequency with prolonged use of topiramate or paracetamol.

CONCLUSIONS

Increased CGRP levels in the blood have been linked to migraine and elevated CGRP can be casued by prolonged sumatriptan exposure. Possible mechanisms that may be common to both migraine and MOH include increased endogenous facilitation of pain and/or diminished diminished endogenous pain inhibition. Neuroanatomical pathways mediating these effects are examined.

摘要

简介

药物过度使用性头痛(MOH)是偏头痛治疗中需要关注的临床问题。MOH 是由于频繁使用原发性头痛治疗药物引起的。可能导致 MOH 的药物包括阿片类镇痛药以及曲坦类、麦角生物碱或含有咖啡因和巴比妥类药物的药物组合等专门用于治疗偏头痛的制剂。

文献综述

研究表明,偏头痛患者更容易发生 MOH,并且这些药物的长期使用会增加慢性偏头痛发展的预后,这表明类似的潜在机制可能会同时导致偏头痛和 MOH。在这篇综述中,我们研究了与偏头痛相关的几种机制之间的联系,并探讨了它们在 MOH 中的潜在作用。例如,与偏头痛发生相关的皮质扩散性抑制(CSD)在使用托吡酯或扑热息痛时间延长时会增加频率。血液中 CGRP 水平升高与偏头痛有关,而延长舒马曲坦暴露也会导致 CGRP 升高。可能与偏头痛和 MOH 都相关的机制包括内源性疼痛易化增加和/或内源性疼痛抑制减少。本文还研究了介导这些作用的神经解剖途径。

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