Opiate-induced persistent pronociceptive trigeminal neural adaptations: potential relevance to opiate-induced medication overuse headache.
Opiate-induced persistent pronociceptive trigeminal neural adaptations: potential relevance to opiate-induced medication overuse headache.
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DOI：
10.1111/j.1468-2982.2009.01873.x
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发表时间：
2009-12
期刊：
影响因子：
--
通讯作者：
Porreca F
中科院分区：
文献类型：
--
作者：
De Felice M;Porreca F
药物过度使用性头痛（MOH）是一种具有挑战性的、使人衰弱的疾病，是由于频繁使用治疗偏头痛的药物而发展起来的。据估计，卫生部影响总人口的3-5%。MOH的发病机制尚不清楚。至少在包括美国在内的一些国家，阿片类药物是治疗偏头痛的主要药物之一。虽然反复使用阿片类药物治疗头痛的影响尚不清楚，但阿片类药物的使用可能导致此类头痛的频率和发生率增加。最近的临床前研究探索了持续暴露于吗啡后的神经适应性变化，可能会对MOH的可能原因有所了解。在外周，这些变化包括三叉神经初级传入神经元中降钙素基因相关肽（CGRP）的表达增加。在中枢，它们包括在背角和尾核水平的兴奋性神经传递增加。关键的是，这些神经适应性变化持续很长一段时间，吗啡预处理后CGRP的释放增强。已知会引起偏头痛的刺激物，如一氧化氮供体或压力，在吗啡中会产生痛觉过敏，但在停用阿片类药物后很长一段时间内，盐水预处理的大鼠不会产生痛觉过敏。CGRP在引发颅内血管舒张和随后的头痛中起重要作用。此外，研究表明偏头痛患者伤害性通路的兴奋性增加，CGRP受体拮抗剂已被证明对偏头痛有效。因此，这种持续的神经适应性变化可能与促进MOH的过程有关。
Medication overuse headache (MOH) is a challenging, debilitating disorder that develops from the frequent use of medications taken for the treatment of migraine headache pain. MOH affects an estimated 3–5% of the general population. The mechanisms underlying the development of MOH remain unknown. Opiates are one of the major classes of medications used for the treatment of migraine at least in some countries, including the USA. Although the effects of repeated opiate use for headache are unknown, it is possible that opiate use may contribute to increased frequency and occurrence of such headaches. Recent preclinical studies exploring the neuroadaptive changes following sustained exposure to morphine may give some insights into possible causes of MOH. Peripherally, these changes include increased expression of calcitonin gene-related peptide (CGRP) in trigeminal primary afferent neurons. Centrally, they include increased excitatory neurotransmission at the level of the dorsal horn and nucleus caudalis. Critically, these neuroadaptive changes persist for long periods of time and the evoked release of CGRP is enhanced following morphine pretreatment. Stimuli known to elicit migraine, such as nitric oxide donors or stress, produce hyperalgesia in morphine- but not in saline-pretreated rats even long after the discontinuation of the opiate. CGRP plays a prominent role in initiating vasodilation of the intracranial blood vessels and subsequent headache. Furthermore, studies have demonstrated increased excitability of the nociceptive pathway in migraine sufferers, and CGRP receptor antagonists have been shown to be efficacious in migraine pain. Thus, such persistent neuroadaptive changes may be relevant to the processes that promote MOH.
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