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慢性偏头痛的教训。

The lesson of chronic migraine.

作者信息

Bonavita V, De Simone R

机构信息

Istituto di Diagnosi e Cura Hermitage Capodimonte, Naples, Italy.

出版信息

Neurol Sci. 2015 May;36 Suppl 1:101-7. doi: 10.1007/s10072-015-2175-4.

Abstract

The hypothesis that central sensitization/allodynia is the common final mechanism responsible for the progression of migraine pain is supported by the possibility of tracing back to allodynic mechanisms the action of the main risk factors for chronic migraine validated by the recent literature. The comorbidity between migraine and idiopathic intracranial hypertension without papilledema is emerging as a new, commonly overlooked risk factor for migraine progression whose putative mechanism might also converge on the sensitization of central pain pathways. If headache progression always occurs at the end of a pathogenetic sequence typical of an individual susceptibility to allodynia, then the primary character of chronic migraine might be debated. Allodynia is not specific to migraine but is implied in the progressive amplification of pain after repeated stimuli, a universal adaptive phenomenon. Being largely conditioned by the individual comorbidity profile, allodynia may only in part be defined as primary in itself. Many migraine comorbid conditions, including a hidden idiopathic intracranial hypertension without papilledema, may emphasize susceptibility to allodynia and promote chronic migraine. These factors and comorbid conditions require to be individually assessed and adequately treated to optimize the therapeutic response.

摘要

中枢敏化/异常性疼痛是偏头痛疼痛进展的共同最终机制这一假说,得到了以下可能性的支持:可将近期文献验证的慢性偏头痛主要危险因素的作用追溯至异常性疼痛机制。偏头痛与无视乳头水肿的特发性颅内高压之间的共病,正成为偏头痛进展的一个新的、常被忽视的危险因素,其假定机制可能也集中于中枢疼痛通路的敏化。如果头痛进展总是发生在个体对异常性疼痛易感性的典型发病序列末尾,那么慢性偏头痛的原发性特征可能会受到质疑。异常性疼痛并非偏头痛所特有,而是在反复刺激后疼痛的渐进性放大中起作用,这是一种普遍的适应性现象。异常性疼痛在很大程度上受个体共病情况的制约,其本身可能只能部分地被定义为原发性。许多偏头痛共病情况,包括隐匿性无视乳头水肿的特发性颅内高压,可能会加重对异常性疼痛的易感性并促进慢性偏头痛。需要对这些因素和共病情况进行个体评估并给予适当治疗,以优化治疗反应。

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