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脑膜感觉神经元的致敏作用与头痛的起源

Sensitization of meningeal sensory neurons and the origin of headaches.

作者信息

Strassman A M, Raymond S A, Burstein R

机构信息

Department of Anesthesia and Critical Care, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA.

出版信息

Nature. 1996 Dec 12;384(6609):560-4. doi: 10.1038/384560a0.

DOI:10.1038/384560a0
PMID:8955268
Abstract

The headaches that accompany certain intracranial pathologies (such as meningitis, subarachnoid haemorrhage and tumour) have been considered to result from mechanical or chemical stimulation of pain-sensitive structures of the intracranial meninges. Although the recurrent headache of migraine is of unknown origin and is not accompanied by an identifiable pathology, it shares with intracranial headaches features that suggest an exaggerated intracranial mechanosensitivity (worsening of the pain by coughing, breath-holding or sudden head movement). One possible basis for such symptoms would be a sensitization of meningeal afferents to mechanical stimuli. Previous studies of neuronal responses to meningeal stimulation have focused primarily on cells in the central portion of the trigeminal pathway, and have not investigated the possible occurrence of sensitization. We have recorded the activity of primary afferent neurons in the rat trigeminal ganglion that innervate the dural venous sinuses. Chemical stimulation of their dural receptive fields with inflammatory mediators both directly excited the neurons and enhanced their mechanical sensitivity, such that they were strongly activated by mechanical stimuli that initially had evoked little or no response. These properties of meningeal afferents (chemosensitivity and sensitization) may contribute to the intracranial mechanical hypersensitivity that is characteristic of some types of clinically occurring headaches, and may also contribute to the throbbing pain of migraine.

摘要

某些颅内病变(如脑膜炎、蛛网膜下腔出血和肿瘤)伴随的头痛被认为是由颅内脑膜疼痛敏感结构受到机械或化学刺激所致。尽管偏头痛的复发性头痛病因不明且无明显可识别的病变,但它与颅内头痛有一些共同特征,提示颅内机械敏感性增强(咳嗽、屏气或突然头部运动可使疼痛加剧)。出现此类症状的一个可能原因是脑膜传入神经对机械刺激的敏感性增加。以往关于神经元对脑膜刺激反应的研究主要集中在三叉神经通路中央部分的细胞,尚未研究是否可能发生敏化现象。我们记录了大鼠三叉神经节中支配硬脑膜静脉窦的初级传入神经元的活动。用炎症介质对其硬脑膜感受野进行化学刺激,既能直接兴奋神经元,又能增强其机械敏感性,使其对最初几乎不引起反应或无反应的机械刺激产生强烈激活。脑膜传入神经的这些特性(化学敏感性和敏化)可能导致某些临床类型头痛所特有的颅内机械超敏反应,也可能导致偏头痛的搏动性疼痛。

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