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TFOS DEWS二期疼痛和感觉报告 TFOS DEWS II pain and sensation report

期刊名称:The Ocular Surface

卷期:2017年第15卷第3期

关键词:
疼痛 感觉 报告

摘要

摘要:由于机械,化学,热刺激引起的眼球表面疼痛是由三叉神经元介导的,而冷温度感受器可以检测湿度且能够灵活的维持基础泪液生成和眨眼率。这些神经元投射到三叉脑干核复合体的两个区域:ViVc 被眼球表面水分变化激活,以及VcC1,调节眼部疼痛和反射眨眼的感觉描述性成分。ViVc眼部神经元投射到控制流泪和自发性眨眼的大脑区域以及感觉丘脑。主要泪腺的分泌主要由反射性的由眼球表面神经元激活的自主交感神经调节。这些也通过不确定的传出神经纤维来唤醒杯状细胞的分泌。调节睑板腺分泌或粘蛋白释放的神经通路尚未被发现。在干眼症中,减少泪液分泌会导致炎症和周围神经损伤。炎症导致多模式和机械痛觉感受器神经末梢的致敏化,并且使冷温度感受器的活性异常升高,这些共同导致了干燥感及疼痛感。长期的炎症反应以及神经损伤改变了三叉神经节细胞和脑干神经元末端以及细胞受体的离子通道和受体基因表达,改变了它们的兴奋性、连接性和冲动性。从而引发存在于眼部感觉通路的分子、结构和功能障碍,最终导致存在于眼球表面的触物感疼痛及神经性疼痛。疼痛程度可以通过一系列问卷调查进行评估,然而角膜神经状态则是通过触觉测量法以及活体共聚焦显微镜来评估。

 

Pain associated with mechanical, chemical, and thermal heat stimulation of the ocular surface is mediated by trigeminal ganglion neurons, while cold thermoreceptors detect wetness and reflexly maintain basal tear production and blinking rate. These neurons project into two regions of the trigeminal brain stem nuclear complex: ViVc, activated by changes in the moisture of the ocular surface and VcC1, mediating sensory-discriminative aspects of ocular pain and reflex blinking. ViVc ocular neurons project to brain regions that control lacrimation and spontaneous blinking and to the sensory thalamus. Secretion of the main lacrimal gland is regulated dominantly by autonomic parasympathetic nerves, reflexly activated by eye surface sensory nerves. These also evoke goblet cell secretion through unidentified efferent fibers. Neural pathways involved in the regulation of meibomian gland secretion or mucin release have not been identified. In dry eye disease, reduced tear secretion leads to inflammation and peripheral nerve damage. Inflammation causes sensitization of polymodal and mechano-nociceptor nerve endings and an abnormal increase in cold thermoreceptor activity, altogether evoking dryness sensations and pain. Long-term inflammation and nerve injury alter gene expression of ion channels and receptors at terminals and cell bodies of trigeminal ganglion and brainstem neurons, changing their excitability, connectivity and impulse firing. Perpetuation of molecular, structural and functional disturbances in ocular sensory pathways ultimately leads to dysestesias and neuropathic pain referred to the eye surface. Pain can be assessed with a variety of questionaires while the status of corneal nerves is evaluated with esthesiometry and with invivo confocal microscopy.


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