TFOS DEWS II pain and sensation report.

TFOS DEWS II pain and sensation report.
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DOI:
10.1016/j.jtos.2017.05.002
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发表时间:
2017-07
期刊:
The ocular surface
影响因子:
--
通讯作者:
Wolffsohn JS
Wolffsohn JS
中科院分区:
其他
文献类型:
--
作者:
Belmonte C;Nichols JJ;Cox SM;Brock JA;Begley CG;Bereiter DA;Dartt DA;Galor A;Hamrah P;Ivanusic JJ;Jacobs DS;McNamara NA;Rosenblatt MI;Stapleton F;Wolffsohn JS

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与眼表面的机械和化学刺激相关的疼痛由三叉神经节机械和多模态伤害感受器神经元介导,而冷的温度感受器检测湿度并反射性地维持基础泪液产生和眨眼率。这些神经元投射到三叉神经脑干核复合体的两个区域:ViVc,由眼表水分和VC1的变化激活,介导眼痛和反射性眨眼的感觉辨别方面。ViVc眼神经元投射到控制流泪和自发眨眼的大脑区域以及感觉丘脑。主泪腺的分泌主要由自主副交感神经调节,由眼表面感觉神经反射激活。这些也引起杯状细胞分泌通过不明传出纤维。参与调节梅波尼亚腺分泌或粘蛋白释放的神经通路尚未确定。在干眼病中,泪液分泌减少导致炎症和外周神经损伤。炎症引起多模态和机械伤害感受器神经末梢的敏感化以及冷温度感受器活性的异常增加,共同引起干燥感觉和疼痛。长期炎症和神经损伤改变三叉神经节和脑干神经元的末端和细胞体的离子通道和受体的基因表达,改变它们的兴奋性、连接性和脉冲放电。眼感觉通路中分子、结构和功能障碍的持续存在最终导致涉及眼表面的感觉障碍和神经性疼痛。疼痛可以通过各种问卷进行评估,而角膜神经的状态可以通过触觉测量法和体内共焦显微镜进行评估。
Pain associated to mechanical and chemical irritation of the eye surface is mediated by trigeminal ganglia mechano- and polymodal nociceptor 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 Meibonian gland secretion or mucins 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 in vivo confocal microscopy.
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