Mechanisms of pain and itch caused by herpes zoster (shingles)
Mechanisms of pain and itch caused by herpes zoster (shingles)
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DOI：
10.1016/j.jpain.2007.10.003
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发表时间：
2008-01-01
期刊：
影响因子：
4
通讯作者：
Oaklander, Anne Louise
中科院分区：
文献类型：
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作者：
Oaklander, Anne Louise
对带状疱疹或带状疱疹后神经痛(PHN)患者的研究为疼痛机制提供了见解。带状疱疹疼痛是一种反映急性组织和神经损伤的正常和神经性疼痛的组合。PHN疼痛在组织愈合后持续，是由持续性神经损伤引起的。虽然还没有带状疱疹或PHN的显微神经学研究，但在痛性多发性神经病中已经记录了自发的C-伤害性感受器活动，也可能发生在带状疱疹中。由于PHN神经和神经节的病理检查显示慢性神经元丢失和无炎症的静止性瘢痕形成，目前还不确定这种情况是否在PHN中持续存在。皮肤活检研究已将PHN的存在与持续性远端伤害性轴突丢失的严重程度相关联，尸检已将疼痛持续性与脊髓背角节段性萎缩联系起来，强调了中枢反应对神经损伤的重要性。对三叉神经痛患者组织的病理学研究表明，短暂的腰间性疼痛反映了相邻裸露轴突之间的触觉神经传递。尽管有大量动物模型的间接证据，但慢性自发性疼痛和机械性痛觉异常的机制仍然不确定。带状疱疹后瘙痒可能是由调节瘙痒的外周和/或中枢神经元无端放电引起的。如果它发生在从带状疱疹严重失去传入的左侧皮肤的神经元中(“麻木”)，患者可能会因为抓挠而给自己造成无痛伤害。进一步的人体研究，通过电生理记录，通过结构和功能成像，以及通过尸检，应该继续提供急需的见解。观点：许多患者带状疱疹后仍有慢性疼痛和/或瘙痒，目前的治疗方法无法缓解。许多人会很乐意自愿参加包括尸检在内的临床研究，试图提高对这些常见和致残疾病的了解。它们的流行使高功率研究成为可能。资金和组织是目前的瓶颈。(C)2008年，由美国疼痛协会提供。
Study of humans with shingles or postherpetic neuralgia (PHN) is providing insights into pain mechanisms. Shingles pain is a combination of normal and neuropathic pain that reflects acute tissue and neural injury. PHN pain, which lasts after tissues have healed, is caused by persistent neural injuries. Spontaneous C-nociceptor activity has been documented in painful polyneuropathies and probably occurs in shingles as well, although there are no microneurographic studies of either shingles or PHN. It is uncertain if this persists in PHN since pathological examination of PHN-affected nerves and ganglia show chronic neuronal loss and quiescent scarring without inflammation. Skin-biopsy study has correlated the presence of PHN with the severity of persistent distal nociceptive axon loss, and autopsy has correlated pain persistence with segmental atrophy of the spinal cord dorsal horn, highlighting the importance of central responses to nerve injury. Pathological studies of tissues from patients with trigeminal neuralgia suggest that brief lancinating pains reflect ephaptic neurotransmission between adjacent denuded axons. The mechanisms of chronic spontaneous pain and mechanical allodynia remain uncertain despite considerable indirect evidence from animal models. Postherpetic itch is presumably caused by unprovoked firing of the peripheral and/or central neurons that mediate itch. if it occurs in neurons innervating skin left severely deafferented from shingles ("numb"), patients can give themselves painless injuries from scratching. Further human study, by electrophysiological recording, by structural and functional imaging, and by autopsy, should continue to provide much-needed insights.Perspective: Many patients continue to have chronic pain and/or itch after shingles that is unrelieved by current treatments. Many will gladly volunteer for clinical studies, including autopsy, to try and improve understanding of these common and disabling conditions. Their prevalence makes highly powered studies feasible. Funding and organization are the current bottlenecks. (c) 2008 by the American Pain Society.