2 0 0 0 OA 帯状疱疹後神経痛
1 0 0 0 OA 帯状疱疹の痛みのメカニズム
- 著者
- 横田 敏勝 檀 健二郎 小山 なつ
- 出版者
- Japan Society of Pain Clinicians
- 雑誌
- 日本ペインクリニック学会誌 (ISSN:13404903)
- 巻号頁・発行日
- vol.5, no.2, pp.112-118, 1998-04-25 (Released:2009-12-21)
- 参考文献数
- 39
After chicken pox, varicella-zoster virus (VZV) establishes latent infection in satellite cells in sensory ganglia and eventually reactivates as acute herpes zoster (AHZ) or shingles. The reactivation leads to infection of other cells within the ganglion and results in inflammation of the posterior spinal cord, peripheral nerve and skin. Pain in AHZ is primarily due to inflammation of the infected structures. Epidural block soothes inflammation in the epineurium and controls the ongoing afferent barrage in the affected nerve fibers, preventing sensitization of second order neurons.Postherpetic neuralgia (PHN) is the commonest and perhaps most-dreaded complication of AHZ. Pain of PHN is often of three types; ongoing pain, superimposed paroxysmal pain and allodynia. An ongoing pain is described as burning, aching or tearing, and a superimposed paroxysmal pain as stabbing or electric shock-like. For many patients, sensations evoked by clothes contact or skin stretching with movement constitute the most unbearable part of PHN. There are sensory deficits affecting all modalities in the involved dermatomes, indicative of partial deafferentation. Intravenous lidocaine produces significant relief for PHN, and pain relief with topically applied lidocaine has also been reported. It is likely that ectopic impulses are generated from surviving axons and induce hypersensitivity of second-order neurons.The ectopic impulses are abolished by concentrations of lidocaine much lower than that required for blocking normal axonal conduction. Unfortunately lidocaine is not always effective. Thus deafferentation hyperactivity of second order neurons is another possible explanation.Allodynia is most often elicited by innocuous moving stimuli, and the mechanical allodynia appears to be mediated by large fibers. This implies abnormal synaptic connectivity at the spinal-cord level between large afferent fibers and the central pain signaling secondary neurons. It has been hypothesized that deafferentation of nociceptive fibers leads to vacancies at the level of second-order neurons, enabling these neurons to create new working synaptic connections with surviving large fibers. This reorganization may involve WDR neurons. Then the wind up response of WDR neurons which normally occurs in response to repetitive C fiber stimulation through activation of NMDA receptors, may be brought about by large fiber inputs. This may account for the wind up of tactile allodynia in PHN.