대상포진후 신경통의 병태생리

Abstract

Postherpetic neuralgia (PHN) is one of the most extensively investigated neuropathic pains. Much clinical and experimental evidence supports both peripheral and central pathophysiological mechanisms contributing to the pain of PHN. If loss of inhibitory interneurons (disinhibition) occurs in herpes zoster, this could lead to enhanced responsiveness to peripheral stimulation, increasing the spontaneous activity of central nervous system pain transmission neurons. There are at least two distinct mechanisms for dynamic mechanical allodynia: central sensitization or sprouting of the spinal terminals of Aβ primary afferents to innervate dorsal horn neurons, which follows loss of their normal C-nociceptor input. When the central sensitization is produced by C-fiber activity, Aβ-fibers become capable of activating central nervous system pain signaling neurons, which leads to allodynia. When the peripheral nerve is damaged, in addition to sensitized peripheral terminals, a region near the dorsal root ganglion begins to generate spontaneous impulses and the damaged nociceptors also develop catecholamine sensitivity. Therefore, several distinct pathophysiological mechanisms contribute to the pain of PHN. It is likely that more than one mechanism is operative in an individual, with each offering the possibility for the development of new therapeutic interventions.