VASODILATATION, LOWERED PAIN THRESHOLD, AND INCREASED TISSUE VULNERABILITY

Abstract

Several observations suggest that neural activity may damage tissues by mechanisms other than those producing ischemia. The phenomenology of herpes zoster, with vasodilation, vesiculation, and necrosis of the skin accompanying damage of the dorsal and ventral horns, was at one time cited as evidence that nerve damage might secondarily cause skin injury. However, since the virus of herpes zoster has been demonstrated not only in the neural structures, but also in the skin, it is uncertain what part the nervous system effects play.* The occurrence of herpes labialis following dorsal root section for trigeminal neuralgia supports the view that alterations in neural function may so change the environment of latent virus forms in the skin that they become active.² Thus, about 90% of persons who have had dorsal root section of the trigeminal nerve near the ganglion, including fibers subserving sensation of the lips, exhibit, as a sequel, herpes