Postherpetic neuralgia (PHN) is a common and often severely painful peripheral neuropathy. Several recent studies in patients with PHN have been performed using quantitative sensory testing of primary afferent function, skin biopsies, and controlled treatment trials. Moreover, our knowledge of the pain generating mechanisms in PHN has been increased by the comparison of PHN with experimental models of neuropathic pain. Studies on PHN patients suggest several pathophysiological mechanisms in both the peripheral and central nervous system: (1) Pathological active or sensitized nociceptors (irritable nociceptors) can induce secondary changes in central processing, leading to spinal cord hyperexcitability that causes input from mechanoreceptive Aβ-fibers (light touching) to be perceived as pain. These patients characteristically have minimal sensory loss and severe allodynia. (2) Nociceptor function may be selectively impaired within the allodynic skin. In such patients pain and temperature sensation are profoundly impaired but light moving mechanical stimuli can often produce severe pain (allodynia). Anatomical reorganization in the dorsal horn resulting from C-fiber degeneration may lead to Aβ-fiber mediated allodynia. (3) Other patients have severe spontaneous pain, profound sensory loss but no hyperalgesia or allodynia. These patients presumably have lost both large and small diameter fibers. The pain is likely due to increased spontaneous activity in deafferented central neurons and/or reorganization of central connections. In one clinical entity with a single etiology several distinct peripheral and central pathophysiological mechanisms can contribute to pain generation. The three types of mechanisms may even coexist in individual patients. The treatment of PHN is currently unsatisfactory. Improved therapeutic outcomes require that mechanism-based interventions for each of the different mechanisms be developed. In recent years several possible predictors for the development of PHN have been evaluated. Besides age, the acute zoster pain intensity and a preexisting polyneuropathy may be important. Based on the pathophysiological mechanisms several therapeutical interventions may be effective in preventing PHN. Until now, an adaquate analgesia in the acute phase and an early therapy with antiviral drugs might be the most successful options.
In summary, the low systemic toxicity of ropivacaine allows it's clinical use in relatively high concentrations and doses for reliable surgical anaesthesia. The separation between sensory and motor block at low concentrations makes ropivacaine an effective and opioid-saving epidural analgesic for the relief of pain after surgery and during labour.