Fields H L, Rowbotham M, Baron R
Department of Neurology, University of California at San Francisco 94143, USA.
Neurobiol Dis. 1998 Oct;5(4):209-27. doi: 10.1006/nbdi.1998.0204.
Postherpetic neuralgia (PHN) is a common and often devastatingly painful condition. It is also one of the most extensively investigated of the neuropathic pains. Patients with PHN have been studied using quantitative testing of primary afferent function, skin biopsies, and controlled treatment trials. Together with insights drawn from an extensive and growing literature on experimental models of neuropathic pain these patient studies have provided a preliminary glimpse of the pain-generating mechanisms in PHN. It is clear that both peripheral and central pathophysiological mechanisms contribute to PHN pain. Some PHN patients have abnormal sensitization of unmyelinated cutaneous nociceptors (irritable nociceptors). Such patients characteristically have minimal sensory loss. Other patients have pain associated with small fiber deafferentation. In such patients pain and temperature sensation are profoundly impaired but light moving mechanical stimuli can often produce severe pain (allodynia). In these patients, allodynia may be due to the formation of new connections between nonnociceptive large diameter primary afferents and central pain transmission neurons. Other deafferentation patients have severe spontaneous pain without hyperalgesia or allodynia and presumably have lost both large and small diameter fibers. In this group the pain is likely due to increased spontaneous activity in deafferented central neurons and/or reorganization of central connections. These three types of mechanism may coexist in individual patients and each offers the possibility for developing new therapeutic interventions.
带状疱疹后神经痛（PHN）是一种常见且往往疼痛剧烈的疾病。它也是神经病理性疼痛中研究最为广泛的疾病之一。已经通过对初级传入功能的定量测试、皮肤活检和对照治疗试验对PHN患者进行了研究。这些患者研究与从大量且不断增加的关于神经病理性疼痛实验模型的文献中获得的见解一起，初步揭示了PHN的疼痛产生机制。很明显，外周和中枢病理生理机制都与PHN疼痛有关。一些PHN患者存在无髓鞘皮肤伤害感受器的异常敏化（易激惹伤害感受器）。这类患者的特征是感觉丧失极小。其他患者的疼痛与小纤维传入阻滞有关。在这类患者中，痛觉和温度觉严重受损，但轻微的移动机械刺激通常会产生剧痛（痛觉过敏）。在这些患者中，痛觉过敏可能是由于非伤害性大直径初级传入纤维与中枢疼痛传递神经元之间形成了新的连接。其他传入阻滞患者有严重的自发痛但无痛觉过敏或痛觉过敏，推测同时失去了大直径和小直径纤维。在这组患者中，疼痛可能是由于传入阻滞的中枢神经元自发活动增加和/或中枢连接重组所致。这三种机制可能在个体患者中共存，每种机制都为开发新的治疗干预措施提供了可能性。
