In the syndrome of post-herpetic neuralgia (PHN), the nature of the sensory disturbance and its relationship both to the severity and cause of the pain is controversial. To address these issues, sensory mapping and quantitative thermal sensory testing was carried out four times in separate sessions on 35 subjects with established PHN. All subjects had pain affecting the torso or extremities and brush-evoked allodynia. Each session included rating of ongoing pain, mapping of the area of any sensory disturbance and the area of greatest pain, grading of allodynia severity within the area of greatest ongoing pain, and quantitative testing of thermal sensation in both the painful and the contralateral unaffected mirror-image skin. The severity of allodynia was positively correlated with reported ongoing pain severity. As a group, subjects had a sensory deficit to thermal stimuli in PHN skin compared with unaffected mirror-image skin. However, the magnitude of the heat pain sensory deficit was inversely correlated with both pain intensity and severity of allodynia. In fact, 12 subjects had heat hyperalgesia in their region of maximum pain. Compared with the 23 subjects with heat hypoalgesia, the group of 12 heat hyperalgesic subjects had significantly higher pain ratings and allodynia severity. Sensory loss was less strongly, but still inversely related to pain severity for the thermal modalities of innocuous warming, cooling and cold pain. This implies that there is no simple relationship between loss of peripheral nerve function and spontaneous or evoked pain. Rather, the preservation of several sensory modalities in their area of maximal pain suggests that in some PHN patients, activity in primary afferent nociceptors that remain connected to both their peripheral and central targets contributes significantly to ongoing pain. Although other mechanisms are likely to contribute to the pain, the demonstrated responsivity of PHN to topical agents including local anaesthetics, capsaicin, and non-steroidal anti-inflammatory drugs, supports this proposed mechanism of pain generation.

译文

在带状疱疹后神经痛 (PHN) 综合征中,感觉障碍的性质及其与疼痛的严重程度和原因的关系是有争议的。为了解决这些问题,在35个已建立PHN的受试者中,分别进行了四次感官映射和定量热感官测试。所有受试者都有影响躯干或四肢的疼痛和刷子诱发的异常性疼痛。每个疗程包括持续疼痛的评分,任何感觉障碍区域和最大疼痛区域的映射,最大持续疼痛区域内的异常性疼痛严重程度的分级,以及对疼痛和对侧未受影响的镜像皮肤的热感觉的定量测试。异常性疼痛的严重程度与报告的持续疼痛严重程度呈正相关。作为一组,与未受影响的镜像皮肤相比,受试者对PHN皮肤的热刺激感觉不足。然而,热痛感觉缺陷的程度与疼痛强度和异常性疼痛的严重程度呈负相关。实际上,有12名受试者在其最大疼痛区域存在热痛觉过敏。与23例热痛觉低下的受试者相比,12例热痛觉过敏受试者的疼痛等级和异常性疼痛严重程度明显更高。感觉损失不那么强烈,但对于无害的变暖,降温和冷痛的热方式,其疼痛程度仍与疼痛严重程度成反比。这意味着周围神经功能丧失与自发性或诱发性疼痛之间没有简单的关系。相反,在其最大疼痛区域保留几种感觉方式表明,在某些PHN患者中,与周围和中心目标保持联系的主要传入伤害感受器的活动显着导致持续的疼痛。尽管其他机制可能会导致疼痛,但已证明PHN对局部药物 (包括局部麻醉剂,辣椒素和非甾体抗炎药) 的反应性支持了这种提出的疼痛产生机制。

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