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冷觉过敏与复杂性区域疼痛综合征 (CRPS) 中的阵发性和诱发机械性疼痛相关。

Cold allodynia is correlated to paroxysmal and evoked mechanical pain in complex regional pain syndrome (CRPS).

机构信息

Section of Clinical Neurophysiology, Department of Neurology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.

Faculty of Medicine, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.

出版信息

Scand J Pain. 2022 Apr 18;22(3):533-542. doi: 10.1515/sjpain-2021-0208. Print 2022 Jul 26.

Abstract

OBJECTIVES

Mechanisms of complex regional pain syndrome (CRPS) are still debated. Identifying subgroups of patients have been attempted in the hope of linking clinical findings to possible mechanisms. The aim of the present study was to investigate whether subgroups of CRPS (based on quantitative sensory testing (QST)-results) differed with respect to different characteristics of pain like spontaneous ongoing or paroxysmal pain and mechanical dynamic allodynia.

METHODS

61 CRPS-patients (type 1 and 2) were examined clinically and with QST, in affected and contralateral extremity, with assessment of thresholds for warmth, cold and heat-and cold pain.

RESULTS

43 patients (20 men, 23 men) were diagnosed with CRPS 1 (70.5%) and 18 patients (8 women and 10 men) with CRPS 2 (29.5%). Three subgroups were defined based on thermal thresholds; A (thermal allodynia 22.9%), B (thermal hyposensitivity 37.3%), C (thermal allodynia and hyposensitivity 39.3%). Paroxysmal pain was more prevalent in patients with thermal allodynia (merging group A + C, 25/38-65.8%) compared to patients without thermal allodynia (group B, 5/23-21.7%) (p-value=0.00085).

CONCLUSIONS

We suggest that cold allodynia is based on hyper-excitability of very superficial skin nociceptors. The correlation between paroxysmal pain, allodynia to light touch and cold allodynia suggests that activity in those peripheral nociceptors can drive both, paroxysmal pain and spinal sensitization leading to stroke evoked allodynia. Mechanistically, the physical cold stimulus can unmask disease-related hyperexcitability by closure of temperature-sensitive potassium channels or induction of resurgent currents. Small fiber degeneration alone may not be the crucial mechanism in CRPS, nor explain pain.

摘要

目的

复杂区域疼痛综合征(CRPS)的发病机制仍存在争议。人们尝试对患者进行亚组分类,希望将临床发现与可能的发病机制联系起来。本研究旨在探讨 CRPS 亚组(基于定量感觉测试(QST)结果)是否在疼痛的不同特征方面存在差异,例如自发性持续性或阵发性疼痛和机械性动态触诱发痛。

方法

对 61 例 CRPS 患者(1 型和 2 型)进行临床检查和 QST 检查,分别在患侧和健侧肢体进行检查,评估温热、寒冷和冷热痛觉的阈值。

结果

43 例患者(20 名男性,23 名女性)被诊断为 CRPS1(70.5%),18 例患者(8 名女性和 10 名男性)被诊断为 CRPS2(29.5%)。根据热阈值将患者分为 3 个亚组;A 组(热感觉过敏 22.9%)、B 组(热感觉迟钝 37.3%)、C 组(热感觉过敏和感觉迟钝 39.3%)。阵发性疼痛在有热感觉过敏的患者中更为常见(合并组 A+C,38/38-65.8%),而在没有热感觉过敏的患者中则较少见(组 B,23/5-21.7%)(p 值=0.00085)。

结论

我们认为冷感觉过敏是基于非常浅表皮肤伤害感受器的超兴奋性。阵发性疼痛、轻触性痛觉过敏和冷感觉过敏之间的相关性表明,这些周围伤害感受器的活动既能引起阵发性疼痛,又能引起脊髓敏化,导致中风诱发的触诱发痛。从机制上讲,物理冷刺激可以通过关闭温度敏感钾通道或诱导再生电流来揭示与疾病相关的超兴奋性。小纤维变性本身可能不是 CRPS 的关键机制,也不能解释疼痛。

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