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脊髓麻醉期间的痛觉过敏和镇痛作用减弱

Hyperalgesia and Reduced Offset Analgesia During Spinal Anesthesia.

作者信息

Sitsen Elske, van Velzen Monique, de Rover Mischa, Dahan Albert, Niesters Marieke

机构信息

Department of Anesthesiology, Leiden University Medical Center, Leiden, RC 2300, the Netherlands.

出版信息

J Pain Res. 2020 Aug 24;13:2143-2149. doi: 10.2147/JPR.S258533. eCollection 2020.

DOI:10.2147/JPR.S258533
PMID:33061546
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7519835/
Abstract

INTRODUCTION

Spinal anesthesia induces short-term deafferentation and causes connectivity changes in brain areas involved in endogenous pain modulation. We determined whether spinal anesthesia alters pain sensitivity and offset analgesia. Offset analgesia is a manifestation of endogenous pain modulation and characterized by profound analgesia upon a small decrease in noxious stimulation.

METHODS

In this randomized controlled crossover trial, static thermal pain responses and offset analgesia were obtained in 22 healthy male volunteers during spinal anesthesia and control conditions (absence of spinal anesthesia). Pain responses and offset analgesia were measured on a remote skin area above the upper level of anesthesia (C8/Th1).

RESULTS

Following spinal injection of the local anesthetic, the average maximum anesthesia level was Th6. Static pain scores at C8/Th1 were higher during spinal anesthesia compared to control: 59.1 ± 15.0 mm (spinal anesthesia) versus 51.7 ± 19.7 mm (control; p = 0.03). Offset analgesia responses were decreased during spinal analgesia: pain score decrease 79 ± 27% (spinal anesthesia) versus 90 ± 17% (control; p = 0.016).

DISCUSSION

We confirmed that spinal anesthesia-induced deafferentation causes hyperalgesic responses to noxious thermal stimulation and reduced offset analgesia at dermatomes remote and above the level of deafferentation. While these data suggest that the reduction of offset analgesia has a central origin, related to alterations in brain areas involved in inhibitory pain control, we cannot exclude alternative (peripheral) mechanisms.

TRIAL REGISTRATION

Dutch Cochrane Center under identifier (www.trialregister.nl) NL3874.

摘要

引言

脊髓麻醉会导致短期传入神经阻滞,并引起参与内源性疼痛调节的脑区连接性变化。我们确定脊髓麻醉是否会改变疼痛敏感性和抵消性镇痛。抵消性镇痛是内源性疼痛调节的一种表现,其特征是在有害刺激稍有减少时就会出现深度镇痛。

方法

在这项随机对照交叉试验中,对22名健康男性志愿者在脊髓麻醉和对照条件下(无脊髓麻醉)进行了静态热痛反应和抵消性镇痛测试。在高于麻醉上界的远隔皮肤区域(C8/Th1)测量疼痛反应和抵消性镇痛。

结果

脊髓注射局部麻醉药后,平均最大麻醉平面为胸6。与对照相比,脊髓麻醉期间C8/Th1处的静态疼痛评分更高:59.1±15.0毫米(脊髓麻醉)对51.7±19.7毫米(对照;p = 0.03)。脊髓镇痛期间抵消性镇痛反应降低:疼痛评分降低79±27%(脊髓麻醉)对90±17%(对照;p = 0.016)。

讨论

我们证实,脊髓麻醉引起的传入神经阻滞会导致对有害热刺激的痛觉过敏反应,并降低传入神经阻滞区域远隔和上方皮节的抵消性镇痛。虽然这些数据表明抵消性镇痛的降低有中枢起源,与参与抑制性疼痛控制的脑区改变有关,但我们不能排除其他(外周)机制。

试验注册

荷兰 Cochrane 中心,标识符为(www.trialregister.nl)NL3874。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2cd/7519835/81c91605d8ec/JPR-13-2143-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2cd/7519835/4b9e313a8da9/JPR-13-2143-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2cd/7519835/b45eb102c380/JPR-13-2143-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2cd/7519835/81c91605d8ec/JPR-13-2143-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2cd/7519835/4b9e313a8da9/JPR-13-2143-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2cd/7519835/b45eb102c380/JPR-13-2143-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2cd/7519835/81c91605d8ec/JPR-13-2143-g0003.jpg

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