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Hyperalgesia and Reduced Offset Analgesia During Spinal Anesthesia

Authors Sitsen E, van Velzen M, de Rover M, Dahan A, Niesters M

Received 16 April 2020

Accepted for publication 11 August 2020

Published 24 August 2020 Volume 2020:13 Pages 2143—2149


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Michael A Überall

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

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

Correspondence: Marieke Niesters
Department of Anesthesiology, Leiden University Medical Center, H5-022, Leiden, RC 2300, the Netherlands

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 ( NL3874.

Keywords: spinal anesthesia, analgesia, pain responses, hyperalgesia, deafferentation

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