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ANALGESIA

Imaging Pain Modulation by Subanesthetic S-(+)-Ketamine

Till Sprenger, MD^*, Michael Valet, MD^*, Ralph Woltmann, MD^*, Claus Zimmer, MD, Rainer Freynhagen, MD, DEAA, Eberhard F. Kochs, MD, Thomas R. Tölle, MD, PhD^*, and Klaus J. Wagner, MD

From the *Neurologische Klinik und Poliklinik, Technische Universität München; Klinik für Anaesthesiologie, Technische Universität München; Institut für Röntgendiagnostik, Technische Universität München; Klinik für Anaesthesiologie, Universität Düsseldorf, Germany.

Address correspondence and reprint requests to Till Sprenger, MD, Neurologische Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universität München, Moehlstr. 28, D-81675 Muenchen, Germany. Address e-mail to sprenger{at}lrz.tu-muenchen.de.

Abstract

Little is known about the effects of low-dose S-(+)-ketamine on the cerebral processing of pain. We investigated the effects of subanesthetic IV S-(+)-ketamine doses on the perception of experimental painful heat stimuli. Healthy volunteers were evaluated with functional magnetic resonance imaging (fMRI) while receiving the painful stimuli in conjunction with placebo and increasing doses (0.05, 0.1, 0.15 mg · kg^–1 · h^–1) of ketamine infusion. Vital variables were monitored and all subjects rated pain intensity and unpleasantness on a numerical rating scale. Alterations in consciousness were measured using a psycho-behavioral questionnaire. Pain unpleasantness declined as ketamine dosage was increased (55.1% decrease, placebo versus 0.15 mg · kg^–1 · h^–1 ketamine). Pain intensity ratings also decreased with increasing ketamine dosage but to a lesser extent (23.1% decrease). During placebo administration, a typical pain activation network (thalamus, insula, cingulate, and prefrontal cortex) was found, whereas decreased pain perception with ketamine was associated with a dose-dependent reduction of pain-induced cerebral activations. Analysis of the dose-dependent ketamine effects on pain processing showed a decreasing activation of the secondary somatosensory cortex (S2), insula and anterior cingulate cortex. This part of the anterior cingulate cortex (midcingulate cortex) has been linked with the affective pain component that underlines the potency of ketamine in modulating affective pain processing.

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				J. G. Bovill Anesthetic Pharmacology: Reflections of a Section Editor Anesth. Analg., November 1, 2007; 105(5): 1186 - 1190. [Full Text] [PDF]

Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999