• Robert K Hofbauer, Pierre Fiset, Gilles Plourde, Steven B Backman, and M Catherine Bushnell.
• Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada.
• Anesthesiology. 2004 Feb 1; 100 (2): 386-94.

BackgroundAnatomic and physiologic data show that multiple regions of the forebrain are activated by pain. However, the effect of anesthetic level on nociceptive input to these regions is not well understood.MethodsThe authors used positron emission tomography to measure the effect of various concentrations of propofol on pain-evoked changes in regional cerebral blood flow. Fifteen volunteers were scanned while warm and painful heat stimuli were presented to the volar forearm using a contact thermode during administration of target propofol concentrations of 0.0 microg/ml (alert control), 0.5 microg/ml (mild sedation), 1.5 microg/ml (moderate sedation), and 3.5 microg/ml (unconsciousness).ResultsDuring the 0.5-microg/ml target propofol concentration (mild sedation), the subjects' pain ratings increased relative to the alert control condition; correspondingly, pain-evoked regional cerebral blood flow increased in the thalamus and the anterior cingulate cortex. In contrast, when subjects lost consciousness (3.5 microg/ml), pain-evoked responses in the thalamus and the anterior cingulate cortex were no longer observed, whereas significant pain-evoked activation remained in the insular cortex.ConclusionThese data show that propofol has a dose-dependent effect on thalamocortical transfer of nociceptive information but that some pain-evoked cortical activity remains after loss of consciousness.

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