Brain activation due to postoperative pain from the right hand measured with regional cerebral blood flow using positron emission tomography.

Background Brain activation resulting from acute postoperative pain has to our knowledge not previously been studied using positron emission tomography, except from one case study. The aim of this study was to monitor activation in brain sensory pathways during acute pain after surgery of the hand. A secondary aim was to compare brain activation in clinical postoperative pain to that previously reported, by the same research group, for a model of experimental pain from the same body area. Increase in regional cerebral blood flow (rCBF) is presumed to indicate neuronal activation and decrease in blood flow decreased neuronal firing. An increase in blood flow in a brain region may represent stimulatory activity as well as inhibitory. Methods Brain activity was measured during clinical postoperative pain and a pain free state in six patients with positron emission tomography (PET) as changes in regional cerebral blood flow (rCBF). rCBF during pain from surgery of the right thumb base was compared with a pain free state achieved by regional anaesthesia of the painful area. Results In postoperative pain, patients had a significantly higher CBF in the contralateral/primary and secondary somatosensory cortices as well as in the contralateral motor cortex compared to the pain free stat during local regional anaesthesia. Relatively lower rCBF during the pain state was observed in clusters in the contralateral tertiary sensory cortex, ipsilateral and contralateral secondary visual cortex, prelimbic cortex, ipsilateral prefrontal as well as anterior cingulate cortex and contralateral secondary somatosensory cortex. The increased rCBF in primary and somatosensory cortices probably correspond to pain localizing processing. We also compared the findings in cerebral activation patterns of the postoperative pain state as described above, with the results from a previously published study by the same research group, using an experimental pain model when pain was inflicted with application of mustard oil in the same location, the thumb base region of the right hand. Since no formal statistical analysis was carried out between the two studies, the data are not very strong, but the differences reported were obvious when comparing the two situations. The comparison gave the following outcome: Digit activation occurred in identical sensory brain areas, i.e. primary and secondary somatosensory cortices, as compared to the changes in this study, supporting that pain localization processes use similar sensory pathways in a nociceptive acute experimental pain model, and in clinical acute postoperative nociceptive pain. Dissimilarities were observed between the models in activation of brain areas coding of the emotional pain qualities, indicating some differences between the experimental and "real" acute nociceptive pain. Conclusion We have reported a distinct cerebral activation pattern produced by acute postoperative pain following hand surgery. The findings were compared to data obtained in a previously published report of the cerebral activation pattern from an acute experimental pain model in volunteers. We found similarities as well as some differences in the activation pattern between the two situations.