• T Giesecke, R H Gracely, D J Clauw, A Nachemson, M H Dück, R Sabatowski, H J Gerbershagen, D A Williams, and F Petzke.
• Klinik für Anästhesiologie und operative Intensivmedizin, Klinikum der Universität Köln. t.giesecke@uni-koeln.de
• Schmerz. 2006 Sep 1;20(5):411-4, 416-7.

IntroductionA study of patients with low back pain (LBP) had revealed altered central pain processing. At an equal pain level LBP patients had considerably more neuronal activation in the somatosensory cortices than controls. In a new analysis of this dataset, we further investigated the differences in central pain processing between LBP patients and controls, looking for possible pathogenic mechanisms.MethodsCentral pain processing was studied by functional magnetic resonance imaging (fMRI), using equally painful pressure stimuli in a block paradigm. In this study, we reanalyzed the fMRI data to statistically compare pain-elicited neuronal activation of both groups.ResultsEqually painful pressure stimulation resulted in a significantly lower increase of regional cerebral blood flow (rCBF) in the periaqueductal gray (PAG) of the LBP patients. The analysis further revealed a significantly higher increase of rCBF in LBP than in HC in the primary and secondary somatosensory cortex and the lateral orbitofrontal cortex (LOFK), elicited by these same stimuli.ConclusionsThese findings support a dysfunction of the inhibitory systems controlled by the PAG as a possible pathogenic mechanism in chronic low back pain.

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