• Tianjiao Li, Shuo Zhang, and Jiro Kurata.
• Department of Anesthesiology, Tokyo Medical and Dental University Graduate School of Medical and Dental Sciences, Tokyo, Japan.
• J Anesth. 2018 Dec 1; 32 (6): 831-843.

PurposeAlthough cerebral structural and functional changes were uncovered by neuroimaging in patients with chronic low back pain (CLBP), their associations remain to be clarified. We co-analyzed anatomical and functional magnetic resonance imaging data in those patients and tested whether cortical gray matter volume changes are associated with altered pain modulatory networks underlying chronification of pain.MethodsIn 16 patients with CLBP and 16 heathy controls, we performed functional magnetic resonance imaging during mechanical pain stimulation on the lower back followed by anatomical imaging. We performed voxel-based morphometry and functional connectivity analysis from the seeds with altered gray matter volume, and examined correlations between imaging and psychophysical parameters.ResultsPatients showed decreases in gray matter volume at the right dorsolateral prefrontal cortex, middle occipital gyrus, and cerebellum, and showed increases at the bilateral primary sensorimotor cortices, left fusiform gyrus, and right cerebellum compared with controls (P < 0.001). Dorsolateral prefrontal and fusiform volumes showed negative associations with affective comorbidity, whereas motor cortex volume with impaired daily activity (P < 0.05). Connectivity was decreased between the cerebellar and limbic, and increased between the bilateral sensorimotor regions (PFDR < 0.05). Higher pain intensity and unpleasantness correlated with enhanced bilateral sensorimotor and dorsolateral-medial prefrontal networks, respectively (P < 0.05).ConclusionPatients showed a decreased volume of cortical center for descending pain modulation and an increased volume of sensorimotor network, in association with suppressed descending pain modulatory and cerebellum-limbic networks and enhanced sensorimotor network during pain. Such structural and functional alterations might be part of cerebral pathophysiology of CLBP.

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