• Yohei Matsuo, Jiro Kurata, Miho Sekiguchi, Katsuhiro Yoshida, Takuya Nikaido, and Shin-Ichi Konno.
• Department of Orthopaedic Surgery, Fukushima Medical University School of Medicine, 1 Hikariga-oka, Fukushima City, 960-1295, Japan.
• J Anesth. 2017 Aug 1; 31 (4): 523-530.

PurposeA considerable portion of chronic low back pain (cLBP) patients lack anatomical abnormality, resist conventional therapeutic interventions, and their symptoms are often complicated with psychological and social factors. Such patients have been reported to show cerebral abnormalities both in anatomy and function by neuroimaging studies. Here we examined differences in cerebral reactivity to a simulated low back pain stimulus between cLBP patients and healthy controls by functional magnetic resonance imaging (fMRI), and their behavioral correlates from a psychophysical questionnaire.MethodsEleven cLBP patients and 13 healthy subjects (HS) were enrolled in this study. After psychophysical evaluation on-going pain with McGill Pain Questionnaire Short Form (MPQ), they underwent whole-brain fMRI in a 3-Tesla MRI scanner while receiving three blocks of 30-s mechanical pain stimuli at the left low back with a 30-s rest in between, followed by a three-dimensional anatomical imaging. Functional images were analyzed with a multi-subject general linear model for blood oxygenation level-dependent (BOLD) signal changes associated with pain. Individual BOLD signal amplitudes at activated clusters were examined for correlation with psychophysical variables. Two in the cLBP and five data sets in the HS groups were excluded from analysis because of deficient or artifactual data or mismatch in age.ResultsThe HS group showed LBP-related activation at the right insular cortex, right dorsolateral prefrontal cortex (DLPFC), left anterior cingulate cortex (ACC), and left precuneus; and deactivation in a large area over the parietal and occipital cortices, including the bilateral superior parietal cortex. On the other hand, the cLBP group did not show any significant activation at those cortical areas, but showed similar deactivation at the bilateral superior parietal cortex and part of the premotor area. An HS > cLBP contrast revealed significantly less activity at the ACC and DLPFC in the cLBP group, which was negatively correlated with higher MPQ scores.ConclusionsThe cLBP patients showed attenuated reactivity to pain at the ACC and DLPFC, known cortical areas mediating affective component, and top-down modulation, of pain. The present results might be associated with possible dysfunction of the descending pain inhibitory system in patients with chronic low back pain, which might possibly play a role in chronification of pain.

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