Chronic pain is a highly prevalent disease with poorly understood pathophysiology. In particular, the brain mechanisms mediating the transition from acute to chronic pain remain largely unknown. Here, we identify a subcortical signature of back pain. Specifically, subacute back pain patients who are at risk for developing chronic pain exhibit a smaller nucleus accumbens volume, which persists in the chronic phase, compared to healthy controls. The smaller accumbens volume was also observed in a separate cohort of chronic low-back pain patients and was associated with dynamic changes in functional connectivity. At baseline, subacute back pain patients showed altered local nucleus accumbens connectivity between putative shell and core, irrespective of the risk of transition to chronic pain. At follow-up, connectivity changes were observed between nucleus accumbens and rostral anterior cingulate cortex in the patients with persistent pain. Analysis of the power spectral density of nucleus accumbens resting-state activity in the subacute and chronic back pain patients revealed loss of power in the slow-5 frequency band (0.01 to 0.027 Hz) which developed only in the chronic phase of pain. This loss of power was reproducible across two cohorts of chronic low-back pain patients obtained from different sites and accurately classified chronic low-back pain patients in two additional independent datasets. Our results provide evidence that lower nucleus accumbens volume confers risk for developing chronic pain and altered nucleus accumbens activity is a signature of the state of chronic pain.

Chronic low back pain (CLBP) and obesity are interrelated, but the physiological mechanisms linking the 2 conditions remain to be determined. Functional brain imaging data from CLBP patients show functional and structural alterations in areas mediating the attribution of hedonic value to food. Accordingly, we hypothesized that CLBP patients would exhibit alteration in the hedonic perception of highly palatable, calorie-containing foods. CLBP patients and matched healthy controls initially rated their perception of highly palatable puddings of varying fat content and sugary drinks of varying sucrose content without ingesting significant amounts of either stimulus. In a subsequent intake test, hungry participants ingested their preferred pudding ad libitum. Compared to healthy controls, CLBP patients exhibited significantly lower ratings of food pleasure when sampling the fat puddings but not when sampling the sugary drinks. In contrast, the patients' sensory evaluation of these stimuli was not different from those of healthy controls. In addition, whereas in healthy controls caloric intake from pudding closely matched hedonic ratings and decreased hunger after ad libitum pudding intake, such effect was totally abolished in CLBP patients. Our data thus reveal a decoupling between hedonic perception and fat calorie intake in CLBP patents, suggesting altered hedonic perception of fat as a potential mechanism linking CLBP to overeating and obesity.

No abstract