Neuroscience researchers have been searching for years using imaging studies to find changes in brain structure and function that correlate with persistent pain. A recent study in Nature Neuroscience studied patients (n=40) with subacute back pain (SBP) lasting 4–16 weeks, with no prior back pain for at least 1 year. Brain scans were conducted on each subject at study entry and their pain and brain markers were followed over four visits for 1 year. The study was looking to identify any causal relationship between brain reorganization and pain persistence or for changes that precede, and therefore predict, the transition to chronicity.
They divided the SBP groups into persistent subacute back pain (SBPp) versus recovering subacute back pain (SBPr) versus a healthy control group. At baseline, SBPp and SBPr patients showed similar pain and mood characteristics except for the affective dimension of pain, which was substantially higher in SBPp than SBPr patients; at visit 4, SBPr subjects showed decreases in most measured parameters which indicated recovery from pain.
Across all measures and time points, SBPr patients resembled healthy controls, whereas specific changes differentiated SBPp patients. Sensorimotor areas (insula, sensorimotor cortex) and a key mesolimbic (nucleus accumbens) region showed decreased gray matter density in subjects with persistent pain. Insular cortex function in pain perception is well documented and insular cortex is activated transiently with pain in patients suffering from chronic back pain. This suggests a direct insular contribution to pain chronification.
According to the authors, “these results provide, to the best of our knowledge, the first temporal profile of brain parameters during pain chronification. Current ideas regarding pain chronification have focused on peripheral nerve and spinal cord reorganization. We found that the corticolimbic medial prefrontal cortex-nucleus accumbens connection is an accurate predictor of the transition from subacute to chronic pain. That motivation-valuation circuitry predicts pain persistence raises the possibility that, as with positive reinforcement learning, the NAc contributes to an aversive teaching signal that leads to sustained pain intensity over time following a static peripheral injury.”