Abstract
The mechanism of brain reorganization in pain chronification is unknown. In a longitudinal brain imaging study, sub–acute back pain (SBP) patients were followed over one year. When pain persisted (SBPp, in contrast to recovering SBP, and healthy controls), brain gray matter density decreased. Importantly, initially greater functional connectivity of nucleus accumbens with prefrontal cortex predicted pain persistence, implying that corticostriatal circuitry is causally involved in the transition from acute to chronic pain.
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