Corticolimbic anatomical characteristics predetermine risk for chronic pain

Abstract

See Tracey (doi: [Related article:]10.1093/brain/aww147) for a scientific commentary on this article.

Why some individuals progress from acute to chronic pain is unclear. Vachon-Presseau et al. monitor patients with subacute pain for three years, and show that pre-existing structural and functional connectivity within dorsal mPFC-amygdala-accumbens corticolimbic circuitry, as well as amygdala and hippocampal volumes, represent risk factors for transition to chronic pain.

Abstract

See Tracey (doi: [Related article:]10.1093/brain/aww147) for a scientific commentary on this article.

Why some individuals progress from acute to chronic pain is unclear. Vachon-Presseau et al. monitor patients with subacute pain for three years, and show that pre-existing structural and functional connectivity within dorsal mPFC-amygdala-accumbens corticolimbic circuitry, as well as amygdala and hippocampal volumes, represent risk factors for transition to chronic pain.

Abstract

See Tracey (doi: [Related article:]10.1093/brain/aww147) for a scientific commentary on this article.

Mechanisms of chronic pain remain poorly understood. We tracked brain properties in subacute back pain patients longitudinally for 3 years as they either recovered from or transitioned to chronic pain. Whole-brain comparisons indicated corticolimbic, but not pain-related circuitry, white matter connections predisposed patients to chronic pain. Intra-corticolimbic white matter connectivity analysis identified three segregated communities: dorsal medial prefrontal cortex–amygdala–accumbens, ventral medial prefrontal cortex–amygdala, and orbitofrontal cortex–amygdala–hippocampus. Higher incidence of white matter and functional connections within the dorsal medial prefrontal cortex–amygdala–accumbens circuit, as well as smaller amygdala volume, represented independent risk factors, together accounting for 60% of the variance for pain persistence. Opioid gene polymorphisms and negative mood contributed indirectly through corticolimbic anatomical factors, to risk for chronic pain. Our results imply that persistence of chronic pain is predetermined by corticolimbic neuroanatomical factors.