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      Corticolimbic anatomical characteristics predetermine risk for chronic pain.

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          Abstract

          SEE TRACEY DOI101093/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.

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          Author and article information

          Journal
          Brain
          Brain : a journal of neurology
          Oxford University Press (OUP)
          1460-2156
          0006-8950
          Jul 2016
          : 139
          : Pt 7
          Affiliations
          [1 ] 1 Department of Physiology, Feinberg School of Medicine, Northwestern University 303 E. Chicago Ave., Chicago, IL 60611, USA.
          [2 ] 2 Department of Psychiatry and Neurobehavioral Sciences, University of Virginia , 2955 Ivy Rd, Suite 210, Charlottesville, VA 22903, USA.
          [3 ] 3 Department of Anesthesia, Pain Management and Perioperative Medicine Dalhousie University, Halifax, NS, Canada B3H 4R2.
          [4 ] 4 Department of Medical Social Sciences, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
          [5 ] 5 Department of Neuroscience, Science for Life Laboratory, Uppsala University, BMC, Pob 593, 75124, Uppsala, Sweden.
          [6 ] 6 Northwestern University Feinberg School of Medicine, Departments of Physical Medicine and Rehabilitation and Internal Medicine/Rheumatology, 710 N. Lake Shore Drive, Room 1020, Chicago, IL 60611, USA.
          [7 ] 1 Department of Physiology, Feinberg School of Medicine, Northwestern University 303 E. Chicago Ave., Chicago, IL 60611, USA 7 Rehabilitation Istitute of Chicago, 345 E Superior St, Chicago, IL 60611, USA a-apkarian@northwestern.edu marwanbaliki2008@u.northwestern.edu.
          [8 ] 1 Department of Physiology, Feinberg School of Medicine, Northwestern University 303 E. Chicago Ave., Chicago, IL 60611, USA a-apkarian@northwestern.edu marwanbaliki2008@u.northwestern.edu.
          Article
          aww100
          10.1093/brain/aww100
          4939699
          27190016
          0ff462ab-c247-48b7-ae39-27d3f0c4163f
          History

          brain network,chronic pain,diffusion tensor imaging (DTI),limbic system,magnetic resonance imaging (MRI)

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