Structural brain changes in chronic pain reflect probably neither damage nor atrophy

PLoS One. 2013;8(2):e54475. doi: 10.1371/journal.pone.0054475. Epub 2013 Feb 6.

Abstract

Chronic pain appears to be associated with brain gray matter reduction in areas ascribable to the transmission of pain. The morphological processes underlying these structural changes, probably following functional reorganisation and central plasticity in the brain, remain unclear. The pain in hip osteoarthritis is one of the few chronic pain syndromes which are principally curable. We investigated 20 patients with chronic pain due to unilateral coxarthrosis (mean age 63.25±9.46 (SD) years, 10 female) before hip joint endoprosthetic surgery (pain state) and monitored brain structural changes up to 1 year after surgery: 6-8 weeks, 12-18 weeks and 10-14 month when completely pain free. Patients with chronic pain due to unilateral coxarthrosis had significantly less gray matter compared to controls in the anterior cingulate cortex (ACC), insular cortex and operculum, dorsolateral prefrontal cortex (DLPFC) and orbitofrontal cortex. These regions function as multi-integrative structures during the experience and the anticipation of pain. When the patients were pain free after recovery from endoprosthetic surgery, a gray matter increase in nearly the same areas was found. We also found a progressive increase of brain gray matter in the premotor cortex and the supplementary motor area (SMA). We conclude that gray matter abnormalities in chronic pain are not the cause, but secondary to the disease and are at least in part due to changes in motor function and bodily integration.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Atrophy / pathology
  • Behavior / physiology
  • Brain / pathology*
  • Brain Mapping / methods
  • Chronic Pain / pathology*
  • Cross-Sectional Studies
  • Female
  • Humans
  • Longitudinal Studies
  • Male
  • Middle Aged
  • Motor Cortex / pathology*
  • Osteoarthritis, Hip / pathology*
  • Prefrontal Cortex / pathology*

Grants and funding

This work was supported by grants from the DFG (German Research Foundation) (MA 1862/2-3) and BMBF (The Federal Ministry of Education and Research) (371 57 01 and NeuroImage Nord). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.