Corticostriatal functional connectivity predicts transition to chronic back pain

• Published in: Nature neuroscience Vol. 15; no. 8; pp. 1117 - 1119
• Main Authors: Baliki, Marwan N, Petre, Bogdan, Torbey, Souraya, Herrmann, Kristina M, Huang, Lejian, Schnitzer, Thomas J, Fields, Howard L, Apkarian, A Vania
• Format: Journal Article
• Language: English
• Published: New York Nature Publishing Group US 01-08-2012; Nature Publishing Group
• Subjects: 631/378/1689/2610; 631/378/1697; Acute Pain - physiopathology; Adult; Animal Genetics and Genomics; Back pain; Back Pain - physiopathology; Backache; Behavioral Sciences; Biological Techniques; Biomarkers; Biomedical and Life Sciences; Biomedicine; Brain; Brain - pathology; Brain - physiopathology; brief-communication; Chronic Pain - physiopathology; Corpus Striatum - physiopathology; Female; Follow-Up Studies; Forecasting - methods; Humans; Magnetic Resonance Imaging - methods; Male; Medical imaging; Neural Pathways - physiopathology; Neurobiology; Neuroimaging; Neurosciences; Nucleus Accumbens - physiopathology; Pain Measurement - instrumentation; Physiological aspects; Prefrontal Cortex - physiopathology; United States; California; Chicago Illinois; United States > US; Illinois
• ISSN: 1097-6256; 1546-1726
• DOI: 10.1038/nn.3153

In a longitudinal brain imaging study, patients with subacute back pain were followed over the course of 1 year. 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.
The mechanism of brain reorganization in pain chronification is unknown. In a longitudinal brain imaging study, subacute back pain (SBP) patients were followed over the course of 1 year. When pain persisted (SBPp, in contrast to recovering SBP and healthy controls), brain gray matter density decreased. 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.