Bogdan Petre and Souraya Torbey contributed equally to this work.
Smoking increases risk of pain chronification through shared corticostriatal circuitry
Version of Record online: 12 OCT 2014
© 2014 Wiley Periodicals, Inc.
Human Brain Mapping
Volume 36, Issue 2, pages 683–694, February 2015
How to Cite
Petre, B., Torbey, S., Griffith, J. W., De Oliveira, G., Herrmann, K., Mansour, A., Baria, A. T., Baliki, M. N., Schnitzer, T. J. and Apkarian, A. V. (2015), Smoking increases risk of pain chronification through shared corticostriatal circuitry. Hum. Brain Mapp., 36: 683–694. doi: 10.1002/hbm.22656
- Issue online: 17 JAN 2015
- Version of Record online: 12 OCT 2014
- Manuscript Accepted: 30 SEP 2014
- Manuscript Revised: 26 SEP 2014
- Manuscript Received: 2 JUL 2014
- National Institutes of Health (National Institutes of Neurological Disorders and Stroke). Grant Number: NS035115
- chronic pain;
- back pain;
- prefrontal cortex
Smoking is associated with increased incidence of chronic pain. However, the evidence is cross-sectional in nature, and underlying mechanisms remain unclear. In a longitudinal observational study, we examined the relationship between smoking, transition to chronic pain, and brain physiology. In 160 subjects with subacute back pain (SBP: back pain lasting 4–12 weeks, and no prior back pain [BP] for at least 1 year) pain characteristics, smoking status, and brain functional properties were measured repeatedly over 1 year. Sixty-eight completed the study, subdivided into recovering (SBPr, n = 31) and persisting (SBPp, n = 37), based on >20% decrease in BP over the year. Thirty-two chronic back pain (CBP: duration > 5 years) and 35 healthy controls were similarly monitored. Smoking prevalence was higher in SBP and CBP but not related to intensity of BP. In SBP, smoking status at baseline was predictive of persistence of BP 1 year from symptom onset (differentiating SBPp and SBPr with 0.62 accuracy). Smoking status combined with affective properties of pain and medication use improved prediction accuracy (0.82). Mediation analysis indicated the prediction of BP persistence by smoking was largely due to synchrony of fMRI activity between two brain areas (nucleus accumbens and medial prefrontal cortex, NAc-mPFC). In SBP or CBP who ceased smoking strength of NAc-mPFC decreased from precessation to postcessation of smoking. We conclude that smoking increases risk of transitioning to CBP, an effect mediated by corticostriatal circuitry involved in addictive behavior and motivated learning. Hum Brain Mapp 36:683–694, 2015. © 2014 Wiley Periodicals, Inc.