​Background

Chronic back pain (CBP) is an important clinical, social, economic, and public health problem. Many risk factors are associated with CBP. However, the evidence is often cross-sectional. In an innovative study, researchers from the Northwestern University of Chicago explored the relationship between smoking, transition to chronic pain and functional characteristics of the brain.

Methods
A longitudinal observational study was conducted. 
160 subacute back pain (SBP) patients were enrolled and were investigated for pain characteristics, smoking status, and brain functional connectivity. These aspects were measured repeatedly over 1 year. In addition, all analyses were performed in 32 chronic back pain (CBP) patients and 35 healthy controls. T1-MPRAGE anatomical data and fMRI data were acquired. Preprocessing procedures were used to analyse strength of information sharing (functional connectivity) between the nucleus accumbens and medial prefrontal cortex.

Results
68 SBP patients completed the study and were allocated to either a recovering (>20% decrease in back pain over the year) or persisting pain group. The researchers revealed a higher smoking prevalence in SBP and CBP patients. Interestingly, smoking prevalence was not related to BP intensity. Smoking status at baseline in SBP was predictive for BP persistence 1 year after the onset of pain symptoms (0.62). When smoking status was combined with medication use and affective characteristics of pain, prediction accuracy for chronification was improved (0.82). Prediction of BP persistence by smoking was strongly influenced by the synchrony of fMRI activity between 2 brain areas (nucleus accumbens and medial prefrontal cortex). In SBP and CBP patients who quit smoking, the strength of nucleus accumbens-medial prefrontal cortex connectivity was decreased from precessation to postcessation of smoking.

Discussion
These results have important clinical implications for the identification of individuals who are more vulnerable for the transition to CBP. Further, this study reveals the importance of anti-smoking campaigns and smoking cessation as one of the factors for the prevention of pain chronification.

Conclusion
Smoking increases risk of transition to CBP. Corticostriatal circuitry involved in motivated learning and addictive behaviour mediates this effect.

Further reading: 
http://www.ncbi.nlm.nih.gov/pubmed/?term=smoking+increases+risk+of+pain+chronification 
http://onlinelibrary.wiley.com/doi/10.1002/hbm.22656/epdf

Coppieters Iris 
Iris.coppieters@ugent.be