Presented at the 2013 AAPM Annual Meeting « Back

Neural Correlates of Effective Cognitive Modulation of Pain

Heather Chapin, PhD, hchapin@stanford.edu¹, Epifanio Bagarinao, PhD¹, Emily K. Hubbard, BA², Eric A. Dixon, BA¹, Gary H. Glover, PhD², Sean Mackey, MD PhD¹, (1) Stanford University, Palo Alto, California, (2) Stanford University School of Medicine, San Francisco, California

The neural mechanisms underlying cognitive pain modulation are poorly understood and previous studies have not focused on clinically meaningful changes in pain. We sought to characterize neural processes underlying clinically significant cognitive pain modulation. This may help us develop more effective interventions that target the relevant neural processes. All participants provided written, informed consent as approved by the Stanford University Institutional Review Board. Fifteen healthy controls that had demonstrated the ability to significantly alter pain were asked to cognitively increase and decrease pain elicited by moderately painful heat stimuli while undergoing fMRI scanning. We hypothesized that pain modulation would be associated with changes in brain areas involved in pain perception and cognitive control. We found activation differences in areas related to pain processing, self-regulation, and cognitive control. Mid-line frontal areas and rostral anterior cingulate showed greater deactivation during increase pain. Dorsal anterior cingulate (dACC) and pre-supplementary motor area showed greater activation during decrease pain. Signal increases in the prefrontal cortex, dACC, and thalamus predicted decreased pain ratings. These results show that successful cognitive modulation of pain involves brain areas associated with pain processing and cognitive control. One area, the dACC, was both correlated with pain ratings and showed a significant difference in activation between conditions. This region has been shown to be important for self-regulation, indicating the dACC may be a key component in modifying pain perception within a clinically significant range. Therefore, the dACC may be an optimal target for the neuromodulatory control of pain using real-time fMRI neurofeedback.

Funding: Supported by a grant from NIH (T32 Institutional Training Grant), NIDA (K24 DA029262 and R21 DA026092), and the Redlich Pain Research Endowment