Cognitive-behavioral therapy increases prefrontal cortex gray matter in patients with chronic pain

Abstract

Several studies have reported reduced cerebral gray matter (GM) volume or density in chronic pain conditions, but there is limited research on the plasticity of the human cortex in response to psychological interventions. We investigated GM changes after cognitive-behavioral therapy (CBT) in patients with chronic pain. We used voxel-based morphometry to compare anatomic magnetic resonance imaging scans of 13 patients with mixed chronic pain types before and after an 11-week CBT treatment and to 13 healthy control participants. CBT led to significant improvements in clinical measures. Patients did not differ from healthy controls in GM anywhere in the brain. After treatment, patients had increased GM in the bilateral dorsolateral prefrontal, posterior parietal, subgenual anterior cingulate/orbitofrontal, and sensorimotor cortices, as well as hippocampus, and reduced GM in supplementary motor area. In most of these areas showing GM increases, GM became significantly higher than in controls. Decreased pain catastrophizing was associated with increased GM in the left dorsolateral prefrontal and ventrolateral prefrontal cortices, right posterior parietal cortex, somatosensory cortex, and pregenual anterior cingulate cortex. Although future studies with additional control groups will be needed to determine the specific roles of CBT on GM and brain function, we propose that increased GM in the prefrontal and posterior parietal cortices reflects greater top-down control over pain and cognitive reappraisal of pain, and that changes in somatosensory cortices reflect alterations in the perception of noxious signals.

Perspective: An 11-week CBT intervention for coping with chronic pain resulted in increased GM volume in prefrontal and somatosensory brain regions, as well as increased dorsolateral prefrontal volume associated with reduced pain catastrophizing. These results add to mounting evidence that CBT can be a valuable treatment option for chronic pain.

Keywords: CBT; Dorsolateral prefrontal cortex; neuroimaging; pain catastrophizing; voxel-based morphometry.

Conflict of interest statement

Disclosures: The authors have no conflicts of interest to declare. This research was supported by grants from the National Institute of Arthritis, Musculoskeletal Diseases (NIAMS)

Copyright © 2013 American Pain Society. Published by Elsevier Inc. All rights reserved.

Figures

Figure 1

All significant clusters from post-CBT vs. pre-CBT repeated measures analysis. The order (left to right) matches the order of clusters shown in Table 2. Note that the SMA cluster on the far right is pre-CBT > post-CBT. MNI coordinates (x,y,z) for each crosshair location are shown for each cluster. DLPFC, dorsolateral prefrontal cortex; M1, primary motor cortex; PPC, posterior parietal cortex; S1, primary somatosensory cortex; S2, second somatosensory cortex; sACC/OFC, subgenual ACC/oribotofrontal cortex; SMA, supplementary motor area. ¥ cluster is not significant when a covariate for pain type is included.

Figure 2

VBM results showing three regions where GM increased (right and left DLPFC) or decreased (Pre-SMA/SMA) in patients post-CBT compared to pre-CBT. The plot to the right shows the means and standard errors for each region shown in the panels to the left. Data for all three groups (patients pre-and post-CBT and controls) are normalized to patients pre-CBT. See Table 2 for details on the SPM statistics. Red asterisks indicate ROIs where controls had significantly less GM than patients post-CBT, and the black asterisk indicates the ROI where controls had less GM than patients pre-CBT, as determined by t-tests on mean values of the ROIs. DLPFC, dorsolateral prefrontal cortex; SMA, supplementary motor area. ¥ cluster is not significant when a covariate for pain type is included.

Figure 3

All significant clusters from regression of change in catastrophizing and change in GM. The order (left to right) matches the order of clusters shown in Table 2. Note that the first four clusters from left to right were negative correlations between GM and catastrophizing, while the 2 right clusters (HC, DLPFC) were positive correlations. MNI coordinates (x,y,z) for each crosshair location are shown for each cluster. ACC, anterior cingulate cortex; DLPFC, dorsolateral prefrontal cortex; IFG, inferior frontal gyrus; PPC, posterior parietal cortex; S1, primary somatosensory cortex; S2, second somatosensory cortex. ¥ cluster is not significant when a covariate for pain type is included.

Figure 4

Three of the four clusters where increased gray matter volume after CBT correlated with decreased pain catastrophizing. The left DLPFC and IFG and the right S2/S1/PPC clusters are shown. Results are cluster corrected at pFWE