Studies on functional and structural changes in the primary somatosensory cortex (S1) have provided important insights into neural mechanisms underlying several
chronic pain conditions. However, the role of S1 plasticity in
postherpetic neuralgia (PHN) remains elusive. Combining psychophysics and magnetic resonance imaging (MRI), we investigated whether
pain in PHN patients is linked to S1 reorganization as compared with healthy controls. Results from voxel-based morphometry showed no structural differences between groups. To characterize functional plasticity, we compared S1 responses to noxious
laser stimuli of a fixed intensity between both groups and assessed the relationship between S1 activation and spontaneous
pain in PHN patients. Although the intensity of evoked
pain was comparable in both groups, PHN patients exhibited greater activation in S1 ipsilateral to the stimulated hand.
Pain-related activity was identified in contralateral superior S1 (SS1) in controls as expected, but in bilateral inferior S1 (IS1) in PHN patients with no overlap between SS1 and IS1. Contralateral SS1 engaged during evoked
pain in controls encoded spontaneous
pain in patients, suggesting functional S1 reorganization in PHN. Resting-state fMRI data showed decreased functional connectivity between left and right SS1 in PHN patients, which scaled with the intensity of spontaneous
pain. Finally, multivariate pattern analyses (MVPA) demonstrated that BOLD activity and resting-state functional connectivity of S1 predicted within-subject variations of evoked and spontaneous
pain intensities across groups. In summary, functional reorganization in S1 might play a key role in
chronic pain related to PHN and could be a potential treatment target in this patient group.