Somatosensory change and pain relief induced by repetitive transcranial magnetic stimulation in patients with central poststroke pain.

OBJECTIVE: To quantify changes in pain and somatosensory function in patients with central poststroke pain (CPSP) syndrome following five sessions of repetitive transcranial magnetic stimulation (rTMS). METHODS: Fourteen CPSP patients underwent MRI-guided TMS mapping to identify the motor hotspot for evoked responses from a muscle corresponding to a painful region (hand, N = 11, or distal leg, N = 3). Targeted rTMS consisting of 2000 stimuli/10 Hz each session was delivered over five sessions. Quantitative somatosensory testing (QST) was performed within the painful area and at the contralateral mirror-image site at baseline and after the rTMS. RESULTS: At baseline there were significant sensory deficits of the affected body side for warm and cold detection and heat/cold pain thresholds. Following rTMS, sensory thresholds showed significant improvements for cold detection threshold (repeated-measures ANOVA, p = 0.04). Subjects' pain reports (numerical rating scale 0-10) showed modest but significant improvements in the first week after rTMS (baseline 7.0 ± 1.5; post-TMS 6.3 ± 1.5; Wilcoxon signed-rank test, p = 0.018), and these were largely maintained for up to four weeks post-rTMS. Improvements in warm detection threshold showed a significant correlation with decrease in pain score (Spearman's rank-order correlation, p = 0.007). CONCLUSIONS: Five sessions of open-label rTMS provided analgesia and improved thermal sensibility. The correlation of reduction of detection threshold for warmth and pain relief suggest that the effect of rTMS may be mediated via circuitries that share the processing of noxious and thermal signals, such as the insula and the somatosensory and anterior cingulate cortices. QST may have a role in the assessment of patients with neuropathic pain for suitability for rTMS treatment and is likely to add to our understanding of how rTMS induces pain relief.

Specific brain morphometric changes in spinal cord injury with and without neuropathic pain.

Why only certain patients develop debilitating pain after spinal chord injury and whether structural brain changes are implicated remain unknown. The aim of this study was to determine if patients with chronic, neuropathic below-level pain have specific cerebral changes compared to those who remain pain-free. Voxel-based morphometry of high resolution, T1-weighted images was performed on three subject groups comprising patients with pain (SCI-P, n = 18), patients without pain (SCI-N, n = 12) and age- and sex-matched controls (n = 18). The SCI-P group was first compared directly with the SCI-N group and then subsequently with controls. Overall, grey and white matter changes dependent on the presence of pain were revealed. Significant changes were found within the somatosensory cortex and also in corticospinal tracts and visual-processing areas. When the SCI-P group was directly compared with the SCI-N group, reduced grey matter volume was found in the deafferented leg area of the somatosensory cortex bilaterally. This region negatively correlated with pain intensity. Relative to controls, grey matter in this paracentral primary sensory cortex was decreased in SCI-P but conversely increased in SCI-N. When compared with controls, discrepant corticospinal tract white matter reductions were found in SCI-P and in SCI-N. In the visual cortex, SCI-N showed increased grey matter, whilst the SCI-N showed reduced white matter. In conclusion, structural changes in SCI are related to the presence and degree of below-level pain and involve but are not limited to the sensorimotor cortices. Pain-related structural plasticity may hold clinical implications for the prevention and management of refractory neuropathic pain.