Chronic pain and evoked responses in the brain: A magnetoencephalographic study in Complex Regional Pain Syndrome I and II

Complex Regional Pain Syndrome (CRPS) type I and II are chronic pain syndromes with comparable symptoms, only in CRPS II a peripheral nerve injury is present. No objective tests are currently available to differentiate the two types which hampers diagnosis and treatment. Non-invasive brain imaging techniques may offer diagnostic tools by tracking perceptual changes and changes in cortical topography in these patients. Using magnetoencephalography, we compared the brain evoked responses after standard electrical median and ulnar nerve stimulation. Three groups were compared; (a) 20 healthy subjects, (b) 20 CRPS I and (c) 20 CRPS II patients, patients suffered from a unilaterally affected upper extremity. In the CRPS II group, after a local anaesthetic block at the injured site of a peripheral nerve and the patient in the pain free condition, another measurement was performed for comparison. The response parameters studied were: peak latencies, number of peaks, compr essed waveform profiles (CWP), global field power (GFP) curves and values, and six dipole parameters. In the healthy subject group the GFP curves, as an indication of the distribution of cortical activation, were highly symmetrical for both nerves. At 30 ms and 70 ms post- trigger major peaks of activation were observed. In CRPS I, at 70 ms post-trigger, a significant decrease of the GFP values in the Affected Hemisphere (contralateral to the affected hand) was found compared to subjects. No significant difference between the AH and the UH (contralateral to the unaffected hand) was found. In CRPS II at 70 ms a significant increase in the AH was observed compared to the UH. In both CRPS groups the UHs demonstrated cortical plasticity changes; cortical activation compared to subjects presented a significant shrinkage of the activated somatosensory area. Compared to healthy subjects, responses in the AH for the CRPS II groups were not significantly different; however the CRPS II GFP AH va lues were significantly larger compared to the AH and UH of the CRPS I group. Brain mapping in the 400 ms post-trigger period, based on polarity reversals, demonstrated altered cortical processing in patients. For all groups at 30 ms and 70 ms, the majority of the equivalent current dipole data (12-14/20) indicated source localization in the primary somatosensory cortex. The latter finding was supported by the data found in the CRPS II groups, before and after a local anaesthetic block and the patient in the pain free condition. After the block the GFP values decreased at 70 ms post stimulus. At this latency, dipoles studied were located in the primary somatosensory cortex. This study presents the first systematic evaluation of CRPS I and II. Involvement of the UHs in both CRPS groups may indicate altered inter-hemispherical transmission in unilaterally affected upper extremities. Since in both CRPS syndromes, a difference in cortical activation exists as compared to healthy subjects , the two syndromes may require a different treatment approach. Our study suggests that evoked magnetic responses may offer an objective clinical tool for future diagnosis of CRPS I and CRPS II