Event-Related Cortical Processing in Neuropathic Pain under Long-Term Spinal Cord Stimulation

Background: Several mechanisms were suggested in the past to explain the beneficial effectof spinal cord stimulation (SCS) in patients suffering from neuropathic pain. Little is known aboutpotential supraspinal mechanisms.Objective: In this study cortical signaling of patients with neuropathic pain and successful longterm treatment with SCS was analyzed.Study Design: Observational study.Setting: University hospital, neurosurgical department, outpatient clinic for movement disordersand pain, institute for cognitive and clinical neuroscience.Methods: Nine patients with neuropathic pain of a lower extremity with a lasting response tochronic SCS were included. Cortical activity was analyzed using event-related potentials of theelectroencephalogram after non-painful and painful stimulation. Each patient was tested underthe effect of long-term SCS and 24 hours after cessation of SCS. Cortical areas involved in thepeaks of evoked potentials were localized using a source localization method based on a fixeddipole model.Results: Detection threshold and intensity of non-painful stimulation did not differ significantlyon both sides. Pain threshold was significantly lower on the neuropathic side under the effect ofSCS (P = 0.03). Bilateral pain thresholds were significantly lower (P = 0.03 healthy side, P = 0.003neuropathic side) in 5 patients with increased pain after cessation of SCS.Under the effect of SCS cortical negativities (N1, N2, N3) and positivities (P1) demonstratedbilaterally comparable amplitudes. After cessation of SCS, decreased threshold for peripheralstimulation resulted in lowered negativities on both sides. The positivity P1 was differentiallyregulated and was reduced more contralateral to the unaffected side. N2 was localized at thesensory representation of the leg within the homunculus. The main vector of P1 was localizedwithin the cingular cortex (CC) and moved more anteriorly under the effect of SCS.Limitations: The exact time span that SCS continues to have an effect is not known. However,due to patient discomfort discontinuation of SCS therapy was not prolonged over a 24 hour period.Further limitations were the low number of patients who agreed to discontinue SCS therapy forresearch purposes.Conclusions: Long-term SCS for treatment of neuropathic pain influenced both pain thresholdsand cortical signalling. Source localization of P1 suggests involvement of regions involved incognitive/associative processing of pain.Key words: Event related cortical processing, neuropathic pain, spinal cord stimulation, SCS