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 effect of spinal cord stimulation (SCS) in patients suffering from neuropathic pain. Little is known about potential supraspinal mechanisms. OBJECTIVE In this study cortical signaling of patients with neuropathic pain and successful long-term treatment with SCS was analyzed. STUDY DESIGN Observational study. SETTING University hospital, neurosurgical department, outpatient clinic for movement disorders and pain, institute for cognitive and clinical neuroscience. METHODS Nine patients with neuropathic pain of a lower extremity with a lasting response to chronic SCS were included. Cortical activity was analyzed using event-related potentials of the electroencephalogram after non-painful and painful stimulation. Each patient was tested under the effect of long-term SCS and 24 hours after cessation of SCS. Cortical areas involved in the peaks of evoked potentials were localized using a source localization method based on a fixed dipole model. RESULTS Detection threshold and intensity of non-painful stimulation did not differ significantly on both sides. Pain threshold was significantly lower on the neuropathic side under the effect of SCS (P = 0.03). Bilateral pain thresholds were significantly lower (P = 0.03 healthy side, P = 0.003 neuropathic side) in 5 patients with increased pain after cessation of SCS. Under the effect of SCS cortical negativities (N1, N2, N3) and positivities (P1) demonstrated bilaterally comparable amplitudes. After cessation of SCS, decreased threshold for peripheral stimulation resulted in lowered negativities on both sides. The positivity P1 was differentially regulated and was reduced more contralateral to the unaffected side. N2 was localized at the sensory representation of the leg within the homunculus. The main vector of P1 was localized within 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 for research purposes. CONCLUSIONS Long-term SCS for treatment of neuropathic pain influenced both pain thresholds and cortical signalling. Source localization of P1 suggests involvement of regions involved in cognitive/associative processing of pain.