Abstract

Objective To evaluate the functional activation of the somatosensory cortical regions in neuropathic pain patients during therapeutic spinal cord stimulation (SCS). Methods In nine failed back surgery syndrome patients, the left tibial and the left sural nerves were stimulated in two sessions with intensities at motor and pain thresholds, respectively. The cortical somatosensory evoked potentials were analyzed using source dipole analysis based on 111 EEG signals. Results The short-latency components of the source located in the right primary somatosensory cortex (SI: 43, 54 and 65 ms) after tibial nerve stimulation, the mid-latency SI component (87 ms) after sural nerve stimulation, and the mid-latency components in the right (≈161 ms) and left (≈168 ms) secondary somatosensory cortices (SII) were smaller in the presence of SCS than in absence of SCS. The long-latency source component arising from the mid-cingulate cortex (≈313 ms) was smaller for tibial and larger for sural nerve stimuli during SCS periods compared to periods without SCS. Conclusions SCS attenuates the somatosensory processing in the SI and SII. In the mid-cingulate cortex, the effect of SCS depends on the type of stimulation and nerve fibers involved. Significance Results suggest that the effects of SCS on cortical somatosensory processing may contribute to a reduction of allodynia during SCS.

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