• Hubert Polácek, Jirí Kozák, Ivan Vrba, Jirí Vrána, and Andrej Stancák.
• Charles University Prague, Department of Normal, Pathological and Clinical Physiology, Third Faculty of Medicine, Ke Karlovu 4, Prague 2, Czech Republic. h.polacek@seznam.cz
• Clin Neurophysiol. 2007 Jun 1;118(6):1291-302.

ObjectiveTo evaluate the functional activation of the somatosensory cortical regions in neuropathic pain patients during therapeutic spinal cord stimulation (SCS).MethodsIn 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.ResultsThe short-latency components of the source located in the right primary somatosensory cortex (SI: 43, 54 and 65ms) after tibial nerve stimulation, the mid-latency SI component (87ms) after sural nerve stimulation, and the mid-latency components in the right (approximately 161ms) and left (approximately 168ms) 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 (approximately 313ms) was smaller for tibial and larger for sural nerve stimuli during SCS periods compared to periods without SCS.ConclusionsSCS 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.SignificanceResults suggest that the effects of SCS on cortical somatosensory processing may contribute to a reduction of allodynia during SCS.

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