Artikel
Cortical processing in neuropathic pain under long-term spinal cord stimulation
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Veröffentlicht: | 4. Juni 2012 |
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Gliederung
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Objective: Several hypothetical mechanisms of spinal cord stimulation (SCS) were described in the past to explain the beneficial effect of this method in patients suffering from neuropathic pain. Little is known about potential cortical mechanisms. In this study cortical signaling of patients with neuropathic pain and successful long-term treatment with SCS was analyzed.
Methods: Nine patients with neuropathic pain of the lower extremities and excellent to fair improvement of pain under SCS were included into the study. Cortical activity was analyzed using event related EEG 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 responsible for 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 Man Whitney rank sum test). Intensities for painful stimulation were significantly lower on both sides (p=0.03 healthy side, p=0.003 neuropathic side) in 6 patients with increased pain after cessation of SCS. Under the effect of SCS cortical negativities (N1 and N2) and positivities (P1) demonstrated bilaterally comparable amplitudes. After cessation of SCS decreased stimulation parameters resulted in decreased negativities on both sides. The positivity P1 was differentially regulated and was reduced on the healthy side but stable on the neuropathic side. N2 was localized at the sensory representation of the leg within the homunculus. Main vector of P1 was localized within the anterior cingulate cortex (ACC) and moved more posteriorly on the neuropathic side after cessation of SCS.
Conclusions: Long-term SCS for treatment of neuropathic pain influenced cortical signaling. Source localization of P1 suggests involvement of cognitive mechanisms.