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CURRENT ISSUEMINERVA ANESTESIOLOGICA

A Journal on Anesthesiology, Resuscitation, Analgesia and Intensive Care


Official Journal of the Italian Society of Anesthesiology, Analgesia, Resuscitation and Intensive Care
Indexed/Abstracted in: Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 2,036

 

Minerva Anestesiologica 2012 March;78(3):297-302

 ORIGINAL ARTICLES

Inhibition of somatosensory evoked potentials during spinal cord stimulation and its possible role in the comprehension of antalgic mechanisms of neurostimulation for neuropathic pain

Buonocore M. 1, 3, Bodini A. 1, Demartini L. 2, Bonezzi C. 2, 3

1 Unit of Clinical Neurophysiology and Neurodiagnostic Skin Biopsy;
2 Unit of Pain Medicine;
3 Centre for Research in Pain Pathophysiology and Therapy, Fondazione Salvatore Maugeri, Scientific Institute of Pavia, Pavia, Italy

BACKGROUND: Spinal cord stimulation (SCS) has been widely used for pain relief of patients with neuropathic chronic pain, frequently with only partial efficacy. Further advancements probably need a better understanding of SCS mechanisms, yet largely unknown. Aims of this paper were to answer the question if the lumbar SCS inhibits the tibial nerve somatosensory evoked potentials (SEPs) and to discuss the role of lemniscal afferents modulation in the antalgic mechanism of SCS.
METHODS: Ten consecutive patients successfully treated with implanted SCS devices for chronic pain in the lower limbs (four males, six females, age range 42-72 years) were enrolled. All the patients had an implanted system with an epidural lead connected to a pulse generator. The vertebral level ranged from T9 to T12. The cortical SEPs complex P39-N50-P60 was recorded at the basal (T0) evaluation, during the stimulation (T1) and immediately after the stimulation (T2).
RESULTS:In two of ten patients (20%) the complex P39–N50-P60 became unrelievable at the T1 control (stimulator on). In the remaining eight patients statistical analysis showed a significant reduction of the P39/N50 amplitude at T1 recording. In all patients considered, T0 and T2 recordings were not significantly different, suggesting a fast recovery of the SCS effect on SEPs.
CONCLUSION: The results obtained in the present study show an inhibitory effect of SCS on SEPs and support the hypothesis that in some forms of neuropathic pain the antalgic effect of SCS could be attributed to the collision of action potentials travelling in opposite direction on peripheral large diameter fibres.

language: English


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