Assessment of chronic peripheral localized neuropathic pain during stimulation of the dorsal root ganglion using laser-evoked potentials

Abstract

The modern era in neuromodulation for the treatment of pain began after Melzack and Wall’s seminal work describing the so-called gate control theory (Melzack and Wall 1965). The first application of neuromodulation in a chronic pain patient was performed by Shealy in 1967 (Shealy, Mortimer et al. 1967). Since then, spinal cord stimulation - traditionally involving the placement of an electrode placed on the dorsal column of the spinal cord - has become a valuable method to treat chronic neuropathic pain. Dorsal root ganglion stimulation (DRGS) appeared in 2011 as an interesting new option in neuromodulation for chronic neuropathic pain. Even though clinical results addressing DRGS have already been published and show encouraging clinical results, limited data concerning mechanisms of action have been released to date. This observation highlights the need for further investigation into DRGS, e.g. by implementing standardized clinical assessment tools or neurophysiological techniques (Forget, Boyer et al. 2015). The primary aim of this study was to assess LEPs and to evaluate pain intensity changes at 1 and 6 months after DRGS onset in comparison to baseline (no stimulation). A secondary aim was to evaluate how DRGS affects different clinical measures, as assessed with a neuropathic pain screening tool questionnaire (PainDETECT), a generic QoL questionnaire (SF-36), and a questionnaire of disability associated with chronic neuropathic pain (PDI). Through an open-label study design, we evaluated seven patients (4 men and 3 women; mean age 50.7 years) diagnosed with unilateral chronic peripheral localized neuropathic pain of the groin, knee or leg who were implanted with DRGS electrodes. LEPs N2/P2 peak-to-peak amplitude values significantly increased after 1 and 6 months of DRGS in comparison to baseline (p < .05). The N2/P2 mean values increased from 3.7 μV at baseline to 11.3 μV and 10.7 μV at 1 and 6 months, respectively. At the end of the sixth month under stimulation, LEPs amplitudes were restored to normal values. On the other hand, pain intensity ratings measured through NRS scores significantly decreased after 1 and 6 months of DRGS in comparison to baseline (p < .05). The scores dropped from a mean of 7.6 at baseline to 2.1 and 2.2 at 1 and 6 months, respectively. We also confirmed a trend for improvement in the PainDETECT, SF-36, and PDI measures. These findings suggest that DRGS increases LEPs amplitude and decreases chronic neuropathic pain, resulting in treatment efficacy. We suggest that the observed LEPs restoration reflects normalization of pain pathway signal transmission. Therefore, a better understanding of the role of the DRG in neuromodulation for chronic neuropathic pain will surely impact the field of neuromodulative techniques. The present work represents a contribution towards this goal.