Association Between Spinal Cord Stimulation and Top-Down Nociceptive Inhibition in People With Failed Back Surgery Syndrome: A Cohort Study

Abstract

BackgroundDescending nociceptive inhibitory pathways often malfunction in people with chronic pain. Conditioned pain modulation (CPM) is an experimental evaluation tool for assessing the functioning of these pathways. Spinal cord stimulation (SCS), a well-known treatment option for people with failed back surgery syndrome (FBSS), probably exerts its pain-relieving effect through a complex interplay of segmental and higher-order structures.ObjectiveTo the best of our knowledge, no clinical studies have thoroughly investigated the associations between SCS and CPM.DesignThis was a prospective cohort study in people with FBSS.MethodsSeventeen people who had FBSS and were scheduled for SCS were enrolled in this study. The CPM model was evaluated at both sural nerves and was induced by electrical stimulation as the test stimulus and the cold pressor test as the conditioning stimulus.ResultsBefore SCS, less than 30% of the participants with FBSS showed a CPM effect. Significant increases in the electrical detection threshold on the symptomatic side and the nonsymptomatic side were found. On the symptomatic side, no differences in the numbers of CPM responders before and after SCS could be found. On the nonsymptomatic side, more participants showed a CPM effect during SCS. Additionally, there were significant differences for CPM activation and SCS treatment.LimitationsLimitations were the small sample size and the subjective outcome parameters in the CPM model.ConclusionsThis study revealed a bilateral effect of SCS that suggests the involvement of higher-order structures, such as the periaqueductal gray matter and rostroventromedial medulla (key regions in the descending pathways), as previously suggested by animal research.

Exploration of the Supraspinal Hypotheses about Spinal Cord Stimulation and Dorsal Root Ganglion Stimulation: A Systematic Review

“…Two articles used an indirect evaluation through experimental pain measurements with Conditioned Pain Modulation (CPM). CPM is an indirect psychophysical measure to assess the functioning of the endogenous descending nociceptive inhibitory system, whereby SCS seemed to activate this descending system [50,66]. Additionally, sensory assessments with mechanical and thermal hypersensitivity indicated that SCS reduced hypersensitivity [5,23,29], indicative for the activation of brainstem structures in the descending inhibition.…”

Heart rate variability is not suitable as a surrogate marker for pain intensity in patients with chronic pain

“…10 Interactions are established by (1) baroreflex activity with an inverse relationship between resting blood pressure levels and acute pain sensitivity, 11 (2) the vagal-nociceptive interactions where sympathetic and parasympathetic preganglionic nuclei receive input from the descending nociceptive inhibitory pathways to exert an influence on pain thresholds and modifying autonomic outflow, 50,58 and (3) projections from the periaqueductal grey neurons to autonomic centers in the medulla, involved in cardiovascular changes during endogenous analgesia. 6,34 Because structural and functional brain alterations are reported in chronic pain patients, 42 as well as a dysregulation of the balance between the sympathetic and parasympathetic system, 17,20 decreased baroreflex sensitivity, 19 and diminished functioning of the descending nociceptive inhibitory pathways, 31,45 both systems demonstrated altered output mechanisms, which points towards a relation between pain intensity and HRV in chronic pain. Nevertheless, despite these anatomical and functional connections, no information is available yet concerning the association between the amount of pain intensity and HRV parameters in patients with chronic pain.…”

“…Because structural and functional brain alterations are reported in chronic pain patients, 42 as well as a dysregulation of the balance between the sympathetic and parasympathetic system, 17,20 decreased baroreflex sensitivity, 19 and diminished functioning of the descending nociceptive inhibitory pathways, 31,45 both systems demonstrated altered output mechanisms, which points towards a relation between pain intensity and HRV in chronic pain. Nevertheless, despite these anatomical and functional connections, no information is available yet concerning the association between the amount of pain intensity and HRV parameters in patients with chronic pain.…”