ArticleEuropean journal of pain (London, England)2022
Anti- and Pro-Nociceptive mechanisms in neuropathic pain after human spinal cord injury.
Article in European journal of pain (London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 14 citations in OpenAlex.
- The role of biopsychosocial factors in classifying pain intensity across various chronic pain conditions.Scientific reports · 2026Article
- Beyond device parameters: psychological predictors of spinal cord stimulation success and their neurobiological mechanisms-a narrative review.Frontiers in psychology · 2026Review
- Intact endogenous pain inhibition in complex regional pain syndrome type 1.Pain reports · 2025Article
- What a Sham(e): Sham-Controlled Conditioned Pain Modulation Effects on Pressure but Not Heat Pain Thresholds in Healthy Volunteers.European journal of pain (London, England) · 2025Article
- Virtual Reality Interventions for Spinal Cord Injury-Related Neuropathic Pain: A Comprehensive Scoping Review of Multidimensional Outcomes.Journal of pain research · 2025Review
- Tonic Cold Pain Temporal Summation and Translesional Cold Pressor Test-Induced Pronociception in Spinal Cord Injury: Association with Spontaneous and Below-Level Neuropathic Pain.Healthcare (Basel, Switzerland) · 2024Article
- Understanding inter-individual variability of experimental pain habituation and conditioned pain modulation in healthy individuals.Scientific reports · 2024Article
- Central neuropathic pain.Nature reviews. Disease primers · 2023Review
- Intrinsic brain connectivity alterations despite intact pain inhibition in subjects with neuropathic pain after spinal cord injury: a pilot study.Scientific reports · 2023Article
- Review
- Anti- and Pro-Nociceptive mechanisms in neuropathic pain after human spinal cord injury.European journal of pain (London, England) · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundDeficient endogenous pain modulation and increased nociceptive excitability are key features of central sensitization and can be assessed in humans by conditioned pain modulation (CPM, anti-nociceptive) and temporal summation of pain (TSP, pro-nociceptive), respectively. This study aimed to investigate these measures as proxies for central sensitization in subjects with chronic neuropathic pain (NP) after spinal cord injury (SCI).
methodsIn paraplegic subjects with NP (SCI-NP; n = 17) and healthy controls (HC; n = 17), parallel and sequential sham-controlled CPM paradigms were performed using pressure pain threshold at the hand, that is, above lesion level, as test stimulus. The conditioning stimulus was a noxious cold (verum) or lukewarm water bath (sham) applied contralaterally. Regarding pro-nociceptive mechanisms, a TSP protocol with individually-adjusted pressure pain stimuli at the thenar eminence was used. CPM and TSP magnitudes were related to intensity and spatial extent of spontaneous NP.
resultsNeither the parallel nor sequential sham-controlled CPM paradigm showed any significant inhibition of above-level pressure pain thresholds for SCI-NP or HC. Accordingly, no group difference in CPM capacity was found, however, subjects with more intense spontaneous NP showed lower inhibitory CPM capacity. TSP was observed for both groups but was not enhanced in SCI-NP.
conclusionsOur results do not support altered above-level anti- or pro-nociceptive mechanisms in SCI-NP compared with HC; however, they also highlight the relevance of spontaneous NP intensity with regards to the capacity of endogenous pain modulation in SCI subjects. SIGNIFICANCE: Central sensitization encompasses deficient endogenous pain modulation and increased nociceptive excitability. These two mechanisms can be assessed in humans by conditioned pain modulation and temporal summation of pain, respectively. Our data demonstrates a lack of descending pain inhibition only in subjects with severe neuropathic pain which may hint towards central sensitization at spinal and/or supra-spinal levels. Disentangling the mechanisms of endogenous pain modulation and neuronal hyperexcitability might improve mechanism-based treatment of neuropathic pain in subjects with spinal cord injury.
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