ReviewCureus2025
Integrated Spinal and Supraspinal Mechanisms of Spinal Cord Stimulation Analgesia: A Systematic Review of Bidirectional Neural Modulation.
Review in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord stimulation (SCS) is an established therapy for refractory neuropathic pain, yet its spinal-level gating and supraspinal modulatory actions have rarely been unified into a single framework. Adhering to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, we conducted a comprehensive search and rigorous selection of animal studies that investigated both spinal and supraspinal circuitry involved in SCS-induced analgesia. Through this process, we identified and systematically reviewed seven rodent studies employing tonic, burst, or sub-perception SCS in mononeuropathy and spared-nerve-injury models, extracting electrophysiological, molecular, lesion, and imaging data. Across these models, SCS consistently restored dorsal-horn inhibitory tone, enhancing GABAergic and glycinergic signaling, suppressing wide-dynamic-range neuron hyperactivity, and attenuating mitogen-activated protein kinase (MAPK) and microglial activation. At the same time, epidural stimulation sent signals up the spinal cord that activated key brainstem pain-control centers: the periaqueductal gray, rostroventromedial medulla, and locus coeruleus. It also normalized abnormal cortical oscillations in somatosensory and limbic regions. Lesion and receptor-blockade experiments revealed that disruption of either ascending afferents or descending tracts halved analgesic efficacy, confirming a bidirectional feedback loop. Functional MRI further showed that burst versus tonic waveforms differentially recruit sensory versus affective networks. Together, these findings support a unified spinal-supraspinal model of SCS-mediated analgesia and highlight opportunities to refine electrode placement, waveform design, and stimulation parameters. While translational implications are tempered by variability in preclinical study designs, this integrated framework provides a roadmap for next-generation, mechanism-driven neuromodulation therapies tailored to individual pain needs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.