ArticleThe journal of pain2018
Pain After Spinal Cord Injury Is Associated With Abnormal Presynaptic Inhibition in the Posterior Nucleus of the Thalamus.
Article in The journal of pain, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Spinal cord stimulation: An emerging strategy for chronic pain relief after spinal cord injury.Neural regeneration research · 2026Article
- Shared Mechanisms and Integrated Management of Post-Stroke Pain and Depression: A Comprehensive Review.Pain and therapy · 2026Review
- Machine learning-driven identification of critical gene programs and key transcription factors in migraine.The journal of headache and pain · 2025Article
- What Links Sleep and Neuropathic Pain?: A Literature Review on the Neural Circuits for Sleep and Pain Control.Nature and science of sleep · 2025Review
- Myeloid Cell Association with Spinal Cord Injury-Induced Neuropathic Pain and Depressive-like Behaviors in LysM-eGFP Mice.The journal of pain · 2024Article
- Up-regulation of LCN2 in the anterior cingulate cortex contributes to neural injury-induced chronic pain.Frontiers in cellular neuroscience · 2023Article
- Corticothalamic Pathways From Layer 5: Emerging Roles in Computation and Pathology.Frontiers in neural circuits · 2021Review
- Regional Hyperexcitability and Chronic Neuropathic Pain Following Spinal Cord Injury.Cellular and molecular neurobiology · 2020Review
- Considerations for Studying Sex as a Biological Variable in Spinal Cord Injury.Frontiers in neurology · 2020Article
- The etiological contribution of GABAergic plasticity to the pathogenesis of neuropathic pain.Molecular painReview
- Patterns of cognitive decline and somatosensory processing in a mouse model of amyloid accumulation.Neurobiology of pain (Cambridge, Mass.)Article
- Pain matrix shift in the rat brain following persistent colonic inflammation revealed by voxel-based statistical analysis.Molecular painArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Pain after spinal cord injury (SCI-Pain) is one of the most debilitating sequelae of spinal cord injury, characterized as relentless, excruciating pain that is largely refractory to treatments. Although it is generally agreed that SCI-Pain results from maladaptive plasticity in the pain processing pathway that includes the spinothalamic tract and somatosensory thalamus, the specific mechanisms underlying the development and maintenance of such pain are yet unclear. However, accumulating evidence suggests that SCI-Pain may be causally related to abnormal thalamic disinhibition, leading to hyperactivity in the posterior thalamic nucleus (PO), a higher-order nucleus involved in somatosensory and pain processing. We previously described several presynaptic mechanisms by which activity in PO is regulated, including the regulation of GABAergic as well as glutamatergic release by presynaptic metabotropic gamma-aminobutyric acid (GABA PERSPECTIVE: This report presents synaptic mechanisms that may underlie the development and maintenance of SCI-Pain. Because of the difficulty in treating SCI-Pain, a better understanding of the underlying neurobiological mechanisms is critical, and may allow development of better treatment modalities.
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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.