ReviewCurrent pain and headache reports2011
Neuronal hyperexcitability: a substrate for central neuropathic pain after spinal cord injury.
Review in Current pain and headache reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04506099 (Transcutaneous Intercostal Nerve Stimulation in Spinal Cord Injury), which is not on this map. Cited by 51 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Transcutaneous Intercostal Nerve Stimulation in Spinal Cord Injury
Who cites it
51 citing papers in PubMed, 103 citations in OpenAlex.
- Spinal cord stimulation: An emerging strategy for chronic pain relief after spinal cord injury.Neural regeneration research · 2026Article
- A predictive corticospinal model for pain perception.Cell reports. Medicine · 2026Article
- Immediate Consequences of a Spinal Cord Injury During Development: Unique Insights From Ex Vivo Models.Neural plasticity · 2026Review
- Isolation, characterization and testing of RNA aptamers targeting glutamate receptors in a rat spinal cord injury pain model.Communications biology · 2025Article
- Opportunities and challenges for deep brain stimulation electrode-guided neurofeedback for symptom mitigation in neurological and psychiatric disorders.Journal of neuroengineering and rehabilitation · 2025Review
- Neuropathic Pain-Like Responses in a Chronic CNS Injury Model Are Mediated by Corticospinal-Targeted Spinal Interneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- The Pathological Role and Therapeutic potential of ALDH2 in acrolein detoxification Following Spinal Cord Injury in Mice.bioRxiv : the preprint server for biology · 2025Article
- Article
- Intraspinal microstimulation of the ventral horn has therapeutically relevant cross-modal effects on nociception.Brain communications · 2024Article
- Central neuropathic pain.Nature reviews. Disease primers · 2023Review
- ST2-Conditioned Medium Fosters Dorsal Horn Cell Excitability and Synaptic Transmission in Cultured Mouse Spinal Cord.Stem cell reviews and reports · 2023Article
- Hmgb1 Silencing in the Amygdala Inhibits Pain-Related Behaviors in a Rat Model of Neuropathic Pain.International journal of molecular sciences · 2023Article
- Autogenic biofeedback training improves autonomic responses in a participant with cervical motor complete spinal cord injury- case report.Spinal cord series and cases · 2023Article
- Phenotypes of Motor Deficit and Pain after Experimental Spinal Cord Injury.Bioengineering (Basel, Switzerland) · 2022Article
- Dorsal horn neuronal sparing predicts the development of at-level mechanical allodynia following cervical spinal cord injury in mice.Experimental neurology · 2022Article
- Mu and Delta Opioid Receptor Targeting Reduces Connexin 43-Based Heterocellular Coupling during Neuropathic Pain.International journal of molecular sciences · 2022Article
- Central Neuropathic Pain Syndromes: Current and Emerging Pharmacological Strategies.CNS drugs · 2022Review
- Article
- Altered synaptic connections and inhibitory network of the primary somatosensory cortex in chronic pain.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Review
- Functional Neurophysiological Biomarkers of Early-Stage Alzheimer's Disease: A Perspective of Network Hyperexcitability in Disease Progression.Journal of Alzheimer's disease : JAD · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Neuronal hyperexcitability produces enhanced pain transmission in the spinal dorsal horn after spinal cord injury (SCI). Spontaneous and evoked neuronal excitability normally are well controlled by neural circuits. However, SCI produces maladaptive synaptic circuits in the spinal dorsal horn that result in neuronal hyperexcitability. After SCI, activated primary afferent neurons produce enhanced release of glutamate, neuropeptides, adenosine triphosphate, and proinflammatory cytokines, which are known to be major components for pain transmission in the spinal dorsal horn. Enhanced neurochemical events contribute to neuronal hyperexcitability, and neuroanatomical changes also contribute to maladaptive synaptic circuits and neuronal hyperexcitability. These neurochemical and neuroanatomical changes produce enhanced cellular signaling cascades that ensure persistently enhanced pain transmission. This review describes altered neurochemical and neuroanatomical contributions on neuronal hyperexcitability in the spinal dorsal horn, which serve as substrates for central neuropathic pain after SCI.
Indexed as
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What OpenQuestion holds
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.