Evidence map›Paper›PMID 24978827›Full record

ArticlePain2014

Early afferent activity from the facet joint after painful trauma to its capsule potentiates neuronal excitability and glutamate signaling in the spinal cord.

Nathan D Crosby, Taylor M Gilliland, Beth A Winkelstein

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Pain, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04542798 (Central Sensitization and Aberrant Nerve Sprouting Possible Explanations for RFA Failure of MBDR in CLBP of FJ Origin), which is not on this map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.1field-weighted citation impact, top 9% of its field
1 · What the graph read from it

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.

2 · The registry

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.

NCT04542798 naunknown statusnot on this mapstarted 2020, after this paper: background citation

Central Sensitization and Aberrant Nerve Sprouting Possible Explanations for RFA Failure of MBDR in CLBP of FJ Origin: CRF Versus WCRF or PRF-DRG Randomized Clinical Trial

TypeinterventionalSponsorHospital General Universitario de ValenciaRan2020 to 2024Enrolled80ConditionsLow Back Pain, Recurrent, Neuropathic Pain, Facet Joint Pain, Central SensitisationArmsRadiofrequency COSMAN
3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Nathan D CrosbyDepartment of Bioengineering, University of Pennsylvania, Philadelphia, PA, USA Department of Neurosurgery, University of Pennsylvania, Philadelphia, PA, USA.
Taylor M Gilliland
Beth A Winkelstein
University of Pennsylvania · US

Funding

Nociceptive Mechanisms In Whiplash InjuryR01AR056288 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI WINKELSTEIN, BETH A · 2009 to 2013
$1.6M
NIAMS NIH HHS AR056288NIAMS NIH HHS R01 AR056288
6 · The paper itself

Abstract

Cervical facet joint injury induces persistent pain and central sensitization. Preventing the peripheral neuronal signals that initiate sensitization attenuates neuropathic pain. Yet, there is no clear relationship among facet joint afferent activity, development of central sensitization, and pain, which may be hindering effective treatments for this pain syndrome. This study investigates how afferent activity from the injured cervical facet joint affects induction of behavioral sensitivity and central sensitization. Intra-articular bupivacaine was administered to transiently suppress afferent activity immediately or 4 days after facet injury. Mechanical hyperalgesia was monitored after injury, and spinal neuronal hyperexcitability and spinal expression of proteins that promote neuronal excitability were measured on day 7. Facet injury with saline vehicle treatment induced significant mechanical hyperalgesia (P<.027), dorsal horn neuronal hyperexcitability (P<.026), upregulation of pERK1/2, pNR1, mGluR5, GLAST, and GFAP, and downregulation of GLT1 (P<.032). However, intra-articular bupivacaine immediately after injury significantly attenuated hyperalgesia (P<.0001), neuronal hyperexcitability (P<.004), and dysregulation of excitatory signaling proteins (P<.049). In contrast, intra-articular bupivacaine at day 4 had no effect on these outcomes. Silencing afferent activity during the development of neuronal hyperexcitability (4 hours, 8 hours, 1 day) attenuated hyperalgesia and neuronal hyperexcitability (P<.045) only for the treatment given 4 hours after injury. This study suggests that early afferent activity from the injured facet induces development of spinal sensitization via spinal excitatory glutamatergic signaling. Peripheral intervention blocking afferent activity is effective only over a short period of time early after injury and before spinal modifications develop, and is independent of modulating spinal glial activation.

Indexed as

AnimalsDown-RegulationGlutamic AcidHyperalgesiaMaleNeurons, AfferentPain MeasurementRatsSignal TransductionSpinal CordUp-RegulationZygapophyseal JointGlutamic AcidBupivacaineFacet jointGlutamateHyperalgesiaNeuronal hyperexcitabilityPain

Identifiers

PMID24978827
PMCPMC4157970
OpenAlexW1974880258

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.