Evidence map›Paper›PMID 31955281›Full record

ReviewCellular and molecular neurobiology2020

Regional Hyperexcitability and Chronic Neuropathic Pain Following Spinal Cord Injury.

Jonghoon Kang, Steve S Cho, Hee Young Kim, Bong Hyo Lee, Hee Jung Cho, Young S Gwak

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
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  14. Neural regeneration research · 2024
    Review
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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

6 authors at 4 institutions in 2 countries.

Jonghoon KangDepartment of Biology, Valdosta State University, Valdosta, GA, 31698, USA.
Steve S ChoDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Hee Young KimDepartment of Physiology, College of Korean Medicine, Daegu Haany University, Daegu, 42158, South Korea.
Bong Hyo LeeDepartment of Acupuncture, Moxibustion and Acupoint, College of Korean Medicine, Daegu Haany University, Daegu, 42158, South Korea.
Hee Jung ChoDepartment of Anatomy, School of Medicine, Kyungpook National University, Daegu, 41944, South Korea. hjcho@knu.ac.kr.
Young S GwakDepartment of Physiology, College of Korean Medicine, Daegu Haany University, Daegu, 42158, South Korea. ysgwak@dhu.ac.kr.ORCID http://orcid.org/0000-0001-7548-5733
Daegu Haany University · KRBoston Children's Hospital · USKyungpook National University · KRValdosta State University · US

Funding

National Research Foundation of Korea 2017R1D1A3B03035303
6 · The paper itself

Abstract

Spinal cord injury (SCI) causes maladaptive changes to nociceptive synaptic circuits within the injured spinal cord. Changes also occur at remote regions including the brain stem, limbic system, cortex, and dorsal root ganglia. These maladaptive nociceptive synaptic circuits frequently cause neuronal hyperexcitability in the entire nervous system and enhance nociceptive transmission, resulting in chronic central neuropathic pain following SCI. The underlying mechanism of chronic neuropathic pain depends on the neuroanatomical structures and electrochemical communication between pre- and postsynaptic neuronal membranes, and propagation of synaptic transmission in the ascending pain pathways. In the nervous system, neurons are the only cell type that transmits nociceptive signals from peripheral receptors to supraspinal systems due to their neuroanatomical and electrophysiological properties. However, the entire range of nociceptive signaling is not mediated by any single neuron. Current literature describes regional studies of electrophysiological or neurochemical mechanisms for enhanced nociceptive transmission post-SCI, but few studies report the electrophysiological, neurochemical, and neuroanatomical changes across the entire nervous system following a regional SCI. We, along with others, have continuously described the enhanced nociceptive transmission in the spinal dorsal horn, brain stem, thalamus, and cortex in SCI-induced chronic central neuropathic pain condition, respectively. Thus, this review summarizes the current understanding of SCI-induced neuronal hyperexcitability and maladaptive nociceptive transmission in the entire nervous system that contributes to chronic central neuropathic pain.

Indexed as

AnimalsChronic PainHumansNeuralgiaNeural InhibitionNeuronsOrgan SpecificitySpinal Cord InjuriesHyperexcitabilityNeuropathic painSpinal cord injury

Identifiers

PMID31955281
PMCPMC11448802
OpenAlexW2999181178

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.