Evidence map›Paper›PMID 22285252›Full record

ReviewExperimental neurology2013

Axonal pathology in traumatic brain injury.

Victoria E Johnson, William Stewart, Douglas H Smith

Registry-linked trialAbstract readReview
In one paragraph

Review in Experimental neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05786729 (Effects of Aerobic Exercise and Rehabilitation After Traumatic Brain Injury), which is not on this map. Cited by 657 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
657citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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.

NCT05786729 phase1 / phase2enrolling by invitationnot on this mapstarted 2022, after this paper: background citation

Effects of Aerobic Exercise and Rehabilitation After Traumatic Brain Injury

TypeinterventionalSponsorCentre for Neuro SkillsRan2022 to 2028Enrolled190ConditionsTraumatic Brain InjuryArmsAerobic Exercise (AER), Rehabilitation
3 · Its place in the literature

Who cites it

657 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Recovery from disorders of consciousness: Lesions and GABAergic modulation in a biologically inspired spiking neural network.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Observational
  13. Review
  14. Article
  15. Article
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  19. Axon Diameter Mapping From Myelin Water Diffusion MRI.IEEE transactions on medical imaging · 2026
    Article
  20. Research progress on biomarkers of traumatic brain injury.Animal models and experimental medicine · 2026
    Review

597 more citing papers are in PubMed but not listed here.

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.

Victoria E JohnsonPenn Center for Brain Injury and Repair and Department of Neurosurgery, University of Pennsylvania, PA 19104, USA.
William Stewart
Douglas H Smith

Funding

TBI: Uncovering Mechanisms of AD-like pathologyR01NS038104 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI SMITH, DOUGLAS HAMILTON · 1999 to 2020
$7.6M
NeuroimagingP01NS056202 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI LEVIN, HARVEY · 2008 to 2012
$6.6M
Alzheimer-Like Pathologies Following Traumatic Brain Injury in Older IndividualsR03AG038911 · NIA · UNIVERSITY OF PENNSYLVANIA · PI SMITH, DOUGLAS HAMILTON · 2011 to 2012
$131k
NIA NIH HHS R03 AG038911NINDS NIH HHS NS038104NINDS NIH HHS NS056202NINDS NIH HHS P01 NS056202NINDS NIH HHS R01 NS038104
6 · The paper itself

Abstract

Over the past 70years, diffuse axonal injury (DAI) has emerged as one of the most common and important pathological features of traumatic brain injury (TBI). Axons in the white matter appear to be especially vulnerable to injury due to the mechanical loading of the brain during TBI. As such, DAI has been found in all severities of TBI and may represent a key pathologic substrate of mild TBI (concussion). Pathologically, DAI encompasses a spectrum of abnormalities from primary mechanical breaking of the axonal cytoskeleton, to transport interruption, swelling and proteolysis, through secondary physiological changes. Depending on the severity and extent of injury, these changes can manifest acutely as immediate loss of consciousness or confusion and persist as coma and/or cognitive dysfunction. In addition, recent evidence suggests that TBI may induce long-term neurodegenerative processes, such as insidiously progressive axonal pathology. Indeed, axonal degeneration has been found to continue even years after injury in humans, and appears to play a role in the development of Alzheimer's disease-like pathological changes. Here we review the current understanding of DAI as a uniquely mechanical injury, its histopathological identification, and its acute and chronic pathogenesis following TBI.

Indexed as

AnimalsAxonsBrain InjuriesComaDiffuse Axonal InjuryHumansNerve DegenerationNerve Fibers, MyelinatedAxonAxonal pathologyDAIDiffuse axonal InjuryHead injuryMicrotubuleNeurodegenerationRotational accelerationTBITraumatic brain injury

Identifiers

PMID22285252
PMCPMC3979341

What OpenQuestion holds

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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.