Literature DB >> 9292874

The diagnosis of diffuse axonal injury: implications for forensic practice.

J F Geddes1, G H Vowles, T W Beer, D W Ellison.   

Abstract

The diagnosis of diffuse axonal injury (DAI), which may be of considerable importance in forensic medicine, necessitates widespread sampling of the brain for histology. Because a limited sampling method for screening brains for axonal damage would be of value for medico-legal work, the authors have tested the findings of an earlier study which suggested that a standard set of three blocks from above and below the tentorium could reliably be used in routine practice as a basis for the diagnosis of DAI. A series of 22 previously diagnosed cases of DAI, with a range of survival times, was studied using immunohistochemistry with antibodies to beta-amyloid precursor protein (beta APP), the microglial-associated antigen CD68 (PG-M1) and for GFAP. Strict histological criteria were used to assess traumatic damage, and the evolution of the histological changes with increasing survival is described. In four cases, the sampling scheme employed yielded evidence of axonal damage in only one block, and a diagnosis of DAI could have been made in only 13/22 cases. In six of the shortest surviving cases, beta APP positivity in the corpus callosum and brainstem outlined areas of early ischaemia, as well as of traumatic damage, so that interpretation of immunolabelling was not always clearcut The findings suggest that DAI cannot be reliably diagnosed on a restricted number of blocks from vulnerable areas, and that the use of beta APP and PG-M1 immunocytochemistry may bring interpretative problems that can only be resolved by taking a larger series of tissue samples for histology.

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Year:  1997        PMID: 9292874

Source DB:  PubMed          Journal:  Neuropathol Appl Neurobiol        ISSN: 0305-1846            Impact factor:   8.090


  25 in total

1.  Real-time PCR quantitation of FE65 a beta-amyloid precursor protein-binding protein after traumatic brain injury in rats.

Authors:  Morio Iino; Masato Nakatome; Yoshiaki Ogura; Harutoshi Fujimura; Hisanaga Kuroki; Hiromasa Inoue; Yukiko Ino; Tasuku Fujii; Toshiyuki Terao; Ryoji Matoba
Journal:  Int J Legal Med       Date:  2003-04-18       Impact factor: 2.686

2.  Partial interruption of axonal transport due to microtubule breakage accounts for the formation of periodic varicosities after traumatic axonal injury.

Authors:  Min D Tang-Schomer; Victoria E Johnson; Peter W Baas; William Stewart; Douglas H Smith
Journal:  Exp Neurol       Date:  2011-11-04       Impact factor: 5.330

3.  The possible role of hypoxia in the formation of axonal bulbs.

Authors:  B Kaur; G N Rutty; W R Timperley
Journal:  J Clin Pathol       Date:  1999-03       Impact factor: 3.411

4.  An unusual case of crossbow homicide.

Authors:  C Pomara; S D'Errico; M Neri
Journal:  Forensic Sci Med Pathol       Date:  2007-05-09       Impact factor: 2.007

Review 5.  Traumatic brain injury and amyloid-β pathology: a link to Alzheimer's disease?

Authors:  Victoria E Johnson; William Stewart; Douglas H Smith
Journal:  Nat Rev Neurosci       Date:  2010-05       Impact factor: 34.870

6.  Mechanical disruption of the blood-brain barrier following experimental concussion.

Authors:  Victoria E Johnson; Maura T Weber; Rui Xiao; D Kacy Cullen; David F Meaney; William Stewart; Douglas H Smith
Journal:  Acta Neuropathol       Date:  2018-02-19       Impact factor: 17.088

7.  CLARITY reveals a more protracted temporal course of axon swelling and disconnection than previously described following traumatic brain injury.

Authors:  Maura T Weber; John D Arena; Rui Xiao; John A Wolf; Victoria E Johnson
Journal:  Brain Pathol       Date:  2018-12-27       Impact factor: 6.508

Review 8.  Traumatic brain injury: cause or risk of Alzheimer's disease? A review of experimental studies.

Authors:  J Szczygielski; A Mautes; W I Steudel; P Falkai; T A Bayer; O Wirths
Journal:  J Neural Transm (Vienna)       Date:  2005-06-15       Impact factor: 3.575

9.  Acute and chronically increased immunoreactivity to phosphorylation-independent but not pathological TDP-43 after a single traumatic brain injury in humans.

Authors:  Victoria E Johnson; William Stewart; John Q Trojanowski; Douglas H Smith
Journal:  Acta Neuropathol       Date:  2011-11-19       Impact factor: 17.088

10.  Inhibition of Endocannabinoid Degradation Improves Outcomes from Mild Traumatic Brain Injury: A Mechanistic Role for Synaptic Hyperexcitability.

Authors:  Jacques Mayeux; Paige Katz; Scott Edwards; Jason W Middleton; Patricia E Molina
Journal:  J Neurotrauma       Date:  2016-06-27       Impact factor: 5.269

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