Traumatic brain injury: Estimate of the age of the injury based on neuroinflammation, endothelial activation markers and adhesion molecules
- PMID: 33625724
- DOI: 10.14670/HH-18-319
Traumatic brain injury: Estimate of the age of the injury based on neuroinflammation, endothelial activation markers and adhesion molecules
Abstract
Studies on traumatic brain injury (TBI) are applicable not only in the clinical context, but also in the forensic field. Over time, the literature has accumulated scientific evidence supporting the use of specific histopathological tests in dating traumatic brain injuries. In primary damage, cell death occurs by necrosis/apoptosis. In secondary injury, the underlying mechanisms are inflammation and ischemia. The inflammatory response of the central nervous system (CNS) follows the common steps of the innate response. In head injury, the blood brain barrier (BBB) undergoes both functional damage and, subsequently, finer structural changes. Scientific evidence has shown modifications of the junctional-endothelial system that favors the extravasation of immunocompetent cells. The histological evaluation of the subdural hematoma, of the cerebral contusions, of the diffuse axonal damage can certainly bring useful elements, with limitations, to the chronological evaluation of the lesions. Many markers have been used to better define the dating of the head injury. Several authors also analyzed the usefulness of secondary damage markers in brain tissue. The progress achieved with immunohistochemistry is significant compared to the use of routine staining. With immunohistochemistry it is possible to identify much narrower and more precise time intervals and, above all, with greater probative reliability. Recently attention has been paid to the modification of structural proteins and miRNAs. Future research is already started and entrusted to multidisciplinary teams that know how to combine their specific skills in search of a reproducible standard of known and sufficient accuracy.
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References
-
- Abdul-Muneer P.M., Chandra N. and Haorah J. (2015). Interactions of oxidative stress and neurovascular inflammation in the pathogenesis of traumatic brain injury. Mol. Neurobiol. 51, 966-979. - PubMed
-
- Balabanov R., Goldman H., Murphy S., Pellizon G., Owen C., Rafols J. and Dore-Duffy P. (2001). Endothelial cell activation following moderate traumatic brain injury. Neurol. Res. 23, 175-182. - PubMed
-
- Biagas K.V., Uhl M.W., Schiding J.K., Nemoto E.M. and Kochanek P.M. (1992). Assessment of posttraumatic polymorphonuclear leukocyte accumulation in rat brain using tissue myeloperoxidase assay and vinblastine treatment. J. Neurotrauma 9, 363-371. - PubMed
-
- Blumbergs P.C., Scott G., Manavis J., Wainwright H., Simpson D.A. and McLean A.J. (1995). Topography of axonal injury as defined by amyloid precursor protein and the sector scoring method in mild and severe closed head injury. J. Neurotrauma 12, 565-572. - PubMed
-
- Böhmer A.E., Oses J.P., Schmidt A.P., Perón C.S., Krebs C.L., Oppitz P.P., D'Avila T.T., Souza D.O., Portela L.V. and Stefani M.A. (2011). Neuron-specific enolase, S100B, and glial fibrillary acidic protein levels as outcome predictors in patients with severe traumatic brain injury. Neurosurgery 68, 1624-1630. - PubMed
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