The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Traumatic Brain Injury: An Overview of Pathobiology with Emphasis on Military Populations
Open accessAbstract
This review considers the pathobiology of non-impact blast-induced neurotrauma (BINT). The pathobiology of traumatic brain injury (TBI) has been historically studied in experimental models mimicking features seen in the civilian population. These brain injuries are characterized by primary damage to both gray and white matter and subsequent evolution of secondary pathogenic events at the cellular, biochemical, and molecular levels, which collectively mediate widespread neurodegeneration. An emerging field of research addresses brain injuries related to the military, in particular blast-induced brain injuries. What is clear from the effort to date is that the pathobiology of military TBIs, particularly BINT, has characteristics not seen in other types of brain injury, despite similar secondary injury cascades. The pathobiology of primary BINT is extremely complex. It comprises systemic, local, and cerebral responses interacting and often occurring in parallel. Activation of the autonomous nervous system, sudden pressure-increase in vital organs such as lungs and liver, and activation of neuroendocrine-immune system are among the most important mechanisms significantly contributing to molecular changes and cascading injury mechanisms in the brain.
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Citations
Cites
Experimental models of traumatic brain injury: do we really need to build a better mousetrap?
Morales, D. M., Marklund, N., Lebold, D., Thompson, H. J., Pitkanen, A., Maxwell, W. L., Longhi, L., Laurer, H., Maegele, M., Neugebauer, E., et al. (2005) · Neuroscience · doi:10.1016/j.neuroscience.2005.08.030 · Cited by 339 · cited 1×
“…this topic in detail, particularly from the perspectives of animal models (Cernak, 2005; Kazanis, 2005; LaPlaca et al, 2007; Manvelyan, 2006; Morales et al, 2005; Potts et al, 2009; Weber, 2007), and the understanding that we have gained from these models with regard to general pathobiology…”
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Cited by
Risdall, J. E., & Menon, D. K. (2011) · Philosophical Transactions of the Royal Society B: Biological Sciences · doi:10.1098/rstb.2010.0230 · Cited by 185
Blood–brain barrier dysfunction following traumatic brain injury
Alluri, H., Wiggins-Dohlvik, K., Davis, M. L., Huang, J. H., & Tharakan, B. (2015) · Metabolic Brain Disease · doi:10.1007/s11011-015-9651-7 · Cited by 149
Repetitive blast exposure in mice and combat veterans causes persistent cerebellar dysfunction
Meabon, J. S., Huber, B. R., Cross, D. J., Richards, T. L., Minoshima, S., Pagulayan, K. F., Li, G., Meeker, K. D., Kraemer, B. C., Petrie, E. C., et al. (2016) · Science Translational Medicine · doi:10.1126/scitranslmed.aaa9585 · Cited by 138
Swanson, T. M., Isaacson, B. M., Cyborski, C. M., French, L. M., Tsao, J. W., & Pasquina, P. F. (2017) · Public Health Reports® · doi:10.1177/0033354916687748 · Cited by 112
Gerson, J., Castillo-Carranza, D. L., Sengupta, U., Bodani, R., Prough, D. S., DeWitt, D. S., Hawkins, B. E., & Kayed, R. (2016) · Journal of Neurotrauma · doi:10.1089/neu.2015.4262 · Cited by 94
Pituitary dysfunction after blast traumatic brain injury: The UK BIOSAP study
Baxter, D., Sharp, D. J., Feeney, C., Papadopoulou, D., Ham, T. E., Jilka, S., Hellyer, P. J., Patel, M. C., Bennett, A. N., Mistlin, A., et al. (2013) · Annals of Neurology · doi:10.1002/ana.23958 · Cited by 81
“The primary blast wave or wind may cause direct injury, or secondary injuries from explosion debris or tertiary injuries from the impact of being thrown by the blast may occur.(28,29) These injuries could affect the hypothalamus, pituitary gland, or pituitary stalk, resulting in damage to cell bodies or white matter c…”
BackgroundBlast TBI models, neuropathology, and implications for seizure risk.
Kovacs, S. K., Leonessa, F., & Ling, G. S. F. (2014) · Frontiers in Neurology · doi:10.3389/fneur.2014.00047 · Cited by 71
Belding, J. N., Englert, R. M., Fitzmaurice, S., Jackson, J. R., Koenig, H. G., Hunter, M. A., Thomsen, C. J., & da Silva, U. O. (2021) · Frontiers in Neurology · doi:10.3389/fneur.2021.628782 · Cited by 53
Vu, P. A., Tucker, L. B., Liu, J., McNamara, E. H., Tran, T., Fu, A. H., Kim, Y., & McCabe, J. T. (2018) · Brain Research · doi:10.1016/j.brainres.2018.08.034 · Cited by 32
Chronic Caffeine Exposure Attenuates Blast-Induced Memory Deficit in Mice
Ning, Y.-L., Yang, N., Chen, X., Zhao, Z.-A., Zhang, X.-Z., Chen, X.-Y., Li, P., Zhao, Y., & Zhou, Y.-G. (2015) · Chinese Journal of Traumatology · doi:10.1016/j.cjtee.2015.10.003 · Cited by 24
Metadata
- Authors
- Cernak, I., & Noble-Haeusslein, L. J.
- Venue
- Journal of Cerebral Blood Flow & Metabolism
- Publisher
- SAGE Publications
- Published
- 2009-10-07
- Volume
- 30
- Issue
- 2
- Pages
- 255-266
- ISSN
- 0271-678X (ISSN-L)
- 1559-7016
- OpenAlex
- W2000489529
- Cited by
- 444
- References
- 1
- FWCI
- 15.94
- Type
- journal article
- Language
- en
- Open access
- green
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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