Morphological features of mild blast-induced traumatic brain injury (literature review)

Authors

DOI:

https://doi.org/10.26641/1997-9665.2025.3.15-21

Keywords:

blast, trauma, brain, morphology, blood-brain barrier, astrogliosis, inflammation, neurodegeneration

Abstract

The article is based on a thorough analysis of contemporary world literature devoted to the morphological study of macroscopic and microscopic markers of mild blast-induced traumatic brain injury (bTBI). The relevance of this analysis stems from the fact that blast-induced traumatic brain injury is one of the most common injuries suffered by military personnel and civilians during military operations, including while Russia's full-scale invasion of Ukraine. Mild bTBI differs from moderate and severe trauma in that there are no external signs of injury from debris or thermal factors, so it often goes undiagnosed and leads to irreversible changes that negatively affect work capacity and life quality. To create this article, an analysis of international scientific publications for the period 2006-2025 was conducted. The search for sources was performed using the keywords “blast, trauma, brain, morphology, blood-brain barrier, astrogliosis, inflammation, neurodegeneration” in the PubMed bibliographic database, the ResearchGate scientific portal, and the ScienceDirect electronic portal. In general, mild blast-induced traumatic brain injury is diffuse damage caused by the effects of a blast wave. The main structure undergoing changes is the blood-brain barrier, damage to which consists in increased vascular permeability, causing pro- and inflammatory biologically active substances to enter the brain, contributing to the development of inflammation and astrogliosis, impaired cerebral circulation and oedema. Morphological signs of neuronal damage also indicate inflammation and metabolic disorders, leading to the development of neurodegeneration in the distant post-traumatic period. Axonal damage is also a characteristic feature of blast-induced traumatic brain injury.

References

  1. Varghese N, Morrison B. Partial depletion of microglia attenuates long-term potentiation deficits following repeated blast traumatic brain injury in organotypic hippocampal slice cultures. J Neurotrauma. 2023;40(5-6):547-560. doi: 10.1089/neu.2022.0284.
  2. Kozlova Y, Kozlov S. Сhanges of trace elements in the cerebellum and their influence on the rats behavior in elevated plus maze in the acute period of mild blast-induced brain injury. J Trace Elem Med Biol. 2023;78:127189. doi: 10.1016/j.jtemb.2023. 127189.
  3. Buchanan BJ, author. Gunpowder, explosives and the state. Aldershot: Ashgate; 2006. 449 p. doi: 10.4324/9781315253725.
  4. Cirincione J, author. Bomb scare: the history and future of nuclear weapons. New York: Columbia University Press; 2008. 232 p. doi: 10.1080/ 14702436.2012.661986.
  5. Zhang L, Yang Q, Yuan R, et al. Single-nucleus transcriptomic mapping of blast-induced traumatic brain injury in mice hippocampus. Scientific Data. 2023;10(1):638. doi: 10.1038/s41597-023-02552-x.
  6. Mac Donald CL, Johnson AM, Wierzechowski L, et al. Prospectively assessed clinical outcomes in concussive blast vs nonblast traumatic brain injury among evacuated US military personnel. JAMA Neurology. 2014;71(8):994-1002. doi: 10.1001/jamaneurol.2014.1114.
  7. Kozlov SV, Mishalov VD, Suloev KM, Kozlova YuV. [Pathomorphological markers of blast-induced brain injury]. Morphologia. 2021;15(3):96–100. Ukrainian. doi: 10.26641/1997-9665.2021.3.96-100.
  8. Song H, Konan LM, Cui J, et al. Nanometer ultrastructural brain damage following low intensity primary blast wave exposure. Neural Regeneretion Research. 2018;13(9):1516-9. doi: 10.4103/1673-5374.237110.
  9. Przekwas A, Somayaji MR, Gupta RK. Synaptic mechanisms of blast-induced brain injury. Frontiers in Neurology. 2016;7:2. doi: 10.3389/ fneur.2016.00002.
  10. Dickerson MR, Murphy SF, Urban MJ, et al. Chronic anxiety- and depression-like behaviors are associated with glial-driven pathology following repeated blast induced neurotrauma. Front Behav Neurosci. 2021;15:787475. doi: 10.3389/ fnbeh.2021.787475.
  11. Govindarajulu M, Patel MY, Wilder DM, et al. Upregulation of multiple toll-like receptors in ferret brain after blast exposure: Potential targets for treatment. Neurosci Lett. 2023;810:137364. doi: 10.1016/j.neulet.2023.137364.
  12. Dennis EL, Rowland JA, Esopenko C, et al. Differences in brain volume in military service members and veterans after blast-related mild TBI: A LIMBIC-CENC Study. JAMA Netw Open. 2024;7(11):e2443416. doi: jamanetworkopen.2024.43416.
  13. Hasanpour-Segherlou Z, Masheghati F, Shakeri-Darzehkanani M, et al. Neurodegenerative disorders in the context of vascular changes after traumatic brain injury. Journal of Vascular disease. 2024;3:319-332. doi: 10.3390/jvd3030025.
  14. Ma J, Wang J, Deng K, et al. The effect of MaxiK channel on regulating the activation of NLRP3 inflammasome in rats of blast-induced traumatic brain injury. Neuroscience. 2022;482:132-142. doi: 10.1016/j.neuroscience.2021.12.019.
  15. Nonaka M, Taylor WW, Bukalo O, et al. Behavioral and myelin-related abnormalities after blast-induced mild traumatic brain injury in mice. J Neurotrauma. 2021;38(11):1551-1571. doi: 10.1089/ neu.2020.7254.
  16. Gama Sosa MA, De Gasperi R, Perez Garcia GS, et al. Low-level blast exposure disrupts gliovascular and neurovascular connections and induces a chronic vascular pathology in rat brain. Acta Neuropathologica Communications. 2019;7(1):6. doi: 10.1186/s40478-018-0647-5.
  17. Uzunalli G, Herr S, Dieterly AM, et al. Structural disruption of the blood-brain barrier in repetitive primary blast injury. Fluids Barriers CNS. 2021;18(1):2. doi: 10.1186/s12987-020-00231-2.
  18. Heyburn L, Abutarboush R, Goodrich S, et al. Repeated low-level blast overpressure leads to endovascular disruption and alterations in TDP-43 and Piezo2 in a rat model of blast TBI. Frontiers in Neurology. 2019;10:766. doi: 10.3389/ fneur.2019.00766.
  19. Kuriakose M, Rama Rao KV, Younger D, et al. Temporal and spatial effects of blast overpressure on blood-brain barrier permeability in traumatic brain injury. Scientific Reports. 2018;8(1):8681. doi: 10.1038/s41598-018-26813-7.
  20. Varatharaj A, Galea I. The blood-brain barrier in systemic inflammation. Brain, Behavior, and Immunity. 2017;60:1-12. doi: 10.1016/ j.bbi.2016.03.010.
  21. Logsdon AF, Meabon JS, Cline MM, et al. Blast exposure elicits blood-brain barrier disruption and repair mediated by tight junction integrity and nitric oxide dependent processes. Scientific Reports. 2018;8(1):11344. doi: 10.1038/s41598-018-29341-6.
  22. Levy M, Arfi Levy E, Marianayagam NJ, et al. Distinctive patterns of sequential platelet counts following blunt traumatic brain injury predict outcomes. Brain Inj. 2024;38(10):818-826. doi: 10.1080/02699052.2024.2347571.
  23. Cao R, Zhang C, Mitkin VV, et al. Comprehensive characterization of cerebrovascular dysfunction in blast traumatic brain injury using photoacoustic microscopy. Journal of Neurotrauma. 2019;36(10):1526-1534. doi: 10.1089/ neu.2018.6062.
  24. Rodriguez UA, Zeng Y, Parsley MA, et al. Effects of blast-induced neurotrauma on pressurized rodent middle cerebral arteries. Journal of Visualized Experiments. 2019;146. doi: 10.3791/58792.
  25. Rodriguez UA, Zeng Y, Deyo D, et al. Effects of mild blast traumatic brain injury on cerebral vascular, histopathological, and behavioral outcomes in rats. Journal of Neurotrauma. 2018;35(2):375-392. doi: 10.1089/neu.2017.5256.
  26. Rama Rao KV, McLean VL, Wilder DM, et al. Comparison of blood-brain barrier permeability changes in gyrencephalic (ferret & non-human primate) and lissencephalic (rat) models following blast overpressure exposures. Exp Neurol. 2025;392:115375. doi: 10.1016/j.expneurol.2025. 115375.
  27. Zhu X, Chu X, Wang H, et al. Investigating neuropathological changes and underlying neurobiological mechanisms in the early stages of primary blast-induced traumatic brain injury: Insights from a rat model. Exp Neurol. 2024;375:114731. doi: 10.1016/j.expneurol.2024.114731.
  28. Kabu S, Jaffer H, Petro M, et al. Blast-associated shock waves result in increased brain vascular leakage and elevated ROS levels in a rat model of traumatic brain injury. PLoS One. 2015;10(5):e0127971. doi: 10.1371/journal.pone. 0127971.
  29. Zhou Y, Song Y, Zhu L. Activation of autophagy after blast-induced traumatic brain injury in mice. Neuroreport. 2023;34(15):759-766. doi: 10.1097/wnr.0000000000001951.
  30. Mohammadi A, Hosseinzadeh Colagar A, Khorshidian A, et al. The functional roles of curcumin on astrocytes in neurodegenerative diseases. Neuroimmunomodulation. 2022;29(1):4-14. doi: 10.1159/ 000517901.
  31. Zhou B, Zuo YX, Jiang RT. Astrocyte morphology: Diversity, plasticity, and role in neurological diseases. CNS Neuroscience & Therapeutics. 2019;25(6):665-673. doi: 10.1111/cns.13123.
  32. Inutsuka A, Hattori A, Yoshida M, et al. Cerebellar damage with inflammation upregulates oxytocin receptor expression in Bergmann Glia. Mol Brain. 2024;17(1):41. doi: 10.1186/s13041-024-01114-5.
  33. Si TE, Li Z, Zhang J, et al. Epigenetic mechanisms of Müller glial reprogramming mediating retinal regeneration. Front Cell Dev Biol. 2023;11:1157893. doi: 10.3389/fcell.2023.1157893.
  34. Ciani C, Falcone C. Interlaminar and varicose-projection astrocytes: toward a new understanding of the primate brain. Front Cell Neurosci. 2024;18:1477753. doi: 10.3389/fncel.2024.1477753.
  35. Zhao Y, Huang Y, Cao Y, et al. Astrocyte-mediated neuroinflammation in neurological conditions. Biomolecules. 2024;14(10):1204. doi: 10.3390/biom14101204.
  36. Smith AM, Davey K, Tsartsalis S, et al. Diverse human astrocyte and microglial transcriptional responses to Alzheimer's pathology. Acta Neuropathologica. 2022;143(1):75-91. doi: 10.1007/s00401-021-02372-6.
  37. Rodriguez-Vieitez E, Kumar A, Malarte ML, et al. Imaging neuroinflammation: quantification of astrocytosis in a multitracer PET approach. Methods in Molecular Biology. 2024;2785:195-218. doi: 10.1007/978-1-0716-3774-6_13.
  38. Tschiffely AE, Statz JK, Edwards KA, et al. Assessing a blast-related biomarker in an operational community: glial fibrillary acidic protein in experienced breachers. Journal of Neurotrauma. 2020;37(8):1091-1096. doi: 10.1089/neu.2019.6512.
  39. Brenner M, Messing A. Regulation of GFAP expression. ASN Neuro. 2021;13: 1759091420981206. doi: 10.1177/ 1759091420981206.
  40. Bishop P, Rocca D, Henley JM. Ubiquitin C-terminal hydrolase L1 (UCH-L1): structure, distribution and roles in brain function and dysfunction. Biochemical Journal. 2016;473(16):2453-2462. doi: 10.1042/bcj20160082.
  41. Thelin EP, Zeiler FA, Ercole A, et al. Serial sampling of serum protein biomarkers for monitoring human traumatic brain injury dynamics: a systematic review. Frontiers in Neurology. 2017;8:300. doi: 10.3389/fneur.2017.00300.
  42. Boutté AM, Thangavelu B, LaValle CR, et al. Brain-related proteins as serum biomarkers of acute, subconcussive blast overpressure exposure: A cohort study of military personnel. PLoS One. 2019;14(8):e0221036. doi: 10.1371/journal.pone. 0221036.
  43. Jitsu M, Niwa K, Suzuki G, et al. Behavioral and histopathological impairments caused by topical exposure of the rat brain to mild-impulse laser-induced shock waves: impulse dependency. Frontiers in Neurology. 2021;12:621546. doi: 10.3389/ fneur.2021.621546.
  44. Przekwas A, Garimella HT, Tan XG, et al. Biomechanics of blast TBI with time-resolved consecutive primary, secondary, and tertiary loads. Military Medicine. 2019;184(1):195-205. doi: 10.1093/ milmed/usy344.
  45. Xia F, Ha Y, Shi S, et al. Early alterations of neurovascular unit in the retina in mouse models of tauopathy. Acta Neuropathologica Communication. 2021;9(1):51. doi: 10.1186/s40478-021-01149-y.
  46. Shirafuji N, Hamano T, Yen SH, et al. Homocysteine increases Tau phosphorylation, truncation and oligomerization. International Journal of Molecular Sciences. 2018;19(3):891. doi: 10.3390/ ijms19030891.
  47. Pan J, Connolly ID, Dangelmajer S, et al. Sports-related brain injuries: connecting pathology to diagnosis. Neurosurgical Focus. 2016;40(4):E14. doi: 10.3171/2016.1.focus15607.
  48. Chang CW, Shao E, Mucke L. Tau: Enabler of diverse brain disorders and target of rapidly evolving therapeutic strategies. Science. 2021;371(6532):eabb8255. doi: 10.1126/science. abb8255.
  49. Lucke-Wold BP, Logsdon AF, Turner RC, et al. Endoplasmic reticulum stress modulation as a target for ameliorating effects of blast induced traumatic brain injury. Journal of Neurotrauma. 2017;34(S1):S62-S70. doi: 10.1089/neu.2016.4680.
  50. Moreno H, Morfini G, Buitrago L, et al. Tau pathology-mediated presynaptic dysfunction. Neuroscience. 2016;325:30-8. doi: 10.1016/j.neuroscience.2016.03.044.
  51. De la Rosa A, Olaso-Gonzalez G, Arc-Chagnaud C, et al. Physical exercise in the prevention and treatment of Alzheimer's disease. Journal of Sport and Health Science. 2020;9(5):394-404. doi: 10.1016/j.jshs.2020.01.004.

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2025-10-30

How to Cite

Kozlova, Y., Kozlova, K., Korzachenko , M., Suloev , K., & Chekan , S. (2025). Morphological features of mild blast-induced traumatic brain injury (literature review). Морфологія / Morphologia / Morfologìâ, 19(3), 15–21. https://doi.org/10.26641/1997-9665.2025.3.15-21

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Vol. 19 No. 3 (2025)

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