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Mechanisms of Blast-Induced Traumatic Brain Injury (bTBI) in Civilian Contexts

Summary

Blast-induced Traumatic Brain Injuries (bTBIs) typically arise from large explosions and can cause detrimental consequences to the victim, including, physical, emotional, and cognitive changes[1][2]. The significance of its risk demands extensive and appropriate research into the mechanism of action of these injuries, facilitating the development of better protective equipment and safety protocols in individual and group settings. Most common cases of this injury occur on militaristic scales or from police-related activities[1][3], however, its prominence in civilian contexts has continued to rise over the years in non-government facing domains, such as with the rise in terrorist attacks and failed attempts at non-lethal crowd control tactics. Thus, further research and analysis into the mechanisms of bTBIs are becoming increasingly necessary[4][5][3].

Damage to the brain tissue can be caused by the blast wave itself or from a range of indirect consequences that arise from this initial explosion[6]. These injuries are influenced by general factors of blast energy, distance, and environment and victim protection that align with mechanical factors of load, pressure, stress and strain[7].

For a person to sustain a bTBI, aside from the factors listed above, a wave of energy exceeding a defined pressure threshold[1] must travel through the layers of the skin, bones, and fluid, to ultimately reach the brain. This can either occur through intense pressure imbalances within the ear, excessive energy absorption by the brain, or vascular cranial systems. Although no universal human threshold exists, this literature review reports intracranial stress transmission beginning at ~16 kilopascals and CSF cavitation and harmful shear strain in models exposed to 50-1000 kilopascals for 1-8 ms[8][9]. 

FE models are extremely useful for studying the effects of physical blast tests and impulse brain loading, with promising advancements becoming increasingly more attainable, along with the continuous development of detection and modelling technologies[9]. While studies disagree on the source of injury, the implementation of a standardized experimental setup and criteria (such that computational and experimental models (animal and hybrid) support each other), will lead to safer and more definitive injury criteria and safety precautions.

Background

Blast-induced Traumatic Brain Injuries (bTBIs) are a critical concern for civilians exposed to both intentional and unintentional explosions.

Despite the severity of these injuries, little research has been conducted on its impacts and mechanisms within a civilian framework[1], as the majority of existing reviews focus on military data and personnel. The scenarios in which these two groups are impacted diverge substantially with regards to explosive power, device types, environment variables, and population characteristics. It is therefore not accurate to apply injury criterion or injury prevention techniques cross-situationally. Civilians are generally unprotected, untrained[4], and located in enclosed or semi-enclosed spaces such as buildings or vehicles, which can amplify blast overpressure and alter injury patterns[5]. Additionally, there is a larger age range for civilian injuries and a higher percentage of women[3] who get injured in these situations, meaning injury tolerance and reaction differ significantly from a military context.

Five injury sections[6] contribute to bTBI individually or in combination:

  1. Primary - damage to brain tissue resulting from the blast-wave induced by changes in atmospheric pressure
  2. Secondary - objects in motion (such as projectile debris) that may hit the head
  3. Tertiary - person being forcefully put in motion by the blast
  4. Quaternary - psychological/burn trauma (heat, chemicals, toxins)
  5. Quinary - infection or radiation contamination

In a large US trauma database, blast injuries accounted for a small fraction of trauma but produced substantial morbidity. Studies of mass-casualty events, such as car bombings[10] or large urban explosions, report head injuries in 25-50% of civilian casualties[11], with children often sustaining higher rates of head and abdominal trauma than adults[12]. Civilian neurosurgical case studies describe substantial early mortality and severe disability caused by bTBI[2].

Blast outcomes are further influenced by factors such as blast energy, the victim’s distance from epicenter[7], whether the blast occurred in an open or confined space[5], and whether the individual was shielded or directly exposed. These sources of variability complicate efforts to define injury tolerances and thus develop robust prevention strategies.

From a biomechanical standpoint, it is critical to account for various characteristics such as the mechanical load of blast overpressure, pressure thresholds that lead to injury and the pathway the energy takes through the body (cranial - through the skull, otologic - through the ear, and thoracoabdominal - through the chest/belly). Methods such as computational models and in-vivo animal testing take the lead in mapping this invisible trauma.

Mechanism

CFD blast wave and FEM biomechanics of a human head
Figure 1: Coupled simulations of CFD blast wave and FEM biomechanics of a human head. Pressure profiles in the air and in the brain during intracranial pressure wave penetration.

There are three primary ways that bTBIs can occur[13][14]. Tympanic membrane perforation allows blast overpressure to enter through the ear canal and middle ear structures. Cranial transmission occurs when the blast wave directly loads the scalp and skull, transmitting pressure into the brain. Thoracic–hydrodynamic loading involves blast compression of the chest, sending a vascular pressure surge toward the brain.

Tympanic Membrane Perforation

The Tympanic Membrane (TM) separates the ear canal from the middle ear, converting sound into mechanical vibrations. Under normal conditions, the TM is very sensitive and responds to pressures between 10⁻⁵ and 10² pascals with ruptures occurring at 10⁵ Pascal. Blast waves can exceed pressures of over 10⁶ pascals[15], which can cause the TM to perforate, resulting in immediate hearing loss and disruption of normal pressure transfer within the ear[15].

Finite element (FE) analyses of the TM[16] showed that stresses were concentrated around the center and lower areas of the membrane (umbo and pars tensa regions). The computational fluid dynamics (CFD) simulation depicting pressure profiles in the air and brain during intracranial pressure wave penetration is shown in Figure 1. Studies using cadavers[17] and animals supported the hypothesis and helped estimate rupture limits of the TM.

Cranial Transmission

In a cranial transmission, the blast wave strikes the head directly, causing the energy to pass through the scalp and skull and consequently reach the brain. Analytical and numerical modeling[8] showed that the scalp can amplify incoming pressure. When the blast pressure exceeds 16kilopascal[8], the pressure within the skull can surpass the incident blast pressure, which causes shear and tensile stresses in the brain - primarily at the gray and white matter boundaries - even without any physical impact from the blast wave. This shearing can tear nerve fibers and cause diffuse axonal injury (DAI)[18] which is a severe form of bTBI.

Thoracic-Hydrodynamic Mechanism

The thoracic hydrodynamic mechanism suggests that the blast wave compresses the chest which sends a sudden rush of blood flow to the cerebral vasculature. This leads to microvascular damage, capillary rupture, and intracranial pressure spikes without direct blast exposure to other areas of the body[19].

Modelling and experimental work[13] further supported the hypothesis by demonstrating that pressure waves can damage small brain vessels and the blood-brain barrier even when the head is shielded[20]. This mechanism helps to explain why civilians can experience mild bTBI symptoms even when shielded from direct blast exposure. However, while rodent studies suggest mild blast-induced neurotrauma (BINT) can occur at incident pressures around 145 kilopascal, animal-to-human scaling has been attempted but no robust human thresholds for this mechanism currently exist.

Across these methods, the cited studies explained how blast energy can reach and damage the brain. FE and experimental work on tympanic membrane failure[16][17] demonstrate how even peripheral structures exhibit predictable pressure-driven injury patterns, consistent with CFD-FEM pressure profiles. Cranial transmission modeling[8] suggests that external blast pressure can be amplified, resulting in intracranial pressures consistent with DAI. Lastly, thoracic hydrodynamic findings[13][19] confirm that pressure waves entering through the chest can disrupt cerebral microvasculature, without direct head exposure. Overall, these studies illustrate that bTBI is a multi-pathway phenomenon: each mechanism supported by complementary computational, cadaveric, and animal evidence explaining how blast waves propagate and cause intracranial injury.

Experimental Modelling

Figure 2: To avoid numerical singularity errors, more than one sensor element was taken at front, middle and rear brain of the human model.

Researchers have used many modelling techniques to study the mechanical trauma caused by blast-induced brain injury (bTBI). These include detailed finite-element simulations of head and brain anatomy, in vivo animal studies, and combined physical and computational test setups.

Computational Modelling: Finite Element

One study used a high-resolution FE head model to show that shear strains and Cerebrospinal Fluid (CSF) cavitation can occur at the brain–skull interface when exposed to 50-1000 kilopascal overpressure for 1-8 ms[9]. CSF is the fluid found between the brain and skull that provides nutrients, protection, and waste-removal capabilities. Another study found that rupturing the tympanic membrane can increase pressure in the cranial cavity by using a CT-based 3D FE model to simulate blast waves traveling through the ear canal[9]. This study used more than one sensor (refer to Figure 2) to minimize the uncertainty of the measurement[9]. Both studies demonstrated that injury thresholds are dependent on pressure strength, direction, and tissue boundaries, regardless of direct head impact.

Figure 3: Representation of the virtual sensors positions on the THUMS applied to the left lung, left lobe of the liver and stomach.

More recently, the Total Human Model for Safety (THUMS) simulation adapted the models to add the accuracy of representing civilian situations by including realistic postures and organ connections to study how blasts affect the whole body.[21] As a result, FE techniques are applicable to full-body models and the THUMS models can link the body’s systems (especially the chest and blood vessels) and their interaction with local brain responses, aiding our understanding of mild bTBI. The virtual sensors of this THUMS can be seen in the corresponding Figure 3. Since most CT based FE models in bTBI research focus on the head[9], using THUMS as a comparison for whole body analysis (for example, studying the full body biomechanics: coupling, strain, compression of an organ[21]) could be useful in bTBI analysis.

Animal and Hybrid Model

Animal models aim to create more realistic FE simulations. In studies with rats, controlled blast exposures allow researchers to directly observe changes in behavior, biomarkers, and tissue[13]. One research paper showed that mechanical load is a strong predictor of axonal injury by using a detailed rat FE model and physical blast tests (≈ 207 kilopascal) to link intracranial pressure patterns with tissue findings[13]. Similarly, to visualize shock-wave movement, gel and plastic head models can be used with computer simulations to confirm computational hypotheses[22]. The hybrid surrogate used for this modelling approach is helpful for better visualizing shock in skull deformation[22], with potential uses in creating specific head surrogates for civilian protection.

Additional research on impulsive brain loading extends mathematical and multiscale models linking mechanical inputs to neurobiological effects[23]. This research showed that blast forces cause brain injury by converting mechanical stress into biological damage. Even moderate overpressure (35-70 kilopascal) can cause blood-brain barrier leakage, while brain strain of 10-20% can injure axons (part of a nerve cell)[23]. It is also noted that blast forces impacting the chest can rapidly increase pressure within the brain[23]. Thus, these results prove mechanical blast input affects the neurobiological seen in bTBI[23].

Despite the fact that the animal studies were conducted in controlled laboratory conditions, they still provide insight into the mechanical and physiological conditions encountered during civilian blast events. The moderate overpressures used in the rodent model are similar to those seen in low-explosive urban blasts, such as gas leaks or improvised explosive devices. Long-term implications have been investigated, with certain experiments revealing changes to sleep and circadian gene expression in the hypothalamus and pineal gland within a month[9] of exposure to the blast waves. Thus, mild or subclinical blast exposure can lead to nervous system disorders, potentially resulting in long-term cognitive and neuropsychiatric deficits[24]. In addition, spectroscopic analysis has detected biochemical changes in brain areas such as the hippocampus[25] in these rodents. These changes in the hippocampus might cause memory problems, inflammation, or other symptoms related to bTBI. Due to similar metabolic disturbances that occur in human bTBIs, this finding might be useful for detecting bTBI for civilians.

Based on the above experimental models, the computational method helps to visualize the simulation during the injury and estimate the probability of pressure, stress, and other potential mechanical factors. Along with the clinical findings of animal and hybrid models, these approaches created an integrated picture of civilian bTBI which hopefully will help to predict and mitigate bTBI in the future.

Future Direction

Limitations

Conceptual illustration of a blast shock wave propagating through air. The expanding concentric waves represent the rapid pressure increase and reflection effects often modeled in blast-induced traumatic brain injury (bTBI) research.
Figure 4: 3D Pressure (Longitudinal) Wave

Current bTBI research faces several key limitations that make it difficult to determine exactly how blast pressure transmits through the skull to the brain. The primary issue is that the mechanism itself (direct or indirect energy transmission) remains debated. Specifically, disagreements between studies on whether injury comes mainly from direct pressure wave transmission, skull flexure, or indirect pathways such as vascular and auditory coupling introduce further issues that need to be addressed.[13][8]Experimental setups also introduce major flaws. Many shock tubes generate unrealistic waveforms with reflected and turbulent waves up to 13 times stronger than the original blast, creating false-positive injury patterns[13]. One of the work results of the 3D model in bTBI research is the model of 3D Pressure longitudinal wave shown in Figure 4. Computational models of the head often oversimplify anatomy, assuming uniform tissue and neglecting 3D complexity, which limits accuracy in predicting pressure movement inside the skull[8].

Another limitation is the lack of an agreed-upon injury threshold for bTBI. No clear pressure or intracranial response defines mild, moderate, or severe injury[8]. This inconsistency prevents reliable comparisons across studies. Differences in anatomy between humans and animal models further complicate interpretation, as scaling errors reduce the applicability of animal data to human injury[26]. Ethical constraints also restrict research realism. For example, anesthesia used in animal testing can be neuroprotective, while isolated head models and cadaver studies fail to mimic the blood flow and cerebrospinal dynamics of living humans[27].

Finally, population and data biases reduce generalizability. Most bTBI research is conducted in Western military contexts, leaving civilian and low-resource blast scenarios underexplored[28]. Civilian blasts, such as industrial or firework accidents, differ significantly in pressure profile and tissue response but remain poorly studied[29]. Clinical studies also suffer from small sample sizes, inconsistent imaging protocols, and overlap between bTBI and PTSD symptoms, with no reliable biomarker yet available[27]. Together, these limitations make it difficult to fully define or model how blast forces reach and damage the brain.

Future Work

Future research on bTBI must focus on improving models and general understanding of blast pressure transmission from the skull to surrounding structures into the brain. Currently, the lack of a standardized experimental setup for studying brain injury has generated huge variability in general findings. For example, traditional shock tubes produce secondary and reflected waves that are significantly higher in intensity than the original blast wave, resulting in misleading reported injury patterns.[13] New and highly controlled experimental systems such as the proposed C4 blast generator should be developed and compared to eliminate inconsistencies and help researchers identify the most accurate injury mechanisms.[13]

Computational modelling must also be advanced. Current FE head models often simplify the skull and brain, leaving out 3D effects, indirect loading from skull flexure, and interactions of internal structures[8]. These models also lack detailed geometry of the meningeal layers and auditory anatomy, which are essential for accurately studying how blast pressure travels through the ear canal and into the brain. Future work should expand these models to include the pinna, auricles, and concha, which were shown to strongly influence reflected blast overpressure in previous studies[30]. The implementation of a standardized experimental setup and injury criteria will lead to more comparable results, which is essential to finally solve the dilemma of accurately weighting the contribution of each proposed injury pathway[13]. Knowing this information could give researchers a better grasp on how the injury mechanism occurs and how to better prevent it.

Another key direction is the standardization of experimental result validation. Many FE predictions do not match cadaver or animal data, making it difficult to confirm whether the models reflect the response of a human head[26]. Comparative work using different species, such as rodents, pigs and non-human primates, would address interspecies scaling issues and improve translation to clinical cases[26]. Similarly, animal research should use standardized exposure settings and restraint conditions so data can be compared across labs[27].

References

  1. ↑ 1.0 1.1 1.2 1.3 DuBose, Joseph (2011). "Isolated severe traumatic brain injuries sustained during combat operations: demographics, mortality outcomes, and lessons to be learned from contrasts to civilian counterparts". The Journal of Trauma. 70(1): 11–18. doi:10.1097/TA.0b013e318207c563. |first2= missing |last2= (help)
  2. ↑ 2.0 2.1 Hoz, Samer (2021). "Blast-Induced Traumatic Brain Injuries: Experience from the Deadliest Double Suicide Bombing Attack in Iraq". World Neurosurgery. 145: e192–e201 – via Elsevier Science Direct. |first2= missing |last2= (help)
  3. ↑ 3.0 3.1 3.2 Nunziato, Carl (2019). "How Common Are Civilian Blast Injuries in the National Trauma Databank, and What Are the Most Common Mechanisms and Characteristics of Associated Injuries?". Clinical Orthopaedics and Related Research. 479(4): 683–691. doi:10.1097/CORR.0000000000001642. |first2= missing |last2= (help)
  4. ↑ 4.0 4.1 McAlister, Chryssa (Dec 2017). "The 1917 Halifax Explosion: the first coordinated local civilian medical response to disaster in Canada". Canadian Journal of Surgery. 60(6): 372–374. doi:10.1503/cjs.016317. |first2= missing |last2= (help)
  5. ↑ 5.0 5.1 5.2 Rozenfeld, Michael. "A New Paradigm of Injuries From Terrorist Explosions as a Function of Explosion Setting Type". Annals of Surgery. 263(6): 1228–1234. doi:10.1097/SLA.0000000000001338. |first2= missing |last2= (help)
  6. ↑ 6.0 6.1 Magnuson, John (2018). Traumatic Brain Injury - Pathobiology, Advanced Diagnostics and Acute Management. London: IntechOpen. doi:10.5772/intechopen.74035. ISBN 978-1-78923-117-5.
  7. ↑ 7.0 7.1 Chan, Raymond. "Base rate of post-concussion symptoms among normal people and its neuropsychological correlates". Clinical Rehabilitation. |first2= missing |last2= (help)
  8. ↑ 8.0 8.1 8.2 8.3 8.4 8.5 8.6 8.7 Panzer, Matthew B. (May 2014). "A theoretical analysis of stress wave propagation in the head under primary blast loading". Proceedings of the Institution of Mechanical Engineers, Part H: Journal of Engineering in Medicine.
  9. ↑ 9.0 9.1 9.2 9.3 9.4 9.5 9.6 Govindarajulu, Manoj; Patel, Mital Y.; Krishnan, Jishnu; Long, Joseph B.; Arun, Peethambaran. "Blast Exposure Induces Acute Alterations in Circadian Clock Genes in the Hypothalamus and Pineal Gland in Rats: An Exploratory Study". Neurotrauma Reports. 4.
  10. ↑ Sobh, Ali. "The pagers explosions in Beirut: Injury profiles, surgical care, and medical interventions—A descriptive study from a tertiary care medical center". The Journal of Trauma and Acute Care Surgery.
  11. ↑ Kakmaz, Omer (2015). "Demographic Properties of Civilians with Blast Injuries in Southeastern Anatolia Region". Turkish Journal of Emergency Medicine. 15(2): 69–74. doi:10.5505/1304.7361.2015.25993.
  12. ↑ Maitland, Laura (2022). "Analysis of 983 civilian blast and ballistic casualties and the generation of a template of injury burden: An observational study". eClinicalMedicine. 54. doi:10.1016/j.eclinm.2022.101676.
  13. ↑ 13.00 13.01 13.02 13.03 13.04 13.05 13.06 13.07 13.08 13.09 Gupta, Rakesh K.; Przekwas, Andrzej J. (March 2013). "Mathematical models of blast-induced TBI: current status, challenges, and prospects". Frontiers in Neurology.
  14. ↑ Chavko, Mikulas (August 2015). "A Two-Model Approach to Investigate the Mechanisms Underlying Blast-Induced Traumatic Brain Injury". Frontiers in Neurology.
  15. ↑ 15.0 15.1 G. Hirsch, Frederic (1966). "Effects of Overpressure on the Ear - A Review" (PDF). Biological Effects of Blast from Bombs.
  16. ↑ 16.0 16.1 Gan, Rong Z. (March 2011). "Biomechanics of the human tympanic membrane and its numerical modeling". Journal of Biomechanics.
  17. ↑ 17.0 17.1 Rosowski, John J. (February 2011). "Cadaveric measurements of human middle-ear responses: Implications for sound transmission and hearing loss". Journal of Biomechanics.
  18. ↑ B Mesin, Fassil; Gupta, Nishant; Shapshak, Angela Hays; Margetis, Konstantinos (2025). Diffuse Axonal Injury. Treasure Island.
  19. ↑ 19.0 19.1 Courtney, Amy C.; Courtney, Michael W. (January 2009). "A thoracic mechanism of mild traumatic brain injury due to blast pressure waves". Medical Hypotheses.
  20. ↑ Sachdeva, Tarun; G Ganpule, Shailesh (March 2024). "Twenty Years of Blast-Induced Neurotrauma: Current State of Knowledge". Neurotrauma Rep. 5(1): 243–253.
  21. ↑ 21.0 21.1 Morena, Alberto; Peroni, Lorenzo; Scapin, Martina (October 2024). "Numerical Investigation of the Blast-Induced Injuries Using an Open-Source Detailed Human Model". International Journal for Numerical Methods in Biomedical Engineering. 40(12).
  22. ↑ 22.0 22.1 F, Zhu; C, Wagner; A, Dal Cengio Leonardi; X, Jin; P, Vandevord; C, Chou; KH, Yang; AI, King (2011 May 18). "Using a gel/plastic surrogate to study the biomechanical response of the head under air shock loading: a combined experimental and numerical investigation". Biomech Model Mechanobiol. 11: 341–353. Check date values in: |date= (help)
  23. ↑ 23.0 23.1 23.2 23.3 Hamidreza, Gharahi; Garimella, Harsha T.; Chen, Zhijian J.; Gupta, Raj K.; Przekwas, Andrzej (05 February 2023). "Mathematical model of mechanobiology of acute and repeated synaptic injury and systemic biomarker kinetics". Frontiers in Cellular Neuroscience. 17. Check date values in: |date= (help)
  24. ↑ GA, Elder; JR, Stone; ST, Alhers (19 December 2014). "Effects of low-level blast exposure on the nervous system: is there really a controversy?". Frontiers in Neurology. 5.
  25. ↑ Ranasinghe, Jeewan C; Wang, Ziyang; Shengxi, Huang (26 December 2023). "Raman Spectroscopy on Brain Disorders: Transition from Fundamental Research to Clinical Applications". Biosensors. 13.
  26. ↑ 26.0 26.1 26.2 Bryden, Daniel (August 2, 2019). "Blast-Related Traumatic Brain Injury: Current Concepts and Research Considerations". SAGE. line feed character in |title= at position 46 (help)
  27. ↑ 27.0 27.1 27.2 Agoston, Denes. "Modeling the Neurobehavioral Consequences of Blast-Induced Traumatic Brain Injury Spectrum Disorder and Identifying Related Biomarkers". 310 Brain Neurotrauma: Molecular, Neuropsychological, and Rehabilitation Aspects.
  28. ↑ Debenham, Luke (6 December 2023). "A systematic review of otologic injuries sustained in civilian terrorist explosions". European Archives of Oto-Rhino-Laryngology. line feed character in |title= at position 73 (help)
  29. ↑ Rozenfeld, Michael. "Injuries From Explosions: More Differences Than Similarities Between Various Types". Cambridge University Press. line feed character in |title= at position 48 (help)
  30. ↑ Praveen, Akula (September 28, 2015). "Blast-induced Mild Traumatic Brain Injury through Ear Canal: A Finite Element Study". University of Nebraska-Lincoln. line feed character in |title= at position 61 (help)

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