Blast traumatic brain injury [Neurosurgery Wiki]

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====== Blast traumatic brain injury ======

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"Blast [[traumatic brain injury]]," often abbreviated as "bTBI," refers to a type of [[brain injury]] that occurs as a result of exposure to a [[blast]] or [[explosion]]. This [[injury]] happens when the force of the blast [[wave]], shockwave, or other effects of the explosion impact the [[head]] and cause damage to the brain. It's a specialized area of study within traumatic brain injuries because the mechanisms and effects of blast-related injuries can be different from those caused by other types of accidents or trauma.

===== Epidemiology =====
Per Defense and Veterans Brain Injury Center
((Defense and Veterans Brain Injury Center (DVBIC). DoD worldwide numbers for TBI. https://dvbic.dcoe.mil/system/files/tbi-numbers/worldwide-totals-2000-2018Q1-total_jun-21-2018_v1.0_2018-07-26_0.pdf. Updated 2019. Accessed April 15, 2019)).
(DVBIC) statistics, 383 947 individuals within the Department of Defense (DoD) sustained a TBI from 2001 to 2018, more than one-third of whom were exposed to a blast event
((Regasa LE, Agimi Y, Stout KC. Traumatic brain injury following military deployment: evaluation of diagnosis and cause of injury. J Head Trauma Rehabil. 2019;34:21-29.))
((External causes of traumatic brain injury, 2000-2011. MSMR. 2013;20:9-14.)).



===== Mechanism of injury =====


In blast traumatic brain injuries, the brain can be injured in various ways, including:

Direct [[Impact]]: The force of the blast can cause the brain to collide with the inside of the skull, leading to damage.

Pressure Changes: The rapid change in air pressure during an explosion can affect the brain's function and structure.

Secondary Injuries: Flying [[debris]], shrapnel, or objects propelled by the blast can also cause head injuries and contribute to brain damage.

Tertiary Injuries: Individuals may be thrown or displaced by the force of the blast, resulting in additional injuries, including head trauma.

These injuries can range from mild [[concussion]]s to severe and life-threatening brain damage. Studying blast traumatic brain injuries is important for developing better treatments and prevention strategies, especially for military personnel, first responders, and individuals exposed to explosive events.
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Blast traumatic brain injury (bTBI) affects civilians, soldiers, and veterans worldwide and presents significant health concerns. The mechanisms of neurodegeneration following bTBI remain elusive and current therapies are largely ineffective.
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[[Injury]] mechanism and treatment of [[blast traumatic brain injury]] has not made a [[breakthrough]] so far. Previous reports demonstrate autophagy is involved in regulating the pathophysiological process after [[traumatic brain injury]]. Therefore, a study explored whether [[autophagy]] was activated after [[blast traumatic brain injury]]. A total of 108 [[mice]] were divided [[random]]ly into six groups: 6 h, 1 d, 3 d, 7 d, 14 d after bTBI groups and sham group. The [[protein]] levels of anti-microtubule associated protein 1 light chain 3B (LC3B, hereafter referred to as [[LC3]]), [[beclin1]], and [[p62]] were detected using [[western blot]]. Moreover, [[HO-1]] and [[Nrf2]] were localized using histologic staining. [[Immunofluorescence]] of [[LC3]] and [[immunohistochemistry]] of [[beclin1]] were performed. The autophagy-related ultrastructure was observed by TEM. LC3-II and beclin1 reached their peak on day 3 after bTBI, while p62 showed a continuous downward trend. [[Immunofluorescence]] and [[immunohistochemistry]] also confirmed that the expression levels of LC3 and beclin1 were the highest at 3 days after bTBI. Autophagic [[vesicle]]s containing [[lysosome]]s or digestive residual structures were observed then. [[Autophagy]] was induced in the [[frontal lobe]] tissues of bTBI mice induced by moderate-intensity [[explosion]], with a peak at 3d and a gradual decline thereafter
((Zhou Y, Song Y, Zhu L. Activation of autophagy after [[blast]]-induced [[traumatic brain injury]] in [[mice]]. Neuroreport. 2023 Aug 30. doi: 10.1097/WNR.0000000000001951. Epub ahead of print. PMID: 37695596.)).
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Modeling this disease in rodents to pre-clinically evaluate potential therapeutics has been challenging because of inconsistency between models. Although the effects of primary blast wave injury have been extensively studied, little is known regarding the effects of noncontact rotational TBIs independent of the blast wave. To model this type of injury, Sabbagh et al., generated an air cannon system that does not produce a blast wave, but generates enough air pressure to cause rotational TBI. Mice exposed to this type of injury showed deficits in cognitive and motor task acquisition within 1-2 weeks post-injury, but mice tested 7-8 weeks post-injury did not retain any deficits. This suggests that the effects of a single, noncontact rotational TBI are not long lasting. Despite the transient nature of the behavioral deficits, increased levels of phosphorylated tau were observed at 2 and 8 weeks post-injury; however, this tau did not adopt typical pathological structures that have been observed in other TBI models that incorporate blast waves. This was possibly attributed to the fact that this injury was insufficient to induce changes in microglial activation, which was not affected at 2 or 8 weeks post-injury. Taken together, these data suggest that exposure to noncontact, rotational head injury only produces transient cognitive anomalies, but elicits some minor lasting neuropathological changes
((Sabbagh JJ, Fontaine SN, Shelton LB, Blair LJ, Hunt JB Jr, Zhang B, Gutmann
JM, Lee DC, Lloyd JD, Dickey CA. Noncontact Rotational Head Injury Produces
Transient Cognitive Deficits but Lasting Neuropathological Changes. J
Neurotrauma. 2016 Oct 1;33(19):1751-1760. Epub 2016 Mar 16. PubMed PMID:
26739819.
)).
----
Miller et al. utilized rat organotypic hippocampal slice cultures (OHCs) as an in vitro system to model bTBI. OHCs were exposed to either 138 ± 22 kPa (low) or 273 ± 23 kPa (high) overpressures using an open-ended helium-driven shock tube, or were assigned to sham control group. At 2 hours (h) following injury, we have characterized the astrocytic response to a blast overpressure. Immunostaining against the astrocytic marker glial fibrillary acidic protein (GFAP) revealed acute shearing and morphological changes in astrocytes, including clasmatodendrosis. Moreover, overlap of GFAP immunostaining and propidium iodide (PI) indicated astrocytic death. Quantification of the number of dead astrocytes per counting area in the hippocampal cornu Ammonis 1 region (CA1), demonstrated a significant increase in dead astrocytes in the low- and high-blast, compared to sham control OHCs. However only a small number of GFAP-expressing astrocytes were co-labeled with the apoptotic marker Annexin V, suggesting necrosis as the primary type of cell death in the acute phase following blast exposure. Moreover, western blot analyses revealed calpain mediated breakdown of GFAP. The dextran exclusion additionally indicated membrane disruption as a potential mechanism of acute astrocytic death. Furthermore, although blast exposure did not evoke significant changes in glutamate transporter 1 (GLT-1) expression, loss of GLT-1-expressing astrocytes suggests dysregulation of glutamate uptake following injury. Our data illustrate the profound effect of blast overpressure on astrocytes in OHCs at 2 h following injury and suggest increased calpain activity and membrane disruption as potential underlying mechanisms
((Miller AP, Shah AS, Aperi BV, Kurpad SN, Stemper BD, Glavaski-Joksimovic A.
Acute death of astrocytes in blast-exposed rat organotypic hippocampal slice
cultures. PLoS One. 2017 Mar 6;12(3):e0173167. doi: 10.1371/journal.pone.0173167.
PubMed PMID: 28264063.
)).
====Case series====
Following an explosion in the civilian setting, 65 patients (38%) with GCS scores of 3 to 14 did not experience [[severe traumatic brain injury]]. The proportion of patients with severe TBI and severe TBI in need of a neurosurgical intervention were similar in patients presenting with GCS scores of 3 to 8 and GCS scores of 9 to 14. 
GCS and Simplified Motor Score did not help identify patients with severe TBI in need of a neurosurgical intervention
((Ashkenazi I, Schecter WP, Peleg K, Givon A, Olsha O, Turegano-Fuentes F,
Alfici R; and the Israeli Trauma Group, Bahouth H, Becker A, Ben Ely M,
Braslavsky A, Jeroukhimov I, Qarawany M, Kessel B, Klein Y, Lin G, Merin O, Bala 
M, Mnouskin Y, Rivkind AI, Shaked G, Soffer D, Stein M, Weiss M. Glasgow Coma
Scale Score in Survivors of Explosion With Possible Traumatic Brain Injury in
Need of Neurosurgical Intervention. JAMA Surg. 2016 Jul 13. doi:
10.1001/jamasurg.2016.1742. [Epub ahead of print] PubMed PMID: 27409973.
)).

===== Blast mild traumatic brain injury =====
[[Blast mild traumatic brain injury]].