Exposure to blast overpressure initiates a cascade of cellular pathologic processes in the brain, including damage to the microvasculature and blood–brain barrier (BBB) integrity, followed by increased BBB permeability. The neurologic injury from bTBI can result both from a direct shock wave effect and an indirect transfer of the shock wave through blood vessels and cerebrospinal fluid to the brain. It is thought that post-TBI accumulations of those proteins in combination with persistent abnormal neuroinflammation might contribute to early-onset neurodegeneration or dementia ( Giza and Kutcher, 2014 Smith, 2013).īlast-induced traumatic brain injury (bTBI) has become a common type of military head injury, although non-blast mechanisms are still common in the military and civilian population (e.g., injuries from car and motorcycle accidents, athletic activities, and military physical training). The destruction of intra-axonal structures can result in abnormal accumulations of neurotoxic proteins such as beta-amyloid and phosphorylated tau. Diffuse microvascular damage combined with BBBD and a loss of autonomic regulation results in both hyper- and hypo-perfusion, contributing to ischemia and cerebral edema. TBI-induced blood–brain barrier dysfunction (BBBD) allows elements of the peripheral immune system to participate in this process. A neuroinflammatory response involving microgliosis starts within hours of the injury and might continue for months or even years. This secondary phase might also involve necrosis and neuronal demyelination. Mitochondrial failure results in an energy crisis for the neuron, leading to a loss of neuronal function and apoptosis (programmed cell death). The secondary injury phase begins immediately after the primary phase and involves a progression of axonal injury, with shifts in ionic flux leading to axonal swelling, a loss of axonal transport, and altered neurotransmission ( Giza and Hovda, 2014). Motor vehicle accidents are particularly injurious because of the sudden deceleration ( Johnson et al., 2017). Thus, the primary injury phase of TBI results in damage to axons (axonal injury) and blood vessels (hemorrhage). Neuronal axons and blood vessels are most susceptible to sheer strain due to their elongated microstructure. If a rotational component is present-which is nearly universal in the case of blunt TBI-intracranial structures will torque and twist, resulting in excessive shear strain (i.e., stretch) ( Morales et al., 2005 Smith, 2013). Thus, the brain will strike both anteriorly and posteriorly against the inner aspect of the skull, and a coup-countercoup lesion will result ( Graham et al., 2002). Because the brain resides within a fluid-filled compartment, the movement of its cellular elements lags behind the skull during rapid deceleration. Direct impact of the brain against the bony cranial vault and shearing of neurovascular structures result in neuronal damage. The primary injury phase is immediate, and its damage, which can cause death almost instantaneously, is often complete by the time emergency care is initiated. The first phase occurs as a direct result of the initiating traumatic event the second involves a cascade of several neuropathologic processes continuing for weeks to months after the initial injury. Brain injury from this mechanism has two phases. Blunt, non-penetrating TBI can result from a direct impact to the head or from rapid head acceleration or deceleration without impact.
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