Abstract
Blast-mediated traumatic brain injuries (bTBI) cause long-lasting physical, cognitive, and psychological disorders, including persistent visual impairment. No known therapies are currently utilized in humans to lessen the lingering and often serious symptoms. With TBI mortality decreasing due to advancements in medical and protective technologies, there is growing interest in understanding the pathology of visual dysfunction after bTBI. However, this is complicated by numerous variables, e.g., injury location, severity, and head and body shielding. This review summarizes the visual outcomes observed by various, current experimental rodent models of bTBI, and identifies data showing that bTBI activates inflammatory and apoptotic signaling leading to visual dysfunction. Pharmacologic treatments blocking inflammation and cell death pathways reported to alleviate visual deficits in post-bTBI animal models are discussed. Notably, techniques for assessing bTBI outcomes across exposure paradigms differed widely, so we urge future studies to compare multiple models of blast injury, to allow data to be directly compared.
Highlights
Cases of traumatic brain injury (TBI) morbidity are increasing as people are more often surviving blast-mediated TBI, an injury especially prevalent among military personnel
The Friedlander waveform consists of the shock front, which is an immediate sharp rise in pressure, followed by the blast wind, which is an exponential decay in pressure (Cullis, 2001)
We reviewed the devices and exposure paradigms employed in blast-mediated TBI (bTBI) research and found notable interstudy variations in techniques and assessment outcomes
Summary
Cases of traumatic brain injury (TBI) morbidity are increasing as people are more often surviving blast-mediated TBI (bTBI), an injury especially prevalent among military personnel. Over the past two decades, 417,503 U.S service members sustained at least one TBI as active military (Defense and Veterans Brain Injury Center, 2020) with nearly 2/3 involving an explosive blast (McKee and Robinson, 2014). Visual impairments are reported by some 75% of TBI patients, including blurry/double vision, difficulties reading, light sensitivity, and decreased peripheral vision (Armstrong, 2018; Frick and Singman, 2019). These visual impairments can arise due to optic neuropathy, axonal injury, and the loss of retinal ganglion cells (RGCs), which transmit visual stimuli to higher-level processing centers in the brain (Sen, 2017). In animal studies, decreased RGC survival and axonal integrity are strongly implicated with the activation of microglia and macrophages, with unregulated oxidative stress further contributing to RGC loss and optic nerve degeneration (Wang et al, 2013; Gupta et al, 2019)
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