Effects Of Blast Exposure Research Articles

Effects of blast exposure on anxiety and symptoms of post-traumatic stress disorder (PTSD) among displaced Ukrainian populations.

Generalized anxiety and symptoms of post-traumatic stress disorder (PTSD) are common among individuals forcibly displaced during war and conflict. Blast exposure may be one important contributor of such symptoms. The aims of this study were to provide data on blast-related experiences of internally displaced persons (IDPs) and refugees following Russia's invasion of Ukraine, and to assess the influence of blast exposure on generalized anxiety, and PTSD flashbacks and nightmares. An online health needs survey was distributed to Ukrainian IDPs and refugees between April and July 2022 using Facebook Ads Manager. Participants reported whether they experienced blast exposure since the beginning of the invasion, and whether they took medication for a mental health condition before the war started. Finally, they completed measures of generalized anxiety (GAD-2), and PTSD flashbacks and nightmares. Analyses included 3253 IDPs and 5073 refugees (N = 8326). Results revealed that 67.6% of total participants- 79.9% of IDPs and 61.7% of refugees-reported blast exposure since Russia's invasion. Further, 69.1% (95% CI: 68.05, 70.15) of total participants met the cut-off for generalized anxiety in which further diagnostic evaluation was warranted. Compared to refugees, IDPs reported higher generalized anxiety and greater frequency of PTSD symptoms, specifically flashbacks and nightmares. Further analyses revealed that the impact of blast exposure on flashback frequency was stronger among IDPs compared to refugees (β = 0.51; t(8322) = 11.88, p < .0001, 95% CI: 0.43, 0.60) and among participants with pre-existing mental health conditions compared to those without (β = 0.18; t(8157) = 2.50, p = .013, 95% CI: 0.04, 0.33). Mental health and psychosocial support must be prioritised within humanitarian relief for both IDPs and refugees and especially among people with underlying mental health conditions.

Blast effects on post-concussive and mental health outcomes: Data from Canadian Armed Forces breachers and snipers

LAY SUMMARY There has been increasing interest in understanding the impact of blast exposure on health and performance in military members and Veterans. This phenomenon has proven difficult to study because personnel diagnosed with blast-induced mild traumatic brain injury (mTBI) typically also exhibit emotional difficulties such as posttraumatic stress disorder (PTSD), likely because the events that led to mTBI in theatre were also emotionally traumatic. In turn, this comorbidity makes it difficult to tease apart symptoms uniquely due to blast-induced mTBI or PTSD. Researchers have therefore explored surrogate settings wherein the effects of blast exposure can be assessed in an operationally realistic, yet scientifically more controlled manner, such as breacher and sniper training. To that aim, researchers administered a measure of post-concussive symptomatology and two mental health scales to breachers and snipers, as well as sex- and age-matched military controls. The breachers and snipers reported greater levels of post-concussive symptoms, but not poorer mental health outcomes. Therefore, post-concussive symptoms and mental health outcomes might be dissociable when the impact of repetitive exposure to low-level blast is assessed in the context of training and operations, rather than following warzone deployment involving primarily high-level blast exposure.

Effects of blast exposure on psychiatric and health symptoms in combat veterans

Blast exposure is common among service members, but the chronic psychiatric effects associated with blast exposure are not well-characterized independent of a resulting mild traumatic brain injury (TBI). This analysis evaluated whether blast exposure severity was independently associated with or exacerbated symptom report beyond posttraumatic stress disorder (PTSD) and mild TBI. Participants were Iraq and Afghanistan combat veterans (N = 275; 86.55% male), 71.27% with history of blast exposure, 29.82% current diagnosis of PTSD, and 45.45% with mild TBI. All participants completed diagnostic interviews for PTSD, lifetime TBI, and lifetime blast exposure. Self-reported psychiatric and health outcomes included posttraumatic stress symptoms, depressive symptoms, neurobehavioral symptoms, sleep quality, pain interference, and quality of life. Blast severity was associated with PTSD (B = 2.00), depressive (B = 0.76), and neurobehavioral (B = 1.69) symptoms beyond PTSD diagnosis and mild TBI history. Further, blast severity accounted entirely (i.e., indirect/mediation effect) for the association between TBI and posttraumatic stress (B = 1.62), depressive (B = 0.61), and neurobehavioral (B = 1.38) symptoms. No interaction effects were present. Exposure to blast is an independent factor influencing psychiatric symptoms in veterans beyond PTSD and mild TBI. Results highlight that blast exposure severity may be a more relevant risk factor than deployment mild TBI in combat veterans and should be considered in the etiology of psychiatric symptom presentation and complaints. Further, severity of psychological distress due to the combat environment may be an explanatory mechanism by which blast exposure mediates the relationship between mild TBI and symptom outcomes.

A-138 Lifetime Repetitive Blast Overpressure Exposure Has Negative Impact on Quality of Life after Traumatic Brain Injury

Abstract Objective The objective of this study was to i) address the impact repetitive blast exposure (RBE) has on recovery from TBI in service members and veterans (SMVs), ii) determine if the relative amount of blast exposure in a career changes this effect, iii) determine if any effects of blast exposure are different than known pre-existing neurotrauma such as pre-injury TBI history (piTBIHx) defined as previous TBI that occurred before the index injury for the study. Methods 341 SMVs with an uncomplicated mild, complicated mild, moderate, or severe TBI. piTBIHx was based on a structured interview and RBE was based on self-report. Participants were divided into six cohorts based on RBE and piTBIHx and given the TBI-Quality of Life (TBI-QOL). Four multivariate analysis of variance were completed for each domain separately (Emotional, Physical, Cognition, and Positive) to correct for multiple comparisons. Results Results indicate that HeavyRBE, in the absence of piTBIHx, was associated with worse QOL on measures of Anger (p = 0.032), Anxiety (p = 0.008), Explosive Behavior (p = 0.038), Headache (p = 0.030), Pain (p = 0.016), Cognitive Complaints-Executive Functioning (p = 0.009), and Cognitive Complaints-General (p = 0.013). ModerateRBE in the absence of piTBIHx was associated with more Cognitive Complaints-Executive Function (p = 0.005). ModerateRBE did not differ from the Heavy RBE group regardless of piTBIHx. Conclusion QOL after a TBI may be negatively impacted by a history of RBE. A lifetime of HeavyRBE was associated with worse QOL on numerous measures, however, Moderate RBE was only associated with worse cognitive complaints related to executive functioning.

Physiological measurements of acoustic trauma following blast-induced traumatic brain injury (TBI) in laboratory mice

Exposure to a high intensity blast from the detonation of improvised explosive devices (IEDs) can lead to a traumatic brain injury (TBI) and concurrent trauma to major auditory structures. Research on whether this trauma is permanent or temporary has been inconclusive due to heterogeneity of injury acquisition. A blast wave system that generates consistent and controllable blast waves has been developed, allowing for investigation into the co-morbidity of auditory damage and TBI. In this study, the effects of blast exposure on auditory brainstem responses (ABRs) and distortion product otoacoustic emissions (DPOAEs) in male and female mice were measured. ABRs and DPOAEs were collected prior to exposure to a blast to represent the baseline auditory capacity of each individual subject. Mice were tested at 3, 30, and 90 days after the exposure to capture initial trauma and the degree of recovery. A shift in ABRs and DPOAEs thresholds was observed in post-exposure mice, indicating trauma to central and peripheral auditory systems. Following the 90 day tests, brains and cochleae were collected for further analysis. [Work supported by R01DC016641.]Exposure to a high intensity blast from the detonation of improvised explosive devices (IEDs) can lead to a traumatic brain injury (TBI) and concurrent trauma to major auditory structures. Research on whether this trauma is permanent or temporary has been inconclusive due to heterogeneity of injury acquisition. A blast wave system that generates consistent and controllable blast waves has been developed, allowing for investigation into the co-morbidity of auditory damage and TBI. In this study, the effects of blast exposure on auditory brainstem responses (ABRs) and distortion product otoacoustic emissions (DPOAEs) in male and female mice were measured. ABRs and DPOAEs were collected prior to exposure to a blast to represent the baseline auditory capacity of each individual subject. Mice were tested at 3, 30, and 90 days after the exposure to capture initial trauma and the degree of recovery. A shift in ABRs and DPOAEs thresholds was observed in post-exposure mice, indicating trauma to central and periphe...

The Effects of Blast Exposure on Protein Deimination in the Brain.

Oxidative stress and calcium excitotoxicity are hallmarks of traumatic brain injury (TBI). While these early disruptions may be corrected over a relatively short period of time, long-lasting consequences of TBI including impaired cognition and mood imbalances can persist for years, even in the absence of any evidence of overt injury based on neuroimaging. This investigation examined the possibility that disordered protein deimination occurs as a result of TBI and may thus contribute to the long-term pathologies of TBI. Protein deimination is a calcium-activated, posttranslational modification implicated in the autoimmune diseases rheumatoid arthritis and multiple sclerosis, where aberrant deimination creates antigenic epitopes that elicit an autoimmune attack. The present study utilized proteomic analyses to show that blast TBI alters the deimination status of proteins in the porcine cerebral cortex. The affected proteins represent a small subset of the entire brain proteome and include glial fibrillary acidic protein and vimentin, proteins reported to be involved in autoimmune-based pathologies. The data also indicate that blast injury is associated with an increase in immunoglobulins in the brain, possibly representing autoantibodies directed against novel protein epitopes. These findings indicate that aberrant protein deimination is a biomarker for blast TBI and may therefore underlie chronic neuropathologies of head injury.

Effects of Blast Exposure on Subjective and Objective Sleep Measures in Combat Veterans with and without PTSD.

This study examined the extent to which self-reported exposure to blast during deployment to Iraq and Afghanistan affects subjective and objective sleep measures in service members and veterans with and without posttraumatic stress disorder (PTSD). Seventy-one medication-free service members and veterans (mean age = 29.47 ± 5.76 years old; 85% men) completed self-report sleep measures and overnight polysomnographic studies. Four multivariate analyses of variance (MANOVAs) were conducted to examine the impact of blast exposure and PTSD on subjective sleep measures, measures of sleep continuity, non-rapid eye movement (NREM) sleep parameters, and rapid eye movement (REM) sleep parameters. There was no significant Blast × PTSD interaction on subjective sleep measures. Rather, PTSD had a main effect on insomnia severity, sleep quality, and disruptive nocturnal behaviors. There was no significant Blast × PTSD interaction, nor were there main effects of PTSD or Blast on measures of sleep continuity and NREM sleep. A significant PTSD × Blast interaction effect was found for REM fragmentation. The results suggest that, although persistent concussive symptoms following blast exposure are associated with sleep disturbances, self-reported blast exposure without concurrent symptoms does not appear to contribute to poor sleep quality, insomnia, and disruptive nocturnal disturbances beyond the effects of PTSD. Reduced REM sleep fragmentation may be a sensitive index of the synergetic effects of both psychological and physical insults.

Close-range blast exposure is associated with altered functional connectivity in Veterans independent of concussion symptoms at time of exposure.

Although there is emerging data on the effects of blast-related concussion (or mTBI) on cognition, the effects of blast exposure itself on the brain have only recently been explored. Toward this end, we examine functional connectivity to the posterior cingulate cortex, a primary region within the default mode network (DMN), in a cohort of 134 Iraq and Afghanistan Veterans characterized for a range of common military-associated comorbidities. Exposure to a blast at close range (<10 meters) was associated with decreased connectivity of bilateral primary somatosensory and motor cortices, and these changes were not different from those seen in participants with blast-related mTBI. These results remained significant when clinical factors such as sleep quality, chronic pain, or post traumatic stress disorder were included in the statistical model. In contrast, differences in functional connectivity based on concussion history and blast exposures at greater distances were not apparent. Despite the limitations of a study of this nature (e.g., assessments long removed from injury, self-reported blast history), these data demonstrate that blast exposure per se, which is prevalent among those who served in Iraq and Afghanistan, may be an important consideration in Veterans' health. It further offers a clinical guideline for determining which blasts (namely, those within 10 meters) are likely to lead to long-term health concerns and may be more accurate than using concussion symptoms alone.

Retinal Ganglion Cell Damage in an Experimental Rodent Model of Blast-Mediated Traumatic Brain Injury

To evaluate retina and optic nerve damage following experimental blast injury. Healthy adult mice were exposed to an overpressure blast wave using a custom-built blast chamber. The effects of blast exposure on retina and optic nerve function and structure were evaluated using the pattern electroretinogram (pERG), spectral domain optical coherence tomography (OCT), and the chromatic pupil light reflex. Assessment of the pupil response to light demonstrated decreased maximum pupil constriction diameter in blast-injured mice using red light or blue light stimuli 24 hours after injury compared with baseline in the eye exposed to direct blast injury. A decrease in the pupil light reflex was not observed chronically following blast exposure. We observed a biphasic pERG decrease with the acute injury recovering by 24 hours postblast and the chronic injury appearing at 4 months postblast injury. Furthermore, at 3 months following injury, a significant decrease in the retinal nerve fiber layer was observed using OCT compared with controls. Histologic analysis of the retina and optic nerve revealed punctate regions of reduced cellularity in the ganglion cell layer and damage to optic nerves. Additionally, a significant upregulation of proteins associated with oxidative stress was observed acutely following blast exposure compared with control mice. Our study demonstrates that decrements in retinal ganglion cell responses can be detected after blast injury using noninvasive functional and structural tests. These objective responses may serve as surrogate tests for higher CNS functions following traumatic brain injury that are difficult to quantify.

Cerebellar White Matter Abnormalities following Primary Blast Injury in US Military Personnel

Little is known about the effects of blast exposure on the human brain in the absence of head impact. Clinical reports, experimental animal studies, and computational modeling of blast exposure have suggested effects on the cerebellum and brainstem. In US military personnel with isolated, primary blast-related ‘mild’ traumatic brain injury and no other known insult, we found diffusion tensor MRI abnormalities consistent with cerebellar white matter injury in 3 of 4 subjects. No abnormalities in other brain regions were detected. These findings add to the evidence supporting the hypothesis that primary blast exposure contributes to brain injury in the absence of head impact and that the cerebellum may be particularly vulnerable. However, the clinical effects of these abnormalities cannot be determined with certainty; none of the subjects had ataxia or other detected evidence of cerebellar dysfunction. The details of the blast events themselves cannot be disclosed at this time, thus additional animal and computational modeling will be required to dissect the mechanisms underlying primary blast-related traumatic brain injury. Furthermore, the effects of possible subconcussive impacts and other military-related exposures cannot be determined from the data presented. Thus many aspects of topic will require further investigation.

Primary blast survival and injury risk assessment for repeated blast exposures

The widespread use of explosives by modern insurgents and terrorists has increased the potential frequency of blast exposure in soldiers and civilians. This growing threat highlights the importance of understanding and evaluating blast injury risk and the increase of injury risk from exposure to repeated blast effects. Data from more than 3,250 large animal experiments were collected from studies focusing on the effects of blast exposure. The current study uses 2,349 experiments from the data collection for analysis of the primary blast injury and survival risk for both long- and short-duration blasts, including the effects from repeated exposures. A piecewise linear logistic regression was performed on the data to develop survival and injury risk assessment curves. New injury risk assessment curves uniting long- and short-duration blasts were developed for incident and reflected pressure measures and were used to evaluate the risk of injury based on blast over pressure, positive-phase duration, and the number of repeated exposures. The risk assessments were derived for three levels of injury severity: nonauditory, pulmonary, and fatality. The analysis showed a marked initial decrease in injury tolerance with each subsequent blast exposure. This effect decreases with increasing number of blast exposures. The new injury risk functions showed good agreement with the existing experimental data and provided a simplified model for primary blast injury risk. This model can be used to predict blast injury or fatality risk for single exposure and repeated exposure cases and has application in modern combat scenarios or in setting occupational health limits.

Treatment of Cognitive-Communicative Disorders Following Blast Injury

Abstract Purpose: Mild traumatic brain injury (mTBI) following exposure to a blast is the signature injury of Operation Iraqi Freedom (OIF) and Operation Enduring Freedom (OEF). The purposes of this article are to describe the characteristics of the service members who experience blast injuries, the cognitive-communicative deficits they present, and the role of the speech-language pathologist (SLP) in managing these deficits. Method: Demographic data for the service members who have experienced blast injuries in OIF/OEF are reviewed and reported. The literature on treating cognitive-communicative disorders following mTBI is reviewed and is discussed in the context of managing the deficits reported by service members returning from Iraq and Afghanistan. Results and conclusions: Information regarding the effects of blast exposure on the human body continues to emerge. Data regarding the most effective treatment for cognitive-communicative deficits following blast injury are needed. For now, SLPs must rely on the best evidence from the civilian mTBI literature, clinical expertise, and the personal values of the individual with TBI to develop effective treatment programs targeting the cognitive-communicative disorders experienced by these individuals.

Effects of blast exposure on exercise performance in sheep.

The effects of blast on maximal exercise performance were investigated in sheep that were trained to perform maximal exercise. Sheep were fully instrumented for determination of pulmonary and systemic hemodynamics. Blast exposure was administered by using a compressed air driven shock tube that was positioned to primarily produce cardiopulmonary injury. Four levels of exposure were used that were known to produce sublethal injury ranging from little or no grossly observable cardiopulmonary injury (level 1) to confluent ecchymosis of the heart, lung, or both (level 4). We evaluated maximal exercise performance 1 hour after exposure to level 1, level 2, and level 3 and 24 hours after level 3 and level 4. VO2max was not significantly decreased 1 hour after exposure to level 1 but was decreased after exposure to level 2 (29.9%) and level 3 (49.3%). Significant improvement in exercise performance was observed in 24 hours, as VO2max was not significantly decreased 24 hour after level 3. VO2max was decreased 24 hour after level 4 injury (30.8%). Cardiovascular data collected during exercise suggested that acute cardiopulmonary injury is responsible for the exercise performance decrement observed 1 hour after exposure and that significant recovery of function is observed 24 hours after blast injury.

Vitamin E and Lipoic Acid, but not Vitamin C Improve Blood Oxygenation after High-Energy IMPULSE Noise (BLAST) Exposure

Exposure to high energy impulse noise (BLAST) caused by explosions, result in structural and functional damage to the hollow organs, especially to the respiratory and auditory systems. Lung damage includes alveolar wall rupture, edema and hemorrhage, and may be fatal. Previous observations at the molecular level using the rat model, suggested that secondary free radical-mediated oxidative stress occurs post exposure resulting in antioxidant depletion and hemoglobin (Hb) oxidation. This study examined whether a short period of pre-exposure supplementation with antioxidants would protect Hb from the effects of BLAST exposure. Six groups of male Sprague-Dawley rats (8/group) were gavaged with 800 IU vitamin E (VE) in 2 ml corn oil, 1000 mg vitamin C (VC) in 2 ml distilled water or 25 mg or (-lipoic acid (LA) in 2 ml corn oil for 3 days. Matched control groups were gavaged with the respective vehicles. On day 4, rats were deeply anesthetized and exposed to a simulated BLAST wave with an average peak pressure of 62 ± 2 kPa. Rats were euthanized one hour post exposure and blood samples were obtained by cardiac puncture and analyzed using a hemoximeter. Post exposure oxygenation states (HbO2, O2saturation, and O2content) were markedly decreased, while reduced-Hb was increased. Supplementation with VE and LA reversed the trend and increased Hb oxygenation, but VC did not. This suggests that a brief dietary loading with pharmacological doses of VE or LA, but not VC shortly before BLAST exposure may be beneficial. Moreover, measurement of blood oxygenation may function as a simple, semi-invasive biomarker of BLAST-induced injury applicable to humans.