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Citations
... [1][2][3] In addition to in-theatre exposures, there are also concerns over potential adverse effects of subclinical blast exposures. [4][5][6] This type of blast exposure, now being referred to as military occupational blast exposure, is common for many service members in combat and non-combat settings. 4 A history of TBI is frequently found in veterans seeking treatment at Department of Veterans Affairs (VA) mental health clinics. ...
... [4][5][6] This type of blast exposure, now being referred to as military occupational blast exposure, is common for many service members in combat and non-combat settings. 4 A history of TBI is frequently found in veterans seeking treatment at Department of Veterans Affairs (VA) mental health clinics. 7 TBI is closely linked to chronic mental health problems in veterans, 1 including anxiety, depression, impulsivity, insomnia, and suicidality. ...
Many military veterans who experienced blast-related traumatic brain injuries (TBIs) in the conflicts in Iraq and Afghanistan suffer from chronic cognitive and mental health problems, including post-traumatic stress disorder (PTSD). Male rats subjected to repetitive low-level blast exposure develop chronic cognitive and PTSD-related traits that develop in a delayed manner. Ketamine has received attention as a treatment for refractory depression and PTSD. (2R,6R)-hydroxynorketamine [(2R,6R)-HNK] is a ketamine metabolite that exerts rapid antidepressant actions. (2R,6R)-HNK has become of clinical interest because of its favorable side-effect profile, low abuse potential, and oral route of administration. We treated three cohorts of blast-exposed rats with (2R,6R)-HNK, beginning 7–11 months after blast exposure, a time when the behavioral phenotype is established. Each cohort consisted of groups (n = 10–13/group) as follows: 1) Sham-exposed treated with saline, 2) blast-exposed treated with saline, and 3) blast-exposed treated with a single dose of 20 mg/kg of (2R,6R)-HNK. (2R,6R)-HNK rescued blast-induced deficits in novel object recognition (NOR) and anxiety-related features in the elevated zero maze (EZM) in all three cohorts. Exaggerated acoustic startle was reversed in cohort 1, but not in cohort 3. (2R,6R)-HNK effects were still present in the EZM 12 days after administration in cohort 1 and 27 days after administration in NOR testing of cohorts 2 and 3. (2R,6R)-HNK may be beneficial for the neurobehavioral syndromes that follow blast exposure in military veterans. Additional studies will be needed to determine whether higher doses or more extended treatment regimens may be more effective.
... There is currently no literature reporting on what is deemed to be a safe level of low-level military occupational blast (MOB), leading to an increasing interest in neurological damage following repetitive low-level MOB. 1 High pressure blast waves can induce a range of injuries. Historically, these have been believed to include mild traumatic brain injury (mTBI), central nervous system damage, internal injuries, or, in extreme cases, death. ...
Background:
There is a need for an objective method to determine a safe level of low-level military occupational blast (MOB) having recognised it can lead to neurological damage.
Purpose:
To evaluate the effect of artillery firing training on the neurochemistry of front-line soldiers using 2D COrrelated SpectroscopY (2D COSY) in a 3T clinical MR scanner.
Methods:
Ten men considered to be of sound health were evaluated by before and after a weeklong live firing exercise in two ways. Prior to the live fire exercise, all participants were screened by a Clinical Psychologist using a combination of clinical interview and psychometric tests and then scanned in a 3T MRI. The protocols included T1 and T2 weighted images for diagnostic reporting and anatomical localisation and a 2D COSY to record any neurochemical effects from the firing.
Results:
No changes to the structural MRI were recorded. Nine substantive and statistically significant changes in the neurochemistry were recorded as a consequence of firing training. Glutamine and glutamate, glutathione and two of the seven Fucose-α (1-2)-Glycans were significantly increased. NAA, myo Inositol+Creatine and glycerol were also increased. Significant decreases were recorded for the glutathione cysteine moiety and tentatively assigned glycan with a 1-6 linkage (F2:4.00, F1:1.31ppm).
Conclusions:
These molecules are part of three neurochemical pathways at the terminus of the neurons providing evidence of early markers of disruption to neurotransmission. Using this technology, the extent of deregulation can now be monitored for each Frontline Defender on a personalised basis. The capacity to monitor early a disruption in neurotransmitters, using the 2D COSY protocol, can monitor the effect of firing and may be used to prevent or limit these events.
... Though we adjusted for injury severity, we could not account for chronic pain resulting from injuries, which may contribute to the association between concussion and poorer physical health. We were also unable to measure exposure to lower yield repetitive blast, such as small arms fire, which may contribute to concussion [65]. Our assessment of PTSD and depression occurred several years after the injury incident, and future studies should better define the temporal relationships between concussion, psychological morbidity, and HRQoL. ...
Purpose
To examine the relationship between deployment-related concussion and long-term health-related quality of life (HRQoL) among injured US military personnel.
Methods
The study sample included 810 service members with deployment-related injuries between 2008 and 2012 who responded to a web-based longitudinal health survey. Participants were categorized into three injury groups: concussion with loss of consciousness (LOC; n = 247), concussion without LOC (n = 317), or no concussion (n = 246). HRQoL was measured using the 36-Item Short Form Health Survey physical and mental component summary (PCS and MCS) scores. Current post-traumatic stress disorder (PTSD) and depression symptoms were examined. Multivariable linear regression models assessed the effects of concussion on PCS and MCS scores, while controlling for covariates.
Results
A lower PCS score was observed in participants with concussion with LOC (B = − 2.65, p = 0.003) compared with those with no history of concussion. Symptoms of PTSD (PCS: B = − 4.84, p < 0.001; MCS: B = − 10.53, p < 0.001) and depression (PCS: B = − 2.85, p < 0.001; MCS: B = − 10.24, p < 0.001) were the strongest statistically significant predictors of lower HRQoL.
Conclusion
Concussion with LOC was significantly associated with lower HRQoL in the physical domain. These findings affirm that concussion management should integrate physical and psychological care to improve long-term HRQoL and warrant a more detailed examination of causal and mediating mechanisms. Future research should continue to incorporate patient-reported outcomes and long-term follow-up of military service members to further define the lifelong impact of deployment-related concussion.
... Veterans deployed to OEF/OIF or OND may be exposed to explosions and war-related events, which lead to traumarelated conditions, such as traumatic brain injury (TBI) or post-traumatic stress disorder (PTSD) (Engel et al., 2018;Hoge et al., 2006). TBI is defined as brain damage by an external force, which is a common combat-related injury among OEF/OIF Veterans. ...
Motor vehicle crashes is a leading cause of death for Veterans. We quantified the efficacy of an Occupational Therapy Driving Intervention (OT-DI) and a Traffic Safety Education (TSE) intervention on real-world driving in combat Veterans. Via a randomized trial, we assessed 42 Veterans’ fitness-to-drive abilities using a CDS-250 driving simulator and driving records, to determine differences in simulated driving and real-world events pre- and post-interventions. The OT-DI group (vs. TSE) had fewer over-speeding errors ( p < .001) and total number of driving errors ( p = .002) post-intervention. At Post-Test 2, the OT-DI (vs. TSE) had a reduction in real-world speeding ( p = .05). While statistically not significant, both interventions showed reductions in real-world speeding, number of violations (OT-DI: 23% and TSE: 46% decrease) and crashes (OT-DI: 25% and TSE: 50% decrease). Veterans showed early evidence of efficacy in improving their real-world fitness-to-drive abilities via an OT-DI and TSE intervention.
... The majority of TBIs suffered by a service member are due at least in part to blast exposure (Connelly et al., 2017;DOD Worldwide TBI Numbers, 2021;Xydakis et al., 2008). Military personnel are often exposed to blasts from improvised explosive devices while deployed in theater and can also receive multiple lowlevel blast exposure during training exercises (Engel et al., 2018). ...
Primary blast injury is caused by the direct impact of an overpressurization wave on the body. Due to limitations of current models, we have developed a novel approach to study primary blast‐induced traumatic brain injury. Specifically, we employ a bioengineered 3D brain‐like human tissue culture system composed of collagen‐infused silk protein donut‐like hydrogels embedded with human IPSC‐derived neurons, human astrocytes, and a human microglial cell line. We have utilized this system within an advanced blast simulator (ABS) to expose the 3D brain cultures to a blast wave that can be precisely controlled. These 3D cultures are enclosed in a 3D‐printed surrogate skull‐like material containing media which are then placed in a holder apparatus inside the ABS. This allows for exposure to the blast wave alone without any secondary injury occurring. We show that blast induces an increase in lactate dehydrogenase activity and glutamate release from the cultures, indicating cellular injury. Additionally, we observe a significant increase in axonal varicosities after blast. These varicosities can be stained with antibodies recognizing amyloid precursor protein. The presence of amyloid precursor protein deposits may indicate a blast‐induced axonal transport deficit. After blast injury, we find a transient release of the known TBI biomarkers, UCHL1 and NF‐H at 6 h and a delayed increase in S100B at 24 and 48 h. This in vitro model will enable us to gain a better understanding of clinically relevant pathological changes that occur following primary blast and can also be utilized for discovery and characterization of biomarkers. In vitro tissue engineering provides a novel approach to investigate the cellular and molecular effects of traumatic brain injury. Here, we describe a bioengineered 3D brain‐like human tissue culture system to study primary blast‐induced traumatic brain injury.
... [6][7][8][9] In addition to the overt exposures associated with clinically recognized TBI, there are also concerns over potential adverse effects of what is now being referred to as military occupational blast exposure, a type of subclinical blast exposure, that is common for many service members in combat as well as non-combat settings. [10][11][12] Transcranial laser therapy (TLT) uses low-power lasers and light-emitting diodes (LEDs) in the far-to near-infrared domain of the light spectrum. 13 The lowlevel lasers and LEDs used do not emit significant heat, but modulate numerous cellular activities, including increasing mitochondrial function, enhancing adenosine triphosphate synthesis, altering intracellular calcium, and modulating reactive oxygen species production. ...
Many military veterans who experienced blast-related traumatic brain injuries (TBIs) in the conflicts in Iraq and Afghanistan suffer from chronic cognitive and mental health problems, including post-traumatic stress disorder (PTSD). Transcranial laser therapy (TLT) uses low-power lasers emitting light in the far- to near-infrared ranges. Beneficial effects of TLT have been reported in neurological and mental-health–related disorders in humans and animal models, including TBI. Rats exposed to repetitive low-level blast develop chronic cognitive and PTSD-related behavioral traits. We tested whether TLT treatment could reverse these traits. Rats received a 74.5-kPa blast or sham exposures delivered one per day for 3 consecutive days. Beginning at 34 weeks after blast exposure, the following groups of rats were treated with active or sham TLT: 1) Sham-exposed rats (n = 12) were treated with sham TLT; 2) blast-exposed rats (n = 13) were treated with sham TLT; and 3) blast-exposed rats (n = 14) were treated with active TLT. Rats received 5 min of TLT five times per week for 6 weeks (wavelength, 808 nm; power of irradiance, 240 mW). At the end of treatment, rats were tested in tasks found previously to be most informative (novel object recognition, novel object localization, contextual/cued fear conditioning, elevated zero maze, and light/dark emergence). TLT did not improve blast-related effects in any of these tests, and blast-exposed rats were worse after TLT in some anxiety-related measures. Based on these findings, TLT does not appear to be a promising treatment for the chronic cognitive and mental health problems that follow blast injury.
... While these TBIs occurred through various mechanisms, blast-related injuries resulting from exposures to mortars, artillery shells and improvised explosive devices were the major causes with repetitive mild injuries common [27]. Concerns also exist over potential adverse effects of subclinical blast exposures, which are common for many service members in combat as well as non-combat settings [29]. ...
Military veterans who experience blast-related traumatic brain injuries often suffer from chronic cognitive and neurobehavioral syndromes. Reports of abnormal tau processing following blast injury have raised concerns that some cases may have a neurodegenerative basis. Rats exposed to repetitive low-level blast exhibit chronic neurobehavioral traits and accumulate tau phosphorylated at threonine 181 (Thr181). Using data previously reported in separate studies we tested the hypothesis that region-specific patterns of Thr181 phosphorylation correlate with behavioral measures also previously determined and reported in the same animals. Elevated p-tau Thr181 in anterior neocortical regions and right hippocampus correlated with anxiety as well as fear learning and novel object localization. There were no correlations with levels in amygdala or posterior neocortical regions. Particularly striking were asymmetrical effects on the right and left hippocampus. No systematic variation in head orientation toward the blast wave seems to explain the laterality. Levels did not correlate with behavioral measures of hyperarousal. Results were specific to Thr181 in that no correlations were observed for three other phospho-acceptor sites (threonine 231, serine 396, and serine 404). No consistent correlations were linked with total tau. These correlations are significant in suggesting that p-tau accumulation in anterior neocortical regions and the hippocampus may lead to disinhibited amygdala function without p-tau elevation in the amygdala itself. They also suggest an association linking blast injury with tauopathy, which has implications for understanding the relationship of chronic blast-related neurobehavioral syndromes in humans to neurodegenerative diseases.
... 11 A recent review of the neurological effects of military occupational LLB found few published human studies and emphasized the need for further research. 13,14 For breachers, the safe standoff distance from controlled blasts is calculated based on an overpressure limit, typically 4 psi (28 kPa), which is considered to be of minimal risk for eardrum rupture. 8,9,11,12 However, the presence of objects within the blast range, including personnel, cause changes in overpressure levels that can be difficult to predict. ...
Introduction
Recently, there has been increasing concern about the adverse health effects of long-term occupational exposure to low-level blast in military personnel. Occupational blast exposure occurs routinely in garrison through use of armaments and controlled blast detonations. In the current study, we focused on a population of breaching instructors and range staff. Breaching is a tactical technique that is used to gain entry into closed spaces, often through the use of explosives.
Materials and Methods
Initial measurements of blast overpressure collected during breaching courses found that up to 10% of the blasts for range staff and up to 32% of the blasts for instructors exceeded the recommended 3 psi exposure limit. Using a cross-sectional design, we used tests of balance, ataxia, and hearing to compare a sample of breachers (n = 19) to age-and sex-matched military controls (n = 19).
Results
There were no significant differences between the two groups on the balance and ataxia tests, although the average scores of both groups were lower than would be expected in a normative population. The prevalence of hearing loss was low in the breacher group (4 of 19), and hearing thresholds were not significantly different from the controls. However, the prevalence of self-reported tinnitus was significantly higher in the breacher group (12 of 19) compared with the controls (4 of 19), and all breachers who were identified as having hearing loss also reported tinnitus.
Conclusions
Our results suggest that basic tests of balance, ataxia, and hearing on their own were not sensitive to the effects of long-term occupational exposure to low-level blast. Some of the blast exposure levels exceeded limits, and there was a significant association of exposure with tinnitus. Future studies should supplement with additional information including exposure history and functional hearing assessments. These findings should be considered in the design of future acute and longitudinal studies of low-level blast exposure.
... [2][3][4]17 There are also concerns over the potential adverse consequences of subclinical blast exposures. [18][19][20] This form of blast exposure, now being referred to as military occupational blast exposure, is common for many service members in combat as well as non-combat settings. 18 Whether occupational repetitive low-level blast exposures may cause later health problems is unknown but is a subject of current concern. ...
... [18][19][20] This form of blast exposure, now being referred to as military occupational blast exposure, is common for many service members in combat as well as non-combat settings. 18 Whether occupational repetitive low-level blast exposures may cause later health problems is unknown but is a subject of current concern. 18,21 This study utilized an animal model that was designed to mimic a blast-related human mild TBI or subclinical blast exposure. ...
... 18 Whether occupational repetitive low-level blast exposures may cause later health problems is unknown but is a subject of current concern. 18,21 This study utilized an animal model that was designed to mimic a blast-related human mild TBI or subclinical blast exposure. Studies using this system established that exposures up to 74.5 kPa (equivalent to 10.8 psi), while representing a level of blast that is transmitted to brain, 22 produce no gross neuropathological effects, and histological examination of the lung shows no hemorrhage or other pathology. ...
Many military veterans who experienced blast-related traumatic brain injuries (TBI) in the conflicts in Iraq and Afghanistan currently suffer from chronic cognitive and mental health problems including post-traumatic stress disorder (PTSD). Besides static symptoms, new symptoms may emerge or existing symptoms may worsen. TBI is also a risk factor for the later development of neurodegenerative diseases. Rats exposed to repetitive low-level blast overpressure (BOP) develop robust and enduring cognitive and PTSD-related behavioral traits that are present for at least one year after blast exposure. Here we determined the time-course of these traits appearance by testing rats in the immediate post-blast period. Three cohorts of rats examined within the first eight weeks exhibited no behavioral phenotype, or in one cohort features of anxiety. None showed the altered cued fear responses, or impaired novel object recognition characteristic of the fully developed phenotype. Two cohorts retested 36 to 42 weeks after blast exposure exhibited the expanded behavioral phenotype including anxiety as well as altered cued fear learning and impaired novel object recognition. Combined with previous work the chronic behavioral phenotype has been observed in six cohorts of blast-exposed rats studied at 3-4 months or longer after blast injury and the three cohorts studied here document the progressive nature of the cognitive/behavioral phenotype. These studies suggest the existence of a latent, delayed emerging, and progressive blast-induced cognitive and behavioral phenotype. The delayed onset has implications for the evolution of post-blast neurobehavioral syndromes in military veterans and its modeling in experimental animals.
... These studies revealed that with torso protection, pressures around 30-psi (~ 207 kPa) provided the least amount of lung injury and greatest survival (unpublished pilot data, see Supplementary Fig. S9 online for lung injury comparison) and the lethality observed in torso protected rats exposed to a single blast between 25-35psi was 6% as compared with a lethality of 29% in torso protected rats exposed to a single blast between 42-50psi. In addition, it has been determined that 30-psi (~ 207 kPa) is also the threshold for lung injury in humans 45 . In the present study, each rat was exposed twice to a 30-psi blast wave, 24 h apart. ...
Traumatic brain injury generated by blast may induce long-term neurological and psychiatric sequelae. We aimed to identify molecular, histopathological, and behavioral changes in rats 2 weeks after explosive-driven double-blast exposure. Rats received two 30-psi (~ 207-kPa) blasts 24 h apart or were handled identically without blast. All rats were behaviorally assessed over 2 weeks. At Day 15, rats were euthanized, and brains removed. Brains were dissected into frontal cortex, hippocampus, cerebellum, and brainstem. Western blotting was performed to measure levels of total-Tau, phosphorylated-Tau (pTau), amyloid precursor protein (APP), GFAP, Iba1, αII-spectrin, and spectrin breakdown products (SBDP). Kinases and phosphatases, correlated with tau phosphorylation were also measured. Immunohistochemistry for pTau, APP, GFAP, and Iba1 was performed. pTau protein level was greater in the hippocampus, cerebellum, and brainstem and APP protein level was greater in cerebellum of blast vs control rats (p < 0.05). GFAP, Iba1, αII-spectrin, and SBDP remained unchanged. No immunohistochemical or neurobehavioral changes were observed. The dissociation between increased pTau and APP in different regions in the absence of neurobehavioral changes 2 weeks after
double blast exposure is a relevant finding, consistent with human data showing that battlefield blasts might be associated with molecular changes before signs of neurological and psychiatric disorders manifest.
