Is conduct after capture training sufficiently stressful?

Conduct after capture (CAC) training is for personnel at risk of being captured. To be effective, it needs to be stressful. But how do we know if it is stressful enough? This study uses biomarkers and cognitive measures to evaluate CAC. Soldiers undergoing CAC were measured by the stress hormone cortisol from saliva samples at baseline and during training. The training consisted of being taken capture and put through a number of realistic and threatening scenarios, targeting survival strategies taught in the preceding week. Between scenarios, the trainees were held in a holding cell where they were monitored by a guard. The saliva samples were taken in conjunction with the scenarios. The whole training took place over a period of ~24 h. Cognitive performance was measured at baseline and after training. Three groups took part Group A (n = 20) was taken after 48 h of intense tasks leaving them in a poor resting state. Group B (n = 23) was well rested at CAC onset. Group C (n = 10) was part of a survival, evasion, resistance, and escape (SERE) instructor course. The CAC training was the same for all groups. Group A exhibited a high increase in cortisol during CAC, compared to baseline levels were multiple times as high as “expected” values. Group B exhibited elevated levels slightly lower than those of group A, they also “dropped” to “normal” levels during the latter part of the exercise. Group C displayed the least increase with only slightly elevated levels. CAC training is stressful and cortisol levels were elevated enough to satisfy the prerequisite for effective stress inoculation. No cognitive performance drop could be identified; however, several participants “froze” during the exercise due to intensive stress

A Comparative Study of Two Blast-Induced Traumatic Brain Injury Models: Changes in Monoamine and Galanin Systems Following Single and Repeated Exposure

Repeated mild blast-induced traumatic brain injury (rmbTBI), caused by recurrent exposure to low levels of explosive blast, is a significant concern for military health systems. However, the pathobiology of rmbTBI is currently poorly understood. Animal models are important tools to identify the molecular changes of rmbTBI, but comparisons across different models can present their own challenges. In this study, we compared two well-established rodent models of mbTBI, the “KI model” and the “USU/WRAIR model.” These two models create different pulse forms, in terms of peak pressure and duration. Following single and double exposures to mild levels of blast, we used in situ hybridization (ISH) to assess changes in mRNA levels of tyrosine hydroxylase (TH), tryptophan hydroxylase (TPH2), and galanin in the locus coeruleus (LC) and dorsal raphe nucleus (DRN). These systems and their transmitters are known to mediate responses to stress and anxiety. We found increased mRNA levels of TH, TPH2 and galanin in the LC and DRN of single-exposed rats relative to sham rats in the KI but not the USU/WRAIR model. Sham mRNA values measured in the USU/WRAIR model were substantially higher than their KI counterparts. Double exposure caused similarly significant increases in mRNA values in the KI model but not the USU/WRAIR model, except TPH2 and galanin levels in the DRN. We detected no cumulative effect of injury in either model at the used inter-injury interval (30 min), and there were no detectable neuropathological changes in any experimental group at 1 day post-injury. The apparent lack of early response to injury as compared to sham in the USU/WRAIR model is likely caused by stressors (e.g., transportation and noise), associated with the experimental execution, that were absent in the KI model. This study is the first to directly compare two established rodent models of rmbTBI, and to highlight the challenges of comparing findings from different animal models. Additional studies are needed to understand the role of stress, dissect the effects of psychological and physical injuries and to identify the window of increased cerebral vulnerability, i.e., the inter-injury interval that results in a cumulative effect following repeated blast exposure

Three Experimental Models for Evaluation of Three Different Mechanisms in Blast TBI

Traumatic Brain Injuries (TBI) induced by blast waves from detonations provides huge diagnostic problems. It may be assumed that several mechanisms contribute to the injury. Thus, the primary blast overpressure, acceleration movements, focal impacts as well as heating could contribute to the injury. In a number of experiments we have evaluated the injuries induced by these mechanisms. Our experimental models include a blast tube in which an anesthetized rat can be exposed to controlled detonations of PETN explosives that result in a pressure wave with a magnitude between 130 and 600 kPa. In this model, the animal is fixed with a metal net to avoid head acceleration forces. The pressure wave is of simple Friedl\ue4nder type, with a duration of less than 0.5 ms. Animals that are exposed side on suffer from lethal bleedings from the lungs if the peak pressure exceeds 300 kPa. In recent experiments we have mounted animals in a rigid metallic body protection that covers all parts of the body except for the head, which rests on a bar that prevents from acceleration movements. With this protection the animals survive 600 kPa. The second model is a controlled penetration of a 2 mm thick needle, which is assumed to represent the focal impact of fragments. In the third model the animal is subjected to a high-speed sagittal rotation angular acceleration. This model is assumed to be relevant for rapid acceleration movements that can occur after explosions. Immunohistochemical labeling for amyloid precursor protein revealed signs of diffuse axonal injury (DAI) in the penetration and rotation models. Signs of punctuate inflammation were observed after focal and rotation injury. Exposure in the blast tube did not induce DAI or detectable cell death, but functional changes. Affymetrix Gene arrays showed changes in the expression in a large number of gene families including cell death, inflammation and neurotransmittors in the hippocampus after both acceleration and penetration injuries. Exposure to primary blast wave induced limited shifts in gene expression in the hippocampus. The most interesting findings were a down regulation of genes involved in neurogenesis and synaptic transmission. These experiments indicate that rotational acceleration may be a critical factor for DAI and other acute changes after blast TBI. The further exploration of the mechanisms of blast TBI will have to include a search for long-term effects. Detailed studies on the anxiety related pathways from the brainstem represent an important part these continued studies

Three Experimental Models for Evaluation of Three Different Mechanisms in Blast TBI

Traumatic Brain Injuries (TBI) induced by blast waves from detonations provides huge diagnostic problems. It may be assumed that several mechanisms contribute to the injury. Thus, the primary blast overpressure, acceleration movements, focal impacts as well as heating could contribute to the injury. In a number of experiments we have evaluated the injuries induced by these mechanisms. Our experimental models include a blast tube in which an anesthetized rat can be exposed to controlled detonations of PETN explosives that result in a pressure wave with a magnitude between 130 and 600 kPa. In this model, the animal is fixed with a metal net to avoid head acceleration forces. The pressure wave is of simple Friedl\ue4nder type, with a duration of less than 0.5 ms. Animals that are exposed side on suffer from lethal bleedings from the lungs if the peak pressure exceeds 300 kPa. In recent experiments we have mounted animals in a rigid metallic body protection that covers all parts of the body except for the head, which rests on a bar that prevents from acceleration movements. With this protection the animals survive 600 kPa. The second model is a controlled penetration of a 2 mm thick needle, which is assumed to represent the focal impact of fragments. In the third model the animal is subjected to a high-speed sagittal rotation angular acceleration. This model is assumed to be relevant for rapid acceleration movements that can occur after explosions. Immunohistochemical labeling for amyloid precursor protein revealed signs of diffuse axonal injury (DAI) in the penetration and rotation models. Signs of punctuate inflammation were observed after focal and rotation injury. Exposure in the blast tube did not induce DAI or detectable cell death, but functional changes. Affymetrix Gene arrays showed changes in the expression in a large number of gene families including cell death, inflammation and neurotransmittors in the hippocampus after both acceleration and penetration injuries. Exposure to primary blast wave induced limited shifts in gene expression in the hippocampus. The most interesting findings were a down regulation of genes involved in neurogenesis and synaptic transmission. These experiments indicate that rotational acceleration may be a critical factor for DAI and other acute changes after blast TBI. The further exploration of the mechanisms of blast TBI will have to include a search for long-term effects. Detailed studies on the anxiety related pathways from the brainstem represent an important part these continued studies

Incidence, Demographics, and Outcomes of Penetrating Trauma in Sweden During the Past Decade

Trauma injury is the sixth leading cause of death worldwide, and interpersonal violence is one of the major contributors in particular regarding injuries to the head and neck. The incidence, demographics, and outcomes of penetrating trauma reaching hospitals in Sweden are not known. We report the largest, nationwide epidemiological study of penetrating injuries in Sweden, using the Swedish Trauma Registry (SweTrau). A multi-center retrospective descriptive study of 4,776 patients was conducted with penetrating injuries in Sweden, between 2012 and 2018. Due to the increase in coverage of the SweTrau registry during the same period, we chose to analyze the average number of cases for the time intervals 2013-2015 and 2016-2018 and compare those trends to the reports of the Swedish National Council for Crime Prevention (Bra) as well. A total of 663 patients had Injury Severity Score (ISS) >= 15 at admission and were included in the study. Three hundred and sixty-eight (55.5%) were stab wounds (SW), 245 (37.0%) gunshot wounds (GSW), and 50 (7.5%) other traumas. A majority of the cases involved injuries to the head, neck, and face. SW increased from 145 during 2013-2015 to 184 during the second period of 2016-2018. The increase was greater for GSW from 92 to 141 during the same respective periods. This trend of increase over time was also seen in head, neck, and face injuries. The 30-day mortality was unaffected (48-47%) in GSW and trended toward lower in SW (24-21%) when comparing 2013-2015 with 2016-2018. Patients with head trauma had 45% mortality compared to 18% for non-head trauma patients. Head trauma also resulted in worse outcomes, only 13% had Glasgow outcome score (GOS) 5 compared to 27% in non-head trauma. The increasing number of cases of both SW and GSW corresponded well with reports from Bra although further studies also are needed to address deaths outside of hospitals and not registered at the SweTrau. The majority of cases had injuries to the head, neck, and face and were associated with higher mortality and poor outcomes. Further studies are needed to understand the contributing factors to these worse outcomes in Sweden and whether more targeted trauma care of these patients can improve outcomes

Muscle pathologies after cervical spine distortion-like exposure-a porcine model

Objective: Histological evaluation of porcine posterior cervical muscles after a forceful translational and extensional head retraction simulating high-speed rear end impact. Methods: Four anesthetized pigs were exposed to a cervical spine distortion (CSD)-like motion in a lying position. After 2 different survival times of 4 and 6 h (posttrauma), the pigs were euthanized and tissue sampling of posterior cervical muscles was performed. A standard histological staining method involving paraffin-embedded sections was used to analyze the muscles, focusing on injury signs like hemorrhage and inflammatory cell reaction. A pig that was not subjected to impact was used as a control pig and was subjected to the same procedure to exclude any potential artifacts from the autopsy. Results: The differentiation of 8 different posterior neckmuscles in the dissection process was successful in more than 50 percent for each muscle of interest. Staining and valid analysis was possible from all extracted samples. Muscle injuries to the deepest posterior neck muscles could be found, especially in the musculus obliquus samples, which showed laminar bleedings in 4 out of 4 samples. In addition, in 4 out of 4 samples we were able to see increased cellular reactions. The splenius muscle also showed bleeding in all 4 samples. All animals showed muscle injury signs in more than three quarters of analyzed neck muscles. Differences between survival times of 4 and 6 h in terms of muscular injury were not of primary interest and could not be found. Conclusions: By simulating a CSD-like motion we were able to confirm injuries in the posterior cervical muscles under severe loading conditions

Mechanisms of Blast Induced Brain Injuries, Experimental Studies in Rats.

Traumatic brain injuries (TBI) potentially induced by blast waves from detonations result in significant diagnostic problems. It may be assumed that several mechanisms contribute to the injury. This study is an attempt to characterize the presumed components of the blast induced TBI. Our experimental models include a blast tube in which an anesthetized rat can be exposed to controlled detonations of explosives that result in a pressure wave with a magnitude between 130 and 260 kPa. In this model, the animal is fixed with a metal net to avoid head acceleration forces. The second model is a controlled penetration of a 2 mm thick needle. In the third model the animal is subjected to a high-speed sagittal rotation angular acceleration. Immunohistochemical labeling for amyloid precursor protein revealed signs of diffuse axonal injury (DAI) in the penetration and rotation models. Signs of punctuate inflammation were observed after focal and rotation injury. Exposure in the blast tube did not induce DAI or detectable cell death, but functional changes. Affymetrix Gene arrays showed changes in the expression in a large number of gene families including cell death, inflammation and neurotransmitters in the hippocampus after both acceleration and penetration injuries. Exposure to the primary blast wave induced limited shifts in gene expression in the hippocampus. The most interesting findings were a downregulation of genes involved in neurogenesis and synaptic transmission. These experiments indicate that rotational acceleration may be a critical factor for DAI and other acute changes after blast TBI. The further exploration of the mechanisms of blast TBI will have to include a search for long-term effects