Health Outcomes Associated With Military Deployment: Mild Traumatic Brain Injury, Blast, Trauma, and Combat Associations in the Florida National Guard.
ABSTRACT Vanderploeg RD, Belanger HG, Horner RD, Spehar AM, Powell-Cope G, Luther SL, Scott SG. Health outcomes associated with military deployment: mild traumatic brain injury, blast, trauma, and combat associations in the Florida National Guard. OBJECTIVES: To determine the association between specific military deployment experiences and immediate and longer-term physical and mental health effects, as well as examine the effects of multiple deployment-related traumatic brain injuries (TBIs) on health outcomes. DESIGN: Online survey of cross-sectional cohort. Odds ratios were calculated to assess the association between deployment-related factors (ie, physical injuries, exposure to potentially traumatic deployment experiences, combat, blast exposure, and mild TBI) and current health status, controlling for potential confounders, demographics, and predeployment experiences. SETTING: Nonclinical. PARTICIPANTS: Members (N=3098) of the Florida National Guard (1443 deployed, 1655 not deployed). INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Presence of current psychiatric diagnoses and health outcomes, including postconcussive and non-postconcussive symptoms. RESULTS: Surveys were completed an average of 31.8 months (SD=24.4, range=0-95) after deployment. Strong, statistically significant associations were found between self-reported military deployment-related factors and current adverse health status. Deployment-related mild TBI was associated with depression, anxiety, posttraumatic stress disorder (PTSD), and postconcussive symptoms collectively and individually. Statistically significant increases in the frequency of depression, anxiety, PTSD, and a postconcussive symptom complex were seen comparing single to multiple TBIs. However, a predeployment TBI did not increase the likelihood of sustaining another TBI in a blast exposure. Associations between blast exposure and abdominal pain, pain on deep breathing, shortness of breath, hearing loss, and tinnitus suggested residual barotrauma. Combat exposures with and without physical injury were each associated not only with PTSD but also with numerous postconcussive and non-postconcussive symptoms. The experience of seeing others wounded or killed or experiencing the death of a buddy or leader was associated with indigestion and headaches but not with depression, anxiety, or PTSD. CONCLUSIONS: Complex relationships exist between multiple deployment-related factors and numerous overlapping and co-occurring current adverse physical and psychological health outcomes. Various deployment-related experiences increased the risk for postdeployment adverse mental and physical health outcomes, individually and in combination. These findings suggest that an integrated physical and mental health care approach would be beneficial to postdeployment care.
- [Show abstract] [Hide abstract]
ABSTRACT: Working memory, which is dependent on higher-order executive function in the prefrontal cortex, is often disrupted in patients exposed to blast overpressure. In this study, we evaluated working memory and medial prefrontal neurochemical status in a rat model of blast neurotrauma. Adult male Sprague Dawley rats were anesthetized with 3% isoflurane and exposed to calibrated blast overpressure (17 psi, 117 kPa) while sham animals received only anesthesia. Early neurochemical effects in the prefrontal cortex included a significant decrease in betaine (trimethylglycine) and an increase in GABA at 24 hours, and significant increases in glycerophosphorylcholine, phosphorylethanolamine, as well as glutamate/creatine and lactate/creatine ratios at 48 hours. Seven days after blast, only myo-inositol levels were altered showing a 15% increase. Compared to controls, short-term memory in the novel object recognition task was significantly impaired in animals exposed to blast overpressure. Working memory in control animals was negatively correlated with myo-inositol levels (r = − .759, p < 0.05), an association that was absent in blast exposed animals. Increased myo-inositol may represent tardive glial scarring in the prefrontal cortex, a notion supported by GFAP changes in this region after blast overexposure as well as clinical reports of increased myo-inositol in disorders of memory.Molecular and Cellular Neuroscience 01/2014; · 3.84 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: We investigate the hypothesis that oxidative damage of the cerebral vascular barrier interface (the blood brain barrier, BBB) causes the development of mild traumatic brain injury (mTBI) during primary blast wave spectrum. The underlying biochemical and cellular mechanisms of this vascular layer-structure injury are examined in a novel animal model of shock tube. We first established that low frequency (123kPa) single or repeated shock wave causes BBB/brain injury through biochemical activation by acute mechanical force that occurs at 6-24h after the exposure. This biochemical damage of the cerebral vasculature is initiated by the induction of free radical generating enzymes NADPH oxidase (NOX1) and inducible nitric oxide synthase (iNOS). Induction of these enzymes by shock wave exposure correlated well with the signatures of oxidative and nitrosative damage (4HNE/3NT) and reduction of the BBB tight junction (TJ) proteins occludin, claudin-5 and zonula occluden 1 (ZO-1) in the brain microvessel. In parallel with TJ protein disruption, the perivascular unit was significantly diminished by single or repeated shock wave exposure coinciding with the kinetic profile. Loosening of the vasculature and perivascular unit was mediated by oxidative stress-induced activation of matrix metalloproteinases and fluid channel aquaporin-4, promoting vascular fluid cavitation/edema, enhanced leakiness of the BBB and progression of neuroinflammation. The BBB leakiness and neuroinflammation were functionally demonstrated in an in vivo model by enhanced permeability of Na-Fl/EB low molecular weight tracers and the infiltration of immune cells across the BBB. The detection of brain cell matters NSE/S100β in the blood samples validated the neuro-astroglial injury in shock wave TBI. Our hypothesis that cerebral vascular injury occurring prior to the development of neurological disorders in mild TBI was further confirmed by the activation of caspase-3 and cell apoptosis mostly around the perivascular region. Thus, induction of oxidative stress and MMPs activation by shock wave underlies the mechanisms of cerebral vascular BBB leakage and neuroinflammation.Free Radical Biology and Medicine 03/2013; · 5.27 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: BACKGROUND:: Both the Departments of Defense and Veterans Health Administration have developed and implemented screening procedures for identification of possible deployment-related traumatic brain injury (TBI). OBJECTIVE:: To review population-based screening procedures for TBI, particularly mild TBIs, and discuss potential harms/costs versus benefits of such TBI screening. METHODS:: The principles commonly used in population-based screening for various medical conditions are identified. These principles are applied to screening for TBI. The potential harms and costs are compared with potential benefits of screening for mild TBI. RESULTS:: The core conditions essential for beneficial medical screening-progressive disease, symptoms related to the identified disease, suitable tests or examinations for accurate diagnosis, and accepted and effective treatment-are not present within the context of TBI screening. Potential harms/costs outweigh any potential benefits of population-based screening for TBI. CONCLUSION:: On the basis of generally accepted medical screening principles and assumptions, population screening for mild TBI is unnecessary at best and potentially harmful at worst. Because nonspecific, postconcussion-like symptoms can be effectively treated in a symptom-specific manner, tying them to concussion through a screening and evaluation process is wasteful and potentially harmful.The Journal of head trauma rehabilitation 28(3):211-218. · 2.39 Impact Factor