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.
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ABSTRACT: Co-morbid mild traumatic brain injury (mTBI) and post-traumatic stress disorder (PTSD) has become the signature disorder for returning combat veterans. The clinical heterogeneity and overlapping symptomatology of mTBI and PTSD underscore the need to develop a preclinical model that will enable the characterization of unique and overlapping features and allow discrimination between both disorders. This study details the development and implementation of a novel experimental paradigm for PTSD and combined PTSD-mTBI. The PTSD paradigm involved exposure to a danger-related predator odor under repeated restraint over a 21 day period and a physical trauma (inescapable footshock). We administered this paradigm alone, or in combination with a previously established mTBI model. We report outcomes of behavioral, pathological and biochemical profiles at an acute timepoint. PTSD animals demonstrated recall of traumatic memories, anxiety and an impaired social behavior. In both mTBI and combination groups there was a pattern of disinhibitory like behavior. mTBI abrogated both contextual fear and impairments in social behavior seen in PTSD animals. No major impairment in spatial memory was observed in any group. Examination of neuroendocrine and neuroimmune responses in plasma revealed a trend toward increase in corticosterone in PTSD and combination groups, and an apparent increase in Th1 and Th17 proinflammatory cytokine(s) in the PTSD only and mTBI only groups respectively. In the brain there were no gross neuropathological changes in any groups. We observed that mTBI on a background of repeated trauma exposure resulted in an augmentation of axonal injury and inflammatory markers, neurofilament L and ICAM-1 respectively. Our observations thus far suggest that this novel stress-trauma-related paradigm may be a useful model for investigating further the overlapping and distinct spatio-temporal and behavioral/biochemical relationship between mTBI and PTSD experienced by combat veterans.Frontiers in Behavioral Neuroscience 06/2014; 8:213. DOI:10.3389/fnbeh.2014.00213 · 4.16 Impact Factor
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ABSTRACT: This study used cluster analysis to examine variability in Trail Making Test (TMT) performance in a sample of Operation Enduring Freedom/Operation Iraqi Freedom/Operation New Dawn (OEF/OIF/OND) veterans referred for mild traumatic brain injury (mTBI). Three clusters were extracted, two of which were characterized by level of performance and the third with a unique performance pattern characterized by slow performance on the TMT B (Low B). Clusters did not differ on demographic or psychiatric variables. The Above Average cluster had better performance on measures of processing speed, working memory, and phonemic fluency compared with the Low B cluster. Results suggest that a subset of patients with mTBI perform poorly on TMT B, which subsequently predicts poorer cognitive functioning on several other neuropsychological measures. This subset may be vulnerable to cognitive changes in the context of mTBI and multiple comorbidities while a number of other patients remain cognitively unaffected under the same circumstances.Archives of Clinical Neuropsychology 10/2013; DOI:10.1093/arclin/act080 · 1.92 Impact Factor
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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; DOI:10.1016/j.freeradbiomed.2013.02.029 · 5.71 Impact Factor