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1.
Qual Life Res ; 32(7): 1971-1980, 2023 Jul.
Article in English | MEDLINE | ID: mdl-36897531

ABSTRACT

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.


Subject(s)
Brain Concussion , Military Personnel , Stress Disorders, Post-Traumatic , Humans , Military Personnel/psychology , Quality of Life/psychology , Longitudinal Studies
2.
Brain Behav Immun ; 51: 258-267, 2016 Jan.
Article in English | MEDLINE | ID: mdl-26365025

ABSTRACT

Proinflammatory cytokines have been implicated in alcohol-induced neurodegeneration, but the role of the neuroimmune system in alcohol related behaviors has only recently come to the forefront. Herein, the effects of binge-like drinking on IL-1ß mRNA and immunoreactivity within the amygdala were measured following the "drinking in the dark" (DID) paradigm, a model of binge-like ethanol drinking in C57BL/6J mice. Moreover, the role of IL-1 receptor signaling in the amygdala on ethanol consumption was assessed. Results indicated that a history of binge-like ethanol drinking promoted a significant increase of IL-1ß mRNA expression within the amygdala, and immunohistochemistry analyses revealed that the basolateral amygdala (BLA), but not central amygdala (CeA), exhibited significantly increased IL-1ß immunoreactivity. However, Fluoro-Jade® C labeling indicated that multiple cycles of the DID paradigm were not sufficient to elicit neuronal death. Bilateral infusions of IL-1 receptor antagonist (IL-1Ra) reduced ethanol consumption when infused into the BLA but not the CeA. These observations were specific to ethanol drinking as the IL-1Ra did not alter either sucrose drinking or open-field locomotor activity. The current findings highlight a specific role for IL-1 receptor signaling in modulating binge-like ethanol consumption and indicate that proinflammatory cytokines can be induced prior to dependence or any evidence of neuronal cell death. These findings provide a framework in which to understand how neuroimmune adaptations may alter ethanol consumption and therein contribute to alcohol abuse.


Subject(s)
Basolateral Nuclear Complex/drug effects , Basolateral Nuclear Complex/metabolism , Binge Drinking/metabolism , Ethanol/administration & dosage , Interleukin-1beta/metabolism , Receptors, Interleukin-1/metabolism , Animals , Encephalitis/metabolism , Locomotion/drug effects , Male , Mice , Mice, Inbred C57BL , RNA, Messenger/metabolism , Receptors, Interleukin-1/antagonists & inhibitors , Signal Transduction/drug effects
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