Journal of neurotrauma
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Journal of neurotrauma · Nov 2016
ReviewPrevalence and risk factors of anxiety and depressive disorders following traumatic brain injury: a systematic review.
This review examined pre- and post-injury prevalence of, and risk factors for, anxiety disorders and depressive disorders after traumatic brain injury (TBI), based on evidence from structured diagnostic interviews. A systematic literature search was conducted in EMBASE, MEDLINE, Cochrane Central, PubMed, PsycINFO, and Google Scholar. We identified studies in civilian adults with TBI reporting on the prevalence of anxiety and depressive disorders using structured diagnostic interviews and assessed their quality. ⋯ Females, those without employment, and those with a psychiatric history before TBI were at higher risk for anxiety and depressive disorders after TBI. We conclude that a substantial number of patients encounter anxiety and depressive disorders after TBI, and that these problems persist over time. All health care settings should pay attention to the occurrence of psychiatric symptoms in the aftermath of TBI to enable early identification and treatment of these disorders and to enhance the recovery and quality of life of TBI survivors.
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Journal of neurotrauma · Nov 2016
Multicenter StudyClinical results and outcome improvement over time in traumatic brain injury.
Prognostic models for traumatic brain injury (TBI) are important tools both in clinical practice and research if properly validated, preferably by external validation. Prognostic models also offer the possibility of monitoring performance by comparing predicted outcomes with observed outcomes. In this study, we applied the prognostic models developed by the International Mission on Prognosis and Analysis of Clinical Trials in TBI (IMPACT) in an Italian multi-center database (Neurolink) with two aims: to compare observed with predicted outcomes and to check for a possible improvement of clinical outcome over the 11 years of patient inclusion in Neurolink. ⋯ Outcomes significantly improved over time. This study shows that the IMPACT models performed reasonably well in the Neurolink data and can be used for monitoring performance. After adjustment for predicted outcomes with the prognostic models, we observed a substantial improvement of patient outcomes over time in the three Neurolink centers.
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Journal of neurotrauma · Nov 2016
Post-injury treatment of 7,8-dihydroxyflavone promotes neurogenesis in the hippocampus of the adult mouse.
Traumatic brain injury (TBI) at the moderate level of impact induces massive cell death and results in extensive dendrite degeneration in the brain, leading to persistent cognitive, sensory, and motor dysfunction. Our previous reports have shown that adult-born immature granular neurons in the dentate gyrus are the most vulnerable cell type in the hippocampus after receiving a moderate TBI with a controlled cortical impact (CCI) device. There is no effective approach to prevent immature neuron death or degeneration following TBI. ⋯ In the present study, we systemically treated moderate CCI-TBI mice or sham surgery mice with DHF once a day for 2 weeks via intraperitoneal injection, and then assessed the immature neurons in the hippocampus the 2nd day after the last DHF injection. We found that post-injury treatment of DHF for 2 weeks not only increased the number of adult-born immature neurons in the hippocampus, but also promoted their dendrite arborization in the injured brain following TBI. Thus, DHF may be a promising compound that can promote neurogenesis and enhance immature neuron development following TBI.
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Journal of neurotrauma · Nov 2016
Glucose-dependent insulinotropic polypeptide ameliorates mild traumatic brain injury-induced cognitive and sensorimotor deficits and neuroinflammation in rats.
Mild traumatic brain injury (mTBI) is a major public health issue, representing 75-90% of all cases of TBI. In clinical settings, mTBI, which is defined as a Glascow Coma Scale (GCS) score of 13-15, can lead to various physical, cognitive, emotional, and psychological-related symptoms. To date, there are no pharmaceutical-based therapies to manage the development of the pathological deficits associated with mTBI. ⋯ GIP was well tolerated and ameliorated mTBI-induced memory impairments, poor balance, and sensorimotor deficits after initiation in the post-injury period. In addition, GIP mitigated mTBI-induced neuroinflammatory changes on GFAP, APP, and BMX protein levels. These findings suggest GIP has significant benefits in managing mTBI-related symptoms and represents a novel strategy for mTBI treatment.
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Journal of neurotrauma · Nov 2016
Observational StudyCerebrovascular signal complexity six hours after ICU admission correlates with outcome following severe traumatic brain injury.
Disease states are associated with a breakdown in healthy interactions and are often characterized by reduced signal complexity. We applied approximate entropy (ApEn) analysis to investigate the correlation between the complexity of heart rate (ApEn-HR), mean arterial pressure (ApEn-MAP), intracranial pressure (ApEn-ICP), and a combined ApEn-product (product of the three individual ApEns) and outcome after traumatic brain injury. In 174 severe traumatic brain injured patients, we found significant differences across groups classified by the Glasgow Outcome Score in ApEn-HR (p = 0.007), ApEn-MAP (p = 0.02), ApEn-ICP (p = 0.01), ApEn-product (p = 0.001), and pressure reactivity index (PRx) (p = 0.004) in the first 6 h. ⋯ Patients in the lowest quartile for ApEn-product were over four times more likely to die (39.5% vs. 9.3%, p < 0.001) than those in the highest quartile. ApEn-ICP was inversely correlated with PRx (r = -0.39, p < 0.000001) indicating unique information related to impaired cerebral autoregulation. Our results demonstrate that as early as 6 h into monitoring, complexity measures from easily attainable vital signs, such as HR and MAP, in addition to ICP, can help triage those who require more intensive neurological management at an early stage.