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 StudySerum tau fragments predict return to play in concussed professional ice hockey players.
The diagnosis of sports-related concussion is mainly based on subjective clinical symptoms and neuropsychological tests. Therefore, reliable brain injury biomarkers to assess when it is safe to return to play are highly desirable. The overall objective of this study was to evaluate the utility of two newly described tau fragments for diagnosis and prognosis of sports-related concussions. ⋯ However, serum levels of Tau-C were significantly higher in post-concussion samples compared with preseason. Further, levels of Tau-A correlated with the duration of post-concussive symptoms. Tau-A in serum, which is newly discovered biomarker, could be used to predict when it is safe to return to play after a sports-related concussion.
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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
ER stress and disrupted neurogenesis in the brain are associated with cognitive impairment and depressive-like behavior after spinal cord injury.
Clinical and experimental studies show that spinal cord injury (SCI) can cause cognitive impairment and depression that can significantly impact outcomes. Thus, identifying mechanisms responsible for these less well-examined, important SCI consequences may provide targets for more effective therapeutic intervention. To determine whether cognitive and depressive-like changes correlate with injury severity, we exposed mice to sham, mild, moderate, or severe SCI using the Infinite Horizon Spinal Cord Impactor and evaluated performance on a variety of neurobehavioral tests that are less dependent on locomotion. ⋯ The potent microglial activator cysteine-cysteine chemokine ligand 21 (CCL21) was elevated in the brain sites after SCI in association with increased microglial activation. These findings indicate that SCI causes chronic neuroinflammation that contributes to neuronal loss, impaired hippocampal neurogenesis and increased neuronal ER stress in important brain regions associated with cognitive decline and physiological depression. Accumulation of CCL21 in brain may subserve a pathophysiological role in cognitive changes and depression after SCI.