Journal of neurotrauma
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The high rates of traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD) diagnoses encountered in recent years by the United States Veterans Affairs Healthcare System have increased public awareness and research investigation into these conditions. In this review, we analyze the neural mechanisms underlying the TBI/PTSD comorbidity. TBI and PTSD present with common neuropsychiatric symptoms including anxiety, irritability, insomnia, personality changes, and memory problems, and this overlap complicates diagnostic differentiation. ⋯ These disturbances produce neuronal death and degeneration, axonal injury, and dendritic spine dysregulation and changes in neuronal morphology. In laboratory studies, various forms of pharmacological or psychological treatments are capable of reversing these detrimental processes and promoting axonal repair, dendritic remodeling, and neurocircuitry reorganization, resulting in behavioral and cognitive functional enhancements. Based on these mechanisms, novel neurorestorative therapeutics using anti-inflammatory, antioxidant, and anticonvulsant agents may promote better outcomes for comorbid TBI and PTSD.
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Journal of neurotrauma · Jan 2018
ReviewMedusa's Head: The Complement System in Traumatic Brain and Spinal Cord Injury.
Traumatic brain injury (TBI) and spinal cord injury (SCI) are critical medical conditions and a public health problem for which limited therapeutic options are available. The complement cascade is activated after TBI and SCI, and the resulting effects have been investigated in gene-knockout and pharmacological models. ⋯ The role of upstream classical, alternative, or extrinsic complement activation cascades remains unclear. Although several issues remain to be investigated, current evidence supports the investigation of a number of complement-targeting agents targeting C3 or C5, such as eculizumab, for repurposing in TBI and SCI treatment.
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Journal of neurotrauma · Jan 2018
A systematic review of psychological interventions for sleep and fatigue after mild traumatic brain injury.
This review evaluated the evidence for psychological interventions to improve sleep and reduce fatigue after mild traumatic brain injury (mTBI). Eight electronic databases were searched up until August 2016 for studies that: 1) included adults; 2) tested intervention effectiveness on sleep quality and fatigue post-acutely; and 3) applied a broadly-defined psychological intervention (e.g., cognitive behavioral therapy [CBT], counseling, or education). Only randomized controlled trials were eligible for inclusion. ⋯ All but one study targeted general post-concussion symptoms rather than sleep or fatigue specifically. This runs the risk that the potential benefits of a targeted approach are underestimated in this literature, and future sleep- and fatigue-focused interventions are recommended. It is tentatively concluded that compared with standard care or the provision of generic advice, small improvements in sleep and fatigue are observed through psychological intervention post-mTBI.
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Journal of neurotrauma · Jan 2018
Effects of mild blast traumatic brain injury on cerebral vascular, histopathological and behavioral outcomes in rats.
To determine the effects of mild blast-induced traumatic brain injury (bTBI), several groups of rats were subjected to blast injury or sham injury in a compressed air-driven shock tube. The effects of bTBI on relative cerebral perfusion (laser Doppler flowmetry [LDF]), and mean arterial blood pressure (MAP) cerebral vascular resistance were measured for 2 h post-bTBI. Dilator responses to reduced intravascular pressure were measured in isolated middle cerebral arterial (MCA) segments, ex vivo, 30 and 60 min post-bTBI. ⋯ Because impact TBI (i.e., non-blast TBI) is often associated with reduced cerebral perfusion and impaired cerebrovascular function in part because of the generation of reactive oxygen and nitrogen species such as peroxynitrite (ONOO-), the effects of the administration of the ONOO- scavenger, penicillamine methyl ester (PenME), on cerebral perfusion and cerebral vascular resistance were measured for 2 h post-bTBI. Mild bTBI resulted in reduced relative cerebral perfusion and MCA dilator responses to reduced intravascular pressure, increases in cerebral vascular resistance and in the numbers of FJC-positive cells in the brain, and significantly impaired working memory. PenME administration resulted in significant reductions in cerebral vascular resistance and a trend toward increased cerebral perfusion, suggesting that ONOO- may contribute to blast-induced cerebral vascular dysfunction.
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Journal of neurotrauma · Jan 2018
Cerebral Blood Flow after Mild Traumatic Brain Injury: Associations between Symptoms and Post-Injury Perfusion.
Arterial spin labeling (ASL) has emerged as a technique for assessing mild traumatic brain injury (mTBI), as it can noninvasively evaluate cerebrovascular physiology. To date, there is substantial variability in methodology and findings of ASL studies of mTBI. While both increased and decreased perfusion are reported after mTBI, more consistency is emerging when perfusion is examined with regard to symptomology. ⋯ Perfusion in the left dorsal ACC was higher in athletes reporting physical symptoms six weeks post-injury compared with asymptomatic athletes and controls. Overall, these findings are inconsistent with reports of reduced rCBF after mTBI but coherent with studies that report increased perfusion in persons with greater or persistent mTBI-related symptomology. Future work should continue to assess how CBF perfusion relates to symptomology and recovery after mTBI.