Journal of neurotrauma
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Journal of neurotrauma · Jan 2017
Review Meta AnalysisSystematic review and meta-analysis: Is pre-injury antiplatelet therapy associated with traumatic intracranial hemorrhage?
The objective of this systematic review and meta-analysis is to evaluate whether the pre-injury use of antiplatelet therapy (APT) is associated with increased risk of traumatic intracranial hemorrhage (tICH) on CT scan. PubMed, Medline, Embase, Cochrane Central, reference lists, and national guidelines on traumatic brain injury were used as data sources. Eligible studies were cohort studies and case-control studies that assessed the relationship between APT and tICH. ⋯ The results were robust to sensitivity analysis on study quality. In summary, APT in patients with head injury is associated with increased risk of tICH; this association is most relevant in patients with mTBI. Whether this association is the result of a causal relationship and whether this relationship also exists for patients receiving aspirin monotherapy cannot be established with the current review and meta-analysis.
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Journal of neurotrauma · Jan 2017
Brain volume, connectivity and neuropsychological performance in mild traumatic brain injury: the impact of post-traumatic stress disorder symptoms.
Post-traumatic stress disorder (PTSD) is commonly associated with mild traumatic brain injury (mTBI). To better understand their relationship, we examined neuroanatomical structures and neuropsychological performance in a sample of individuals with mTBI, with and without PTSD symptoms. Thirty-nine subjects with mTBI were dichotomized into those with (n = 12) and without (n = 27) significant PTSD symptoms based on scores on the PTSD Checklist. ⋯ Increased volume and white matter disruptions in these areas, commonly associated with memory functions, may be related to functional disturbances during cognitively demanding tasks. Differences in brain volume and white matter integrity between mTBI subjects and those with mTBI and co-morbid PTSD symptoms point to neuroanatomical differences that may underlie poorer recovery of mTBI subjects who experience PTSD symptoms. These findings support theoretical models of PTSD and its relationship to learning deficits.
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Journal of neurotrauma · Jan 2017
TBI induces alterations in cortical glutamate uptake without a reduction in GLT-1 protein expression.
We hypothesize that the primary mechanism for removal of glutamate from the extracellular space is altered after traumatic brain injury (TBI). To evaluate this hypothesis, we initiated TBI in adult male rats using a 2.0 atm lateral fluid percussion injury (LFPI) model. In the ipsilateral cortex and hippocampus, we found no differences in expression of the primary glutamate transporter in the brain (GLT-1) 24 h after TBI. ⋯ Exploratory studies using an inhibitor of Akt suggest selective activation of kinases in LFPI versus controls. Ingenuity pathway analyses of implicated kinases from our network model found apoptosis and cell death pathways as top functions in acute LFPI. Taken together, our data suggest diminished activity of glutamate transporters in the prefrontal cortex, with no changes in protein expression of the primary glutamate transporter GLT-1, and global alterations in signaling networks that include serine-threonine kinases that are known modulators of glutamate transport activity.
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Journal of neurotrauma · Jan 2017
Early and Persistent Dendritic Hypertrophy in the Basolateral Amygdala Following Experimental Diffuse Traumatic Brain Injury.
In the pathophysiology of traumatic brain injury (TBI), the amygdala remains understudied, despite involvement in processing emotional and stressful stimuli associated with anxiety disorders, such as post-traumatic stress disorder (PTSD). Because the basolateral amygdala (BLA) integrates inputs from sensory and other limbic structures coordinating emotional learning and memory, injury-induced changes in circuitry may contribute to psychiatric sequelae of TBI. This study quantified temporal changes in dendritic complexity of BLA neurons after experimental diffuse TBI, modeled by midline fluid percussion injury. ⋯ However, the BLA was relatively spared from neuropathology, demonstrated by an absence of argyrophilic accumulation over time, in contrast to other brain regions. These data suggest an early and persistent enhancement of dendritic complexity within the BLA after a single diffuse TBI. Increased dendritic complexity would alter information processing into and through the amygdala, contributing to emotional symptoms post-TBI, including PTSD.
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Journal of neurotrauma · Jan 2017
Adolescent Traumatic Brain Injury Induces Chronic Mesolimbic Neuroinflammation with Concurrent Enhancement in the Rewarding Effects of Cocaine in Mice during Adulthood.
Clinical psychiatric disorders of depression, anxiety, and substance abuse are most prevalent after traumatic brain injury (TBI). Pre-clinical research has focused on depression and anxiety post-injury; however, virtually no data exist examining whether the preference for illicit drugs is affected by traumatic injury in the developing adolescent brain. Using the controlled cortical impact (CCI) model of TBI and the conditioned place preference (CPP) assay, we tested the underlying hypothesis that brain injury during adolescence exacerbates the rewarding properties of cocaine in adulthood possibly through an active inflammatory status in the mesolimbic pathway. ⋯ Significant increases in both astrocytic, glial fibrillary acidic protein, and microglial, ionization basic acid 1, markers were observed in the NAc at the end of CPP testing. Moreover, analysis using focused array gene expression panels identified the upregulation of numerous inflammatory genes in moderate CCI-TBI animals, compared to naïve controls, both in the cortex and NAc at 2 weeks post-TBI, before onset of cocaine administration. These results suggest that sustaining moderate TBI during adolescence may augment the rewarding effects of psychostimulants in adulthood, possibly by induction of chronic mesolimbic neuroinflammation.