Journal of neurotrauma
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Journal of neurotrauma · Mar 2015
Intraventricular Hemorrhage on Initial Computed Tomography as Marker of Diffuse Axonal Injury after Traumatic Brain Injury.
Intraventricular hemorrhage (IVH) on initial computed tomography (CT) was reported to predict lesions of diffuse axonal injury (DAI) in the corpus callosum (CC) on subsequent magnetic resonance imaging (MRI). We aimed to examine the relationship between initial CT findings and DAI lesions detected on MRI as well as the relationship between the severity of IVH (IVH score) and severity of DAI (DAI staging). A consecutive 140 patients with traumatic brain injury (TBI) who underwent MRI within 30 days after onset were revisited. ⋯ The IVH score and DAI staging showed significant positive correlation (p<0.0003). IVH score in DAI stage 3 (with DAI involving the brain stem; p=0.0025) or stage 2 (with DAI involving CC; p=0.0042) was significantly higher than that of DAI stage 0 (no DAI lesions). In conclusion, IVH on initial CT is the only marker of DAI on subsequent MRI, specifically severe DAI (stage 2 or 3).
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Journal of neurotrauma · Mar 2015
A Novel, Ultrasensitive Assay for Tau: Potential for Assessing Traumatic Brain Injury in Tissues and Biofluids.
Traumatic brain injury (TBI) is a cause of death and disability and can lead to tauopathy-related dementia at an early age. Pathologically, TBI results in axonal injury that is coupled to tau hyperphosphorylation, leading to microtubule instability and tau-mediated neurodegeneration. This suggests that the forms of this protein might serve as neuroinjury-related biomarkers for diagnosis of injury severity and prognosis of the neurological damage prior to clinical expression. ⋯ In human CSF samples, T-tau and P-tau increased during the sampling period (5-6 d). T-tau and P-tau in human serum rose during the acute phase and decreased during the chronic stage but was still detectable beyond six months post sTBI. Thus, EIMAF has the potential for assessing both the severity of the proximal injury and the prognosis using easily accessible samples.
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Journal of neurotrauma · Feb 2015
Chronology and chronicity of altered resting-state functional connectivity after traumatic brain injury.
Whereas traumatic brain injury (TBI) results in widespread disruption of neural networks, changes in regional resting-state functional connectivity patterns after insult remain unclear. Specifically, little is known about the chronology of emergent connectivity alterations and whether they persist after a critical recovery window. We used resting-state functional magnetic resonance imaging and seed-voxel correlational analyses in both cross-sectional and longitudinal designs to probe intrinsic connectivity patterns involving the posterior cingulate cortex (PCC) and hippocampi, regions shown to be important in the default mode network (DMN) and vulnerable to neuropathology. ⋯ Antiphase synchrony of the hippocampus and dorsolateral prefrontal cortex at the subacute stage of TBI was positively associated with attentional performance on neuropsychological tests at both the subacute and chronic stages. Our findings highlight the heterogeneity of regional whole-brain connectivity changes after TBI, and suggest that residual connectivity alterations exist in the clinically stable phase of TBI. Parallels between the chronicity of the observed effects and findings in neurodegenerative disease are discussed in the context of potential long-term outcomes of TBI.
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Journal of neurotrauma · Feb 2015
ReviewAging, neurodegenerative disease and traumatic brain injury: the role of neuroimaging.
Traumatic brain injury (TBI) is a highly prevalent condition with significant effects on cognition and behavior. While the acute and sub-acute effects of TBI recover over time, relatively little is known about the long-term effects of TBI in relation to neurodegenerative disease. ⋯ We also review the evidence for neuroimaging changes associated with unhealthy brain aging in the context of remote TBI. We conclude that neuroimaging biomarkers have significant potential to increase understanding of the mechanisms of unhealthy brain aging and neurodegeneration following TBI, with potential for identifying those at risk for unhealthy brain aging prior to the clinical manifestation of neurodegenerative disease.
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Journal of neurotrauma · Feb 2015
Effect of small molecule vasopressin V1a and V2 receptor antagonists on brain edema formation and secondary brain damage following traumatic brain injury in mice.
The attenuation of brain edema is a major therapeutic target after traumatic brain injury (TBI). Vasopressin (AVP) is well known to play a major role in the regulation of brain water content and vasoendothelial functions and to be involved in brain edema formation. Therefore, the aim of the current study was to analyze the antiedematous efficacy of a clinically relevant, nonpeptidic AVP V1a and V2 receptor antagonists. ⋯ In contrast, ICV administration of AVP V1a receptor antagonist decreased brain edema formation by 68%, diminished post-traumatic increase of ICP by 46%, and reduced secondary contusion expansion by 43% 24 h after CCI. The ICV inhibition of V2 receptors resulted in significant reduction of post-traumatic brain edema by 41% 24 h after CCI, but failed to show further influence on ICP and lesion growth. Hence, centrally applied vasopressin V1a receptor antagonists may be used to reduce brain edema formation after TBI.