Journal of neurotrauma
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Journal of neurotrauma · Sep 2013
Dose- and Time-Dependent Neuroprotective Effects of Pycnogenol(®) following Traumatic Brain Injury.
After traumatic brain injury (TBI), both primary and secondary injury cascades are initiated, leading to neuronal death and cognitive dysfunction. We have previously shown that the combinational bioflavonoid, Pycnogenol (PYC), alters some secondary injury cascades and protects synaptic proteins when administered immediately following trauma. The purpose of the present study was to explore further the beneficial effects of PYC and to test whether it can be used in a more clinically relevant fashion. ⋯ PYC treatment significantly protected both the cortex and hippocampus from injury-related declines in pre- and post-synaptic proteins. These results demonstrate that a single i.v. treatment of PYC is neuroprotective after TBI with a therapeutic window of at least 4 h post trauma. The natural bioflavonoid PYC may provide a possible therapeutic intervention in neurotrauma.
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Journal of neurotrauma · Sep 2013
Why Is CA3 More Vulnerable Than CA1 in Experimental Models of Controlled Cortical Impact-Induced Brain Injury?
One interesting finding of controlled cortical impact (CCI) experiments is that the CA3 region of the hippocampus, which is positioned further from the impact than the CA1 region, is reported as being more injured. The current literature has suggested a positive correlation between brain tissue stretch and neuronal cell loss. However, it is counterintuitive to assume that CA3 is stretched more during CCI injury. ⋯ Simulation results demonstrated that for CCI with a 5-mm diameter, flat shape impactor, CA3 experienced increased tensile strains over a larger area and to a greater magnitude than did CA1 for group 1, which best explained why CA3 is more sensitive to CCI injury. However, for groups 2-4, the total volume with high strain (>30%) in CA3 was smaller than that in CA1. The FE rat brain model, with detailed hippocampal structures presented here, will help to engineer desired experimental neurotrauma models by virtually characterizing brain biomechanics before testing.
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Aquaporin-4 (AQP4) is an astroglial water channel protein that plays an important role in the transmembrane movement of water within the central nervous system. AQP4 has been implicated in numerous pathological conditions involving abnormal fluid accumulation, including spinal cord edema following traumatic injury. AQP4 has not been studied in post-traumatic syringomyelia, a condition that cannot be completely explained by current theories of cerebrospinal fluid dynamics. ⋯ Immunostaining showed that AQP4 was expressed around all syrinx cavities, most notably adjacent to a mature syrinx (six- and 12-week time-point). This suggests a relationship between AQP4 and fluid accumulation in post-traumatic syringomyelia. However, whether this is a causal relationship or occurs in response to an increase in fluid needs to be established.
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Journal of neurotrauma · Aug 2013
Influence of combat blast-related mild traumatic brain injury acute symptoms on mental health and service discharge outcomes.
Assessment of acute mild traumatic brain injury (mTBI) symptoms after a combat blast could aid diagnosis and guide follow-up care. Our objective was to document acute mTBI symptoms following a combat blast and to examine associations between acute symptoms and mental health and service discharge outcomes. A retrospective cohort study was conducted with 1656 service personnel who experienced a combat blast-related mTBI in Iraq. ⋯ While no acute mTBI symptoms were associated with discharge outcomes, injury severity was associated with disability discharge. LOC after blast-related mTBI was associated with PTSD and PCS, and injury severity was predictive of disability discharge. The assessment of cognitive status immediately after a blast could assist in diagnosing mTBI and indicate a need for follow-up care.
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Journal of neurotrauma · Aug 2013
Arginine vasopressin V1a receptor-deficient mice have reduced brain edema and secondary brain damage following traumatic brain injury.
The formation of brain edema and subsequent intracranial hypertension are major predictors of unfavorable outcome following traumatic brain injury (TBI). Previously, we reported that arginine vasopressin (AVP) receptor antagonists reduce post-traumatic and post-ischemic brain edema in mice. The aim of the current study was to investigate further the contribution of arginine vasopressin V1a receptors to TBI-induced secondary brain damage in V1a receptor knock-out mice. ⋯ Furthermore, the V1a receptor knock-out mice had less neurological dysfunction (3.2±0.8 vs. 7.0±1.4 in wild-type mice) and weight loss (1.0±1.0% vs. 4.9±1.8% in wild-type mice) seven days after CCI. Our data show that mice lacking V1a receptors have less secondary brain damage following experimental traumatic brain injury. We therefore conclude that V1a receptors may represent a novel drug target for preventing post-traumatic brain edema.