Journal of neurotrauma
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Journal of neurotrauma · Nov 2012
Multivariate outcome prediction in traumatic brain injury with focus on laboratory values.
Traumatic brain injury (TBI) is a major cause of morbidity and mortality. Identifying factors relevant to outcome can provide a better understanding of TBI pathophysiology, in addition to aiding prognostication. Many common laboratory variables have been related to outcome but may not be independent predictors in a multivariate setting. ⋯ A worse outcome related to increasing osmolarity may warrant further study. Importantly, hemoglobin was not found significant when adjusted for post-resuscitation GCS as opposed to an admission GCS, and timing of GCS can thus have a major impact on conclusions. In total, laboratory variables added an additional 1.3-4.4% to pseudo R².
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Journal of neurotrauma · Nov 2012
Deficits in social behavior emerge during development after pediatric traumatic brain injury in mice.
The pediatric brain may be particularly vulnerable to social deficits after traumatic brain injury (TBI) due to the protracted nature of psychosocial development through adolescence. However, the majority of pre-clinical studies fail to assess social outcomes in experimental pediatric TBI. The current study evaluated social behavior in mice subjected to TBI at post-natal day (p)21. ⋯ Together these findings reveal reduced social interaction and a tendency towards increased aggression, which evolves across development to adulthood. This emergence of aberrant social behavior, which parallels the development of other cognitive deficits in this model and behaviors seen in brain-injured children, is consistent with the hypothesis that the full extent of deficits is not realized until the associated skills reach maturity. Thus, efficacy of therapeutics for pediatric TBI should take into account the time-dependent emergence of abnormal behavioral patterns.
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Journal of neurotrauma · Nov 2012
Cerebellar gene expression following human traumatic brain injury.
Gene expression of specific brain biomarkers offers the possibility of shedding light on the difficult molecular pathways of traumatic brain injury (TBI) and may be useful to estimate the age of trauma. Gene expression rates of cerebellar injuries are not yet sufficiently established. In 12 cases (mean age 42 years) of TBI including a pathological change in cerebellum (with known survival times ranging from immediate death to 96 h), brain tissue samples from different brain regions were analyzed with real-time polymerase chain reaction (PCR) for expression of caspase-3, tyrosine kinase receptor B (TrkB), S100B, and glial fibrillary acidic protein (GFAP) mRNA. ⋯ For short survival times, the expression changes of caspase-3 (p<0.05) and the expression changes of TrkB (p<0.1) in the cerebellum show a significant increase compared to the controls. The cerebellar gene expression changes seem to occur much faster and stronger compared to the other investigated regions, in particular the cerebral trauma site. These findings could make the cerebellum an important target area to study the expression changes after TBI.
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Journal of neurotrauma · Nov 2012
Functional and histological outcome after focal traumatic brain injury is not improved in conditional EphA4 knockout mice.
We investigated the role of the axon guidance molecule EphA4 following traumatic brain injury (TBI) in mice. Neutralization of EphA4 improved motor function and axonal regeneration following experimental spinal cord injury (SCI). We hypothesized that genetic absence of EphA4 could improve functional and histological outcome following TBI. ⋯ TBI increased cortical and hippocampal astrocytosis (GFAP immunohistochemistry, p<0.05) and hippocampal sprouting (Timm stain, p<0.05) and induced a marked loss of hemispheric tissue (p<0.05). EphA4 cKO did not alter the histological outcome. Although our results may argue against a beneficial role for EphA4 in the recovery process following TBI, further studies including post-injury pharmacological neutralization of EphA4 are needed to define the role for EphA4 following TBI.
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Journal of neurotrauma · Nov 2012
A relatively brief exposure to environmental enrichment after experimental traumatic brain injury confers long-term cognitive benefits.
It is well established that a relatively brief exposure to environmental enrichment (EE) enhances motor and cognitive performance after experimental traumatic brain injury (TBI), but it is not known whether the benefits can be sustained after EE is discontinued. To address this important rehabilitation-relevant concern, anesthetized rats received a controlled cortical impact (CCI) or sham injury, and for phase 1 of the experiment were randomly assigned to either 3 weeks of EE or standard (STD) housing. Neurobehavioral outcome was assessed by established motor and cognitive tests on postoperative days 1-5 and 14-18, respectively. ⋯ The TBI + EE and TBI + EE + STD groups performed markedly better in the water maze than the TBI + STD group (p<0.0001), and did not differ from one another (p=0.53). These data replicate those of several studies from our laboratory showing that EE enhances recovery after CCI injury, and extend those findings by demonstrating that the cognitive benefits are maintained for at least 6 months post-rehabilitation. The persistent benefits shown with this paradigm provide further support for EE as a pre-clinical model of rehabilitation that can be further explored, either alone or in combination with pharmacotherapies, for optimal neurorehabilitation after TBI.