Articles: traumatic-brain-injuries.
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Animal models of traumatic brain injury (TBI) are essential for testing novel hypotheses and therapeutic interventions. Unfortunately, due to the broad heterogeneity of TBI in humans, no single model has been able to reproduce the entire spectrum of these injuries. The controlled cortical impact (CCI) model is one of the most commonly used models of contusion TBI. ⋯ Furthermore, adhesive removal test showed significant somatosensory and motor deficits only in the S-CCI groups. Histological analysis showed a large extent of cortical contusion lesions, including both the sensory and motor cortex, and hippocampal damage in the S-CCI. These findings collectively suggest that the current model may offer sensitive, reliable, and clinically relevant outcomes for assessments of therapeutic strategies for TBI.
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Neuroscience letters · Aug 2014
Neuroglobin overexpression improves sensorimotor outcomes in a mouse model of traumatic brain injury.
There is a significant need for novel treatments that will improve traumatic brain injury (TBI) outcomes. One potential neuroprotective mechanism is to increase oxygen binding proteins such as neuroglobin. Neuroglobin has a high affinity for oxygen, is an effective free radical scavenger, and is neuroprotective within the brain following hypoxia and ischemia. ⋯ Immunostaining showed neuroglobin primarily localized to neurons and glial cells in the injured cortex and ipsilateral hippocampus of WT mice, while neuroglobin was present in all brain regions of NGB mice at 7 days post-TBI. These results showed that overexpression of neuroglobin reduced sensorimotor deficits following TBI, and that an endogenous increase in neuroglobin expression occurs during the subacute period. Increasing neuroglobin expression through novel therapeutic interventions during the acute period after TBI may improve recovery.
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Experimental neurology · Aug 2014
Review Comparative StudyIs neuroinflammation in the injured spinal cord different than in the brain? Examining intrinsic differences between the brain and spinal cord.
The field of neuroimmunology is rapidly advancing. There is a growing appreciation for heterogeneity, both in inflammatory composition and region-specific inflammatory responses. This understanding underscores the importance of developing targeted immunomodulatory therapies for treating neurological disorders. ⋯ The question therefore remains as to whether inflammatory cells responding to spinal cord vs. brain injury adopt similar functions and are therefore amenable to common therapies. In this review, we address this question while revisiting and modernizing the conclusions from publications that have directly compared inflammation across brain and spinal cord injuries. By examining molecular differences, anatomical variations, and inflammatory cell phenotypes between the injured brain and spinal cord, we provide insight into how neuroinflammation relates to neurotrauma and into fundamental differences between the brain and spinal cord.
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Clin Neurol Neurosurg · Aug 2014
ReviewChemoprophylaxis for venous thromboembolism in traumatic brain injury: a review and evidence-based protocol.
Venous thromboembolism (VTE) is a recognized source of morbidity and mortality in patients suffering traumatic brain injury (TBI). While traumatic brain injury is a recognized risk factor for the development of VTE, its presence complicates the decision to begin anticoagulation due to fear of exacerbating the intracranial hemorrhagic injury. ⋯ The review reveals robust evidence regarding the safety and efficacy of chemoprophylaxis in the setting of TBI following demonstration of a stable intracranial injury. In light of this data, a protocol is assembled that, in the absence of predetermined exclusion criteria, will initiate chemoprophylaxis within 24h after the demonstration of a stable intracranial injury by computed tomography (CT).
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Clinical Trial Observational Study
Prognostic value of neuropeptide proenkephalin A in patients with severe traumatic brain injury.
High plasma proenkephalin A levels have been associated with poor clinical outcome of aneurysmal subarachnoid hemorrhage. This prospective observatory study was designed to investigate the relationship between plasma proenkephalin A levels and 1-week mortality, 6-month mortality and 6-month unfavorable outcome (defined as Glasgow Outcome Scale score of 1-3) in patients with severe traumatic brain injury. This study recruited 128 patients and 128 sex- and age-matched healthy controls. ⋯ Furthermore, its predictive value was similar to Glasgow Coma Scale score's (all P>0.05). Yet, a combined logistic-regression model did not show that it statistically significantly improved the predictive value of Glasgow Coma Scale score (all P>0.05). Thus, it was proposed that enhanced plasma proenkephalin A could be a useful, complementary tool to predict short- or long-term clinical outcome after severe traumatic brain injury.