Journal of neurotrauma
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Journal of neurotrauma · Aug 2014
ReviewALTERATION IN SYNAPTIC JUNCTION PROTEINS FOLLOWING TRAUMATIC BRAIN INJURY.
Extensive research and scientific efforts have been focused on the elucidation of the pathobiology of cellular and axonal damage following traumatic brain injury (TBI). Conversely, few studies have specifically addressed the issue of synaptic dysfunction. ⋯ A Synapse Protein Database on synapse ontology identified 109 domains implicated in synaptic activities and over 5000 proteins, but few of these demonstrated to play a role in the synaptic dysfunction after TBI. These proteins are involved in neuroplasticity and neuromodulation and, most importantly, may be used as novel neuronal markers of TBI for specific intervention.
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Journal of neurotrauma · Aug 2014
Subtypes of Post-Traumatic Epilepsy: Clinical, Electrophysiologic, and Imaging Features.
Post-traumatic epilepsy (PTE) is a consequence of traumatic brain injury (TBI), occurring in 10-25% of patients with moderate to severe injuries. The development of animal models for testing antiepileptogenic therapies and validation of biomarkers to follow epileptogenesis in humans necessitates sophisticated understanding of the subtypes of PTE, which is the objective of this study. In this study, retrospective review was performed of patients with moderate to severe TBI with subsequent development of medically refractory epilepsy referred for video-electroencephalography (EEG) monitoring at a single center over a 10-year period. ⋯ At a mean follow-up of 2.5 years, Engel Class I outcomes were seen in 69% of those with TLE and 33% of those with FLE. Our findings suggest PTE is a heterogeneous condition, and careful evaluation with video-EEG monitoring and high resolution MRI can identify distinct syndromes. These results have implications for the design of clinical trials of antiepileptogenic therapies for PTE.
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Journal of neurotrauma · Aug 2014
Therapeutic Effects of Pharmacologically induced Hypothermia against Traumatic Brain Injury in Mice.
Preclinical and clinical studies have shown therapeutic potential of mild-to-moderate hypothermia for treatments of stroke and traumatic brain injury (TBI). Physical cooling in humans, however, is usually slow, cumbersome, and necessitates sedation that prevents early application in clinical settings and causes several side effects. Our recent study showed that pharmacologically induced hypothermia (PIH) using a novel neurotensin receptor 1 (NTR1) agonist, HPI-201 (also known as ABS-201), is efficient and effective in inducing therapeutic hypothermia and protecting the brain from ischemic and hemorrhagic stroke in mice. ⋯ HPI-363 decreased the mRNA expression of tumor necrosis factor-α and interleukin-1β (IL-1β), but increased IL-6 and IL-10 levels. Compared with TBI control mice, HPI-363 treatments improved sensorimotor functional recovery after TBI. These findings suggest that the second generation NTR-1 agonists, such as HPI-363, are efficient hypothermic-inducing compounds that have a strong potential in the management of TBI.
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Journal of neurotrauma · Aug 2014
Risk factors for posttraumatic massive cerebral infarction secondary to space-occupying epidural haematoma.
Post-traumatic massive cerebral infarction (MCI) is a fatal complication of concurrent epidural hematoma (EDH) and brain herniation that commonly requires an aggressive decompressive craniectomy. The risk factors and surgical indications of MCI have not been fully elucidated. In this retrospective study, post-traumatic MCI was diagnosed in 32 of 176 patients. ⋯ Incidence of post-traumatic MCI increased from 16.4% in those having any two of the six risk factors to 47.7% in those having any three or more of the six risk factors (p<0.001). Patients with concurrent EDH and brain herniation exhibited an increased risk for post-traumatic MCI with the accumulation of several critical clinical factors. Early decompressive craniectomy based on accurate risk estimation is recommended in efforts to improve patient functional outcomes.
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Journal of neurotrauma · Aug 2014
Neurotherapeutic Effect of Cord Blood Derived CD45+ Hematopoietic Cells in Mice after Traumatic Brain Injury.
Treatment of traumatic brain injury (TBI) is still an unmet need. Cell therapy by human umbilical cord blood (HUCB) has shown promising results in animal models of TBI and is under evaluation in clinical trials. HUCB contains different cell populations but to date, only mesenchymal stem cells have been evaluated for therapy of TBI. ⋯ At the site of brain injury, 1.5-2 h after transplantation, HUCB-derived cells were identified by near infrared scanning and immunohistochemistry using anti-human-CD45 and anti-human-nuclei antibodies. Nerve growth factor and vascular endothelial growth factor levels were differentially expressed in both ipsilateral and contralateral brain hemispheres, thirty-five days after CHI, measured by enzyme-linked immunosorbent assay. These findings indicate the neurotherapeutic potential of HUCB-derived CD45(+) cell population in a mouse model of TBI and propose their use in the clinical setting of human TBI.