Journal of neurotrauma
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Journal of neurotrauma · Jan 2012
High-strain-rate brain injury model using submerged acute rat brain tissue slices.
Blast-induced traumatic brain injury (bTBI) has received increasing attention in recent years due to ongoing military operations in Iraq and Afghanistan. Sudden impacts or explosive blasts generate stress and pressure waves that propagate at high velocities and affect sensitive neurological tissues. The immediate soft tissue response to these stress waves is difficult to assess using current in vivo imaging technologies. ⋯ Injury at 4 and 6 h was quantified using Fluoro-Jade C. Neuronal injury due to PSHPB testing was found to be significantly greater than injury associated with the tissue slice paradigm alone. While large pressures and strains were encountered for these tests, this system provides a controllable test environment to study injury to submerged brain slices over a range of strain rate, pressure, and strain loads.
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Journal of neurotrauma · Jan 2012
Traumatic brain injury causes an FK506-sensitive loss and an overgrowth of dendritic spines in rat forebrain.
Traumatic brain injury (TBI) causes both an acute loss of tissue and a progressive injury through reactive processes such as excitotoxicity and inflammation. These processes may worsen neural dysfunction by altering neuronal circuitry beyond the focally-damaged tissue. One means of circuit alteration may involve dendritic spines, micron-sized protuberances of dendritic membrane that support most of the excitatory synapses in the brain. ⋯ These results, together with those of a companion study, indicate an FK506-sensitive mechanism of dendritic spine loss in the TBI model. Furthermore, by 1 week after TBI, spine density had increased substantially above control levels, bilaterally in CA1 and CA3 and ipsilaterally in dDG. The apparent overgrowth of spines in CA1 is of particular interest, as it may explain previous reports of abnormal and potentially epileptogenic activity in this brain region.
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Journal of neurotrauma · Jan 2012
Progesterone increases circulating endothelial progenitor cells and induces neural regeneration after traumatic brain injury in aged rats.
Vascular remodeling plays a key role in neural regeneration in the injured brain. Circulating endothelial progenitor cells (EPCs) are a mediator of the vascular remodeling process. Previous studies have found that progesterone treatment of traumatic brain injury (TBI) decreases cerebral edema and cellular apoptosis and inhibits inflammation, which in concert promote neuroprotective effects in young adult rats. ⋯ Progesterone treatment significantly improved neurological outcome after TBI measured by the modified neurological severity score, Morris Water Maze and the long term potentiation in the hippocampus as well as increased the circulating EPC levels compared to TBI controls (p<0.05). Progesterone treatment also significantly increased CD34 and CD31 positive cell number and vessel density in the injured brain compared to TBI controls (p<0.05). These data indicate that progesterone treatment of TBI improves multiple neurological functional outcomes, increases the circulating EPC level, and facilitates vascular remodeling in the injured brain after TBI in aged rats.
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Journal of neurotrauma · Jan 2012
Failure of delayed intravenous administration of bone marrow stromal cells after traumatic brain injury.
Traumatic brain injury (TBI) is a leading cause of mortality and morbidity worldwide. Currently, there is no effective strategy to treat the functional sequelae associated with TBI. Experimental evidence shows that the intravenous administration of bone marrow stromal cells (BMSC) during the first week after TBI prevents neurological deficits, but no experimental studies have shown evidence of the effect of intravenous BMSC on chronic brain injury sequelae. ⋯ At the end of the study period the animals were sacrificed and their brains were studied to evaluate possible differences between groups. Two months after BMSC administration no significant differences were detected in the motor and sensory evaluation between animals treated with BMSC and controls, and no differences were detected after histological study of the brains. Our present results suggest that intravenous administration of BMSC after TBI, when the neurological deficits are well established, has no beneficial effect in neurological outcomes or on brain tissue.
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Journal of neurotrauma · Jan 2012
Lasting pituitary hormone deficiency after traumatic brain injury.
Pituitary deficiencies have been reported after traumatic brain injury (TBI) and may contribute to lasting cognitive disorders in this context. In a population of TBI patients with persistent cognitive and/or behavioral disorders, we sought to determine the prevalence of lasting pituitary deficiency and relationships with TBI severity, cognitive disorders, and impairments in activities of daily living (ADL). Fifty-five patients were included (mean age 36.1 years; 46 men) at least 1 year after TBI. ⋯ We did not find any relationship between pituitary deficiency and the TBI's initial severity. In a multivariate analysis, the TBI severity was introduced as a first factor, and pituitary deficits as a secondary factor for explaining the late outcome (ADL and QoL). In conclusion, TBI patients with cognitive sequelae must undergo pituitary screening because growth hormone, corticotropin, and thyrotropin deficits are particularly common and can adversely affect ADL and reduce QoL.