Articles: traumatic-brain-injuries.
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Following a traumatic brain injury (TBI), 5-50% of patients will develop posttraumatic epilepsy (PTE) with children being particularly susceptible. Currently, PTE cannot be prevented and there is limited understanding of the underlying epileptogenic mechanisms. We hypothesize that early after TBI the brain undergoes distinct cellular and synaptic reorganization that facilitates cortical excitability and promotes the development of epilepsy. ⋯ Our results demonstrate that CCI in juvenile rats rapidly induces epileptiform activity and enhanced cortical synaptic bursting. Detection of epileptiform activity early after injury suggests it may be an important pathophysiological component and potential indicator of developing PTE.
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Neurorehabil Neural Repair · Feb 2015
Effect of intrathecal baclofen bolus injection on ankle muscle activation during gait in patients with acquired brain injury.
Intrathecal baclofen (ITB) bolus injection effectively decreases spinal excitability but the impact on lower limb muscle activation during gait has not been thoroughly investigated. ⋯ ITB bolus injection alters the activation of MG and TA during gait. However, the changes in muscle activation are not closely related to the changes in gait speed or resting muscle hypertonia. The analysis of ankle muscle activation during gait better characterizes the response to ITB bolus injection than gait kinematics.
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Both aspirin therapy and trauma impair platelet function. Platelet dysfunction is associated with worse outcomes in patients with traumatic intracranial hemorrhage (ICH). Platelet transfusion is often used to limit progression of ICH in patients on aspirin, but has not been shown to improve platelet function or outcomes. We hypothesized that platelet transfusion would improve aspirin-induced, but not trauma-induced, platelet dysfunction. ⋯ Patients with isolated ICH have trauma-induced platelet dysfunction. In addition, patients on aspirin have drug-induced abnormalities in platelet response to AA. Platelet transfusion improves aspirin-induced, but not trauma-induced, platelet dysfunction.
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Iran J Basic Med Sci · Feb 2015
Estrogen provides neuroprotection against brain edema and blood brain barrier disruption through both estrogen receptors α and β following traumatic brain injury.
Estrogen (E2) has neuroprotective effects on blood-brain-barrier (BBB) after traumatic brain injury (TBI). In order to investigate the roles of estrogen receptors (ERs) in these effects, ER-α antagonist (MPP) and, ER-β antagonist (PHTPP), or non-selective estrogen receptors antagonist (ICI 182780) were administered. ⋯ A combined administration of MPP and PHTPP or ICI inhibited the E2-induced decrease in brain edema and BBB disruption; this may suggest that these effects were mediated via both receptors.
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J Tissue Eng Regen Med · Feb 2015
Treatment of penetrating brain injury in a rat model using collagen scaffolds incorporating soluble Nogo receptor.
Injuries and diseases of the central nervous system (CNS) have the potential to cause permanent loss of brain parenchyma, with severe neurological consequences. Cavitary defects in the brain may afford the possibility of treatment with biomaterials that fill the lesion site while delivering therapeutic agents. This study examined the treatment of penetrating brain injury (PBI) in a rat model with collagen biomaterials and a soluble Nogo receptor (sNgR) molecule. sNgR was aimed at neutralizing myelin proteins that hinder axon regeneration by inducing growth cone collapse. ⋯ Immunohistochemical staining demonstrated the composition of the cellular infiltrate to include macrophages, astrocytes and vascular endothelial cells. Isolated regions of the scaffold borders showed integration with surrounding viable brain tissue that included neurons and oligodendrocytes. While axon regeneration was not detected in the scaffolds, the cellular infiltration and vascularization of the lesion site demonstrated a modification of the injury environment with implications for regenerative strategies.