Journal of neurotrauma
-
Journal of neurotrauma · Jul 2019
Cost Effectiveness of Biomarker Screening for Traumatic Brain Injury.
Intracranial hemorrhage after traumatic brain injury (TBI) can be life threatening and requires prompt diagnosis. Computed tomography (CT) scans are a rapid and accurate way to evaluate for hemorrhage. In patients with mild and moderate TBI, however, in whom the incidence of intracranial pathology is low, scanning every patient with CT can be costly. ⋯ We performed cost analyses of the BTI screen to determine the threshold of cost-effectiveness, compared with application of clinical decision rules or routine CT scans, for cases of mild or moderate TBI. With a 0.104 probability of an intracranial lesion in mild TBI, the biomarker screen is cost-effective if the cost is $308.96 or below per test. In moderate TBI, because of the greater prevalence of intracranial lesions at 0.663, there is a lower need for screening, and BTI becomes cost-effective up to $73.41 per test.
-
Journal of neurotrauma · Jul 2019
A Role for Postsynaptic Density 95 and its Binding Partners in Models of Traumatic Brain Injury.
Postsynaptic density 95 (PSD-95), the major scaffold protein at excitatory synapses, plays a major role in mediating intracellular signaling by synaptic N-methyl-d-aspartate (NMDA) type glutamate receptors. Despite the fact that much is known about the role of PSD-95 in NMDA-mediated toxicity, less is known about its role in mechanical injury, and more specifically, in traumatic brain injury (TBI). Given that neural circuitry is disrupted after TBI and that PSD-95 and its interactors end-binding protein 3 (EB3) and adenomatous polyposis coli (APC) shape dendrites, we examined whether changes to these proteins and their interactions occur after brain trauma. ⋯ Rapid deformation of cortical neurons leads to neuronal death 72 h after injury, but this outcome is not dependent on PSD-95 expression. However, disruptions in dendritic arborization following stretch injury in vitro require PSD-95 expression, and these changes in arborization can be mimicked with expression of PSD-95 mutants lacking the second PDZ domain. Thus, PSD-95 and its interactors may serve as therapeutic targets for repairing dendrites after TBI.