Enhanced neurotrauma services: physician input into traumatic brain injury care.

Elderly trauma victims whose care is shared between surgeons and physicians have improved clinical outcomes and shorter hospital lengths of stay (LOS). To test whether a similar benefit can be gained for patients suffering traumatic brain injury (TBI), a quality improvement project (QIP) was run in which a neurologist was enrolled into the pre-existing neurotrauma team. Mortality rates, LOS and rates of readmission within 30 days of discharge were compared between two cohorts of TBI patients: 80 admittedly prior to the QIP and 80 admitted during the QIP. The two cohorts were well matched for age, gender, mechanism of injury, Glasgow coma score and types of injury. The QIP was not associated with a reduction in mortality but was associated with a significant reduction in mean LOS (from 25.7 days to 17.5 days; p=0.04) and a reduction in readmissions (from seven to zero patients; p=0.01).

Cognition based bTBI mechanistic criteria; a tool for preventive and therapeutic innovations.

Blast-induced traumatic brain injury has been associated with neurodegenerative and neuropsychiatric disorders. To date, although damage due to oxidative stress appears to be important, the specific mechanistic causes of such disorders remain elusive. Here, to determine the mechanical variables governing the tissue damage eventually cascading into cognitive deficits, we performed a study on the mechanics of rat brain under blast conditions. To this end, experiments were carried out to analyse and correlate post-injury oxidative stress distribution with cognitive deficits on a live rat exposed to blast. A computational model of the rat head was developed from imaging data and validated against in vivo brain displacement measurements. The blast event was reconstructed in silico to provide mechanistic thresholds that best correlate with cognitive damage at the regional neuronal tissue level, irrespectively of the shape or size of the brain tissue types. This approach was leveraged on a human head model where the prediction of cognitive deficits was shown to correlate with literature findings. The mechanistic insights from this work were finally used to propose a novel protective device design roadmap and potential avenues for therapeutic innovations against blast traumatic brain injury.

Contribution of Fibrinogen to Inflammation and Neuronal Density in Human Traumatic Brain Injury.

Traumatic brain injury (TBI) is a leading cause of death and disability, particularly among the young. Despite this, no disease-specific treatments exist. Recently, blood-brain barrier disruption and parenchymal fibrinogen deposition have been reported in acute traumatic brain injury and in long-term survival; however, their contribution to the neuropathology of TBI remains unknown. The presence of fibrinogen-a well-documented activator of microglia/macrophages-may be associated with neuroinflammation, and neuronal/axonal injury. To test this hypothesis, cases of human TBI with survival times ranging from 12 h to 13 years (survival <2 months, n = 15; survival >1 year, n = 6) were compared with uninjured controls (n = 15). Tissue was selected from the frontal lobe, temporal lobe, corpus callosum, cingulate gyrus, and brainstem, and the extent of plasma protein (fibrinogen and immunoglobulin G [IgG]) deposition, microglial/macrophage activation (CD68 and ionized calcium-binding adapter molecule 1 [Iba-1] immunoreactivity), neuronal density, and axonal transport impairment (ß-amyloid precursor protein [ßAPP] immunoreactivity) were assessed. Quantitative analysis revealed a significant increase in parenchymal fibrinogen and IgG deposition following acute TBI compared with long-term survival and control. Fibrinogen, but not IgG, was associated with microglial/macrophage activation and a significant reduction in neuronal density. Perivascular fibrinogen deposition also was associated with microglial/macrophage clustering and accrual of ßAPP in axonal spheroids, albeit rarely. These findings mandate the future exploration of causal relationships between fibrinogen deposition, microglia/macrophage activation, and potential neuronal loss in acute TBI.