Articles: traumatic-brain-injuries.
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Comparative Study
A comparison of the Full Outline of UnResponsiveness (FOUR) score and Glasgow Coma Score (GCS) in predictive modelling in traumatic brain injury.
To compare the performance of multivariate predictive models incorporating either the Full Outline of UnResponsiveness (FOUR) score or Glasgow Coma Score (GCS) in order to test whether substituting GCS with the FOUR score in predictive models for outcome in patients after TBI is beneficial. ⋯ Results showed that FOUR score and GCS perform equally well in multivariate predictive modelling in TBI.
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Brain injury : [BI] · Jan 2016
Tracheostomy risk factors and outcomes after severe traumatic brain injury.
To determine risk factors associated with tracheostomy placement after severe traumatic brain injury (TBI) and subsequent outcomes among those who did and did not receive a tracheostomy. ⋯ Age and insurance status are independently associated with tracheostomy placement, but not with mortality after severe TBI. Tracheostomy placement is associated with increased survival after severe TBI.
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Acta Neurochir. Suppl. · Jan 2016
Characterization of Cerebral Vascular Response to EEG Bursts Using ICP Pulse Waveform Template Matching.
Neurovascular coupling is the relationship between the activity of the brain and the subsequent change in blood flow to the active region. The most common methods of detecting neurovascular coupling are cumbersome and noncontinuous. However, the integration of intracranial pressure (ICP) and electroencephalography (EEG) may serve as an indirect measure of neurovascular coupling. ⋯ These changes were compared using a template obtained from patients undergoing CO2-induced vasodilation. All segments exhibited a significant period of vasodilation within 1-2 s after burst, and 4 of 5 had a significant period of vasoconstriction within 4-11 s of the EEG burst, suggesting that there might be a characteristic response of vasodilation and subsequent vasoconstriction after a spontaneous EEG burst. Furthermore, these findings demonstrate the potential of integrated EEG and ICP as an indirect measure of neurovascular coupling.
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Journal of neurotrauma · Jan 2016
Traumatic Brain Injury Impairs SNARE Complex Formation and Alters Synaptic Vesicle Distribution in the Hippocampus.
Traumatic brain injury (TBI) impairs neuronal function and can culminate in lasting cognitive impairment. While impaired neurotransmitter release has been well established after experimental TBI, little is understood about the mechanisms underlying this consequence. In the synapse, vesicular docking and neurotransmitter release requires the formation of the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex. ⋯ Synapses in the hippocampus were imaged at 100k magnification, and vesicle distribution was assessed in pre-synaptic terminals at the active zone. CCI resulted in a significant reduction in vesicle number within 150 nm of the active zone. These findings provide the first evidence of TBI-induced impairments in synaptic vesicle docking, and suggest that reductions in the pool of readily releasable vesicles and impaired SNARE complex formation are two novel mechanisms contributing to impaired neurotransmission after TBI.
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Unique from other brain disorders, traumatic brain injury (TBI) generally results from a discrete biomechanical event that induces rapid head movement. The large size and high organization of the human brain makes it particularly vulnerable to traumatic injury from rotational accelerations that can cause dynamic deformation of the brain tissue. Therefore, replicating the injury biomechanics of human TBI in animal models presents a substantial challenge, particularly with regard to addressing brain size and injury parameters. ⋯ Through a range of head rotational kinematics, this model can produce functional and neuropathological changes across the spectrum from concussion to severe TBI. Notably, however, the model is very difficult to employ, requiring a highly skilled team for medical management, biomechanics, neurological recovery, and specialized outcome measures including neuromonitoring, neurophysiology, neuroimaging, and neuropathology. Nonetheless, while challenging, this clinically relevant model has proven valuable for identifying mechanisms of acute and progressive neuropathologies as well as for the evaluation of noninvasive diagnostic techniques and potential neuroprotective treatments following TBI.