Articles: traumatic-brain-injuries.
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Prehospital care providers are usually the first responders for patients with traumatic brain injury (TBI). Early identification of patients with TBI enables them to receive trauma centre care, which improves outcomes. Two recent systematic reviews concluded that prehospital triage tools for undifferentiated major trauma have low accuracy. However, neither review focused specifically on patients with suspected TBI. Therefore, we aimed to systematically review the existing evidence on the diagnostic performance of prehospital triage tools for patients with suspected TBI. ⋯ Further efforts are needed to improve and optimise prehospital triage tools. Consideration of additional predictors (e.g., biomarkers, clinical decision aids and paramedic judgement) may be required to improve diagnostic accuracy.
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Traumatic brain injury (TBI) is an underrecognized public health threat. Survivors of TBI often suffer long-term neurocognitive deficits leading to the progressive onset of neurodegenerative disease. Recent data suggests that the gut-brain axis is complicit in this process. However, no study has specifically addressed whether fecal microbiota transfer (FMT) attenuates neurologic deficits after TBI. ⋯ These data suggest that restoring a pre-injury gut microbial community structure may be a promising therapeutic intervention after TBI.
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Within 2 min of severe ischemia, spreading depolarization (SD) propagates like a wave through compromised gray matter of the higher brain. More SDs arise over hours in adjacent tissue, expanding the neuronal damage. This period represents a therapeutic window to inhibit SD and so reduce impending tissue injury. Yet most neuroscientists assume that the course of early brain injury can be explained by glutamate excitotoxicity, the concept that immediate glutamate release promotes early and downstream brain injury. There are many problems with glutamate release being the unseen culprit, the most practical being that the concept has yielded zero therapeutics over the past 30 years. But the basic science is also flawed, arising from dubious foundational observations beginning in the 1950s METHODS: Literature pertaining to excitotoxicity and to SD over the past 60 years is critiqued. ⋯ Spreading depolarizations better account for the acute neuronal injury arising from brain ischemia than does the early and excessive release of glutamate.
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Observational Study
The Relationship Between Seizures and Spreading Depolarizations in Patients with Severe Traumatic Brain Injury.
Both seizures and spreading depolarizations (SDs) are commonly detected using electrocorticography (ECoG) after severe traumatic brain injury (TBI). A close relationship between seizures and SDs has been described, but the implications of detecting either or both remain unclear. We sought to characterize the relationship between these two phenomena and their clinical significance. ⋯ In patients with severe TBI requiring neurosurgery, seizures were half as common as SDs. Seizures would have gone undetected without ECoG monitoring in 20% of patients. Although seizures alone did not influence 6-month functional outcomes in this cohort, they were independently associated with electrographic worsening and a lack of motor improvement following surgery. Temporal interactions between ECoG-detected seizures and SDs were common and held prognostic implications. Together, seizures and SDs may occur along a dynamic continuum of factors critical to the development of secondary brain injury. ECoG provides information integral to the clinical management of patients with TBI.
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Journal of neurotrauma · Jun 2022
ReviewNeuroimaging correlates of depression after traumatic brain injury: A systematic review.
Depression is the most frequent neuropsychiatric complication after traumatic brain injury (TBI) and is associated with poorer outcomes. Neuroimaging has the potential to improve our understanding of the neural correlates of depression after TBI and may improve our capacity to accurately predict and effectively treat this condition. We conducted a systematic review of structural and functional neuroimaging studies that examined the association between depression after TBI and neuroimaging measures. ⋯ Findings that were replicated in more than one study included reduced gray matter in the rostral anterior cingulate cortex, pre-frontal cortex, and hippocampus, and damage in five white matter tracts (cingulum, internal capsule, superior longitudinal fasciculi, and anterior and posterior corona radiata). This systematic review found that the available data did not converge on a clear neuroimaging biomarker for depression after TBI. However, there are promising targets that warrant further study.