Journal of neurotrauma
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Journal of neurotrauma · Apr 2017
ReviewNatural compounds as a therapeutic intervention following traumatic brain injury: the role of phytochemicals.
There has been a tremendous focus on the discovery and development of neuroprotective agents that might have clinical relevance following traumatic brain injury (TBI). This type of brain injury is very complex and is divided into two major components. The first component, a primary injury, occurs at the time of impact and is the result of the mechanical insult itself. ⋯ Here, we review 33 different plant-derived natural compounds, phytochemicals, which have been investigated in experimental animal models of TBI. Some of these phytochemicals appear to have potential as possible therapeutic interventions to offset key components of the secondary injury cascade. However, not all studies have used the same scientific rigor, and one should be cautious in the interpretation of studies using naturally occurring phytochemical in TBI research.
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Journal of neurotrauma · Apr 2017
Natural History of Headache Five Years after Traumatic Brain Injury.
Headache is one of the most frequently reported symptoms following traumatic brain injury (TBI). Little is known about how these headaches change over time. We describe the natural history of headache in individuals with moderate to severe TBI over 5 years after injury. ⋯ More than half of classifiable headaches matched the profile of migraine or probable migraine. Headache is a substantial problem after TBI. Results suggest that ongoing assessment and treatment of headache after TBI is needed, as this symptom may be a problem up to 5 years post-injury.
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Journal of neurotrauma · Apr 2017
Acute or delayed treatment with anatabine improves spatial memory and reduces pathological sequelae at chronic timepoints after repetitive mild TBI.
Traumatic brain injury (TBI) has chronic and long-term consequences for which there are currently no approved pharmacological treatments. We have previously characterized the chronic neurobehavioral and pathological sequelae of a mouse model of repetitive mild TBI (r-mTBI) through to 2 years post-TBI. Despite the mild nature of the initial insult, secondary injury processes are initiated that involve neuroinflammatory and neurodegenerative pathways persisting and progressing for weeks and months post-injury and providing a potential window of opportunity for therapeutic intervention. ⋯ Nine months following crossover the remaining mice showed no effect of injury on their spatial memory, and whereas pathological analysis showed improvements in mice that had received delayed treatment, corpus callosum IBA1 increased in post-crossover placebo r-mTBI mice. These data demonstrate efficacy of both early and late initiation of treatment with anatabine in improving long term behavioral and pathology outcomes after mild TBI. Future studies will characterize the treatment window, the time course of treatment needed, and the dose needed to achieve therapeutic levels of anatabine in humans after injury.
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Journal of neurotrauma · Apr 2017
Experimental Investigation of Cavitation as a Possible Damage Mechanism in Blast-Induced Traumatic Brain Injury in Post-mortem Human Subject Heads.
The potential of blast-induced traumatic brain injury from the mechanism of localized cavitation of the cerebrospinal fluid (CSF) is investigated. While the mechanism and criteria for non-impact blast-induced traumatic brain injury is still unknown, this study demonstrates that local cavitation in the CSF layer of the cranial volume could contribute to these injuries. The cranial contents of three post-mortem human subject (PMHS) heads were replaced with both a normal saline solution and a ballistic gel mixture with a simulated CSF layer. ⋯ Sensor data indicates that cavitation may have occurred in the PMHS models at pressure levels below those for a 50% risk of blast lung injury. This study points to skull flexion, the result of the shock wave on the front of the skull leading to a negative pressure in the contrecoup, as a possible mechanism that contributes to the onset of cavitation. Based on observation of intracranial pressure transducer data from the PMHS model, cavitation onset is thought to occur from approximately a 140 kPa head-on incident blast.
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Journal of neurotrauma · Apr 2017
The Estimated Verbal GCS-Sub-Score in Intubated Traumatic Brain Injury Patients - Is it Really Better?
The Glasgow Coma Scale (GCS) has limited utility in intubated patients due to the inability to assign verbal subscores. The verbal subscore can be derived from the eye and motor subscores using a mathematical model, but the advantage of this method and its use in outcome prognostication in traumatic brain injury (TBI) patients remains unknown. We compared the validated "Core+CT"-IMPACT-model performance in 251 intubated TBI patients prospectively enrolled in the longitudinal OPTIMISM study between November 2009 and May 2015 when substituting the original motor GCS (mGCS) with the total estimated GCS (teGCS; with estimated verbal subscore). ⋯ At both time-points, motor GCS contributed more to the variability of outcome (Nagelkerke ΔR(2)) than teGCS (3 months: 5.8% vs. 0.4%; 12 months: 5% vs. 2.6%). The sensitivity analysis with imputed missing outcomes yielded similar results, with improved calibration for both GCS variants. In our cohort of intubated TBI patients, there was no statistically or clinically meaningful improvement in the IMPACT-model performance by substituting the original mGCS with teGCS.