Journal of neurotrauma
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Journal of neurotrauma · Apr 2012
Characterization of a novel rat model of penetrating traumatic brain injury.
A penetrating traumatic brain injury (pTBI) occurs when an object impacts the head with sufficient force to penetrate the skin, skull, and meninges, and inflict injury directly to the brain parenchyma. This type of injury has been notoriously difficult to model in small laboratory animals such as rats or mice. To this end, we have established a novel non-fatal model for pTBI based on a modified air rifle that accelerates a pellet, which in turn impacts a small probe that then causes the injury to the experimental animal's brain. ⋯ We also used a battery of behavioral models to examine the neurological outcome, with the most noteworthy finding being impairment of reference memory function. In conclusion, we have described a number of events taking place after pTBI in our model. We expect this model will prove useful in our efforts to unravel the biological events underlying injury and regeneration after pTBI and possibly serve as a useful animal model in the development of novel therapeutic and diagnostic approaches.
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Journal of neurotrauma · Apr 2012
Caffeic Acid phenethyl ester protects blood-brain barrier integrity and reduces contusion volume in rodent models of traumatic brain injury.
A number of studies have established a deleterious role for inflammatory molecules and reactive oxygen species (ROS) in the pathology of traumatic brain injury (TBI). Caffeic acid phenethyl ester (CAPE) has been shown to exert both antioxidant and anti-inflammatory effects. The primary objective of the present study was to examine if CAPE could be used to reduce some of the pathological consequences of TBI using rodent models. ⋯ CAPE treatment did not improve performance in either vestibulomotor/motor function (tested using beam balance and foot-fault tests), or in learning and memory function (tested using the Morris water maze and associative fear memory tasks). However, animals treated with CAPE were found to have significantly less cortical tissue loss than vehicle-treated controls. These findings suggest that CAPE may provide benefit in the treatment of vascular compromise following central nervous system injury.
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Journal of neurotrauma · Apr 2012
Validity of a pediatric version of the Glasgow Outcome Scale-Extended.
The Glasgow Outcome Scale (GOS) and its most recent revision, the GOS-Extended (GOS-E), provide the gold standard for measuring traumatic brain injury (TBI) outcome. The GOS-E exhibits validity when used with adults and some adolescents, but validity with younger children is not established. Because the GOS-E lacks the developmental specificity necessary to evaluate children, toddlers, and infants, we modified the original version to create the GOS-E Pediatric Revision (GOS-E Peds), a developmentally appropriate structured interview, to classify younger patients. ⋯ The GOS-E Peds is sensitive to severity of injury and is associated with changes in TBI sequelae over time. This pediatric revision provides a valid outcome measure in infants, toddlers, children, and adolescents through age 16. Findings support using the GOS-E Peds as the primary outcome variable in pediatric clinical trials.
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Journal of neurotrauma · Apr 2012
Case ReportsFrontal cortex neuropathology in dementia pugilistica.
Dementia pugilistica (DP) is associated with chronic traumatic brain injury (CTBI), and leads to a "punch drunk" syndrome characterized by impairments in memory and executive function, behavioral changes, and motor signs. Microscopic features include the accumulation of neurofibrillary tangles (NFTs), beta-amyloid (Aβ), and TAR DNA binding protein 43 (TDP-43) pathology. Here we describe detailed clinical and neuropathological data about a 55-year-old retired boxer (ApoE3/4), who presented with executive dysfunction and behavioral impairments. ⋯ Inflammation was another key feature, including microglial activation and significant C1q labeling of neurons, along with NFTs. TDP-43-positive pathology was also observed. Inflammation may be a key inciting as well as propagating feature of DP neuropathology.
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Journal of neurotrauma · Apr 2012
Randomized Controlled TrialCerebral microdialysis effects of propofol versus midazolam in severe traumatic brain injury.
Propofol, an anesthetic agent acting as an analogue of vitamin E, has been advocated to be an ideal neuroprotective agent both in animal models and in clinical practice, due to its positive effects on oxidative stress. Nevertheless, no studies have compared this agent to another sedative agent used for sedation after traumatic brain injury (TBI). The objective was to compare the effects of propofol to midazolam on cerebral biomarkers at the acute phase of severe TBI patients. ⋯ No difference between groups was observed for the L:P ratio (time effect p=0.201, treatment effect p=0.401, time×treatment interaction p=0.101). Similarly, no difference was observed for glutamate (time effect p=0.930, treatment effect p=0.651, time×treatment interaction p=0.353), glycerol (time effect p=0.223, treatment effect p=0.922, time×treatment interaction p=0.308), or glucose (time effect p=0.116, treatment effect p=0.088, time×treatment interaction p=0.235). These results do not support a difference between propofol and midazolam for sedation for the cerebral metabolic profile in severe TBI.