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
Insulin-regulated aminopeptidase deficiency provides protection against ischemic stroke in mice.
Recent studies have demonstrated that angiotensin IV (Ang IV) provides protection against brain injury caused by cerebral ischemia. Ang IV is a potent inhibitor of insulin-regulated aminopeptidase (IRAP). Therefore, we examined the effect of IRAP gene inactivation on neuroprotection following transient middle cerebral artery occlusion (MCAo) in mice. ⋯ An increase in compensatory cerebral blood flow during MCAo was observed in the IRAP knockout animals with no differences in cerebral vascular anatomy detected. The current study demonstrates that deletion of the IRAP gene protects the brain from ischemic damage analogous to the effect of the IRAP inhibitor, Ang IV. This study indicates that IRAP is potentially a new therapeutic target for the development of treatment for ischemic stroke.
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Journal of neurotrauma · Apr 2012
Glial neuronal ratio: a novel index for differentiating injury type in patients with severe traumatic brain injury.
Neurobiochemical marker levels in blood after traumatic brain injury (TBI) may reflect structural changes detected by neuroimaging. This study evaluates whether correlations between neuronal (ubiquitin carboxy-terminal hydrolase-L1 [UCH-L1]) and glial (glial fibrillary acidic protein [GFAP]) biomarkers may be used as an indicator for differing intracranial pathologies after brain trauma. In 59 patients with severe TBI (Glasgow Coma Scale [GCS] score≤8) serum samples were obtained at the time of hospital admission and analyzed for UCH-L1 and GFAP. ⋯ GNR was significantly higher in patients who died, but was not an independent predictor of death. The data from the present study indicate that GNR provides valuable information about different injury pathways, which may be of diagnostic significance. In addition, GNR may help to identify different pathophysiological mechanisms following different types of brain trauma, with implications for therapeutic interventions.
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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.