Journal of neurotrauma
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Journal of neurotrauma · Dec 2012
Do traumatic brain contusions increase in size after decompressive craniectomy?
Hemorrhagic contusions (HC) represent a common consequence of traumatic brain injury (TBI) and usually evolve during the first 12 h after trauma. The relationship between decompressive craniectomy (DC) and evolution of the post-traumatic HC is still unclear. The aim of the present study was to evaluate the impact of DC on HC evolution. ⋯ A significant increase (≥2 cc) of any HC during the observation period was detected in 8 patients (14%): 4/25 patients (16%) of Group 1 and 4/32 patients (12.5%) of Group 2 (Fisher exact test two-sided p=0.72). Univariate and multivariate analyses showed that none of the analyzed factors was associated with increased or de novo appearance of any HC. DC does not seem to constitute a risk factor for the evolution of HC.
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Journal of neurotrauma · Dec 2012
Motor vehicle crash-related subdural hematoma from real-world head impact data.
Abstract Approximately 1,700,000 people sustain a traumatic brain injury (TBI) each year and motor vehicle crashes (MVCs) are a leading cause of hospitalization from TBI. Acute subdural hematoma (SDH) is a common intracranial injury that occurs in MVCs associated with high mortality and morbidity rates. In this study, SDH volume and midline shift have been analyzed in order to better understand occupant injury by correlating them to crash and occupant parameters. ⋯ Age and fracture type were found to be significant contributors to SDH volume. This study is a volumetric analysis of real world brain injuries and known MVC impacts. The results of this study demonstrate a relationship among SDH volume, crash mechanics, and occupant characteristics that provide a better understanding of the injury mechanisms of MVC-associated TBI.
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Journal of neurotrauma · Dec 2012
Comparative StudyA comparison of the effects of nicotinamide and progesterone on functional recovery of cognitive behavior following cortical contusion injury in the rat.
The primary goal of this study was to compare clinically relevant doses of progesterone and nicotinamide within the same injury model. Progesterone has been shown to reduce edema and inflammation and improve functional outcomes following brain injury. Nicotinamide has also been shown to be an effective neuroprotective agent in a variety of neurological injury models. ⋯ The beneficial effects of progesterone appear to be dose dependent with the lower 10 mg/kg dose producing significant effects that were not observed at the higher dose. Direct comparison between nicotinamide and low dose progesterone appears to suggest that both are equally effective. The general findings of this study suggest that both nicotinamide and progesterone produce significant improvements in recovery of function following CCI.
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Journal of neurotrauma · Dec 2012
Repetitive mild traumatic brain injury in a mouse model produces learning and memory deficits accompanied by histological changes.
Concussion or mild traumatic brain injury (mTBI) represents the most common type of brain injury. However, in contrast with moderate or severe injury, there are currently few non-invasive experimental studies that investigate the cumulative effects of repetitive mTBI using rodent models. Here we describe and compare the behavioral and pathological consequences in a mouse model of single (s-mTBI) or repetitive injury (r-mTBI, five injuries given at 48 h intervals) administered by an electromagnetic controlled impactor. ⋯ Axonal injury, manifest as amyloid precursor protein immunoreactive axonal profiles, was present in the corpus callosum of both injury groups, though more evident in the r-mTBI animals. Our data demonstrate that this mouse model of mTBI is reproducible, simple, and noninvasive, with behavioral impairment after a single injury and increasing deficits after multiple injuries accompanied by increased focal and diffuse pathology. As such, this model may serve as a suitable platform with which to explore repetitive mTBI relevant to human brain injury.
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Journal of neurotrauma · Dec 2012
Carvacrol together with TRPC1 elimination improve functional recovery after traumatic brain injury in mice.
Death of Central Nervous System (CNS) neurons following traumatic brain injury (TBI) is a complex process arising from a combination of factors, many of which are still unknown. It has been found that inhibition of transient receptor potential (TRP) channels constitutes an effective strategy for preventing death of CNS neurons following TBI. TRP channels are classified into seven related subfamilies, most of which are Ca(2+) permeable and involved in many cellular functions, including neuronal cell death. ⋯ To better define the type of the specific channel involved, the effect of carvacrol on the extent and speed of recovery after TBI was compared among mice lacking TRPC1, TRPC3, or TRPC5, relative to wild type controls. We found that neurological recovery after TBI was significantly enhanced by combining carvacrol with TRPC1 elimination, but not by the absence of TRPC3 or TRPC5, showing a synergistic effect between carvacrol application and TRPC1 elimination. We conclude that TRPC1-sensitive mechanisms are involved in TBI pathology, and that inhibition of this channel by carvacrol enhances recovery and should be considered for further studies in animal models and humans.