Journal of neurotrauma
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Journal of neurotrauma · Oct 2010
Effects of traumatic brain injury of different severities on emotional, cognitive, and oxidative stress-related parameters in mice.
Cognitive deficits and psychiatric disorders are significant sequelae of traumatic brain injury (TBI). Animal models have been widely employed in TBI research, but few studies have addressed the effects of experimental TBI of different severities on emotional and cognitive parameters. In this study, mice were subjected to weight-drop TBI to induce mild, intermediate, or severe TBI. ⋯ Intermediate and severe TBI caused extensive macroscopic and microscopic brain damage, while mild TBI typically had no histological abnormalities. Moreover, a significant increase in TBARS in the ipsilateral cortex and GPx in the ipsilateral hippocampus was observed at 24 h and 14 days, respectively, following intermediate TBI. The current experimental TBI model induced emotional and cognitive changes comparable to sequelae seen in human TBI, and it might therefore represent a useful approach to the study of mechanisms of and new treatments for TBI and related disorders.
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Journal of neurotrauma · Sep 2010
Multicenter Study Comparative StudyOutcomes of patients with severe traumatic brain injury who have Glasgow Coma Scale scores of 3 or 4 and are over 65 years old.
The goal of this study was to investigate the outcomes of patients with traumatic brain injury (TBI) who had Glasgow Coma Scale (GCS) scores of 3 or 4, and were aged 66 years or older. Between January 2001 and December 2005, 13 European centers enrolled patients with severe brain trauma. Data sets of all patients who had a GCS score of 3 or 4 and were 66 years of age or older were analyzed. ⋯ Patients with GCS scores of 3 or 4 who are older than 65 years have a poor, but not hopeless, prognosis. Confirmed factors predicting poor prognosis for this group of patients were closed basal cisterns and midline shift >15 mm on the first CT scan. Factors possibly related to favorable outcomes were female gender, lower trauma severity, open or partially open basal cisterns, and no midline shift on the first CT scan.
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Journal of neurotrauma · Sep 2010
Multicenter Study Comparative StudyClinical evaluation of a portable near-infrared device for detection of traumatic intracranial hematomas.
The purpose of this multicenter observational clinical study was to evaluate the performance of a near-infrared (NIR)-based, non-invasive, portable device to screen for traumatic intracranial hematomas. Five trauma centers collected data using the portable NIR device at the time a computed tomography (CT) scan was performed to evaluate a suspected traumatic brain injury (TBI). The CT scans were read by an independent neuroradiologist who was blinded to the NIR measurements. ⋯ For all 96 cases with intracranial hemorrhage, regardless of size and type of hemorrhage, the sensitivity was 68.7% (CI 58.3,77.6%), and specificity was 90.7% (CI 86.4,93.7%). These results confirm the results of previous studies that indicate that a NIR-based portable device can reliably screen for intracranial hematomas that are superficial and of a size likely to be of clinical importance. The NIR device cannot replace CT scanning in the diagnosis of TBI, but the device might be useful to supplement clinical information used to triage TBI patients, and in situations in which CT scanning is not readily available.
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Journal of neurotrauma · Sep 2010
Comparative StudyCompression alters kinase and phosphatase activity and tau and MAP2 phosphorylation transiently while inducing the fast adaptive dendritic remodeling of underlying cortical neurons.
In traumatic brain injury (TBI) there is often compression of the cerebral cortex. Using a rat epidural bead implantation model we found that mechanical compression distorted the dendrites of underlying cortical pyramidal neurons, and that the deformed dendrites regained straight morphology in 3 days. This was accompanied by a transient increase in the phosphorylation of microtubule-associated proteins (MAPs) at sites known to destabilize microtubules, including MAP2 from 30 min to 1 h, and tau from 10 min to 12 h following compression. ⋯ The temporal coincidence of these events suggests that alterations of phosphatase and kinase activity underlie MAP2 and tau phosphorylation, thus causing the compressed cortical neurons to remodel their dendrites, including the proximal segments. The rapid onset of these molecular changes demonstrates that compression causes cortical neurons to undergo active changes much early than expected. The large-scale structural changes that result can alter cortical function for an extended period of time.
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Journal of neurotrauma · Sep 2010
Comparative StudyAntagonism of R-type calcium channels significantly improves cerebral blood flow after subarachnoid hemorrhage in rats.
The effects of R-type calcium channels on cerebral blood flow (CBF) and vasospasm pathways following subarachnoid hemorrhage (SAH) have not been well studied. The aim of this study was to investigate the role of R-type calcium channels in vasospasm development and treatment. Sixty-five rats were randomly divided into four groups: sham (n = 14), SAH (n = 17), SAH + nimodipine (n = 17), and SAH + SNX-482 (n = 17). ⋯ Nimodipine had no significant effect on CBF reduction compared to the SAH group (p > 0.008), whereas SNX-482 significantly inhibited CBF reduction (p < 0.008). Both MLC2 phosphorylation and calponin degradation appeared to be inhibited by SNX-482, whereas the effects of nimodipine were relatively blunted. We concluded that an R-type calcium channel antagonist may improve CBF following SAH by partially inhibiting MLC2 phosphorylation and calponin degradation, and may exceed the potential of an L-type calcium channel antagonist, which suggests a more crucial role for R-type calcium channels in the development of SAH vasospasm and its treatment.