Journal of neurotrauma
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Journal of neurotrauma · Jun 2016
Randomized Controlled Trial Multicenter StudyFever control management is preferable to mild therapeutic hypothermia in traumatic brain injury patients with Abbreviated Injury Scale 3-4: a multicenter, randomised controlled trial.
In our prospective, multi-center, randomized controlled trial (RCT)-the Brain Hypothermia (B-HYPO) study-we could not show any difference on neurological outcomes in patients probably because of the heterogeneity in the severity of their traumatic condition. We therefore aimed to clarify and compare the effectiveness of the two therapeutic temperature management regimens in severe (Abbreviated Injury Scale [AIS] 3-4) or critical trauma patients (AIS 5). In the present post hoc B-HYPO study, we re-evaluated data based on the severity of trauma as AIS 3-4 or AIS 5 and compared Glasgow Outcome Scale score and mortality at 6 months by per-protocol analyses. ⋯ The fever control group demonstrated a significant reduction of TBI-related mortality compared with the MTH group (9.7% vs. 34.0%, p = 0.02) and an increase of favorable neurological outcomes (64.5% vs. 51.1%, p = 0.26) in patients with AIS 3-4, although the latter was not statistically significant. There was no difference in mortality or favorable outcome in patients with AIS 5. Fever control may be considered instead of MTH in patients with TBI (AIS 3-4).
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Journal of neurotrauma · Jun 2016
Clinical application of a novel clinical scale for the pre-operative risk evaluation of cerebral herniation from traumatic epidural hematoma.
Secondary massive cerebral infarction (MCI) is the predominant prognostic factor for cerebral herniation from epidural hematoma (EDH) and determines the need for decompressive craniectomy. In this study, we tested the clinical feasibility and reliability of a novel pre-operative risk scoring system, the EDH-MCI scale, to guide surgical decision making. It is comprised of six risk factors, including hematoma location and volume, duration and extent of cerebral herniation, Glasgow Coma Scale score, and presence of preoperative shock, with a total score ranging from 0 to 18 points. ⋯ Results suggested that simple hematoma evacuation craniotomy was sufficient for patients with low risk scores (≤9 points), whereas decompressive craniectomy in combination with duraplasty were necessary only for those with high risk scores (≥13 points). In patients with borderline risk scores (10-12 points), those having unstable vital signs, coexistence of severe secondary brainstem injury, and unresponsive dilated pupils after emergent burr hole hematoma drainage had a significantly increased incidence of post-traumatic MCI and necessity of radical surgical treatments. In conclusion, the novel pre-operative risk EDH-MCI evaluation scale has a satisfactory predictive and discriminative performance for patients who are at risk for the development of secondary MCI and therefore require decompressive craniectomy.
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Journal of neurotrauma · Jun 2016
Fractalkine receptor deficiency is associated with early protection, but late worsening of outcome following brain trauma in mice.
An impaired ability to regulate microglia activation by fractalkine (CX3CL1) leads to microglia chronic sub-activation. How this condition affects outcome after acute brain injury is still debated, with studies showing contrasting results depending on the timing and the brain pathology. Here, we investigated the early and delayed consequences of fractalkine receptor (CX3CR1) deletion on neurological outcome and on the phenotypical features of the myeloid cells present in the lesions of mice with traumatic brain injury (TBI). ⋯ Gene expression on CD11b(+) sorted cells revealed an increase of interleukin 10 and insulin-like growth factor 1 (IGF1) at 1 day and a decrease of IGF1 4 days and 5 weeks post-TBI in CX3CR1(-/-), compared with WT mice. These data show an early protection followed by a chronic exacerbation of TBI outcome in the absence of CX3CR1. Thus, longitudinal effects of myeloid cell manipulation at different stages of pathology should be investigated to understand how and when their modulation may offer therapeutic chances.
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Journal of neurotrauma · Jun 2016
Using post-traumatic amnesia to predict outcome following traumatic brain injury.
Duration of post-traumatic amnesia (PTA) has emerged as a strong measure of injury severity after traumatic brain injury (TBI). Despite the growing international adoption of this measure, there remains a lack of consistency in the way in which PTA duration is used to classify severity of injury. This study aimed to establish the classification of PTA that would best predict functional or productivity outcomes. ⋯ This finding indicates that the greatest accuracy in prognosis is likely to be achieved using PTA as a continuous variable. This enables the probability of productive outcomes to be estimated with far greater precision than that possible using a classification system. Categorizing PTA to classify severity of injury may be reducing the precision with which clinicians can plan the treatment of patients after TBI.
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Journal of neurotrauma · Jun 2016
Neuroprotective effects of the glutamate transporter activator, MS-153, following traumatic brain injury in the adult rat.
Traumatic brain injury (TBI) in humans and in animals leads to an acute and sustained increase in tissue glutamate concentrations within the brain, triggering glutamate-mediated excitotoxicity. Excitatory amino acid transporters (EAATs) are responsible for maintaining extracellular central nervous system glutamate concentrations below neurotoxic levels. Our results demonstrate that as early as 5 min and up to 2 h following brain trauma in brain-injured rats, the activity (Vmax) of EAAT2 in the cortex and the hippocampus was significantly decreased, compared with sham-injured animals. ⋯ Administration of (R)-(-)-5-methyl-1-nicotinoyl-2-pyrazoline (MS-153), a GLT-1 activator, beginning immediately after injury and continuing for 24 h, significantly decreased neurodegeneration, loss of microtubule-associated protein 2 and NeuN (+) immunoreactivities, and attenuated calpain activation in both the cortex and the hippocampus at 24 h after the injury; the reduction in neurodegeneration remained evident up to 14 days post-injury. In synaptosomal uptake assays, MS-153 up-regulated GLT-1 activity in the naïve rat brain but did not reverse the reduced activity of GLT-1 in traumatically-injured brains. This study demonstrates that administration of MS-153 in the acute post-traumatic period provides acute and long-term neuroprotection for TBI and suggests that the neuroprotective effects of MS-153 are related to mechanisms other than GLT-1 activation, such as the inhibition of voltage-gated calcium channels.