Journal of neurotrauma
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Journal of neurotrauma · Jun 2016
The UCLA Study of Children with Moderate to Severe Traumatic Brain Injury: Event-Related Potential Measure of Interhemispheric Transfer Time.
Traumatic brain injury (TBI) frequently results in diffuse axonal injury and other white matter damage. The corpus callosum (CC) is particularly vulnerable to injury following TBI. Damage to this white matter tract has been associated with impaired neurocognitive functioning in children with TBI. ⋯ This subgroup of TBI children with slow IHTT also had significantly poorer neurocognitive functioning than healthy controls-even after correction for premorbid intellectual functioning. We discuss alternative models for the relationship between IHTT and neurocognitive functioning following TBI. Slow IHTT may be a biomarker that identifies children at risk for poor cognitive functioning following moderate/severe TBI.
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Journal of neurotrauma · Jun 2016
Contusion contrast extravasation depicted on multidetector computed tomography angiography predicts growth and mortality in traumatic brain contusion.
Traumatic brain injury (TBI) is the main cause of death in trauma victims and causes high rates of disability and neurological sequelae. Approximately 38-65% of traumatic brain contusions (TBC) demonstrate hemorrhagic expansion on serial computed tomography (CT) scans. Thus far, however, no single variable can accurately predict the hemorrhage expansion of a TBC. ⋯ In addition, expansion of the hemorrhagic component of the TBC was detected in 61.1% of the CE-positive patients, whereas expansion was only observed in 10% of the CE-negative patients (p < 0.001). Poor outcome was observed in 24.2% of the patients in the CE-negative group, but in the presence of CE, 72.7% evolved with poor outcome (p < 0.001). The CE was a strong independent predictor of expansion, poor outcome, and increased risk of in-hospital mortality in our series of patients with TBC.
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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.