Journal of neurotrauma
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Journal of neurotrauma · Mar 2003
Cerebrospinal fluid apolipoprotein E concentration decreases after traumatic brain injury.
The APOE epsilon4 allele has been associated with unfavorable outcome after several types of acute brain injury, yet the biological mechanisms underlying this observation are poorly understood. Postmortem and experimental brain injury studies suggest the presence of increased amounts of apolipoprotein E (apoE) within the neuropil after acute brain injury. We assayed the concentration of apolipoprotein E in the cerebrospinal fluid (CSF) of non-injured controls and patients with traumatic brain injury (TBI) to determine whether differences exist, and if these differences correlate with injury severity and clinical outcome. ⋯ The average concentration of apoE in the CSF of controls was 12.4 mg/L (95% CI: 10.5-14.3 mg/L) and in TBI patients was 3.7 mg/L (95% CI: 2.1-4.1 mg/L; Mann-Whitney: p < 0.0001). In contrast, the concentration of S100B in the CSF of TBI patients was significantly higher than that of controls (Mann-Whitney: p < 0.0001). We speculate that apoE is retained within the parenchyma of the central nervous system in response to injury where in view of previous data, it may have a protective role.
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Journal of neurotrauma · Mar 2003
Pre- and inter-hospital transport of severely head-injured patients in rural Northern Norway.
The purpose of this study was to survey the time consumed during the pre- and inter-hospital transport of severely head injured patients in Northern Norway. All patients (n = 85) operated for an intracranial mass lesions within 48 h after injury during the 10-year period 1986-1995 were included in this retrospective analysis. Ambulance records, transfer notes, and hospital records were reviewed. ⋯ The inter-hospital transfer time was < or = 3 h in 17%. Clearly, the advanced air ambulance service in Northern Norway makes rapid inter-hospital transfer possible despite extremely long geographical distances. Our findings indicate that this possibility is not always utilized.
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Journal of neurotrauma · Mar 2003
Preinjury administration of the calpain inhibitor MDL-28170 attenuates traumatically induced axonal injury.
Traumatic brain injury (TBI) evokes diffuse (traumatic) axonal injury (TAI), which contributes to morbidity and mortality. Damaged axons display progressive alterations gradually evolving to axonal disconnection. In severe TAI, the tensile forces of injury lead to a focal influx of Ca2+, initiating a series of proteolytic processes wherein the cysteine proteases, calpain and caspase modify the axonal cytoskeleton, causing irreversible damage over time postinjury. ⋯ Brains were processed for immunohistochemical localization of damaged axonal profiles displaying either amyloid precursor protein (APP)- or RMO-14-immunoreactivity (IR), both considered markers of specific features of TAI. Digital data acquisition and statistical analysis demonstrated that preinjury administration of MDL-28170 significantly reduced the mean number of damaged RMO-14- as well as APP-IR axonal profiles in the brainstem fiber tracts analyzed. These results further underscore the role of calpain-mediated proteolytic processes in the pathogenesis of DAI and support the potential use of cell permeable calpain-inhibitors as a rational therapeutic approach in TBI.