Journal of neurotrauma
-
Journal of neurotrauma · May 2007
Apolipoprotein E4 allele presence and functional outcome after severe traumatic brain injury.
Presence of the apolipoprotein E (APOE) 4 allele has been associated with increased incidence and faster progression of neurodegenerative diseases, poorer recovery from neurologic insult, and decreased cognitive function in the well-elderly. The specific association between APOE genotype and recovery from severe traumatic brain injury (TBI) is conflicting with many groups finding the APOE 4 allele to be associated with poorer outcome while others have found no association. The purpose of this study was to investigate the association between APOE 4 allele presence and recovery during the two years after injury from severe TBI in light of other potential covariates, such as age, race, gender, hypotension or hypoxia before hospital admission and severity of injury. ⋯ We did not however find significant differences in GOS at individual time points when controlling for other covariates. Our findings suggest that APOE 4 allele presence influences recovery rate from severe TBI independent of other covariates. The findings of this study are unique in that they address not only the relationship between APOE 4 allele presence and outcome from severe TBI, but also describe differences in trajectory of recovery by APOE 4 allele presence.
-
Journal of neurotrauma · May 2007
Proteomic identification of oxidized mitochondrial proteins following experimental traumatic brain injury.
Experimental traumatic brain injury (TBI) results in a significant loss of cortical tissue at the site of injury, and in the ensuing hours and days a secondary injury exacerbates this primary injury, resulting in significant neurological dysfunction. The mechanism of the secondary injury is not well understood, but evidence implicates a critical role for mitochondria in this cascade. This mitochondrial dysfunction is believed to involve excitotoxicity, disruption of Ca(2+) homeostasis, production of reactive oxygen species (ROS), ATP depletion, oxidative damage of mitochondrial proteins, and an overall breakdown of mitochondrial bioenergetics. ⋯ In addition, we have also shown that, following TBI, there is a reduction in the activities of pyruvate dehydrogenase (PDH), complex I, and complex IV. These findings demonstrate that, following TBI, several proteins involved in mitochondrial bioenergetics are highly oxidatively modified, which may possibly underlie the massive breakdown of mitochondrial energetics and eventual cell death known to occur in this model. The identification of these proteins provides new insights into the mechanisms that take place following TBI and may provide avenues for possible therapeutic interventions after TBI.
-
In peripheral nerve injury, end-to-side neurorrhaphy has been reported as an alternative in cases that the proximal nerve stump is not accessible. Several hypotheses have been proposed to explain peripheral nerve regeneration after end-to-side neurorrhaphy. Recent evidence suggests that nerve regeneration occurs by collateral sprouting. ⋯ The goal of this technique is to provide satisfactory functional recovery for the recipient nerve, without any deterioration of the donor nerve function. End-to-side technique has been investigated in detail in both experimental and clinical studies. Only a limited number of reported cases in clinical practice, until today, can reveal that end-to-side technique may become a viable means of repairing peripheral nerves in certain clinical situations.
-
Journal of neurotrauma · May 2007
FasL, Fas, and death-inducing signaling complex (DISC) proteins are recruited to membrane rafts after spinal cord injury.
The Fas/CD95 receptor-ligand system plays an essential role in apoptosis that contributes to secondary damage after spinal cord injury (SCI), but the mechanism regulating the efficiency of FasL/Fas signaling in the central nervous system (CNS) is unknown. Here, FasL/Fas signaling complexes in membrane rafts were investigated in the spinal cord of adult female Fischer rats subjected to moderate cervical SCI and sham operation controls. In sham-operated animals, a portion of FasL, but not Fas was present in membrane rafts. ⋯ Moreover, SCI induced expression of Fas in clusters around the nucleus in both neurons and astrocytes. The formation of the DISC signaling platform leads to rapid activation of initiator caspase-8 and effector caspase-3, and the modification of signaling intermediates such as FADD and cFLIP(L). Thus, FasL/Fas-mediated signaling after SCI is similar to Fas expressing Type I cell apoptosis.
-
Journal of neurotrauma · May 2007
Diffuse axonal injury in severe traumatic brain injury visualized using high-resolution diffusion tensor imaging.
Traumatic brain injury (TBI) is the most common cause of death and disability in young people. The functional outcome in patients with TBI cannot be explained by focal pathology alone, and diffuse axonal injury (DAI) is considered a major contributor to the neurocognitive deficits experienced by this group. The aim of the present study was to investigate whether diffusion tensor imaging (DTI) offers additional information as to the extent of damage not visualized with standard magnetic resonance imaging (MRI) in patients with severe TBI. ⋯ The findings of this study support the hypothesis that severe TBI is accompanied by DAI. The DTI changes were more prominent on the right side that contained the focal pathology in most of the patients and accurately reflected differences in both hemispheres. In conclusion, DTI holds great promise as a diagnostic tool to identify and quantify the degree of white matter injury in TBI patients.