Journal of neurotrauma
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Journal of neurotrauma · Dec 2013
Multicenter StudySevere Traumatic Brain Injury in a High-Income Country: An Epidemiological Study.
This adult cohort determined the incidence and patients' short-term outcomes of severe traumatic brain injury (sTBI) in Switzerland and age-related differences. A prospective cohort study with a follow-up at 14 days was performed. Patients ≥16 years of age sustaining sTBI and admitted to 1 of 11 trauma centers were included. sTBI was defined by an Abbreviated Injury Scale of the head (HAIS) score >3. ⋯ Median GCS at 14 days was 15 (IQR, 14-15) without differences among subgroups. Estimated incidence of sTBI in Switzerland was low, age was high, and mortality considerable. The elderly had higher initial GCS and a higher death rate, but high GCS at 14 days.
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Journal of neurotrauma · Dec 2013
The complement terminal pathway is activated in focal penetrating but not in mild diffuse Traumatic Brain Injury.
The complement system plays an important role in the inflammatory response activated by many central nervous system disorders. However, its significance in traumatic diffuse traumatic axonal injury (TAI) is not fully known. Here we analyze the complement activity in two rat models of traumatic brain injury (TBI); a focal penetration injury (pen-TBI) and a rotational acceleration injury (rot-TBI) that leads to a mild TAI. ⋯ Our findings suggest that the terminal complement pathway is progressed to the formation of the C5b-9 membrane attack complex only in the penetrating TBI but not in isolated TAI model. This indicates that the complement activation does not lead to membrane-damaging effects and a subsequent secondary axotomy in TAI by the terminal complex C5b-9. The role of complement activation in TAI is unclear, but might indicate an alternative function following rot-TBI, such as opsonizing the synapses for elimination.
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Journal of neurotrauma · Dec 2013
Review Meta AnalysisTraumatic Brain Injury: Methodological Approaches to Estimate Health- and Economic Outcomes.
The effort to standardize the methodology and adherence to recommended principles for all economic evaluations has been emphasized in medical literature. The objective of this review is to examine whether economic evaluations in traumatic brain injury (TBI) research have been compliant with existing guidelines. Medline search was performed between January 1, 1995 and August 11, 2012. ⋯ On average, about six of the 10 criteria were followed in these publications, and only two articles met all 10 criteria. These findings call for an increased awareness of the methodological standards that should be followed by investigators both in performance of economic evaluation and in reviews of evaluation reports prior to publication. The results also suggest that all economic evaluations should be made by following the guidelines within a conceptual framework, in order to facilitate evidence-based practices in the field of TBI.
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Journal of neurotrauma · Dec 2013
Mild Traumatic Brain Injury Results in Depressed Cerebral Glucose Uptake: An (18)FDG PET Study.
Moderate to severe traumatic brain injury (TBI) in humans and rats induces measurable metabolic changes, including a sustained depression in cerebral glucose uptake. However, the effect of a mild TBI on brain glucose uptake is unclear, particularly in rodent models. This study aimed to determine the glucose uptake pattern in the brain after a mild lateral fluid percussion (LFP) TBI. ⋯ Using reference region normalization, PET imaging revealed that mild LFP-induced TBI depresses glucose uptake in both the ipsilateral and contralateral hemispheres in comparison with sham-injured and naïve controls from 3 h to 5 days post-injury. Further, areas of depressed glucose uptake were associated with regions of glial activation and axonal damage, but no measurable change in neuronal loss or gross tissue damage was observed. In conclusion, we show that mild TBI, which is characterized by transient impairments in function, axonal damage, and glial activation, results in an observable depression in overall brain glucose uptake using (18)FDG-PET.
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Journal of neurotrauma · Dec 2013
Controlled cortical impact results in an extensive loss of dendritic spines that is not mediated by injury-induced amyloid-beta accumulation.
The clinical manifestations that occur after traumatic brain injury (TBI) include a wide range of cognitive, emotional, and behavioral deficits. The loss of excitatory synapses could potentially explain why such diverse symptoms occur after TBI, and a recent preclinical study has demonstrated a loss of dendritic spines, the postsynaptic site of the excitatory synapse, after fluid percussion injury. The objective of this study was to determine if controlled cortical impact (CCI) also resulted in dendritic spine retraction and to probe the underlying mechanisms of this spine loss. ⋯ To determine if Aβ contributes to spine loss after brain injury, we administered a γ-secretase inhibitor LY450139 after TBI. We found that while LY450139 administration could attenuate the TBI-induced increase in Aβ, it had no effect on dendritic spine loss after TBI. We conclude that the acute, global loss of dendritic spines after TBI is independent of γ-secretase activity or TBI-induced Aβ accumulation.