Journal of neurotrauma
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Journal of neurotrauma · Oct 2016
Non-contact rotational head injury produces transient cognitive deficits but lasting neuropathological changes.
Traumatic brain injury (TBI) caused by improvised explosive devices (IEDs) is a growing problem in military settings, but modeling this disease in rodents to pre-clinically evaluate potential therapeutics has been challenging because of inconsistency between models. Although the effects of primary blast wave injury have been extensively studied, little is known regarding the effects of noncontact rotational TBIs independent of the blast wave. To model this type of injury, we generated an air cannon system that does not produce a blast wave, but generates enough air pressure to cause rotational TBI. ⋯ Despite the transient nature of the behavioral deficits, increased levels of phosphorylated tau were observed at 2 and 8 weeks post-injury; however, this tau did not adopt typical pathological structures that have been observed in other TBI models that incorporate blast waves. This was possibly attributed to the fact that this injury was insufficient to induce changes in microglial activation, which was not affected at 2 or 8 weeks post-injury. Taken together, these data suggest that exposure to noncontact, rotational head injury only produces transient cognitive anomalies, but elicits some minor lasting neuropathological changes.
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Journal of neurotrauma · Oct 2016
Excitotoxicity and Metabolic Crisis Are Associated with Spreading Depolarizations in Severe Traumatic Brain Injury Patients.
Cerebral microdialysis has enabled the clinical characterization of excitotoxicity (glutamate >10 μM) and non-ischemic metabolic crisis (lactate/pyruvate ratio [LPR] >40) as important components of secondary damage in severe traumatic brain injury (TBI). Spreading depolarizations (SD) are pathological waves that occur in many patients in the days following TBI and, in animal models, cause elevations in extracellular glutamate, increased anaerobic metabolism, and energy substrate depletion. Here, we examined the association of SD with changes in cerebral neurochemistry by placing a microdialysis probe alongside a subdural electrode strip in peri-lesional cortex of 16 TBI patients requiring neurosurgery. ⋯ In patients with SD, both glutamate and LPR increased in a dose-dependent manner with the number of SDs in the microdialysis sampling period (0, 1, ≥2 SD) [glutamate: 2.1→7.0→52.3 μmol/L; LPR: 27.8→29.9→45.0, p values <0.05]. In these patients, there was a 10% probability of SD occurring when glutamate and LPR were in normal ranges, but a 60% probability when both variables were abnormal (>10 μmol/L and >40 μmol/L, respectively). Taken together with previous studies, these preliminary clinical results suggest SDs are a key pathophysiological process of secondary brain injury associated with non-ischemic glutamate excitotoxicity and severe metabolic crisis in severe TBI patients.
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Journal of neurotrauma · Oct 2016
Role of Pre-Morbid Factors and Exposure to Blast Mild Traumatic Brain Injury on Post-Traumatic Stress in United States Military Personnel.
Mild traumatic brain injury (mTBI), the signature injury of the recent wars in Afghanistan and Iraq, is a prevalent and potentially debilitating condition that is associated with symptoms of post-traumatic stress/post-traumatic stress disorder (PTS/PTSD). Prior mTBI, severity and type of injury (blast vs. non-blast), and baseline psychiatric illness are thought to impact mTBI outcomes. It is unclear if the severity of pre-morbid PTS/PTSD is a risk factor of post-injury levels of PTS and mTBI symptoms. ⋯ Pre-morbid PTS symptoms are associated with an increased risk for clinical levels of PTS following a subsequent mTBI. Symptom severity and positive radiologic findings may amplify this risk. At-risk personnel may benefit from early identification and intervention.
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Journal of neurotrauma · Oct 2016
Injury of the corticospinal tract in patients with mild traumatic brain injury: A diffusion tensor tractography study.
Motor weakness is an important sequela after traumatic brain injury (TBI). Although the majority of cases of TBI are classified as mild TBI, little is known about motor weakness in mild TBI. In this study, we attempted to investigate injury of the corticospinal tract (CST), an important neural tract for motor function, in patients with mild TBI, using diffusion tensor tractography (DTT). ⋯ On configurational analysis of DTT for the left CST in patient group A, 80% showed partial tearing at the subcortical white matter and 20% showed narrowing. We found that in terms of DTT parameters and configuration, a significant portion of patients with mild TBI showed injury of the CST. These results suggest that DTT could provide useful information in detecting injury of the CST, and evaluation of the CST using DTT would be necessary for patients who complain of hand weakness after mild TBI.