Journal of neurotrauma
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Journal of neurotrauma · May 2016
Multicenter StudyTensor-Based Morphometry Reveals Volumetric Deficits in Moderate/Severe Pediatric Traumatic Brain Injury.
Traumatic brain injury (TBI) can cause widespread and prolonged brain degeneration. TBI can affect cognitive function and brain integrity for many years after injury, often with lasting effects in children, whose brains are still immature. Although TBI varies in how it affects different individuals, image analysis methods such as tensor-based morphometry (TBM) can reveal common areas of brain atrophy on magnetic resonance imaging (MRI), secondary effects of the initial injury, which will differ between subjects. ⋯ We found a number of smaller clusters of volume reduction in the cingulate gyrus, thalamus, and fusiform gyrus, and throughout the frontal, temporal, and parietal cortices. Additionally, we found extensive associations between our cognitive performance measure and regional brain volume. Our results indicate a pattern of atrophy still detectable 1-year post-injury, which may partially underlie the cognitive deficits frequently found in TBI.
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Journal of neurotrauma · May 2016
The Evolution of Posttraumatic Stress Disorder following Moderate to Severe Traumatic Brain Injury.
Increasing evidence indicates that post-traumatic stress disorder (PTSD) may develop following traumatic brain injury (TBI), despite most patients having no conscious memory of their accident. This prospective study examined the frequency, timing of onset, symptom profile, and trajectory of PTSD and its psychiatric comorbidities during the first 4 years following moderate-to-severe TBI. Participants were 85 individuals (78.8% male) with moderate or severe TBI recruited following admission to acute rehabilitation between 2005 and 2010. ⋯ The majority of subjects with PTSD experienced a chronic symptom course and all developed one or more than one comorbid psychiatric disorder, with mood, other anxiety, and substance-use disorders being the most common. Despite event-related amnesia, post-traumatic stress symptoms, including vivid re-experiencing phenomena, may develop following moderate-to-severe TBI. Onset is typically delayed and symptoms may persist for several years post-injury.
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Journal of neurotrauma · May 2016
A propensity score analysis of the impact of invasive intracranial pressure monitoring on outcomes following severe traumatic brain injury.
Although a recent clinical trial (BEST TRIP) demonstrated no improvement in outcomes with invasive intracranial pressure (ICP) monitoring (ICPM) following severe traumatic brain injury (TBI), its generalizability has been called into question. In several global settings ICPM is not the standard of care and is used at the discretion of the attending neurosurgeon. Our objective was to determine the impact of ICPM on mortality and 6-month functional outcomes following severe TBI. ⋯ Following propensity score analysis ICPM use was associated with an 8% (p = 0.002) decrease in mortality but no significant effect (p = 0.2) on functional outcome. The use of ICPM following severe TBI was associated with decreased in-hospital mortality. Further clinical trials of ICPM in TBI may be warranted.
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Journal of neurotrauma · May 2016
Nodal versus Total Axonal Strain and the Role of Cholesterol in Traumatic Brain Injury.
Traumatic brain injury (TBI) is a health threat that affects every year millions of people involved in motor vehicle and sporting accidents, and thousands of soldiers in battlefields. Diffuse axonal injury (DAI) is one of the most frequent types of TBI leading to death. In DAI, the initial traumatic event is followed by a cascade of biochemical changes that take time to develop in full, so that symptoms may not become apparent until days or weeks after the original injury. ⋯ Here, we present preliminary evidence from micro-finite element (FE) simulations that the mechanical response of central nervous system myelinated fibers is dependent on the axonal diameter, the ratio between axon diameter and fiber diameter (g-ratio), the microtubules density, and the cholesterol concentration in the axolemma and myelin. A key outcome of the simulations is that there is a significant difference between the overall level of strain in a given axonal segment and the level of local strain in the Ranvier nodes contained in that segment, with the nodal strain being much larger than the total strain. We suggest that the acquisition of this geometric and biochemical information by means of already available high resolution magnetic resonance imaging techniques, and its incorporation in current FE models of the brain will enhance the models capacity to predict the site and magnitude of primary axonal damage upon TBI.
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Journal of neurotrauma · May 2016
Juvenile Traumatic Brain Injury Increases Alcohol Consumption and Reward in Female Mice.
Traumatic brain injury (TBI) is closely and bi-directionally linked with alcohol use, as by some estimates intoxication is the direct or indirect cause of one-third to one-half of all TBI cases. Alcohol use following injury can reduce the efficacy of rehabilitation and increase the chances for additional injury. Finally, TBI itself may be a risk factor for the development of alcohol use disorders. ⋯ Environmental enrichment administered after injury reduced axonal degeneration and prevented the increase in drinking behavior. Additionally, brain-derived neurotrophic factor gene expression, which was reduced by TBI, was normalized by environmental enrichment. Together, these results suggest a novel model of alterations in reward circuitry following trauma during development.