Journal of neurotrauma
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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.
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Journal of neurotrauma · May 2016
Coated-platelet levels increase with number of injuries in patients with mild traumatic brain injury.
Coated-platelets are procoagulant platelets that are elevated in stroke and are associated with stroke recurrence. In a previous study, prompted by data showing an increased risk for stroke following traumatic brain injury (TBI), we found that coated-platelet levels are elevated in patients with combat-related mild TBI (mTBI) several years after the injury, compared with controls. We now investigate in an expanded patient population whether parameters commonly recorded in mTBI are related to increased coated-platelet potential. ⋯ A multi-variable linear model analysis, including these three parameters and an additional three parameters (race/ethnicity, smoking, and mechanism of injury) that reached a p value of <0.2, showed that the number of injuries were predictive of coated-platelet levels (p = 0.004). These results support a mechanistic link between increased coated-platelet levels and repeated injuries in mTBI. Long-term studies will be required to determine the impact of increased prothrombotic potential in mTBI patients.
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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.