Journal of neurotrauma
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Journal of neurotrauma · Oct 2016
Minor Functional Deficits in Basic Response Patterns for Reinforcement following Frontal Traumatic Brain Injury in Rats.
Traumatic brain injury (TBI) is a major contributor to numerous psychiatric conditions and chronic behavioral dysfunction. Recent studies in experimental brain injury have begun to adopt operant methodologies to assess these deficits, all of which rely on the process of reinforcement. No studies have directly examined how reinforced behaviors are affected by TBI, however. ⋯ Further, injured rats were specifically impaired at lower response requirements on the progressive ratio. Taken together, these findings indicate that simple reinforced behaviors are mostly unaffected after TBI, except in the case of variable ratio schedules, but the altered performance on the higher-order progressive ratio schedule suggests changes involving motivation or potentially perseveration. These findings validate operant measures of more complex behaviors for brain injury, all of which rely on reinforcement and can be taken into consideration when adapting and developing novel functional assessments.
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Journal of neurotrauma · Oct 2016
Three months follow-up of rat mild traumatic brain injury: a combined [18F]FDG and [11C]PK11195 PET study.
Mild traumatic brain injury (mTBI) is the most common cause of head trauma. The time course of functional pathology is not well defined, however. The purpose of this study was to evaluate the consequences of mTBI in rats over a period of 3 months by determining the presence of neuroinflammation ([11C]PK11195) and changes in brain metabolism ([18F]FDG) with positron emission tomography (PET) imaging. ⋯ Alterations in glucose metabolism were detected over the 3 month period, with increased uptake in the medulla (p < 0.04, d ≥ 1.2), and decreased uptake in the globus pallidus, striatum, and thalamus (p < 0.04, d ≤ 1.2). Similar findings were observed in the voxel-based analysis (p < 0.05 at corrected cluster level). As a consequence of the mTBI, and in the absence of apparent behavioral alterations, relative brain glucose metabolism was found altered in several brain regions, which mostly correspond with those presenting neuroinflammation in the subacute stage.
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Journal of neurotrauma · Oct 2016
Ultrastructure of diaschisis lesions following traumatic brain injury.
We used controlled cortical impact in mice to model human traumatic brain injury (TBI). Local injury was accompanied by distal diaschisis lesions that developed within brain regions anatomically connected to the injured cortex. At 7 days after injury, histochemistry documented broadly distributed lesions, particularly in the contralateral cortex and ipsilateral thalamus and striatum. ⋯ Cell bodies and processes that were silver positive at the light microscopy level showed hydropic disintegration consisting of: loss of nuclear heterochromatin; dilated somal and neuritic processes with a paucity of filaments, tubules, and mitochondria; and increased numbers of electron-dense membranous structures. Importantly the cell membrane itself was still intact 3 weeks after injury. Although the full biochemical nature of these lesions remains to be deciphered, the morphological preservation of damaged neurons and processes raises the question of whether this is a reversible process.
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Journal of neurotrauma · Oct 2016
Randomized Controlled TrialCortical Thickness in Mild Traumatic Brain Injury.
Magnetic resonance imaging data were acquired at ∼24 h and ∼3 months post-injury on mild traumatic brain injury (mTBI; n = 75) and orthopedic injury (n = 60) cohorts. The mTBI subjects were randomly assigned to a treatment group with atorvastatin or a non-treatment mTBI group. The treatment group was further divided into drug and placebo subgroups. ⋯ Further analysis revealed significant cortical thinning only in the non-treatment group relative to the control group. In the follow-up, small regions with significant but subtle cortical thinning and thickening were seen in the frontal, temporal, and parietal lobes in the left hemisphere in the non-treatment group only. Our results indicate that cortical thickness could serve as a useful measure in identifying subtle changes in mTBI patients.
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Journal of neurotrauma · Oct 2016
White matter injury susceptibility via fiber strain evaluation using whole-brain tractography.
Microscale brain injury studies suggest axonal elongation as a potential mechanism for diffuse axonal injury (DAI). Recent studies have begun to incorporate white matter (WM) structural anisotropy in injury analysis, with initial evidence suggesting improved injury prediction performance. In this study, we further develop a tractography-based approach to analyze fiber strains along the entire lengths of fibers from voxel- or anatomically constrained whole-brain tractography. ⋯ As an illustration, we evaluate the DAI susceptibilities of WM voxels and transcallosal fiber tracts in three idealized head impacts. Findings suggest the potential importance of the tractography-based approach for injury prediction. These efforts may enable future studies to correlate WM mechanical responses with neuroimaging, cognitive alteration, and concussion, and to reveal the relative vulnerabilities of neural pathways and identify the most vulnerable ones in real-world head impacts.