Journal of neurotrauma
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Journal of neurotrauma · Jan 2017
Early changes in cortical emotion processing circuits after mild traumatic brain injury following motor vehicle collision.
Mild traumatic brain injury (mTBI) patients frequently experience emotion dysregulation symptoms, including post-traumatic stress. Although mTBI likely affects cortical activation and structure, resulting in cognitive symptoms after mTBI, early effects of mTBI on cortical emotion processing circuits have rarely been examined. To assess early mTBI effects on cortical functional and structural components of emotion processing, we assessed cortical activation to fearful faces within the first 2 weeks after motor vehicle collision (MVC) in survivors who did and did not experience mTBI. ⋯ SPG activation in mTBI survivors within 2 weeks after MVC was negatively correlated with subsequent post-traumatic stress symptom severity at 3 months (r = -0.68, p = 0.03). Finally, the SPG region was thinner in the mTBI survivors than in the non-mTBI survivors (F = 11.07, p = 0.002). These results suggest that early differences in activation and structure in cortical emotion processing circuits in trauma survivors who sustain mTBI may contribute to the development of emotion-related symptoms.
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Journal of neurotrauma · Jan 2017
Lack of influence of APoE status on cognition or brain structure in professional fighters.
The role of the apolipoprotein e4 allele in moderating cognitive and neuroanatomical degeneration following repeated traumatic brain injury is controversial. Here we sought to establish the presence or absence of such a moderating relationship in a prospective study of active and retired boxers and mixed martial arts fighters. ⋯ No moderating relationship was detected in any of the analyses. The results of this study suggest that there is no impact of apolipoprotein genotype on the apparent negative association between exposure to professional fighting and brain structure volume or aspects of cognition.
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Journal of neurotrauma · Jan 2017
Combining the antipsychotic drug haloperidol and environmental enrichment after traumatic brain injury is a double-edged sword.
Environmental enrichment (EE) confers significant benefits after experimental traumatic brain injury (TBI). In contrast, the antipsychotic drug (APD) haloperidol (HAL) exerts deleterious effects on neurobehavioral and cognitive recovery. Neurorehabilitation and management of agitation, however, are integral components of the treatment strategy for patients with TBI. ⋯ What was surprising was that the therapeutic effects of EE were greatly reduced by concomitant administration of HAL. No differences in cortical lesion volumes were observed among the groups (p > 0.05). The potential clinical implications of these findings suggest that administering HAL to patients undergoing neurorehabilitation may be a double-edged sword because agitation must be controlled before rehabilitation can be safely initiated and executed, but its use may compromise therapeutic efficacy.
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Journal of neurotrauma · Jan 2017
Unfolded Maps for Quantitative Analysis of Cortical Lesion Location and Extent after Traumatic Brain Injury.
We aimed to generate two-dimensional (2D) unfolded cortical maps from magnetic resonance (MR) images to delineate the location of traumatic brain injury (TBI)-induced cortical damage in functionally diverse cytoarchitectonic areas of the cerebral cortex, and to predict the severity of functional impairment after TBI based on the lesion location and extent. Lateral fluid-percussion injury was induced in adult rats and T2 maps were acquired with magnetic resonance imaging (MRI) at 3 days post-TBI. Somatomotor deficits were assessed based on the composite neuroscore and beam balance test, and spatial learning was assessed in the Morris water maze. ⋯ Subsequent receiver operating characteristic analysis indicated that severity of the MRI lesion in S1ULp and S2 was a sensitive and specific predictor of poor performance in the beam balance test. Moreover, MRI lesions in the S1ULp, S2, S1BF, and Ect and PRh cortices predicted poor performance in the Morris water maze test. Our findings indicate that 2D-unfolded cortical maps generated from MR images delineate the distribution of cortical lesions in functionally different cytoarchitectonic regions, which can be used to predict the TBI-induced functional impairment.
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Journal of neurotrauma · Jan 2017
TREM2 deficiency alters acute macrophage distribution and improves recovery after TBI.
Traumatic brain injury (TBI) affects 1.7 million persons annually in the United States (Centers for Disease Control and Prevention). There is increasing evidence that persons exposed to TBI have increased risk of the development of multiple neurodegenerative conditions, including Alzheimer disease (AD). TBI triggers a strong neuroinflammatory response characterized by astrogliosis, activation of microglia, and infiltration of peripheral monocytes. ⋯ Further, Trem2-/- mice exposed to TBI exhibited enhanced macrophage activation near the lesion, but significantly less macrophage activation away from the lesion when compared with B6 mice exposed to TBI. In addition, at 120 DPI, Trem2-/- mice exposed to TBI demonstrated reduced hippocampal atrophy and rescue of TBI-induced behavioral changes when compared with B6 mice exposed to TBI. Taken together, this study suggests that TREM2 deficiency influences both acute and chronic responses to TBI, leading to an altered macrophage response at early time points, and improved pathological and functional outcomes at later time points.