Articles: traumatic-brain-injuries.
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Journal of neurotrauma · Jan 2017
Striatal Mitochondrial Disruption Following Severe Traumatic Brain Injury.
Traumatic brain injury (TBI) results in oxidative stress and calcium dysregulation in mitochondria. However, little work has examined perturbations of mitochondrial homeostasis in peri-injury tissue. We examined mitochondrial homeostasis after a unilateral controlled cortical impact over the sensorimotor cortex in adult male rats. ⋯ We detected an acute increase in superoxide dismutase 2 mRNA expression, as well as an induction of microRNA (miR)-21 and miR-155, which have been previously demonstrated to disrupt mitochondrial homeostasis. Behaviorally, rats with TBI exhibited marked error rates in contrainjury forelimb performance on the ladder test. These findings reveal that there may be differential susceptibilities of various peri-injury brain structures to mitochondrial dysfunction and associated behavioral deficits, and that molecular pathways demonstrated to interfere with mitochondrial homeostasis and function are activated subacutely post-TBI.
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Journal of neurotrauma · Jan 2017
Long-Term Neuropsychological Profiles and their Role as Mediators of Adaptive Functioning following Traumatic Brain Injury in Early Childhood.
The objectives of the study were to characterize long-term neuropsychological outcomes following traumatic brain injury (TBI) sustained during early childhood, and determine whether identified neuropsychological impairments mediated the effect of TBI on long-term adaptive functioning. Participants included 16 children with severe TBI, 42 children with moderate TBI, and 72 children with orthopedic injuries (OI) sustained between ages 3 and 7 years. Children completed neuropsychological tests and caregivers completed a structured interview of child adaptive functioning at 6.9 (±1.10) years post-injury. ⋯ No neuropsychological measure significantly mediated the effect of moderate TBI on adaptive functioning. Children sustaining early severe TBI demonstrate persisting neuropsychological impairments into adolescence and young adulthood. The impact of severe TBI on children's long-term adaptive functioning is mediated in part by its effects on fluid reasoning and processing speed.
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Journal of neurotrauma · Jan 2017
Long-term motor deficits after controlled cortical impact in rats can be detected by fine motor skill tests but not by automated gait analysis.
Animal models with constant, long-lasting motor deficits together with the right tests to assess behavioral abnormalities are needed to study the effectiveness of potential therapies to restore motor functions. In the current study, controlled cortical impact (CCI) was applied in rats to induce damage to the forelimb area of the motor cortex and the dorsal striatum. ⋯ In striking contrast to previous studies on CCI in mice, neither forelimb impairments, nor general changes in gait, were detected with the CatWalk XT. These data suggest that the adhesive removal test, the cylinder test, and the Montoya staircase test are the methods of choice to detect long-term unilateral motor deficits in rats after CCI, whereas the use of automated gait analysis systems might not be suitable to measure these behavioral deviations.
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Journal of neurotrauma · Jan 2017
Adolescent Mice Demonstrate a Distinct Pattern of Injury after Repetitive Mild Traumatic Brain Injury.
Recently, there has been increasing interest in outcomes after repetitive mild traumatic brain injury (rmTBI) (e.g., sports concussions). Although most of the scientific attention has focused on elite athlete populations, the sequelae of rmTBI in children and young adults have not been well studied. Prior TBI studies have suggested that developmental differences in response to injury, including differences in excitotoxicity and inflammation, could result in differences in functional and histopathological outcomes after injury. ⋯ Three months after injury, adolescent and adult mice demonstrated increased ionized calcium binding adaptor 1 (IbA1) immunolabeling compared with sham controls. Compared with sham controls, NMDA receptor subtype 2B (NR2B) expression in the hippocampus was reduced by ∼20% in both adolescent and adult injured mice. The data suggest that injured adolescent mice may show a distinct pattern of functional deficits after injury that warrants further mechanistic studies.
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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.