Journal of neurotrauma
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Journal of neurotrauma · Apr 2014
Attentional control 10 years post childhood traumatic brain injury: the impact of lesion presence, location and severity in adolescence and early adulthood.
The relationship between brain injury and attentional control (AC) long after a childhood traumatic brain injury (TBI) has received limited investigation. The aim of this article was to investigate the impact that lesion presence, location, and severity has on AC in a group of young persons who had sustained a moderate to severe TBI 10 years earlier during childhood. The participants in this study were a subset of a larger 10-year, follow-up assessment comprised of 31 persons in late adolescence and early adulthood (21 males), with a mean age at testing of 15.4 years (standard error 0.6; range 10.7-21.2 years). ⋯ When using standardized testing with subtests of the TEA-ch, no differences in performance between those with and those without a lesion at 10 years post-TBI were found. On standardized behavioral measures such as parental reports of perceived AC (Behavior Rating Inventory of Executive Function), however, the presence of a lesion was found to have a detrimental effect on the ability to self-regulate and monitor behavior in late adolescence and the early stages of adulthood. We discuss these results and propose that there is a network of brain regions associated with AC, and generalized lesions have the greatest influence on such abilities.
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Journal of neurotrauma · Apr 2014
Traumatic brain injury in vivo and in vitro contributes to cerebral vascular dysfunction through impaired gap junction communication between vascular smooth muscle cells.
Gap junctions (GJs) contribute to cerebral vasodilation, vasoconstriction, and, perhaps, to vascular compensatory mechanisms, such as autoregulation. To explore the effects of traumatic brain injury (TBI) on vascular GJ communication, we assessed GJ coupling in A7r5 vascular smooth muscle (VSM) cells subjected to rapid stretch injury (RSI) in vitro and VSM in middle cerebral arteries (MCAs) harvested from rats subjected to fluid percussion TBI in vivo. Intercellular communication was evaluated by measuring fluorescence recovery after photobleaching (FRAP). ⋯ In isolated MCAs from rats treated with the ONOO(-) scavenger, penicillamine, GJ coupling was not impaired by fluid percussion TBI. In addition, penicillamine treatment improved vasodilatory responses to reduced intravascular pressure in MCAs harvested from rats subjected to moderate fluid percussion TBI. These results indicate that TBI reduced GJ coupling in VSM cells in vitro and in vivo through mechanisms related to generation of the potent oxidant, ONOO(-).
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Journal of neurotrauma · Apr 2014
Assessment of an Experimental Rodent Model of Pediatric Mild Traumatic Brain Injury.
Childhood is one the highest risk periods for experiencing a mild traumatic brain injury (mTBI) from sports-related concussions, motor vehicle accidents, and falls. In addition, many children experience lingering symptomology (post-concussion syndrome) from these closed head injuries. Although the negative sequel of mTBI has been described, a clinically reliable animal model of mild pediatric brain injury has not. ⋯ Juvenile rats who experienced a single mTBI displayed significant motor/balance impairments when tested on the beam walking task and in the open field, as well as deficits of executive functioning as measured with the novel context mismatch task and the probe trial of the Morris water task. In addition, both male and female rats showed depression-like behavior in the forced swim task, with male rats also exhibiting decreased anxiety-related behaviors in the elevated plus maze. The results from this study suggest that the modified weight-drop technique induces a clinically relevant behavioral phenotype in juvenile rats, and may provide researchers with a reliable animal model of mTBI/concussion from which clinical therapeutic strategies could be developed.
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Journal of neurotrauma · Apr 2014
CSF Cortisol and Progesterone Profiles and Outcomes Prognostication after Severe TBI.
Despite significant advances in the management of head trauma, there remains a lack of pharmacological treatment options for traumatic brain injury (TBI). While progesterone clinical trials have shown promise, corticosteroid trials have failed. The purpose of this study was to (1) characterize endogenous cerebrospinal fluid (CSF) progesterone and cortisol levels after TBI, (2) determine relationships between CSF and serum profiles, and (3) assess the utility of these hormones as predictors of long-term outcomes. ⋯ As a precursor to cortisol, progesterone mediated these effects. Serum and CSF levels for both cortisol and progesterone were strongly correlated after TBI relative to controls, possibly because of blood-brain barrier disruption. Also, differentially impaired hormone transport and metabolism mechanisms after TBI, potential de novo synthesis of steroids within the brain, and the complex interplay of cortisol and pro-inflammatory cytokines may explain these acute hormone profiles and, when taken together, may help shed light on why corticosteroid trials have previously failed and why progesterone treatment after TBI may be beneficial.
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Journal of neurotrauma · Apr 2014
Evidence for the therapeutic efficacy of either mild hypothermia or oxygen radical scavengers following repetitive mild traumatic brain injury.
Repetitive brain injury, particularly that occurring with sporting-related injuries, has recently garnered increased attention in both the clinical and public settings. In the laboratory, we have demonstrated the adverse axonal and vascular consequences of repetitive brain injury and have demonstrated that moderate hypothermia and/or FK506 exerted protective effects after repetitive mild traumatic brain injury (mTBI) when administered within a specific time frame, suggesting a range of therapeutic modalities to prevent a dramatic exacerbation. In this communication, we revisit the utility of targeted therapeutic intervention to seek the minimal level of hypothermia needed to achieve protection while probing the role of oxygen radicals and their therapeutic targeting. ⋯ Whereas complete impairment of vascular reactivity was observed in group 1 (without intervention), significant preservation of vascular reactivity was found in the other groups. Similarly, whereas remarkable increase in the APP-positive axon was observed in group 1, there were no significant increases in the other groups. Collectively, these findings indicate that even mild hypothermia or the blunting free radical damage, even when performed in a delayed period, is protective in repetitive mTBI.