Articles: brain-injuries.
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The prevalence and correlates of depressive symptoms following childhood traumatic brain injuries (TBI) were examined using data drawn from a prospective longitudinal study. Participants included 38 children with severe TBI, 51 with moderate TBI, and 55 with orthopedic injuries (OI). Assessments occurred shortly after injury (baseline) and at 6- and 12-month follow-ups. ⋯ Socioeconomic status also was a significant moderator of group differences, such that the effects of TBI were exacerbated in children from more disadvantaged homes. Although self-reports of depressive symptoms were related inconsistently to children's verbal memory, parent reports of depressive symptoms were unrelated to IQ or verbal memory. The findings suggest that TBI increases the risk of depressive symptoms, especially among more socially disadvantaged children, and that depressive symptoms are not strongly related to post-injury neurocognitive deficits.
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Journal of neurotrauma · Sep 2000
Role of nociceptin/orphanin FQ in age-dependent cerebral hemodynamic effects of brain injury.
This study was designed to compare the role of the newly described endogenous opioid nociceptin/orphanin FQ (NOC/oFQ) in the reductions of cerebral blood flow (CBF) and pial artery diameter observed following fluid percussion brain injury (FPI) in chloralose anesthetized newborn and juvenile pigs as a function of time postinsult. FPI elevated CSF NOC/oFQ concentration from 70 +/- 3 to 444 +/- 51 within 1 h and to 1,931 +/- 112 pg/mL (n = 7) within 8 h, whereas concentrations returned to control value within 168 h in the newborn. In contrast, FPI elevated CSF NOC/oFQ from 77 +/- 4 to 202 +/- 16 pg/mL (n = 7) within 1 h, while values returned to control value within 8 h in the juvenile. ⋯ Similar observations for reductions in pial artery diameter were made in untreated and treated newborns and juveniles. These data suggest that an elevated CSF NOC/oFQ concentration and altered vascular responsiveness to this opioid contribute to reductions in CBF and pial artery diameter observed following FPI. Because such NOC/oFQ changes were greater in newborns versus juveniles, these data further suggest that NOC/oFQ contributes to age-related cerebral hemodynamic differences in the effects of FPI.
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Long-term outcome is important in managing traumatic brain injury (TBI), an epidemic in the United States. Many injury severity variables have been shown to predict major morbidity and mortality. Less is known about their relationship with specific long-term outcomes. ⋯ Injury severity variables are significant single outcome predictors and, in combination with premorbid and demographic variables, help predict long-term disability and community integration for individuals hospitalized with TBI.
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The purpose of this study was to determine the validity and reliability of the SjO2 catheter in neurologically impaired patients. Cerebral hypoxia and ischemia are two of the most important causes of secondary injury after brain trauma. Early detection and treatment of cerebral ischemia may prevent additional damage to the injured brain. ⋯ The initial milestones by Myerson et al. and Gibbs et al. have served as the basis for more refined research on cerebral tissue oxygenation and metabolism. The unreliability of the SjO2 catheter demonstrates how little we still know about cerebral physiology. In spite of the many advancements in healthcare technology, limiting secondary brain injury and improving neurologic outcome have remained elusive.
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The identification of a serum marker to assist in the diagnosis of cerebral injury after cardiac surgery is potentially useful. S100 protein is an early marker of cerebral damage. It is released after cardiac surgery performed under cardiopulmonary bypass (CPB). ⋯ Patients undergoing intracardiac operations combined with coronary artery bypass surgery are more susceptible to brain injury and have higher levels of S100 after CPB. Furthermore, adults and children undergoing deep circulatory arrest are more susceptible to brain injury, in terms of higher S100 protein release after CPB. Serum S100 protein levels are reduced after using arterial line filtration and covalent-bonded heparin to coat the inner surface of the CPB circuit.