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 neurosurgery · Sep 2000
Maturation-dependent response of the piglet brain to scaled cortical impact.
The goal of this study was to investigate the relationship between maturational stage and the brain's response to mechanical trauma in a gyrencephalic model of focal brain injury. Age-dependent differences in injury response might explain certain unique clinical syndromes seen in infants and young children and would determine whether specific therapies might be particularly effective or even counterproductive at different ages. ⋯ These results demonstrate that, for this particular focal injury type and severity, vulnerability to mechanical trauma increases progressively during maturation. Because of its developmental and morphological similarity to the human brain, the piglet brain provides distinct advantages in modeling age-specific responses to mechanical trauma. Differences in pathways leading to cell death or repair may be relevant to designing therapies appropriate for patients of different ages.
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Am. J. Physiol. Heart Circ. Physiol. · Sep 2000
Chronic metabolic sequelae of traumatic brain injury: prolonged suppression of somatosensory activation.
Injuries to the brain acutely disrupt normal metabolic function and may deactivate functional circuits. It is unknown whether these metabolic abnormalities improve over time. We used 2-deoxyglucose (2-DG) autoradiographic image-averaging to assess local cerebral glucose utilization (lCMR(Glc)) of the rat brain 2 mo after moderate (1.7-2.1 atm) fluid-percussion traumatic brain injury (FPI). ⋯ Whisker stimulation in rats with prior trauma failed to induce metabolic activation of either cortex or thalamus. Image-mapping of histological material obtained in the same injury model was undertaken to assess the possible influence of injury-induced regional brain atrophy on computed lCMR(Glc); an effect was found only in the lateral cortex at the trauma epicenter. Our results show that, 2 mo after trauma, resting cerebral metabolic perturbations persist, and the whisker-barrel somatosensory circuit shows no signs of functional recovery.
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Traumatic brain injuries (TBIs) are the most common disabling injuries in the United States, accounting for 44% of all deaths due to trauma. Once inflicted, primary cerebral injury is immutable and irreversible. ⋯ Relationships exist between therapeutic positioning, multisystemic stability, and prevention of secondary cerebral injury in severe TBI. A critical review and synthesis of current research literature on multisystem responses to positioning led to development of clinical recommendations based on currently available evidence and generated best practices for positioning patients with severe TBI.
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The Journal of pediatrics · Aug 2000
Increases in bcl-2 protein in cerebrospinal fluid and evidence for programmed cell death in infants and children after severe traumatic brain injury.
To determine whether bcl-2, a protein that inhibits apoptosis, would be increased in cerebrospinal fluid (CSF) in infants and children after traumatic brain injury (TBI) and to examine the association of bcl-2 concentration with clinical variables. ⋯ Bcl-2 may participate in the regulation of cell death after TBI in infants and children. The increase in bcl-2 seen in patients who survived is consistent with a protective role for this anti-apoptotic protein after TBI.