Articles: brain-injuries.
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Arch Phys Med Rehabil · Sep 1993
Comparative StudyUndetected musculoskeletal trauma in children with traumatic brain injury or spinal cord injury.
A prospective study of 82 traumatically injured patients was conducted to determine the frequency with which skeletal trauma was undetected at acute care facilities. The clinical significance of each instance of undetected trauma on the patient's rehabilitation programs was assessed. Between May 1987 and October 1988, all trauma patients who sustained a spinal cord injury (SCI) or a severe traumatic brain injury (TBI) had total body bone scans (Tc-99mMDP) prior to beginning rehabilitation. ⋯ Additionally, heterotopic ossification was detected in 14 children, of which only two sites were previously known. In three children with TBI, the area of heterotopic ossification impeded functional range of motion. Based upon this data we conclude that a total body bone scan is useful in the child with TBI for the detection of undiagnosed skeletal or soft tissue trauma and heterotopic ossification not recognized during acute care.
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Journal of neurosurgery · Sep 1993
Traumatic brain injury, hemorrhagic shock, and fluid resuscitation: effects on intracranial pressure and brain compliance.
Intracranial hypertension following traumatic brain injury is associated with considerable morbidity and mortality. Hemorrhagic hypovolemia commonly coexists with head injury in this population of patients. Therapy directed at correcting hypovolemic shock includes vigorous volume expansion with crystalloid solutions. ⋯ Elevated CVP following resuscitation from hemorrhage to a high CVP significantly worsened intracranial hypertension in animals with concurrent traumatic brain injury, as compared to animals subjected to traumatic brain injury alone (mean +/- standard error of the mean: 33.0 +/- 2.0 vs. 20.0 +/- 2.0 mm Hg, p < 0.05) or to animals subjected to the combination of traumatic brain injury, hemorrhage, and resuscitation to a low CVP (33.0 +/- 2.0 vs. 24.0 +/- 2.0 mm Hg, p < 0.05). These data support the hypothesis that reduction in brain compliance can occur secondary to elevation of CVP following resuscitation from hemorrhagic shock. This may worsen intracranial hypertension in patients with traumatic brain injury and hemorrhagic shock.
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Shock increases mortality from brain injuries, but the mechanism is poorly understood. We hypothesized that brain injury followed by shock and resuscitation leads to a secondary reperfusion injury mediated in part by polymorphonuclear leukocytes (PMNs). To validate this hypothesis, we studied cerebral perfusion pressure (CPP), intracranial pressure (ICP), cerebral blood flow (CBF), cortical water content (CWC), and hemodynamic variables in a porcine model of focal cryogenic brain injury and hemorrhagic shock. ⋯ The CPMN in both hemispheres in group 3 was significantly greater than in either group 2 or group 4. There was a significant positive correlation between CPMN and both ICP and CWC, and a significant negative correlation between CPMN and CBF. These data suggest an association between CPMN accumulation and secondary brain injury.
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J. Cereb. Blood Flow Metab. · Sep 1993
Comparative StudyHypothermia attenuates the loss of hippocampal microtubule-associated protein 2 (MAP2) following traumatic brain injury.
Traumatic brain injury (TBI) produces a tissue-specific decrease in protein levels of microtubule-associated protein 2 (MAP2), an important cross-linking component of the neuronal cytoskeleton. Because moderate brain hypothermia (30 degrees C) reduces certain neurobehavioral deficits produced by TBI, we examined the efficacy of moderate hypothermia (30 degrees C) in reversing the TBI-induced loss of MAP2 protein. Naive, sham-injured, and moderate (2.1 atm) fluid percussion-injured rats were assessed for MAP2 protein content 3 h post injury using quantitative immunoreactivity measurements. ⋯ Fluid percussion injury dramatically reduced MAP2 levels in the normothermic group (44.3 +/- 5.9%; p < 0.0005) compared with normothermic sham-injured controls. No significant reduction of MAP2 was seen in the hypothermic injured group (95.2 +/- 4.6%; compared with hypothermic sham-injured controls, p > 0.20). Although it is premature to infer any causal link, the data suggest that the attenuation of injury-induced MAP2 loss by hypothermia may contribute to its overall neuroprotective action.