Articles: brain-injuries.
-
Biography Historical Article
Good Samaritan surgeon wrongly accused of contributing to President Lincoln's death: an experimental study of the President's fatal wound.
When President Abraham Lincoln was shot in the back of the head at Ford's Theater in Washington, D.C., on April 14, 1865, he was immediately rendered unconscious and apneic. Doctor Charles A. Leale, an Army surgeon, who had special training in the care of brain injuries, rushed to Lincoln's assistance. When Doctor Leale probed the wound in Lincoln's thickened scalp, feeling for the bullet, he dislodged a blood clot, and Lincoln began to breathe again. However, Lincoln progressively deteriorated and died at 7:22 AM on April 15, 1865. During the postmortem examination of Lincoln's body, numerous secondary missiles of bone and metal were found in the track of pultaceous brain tissue, extending completely through the brain to the front of the skull. In February 1995, an article in a popular magazine alleged that Doctor Leale had caused further (fatal) damage to Lincoln's brain by thrusting his finger into the brain through the bullet hole. The article alleged (wrongly) that most bullet wounds of the brain incurred in Civil War times were not fatal. ⋯ The wound made by John Wilkes Booth's derringer ball in Lincoln's brain was devastating; it was clearly the cause of his death. Good Samaritan surgeon Leale has been falsely accused of contributing to Lincoln's death.
-
There is abundant evidence that after in vivo traumatic brain injury, oxygen radicals contribute to changes in cerebrovascular structure and function; however, the cellular source of these oxygen radicals is not clear. The purpose of these experiments was to use a newly developed in vitro tissue culture model to elucidate the effect of strain, or stretch, on neuronal, glial, and endothelial cells and to determine the effect of the free radical scavenger polyethylene glycol-conjugated superoxide dismutase (PEG-SOD; pegorgotein, Dismutec) on the response of each cell type to trauma. ⋯ These studies further document the utility of the model for studying cell injury and repair and further support the vascular endothelial cell as a site of free radical generation and radical-mediated injury. On the assumption that, like aortic endothelial cells, stretch-injured cerebral endothelial cells also produce oxygen radicals, our results further suggest the endothelial cell as a site of therapeutic action of free radical scavengers after traumatic brain injury.
-
J. Cereb. Blood Flow Metab. · May 1996
Widespread hemodynamic depression and focal platelet accumulation after fluid percussion brain injury: a double-label autoradiographic study in rats.
Cerebrovascular damage leading to subsequent reductions in local cerebral blood flow (lCBF) may represent an important secondary injury mechanism following traumatic brain injury (TBI). We determined whether patterns of 111-indium-labeled platelet accumulation were spatially related to alterations in lCBF determined autoradiographically 30 min after TBI. Sprague-Dawley rats (n = 8), anesthetized with halothane and maintained on a 70:30 (vol/vol) mixture of nitrous oxide/oxygen and 0.5% halothane, underwent parasagittal fluid percussion brain injury (1.7-2.2 atm). 111-Indium-tropolone-labeled platelets were injected 30 min prior to TBI while [14C]-iodoantipyrine was infused 30 min after trauma. ⋯ Significant flow reductions were also seen in remote cortical and subcortical areas, including the right frontal cortex and striatum. These results indicate that focal platelet accumulation and widespread hemodynamic depression are both early consequences of TBI. Therapeutic strategies directed at these early microvascular consequences of TBI may be neuroprotective by attenuating secondary ischemic processes.
-
Arch Phys Med Rehabil · May 1996
Randomized Controlled Trial Clinical TrialProspective study on the use of bolus intrathecal baclofen for spastic hypertonia due to acquired brain injury.
To determine if the intrathecal delivery of baclofen will decrease spastic hypertonia caused by brain injury. ⋯ Intrathecal injection of baclofen is capable of reducing the spastic hypertonia associated with brain injury.
-
To longitudinally evaluate unbound and total serum phenytoin concentrations during intravenous phenytoin maintenance dosage and to determine the relationship among phenytoin protein binding, serum albumin, and unbound fatty acid concentrations in patients with head injuries during intensive care unit (ICU) and convalescent care. ⋯ Phenytoin protein binding was significantly correlated with albumin and was more variable in ICU and convalescent patients with brain injuries than in healthy volunteers. The high dosage requirements and subtherapeutic unbound phenytoin concentrations observed during acute care are best explained by increased metabolism. Phenytoin dosage requirements decreased during convalescence.