Articles: brain-injuries.
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Traumatic brain injury (TBI) contributes significantly to the mortality and morbidity rates of traumatized patients. This article presents current concepts in the pathophysiology of TBI, including mechanisms of injury, biomolecular mediators of injury, and the occurrence of secondary injury. Emergency management, monitoring, and imaging of TBI also are reviewed.
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Journal of neurotrauma · Feb 1996
Lesion volume, injury severity, and thalamic integrity following head injury.
Magnetic resonance (MR) scans of 63 traumatic brain injury (TBI) patients were analyzed to examine the relationship between injury severity, lesion volume (nonthalamic cortical/subcortical lesions), ventricle-to-brain ratio (VBR), and thalamic volume. For comparison, 33 normal control subjects were used. Patients with visible nonthalamic structural lesions showed significantly smaller thalamic volumes than patients without visible lesions or control subjects. ⋯ Patients with moderate-severe injuries had significantly smaller thalamic volumes and greater VBRs than patients with mild-moderate injuries. Although several variables related to thalamic volume, the presence of nonthalamic lesions was sufficient to result in smaller thalamic volume. Decreased thalamic volume following head injury suggests that subcortical brain structures may be susceptible to transneuronal degeneration following cortical lesions, and that this can be detected by in vivo MR-based volumetric analysis.
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Journal of neurotrauma · Feb 1996
The effect of lesion volume on cerebral vasomotor tone after focal brain injury and shock.
We have previously shown that the volume of a focal brain injury influences cerebral blood flow. We hypothesized that the cerebral vasomotor tone after traumatic brain injury and shock is related to lesion volume and that the size of the lesion would affect vasomotor reactivity. Swine were randomized to receive either a large or small cryogenic injury followed by shock, and were studied for 5 h postresuscitation. ⋯ A large brain injury and shock resulted in a significant decrease in the pial arteriolar diameter in the injured hemisphere. We also noted significant differences between and within groups in interhemispheric pial arteriolar diameter and pial arteriolar reactivity to acetylcholine and hypocarbia. These data suggest that the volume of injured tissue influences cerebral blood flow by a vascular mechanism, which may be due in part to an alteration in cerebral endothelial cell function.
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Critical care medicine · Feb 1996
Review Case ReportsTreatment modalities for hypertensive patients with intracranial pathology: options and risks.
To review the cerebrovascular pathophysiology of hypertension, and the risks and benefits of antihypertensive therapies in the patient with intracranial ischemic or space-occupying pathology. ⋯ The treatment of acute hypertension in the patient with intracranial ischemic or space-occupying pathology requires an understanding of the pathophysiology of hypertension and determinants of cerebral perfusion pressure. Individual agents should be selected based on their ability to promptly and reliably decrease blood pressure, while considering effects on cerebral blood flow and intracranial pressure.
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Anasthesiol Intensivmed Notfallmed Schmerzther · Feb 1996
[Continuous fiberoptic monitoring of oxygen saturation in cerebral veins in severe craniocerebral trauma--experiences and results].
Monitoring of jugular-venous O2-saturation (SjO2) enables the assessment of cerebral oxygen supply and the rapid detection of cerebral desaturation in patients with severe head injury. Furthermore, it may help to optimize circulation, ventilation, and intracranial hypertension therapy in these patients. This study was performed to evaluate the reliability of SjO2-monitoring as well as to measure cerebral O2-extraction and the frequency of episodes of cerebral desaturation after traumatic brain injury. ⋯ Monitoring of SjO2 in severe head injury provides an estimate of cerebral oxygen supply and may improve the assessment of therapeutic measures in these patients. The high incidence of erroneous readings of the SjO2 is a major drawback of this method. Initially after trauma, a high extraction of oxygen was found, followed by a marked decrease in the subsequent days, presumably reflecting an early, decreased cerebral blood flow and a hyperaemic flow pattern thereafter. Continuous measurements of SjO2 may contribute to advanced, organ-specific cerebral monitoring in severe craniocerebral trauma. The reliability of data, however, should be considerably improved for common clinical use.