Articles: brain-injuries.
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J. Cereb. Blood Flow Metab. · Jun 1998
Randomized Controlled Trial Clinical TrialQuinolinic acid is increased in CSF and associated with mortality after traumatic brain injury in humans.
We tested the hypothesis that quinolinic acid, a tryptophan-derived N-methyl-D-aspartate agonist produced by macrophages and microglia, would be increased in CSF after severe traumatic brain injury (TBI) in humans, and that this increase would be associated with outcome. We also sought to determine whether therapeutic hypothermia reduced CSF quinolinic acid after injury. Samples of CSF (n = 230) were collected from ventricular catheters in 39 patients (16 to 73 years old) during the first week after TBI, (Glasgow Coma Scale [GCS] < 8). ⋯ There was a powerful association between time after TBI and increased quinolinic acid (P < 0.00001), and quinolinic acid was higher in patients who died than in survivors (P = 0.003). Age, gender, GCS, and treatment (32 degrees C versus 37 degrees C) did not correlate with CSF quinolinic acid. These data reveal a large increase in quinolinic acid concentration in CSF after TBI in humans and raise the possibility that this macrophage-derived excitotoxin may contribute to secondary damage.
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Despite increasing understanding of the cellular and molecular mechanisms that cause pathology in children who suffer traumatic brain injury, few advances have been made in developing new effective therapies for such injury. In the past, clinicians treated some neurologically injured patients with the sustained application of systemic hypothermia. This practice was largely abandoned when patients experienced complications; however, interest has been renewed in treatment with milder forms of hypothermia. ⋯ Promising results from two clinical trials are presented. Moreover, evidence is discussed in support of the notion that some children with traumatic brain injury, more so than adults, may benefit from hypothermic therapy. Lastly, putative mechanisms for the effects of hypothermia, including attenuation of injury caused by inflammation, excitotoxic amino acids, nitric oxide, and free radicals, are discussed.
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Journal of neurotrauma · Jun 1998
Soluble ICAM-1 in CSF coincides with the extent of cerebral damage in patients with severe traumatic brain injury.
The intercellular adhesion molecule-1 (ICAM-1) expressed by endothelial cells is crucial in promoting adhesion and transmigration of circulating leukocytes across the blood-brain barrier (BBB). Migrated immunocompetent cells, in turn, release mediators that stimulate glial and endothelial cells to express ICAM-1 and release cytokines, possibly sustaining cerebral damage. Following activation, proteolytic cleavage of membrane-anchored ICAM-1 results in measurable levels of a soluble form, sICAM-1. ⋯ In addition, overall analysis showed that sICAM-1 in CSF correlated with the extent of BBB damage as indicated by the QA (r = 0.76; p < 0.001). These results suggest that increased sICAM-1 levels in CSF might depict ongoing immunologic activation and that sICAM-1 correlates with the extent of tissue and BBB damage. The origin of soluble ICAM-1 in CSF and its pathophysiologic role after TBI remains to be clarified.
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Comparative Study
A clinical evaluation of the Codman MicroSensor for intracranial pressure monitoring.
The strain-gauge Codman MicroSensor intracranial pressure (ICP) transducer has shown consistently good laboratory performance. To assess the practical performance of the system in patients following acute brain injury, 10 patients were fitted with a MicroSensor and a second ICP monitor. In five cases this was a fibre-optic transducer and in five cases an intraventricular fluid-filled device. ⋯ Comparison traces of ICP in individual patients show high agreement in timing and size of changes. The unexplained constant offset leads to uncertainty about the true ICP. Treatment decisions are often based upon absolute levels of ICP and patient care may therefore differ depending upon the monitor used.