Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2008
Assessment of mitochondrial impairment and cerebral blood flow in severe brain injured patients.
We believe that in traumatic brain injury (TBI), the reduction of N-acetyl aspartate (NAA) occurs in the presence of adequate cerebral blood flow (CBF) which would lend support to the concept of mitochondrial impairment. The objective of this study was to test this hypothesis in severely injured patients (GCS 8 or less) by obtaining simultaneous measures of CBF and NAA. ⋯ Considering the direct link between energy metabolism and NAA synthesis in the mitochondria, this study showed that in the absence of an ischemic insult, reductions in NAA concentration reflects mitochondrial dysfunction.
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Acta Neurochir. Suppl. · Jan 2008
Evaluation of optimal cerebral perfusion pressure in severe traumatic brain injury.
Traumatic brain injury (TBI) is a major cause of death and disability. In the 2000 guidelines, one of the suggestions for TBI treatment was to maintain cerebral perfusion pressure (CPP) < or = 70 mmHg. But in the 2003 guidelines, the suggestion was changed to < or = 60 mmHg. ⋯ The patients < 50-year-old, with higher GCS level, with ICP monitoring, and with ICP levels < 20 mmHg had lower mortality rates and better prognosis (GOS) (p < 0.05 or 0.001). The patients in the GCS 3-5 subgroup had a significantly lower mortality and better prognosis if the CPP value was maintained higher than 70 mmHg (p < 0.05) The optimal CPP maintained < or = 60 mmHg did not fit in all STBI patients. Our study concludes that it is critical to maintain CPP substantially higher in lower GCS level patients.
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Acta Neurochir. Suppl. · Jan 2008
Microglial activation and brain injury after intracerebral hemorrhage.
Microglial activation and thrombin formation contribute to brain injury after intracerebral hemorrhage (ICH). Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1beta) are 2 major proinflammatory cytokines. In this study, we investigated whether thrombin stimulates TNF-alpha and IL-1beta secretion in vitro, and whether microglial inhibition reduces ICH-induced brain injury in vivo. ⋯ Tuftsin reduced thrombin-induced upregulation of TNF-alpha and IL-1beta. In vivo, microglia were activated after ICH, and intracerebral injection of tuftsin reduced brain edema in the ipsilateral basal ganglia (81.1 +/- 0.7% vs. 82.7 +/- 1.3% in vehicle-treated group; p < 0.05) after ICH. These results suggest a critical role of microglia activation in ICH-related brain injury.
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Acta Neurochir. Suppl. · Jan 2008
Predictive values of age and the Glasgow Coma Scale in traumatic brain injury patients treated with decompressive craniectomy.
The use of decompressive craniectomy (DC) as an aggressive therapy for traumatic brain injury (TBI) has gained renewed interest. While age and the Glasgow Coma Scale (GCS) are frequently correlated with outcome in TBI, their prognostic values after decompressive craniectomy are ill-defined. ⋯ This data suggests that in TBI patients treated with DC, age correlates with outcome while the correlation between GCS and outcome is age-dependent.
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Acta Neurochir. Suppl. · Jan 2008
Accuracy of non-invasive ICP assessment can be increased by an initial individual calibration.
In a formerly introduced mathematical model, intracranial pressure (ICP) could be non-invasively assessed using cerebral blood flow velocity (FV) and arterial blood pressure (ABP). The current study attempts to check whether the accuracy of the non-invasive ICP assessment (nICP) improves after an initial individual calibration by implanted ICP probes. ⋯ Initial individual calibration of nICP assessment method significantly improves the accuracy of nICP estimation on subsequent days. This hybrid method of ICP assessment may be used in intensive care units in patients with initially implanted ICP probes. After removal of the probes, ICP monitoring can be continued using the calibrated nICP assessment procedure.