Neurocritical care
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Historically, the prognosis for poor grade subarachnoid hemorrhage patients has been considered dismal. As a result, many hospitals have chosen conservative management over aggressive therapy. This guarded approach, however, is based on studies that do not take into account newer, more effective, management protocols and more recent long-term evidence that significant neurological recovery occurs in the months to years following discharge. More accurate and predictive methods are needed to decide when aggressive therapy is warranted. ⋯ This study demonstrates that significant recovery occurs in the weeks to months after poor grade aSAH. Pupillary reactivity on admission can be used as a predictor of survival and recovery at intermediate and long-term time points, more so than Hunt and Hess grade.
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This study compares the effect of mild and severe cerebral ischemia on neuronal damage and neurogenesis. ⋯ These data indicate that histopathological damage depends on the severity of the ischemic insult and that forebrain ischemia activates generation of new neurons. A mild ischemic challenge appears to be a more potent neurogenic stimulus than severe ischemia. The new neurons survive at least 28 days. This may relate to delayed histopathological and functional recovery after cerebral ischemia.
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Clinical Trial
Stereotactic aspiration-thrombolysis of intracerebral hemorrhage and its impact on perihematoma brain edema.
Recent reports suggest that when thrombolytic agents are administered within the clot, lysis rate accelerates at the expense of increased risk of worsening edema. To test this hypothesis, we report on the volumetric analysis of (1) the intraparenchymal hematoma and, (2) perihematomal edema in a cohort of ICH patients treated with intraclot rtPA. ⋯ In this cohort of ICH patients treated using FAST, volumetric analysis of ICH and perihematomal edema seems to suggest that local use of rtPA does not exacerbate brain edema formation. Furthermore, there seems to be a strong association between reduction in ICH volume and reduction in edema volume, as would be expected following the concept of "hemotoxicity" postulated by some investigators.
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Hyperammonemia causes brain edema and high intracranial pressure (ICP) in acute liver failure (ALF) by accumulation of glutamine in brain. Since a high-level glutamine may compromise mitochondrial function, the aim of this study was to determine if the lactate-pyruvate ratio is associated with a rise in the glutamine concentration and ICP. ⋯ ICP and the cerebral glutamine concentration in patients with ALF correlate to the lactate-pyruvate ratio. Since CPP was sufficient in all patients the rise in lactate-pyruvate ratio indicates that accumulation of glutamine compromises mitochondrial function and causes intracranial hypertension.
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Subarachnoid hemorrhage (SAH) can trigger immune activation sufficient to induce the systemic inflammatory response syndrome (SIRS). This may promote both extra-cerebral organ dysfunction and delayed cerebral ischemia, contributing to worse outcome. We ascertained the frequency and predictors of SIRS after spontaneous SAH, and determined whether degree of early systemic inflammation predicted the occurrence of vasospasm and clinical outcome. ⋯ Systemic inflammatory activation is common after SAH even in the absence of infection; it is more frequent in those with more severe hemorrhage and in those who undergo surgical clipping. Higher burden of SIRS in the initial four days independently predicts symptomatic vasospasm and is associated with worse outcome.