Stroke; a journal of cerebral circulation
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Clinical Trial Controlled Clinical Trial
Unexpected nocturnal hypoxia in patients with acute stroke.
Patients who have had a stroke are at risk of hypoxia through alterations in the central regulation of respiration, through aspiration, and through respiratory muscle weakness. Sleep-related breathing disorders are common and may lead to episodes of nocturnal hypoxia even when daytime oxygenation is normal. The aim of this study was to assess the prevalence of unexpected nocturnal hypoxia in stroke patients. ⋯ Oxygen saturation at night is approximately 1% lower than when awake. Almost a quarter of stroke patients who are normoxic at screening during the day spend >30 minutes with an oxygen saturation <90%.
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Although several studies have demonstrated the effectiveness of specialist Stroke Unit (SU) care of stroke patients, there is still disagreement over how these units are best organized. We sought to clarify the role of continuous monitoring of physiological parameters in acute ischemic stroke. ⋯ Admission of acute stroke patients to a monitoring SU may positively influence their outcome at discharge. Confirmation of our findings in larger trials will indicate the need for a revision of the minimum requirements of SUs, with the addition of monitoring as a new requirement.
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The goal of this work was to determine the effect of age at initial presentation on clinical and morphological characteristics in patients with brain arteriovenous malformation (AVM). ⋯ Our data suggest a significant interaction of patient age and clinical and morphological AVM features and argue against uniform AVM characteristics across different age classes at initial presentation. In particular, AVM patients diagnosed at a higher age show a higher fraction of AVM hemorrhage and are more likely to harbor additional risk factors such as concurrent arterial aneurysms and small AVM diameter. Longitudinal population-based AVM data are necessary to confirm these findings.
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We have previously shown that delivery of brain-derived neurotrophic factor (BDNF) through direct intrahippocampal gene transduction with a viral vector suppresses the formation of new dentate granule cells triggered by global forebrain ischemia. Here, we investigated whether inhibition of endogenous BDNF alters ischemia-induced neurogenesis in the dentate gyrus. ⋯ Our findings provide evidence that endogenous BDNF counteracts neuronal differentiation, but not cell proliferation or survival, in ischemia-induced dentate gyrus neurogenesis.