Stroke; a journal of cerebral circulation
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Cerebrospinal fluid drainage is often indicated in patients with acute hydrocephalus after aneurysmal subarachnoid hemorrhage but is believed to increase the risk of rebleeding. We studied the risk of rebleeding in patients with subarachnoid hemorrhage during treatment for acute hydrocephalus. ⋯ This study does not confirm an importantly increased risk of rebleeding during external ventricular drainage or lumbar punctures for acute hydrocephalus after aneurysmal subarachnoid hemorrhage.
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To study cerebrovascular autoregulation and its impact on clinical course in patients with impending malignant middle cerebral artery infarction, we used invasive multimodal neuromonitoring, including measurement of cerebral perfusion pressure, tissue oxygen pressure, and microdialysis. ⋯ We found early impairment of cerebrovascular autoregulation in peri-infarct tissue of patients who developed malignant brain edema, whereas autoregulation was preserved in patients with a benign course. Impaired cerebral autoregulation seems to play a key role for development of a malignant course and might serve as a predictive marker. Impaired cerebral autoregulation also accentuates the need for consequent adjustment of cerebral perfusion pressure in patients with impaired autoregulation.
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The objective was to analyze the feasibility of a lumbar drainage (LD) for a communicating malresorptive hydrocephalus in patients with supratentorial hemorrhage (intracerebral hemorrhage) accompanied by severe ventricular involvement (intraventricular hemorrhage) who required an external ventricular drain (EVD). ⋯ Our data suggest that LD is safe and feasible for treatment of nonpersistent communicating hydrocephalus after intracerebral hemorrhage. After adequate treatment of the occlusive hydrocephalus using an EVD in the acute phase, LD discloses an alternative for further extracorporal cerebrospinal fluid drainage.
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Evidence suggests that activated microglia are detrimental to the survival of new hippocampal neurons, whereas blocking inflammation has been shown to restore hippocampal neurogenesis after cranial irradiation and seizure. The aim of this current study is to determine the effect of minocycline on neurogenesis and functional recovery after cerebral focal ischemia. ⋯ Minocycline reduces functional impairment caused by cerebral focal ischemia. The improved function is associated with enhanced neurogenesis and reduced microglia activation in the dentate gyrus and possibly improved neural environment after chronic treatment with minocycline.
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Astrocytic glutamate transporter protein, GLT-1 (EAAT2), recovers extracellular glutamate and ensures that neurons are protected from excess stimulation. Recently, beta-lactam antibiotics, like ceftriaxone (CTX), were reported to induce the upregulation of GLT-1. Here, we investigated ischemic tolerance induction by CTX in an experimental model of focal cerebral ischemia. ⋯ This study presents evidence that CTX induces ischemic tolerance in focal cerebral ischemia and that this is mediated by GLT-1 upregulation.