Neurocritical care
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Calculating the risk benefit equation for aggressive treatment of non-convulsive status epilepticus.
To address the question: does non-convulsive status epilepticus warrant the same aggressive treatment as convulsive status epilepticus? ⋯ Determination of the optimal management approach to non-convulsive status epilepticus is complex and is ultimately determined by the inciting etiology.
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Red blood cell (RBC) transfusion after aneurysmal subarachnoid hemorrhage (aSAH) has been associated with increased mortality but prior studies have not adequately adjusted for transfusion-indication bias. ⋯ Among patients with aSAH, RBC transfusion was independently associated with an increased mortality after adjustment for the most common clinical indications for transfusion.
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Comparative Study
Outcome of poor-grade subarachnoid hemorrhage as determined by biomarkers of glucose cerebral metabolism.
The aim of this study was to determine if the measurement of blood biomarkers of glucose cerebral metabolism, performed with retrograde jugular catheter, could predict the outcome of poor-grade aneurysmal subarachnoid hemorrhage (aSAH) patients. ⋯ Our data provide additional support to the view that the MR is a reliable marker for predicting the outcome of poor-grade aSAH patients. Prospective studies are needed to confirm its value in multimodal monitoring.
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Comparative Study
Factors associated with favorable response to hyperbaric oxygen therapy among patients presenting with iatrogenic cerebral arterial gas embolism.
Iatrogenic cerebral arterial gas embolism (CAGE) is an uncommon but potentially a fatal condition. Hyperbaric oxygen (HBO2) therapy is the only definitive treatment for patients with CAGE presenting with acute neurologic deficits. ⋯ A high proportion of CAGE patients treated with HBO2 had favorable outcomes. Time-to-HBO2 ≤ 6 h increased the odds of favorable outcome, whereas the presence of infarct/edema on CT/MRI scan before HBO2 reduced the odds of a favorable outcome. Timely diagnosis and differentiation from thrombo-embolic ischemic events appears to be an important determinant of successful HBO2 treatment.
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Spontaneous intracranial hypotension has become a well-recognized cause of headaches and a wide variety of other manifestations have been reported. Recently, several patients with asymptomatic spontaneous intracranial hypotension were reported. I now report two patients with spontaneous intracranial hypotension who developed multiple arterial strokes associated with death in one patient, illustrating the spectrum of disease severity in spontaneous intracranial hypotension. ⋯ Arterial cerebral infarcts are rare, but potentially life-threatening complications of spontaneous intracranial hypotension. The strokes are due to downward displacement of the brain and can be precipitated by craniotomy for evacuation of associated subdural hematomas.