Neurocritical care
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We report four patients who developed periodic eyelid opening following hypoxic ischemic injury. This manuscript reviews the clinical course of our patients as well as previously published cases and discusses the neuroanatomical basis of eyelid opening. ⋯ Our experience and prior reports suggest that periodic eyelid opening following cardiac arrest is associated with a burst-suppression pattern on EEG. Since burst-suppression is highly (though not invariably) predictive of a poor outcome in this patient population, intensivists should be familiar with this neurological sign. Prospective studies are needed to define the neurophysiology of this phenomena and clarify its clinical significance.
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As intravenous thrombolysis frequently fails to recanalize occluded proximal intracerebral arteries, interventional recanalization therapy is increasingly being considered as treatment option in acute ischemic stroke patients. The optimal periprocedural patient management for these interventions is currently unknown. The aim of this study was to identify factors delaying door-to-treatment times, and to evaluate the effect of a fast-track intubation standard operating procedure (I-SOP) on door-to-angiography time. ⋯ In acute stroke patients, intubation prior to interventional recanalization therapy can delay treatment initiation. The implementation of an I-SOP accelerates interventional treatment initiation.
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Case Reports
Cognitive decline and hypersomnolence: thalamic manifestations of a tentorial dural arteriovenous fistula (dAVF).
Intracranial dural arteriovenous fistulas (dAVFs) often present with pulsatile tinnitus, orbital congestion, and headache. Occasionally, they present with focal neurologic deficits, a dementia-like syndrome, hemorrhage, or ischemic infarction. ⋯ We conclude that intracranial dAVFs with thalamic venous congestion should be considered in the diagnostic differential for patients who present with subacute cognitive decline and T2 hyperintense thalamic signal change.
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Early secondary neurologic deterioration after aneurysmal subarachnoid hemorrhage (SAH) may have many causes including rebleeding, hydrocephalus, parenchymal hematoma, or seizures. ⋯ Sudden clinical deterioration after SAH with coma and a fixed "blown" pupil may result from hemorrhage extension into the brainstem parenchyma rather than oculomotor nerve injury from compression or stretch.