Neurocritical care
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Midline shift (MLS) has been associated with unfavorable outcome in patients with intracerebral hemorrhage (ICH). However, the optimal criteria to define the MLS measurements that indicate future outcome in ICH patients are absent, and the quantitative threshold of MLS that differentiates favorable and poor clinical outcome should be further explored. ⋯ MLS(max) can be a good independent predictor of clinical outcome, and MLS(max) > 4 mm is an optimal threshold associated with poor outcome in patients with ICH.
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Review Case Reports
Heart-Shaped Bilateral Medullary Pyramidal Infarction as a Pathognomonic Finding of Anterior Spinal Artery Occlusion.
Unilateral anterior spinal artery (ASA) occlusion resulting in bilateral medullary pyramidal (BMP) infarction is a rare and devastating stroke subtype. We present two cases highlighting the diagnostic and clinical challenges of BMP infarction. ⋯ Acute BMP infarction may present with flaccid tetraplegia mimicking neuromuscular disorders. When the infarction is recognized early, intravenous thrombolysis can be considered to reduce morbidity of this rare stroke subtype.
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Review
Cerebral Edema After Cardiopulmonary Resuscitation: A Therapeutic Target Following Cardiac Arrest?
We sought to review the role that cerebral edema plays in neurologic outcome following cardiac arrest, to understand whether cerebral edema might be an appropriate therapeutic target for neuroprotection in patients who survive cardiopulmonary resuscitation. Articles indexed in PubMed and written in English. Following cardiac arrest, cerebral edema is a cardinal feature of brain injury and is a powerful prognosticator of neurologic outcome. ⋯ Neuroprotection after cardiac arrest generally has focused on protecting neurons, not the microvascular endothelium or blood-brain barrier. Limited preclinical data suggest that strategies to reduce cerebral edema may improve neurologic outcome. Ongoing research will be necessary to determine whether targeting cerebral edema will improve patient outcomes after cardiac arrest.
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Mast cells are first responders to intracerebral hemorrhage. They release potent mediators that can disrupt the blood-brain barrier promoting injury, vasogenic edema formation, and hematoma exacerbation. Also, mast cells recruit other inflammatory cells that maintain and amplify brain damage. Given their early role in the cascade of events in intracerebral hemorrhage, mast cells may offer an alternative target for antichemotactic interventions.