Neurocritical care
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Guillain-Barre syndrome (GBS) is a well known entity that has many infectious agents reported as antecedent events. The spectrum of GBS includes acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), acute motor sensory axonal neuropathy (AMSAN), and some other variants like Miller-Fisher syndrome (MFS). ⋯ We report a case of AMAN variant of GBS associated with proven H1N1 influenza A infection. This virus has not been reported previously as the agent of antecedent infection that induced this disorder. Risk factors for other causes of ICU neuromuscular weakness are usually present in the ICU patients and should not be the reason for reluctance in active quest for GBS. Once the diagnosis of GBS is established or suspected the treatment with plasma exchange or intravenous immune globulin is indicated.
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Refractory intracranial hypertension (RIH) frequently complicates severe traumatic brain injury (TBI) and is associated with worse outcomes. Aggressive fluid resuscitation contributes to the development of peripheral and pulmonary edema, but an effect on cerebral edema is not well established. Some clinicians, including advocates of the "Lund Concept", practice fluid restriction as a means of limiting cerebral edema and reducing intracranial pressure (ICP). ⋯ We found no association between cumulative fluid balance and the development of RIH. However, more judicious volume management has the potential to reduce the occurrence of pulmonary complications. Further research is needed to clarify optimal approaches to fluid management among patients with severe TBI and to guide the interpretation and integration of information derived from P(bt)O(2) monitors.
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The Na(+)-K(+)-2Cl(-) cotransporter localized in the brain vascular endothelium has been shown to be important in the evolution of cerebral edema following experimental stroke. Previous in vivo studies have demonstrated that bumetanide, a selective Na(+)-K(+)-2Cl(-) cotransport inhibitor, attenuates ischemia-evoked cerebral edema. Recently, bumetanide has been shown to also inhibit water permeability via aquaporin-4 (AQP4) expressed in Xenopus laevis oocytes. We tested the hypothesis that the perivascular pool of AQP4 plays a significant role in the anti-edema effect of bumetanide by utilizing wild-type (WT) mice as well as mice with targeted disruption of alpha-syntrophin (alpha-Syn(-/-)) that lack the perivascular pool of AQP4. ⋯ These data suggest that bumetanide exerts its neuroprotective and anti-edema effects partly via blockade of the perivascular pool of AQP4 and may have therapeutic potential for ischemic stroke in the clinical setting.