Neurocritical care
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Benzodiazepine treatment of life-threatening gamma-hydroxybutyrate (GHB) withdrawal is frequently unsatisfactory. Animal studies suggest strongly that treatment with GABA(B) agonists, such as baclofen, will be a more effective strategy. ⋯ Baclofen, a GABA(B) agonist, may be a useful agent in the treatment of severe GHB withdrawal.
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Perihemorrhagic pathophysiology of spontaneous intracerebral hemorrhages (ICH) remains unclear. Recently, ischemic changes in the perihemorrhagic zone (PHZ) have been discussed as a potential source of secondary damage. In this study, we focussed on diffusion and perfusion characteristics of experimental ICH. ⋯ We demonstrated vasogenic edema and mild perfusion reduction in the PHZ above the ischemic threshold. The existence of a perihemorrhagic "penumbra" indicating critically ischemic tissue analogous to ischemic stroke is unlikely.
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Multicenter Study Clinical Trial
Effect of endovascular hypothermia on acute ischemic edema: morphometric analysis of the ICTuS trial.
Pilot studies of hypothermia for stroke suggest a potential benefit in humans. We sought to test whether hypothermia decreases post-ischemic edema using CT scans from a pilot trial of endovascular hypothermia for stroke. ⋯ Endovascular hypothermia decreases acute post-ischemic cerebral edema. A larger trial is warranted to determine if it affects final infarct volume and outcome in stroke.
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Thrombolysis heralded a new era of acute intervention for ischemic stroke, accompanied by an increasing need for comprehensive acute critical care support. There remains the prospect of novel cerebral protection strategies. Cerebral ischemia initiates a complex cascade of events at genomic, molecular, and cellular levels, and inflammation is important in this cascade, both in the CNS and in the periphery. ⋯ A promising novel therapeutic approach is the interleukin-1 receptor antagonist (IL-1ra), which limits the action of the cytokine IL-1, a pivotal mediator in the pathophysiology of acute neurodegeneration. Critical care has much to offer some patients after acute ischemic stroke, including the delivery of acute interventions, often with very short therapeutic time windows, physiological support, and the management of complications. We discuss inflammation and its mediators in acute ischemic stroke, the systemic stress, and acute phase protein responses to acute ischemic stroke, how inflammation is relevant in deteriorating ischemic stroke, the impact of physiological variables, and both current and emerging interventions for acute ischemic stroke.