Neurocritical care
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Management of refractory status epilepticus (SE) involves administration of intravenous γ-aminobutyric acid (GABA(A)) receptor agonists, such as benzodiazepines, barbiturates, or propofol. Animal models suggest that reductions in synaptic GABA(A) receptors may cause these drugs to become less effective as the duration of SE increases. This may explain the large doses that are commonly required to control seizures, which in turn contributes to a high incidence of complications, including hypotension and the need for vasopressors. In contrast, expression of excitatory N-methyl-D-aspartate (NMDA) receptors increases with prolonged SE and their stimulation by glutamate may propagate seizure activity. Ketamine is a NMDA-receptor antagonist that is considered promising as treatment for refractory SE. Compared with other anaesthetic drugs, ketamine produces less hypotension. ⋯ Larger series and phase I clinical trial(s) of ketamine for treatment of refractory SE seem warranted.
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Temporal patterns in aneurysmal subarachnoid hemorrhage (aSAH) may provide insight into modulation, and therefore, prevention of hemorrhage. We investigated the time of hemorrhage and its relationship to traditional risk factors among patients admitted with aSAH. ⋯ aSAH occur in a diurnal, morning prevalent pattern regardless of traditional aSAH risk factors. The association of these risk factors with existing onset patterns should be investigated in future studies.
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Apolipoprotein E has previously been demonstrated to modulate acute brain injury responses, and administration of COG1410, an apoE-mimetic peptide derived from the receptor-binding region of apoE, improves outcome in preclinical models of acute neurological injury. In the current study, we sought to establish the optimal dose and timing of peptide administration associated with improved functional outcome in a murine model of intracerebral hemorrhage (ICH). ⋯ COG1410 administered at a dose of 2 mg/kg within 2 h after injury improves functional recovery in a murine model of ICH.
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Delayed deterioration associated with vasospasm (DDAV) after aneurismal subarachnoid hemorrhage (SAH) is a major cause of morbidity. We have previously shown that myeloid cell depletion before experimental SAH in a murine model ameliorates DDAV. In this study, we address whether systemic administration of lipopolysaccharide (LPS) worsens DDAV in a myeloid cell-dependent fashion. ⋯ LPS administration before SAH worsens DDAV through a myeloid cell-dependent mechanism supporting studies in humans which show that systemic inflammation increases the likelihood of developing DDAV.