Neurocritical care
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To compare in-hospital mortality between intracerebral hemorrhage (ICH) patients in rural hospitals to those in urban hospitals of the USA. ⋯ Despite current efforts to reduce disparity in stroke care, ICH patients hospitalized in rural hospitals had two times the odds of dying compared to those in urban hospitals. In addition, the ICH mortality gap between rural and urban centers is increasing. Further studies are needed to identify and reverse the causes of this disparity.
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Mild obesity is associated with a survival benefit in cardiovascular and cerebrovascular disease. Only a few studies have analyzed the effect of obesity on outcomes after spontaneous intracerebral hemorrhage (ICH), and none have used a national US database. We sought to determine whether or not obesity was associated with outcomes and in-hospital complications following ICH. ⋯ In patients with spontaneous ICH, obesity is associated with decreased in-hospital mortality but higher rates of in-hospital complications and greater total hospital charges. Non-morbid obesity carries lower odds of non-routine hospital discharge.
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In studies on cardiac arrest (CA)/resuscitation (R) injury, Purkinje cell degeneration was described, however, with inconsistent data concerning severity and time point of manifestation. Moreover, CA/R studies paid only limited attention to inhibitory stellate interneurons. To this aim, the hypothesis that cerebellar could be relatively resilient toward CA/R because of diverse cellular defense mechanisms including interaction with stellate cells was tested. ⋯ Comparative analysis of hippocampal CA1 pyramidal cells and cerebellar Purkinje cells confirmed a relative resil-ience of Purkinje cells to CA/R. We found only a notable degeneration of Purkinje cell neuronal fiber network, which, however, not necessarily led to neuronal cell death. To induce significant Purkinje cell loss, a stronger ischemic trigger seems to be needed. As possible Purkinje cell-protecting mechanisms, we would propose: (1) activation of inhibitory stellate cells, shown by cfos, MnSOD, and Bcl2 expression, balancing out ischemia-induced excitation and inhibition of Purkinje cells; (2) translocation of the calcium-buffering system, shown by parvalbumin and calbindin D28 k expression, protecting Purkinje cells from detrimental calcium overload; (3) activation of the neuron-astrocyte cross talk, protecting Purkinje cells from over-excitation by removing potassium and neurotransmitters from the extracellular space; (4) activation of the effective and long-lasting MnSOD defense system; and (5) of the anti-apoptotic protein Bcl2 in Purkinje cells itself. Moreover, the results emphasize the limited comparability of animal CA/R studies because of the heterogeneity of the used experimental regimes.