Oligodendroglial reactions to compression injury of spinal cord include apoptosis, secondary demyelination, and remyelination failure. Within hours after contusion, the membrane lipid peroxidation (MLP) byproduct, 4-hydroxynonenal (HNE), increases rapidly in gray matter and thereafter in white matter tracts beyond the initial lesion level. Considering that HNE is a mediator and marker of neuronal MLP toxicity in various neurodegenerative conditions, the present study examined its effect on the regeneration potential of oligodendrocyte progenitors, as defined by their capacity to survive, proliferate and migrate in primary culture. Treatment of oligodendroblasts with HNE evoked a time- and dose-dependent cytotoxicity resembling apoptosis at aldehyde concentrations known to be produced by neurons and achieved in tissue undergoing peroxidative injury. In addition, sublethal concentrations of HNE inhibited the mitogenic and chemotactic responses of more immature progenitors to platelet-derived growth factor. These effects appear to be mediated in part by the formation of HNE adducts with progenitor proteins located within the plasma membrane and cytoplasmic compartments. Our data are the first to show that HNE can have direct, deleterious effects on oligodendrocyte precursors. The present study also suggests a mechanism by which the striking accumulation of HNE in white matter tracts surrounding the site of spinal cord compression injury and in other ischemic-hypoxic insults associated with MLP could suppress the potential regenerative response of endogenous oligodendrocyte progenitor cells.
It is important to be cognizant of the possibility of pheochromocytoma in patients presenting with hypertension and cerebrovascular manifestations, as commonly used investigations (e.g. catheter angiography) and treatment modalities (e.g. beta-blockers to treat hypertension, corticosteroids to treat suspected vasculitis, etc.) can lead to life threatening complications.
Burst-suppression pattern on electroencephalography (EEG) occurs upon dissociation of the cortex from underlying brain structures. Unless the pattern is a physiologic consequence of administered sedatives, this electroencephalographic pattern is indicative of a poor neurologic outcome and high mortality. We report a case of a 29-year-old female thought to be brain dead based on initial physical examination and EEG findings of burst-suppression, who was later found to have supratherapeutic serum levels of bupropion. This is the second documented case of burst-suppression pattern on EEG in a patient who overdosed on bupropion. We propose that burst-suppression in the setting of bupropion toxicity may revert with drug clearance.
BackgroundAneurysmal subarachnoid hemorrhage (aSAH) is the most severe type of stroke. In 2012, the Joint Commission, in collaboration with the American Heart Association/American Stroke Association (AHA/ASA), launched the Advanced Certification for Comprehensive Stroke Centers (CSCs). This new level of certification was designed to promote higher standard of care for patients with complex stroke.ObjectiveThe goal of this study was to examine the treatment modality and quality benchmarks of aSAH at one of the first five certified CSCs in the United States.MethodsConsecutive patients with aSAH at Cedars-Sinai Medical Center between April 1, 2012 and May 30, 2014 were included for this retrospective study. The ruptured aneurysm was treated with coiling or clipping within 24 h. All patients were managed per AHA guidelines. Discharge outcomes were assessed using modified Rankin Scale (mRS). The rate of aneurysm treatment, door-to-treatment time, rate of posttreatment rebleed, hospital length of stay (LOS), discharge outcome, and mortality rates were evaluated as quality indicators.ResultsThe median age (interquartile range) of the 118 patients with aSAH was 55 (19). Among them, 84 (71.2%) were females, 94 (79.7%) were transfers from outside hospitals, and 74 (62.7%) had Hunt and Hess grades 1–3. Sixty patients (50.8%) were treated with coiling, 52 (44.1%) with clipping, and 6 (5.1%) untreated due to ictal cardiac arrest or severe comorbidities. The rate of aneurysm treatment was 95% (112/118) with median door-to-treatment time at 12.5 (8.5) h and 0.9% (1/112) posttreatment rebleed. The median ICU and hospital LOS were 12.5 (7) and 17.0 (14.5) days, respectively. Coiling was associated with significantly shorter LOS than clipping. There were 59 patients (50%) with favorable outcome and 19 deaths (16.1%) at hospital discharge. There was no significant difference in discharge outcome between coiling and clipping.ConclusionCare of aSAH at one of the early CSCs in the United States was associated with high rate of aneurysm treatment, fast door-to-treatment time, low posttreatment rebleed, excellent outcome, and low mortality rate. Coiling was associated with significant shorter LOS than clipping. There was no significant difference in discharge outcomes between treatment modalities.
Ischemic infarcts in the setting of CABG or ECMO are often presumed to be thromboembolic from the heart or device, related to underlying hemodynamic instability, or due to a clinically apparent systemic infection such as endocarditis. This report suggests that invasive cerebral aspergillosis should be considered in seemingly immunocompetent patients following CABG or ECMO. The mechanism is unclear, but may be related to systemic inflammatory dysregulation resulting in increased susceptibility to uncommon pathogens.
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