Management of the Patient with Malignant Hemispheric Stroke.

Malignant hemispheric stroke occurs in 10% of ischemic strokes and has one of the highest mortality and morbidity rates. This stroke, also known as malignant middle cerebral artery stroke, may cause ischemia to an entire hemisphere causing edema, herniation, and death. A collaborative interdisciplinary team approach is needed to manage these complex stroke patients. The nurse plays a vital role in bedside management and support of the patient and family through this complex course of care. This article discusses malignant middle cerebral artery stroke pathophysiology, techniques to predict patients at risk for herniation, collaborative care strategies, and nursing care.

Enriched Environment Elicits Proangiogenic Mechanisms After Focal Cerebral Ischemia.

Brain has limited capacity for spontaneous recovery of lost function after stroke. Exposure to enriched environment (EE) can facilitate functional recovery, but mechanisms underlying this effect are poorly understood. Here, we used a middle cerebral artery occlusion (MCAO) model to investigate the impact of EE on angiogenesis in the post-ischemic brain in adult male Sprague Dawley rats, and examined whether blood-borne factors may contribute. Compared with standard cage (SC), exposure to EE was associated with greater improvement in neurological function, higher peri-infarct vascular density, and higher chronic post-ischemic cerebral blood flow assessed by laser speckle imaging. The effect persisted for at least 28 days. EE also enhanced the expression of hepatocyte growth factor in the peri-ischemic cortex when measured 15 days after MCAO. Interestingly, serum from rats exposed to EE after MCAO showed elevated levels of hepatocyte growth factor, and plasma or serum from rats exposed to EE after MCAO enhanced the survival and proliferation of cultured endothelial cells, in vitro, when compared with control plasma or serum from SC group after MCAO. Together, our data suggest that exposure to EE promotes angiogenesis in the ischemic brain that may in part be mediated by blood-borne factors.

Enriched environment promotes post-stroke neurogenesis through NF-κB-mediated secretion of IL-17A from astrocytes.

Enriched environment (EE) has been shown to promote post-stroke neurogenesis and functional recovery. However, the underlying molecular mechanisms remains poorly understood. Male C57BL/6 mice underwent 60-min middle cerebral artery occlusion (MCAO) followed by reperfusion, after which mice were housed in either standard environment (SE) or EE. We found that post-ischemic EE exhibited reduced protein level of nuclear factor κB (NF-κB)/p65 in cytoplasm and increased its expression correspondingly in nucleus at 28 days post-ischemia (dpi). However, post-ischemic EE had no effects on terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL)-positive cells in ischemic hemisphere at 28dpi. EE mice treated with NF-kB inhibitor Bay11-7082 had decreased subventricular zone (SVZ) neural precursor cells (NPCs) proliferation, neuronal differentiation and subsequent functional recovery after stroke at 28dpi. Bay11-7082 treatment attenuated the promoting effects of post-ischemic EE on interleukin 17A (IL-17A) messenger RNA (mRNA) and protein expression at 28dpi. Furthermore, our in vitro data revealed that in primary astrocyte cultures addition of Bay11-7082 markedly decreased the expression of IL-17A in both the cell lysate and culture supernatant of activated astrocytes. Blockade of IL-17A with neutralizing antibody abrogated the promoting role of EE in NPCs proliferation derived from SVZ, neuronal differentiation and subsequent functional recovery after stroke. Thus, our results reveal a previously uncharacterized property of NF-κB/IL-17A signaling pathway in EE-mediated neurogenesis and functional recovery after ischemic stroke.

Predictive value of the bispectral index for burst suppression on diagnostic electroencephalogram during drug-induced coma.

STUDY PURPOSE: To determine correlation and predictive value between data obtained with the bispectral index (BIS) and diagnostic electroencephalogram (EEG) in determining degree of burst suppression during drug-induced coma. This study seeks to answer the question: "To what degree can EEG suppression and burst count as measured by diagnostic EEG during drug-induced coma be predicted from data obtained from the BIS such as BIS value, suppression ratio (SR), and burst count?" BACKGROUND/SIGNIFICANCE: During drug-induced coma, cortical EEG is the gold standard for real-time monitoring and drug titration. Diagnostic EEG is, from setup through data analysis, labor intensive, costly, and difficult to maintain uniform clinician competency. BIS monitoring is less expensive, less labor-intensive, and easier to interpret data and establish/maintain competency. Validating BIS data versus diagnostic EEG facilitates effective brain monitoring during drug-induced coma at lower cost with similar outcomes. METHOD: This is a prospective, observational cohort study. Four consecutive patients receiving drug-induced coma/EEG monitoring were enrolled. BIS was initiated after informed consent. Variables recorded per minute included presence or absence of EEG burst suppression, burst count, BIS value over time, burst count, and SR. Pearson's product-moment and Spearman rank coefficient for BIS value and SR versus burst count were performed. Regression analysis was utilized to plot BIS values versus bursts/minute on EEG as well as SR versus burst count on EEG. EEG/BIS data were collected from digital data files and transcribed onto data sheets for corresponding time indices. RESULTS: Four patients yielded 1,972 data sets over 33 hours of EEG/BIS monitoring. Regression coefficient of 0.6673 shows robust predictive value between EEG burst count and BIS SR. Spearman rank coefficient of -0.8727 indicates strong inverse correlation between EEG burst count and BIS SR. Pearson's correlation coefficient between EEG versus BIS burst count was .8256 indicating strong positive correlation. Spearman's rank coefficient of 0.8810 and Pearson's correlation coefficient of .6819 showed strong correlation between BIS value versus EEG burst count. Number of patients (4) limits available statistics and ability to generalize results. Graphs and statistics show strong correlation/predictive value for BIS parameters to EEG suppression. CONCLUSIONS: This study is the first to measure correlation and predictive value between BIS monitoring and diagnostic EEG for degree of EEG suppression and burst count in the adult population. Available statistic tests and graphing of variables from BIS and diagnostic EEG show strong correlation and predictive value between both monitoring technologies during drug-induced coma. These support using BIS value, SR, and burst count to predict degree of EEG suppression in real time for titrating metabolic suppression therapy.

Gene and protein analysis of brain derived neurotrophic factor expression in relation to neurological recovery induced by an enriched environment in a rat stroke model.

Although an enriched environment enhances functional recovery after ischemic stroke, the mechanism underlying this effect remains unclear. We previously reported that brain derived neurotrophic factor (BDNF) gene expression decreased in rats housed in an enriched environment for 4 weeks compared to those housed in a standard cage for the same period. To further clarify the relationship between the decrease in BDNF and functional recovery, we investigated the effects of differential 2-week housing conditions on the mRNA of BDNF and protein levels of proBDNF and mature BDNF (matBDNF). After transient occlusion of the right middle cerebral artery of male Sprague-Dawley rats, we divided the rats into two groups: (1) an enriched group housed multiply in large cages equipped with toys, and (2) a standard group housed alone in small cages without toys. Behavioral tests before and after 2-week differential housing showed better neurological recovery in the enriched group than in the standard group. Synaptophysin immunostaining demonstrated that the density of synapses in the peri-infarct area was increased in the enriched group compared to the standard group, while infarct volumes were not significantly different. Real-time reverse transcription polymerase chain reaction, Western blotting and immunostaining all revealed no significant difference between the groups. The present results suggest that functional recovery cannot be ascribed to an increase in matBDNF or a decrease in proBDNF but rather to other underlying mechanisms.