RESUMO
Background@#Post-cardiac arrest syndrome (PCAS) is one of the critical conditions which can result in a more serious brain injury. Early and accurate prognostication is crucial for deciding the patient’s therapeutic plan and setting the treatment goal. This study aimed to establish the prognostication values of quantitative electroencephalography (QEEG) in PCAS patients. @*Methods@#We recruited 183 PCAS patients treated with therapeutic hypothermia. Electroencephalography (EEG) data within 72 hours after cardiac arrest (CA) and clinical data were collected. QEEG analysis including power spectral density (PSD) and connectivity analysis of default mode network (DMN) with imaginary coherence were performed. @*Results@#There were significantly different patterns of PSD between neurologic good and poor outcome groups; absolute and relative power of the alpha 2 and beta 1 frequency (10-15 Hz) bands were increased in all brain regions of good outcome group. However, the relative power of the delta band and higher frequency bands over fast alpha (beta 3 and gamma bands over 20 Hz) were poor outcome markers. We found out that connectivity of DMN were significantly decreased in the poor outcome group compared with the good outcome group. @*Conclusions@#These findings suggest that QEEG analysis could quantify and automate the interpretation of EEG. Furthermore, they can improve the prognostic values for neurologic outcomes relatively accurately and objectively in PCAS patients treated with hypothermia compared with traditional visual grading.
RESUMO
Acute cerebral infarction secondary to glioblastoma is rarely reported, and its mechanism is still controversial. Vascular infiltration of malignant cell, direct mass effect and local procoagulant effect were considered as main pathophysiology. We report a case of glioblastoma-related cerebral infarction documented by high resolution vessel wall magnetic resonance imaging, which reveals concentric enhancement of arterial wall and intraluminal thrombus without direct compression. These findings suggest tumor cell infiltration of intracranial vessels is one of the important mechanisms of glioblastoma-related cerebral infarction.