Abstract TP43: Transient Global Brain Ischemia Induces Striatal Neuronal Death of T1-Hyperintensity without Hemorrhage: Susceptibility-Weighted Imaging Study on Cardiac Arrest Survivors
Background: Global brain ischemia-reperfusion leads to selective neuronal death in the hippocampal CA1 area, cerebellar cortex, dorsolateral striatum, and/or neocortical layers 3, 5, and 6 in animal models and in humans. We have reported a delayed neurodegeneration of late-onset neuroimaging change in such brain areas vulnerable to ischemia (Stroke.1994;25:2091-95., Stroke.1999;30:1038-42., Stroke.1999;30:1043-46., Cerebrovasc Dis.2000;10:2-7., Ann Neurol.2003;54:732-7.). The magnetic resonance imaging (MRI) studies on patients after cardiac arrest showed 1) bilateral neurodegeneration with hyperintensity on T1-weighted MRI in the striatum, thalamus, and/or substantia nigra (Stroke.1994;25:2091-5., Neuroradiology.1994;36:605-7.), and 2) specific hippocampal atrophy in the chronic stage (MRI volumetry) (Cerebrovascular Dis.2000;10:2-7.). In the current study with susceptibility-weighted MRI (SWI), we investigated if the delayed T1-hyperintensity in the dorsolateral striatum consistently observed in cardiac arrest survivors represents minor hemorrhage (methemoglobin) or signifies selective neuronal death without bleeding reported as a specific type of ischemic neurodegeneration (Ann Neurol.2003;54:732-47.).
Methods: We studied 11 patients in a vegetative state after unexpected out-of-hospital cardiac arrest who were able to undergo multiple brain MRI. We performed SWI to evaluate if the late-onset striatal T1-hyperintensity represents iron accumulation derived from hemoglobin degradation products or not.
Results: In the 11 patients, serial MR images demonstrated delayed T1-hyperintesity in the bilateral striatum from one to two weeks after the onset. The SWI study showed no hypointense change in the striatal T1-hyperintensity.
Conclusion: The striatal T1-hyperintensity after cardiac arrest seems to correspond to selective neuronal death and glial proliferation with paramagnetic effects but not hemoglobin degradation due to erythrocyte-extravasation.
- © 2012 by American Heart Association, Inc.