A LMOST half a century has passed since the first experimental and clinical use of cardiopulmonary bypass (CPB) with deep hypothermic circulatory arrest (DHCA) for the surgical correction of congenital cardiac defects. 1 In those 50 years, a marked advance in the understanding of the physiology and improvement in the technical conduct of hypothermic CPB have enabled surgeons to perform repairs on the most difficult congenital cardiac defects with ever-decreasing morbidity and mortality. However, neurologic injury with residual motor and neuropsychologic deficit attributed to DHCA has long been identified as a major morbidity 2 that has yet to be overcome. The incidence of neurologic complications in children after DHCA ranges from 20% to 80%, including developmental delays, diminished intelligence, pyramidal deficits, severe hypotonia, focal seizures, and choreoathetosis. 3,4 These neurologic deficits increase the mortality rate from 7.2% to 19.6% after pediatric cardiac surgery. The incidence of electroencephalographic (EEG) seizures (20%) post-DHCA far exceeds clinically detected seizures (6%) and correlates with a worse motor function, neuropsychologic development, and more abnormalities on magnetic resonance imaging in a 1-year follow-up. 5