Pediatric cardiac surgery with cardiopulmonary bypass (CPB) is frequently associated with neurologic deficits. We describe the postoperative EEG changes, assess their possible causes, and evaluate their relevance to neurologic outcome. Thirty-one children and five neonates with congenital heart disease were included. EEG recording started after intubation and continued until 22-96 h after CPB. In addition to conventional analysis, spectral analysis was performed for occipital and frontal electrodes, and differences between pre-and postoperative delta power (delta-␦P) were calculated. Maximum values of occipital delta-␦P that occurred within 48 h after CPB were correlated with clinical variables and with perioperative markers of oxidative stress and inflammation. Occipital delta-␦P correlated with frontal delta-␦P, and maximum delta-␦P correlated with conventional rating. Distinct rise of ␦P was detected in 18 of 21 children without any acute or long-term neurologic deficits but only in five of 10 children with temporary or permanent neurologic deficits. Furthermore, maximally registered delta-␦P was inversely associated with duration of CPB and postoperative ventilation. Maximal delta-␦P was also inversely associated with the loss of plasma ascorbate (as an index of oxidative stress) and plasma levels of IL-6 and IL-8. Slow wave activity frequently occurs within 48 h after CPB. However, our data do not support the notion that EEG slowing is associated with adverse neurologic outcome. This is supported by the fact that EEG slowing was associated with less oxido-inflammatory stress. Abbreviations AC, aortic cross-clamping CPB, cardiopulmonary bypass FFT, fast Fourier transformation max delta-␦P, maximum difference between pre-and postoperative delta power MDA, malondialdehyde MDA-TNL, malondialdehyde corrected for total neutral lipids ␦P, delta power delta-␦P, difference between pre-and postoperative delta power Cardiac surgery with cardiopulmonary bypass (CPB) in children and neonates is frequently associated with acute neurologic symptoms and long-term neurologic deficits (1-4). Neuropsychological deficits persist in a substantial number of patients. During the intraoperative period, a global decrease in perfusion and oxygen delivery and focal ischemia related to embolic insults or diffuse microvascular changes are the principal mechanisms of brain damage (5). Systemic inflammation and reactive oxygen species generated by CPB might contribute to postoperative neurologic dysfunction (6,7). Impaired cerebral vasoregulation and ischemia/reperfusion injury continues in the early postoperative period (8,9). Postoperative cardiopulmonary dysfunction may additionally threaten cerebral perfusion pressure and oxygen delivery. However, there is an increased energy demand to restore neuronal membrane function and ionic gradients that are compromised by CPB.Events that affect the brain are usually followed by neuronal dysfunction, which can often be detected by EEG changes.