Abstract
To examine the origin of seizures induced by severe neonatal hyperbilirubinemia, The EEG characteristics of seizures were analyzed in newborns with and without severe neonatal hyperbilirubinemia. Fisher’s exact test was used to determine the specificity. In total, 931 patients had a total serum bilirubin (TSB) level of 340–425 μmol/L, only 2 of whom had seizures. Compared to patients with hyperbilirubinemia and a TSB level of 340–425 μmol/L, those with a TSB level >425 μmol/L had a significant risk of seizure (OR = 213.2, 95% CI = 113.0–405.8, P<0.001). Of all 28 patients with severe hyperbilirubinemia and seizure, 26 had seizures that originated in the temporal and/or occipital lobe. In seizure patients without severe hyperbilirubinemia, origination in the temporal/occipital and other lobes occurred in 19 and 117 cases, respectively. Compared to the risk of seizure origination in the temporal and/or occipital lobe in other diseases, the risk in patients with severe hyperbilirubinemia was increased by approximately 80 times (OR = 80.1, 95% CI = 28.3–226.4, P<0.001). Severe neonatal hyperbilirubinemia can selectively induce temporal and occipital lobe seizures. This is the first report of a new syndrome with the same etiology and electrophysiological features as epilepsy.
Highlights
Severe neonatal hyperbilirubinemia can lead to brain damage, including bilirubin encephalopathy and kernicterus
Novel seizures induced by severe neonatal hyperbilirubinemia for total serum bilirubin (TSB) greater than 30 mg/dL remained relatively stable from 2007–2012 in California[3] along with the incidence of the newborns who underwent exchange transfusion
Novel seizures induced by severe neonatal hyperbilirubinemia and axial FLAIR (TR: 6000 ms; TE: 100 ms) images were obtained
Summary
Severe neonatal hyperbilirubinemia can lead to brain damage, including bilirubin encephalopathy and kernicterus. These long-term outcomes are not common nowadays due to the availability of timely and effective interventions for hyperbilirubinemia, for example, exchange transfusion, maternal rhesus immunoglobulin prophylaxis and phototherapy[1]. Kernicterus can occur in healthy near-term and term infants without hemolytic disease or risk factors for hemolysis[2]. Some of the associated risk factors for severe hyperbilirubinemia are: jaundice in the first day of life or before discharge, having a compatriot who had jaundice underwent phototherapy, late preterm with the gestational age of 35–36 weeks, Asian race, the presence of infant bruising or cephalhematoma, rhesus and ABO incompatibility, as well as glucose-6-phosphate dehydrogenase (G6PD) deficiency[1].
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