Abstracts

COMPARISON OF FEATURES OF SUPPRESSION-BURST ELECTROENCEPHALOGRAPHIC PATTERN WITH DIFFERENT ETIOLOGIES

Abstract number : 3.095
Submission category : 3. Neurophysiology
Year : 2013
Submission ID : 1747366
Source : www.aesnet.org
Presentation date : 12/7/2013 12:00:00 AM
Published date : Dec 5, 2013, 06:00 AM

Authors :
T. Fukasawa, T. Kubota, T. Negoro

Rationale: The suppression-burst (SB) electroencephalographic pattern is observed in infants with two seizure syndromes: Ohtahara syndrome (OS) and early myoclonic encephalopathy (EME). The SB pattern is also observed in neonates with neonatal hypoxic ischemic encephalopathy (HIE), but is usually transient in such cases. There is variability in the electroencephalographic features of the SB pattern. We analyzed the characteristics of the SB pattern caused by hemimegalencephaly (HME), nonketotic hyperglycinemia (NKH), and HIE.Methods: The subjects of this study were two infants with seizures demonstrating an SB pattern. Their etiologies were HME and NKH. We also examined one neonate with HIE showing an SB pattern. The infant with HME developed OS, and the infant with NKH developed EME. In both infants with HME and NKH, we measured the durations of 30 burst phases, suppression phases, and intervals from the beginning of one burst to the beginning of the next burst in the initial electroencephalograms. In the patient with HIE, we measured the same durations and intervals in the electroencephalogram recorded after therapeutic hypothermia and the cessation of sedative drugs. Differences among the patients were statistically analyzed using the Kruskal-Wallis test and Mann-Whitney s U-test. A p-value of <0.05 was considered significant.Results: When electroencephalography was performed, the infant with HME and with NKH were both 3 days of age, and neither of them was administered anticonvulsant drugs. The infant with HIE was 7 days of age and was administered no anticonvulsant drugs. In the infant with HME, the median durations (range) of the burst phase, suppression phase, and intervals from the beginning of one burst to the beginning of the next burst were 5 (2 7), 8 (3 17), and 13 (7 19) seconds, respectively. In the infant with NKH, they were 3 (1 5), 7 (2 16), and 9.5 (4 19) seconds, respectively. Finally, in the infant with HIE, they were 4 (2 7), 28 (7 60), and 32 (11 65) seconds, respectively.Conclusions: The durations of the burst phase, suppression phase, and intervals from the beginning of one burst to the beginning of the next burst were significantly different among the patients. In the patient with HIE, the suppression phases were significantly longer than those in the other two patients. The suppression phase may become prolonged depending on the extent of brain activity suppression. According to Ohtahara, the durations of the burst phase, suppression phase, and intervals from the beginning of one burst to the beginning of the next burst in patients with OS are 2 6, 3 5, and 5 10 seconds, respectively, and the durations of the burst phase and suppression phase in patients with EME are 1 5 and 3 10 seconds, respectively. In the infants with HME and NKH, the durations of the burst phases were almost concordant with those described by Ohtahara, but the durations of the suppression phases were longer than those described by Ohtahara. In actuality, these durations may vary depending on etiology, epileptogenicity, general status, brain activity suppression, and other factors.
Neurophysiology