Revista de neurologia · 2001
[Neonatal EEG trace of burst suppression. Etiological and evolutionary factors].
Аннотация на английскомСтатьяНазвание и аннотация: Перевод в очереди
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Martínez-Bermejo A, Roche C, López-Martín V, Arcas J, Tendero A
Аннотация
INTRODUCTION: The electroencephalographic (EEG) trace seen during the neonatal period which shows so called discharges of burst suppression, is caused by a severe disorder of cerebral electrogenesis occurring at this time.
OBJECTIVE: To determine the aetiology, clinical significance and evolution of a group of newborn babies with this type of EEG trace.
PATIENTS AND METHODS: We made a retrospective study of fullterm babies in whom burst suppression EEG recordings had been obtained during the neonatal period.
RESULTS: We studied 34 patients. In 14 cases the trace was associated with hypoxic ischemic encephalopathy; 4 with meningitis; another 4 with early infantile epileptic encephalopathy (Ohtahara syndrome); 4 cases were attributed to drugs (4 with fentanyl associated in one case with phenobarbitone and in another with midazolam); 2 cases were due to early myoclonic epilepsy; 3 to multiple organ failure; one to non ketotic hyperglycinemia and another to leucinosis. In one patient the aetiology could not be determined. Seven patients died before the age of 6 months. Severe neurological sequelae were seen in all the others except for four cases (3 treated with fentanyl and one case with hypoxic ischemic encephalopathy).
CONCLUSIONS: The presence of a burst suppression EEG trace in a neonate makes extensive study to determine the aetiology necessary. Although associated with a worse prognosis, those not treated with piperidine derivatives should be classified separately. Those treated with piperidine derivatives have a good prognosis.
OBJECTIVE: To determine the aetiology, clinical significance and evolution of a group of newborn babies with this type of EEG trace.
PATIENTS AND METHODS: We made a retrospective study of fullterm babies in whom burst suppression EEG recordings had been obtained during the neonatal period.
RESULTS: We studied 34 patients. In 14 cases the trace was associated with hypoxic ischemic encephalopathy; 4 with meningitis; another 4 with early infantile epileptic encephalopathy (Ohtahara syndrome); 4 cases were attributed to drugs (4 with fentanyl associated in one case with phenobarbitone and in another with midazolam); 2 cases were due to early myoclonic epilepsy; 3 to multiple organ failure; one to non ketotic hyperglycinemia and another to leucinosis. In one patient the aetiology could not be determined. Seven patients died before the age of 6 months. Severe neurological sequelae were seen in all the others except for four cases (3 treated with fentanyl and one case with hypoxic ischemic encephalopathy).
CONCLUSIONS: The presence of a burst suppression EEG trace in a neonate makes extensive study to determine the aetiology necessary. Although associated with a worse prognosis, those not treated with piperidine derivatives should be classified separately. Those treated with piperidine derivatives have a good prognosis.