Brain & development · 2014
Study of epileptic drop attacks in symptomatic epilepsy of early childhood - differences from those in myoclonic-astatic epilepsy.
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Itoh Yasushi, Oguni Hirokazu, Hirano Yoshiko, Osawa Makiko
Аннотация
OBJECTIVES: We studied epileptic drop attacks (EDA) in symptomatic epilepsy of early childhood by means of video-polygraphic recordings and compared clinico-electrical differences in EDA among patients with idiopathic myoclonic-astatic epilepsy (MAE).
SUBJECTS AND METHODS: Subjects consisted of 21 children with symptomatic epilepsy and 20 with idiopathic MAE whose EDA were documented at an age between 7 months and 6 years. The seizure types causing EDA as well as other demographic data were compared between the two epilepsy types.
RESULTS: A video-polygraphic study captured a total of 188 EDA (median: 8) in patients with symptomatic epilepsy and 182 EDA (median: 7) in those with idiopathic MAE. In the former, EDA were caused by epileptic spasms (ES) corresponding to generalized biphasic slow discharges, sharp-and-slow wave complexes, or the flattening of ongoing background activity in 15 patients, atonic seizures associated with runs of generalized spike-and-wave complexes in four patients, and myoclonic-atonic seizures in the remaining two patients. The mode of occurrence of EDA in ES was periodic clustering in eight of 15 patients. Interictal EEG revealed generalized irregular multiple spikes-and-waves with focal or multifocal accentuations. Sixteen idiopathic MAE patients had myoclonic-atonic seizures while the remaining four had myoclonic-flexor seizures, all corresponding to generalized high amplitude spikes or polyspike-and-wave complexes and occurring singly.
CONCLUSION: EDA often seen in young children with symptomatic epilepsy were most frequently caused by flexor type ES and rarely by myoclonic-atonic seizures, a hallmark seizure type of MAE. In a clinical setting, the occurrence of periodic clusters and independent focal or multifocal accentuations of generalized spike-and-wave complexes in interictal EEG may indicate EDA caused by ES.
SUBJECTS AND METHODS: Subjects consisted of 21 children with symptomatic epilepsy and 20 with idiopathic MAE whose EDA were documented at an age between 7 months and 6 years. The seizure types causing EDA as well as other demographic data were compared between the two epilepsy types.
RESULTS: A video-polygraphic study captured a total of 188 EDA (median: 8) in patients with symptomatic epilepsy and 182 EDA (median: 7) in those with idiopathic MAE. In the former, EDA were caused by epileptic spasms (ES) corresponding to generalized biphasic slow discharges, sharp-and-slow wave complexes, or the flattening of ongoing background activity in 15 patients, atonic seizures associated with runs of generalized spike-and-wave complexes in four patients, and myoclonic-atonic seizures in the remaining two patients. The mode of occurrence of EDA in ES was periodic clustering in eight of 15 patients. Interictal EEG revealed generalized irregular multiple spikes-and-waves with focal or multifocal accentuations. Sixteen idiopathic MAE patients had myoclonic-atonic seizures while the remaining four had myoclonic-flexor seizures, all corresponding to generalized high amplitude spikes or polyspike-and-wave complexes and occurring singly.
CONCLUSION: EDA often seen in young children with symptomatic epilepsy were most frequently caused by flexor type ES and rarely by myoclonic-atonic seizures, a hallmark seizure type of MAE. In a clinical setting, the occurrence of periodic clusters and independent focal or multifocal accentuations of generalized spike-and-wave complexes in interictal EEG may indicate EDA caused by ES.