TY - JOUR
T1 - Epilepsy with Electrical Status Epilepticus During Slow Sleep and Secondary Bilateral Synchrony
AU - Kobayashi, Katsuhiro
AU - Nishibayashi, Naohiro
AU - Ohtsuka, Yoko
AU - Oka, Eiji
AU - Ohtahara, Shunsuke
PY - 1994/9
Y1 - 1994/9
N2 - Summary: In 3 children with “epilepsy with electrical status epilepticus during slow sleep” (ESES), we estimated interhemispheric small time differences (TDs) during spike‐wave activity in EEG by coherence and phase analysis by the two‐dimensional autoregressive model to differentiate their continuous diffuse spike‐waves during slow‐wave sleep (CSWS) between primary bilateral synchrony and secondary bilateral synchrony (SBS). Maximal TDs at onset of apparently bilateral synchronous spike‐wave bursts (BSSWs) during slow‐wave sleep were 12·0–26·5 ms (mean 20·3 ms) with consistent leading hemispheres in eight bursts of the 3 patients, indicating SBS as pathophysiology of their CSWS. This suggestion was supported by their clinico‐EEG findings, including the effect of a single oral dose of clobazam (CLB) on EEG. Three ictal BSSWs of atypical absence seizures in 2 patients were also analyzed to obtain maximal TDs of 17·9–41·7 ms (mean 26·3 ms) at onset, with the same leading sides as in sleep, also indicating SBS. Examination of intraburst TD variations showed no consistent disappearance of TDs during the latter part of the bursts, in either sleep or the ictal EEGs of atypical absences, and a role of the corpus callosum was suggested in the generation of SBS in ESES.
AB - Summary: In 3 children with “epilepsy with electrical status epilepticus during slow sleep” (ESES), we estimated interhemispheric small time differences (TDs) during spike‐wave activity in EEG by coherence and phase analysis by the two‐dimensional autoregressive model to differentiate their continuous diffuse spike‐waves during slow‐wave sleep (CSWS) between primary bilateral synchrony and secondary bilateral synchrony (SBS). Maximal TDs at onset of apparently bilateral synchronous spike‐wave bursts (BSSWs) during slow‐wave sleep were 12·0–26·5 ms (mean 20·3 ms) with consistent leading hemispheres in eight bursts of the 3 patients, indicating SBS as pathophysiology of their CSWS. This suggestion was supported by their clinico‐EEG findings, including the effect of a single oral dose of clobazam (CLB) on EEG. Three ictal BSSWs of atypical absence seizures in 2 patients were also analyzed to obtain maximal TDs of 17·9–41·7 ms (mean 26·3 ms) at onset, with the same leading sides as in sleep, also indicating SBS. Examination of intraburst TD variations showed no consistent disappearance of TDs during the latter part of the bursts, in either sleep or the ictal EEGs of atypical absences, and a role of the corpus callosum was suggested in the generation of SBS in ESES.
KW - Children
KW - Electroencephalog
KW - Epilepsy with continuous spike waves during slow wave sleep
KW - Epilepsy with electrical status epilepticus during slow sleep
KW - Sleep
KW - raphy
UR - http://www.scopus.com/inward/record.url?scp=0027986828&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0027986828&partnerID=8YFLogxK
U2 - 10.1111/j.1528-1157.1994.tb02561.x
DO - 10.1111/j.1528-1157.1994.tb02561.x
M3 - Article
C2 - 7925158
AN - SCOPUS:0027986828
SN - 0013-9580
VL - 35
SP - 1097
EP - 1103
JO - Epilepsia
JF - Epilepsia
IS - 5
ER -