<abstract xmlns="http://www.w3.org/1999/xhtml"><sec id="j_joepi-2015-0001_s_001"><h3>Aim</h3><p>The aim of this article is to review criticaly the Electrical Status Epilepticus in Slow Sleep (ESES) phenomenon from a neurophysiological mechanisms aspect as well as terminological and classification issues.</p></sec><sec id="j_joepi-2015-0001_s_002"><h3>Methods</h3><p>The review includes all the relevant papers published during the last 43 years on the subject of ESES and Continous Spike – Wave in Sleep (CSWS).These papers were identified in various large databases via the internet.</p></sec><sec id="j_joepi-2015-0001_s_003"><h3>Rewiev and remarks</h3><p>ESES/CSWS phenomena can be held as a common final pathway originating from different etiologies, including patients with early brain damage (probably involving thalamic structures), but also patients without structural pathology as in atypical evolution of idiopathic regional childhood hyperexcitability syndromes (with Rolandic epilepsy as a prototype). There are hints that genetic predisposition might be an important factor in the development of this process. The two large patient groups (lesional and non-lesional) show the same EEG evolution and encephalopathic cognitive consequences. The sleep EEG activation can be held as a common endophenotype. ESES represents an extreme sleep activation/potentiation of the local/regional interictal discharges, enhancing them in frequency, territorial extension, intra and trans-hemispherial propagation, synchrony and continuity. This process is most probably not identical with the development of bilateral spike-wave pattern in ,,generalized” epilepsies which involves primarily or secondarily the thalamocortical system as it had been explored by Gloor (1979) for idiopathic generalized rpilepsy and Steriade and Amzica (2003) for different types of generalized spike and wave discharges.</p></sec><sec id="j_joepi-2015-0001_s_004"><h3>Conclusions and syndromological embedding of ESES</h3><p>In an overwhelming majority of the investigated cases, the maps of the single discharges constituting sleep activation are identical; with focal/regional interictal spikes followed by slow closing wave, as it is seen in childhood regional age dependent hyperexcitability syndromes (prototype of the centro-temporal spikes of Rolandic epilepsy). The main mechanism of the developing cognitive impairment is most probably the consequence of interference with plastic function of slow wave sleep by obliterating synaptic decline during sleep. Presently, the consensus and co-operative research is highly obstacled by the terminological chaos, the controversial definitions and views around this still striking and enigmatic phenomenon.</p></sec></abstract>

AimThe aim of this article is to review criticaly the Electrical Status Epilepticus in Slow Sleep (ESES) phenomenon from a neurophysiological mechanisms aspect as well as terminological and classification issues.MethodsThe review includes all the relevant papers published during the last 43 years on the subject of ESES and Continous Spike – Wave in Sleep (CSWS).These papers were identified in various large databases via the internet.Rewiev and remarksESES/CSWS phenomena can be held as a common final pathway originating from different etiologies, including patients with early brain damage (probably involving thalamic structures), but also patients without structural pathology as in atypical evolution of idiopathic regional childhood hyperexcitability syndromes (with Rolandic epilepsy as a prototype). There are hints that genetic predisposition might be an important factor in the development of this process. The two large patient groups (lesional and non-lesional) show the same EEG evolution and encephalopathic cognitive consequences. The sleep EEG activation can be held as a common endophenotype. ESES represents an extreme sleep activation/potentiation of the local/regional interictal discharges, enhancing them in frequency, territorial extension, intra and trans-hemispherial propagation, synchrony and continuity. This process is most probably not identical with the development of bilateral spike-wave pattern in ,,generalized” epilepsies which involves primarily or secondarily the thalamocortical system as it had been explored by Gloor (1979) for idiopathic generalized rpilepsy and Steriade and Amzica (2003) for different types of generalized spike and wave discharges.Conclusions and syndromological embedding of ESESIn an overwhelming majority of the investigated cases, the maps of the single discharges constituting sleep activation are identical; with focal/regional interictal spikes followed by slow closing wave, as it is seen in childhood regional age dependent hyperexcitability syndromes (prototype of the centro-temporal spikes of Rolandic epilepsy). The main mechanism of the developing cognitive impairment is most probably the consequence of interference with plastic function of slow wave sleep by obliterating synaptic decline during sleep. Presently, the consensus and co-operative research is highly obstacled by the terminological chaos, the controversial definitions and views around this still striking and enigmatic phenomenon.

Encephalopathy with Electrical Status Epilepticus in Slow Wave Sleep – a review with an emphasis on regional (perisylvian) aspects

Journal of Epileptology

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

AimThe aim of this article is to review criticaly the Electrical Status Epilepticus in Slow Sleep (ESES) phenomenon from a neurophysiological mechanisms aspect...

Encephalopathy with Electrical Status Epilepticus in Slow Wave Sleep – a review with an emphasis on regional (perisylvian) aspects

Online veröffentlicht: 09. Dez. 2014

Seitenbereich: 71 - 87

Eingereicht: 16. Sept. 2014

Akzeptiert: 03. Dez. 2014

DOI: https://doi.org/10.21307/joepi-2015-0015

Schlüsselwörter
Electrical Status Epilepticus in Slow Sleep, Continuous Spike-Wave in slow Sleep, perisylvian epileptic network, cognitive impairment, sleep plastic functions, synaptic decline during slow wave sleep, atypical Rolandic epilepsy, early thalamic lesions

© 2014 Peter Halász et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Encephalopathy with Electrical Status Epilepticus in Slow Wave Sleep – a review with an emphasis on regional (perisylvian) aspects

Online veröffentlicht: 09. Dez. 2014

Seitenbereich: 71 - 87

Eingereicht: 16. Sept. 2014

Akzeptiert: 03. Dez. 2014

DOI: https://doi.org/10.21307/joepi-2015-0015

SchlüsselwörterElectrical Status Epilepticus in Slow Sleep, Continuous Spike-Wave in slow Sleep, perisylvian epileptic network, cognitive impairment, sleep plastic functions, synaptic decline during slow wave sleep, atypical Rolandic epilepsy, early thalamic lesions

© 2014 Peter Halász et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Schlüsselwörter
Electrical Status Epilepticus in Slow Sleep, Continuous Spike-Wave in slow Sleep, perisylvian epileptic network, cognitive impairment, sleep plastic functions, synaptic decline during slow wave sleep, atypical Rolandic epilepsy, early thalamic lesions