title: The effect of surgery in encephalopathy with electrical status epilepticus during sleep.
abstract: OBJECTIVE
  We analyzed clinical and electroencephalography (EEG) outcomes of 13 patients with pharmacoresistant encephalopathy with electrical status epilepticus during sleep (ESES) following epilepsy surgery.
  
  
  METHODS
  All patients had symptomatic etiology of ESES and preoperative neuropsychological deterioration. Ten patients had daily atypical absences. Clinical outcome was assessed at 6 months and at 2 years after surgery. Clinical and EEG data were reviewed retrospectively. The spike propagation pattern and area and source strength in source montage were analyzed from preoperative and postoperative EEG studies.
  
  
  RESULTS
  Preoperative sleep EEG showed electrical status epilepticus during sleep (SES) with one-way interhemispheric propagation in nine patients and with two-way interhemispheric propagation in four. The age of the patients at the time of surgery ranged from 3.6-9.9 years. Focal resection (two patients) or hemispherotomy (one patient with postoperative EEG) either terminated SES or restricted the discharge to one region. Either reduced SES propagation area or source strength was found in four of eight callosotomy patients with postoperative EEG. Of patients who had seizures preoperatively, Engel class I-II seizure outcome was observed in two of three children after focal resection or hemispherotomy and in two of eight children after callosotomy. None of these patients with Engel class I-II outcome had SES with two-way interhemispheric propagation on preoperative EEG. Cognitive deterioration was halted postoperatively in all except one patient. Cognitive catch-up of more than 10 IQ points was seen in three patients, all of whom had shown a first measured IQ of >75.
  
  
  CONCLUSIONS
  Patients with pharmacoresistant ESES based on symptomatic etiology may benefit from resective surgery or corpus callosotomy regarding both seizure outcome and cognitive prognosis.
authors.affiliation: Department of Clinical Neurophysiology, Turku University Hospital, Turku, Finland. maria.peltola@utu.fi
authors.forename: Maria E
authors.initials: ME
authors.lastname: Peltola
authors.forename: Elina
authors.initials: E
authors.lastname: Liukkonen
authors.forename: Marja-Liisa
authors.initials: ML
authors.lastname: Granström
authors.forename: Ritva
authors.initials: R
authors.lastname: Paetau
authors.forename: Elisa
authors.initials: E
authors.lastname: Kantola-Sorsa
authors.forename: Leena
authors.initials: L
authors.lastname: Valanne
authors.forename: Björn
authors.initials: B
authors.lastname: Falck
authors.forename: Göran
authors.initials: G
authors.lastname: Blomstedt
authors.forename: Eija
authors.initials: E
authors.lastname: Gaily
mesh_terms: D000927:Anticonvulsants / Q000627:therapeutic use; D002540:Cerebral Cortex / Q000503:physiopathology / Q000601:surgery; D002648:Child; D002675:Child, Preschool; D003337:Corpus Callosum / Q000503:physiopathology / Q000601:surgery*; D004292:Dominance, Cerebral / Q000502:physiology; D004351:Drug Resistance; D004569:Electroencephalography; D004832:Epilepsy, Absence / Q000503:physiopathology / Q000601:surgery*; D004830:Epilepsy, Tonic-Clonic / Q000503:physiopathology / Q000601:surgery*; D005071:Evoked Potentials / Q000502:physiology; D005260:Female; D005500:Follow-Up Studies; D038421:Hemispherectomy; D006801:Humans; D008607:Intellectual Disability / Q000503:physiopathology / Q000601:surgery; D065768:Lennox Gastaut Syndrome; D015225:Magnetoencephalography; D008297:Male; D009483:Neuropsychological Tests; D017286:Polysomnography; D012189:Retrospective Studies; D012815:Signal Processing, Computer-Assisted; D012893:Sleep Wake Disorders / Q000503:physiopathology* / Q000601:surgery*; D013036:Spasms, Infantile / Q000503:physiopathology / Q000601:surgery; D013226:Status Epilepticus / Q000503:physiopathology* / Q000601:surgery*
chemical_list: D000927:Anticonvulsants