title: Early thalamic lesions in patients with sleep-potentiated epileptiform activity.
abstract: OBJECTIVE
  To compare the prevalence and type of early developmental lesions in patients with a clinical presentation consistent with electrical status epilepticus in sleep either with or without prominent sleep-potentiated epileptiform activity (PSPEA).
  
  
  METHODS
  We performed a case-control study and enrolled patients with 1) clinical features consistent with electrical status epilepticus in sleep, 2) ≥1 brain MRI scan, and 3) ≥1 overnight EEG recording. We quantified epileptiform activity using spike percentage, the percentage of 1-second bins in the EEG tracing containing at least 1 spike. PSPEA was present when spike percentage during non-REM sleep was ≥50% than spike percentage during wakefulness.
  
  
  RESULTS
  One hundred patients with PSPEA (cases) and 47 patients without PSPEA (controls) met the inclusion criteria during a 14-year period. Both groups were comparable in terms of clinical and epidemiologic features. Early developmental lesions were more frequent in cases (48% vs 19.2%, p = 0.002). Thalamic lesions were more frequent in cases (14% vs 2.1%, p = 0.037). The main types of early developmental lesions found in cases were vascular lesions (14%), periventricular leukomalacia (9%), and malformation of cortical development (5%). Vascular lesions were the only type of early developmental lesions that were more frequent in cases (14% vs 0%, p = 0.005).
  
  
  CONCLUSIONS
  Patients with PSPEA have a higher frequency of early developmental lesions and thalamic lesions than a comparable population of patients without PSPEA. Vascular lesions were the type of early developmental lesions most related to PSPEA.
authors.affiliation: Department of Neurology, Children’s Hospital Boston, Harvard Medical School, Boston, MA, USA.
authors.forename: I
authors.initials: I
authors.lastname: Sánchez Fernández
authors.forename: M
authors.initials: M
authors.lastname: Takeoka
authors.forename: E
authors.initials: E
authors.lastname: Tas
authors.forename: J M
authors.initials: JM
authors.lastname: Peters
authors.forename: S P
authors.initials: SP
authors.lastname: Prabhu
authors.forename: K M
authors.initials: KM
authors.lastname: Stannard
authors.forename: M
authors.initials: M
authors.lastname: Gregas
authors.forename: Y
authors.initials: Y
authors.lastname: Eksioglu
authors.forename: A
authors.initials: A
authors.lastname: Rotenberg
authors.forename: J J
authors.initials: JJ
authors.lastname: Riviello
authors.forename: S V
authors.initials: SV
authors.lastname: Kothare
authors.forename: T
authors.initials: T
authors.lastname: Loddenkemper
mesh_terms: D000293:Adolescent; D016022:Case-Control Studies; D002540:Cerebral Cortex / Q000002:abnormalities* / Q000503:physiopathology; D002648:Child; D002675:Child, Preschool; D004569:Electroencephalography; D005260:Female; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007969:Leukomalacia, Periventricular / Q000150:complications* / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D008297:Male; D008487:Medical History Taking; D017286:Polysomnography; D047928:Premature Birth; D012890:Sleep; D013226:Status Epilepticus / Q000175:diagnosis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D020521:Stroke / Q000150:complications* / Q000503:physiopathology; D013788:Thalamus / Q000473:pathology* / Q000503:physiopathology; D055815:Young Adult