title: Epileptogenicity of focal malformations due to abnormal cortical development: direct electrocorticographic-histopathologic correlations.
abstract: OBJECTIVE
  Malformations due to abnormal cortical development (MCDs) are common pathologic substrates of medically intractable epilepsy. The in situ epileptogenicity of these lesions as well as its relation to histopathologic changes remains unknown. The purpose of this study was to correlate the cellular patterns of MCDs with the expression of focal cortical epileptogenicity as assessed by direct extraoperative electrocorticographic (ECoG) recordings by using subdural grids.
  
  
  METHODS
  Fifteen patients with drug-resistant focal epilepsy due to pathologically confirmed MCD who underwent subdural electrode placement for extraoperative seizure localization and cortical mapping between 1997 and 2000 were included in the study. Areas of interictal spiking and ictal-onset patterns were identified and separated during surgery for further pathologic characterization (cellular and architectural). Three pathologic groups were identified: type I; architectural disorganization with/without giant neurons, type IIA; architectural disorganization with dysmorphic neurons, and type IIB; architectural disorganization, dysmorphic neurons, and balloon cells (BCs). The focal histopathologic subtypes of MCDs in cortical tissue resected were then retrospectively correlated with in situ extraoperative ECoG patterns.
  
  
  RESULTS
  Cortical areas with histopathologic subtype IIA showed significantly higher numbers of slow repetitive spike pattern in comparison with histopathologic type I (p = 0.007) and normal pathology (p = 0.002). The ictal onset came mainly from cortical areas with histopathologic type IIA (nine of 15 patients). None of the seizures originated from neocortical areas that showed BC-containing MCD (type IIB).
  
  
  CONCLUSIONS
  This study shows that areas containing BCs are less epileptogenic than are closely located dysplastic regions. These results suggest a possible protective effect of BCs or a severe disruption in the neuronal networks in BCs containing dysplastic lesions. Further studies are needed to elucidate the nature and the potential role(s) of balloon cells in MCD-induced epileptogenicity.
authors.affiliation: Department of Neurology, The Cleveland Clinic Foundation, Cleveland, Ohio, USA.
authors.forename: Kanokwan
authors.initials: K
authors.lastname: Boonyapisit
authors.forename: Imad
authors.initials: I
authors.lastname: Najm
authors.forename: George
authors.initials: G
authors.lastname: Klem
authors.forename: Zhong
authors.initials: Z
authors.lastname: Ying
authors.forename: Candice
authors.initials: C
authors.lastname: Burrier
authors.forename: Eric
authors.initials: E
authors.lastname: LaPresto
authors.forename: Dileep
authors.initials: D
authors.lastname: Nair
authors.forename: William
authors.initials: W
authors.lastname: Bingaman
authors.forename: Richard
authors.initials: R
authors.lastname: Prayson
authors.forename: Hans
authors.initials: H
authors.lastname: Lüders
mesh_terms: D000293:Adolescent; D000328:Adult; D002540:Cerebral Cortex / Q000002:abnormalities* / Q000473:pathology / Q000601:surgery; D002648:Child; D004569:Electroencephalography; D004828:Epilepsies, Partial / Q000151:congenital* / Q000175:diagnosis / Q000473:pathology / Q000601:surgery; D005071:Evoked Potentials / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D009474:Neurons / Q000473:pathology