Abstracts

RATIONALE: Malformations due to abnormal cortical development (MCDs) are common pathological substrates of medically intractable epilepsy. The in situ epileptogenicity of these lesions as well as its relationship with histopathological changes remains unknown. The purpose of this study is to correlate the cellular patterns of MCDs with the expression of focal cortical epileptogenicity as assessed by direct extraoperative electrocorticographic (ECoG) recordings using subdural grids.
METHODS: Cortical areas with presence of interictal spiking and ictal onset patterns were identified and separated during surgery from 15 patients with medically intractable epilepsy due to MCDs. The resected cortical tissue were analyzed and classified into 3 groups based on the histopathological subtypes. (Type I: presence of architectural disorganization of cortical layers with/without giant neurons, Type II: presence of architectural disorganization with dysmorphic neurons, and Type III: presence of architectural disorganizations and balloon cells) The focal histopathological subtypes of MCDs in cortical tissue resected were then correlated with in situ ECoG patterns recorded extraoperatively from subdural grids.
RESULTS: Comparison of the interictal EcoG from cortical areas with 3 histopathological subtypes showed significantly higher number of total interictal spikes from areas with histopathological type IIA in comparison with type I and IIB. Repetitive spikes and paroxysmal fast pattern were more frequent in histopathological type IIA in comparison to type I and IIB. Hippocampal sclerosis had higher number of total interictal spikes, repetitive spikes and paroxysmal fast pattern as compared to neocortical areas with MCDs. The ictal onset came mainly from cortical area with histopathological type IIA (9/15 patients) and hippocampal sclerosis (2/15 patients). Only a small number of the cases (3/15 patients) had ictal onset localized to cortical areas with type I pathology. None of the seizures originated from neocortical areas that showed BC-containing MCD (type IIB). The most commonly seen ictal ECoG pattern in cortical area with histopathological subtype IIA and in hippocampal sclerosis was paroxysmal fast pattern with or without repetitive spikes. The ictal onset pattern seen in type I showed only repetitive spikes with no paroxysmal fast pattern.
CONCLUSIONS: This study shows that areas containing BCs are less epileptogenic than 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 CD-induced epileptogenicity.