Abstracts

Rationale: Malformations of cortical development (MCDs), and focal cortical dysplasia (FCD) in particular, are an important cause of medically intractable epilepsy. Recent research suggests that distinct subtypes of FCDs result from disturbances at the different stages of cerebral cortical development, which may imply variability in seizure generation mechanisms. Identifying unique electrographic patterns, which potentially reflect epileptogenic mechanisms of different FCD subtypes, could have implications for their medical and surgical management. The purpose of this study was to investigate the correlation of intracranial EEG ictal and interictal patterns associated with the different subtypes of FCD lesions as defined by three-tiered ILAE classification system. Methods: We retrospectively analyzed all available interictal and ictal intracranial EEG recordings from 2002-2015 for patients with pathology-proven FCD who subsequently underwent resective epilepsy surgery at Yale New Haven Hospital. The first seizure per day of each patient was reviewed resulting in a minimum of one and a maximum of five seizures per patient, excluding any seizure which was a part of a seizure cluster. Subsequently, observed EEG patterns were categorized into several types based on their morphology and correlated with histopathological findings of resected tissue. Results: A total of 12 patients were included in the study and 37 discrete seizures were analyzed. The majority of patients had Type II FCD (10) with the rest having Type I FCD (2). Five ictal-onset patterns were observed: low-voltage fast activity (40%), single delta wave with superimposed low-voltage fast activity (22%), spiking with low-voltage fast activity (16%), repetitive spiking (11%), and rhythmic sharp wave activity (11%). These ictal patterns were seen across different subtypes of FCDs, with low-voltage fast activity being the most common seizure-onset pattern. Five interictal waveform morphologies were described: isolated spikes, repetitive spiking, repetitive bursts of spikes, paroxysmal fast activity, and slow repetitive spike pattern. In general, all FCD subtypes demonstrated multiple interictal discharge morphologies. However, a specific interictal pattern of slow repetitive polyspike wave was observed in the majority (70%) of the patients with Type 2 FCD, although not reaching statistical significance in being a unique interictal pattern specifically to Type 2 FCD (p=0.15). However, this interictal pattern was located exclusively within the seizure onset region when it was observed (p=0.015). Conclusions: Overall, our data suggest that different FCD subtypes do not demonstrate markedly distinct intracranial electrographic patterns which is in concordance with previous studies; suggesting that all FCD subtypes may share common mechanisms of seizure generation. An interesting finding from this analysis is that a majority of Type II FCDs appear to demonstrate a unique interictal pattern consisting of repetitive polyspike slow wave discharges that has not been described previously. Although this finding did not reach statistical significance due to our small sample size a trend toward significance was suggested. However, the most notable observation of this study is that this pattern co-localized with the seizure onset region which did reach statistical significance. This suggests that the presence of this particular pattern on interictal intracranial EEG recording may help in identifying the epileptogenic focus. Determining whether this pattern is correlated with surgical outcomes or observed in seizure onset foci in other dysplastic lesions of a similar developmental origin will need to be further elucidated with a larger study. Funding: None