Abstracts

Rationale: Focal cortical dysplasia (FCD) type II has a close relationship with sleep-related epilepsy (SRE). However, the mechanism underlying the genesis of the SRE in FCD type II is not well understood. The current study aims at evaluating the association between volume of FCD lesion, volume of thalamus, as well as the location of FCD with SRE. Methods: Patients with histopathologically confirmed FCD type II from three epilepsy centers, Second Affiliated Hospital of Zhejiang University, Beijing Tiantan Hospital of Capital Medical University and Cleveland Clinic Epilepsy Center were included in this study. Cortical surface reconstructions and volume calculations were performed using FreeSurfer. The lesions were delineated independently on T1 volumetric MRI by two trained raters using the ITK-SNAP software. To correct for different head sizes, the lesion volumes were normalized by intracranial volumes of each individual. Lesions were also classified into small and large using quantitative (volume) criteria following methods from Besson et al., Brain 2006. All patients underwent video-EEG monitoring and whether the epilepsy was sleep-related was extracted from the monitoring report and history. Results: A total of 77 consecutive patients were included. Of them, 36 (46.7%) were SRE and 41 were not non-SRE. The normalized FCD type II volume ranged from 291 mm3 to 29990 mm3. To correct for non-normal distribution, the normalized volumes of FCD type II were log-transformed. Analysis of covariance showed that SRE was significantly associated with smaller lesion volume (Table 1, p=0.015). Small lesions were defined as those having a volume smaller than 3291 mm3. Twenty-seven (27/36 = 75%) patients with SRE had small FCD lesions, which were significantly higher than non-SRE group (17/41=41.5%, P=0.003). The location of FCD lesion and thalamic volume were not statistically different between the SRE and non-SRE group(Figure 1). There is no particular seizure semiology that characterized patients with SRE compared with those with non-SRE. Conclusions: Interaction between sleep rhythm and peri-lesional epileptic network is required for ictogenesis in patients with FCD. Our data suggests that the modulation is seen more significantly in small FCD lesions, rather than large FCD lesions, suggesting different peri-lesional network recruitment between the two groups. Funding: none