Abstracts

Rationale: Executive dysfunction is a common comorbidity in focal epilepsy. Children with focal cortical dysplasia (FCD)-related epilepsy have high rates of executive dysfunction that is thought to be multifactorial in etiology, and likely to be related to underlying cortical functional network disruptions.¹ The Behavior Rating Inventory of Executive Function (BRIEF) is a validated tool to assess for executive dysfunction. We hypothesized that FCD co-localization to the frontoparietal control network would have increased risk of executive dysfunction in children with pediatric FCD-related epilepsy.

Methods: This was an IRB-approved, retrospective cohort selected from the epilepsy surgery database at Children’s National Hospital in Washington, DC. Inclusion criteria: 3T or 1.5T MRI-confirmed FCD with pharmacoresistant epilepsy (PRE) from January, 2000-January, 2022; BRIEF-global executive composite (GEC) score obtained during presurgical neuropsychological work-up; confirmed FCD pathology. Patients were excluded if there was dual pathology (except for mesial temporal sclerosis), tuberous sclerosis, hemimegalencephaly from imaging or history. Structural MRIs were segmented² to determine FCD dominant network (Yeo 7-network³ with most overlap). We used multivariate linear regression to evaluate factors contributing to BRIEF-GEC T-score.

Results: Of 48 FCD-PRE patients, n=11 (23%) had executive dysfunction. Clinico-patho-radiologic and demographic data are in Table 1. Multivariate linear regression showed FCD Type I pathology (Estimate 9.33, 95%CI 0.91-17.76, p=0.03) is associated with BRIEF-GEC T-score. Lesion size, hemisphere, lobe, epilepsy duration and dominant network are not (Figure 1). Our initial hypothesis that FCD co-localization to the control network is associated with executive dysfunction was not confirmed with these data.

Conclusions: We show in FCD pharmacoresistant epilepsy that FCD Type I pathology is associated with increased risk of executive dysfunction. FCD size, cortical lobar location, structural co-localization to attentional networks and epilepsy duration did not clearly predict BRIEF-GEC T-score. Executive dysfunction in FCD-PRE may relate to lesion interaction with functional networks better explored with connectomics. These results expand on the severity of FCD Type I pathology, already associated with worse surgical outcomes and intellectual disability⁴, to include risk of executive dysfunction.

Funding: MA is supported by a GWU Gill Summer Research Fellowship. NTC is funded by an AAN Career Development Award and the Hess Foundation.


References:

1. Sepeta LN et al. The role of executive functioning in memory performance in pediatric focal epilepsy. Epilepsia. 2017 Feb;58:300-310.

2. Cohen NT et al. Networks Underlie Temporal Onset of Dysplasia-Related Epilepsy: A MELD Study. Annals of neurology. 2022 Sep;92:503-511.

3. Yeo BT et al. The organization of the human cerebral cortex estimated by intrinsic functional connectivity. Journal of neurophysiology. 2011 Sep;106:1125-1165.

4. Krsek P et al. Different presurgical characteristics and seizure outcomes in children with focal cortical dysplasia type I or II. Epilepsia. 2009 Jan;50:125-137.