Authors :
Presenting Author: Xiaotong Li, BA – Children's National Hospital
Priyanka Venkata Sita Illapani, MSc – Children's National Hospital
Sonya Leikin, BS – Children's National Hospital
Hua Xie, PhD – Children's National Hospital
Chima Oluigbo, MD – Children's National Hospital, George Washington University
Gilbert Vezina, MD – Children's National Hospital
William Gaillard, MD – Children's National Hospital
Hayley Loblein, PhD – Children's National Hospital
Perrine Heymann, PhD – Children's National Hospital
Leigh Sepeta, PhD – Children's National Hospital
Madison Berl, PhD – Children's National Hospital
Nathan Cohen, MD – Children's National Hospital
Rationale:
Focal cortical dysplasia (FCD) is the most common cause of surgically-treatable, drug-resistant epilepsy in children. Depression and anxiety are common comorbidities in epilepsy. Mounting evidence from functional imaging studies implicates limbic and/or default mode network (DMN) connectivity abnormalities associated with anxiety and depression: increased DMN and decreased limbic connectivity in temporal lobe epilepsy with depression; and limbic and/or DMN hyperconnectivity in anxiety. The Child Behavior Checklist (CBCL) is a parent-reported measure designed to assess emotional, behavioral, and social problems in children and adolescents. FCD co-localization (maximum overlap with one of the seven Yeo functional networks) links to several features of FCD-related epilepsy. We proposed three hypotheses: FCD with limbic or DMN co-localization have 1) elevated CBCL anxiety scores; 2) elevated CBCL depression scores; and 3) elevated CBCL internalizing scores (composite score).
Methods:
This is a retrospective review of pediatric patients from Children’s National Hospital with 3T or 1.5T MRI-confirmed FCD with or without drug-resistant epilepsy from January 2000 to January 2022 who have a presurgical parent-reported CBCL. MRIs were obtained by standard clinical evaluation. We examined CBCL anxiety, depression and internalizing scales with T-score of 65 or higher as clinically elevated. Chi-square was used to examine association between FCD co-localization and elevated scores. Independent sample t-test was used to examine relationships between FCD co-localization and CBCL scales as continuous T-scores.
Results:
70 pediatric patients with FCD-related epilepsy were selected. There was no association between limbic/DMN and elevated anxiety (χ², p = 0.37); limbic/DMN and elevated depression (χ², p = 0.47); or limbic/DMN and elevated internalizing symptoms (χ², p = 0.48). Independent t-test also showed no associations with T-scores: between limbic/DMN and anxiety (p = 0.5); depression (p = 0.89); or internalizing (p = 0.75).
Conclusions:
This study showed no association between FCD co-localization to limbic or default mode networks and CBCL anxiety, depression, or internalizing symptoms. These results may be confounded by variable antiseizure medication regimens, seizure frequency, or timepoints of CBCL acquisition. While DMN or limbic networks are altered in depression/anxiety, the impairments may be specific to certain subregions not captured by this network co-localization method. Future multicenter and prospective studies should incorporate multimodal connectivity explorations to fully assess lesion-network interactions in the neural underpinning of mood disorder comorbidities in FCD-related epilepsy.
Funding:
NTC is funded by an AAN Career Development Award and the Hess Foundation. This work is partially supported by the District of Columbia Intellectual and Developmental Disabilities Research Center (DC-IDDRC) NIH P50 HD105328.