CBCL公司
癫痫
焦虑
萧条(经济学)
儿童行为检查表
心理学
皮质发育不良
精神科
医学
默认模式网络
听力学
颞叶
临床心理学
神经科学
精神病理学
癫痫发生
钩束
共病
儿科
共域化
发病年龄
边缘系统
作者
Xinwei Li,Ty Charde,Venkata Sita Priyanka Illapani,Sonya Leikin,Hua Xie,Chima O. Oluigbo,L. Gilbert Vezina,William D. Gaillard,Hayley J. Loblein,Perrine Heymann,Leigh Sepeta,Madison M. Berl,Adelaide S. Robb,Nathan T. Cohen
摘要
Objective Focal cortical dysplasia (FCD) is the most common cause of surgically treatable, drug‐resistant epilepsy in children. Anxiety and depression are frequent comorbidities in epilepsy. This study examined whether FCD overlap with large‐scale functional networks, the default mode network (DMN) and the limbic network, is associated with parent‐reported anxiety or depressive symptoms. Methods Sixty‐nine patients with FCD‐related epilepsy completed the Child Behavior Checklist (CBCL), among whom 56 finished the 6 to 18 years version of CBCL (CBCL 6–18 ). FCD overlap (%) with Yeo 7‐networks was calculated. General linear models tested FCD DMN or FCD limbic overlap with CBCL Diagnostic and Statistical Manual of Mental Disorders – Fifth Edition (DSM)‐Anxiety Problems or DSM‐Depressive Problems Scores controlling for age and gender. Results Fifty‐six patients had preoperative CBCL 6–18 (median age = 12.8 years, 55% male patients). FCD DMN overlap (B = 0.08, 95% confidence interval [CI] = 0.002–0.16, partial η 2 = 0.086, p = 0.045) and female gender were associated with higher DSM‐Depressive Problems T‐scores. This lesion‐network depressive‐symptoms effect was stronger in an adolescent‐only model (52% male patients): FCD DMN overlap (B = 0.19, 95% CI = 0.068–0.32, partial η 2 = 0.37, p = 0.004). Network overlap was not associated with DSM‐Anxiety Problems in any age group. Interpretation FCD DMN overlap is associated with increased depressive symptoms, particularly for adolescents, whereas FCD limbic overlap is not. These findings underscore the importance of lesion‐network colocalization contributing to depression vulnerability in developmental epilepsy and highlight DMN colocalization involvement as a potential neurobiological marker of depressive risk. ANN NEUROL 2026
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