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Brain functional connectivity patterns in focal cortical dysplasia related epilepsy

皮质发育不良 癫痫 功能连接 神经科学 功能磁共振成像 默认模式网络 小脑 病态的 磁共振成像 连接体 癫痫外科 心理学 医学 病理 放射科
作者
Wenyu Liu,Mintao Lin,Qiang Yue,Qiyong Gong,Dong Zhou,Xintong Wu
出处
期刊:Seizure-european Journal of Epilepsy [Elsevier]
卷期号:87: 1-6 被引量:16
标识
DOI:10.1016/j.seizure.2021.02.009
摘要

Abstract

Objective

Focal cortical dysplasia (FCD) appears to be strongly associated with intractable epilepsy. Although patients with FCD are candidates for epilepsy surgery, gray matter structural abnormalities can extend beyond the primary lesion, which makes surgery less effective. The objective of this study was to evaluate functional connectivity patterns in epilepsy associated with FCD to explore the underlying pathological mechanism of this disorder.

Methods

A total of 34 patients (14 men) with FCD and epilepsy [mean age ± standard deviation (SD), 24.5 ± 9.8 years; range, 8–47 years] and 34 age-matched healthy controls (14 men, 24.6 ± 9.7 years) underwent functional magnetic resonance imaging. Independent component analysis (ICA), seed-based functional connectivity, and graph theory were applied to analyze functional connectivity patterns in the brain.

Results

Patients showed more connections among dorsal attention network, anterior default mode network, and sensorimotor brain networks than healthy controls based on ICA. Analysis of connectivity between regions of interest (ROIs) showed greater functional connectivity in patients between frontal and temporal regions, but lower connectivity between the cerebellum and frontal regions. The normalized characteristic path length was significantly higher in group of patients, but the two groups showed no significant differences in global or regional efficiency, clustering coefficient or characteristic path length.

Conclusions

Analysis of ICA-derived and ROI-based functional connectivity suggests that disrupted interactions and dysconnectivity in large-scale neural networks and frontotemporal-cerebellar regions may contribute to underlying pathological mechanisms in FCD-related epilepsy.
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