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Updated: Aug 8, 2025

Network Analysis of the Default Mode Network Using Functional Connectivity MRI in Temporal Lobe Epilepsy
Published on: August 5, 2014
Brain network properties of clinical versus subclinical seizures among critically ill children
Laura K Koster1, Rouzbeh Zamyadi2, Luowei Yan2
1Division of Neurology, The Hospital for Sick Children and Department of Paediatrics, University of Toronto, Toronto, Canada; Neurosciences & Mental Health Program, The Hospital for Sick Children Research Institute, Toronto, Canada.
Objective:
Electrographic seizures are common among critically ill children, and have been associated with worse outcomes. Despite their often-widespread cortical representation, most of these seizures remain subclinical, a phenomenon which remains poorly understood. We compared the brain network properties of clinical versus subclinical seizures to gain insight into their relative potential deleterious effects.
Methods:
Functional connectivity (phase lag index) and graph measures (global efficiency and clustering coefficients) were computed for 2178 electrographic seizures recorded during 48-hours of 19-channel continuous EEG monitoring obtained in 20 comatose children. Frequency-specific group differences in clinical versus subclinical seizures were analyzed using a non-parametric ANCOVA, adjusting for age, sex, medication exposure, treatment intensity and seizures per subject.
Results:
Clinical seizures demonstrated greater functional connectivity than subclinical seizures at alpha frequencies, but less connectivity than subclinical seizures at delta frequencies. Clinical seizures also demonstrated significantly higher median global efficiency than subclinical seizures (p < 0.01), and significantly higher median clustering coefficients across all electrodes at alpha frequencies.
Conclusions:
Clinical expression of seizures correlates with greater alpha synchronization of distributed brain networks.
Significance:
The stronger global and local alpha-mediated functional connectivity observed during clinical seizures may indicate greater pathological network recruitment. These observations motivate further studies to investigate whether the clinical expression of seizures may influence their potential to cause secondary brain injury.
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