Evidence of thalamocortical network activation during epileptic spasms: A thalamic stereotactic EEG study

Although the role of subcortical structures in the generation of epileptic spasms has been proposed, supporting evidence remains limited. This study aimed to provide neurophysiological evidence of thalamocortical network involvement during epileptic spasms.

We analyzed four patients (ages 2.7-16.9 years) with epileptic spasms who underwent intracranial electroencephalography (EEG) monitoring with thalamic sampling in preparation for potential neurostimulation. Epileptic spasms were initially assessed using visual inspection and time-frequency analysis. We then evaluated undirected connectivity through coherence analysis and directed connectivity using spectral Granger causality analysis between the thalamus and the seizure-onset zone, focusing on ictal connectivity changes in both slow (0.5-10 Hz) and fast (10-80 Hz) frequency bands. In addition, phase-amplitude coupling was assessed with a modulation index to examine the interaction between ictal slow and fast band activities.

A total of 84 epileptic spasms were analyzed. Ictal EEG changes of slow wave complex were visually confirmed in the thalamic channels. There was an increase in signal power in both the slow and fast bands at the thalamus. Undirected (coherence) and directed (spectral Granger causality) connectivity analyses showed a significant increase in connectivity between the thalamus and seizure-onset zone in both the slow and fast bands compared to baseline. Directed connectivity in the slow bands increased equally from the thalamus to the seizure-onset zone (outflow) and vice versa (inflow). However, fast band inflow was more pronounced than outflow. The modulation index increased significantly during epileptic spasms at the thalamus. Furthermore, a higher modulation index in the cortex correlated with more pronounced clinical manifestations of epileptic spasms.

Ictal slow-wave complexes on EEG during epileptic spasms may reflect long-range thalamocortical network activation, highlighting the critical role of subcortical structures in ictogenesis and the potential treatment implications for thalamic neuromodulation.