# Static and dynamic intracerebral signal analysis reveals protective networks against seizures in drug-resistant focal epilepsy

**Authors:** Roberta Di Giacomo, Pablo Núñez, Jesús Poza, Victor Rodríguez-González, Carlos Gómez, Alessandra Burini, Laura Castana, Marco de Curtis, Laura Tassi, Giulia Varotto

PMC · DOI: 10.1093/braincomms/fcag047 · Brain Communications · 2026-02-20

## TL;DR

This study explores brain network dynamics in drug-resistant epilepsy to identify protective mechanisms that prevent minor electrical discharges from becoming seizures.

## Contribution

The study introduces novel insights into static and dynamic brain network changes preceding seizures, highlighting protective roles of non-epileptogenic zones.

## Key findings

- Static connectivity analysis showed altered network properties before minor discharges and seizures.
- Dynamic analysis revealed lower complexity and longer stability of brain states before minor discharges.
- Non-epileptogenic zones exhibited protective patterns preventing escalation to major seizures.

## Abstract

Epilepsy research increasingly emphasizes the role of brain network dynamics in seizure generation and propagation. Nevertheless, the interplay between the mechanisms that enhance or inhibit seizure initiation remains poorly understood. In this study, we explore both static and dynamic functional brain networks preceding ictal minor electrical discharges and major seizures, within epileptogenic and non-epileptogenic zones, using intracerebral recordings from patients with drug-resistant focal epilepsy. Stereo-electroencephalographic signals were recorded from 39 patients with focal drug-resistant epilepsy during pre-surgical monitoring. Static functional connectivity was quantified using graph theory metrics, whereas dynamic connectivity was characterized through the analysis of the complexity and dwell times of brain meta-state activations. Static connectivity analysis revealed significant alterations in network centrality, integration, and segregation properties, with distinct patterns characterizing resting conditions, minor electrical discharges and major seizures. Specifically, network analysis before minor electrical discharges exhibited increased nodal strength and reduced betweenness centrality in the epileptogenic zone, associated with greater integration and reduced segregation in non-epileptogenic zones. Dynamic connectivity analysis showed lower complexity and longer stability of meta-states before minor electrical discharges, particularly in high-frequency signals of non-epileptogenic zones. Taken together, our findings provide novel and valuable insights into the topological organization and the dynamic changes of brain networks before epileptic seizures, suggesting the presence of a protective mechanism, mainly involving non-epileptogenic zones, able to prevent minor electrical discharges to evolve into a mayor seizure. A better understanding of these network changes is pivotal for improving therapeutic strategies in epilepsy, particularly those targeting dynamic network alterations.

Di Giacomo et al. applied static and dynamic functional connectivity analysis to stereo electroencephalography (SEEG) in drug-resistant epilepsy, investigating differences in networks preceding minor electrical discharges and major seizures. Results reveal regulatory mechanisms, mainly involving regions beyond the epileptogenic zone, which may prevent minor electrical discharges from evolving into full seizures.

Graphical AbstractFor image description, please refer to the figure legend and surrounding text.

## Linked entities

- **Diseases:** epilepsy (MONDO:0005027)

## Full-text entities

- **Genes:** IGKV5-2 (immunoglobulin kappa variable 5-2) [NCBI Gene 28907] {aka B2, IGKV52}, THAS (thoracoabdominal syndrome) [NCBI Gene 7055] {aka TAS}, PRB1 (proline rich protein BstNI subfamily 1) [NCBI Gene 5542] {aka PM, PMF, PMS, PRB1L, PRB1M}
- **Diseases:** temporal lobe epilepsy (MESH:D004833), Alzheimer's disease (MESH:D000544), schizophrenia (MESH:D012559), neurological diseases (MESH:D020271), focal epilepsies (MESH:D004828), polymicrogyria (MESH:D065706), DRE (MESH:D000069279), MED (MESH:D004556), Seizure (MESH:D012640), Epilepsy (MESH:D004827), gliosis (MESH:D005911), hippocampal sclerosis (MESH:D000092223), sFC (MESH:D014202), MS (MESH:D004830), nodular heterotopia (MESH:D054091), FCD type IIa (MESH:C537067), depression (MESH:D003866), epileptiform discharges (MESH:D019522), cortical dysplasia (MESH:D054220), oligodendroglial hyperplasia (MESH:D006965), generalized epilepsy (MESH:D004829), cognitive impairment (MESH:D003072)
- **Chemicals:** MED (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12954387/full.md

## References

87 references — full list in the complete paper: https://tomesphere.com/paper/PMC12954387/full.md

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Source: https://tomesphere.com/paper/PMC12954387