# The Dual Associations of Peripheral Inflammatory Cells With Brain Reorganization in Insular Gliomas With/Without Epilepsy: An Exploratory Analysis

**Authors:** Hongfang Zhao, Bohan Zhang, Qifeng He, Zhenghai Deng, Zonggang Hou, Jian Xie

PMC · DOI: 10.1002/cns.70788 · CNS Neuroscience & Therapeutics · 2026-02-20

## TL;DR

This study explores how brain reorganization in insular glioma patients with and without epilepsy is linked to peripheral inflammatory cells, suggesting potential biomarkers for treatment.

## Contribution

The study identifies distinct brain reorganization patterns and their associations with peripheral inflammatory cells in insular glioma subtypes.

## Key findings

- Increased toroidal gyrification in IRE patients correlates with lower white blood cell counts.
- Contralateral gyrification in IRnE patients is not linked to inflammatory cell counts.
- Toro GI shows initial predictive value for postoperative epilepsy control.

## Abstract

The insula was invaded by gliomas and epilepsy occurred frequently. Our study aimed to reveal brain reorganization and explore potential peripheral biomarkers that reflect these processes.

51 insular glioma‐related epilepsy (IRE) and 52 without epilepsy (IRnE) patients were included. Deep learning was used for tumor segmentation to generate masks for subsequent analyses. Virtual brain grafting was applied to eliminate the mass effect. Morphological analyses relied on MATLAB, SPM, and CAT12. Statistical analyses included χ2 test, t test, one‐way ANOVA, regression, principal component, and correlation analysis.

Increased gyrification (GI) occurred on the contralateral side of IRnE. Increased gray matter volume and toroidal GI (Toro GI) appeared on the same and contralateral sides of IRE, respectively. Elevated Toro GI showed an initial predictive value for the control of postoperative epilepsy and was negatively associated with blood white cell, monocyte, and neutrophil counts in IRE. The opposite relationship was observed for GI in IRnE.

The brain would conduct different reorganization models to adapt to IRE and IRnE. These processes may be associated with specific peripheral inflammatory cells. Longitudinal studies and explorations of more specific biomarkers are necessary for elucidating the causal relationships and providing suggestions for therapeutic concepts of different insular glioma subtypes.

Legend process. (A,B) Based on deep learning and virtual brain grafting, we revealed that the brain could conduct reorganization to adopt insular glioma with/without epilepsy, which was not influenced by tumor features and was associated with peripheral inflammatory cells. (C) Exploring causal links of the associations may provide personal suggestions for insular glioma.

## Linked entities

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

## Full-text entities

- **Genes:** IDH1 (isocitrate dehydrogenase (NADP(+)) 1) [NCBI Gene 3417] {aka HEL-216, HEL-S-26, IDCD, IDH, IDP, IDPC}, MGMT (O-6-methylguanine-DNA methyltransferase) [NCBI Gene 4255], GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, TP53 (tumor protein p53) [NCBI Gene 7157] {aka BCC7, BMFS5, LFS1, P53, TRP53}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, TERT (telomerase reverse transcriptase) [NCBI Gene 7015] {aka CMM9, DKCA2, DKCB4, EST2, PFBMFT1, TCS1}, ATRX (ATRX chromatin remodeler) [NCBI Gene 546] {aka JMS, MRX52, RAD54, RAD54L, XH2, XNP}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, SLC1A2 (solute carrier family 1 member 2) [NCBI Gene 6506] {aka DEE41, EAAT2, EIEE41, GLT-1, GLT1, HBGT}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}
- **Diseases:** depression (MESH:D003866), inflammatory drugs (MESH:D000081015), brain edema (MESH:D001929), bipolar (MESH:D001714), seizure (MESH:D012640), multiple sclerosis (MESH:D009103), absence seizures (MESH:D004832), Alpha Thalassemia/Mental Retardation Syndrome X-linked (MESH:C538258), long-COVID (MESH:D000094024), cognitive decline (MESH:D003072), damage (MESH:D020263), Epilepsy (MESH:D004827), glioma (MESH:D005910), headaches (MESH:D006261), Inflammation (MESH:D007249), Parkinson's disease (MESH:D010300), brain (MESH:D001927), psychosis (MESH:D011618), intracranial malignant tumor (MESH:D009369), SBM (MESH:D019292), Alzheimer's disease (MESH:D000544), mental disorders (MESH:D001523), brain atrophy (MESH:C566985), neuroinflammation (MESH:D000090862)
- **Chemicals:** prednisone (MESH:D011241), aspirin (MESH:D001241), glutamate (MESH:D018698), levetiracetam (MESH:D000077287), creatinine (MESH:D003404), nitrogen (MESH:D009584), Cr (MESH:D002857), uric acid (MESH:D014527), Urea (MESH:D014508), bilirubin (MESH:D001663), cephalosporins (MESH:D002511)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12927981/full.md

## References

57 references — full list in the complete paper: https://tomesphere.com/paper/PMC12927981/full.md

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Source: https://tomesphere.com/paper/PMC12927981