NIMG-13. CHANGES IN CORTICAL ARCHITECTURE ASSOCIATED WITH GLIOBLASTOMA ASSOCIATED EPILEPSY

Abstract BACKGROUND Emerging evidence suggests both local hyper-excitability promoting epilepsy, and synaptic and paracrine mediated integration of Glioblastoma into brain-wide neural networks. In this study we sought clinical evidence of disease progression, and concurrent radiological evidence of differences in remote cortical architecture, in Glioblastoma patients with and without epilepsy. METHODS 55 patients with biopsy-confirmed Glioblastoma, mean-age 59.4yrs±10.9yrs, were studied. 23 patients had a diagnosis of Glioblastoma-related epilepsy on presentation. We compared clinical markers of disease progression in individuals with and without epilepsy. Further, we explored differences in cortical architecture between both groups. Utilising pre-operative T1-weighted, contrast-enhanced MRI scans (n=45), we performed vertex-wise measurements of cortical thickness (CT) and cortical surface area (CSA) using the Virtual Brain Grafting Toolbox and FreeSurfer v.7.0. Radiologically-identifiable tumour and oedema was masked and excluded from analysis. Scans with right-hemispheric tumours were flipped to the left. Linear mixed-effects models were applied to pre-processed imaging-data. RESULTS Individuals with epilepsy had shorter progression-free survival (median 4.2 months) than those without seizures (9.3 months, p<0.05) with gold-standard treatment. No significant difference between lesion volumes (tumour and oedema) existed between the two groups (unpaired t-test, p>0.05). Controlling for age and tumour location, significant increases (p<0.01) in CT and CSA were observed in patients with Glioblastoma-related epilepsy in lesion-ipsilateral supramarginal gyrus, superior parietal lobule, precuneus/cuneus and temporal lobe compared to those without epilepsy. Interestingly, significant (p<0.05) increases in CT in lesion-contralateral supramarginal gyrus were additionally observed in those with epilepsy compared to those without. CONCLUSIONS Glioblastoma-related epilepsy was associated with poorer survival outcomes and changes in remote cortical architecture. Implicated regions form part of the default mode network, which has previously been identified as a crucial hub for epilepsy. Biological underpinnings of cortical network alterations, and their possible role in promoting not only hyper-excitability but also Glioblastoma progression, require correlation with histopathological characteristics and validation in larger study cohorts.