---
title: "Longitudinal Imaging in FCD II Model Shows Lesion Growth and Loss of Pre-Discharge Recruitment"
id: "biorxiv-1-longitudinal-imaging-in-a-mouse-model-of-focal-cortical-dysplasia-reveals"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-1-longitudinal-imaging-in-a-mouse-model-of-focal-cortical-dysplasia-reveals"
content_type: "clinical_feed_article"
specialty: "Neurology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.10.24.761526v1?rss=1"
published_at: "2026-10-25T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Longitudinal Imaging in FCD II Model Shows Lesion Growth and Loss of Pre-Discharge Recruitment
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-1-longitudinal-imaging-in-a-mouse-model-of-focal-cortical-dysplasia-reveals
- **Specialty:** [Neurology](https://medichelpline.com/clinical-feed/neurology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.10.24.761526v1?rss=1)
- **Published At:** 2026-10-25T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- Investigators used a mouse model of **Focal cortical dysplasia type II** carrying the patient-derived **mTORp.L2427P** gain-of-function variant introduced by in utero electroporation. - The team implanted a chronic cranial window and performed repeated in vivo two-photon calcium imaging at defined time points; they combined imaging with video-EEG monitoring to define seizure status and interictal discharges. - The lesional cortex expanded over time in adulthood; dysplastic tissue was not static but showed progressive enlargement. - The observed expansion occurred without accumulation of tenascin R/C reported in some human lesions; the authors reported that continued somatic growth of dysmorphic neurons partially explained enlargement. - Cellular activity patterns shifted in a cell-type-specific manner: **dysmorphic neurons** were generally hypoactive across stages. - In animals that developed seizures, activity of dysmorphic neurons and pyramidal cells declined progressively over disease course. - In animals that did not seize, VIP interneuron activity increased slightly, while pre-discharge recruitment of lesional neurons remained reliable at earlier stages. - At later disease stages the lesion lost its temporal lead: layer 2/3 lesional neurons were no more active before interictal discharges than expected by chance. - Authors conclude FCD II continues to remodel structurally and functionally through adulthood, with the most marked changes in animals with seizures. - The data suggest a finite window during which removing the lesion might arrest disease; the manuscript cites clinical evidence that earlier surgery is favored. - The source did not report specific numbers for cell counts, exact imaging timepoints, sample sizes, or statistical values in the abstract; those methodological details were not provided in the abstract text supplied here.
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Monika Rehorova 1 Institute of Physiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic; Epilepsy Research Centre Prague (EpiReC); * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Monika%2BRehorova%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Rehorova%20M&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AMonika%2BRehorova%2B) * [ORCID record for Monika Rehorova](http://orcid.org/0000-0002-8658-1728 "Open in new tab") Jana Thao Rozlivkova 2 Institute of Physiology, Second Faculty of Medicine, Charles University; Epilepsy Research Centre Prague (EpiReC) * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Jana%2BThao%2BRozlivkova%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Rozlivkova%20JT&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AJana%2BThao%2BRozlivkova%2B) * [ORCID record for Jana Thao Rozlivkova](http://orcid.org/0009-0003-5649-9867 "Open in new tab") Jana Populova 1 Institute of Physiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic; Epilepsy Research Centre Prague (EpiReC); * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Jana%2BPopulova%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Populova%20J&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AJana%2BPopulova%2B) * [ORCID record for Jana Populova](http://orcid.org/0009-0000-7250-5049 "Open in new tab") Natalie Prochazkova 1 Institute of Physiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic; Epilepsy Research Centre Prague (EpiReC); * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Natalie%2BProchazkova%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Prochazkova%20N&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ANatalie%2BProchazkova%2B) * [ORCID record for Natalie Prochazkova](http://orcid.org/0009-0001-0320-8806 "Open in new tab") Carl VL Olson 1 Institute of Physiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic; Epilepsy Research Centre Prague (EpiReC); * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Carl%2BVL%2BOlson%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Olson%20CV&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ACarl%2BVL%2BOlson%2B) * [ORCID record for Carl VL Olson](http://orcid.org/0000-0002-1333-2392 "Open in new tab") Niki Shariati 1 Institute of Physiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic; Epilepsy Research Centre Prague (EpiReC); * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Niki%2BShariati%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Shariati%20N&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ANiki%2BShariati%2B) * [ORCID record for Niki Shariati](http://orcid.org/0009-0008-9252-8721 "Open in new tab") Jan Kudlacek 1 Institute of Physiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic; Epilepsy Research Centre Prague (EpiReC); * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Jan%2BKudlacek%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Kudlacek%20J&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AJan%2BKudlacek%2B) * [ORCID record for Jan Kudlacek](http://orcid.org/0000-0001-5597-8709 "Open in new tab") Premysl Jiruska 1 Institute of Physiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic; Epilepsy Research Centre Prague (EpiReC); * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Premysl%2BJiruska%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Jiruska%20P&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3APremysl%2BJiruska%2B) * [ORCID record for Premysl Jiruska](http://orcid.org/0000-0003-4955-8577 "Open in new tab") Ondrej Novak 1 Institute of Physiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic; Epilepsy Research Centre Prague (EpiReC); * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Ondrej%2BNovak%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Novak%20O&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AOndrej%2BNovak%2B) * [ORCID record for Ondrej Novak](http://orcid.org/0000-0002-8874-4252 "Open in new tab") * For correspondence: ondrej.novak@lfmotol.cuni.cz * [Abstract](https://www.biorxiv.org/content/10.64898/2026.10.24.761526v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5901377/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.10.24.761526v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5901377/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.10.24.761526v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5901377/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.10.24.761526v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5901377/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.10.24.761526v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5901377/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract ABSTRACT Objective: Focal cortical dysplasia type II (FCD II) is a leading cause of drug-resistant focal epilepsy, yet how its lesional circuits behave and change over time in vivo has not been directly observed. Methods: We used a mouse model of FCD II carrying the patient-derived gain-of-function mTORp.L2427P variant introduced by in utero electroporation. Through a chronic cranial window over the lesion, we performed repeated in vivo two-photon calcium imaging of identified dysmorphic neurons, pyramidal cells, and VIP interneurons at defined time points, combined with video-EEG monitoring, to determine seizure status and relate cellular activity to interictal discharges. Results: The lesion was not static in adulthood. Dysplastic cortex expanded progressively. This expansion occurred without the tenascin R/C accumulation reported in human FCD II, and was partly explained by continued somatic growth of dysmorphic neurons. Dysmorphic neurons were generally hypoactive; in seizing mice, both dysmorphic and pyramidal cell activity progressively declined, whereas VIP interneuron activity increased slightly in non-seizing animals. In non-seizing lesional cortex, neurons were reliably recruited immediately before interictal discharges. By late disease stages, pre-discharge recruitment had weakened to the point that lesional layer 2/3 neurons were no more active before discharges than expected by chance. Significance: These findings recast FCD II as a lesion that continues to remodel structurally and functionally throughout adulthood, and does so most markedly in animals with seizures. Growth, a cell-type-specific shift in spontaneous activity, and a progressive loss of the lesion's temporal lead over interictal discharges together suggest that FCD II is a dynamically evolving lesion whose relationship to epileptiform activity changes over time. If the lesion progressively loses its generative role, the window in which removing it can arrest the disease is finite, consistent with clinical evidence favoring earlier surgery. ### Competing Interest Statement The authors have declared no competing interest. ## Funder Information Declared Ministry of Health of the Czech Republic, Prague, CZ, NW24-04-00041 Ministry of Education, Youth and Sports of the Czech Republic, Prague, CZ, EU – Next Generation EU: LX22NPO5107 Charles University, Prague, CZ, UNCE24/MED/021 - EXCITE, PRIMUS/23/MED/011, Returns at CU - CZ.02.01.01/00/24_037/0013839– RTNS25-022, GAUK 254122, GAUK 423325 Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a [CC-BY 4.0 International license](http://creativecommons.org/licenses/by/4.0/). bioRxiv and medRxiv thank the following for their generous financial support: > The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. [Donate to openRxiv ](https://www.zeffy.com/en-US/donation-form/donate-to-make-a-difference-10981) [ Back to top](https://www.biorxiv.org/content/10.64898/2026.10.24.761526v1?rss=1#page) [ Previous](https://www.
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