Norby, J. H. | bioRxiv Science

bioRxiv2026

Seize the Data: A User-Friendly GUI for High-Resolution Analysis of Seizure Dynamics in HD-MEA Recordings

High-density multi-electrode arrays (HD-MEAs) generate large, complex datasets that are challenging to efficiently manage and analyze with existing tools, especially in open-source environments. To address this, we developed the BYU Seizure and Analytics Tool (YSA), an open-source graphical user interface (GUI) built in Python and C++ for efficient analysis and visualization of HD-MEA recordings. The YSA features raster plots, automated discharge detection and tracking, downsampling, playback, and export functions, enabling streamlined workflows for large-scale neural data. We demonstrate the utility of the tool in the context of seizure and status epilepticus (SE)-like activity, highlighting how the YSA facilitates rapid exploration of the spatiotemporal dynamics in brain networks. This platform provides an accessible and practical solution for HD-MEA data analysis, supporting a range of neuroscience applications. Significance StatementHigh-density multi-electrode arrays (MEAs) generate rich spatiotemporal datasets ideal for studying complex brain dynamics such as seizure activity. However, the size and complexity of these data often pose challenges for efficient analysis and interpretation. We present the BYU Seizure and Analytics Tool (YSA), an open-source graphical interface for intuitive visualization and exploration of MEA data. YSA enables users to navigate activity across the entire brain slice, identify relevant patterns, and easily export subsets for targeted analyses such as individual discharges. By making high-density seizure data more accessible and actionable, YSA streamlines analysis workflows and supports deeper insights into the spatiotemporal dynamics underlying seizure initiation and propagation in models of status epilepticus, pharmacoresistant epilepsy, and broader neural activity.

neuroscience↗

bioRxiv2025

Human and Rodent Seizures Demonstrate a Dynamic Interplay with Spreading Depolarizations

Seizure termination has been linked to spreading depolarizations (SDs) in experimental epilepsy models, and SDs have recently been suggested to protect against seizures. The precise mechanism, however, remains unclear. Additionally, the co-occurrence of SDs with human seizures remains debated. In this study, we found that SDs are a prominent feature following ictal events in both human clinical recordings (n=20 seizures from 7 epilepsy patients) using direct-current amplifiers and in the 0 Mg2+ model of ictogenesis from rodent brain slices (n=17). Approximately one-third of rodent seizure-like events (SLEs) were associated with SDs, while all human seizures analyzed had associated infraslow shifts, a hallmark of SDs. SDs were more prominent in the lateral frontal, medial frontal, and lateral temporal lobes, as well as the insular cortex in human patients, but were observed in all recorded brain regions. In rodents, SDs clustered toward the end of ictal events, resulting in significantly shorter SLEs (SLE without SD: 32.60 {+/-} 5.31 s; SLE with SD: 16.03 {+/-} 4.45 s) and delayed onset of subsequent SLEs. These SDs also caused significant AC band silencing compared to SLEs without SDs. Interestingly, SLEs with SDs displayed significantly more low gamma activity during ictal events. Using ion- selective microelectrodes, we found no significant correlation between extracellular [K+] levels and SLEs ending in SDs, questioning the role of [K+]o in SD induction during seizures. We observed more heterogeneity in human seizures than in rodent SLEs, with some human seizures showing SD-associated termination and others demonstrating SDs in the middle of ictal events; such intra-seizure SDs were never observed in our rodent model. The human data, collected from patients with intractable epilepsy, demonstrate clear SD propagation during seizures and show that SDs appear and propagate, in multiple brain regions simultaneously with ictal events. Collectively, these results indicate that SDs are a hallmark of ictal activity and may contribute to seizure termination in both experimental and clinical settings. Furthermore, these findings provide unique insight into the neuronal dynamics that promote SD induction by showing that increased low gamma activity during SLEs is more predictive of SD induction than extracellular [K+] levels. We also add further support for the hypothesis that SDs are both anti- seizure and anti-ictogenic as they not only limit and delay subsequent ictal activity but also reduce the duration of SLEs. Taken together, these findings provide rationale for further exploration of SDs as a means to prematurely terminate life-threatening seizures.

neuroscience↗