arXiv subjects

Aaron Struck

Publications and source records attributed to Aaron Struck.

4 recordsLinked to original sources

arXiv2026

Poisson Flow of Cortical Folding in Juvenile Myoclonic Epilepsy

Cortical folding reflects coordinated neurodevelopmental processes and is increasingly recognized as a sensitive marker of neurological disease. However, most existing analyses rely on indirect scalar summaries that do not explicitly model folding geometry itself. In juvenile myoclonic epilepsy (JME), a common genetic epilepsy, cortical abnormalities are often subtle, spatially distributed, and difficult to detect using conventional morphometric measures. We introduce a Poisson-equation--based framework that models cortical folding as a geometry-driven flow derived from mean curvature on the cortical manifold. By treating folding patterns as a stationary source--sink structure, the proposed approach yields a smooth, globally balanced potential field whose surface gradient defines a physically interpretable flux. This framework enables spatially coherent analysis of sulcal--gyral folding organization and provides a principled representation of geometry-driven cortical structure in JME.

cs.CV↗

arXiv2026

Poisson Flow Model of Cortical Folding Pattern

Cortical folding reflects coordinated neurodevelopmental processes and provides a sensitive marker of neurological disease. In juvenile myoclonic epilepsy (JME), structural abnormalities are subtle and spatially distributed, limiting the sensitivity of conventional morphometric measures such as cortical thickness. We introduce a Poisson flow model derived from gradients of the mean curvature field on the cortical surface. The method yields a smooth scalar field obtained from a Poisson equation, whose surface gradient defines a flow representation of folding organization. This representation enables spatially coherent characterization of sulcal--gyral patterns and provides a principled geometric framework for studying distributed cortical alterations in JME.

q-bio.NC↗

arXiv2026

Counterfactual Analysis of Brain Network Dynamics

Causal inference in brain networks has traditionally relied on regression-based models such as Granger causality, structural equation modeling, and dynamic causal modeling. While effective for identifying directed associations, these methods remain descriptive and acyclic, leaving open the fundamental question of intervention: what would the causal organization become if a pathway were disrupted or externally modulated? We introduce a unified framework for counterfactual causal analysis that models both pathological disruptions and therapeutic interventions as an energy-perturbation problem on network flows. Grounded in Hodge theory, directed communication is decomposed into dissipative and persistent (harmonic) components, enabling systematic analysis of how causal organization reconfigures under hypothetical perturbations. This formulation provides a principled foundation for quantifying network resilience, compensation, and control in complex brain systems.

q-bio.NC↗

arXiv2023

Effects of Epileptiform Activity on Discharge Outcome in Critically Ill Patients

Epileptiform activity (EA) is associated with worse outcomes including increased risk of disability and death. However, the effect of EA on the neurologic outcome is confounded by the feedback between treatment with anti-seizure medications (ASM) and EA burden. A randomized clinical trial is challenging due to the sequential nature of EA-ASM feedback, as well as ethical reasons. However, some mechanistic knowledge is available, e.g., how drugs are absorbed. This knowledge together with observational data could provide a more accurate effect estimate using causal inference. We performed a retrospective cross-sectional study with 995 patients with the modified Rankin Scale (mRS) at discharge as the outcome and the EA burden defined as the mean or maximum proportion of time spent with EA in six-hour windows in the first 24 hours of electroencephalography as the exposure. We estimated the change in discharge mRS if everyone in the dataset had experienced a certain EA burden and were untreated. We combined pharmacological modeling with an interpretable matching method to account for confounding and EA-ASM feedback. Our matched groups' quality was validated by the neurologists. Having a maximum EA burden greater than 75% when untreated had a 22% increased chance of a poor outcome (severe disability or death), and mild but long-lasting EA increased the risk of a poor outcome by 14%. The effect sizes were heterogeneous depending on pre-admission profile, e.g., patients with hypoxic-ischemic encephalopathy (HIE) or acquired brain injury (ABI) were more affected. Interventions should put a higher priority on patients with an average EA burden higher than 10%, while treatment should be more conservative when the maximum EA burden is low.

stat.ME↗