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Luigi Maccotta

Publications and source records attributed to Luigi Maccotta.

3 recordsLinked to original sources

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

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

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