Focal cortical dysplasia (FCD) is a leading cause of pharmacoresistant epilepsy in pediatric populations, yet its role in epileptogenesis remains incompletely understood. Recent findings suggest that hyperexcitability may originate in non-dysplastic peripheral areas rather than the malformation itself. However, given the significant variability across FCD cases, clarifying whether cytoarchitectural disorganization drives activity changes remains challenging. Using the carmustine-induced animal model, we investigated how varying degrees of cortical malformation influence neural dynamics. Local field potentials were recorded via multielectrode arrays during spontaneous activity and external perturbation. We introduced a novel metric to quantify spatial heterogeneity in signal organization and assessed its association with excitation-inhibition balance. Results show that alterations in signal structure correlate with the extent and distribution of cortical abnormalities, highlighting the functional relevance of cytoarchitectural variability. This work advances understanding of FCD-related network dysfunction and offers analytical tools with potential translational value for pre-surgical evaluation.