Cortical-fluidic dimensional mapping isolates GRIN2A-driven dysconnectivity and pharmacological network degradation in schizophrenia

Standard connectivity models fail to capture the transient spatial kinematics underlying schizophrenia pathophysiology. The present study introduces Cortical-Fluidic Dimensional Mapping to resolve this analytical limitation. The framework translates continuous high-density electroencephalography into a dynamic fluid system to quantify instantaneous spatial turbulence. The algorithm processed over 7000 memory testing sessions from 364 healthy participants. The validation phase evaluated a pre-existing clinical repository comprising 300 de-identified psychiatric records. The investigation isolated functional dysconnectivity driven by the GRIN2A genetic variant and specific neurochemical modulations. The C-C genotype triggers a profound inversion of functional connectivity in the cuneus to caudate pathway, indicating a critical collapse in sensory gating mechanisms. Midazolam suppresses network turbulence heavily. Ketamine induces widespread hyperconnectivity across the networks. Lamotrigine mitigates this aberrant ketamine-driven state successfully. The physiological parameters directly mirror the cognitive deficits. Cuneus dysconnectivity links strictly to global symptom severity. The methodology establishes an objective biomarker. The framework maps the exact spatial consequences of N-methyl-D-aspartate receptor hypofunction. The metrics quantify the dysconnection hypothesis directly. The system links molecular glutamatergic vulnerabilities to macroscopic neural degradation in treatment-resistant psychiatric conditions.