Abstract / Summary
Abstract Background Acute cerebral ischemia presents a critical dissociation between hyperacute synaptic failure and macrostructural tissue necrosis. Conventional linear screening instruments (e.g., MMSE, MoCA) exhibit pronounced ceiling effects and obscure modular neurodynamic disconnection. Modern connectomics posits that focal ischemia triggers acute network diaschisis across distributed large-scale circuits—specifically the default mode and frontoparietal control networks – prior to the emergence of radiologically visible cytotoxic edema on non-contrast computed tomography (CT). We evaluated a digital adaptation of Luria’s qualitative syndromic process approach to quantify this functional-structural dissociation during early post-stroke triage. Methods In this observational audit at a tertiary stroke center, 124 patients with verified acute stroke were stratified by emergent neuroimaging into an acute CT-negative presentation group (n = 56) and a macrostructural lesion-verified necrosis group (n = 68). Bedside neuropsychological testing (24–48 hours post-ICU stabilization) was conducted via the NeuroDraft platform across 10 independent cognitive domains using the continuous Luria Raw metric (0.0–5.0 penalty scale). Latent dimensionality was examined via complete-case Principal Component Analysis (PCA) with orthogonal Varimax rotation (n = 121), following the predefined methodological exclusion of 3 individuals with early-stage extrapyramidal pathology to prevent motor-slowing confounds. Results Memory and attention deficits exhibited striking cross-cohort statistical equivalence. Memory impairment showed near-identical severity (M = 1.69 ± 0.91 vs. 1.80 ± 0.93; U = 1870.5, p = 0.87), and complex attention diverged minimally (M = 1.19 ± 0.95 vs. 1.43 ± 0.94; U = 1677.0, p = 0.25), demonstrating early network-level vulnerability preceding macroscopic cytotoxic alterations. Conversely, language functions demonstrated significant resilience in the CT-negative cohort (M = 0.69 ± 0.98 vs. 1.14 ± 1.20; U = 1465.5, p = 0.03). Intra-individual profile variability revealed a trend toward syndromic flattening as structural damage consolidated (coefficient of variation: 1.26 vs. 1.09; U = 1344.0, p = 0.06). Factor decomposition resolved two independent axes: posterior instrumental-operational integrity and anterior-subcortical dynamic-regulatory control. Conclusions Network-level functional collapse outpaces visible parenchymal necrosis in emergent stroke. Digital Lurian profiling provides sensitive, deterministic quantification of early diaschisis, supporting bedside decision-making without replacing macrostructural neuroimaging.