COMPARATIVE ANALYSIS OF CLINICAL-NEUROLOGICAL AND COGNITIVE CHARACTERISTICS OF SPEECH DELAY IN CHILDREN WITH AND WITHOUT RESIDUAL BRAIN PATHOLOGY

Abstract

Speech delay is a multifactorial neurodevelopmental disorder resulting from the combined influence of perinatal cerebral damage, immune dysregulation, and genetic susceptibility. Increasing evidence indicates that neuroinflammatory mechanisms and functional polymorphisms of cytokine genes play a crucial role in impaired neuronal differentiation, synaptic plasticity, and speech development.The present study aimed to investigate serum inflammatory cytokine profiles and polymorphic variants of the IL1β, IL6, and TNFα genes in children with speech delay, stratified according to the presence or absence of residual brain pathology, and to determine their pathogenetic and prognostic significance.The study included three groups: children with speech delay and residual brain pathology (n = 30), children with speech delay without residual cerebral abnormalities (n = 46), and a control group of neurologically healthy children (n = 20). Serum levels of IL-1β, IL-6, TNF-α, and IL-10 were measured using multiplex enzyme-linked immunosorbent assay, and genetic polymorphisms (IL1β −31 C>T, IL6 −174 C>G, TNFα −308 G>C) were analyzed by molecular genetic methods. Statistical analysis was performed using Welch’s ANOVA, Student’s t-test, Pearson’s χ² test, Fisher’s exact test, and odds ratio calculations.Children with speech delay demonstrated significantly elevated concentrations of both proinflammatory and anti-inflammatory cytokines compared to healthy controls (p < 0.001). Increased IL-6 levels were more frequently associated with residual brain pathology, whereas elevated TNF-α concentrations were predominantly observed in children without structural brain abnormalities, suggesting the presence of distinct inflammatory response phenotypes.