1. Introduction

In modern pediatric neurology, delayed speech development (DSD) is considered one of the most common neuropsychological disorders of early childhood. The formation of speech in children is a complex, multilevel, and multifactorial process based on physiological mechanisms and closely linked with social, cultural, and psychological conditions [7,9].

Speech function is highly sensitive to various adverse influences, and its disturbances often lead to significant consequences, including difficulties in cognitive and communicative activities, as well as deviations in neuropsychological and social development. These factors are especially critical during early childhood, when the fundamental mechanisms of speech are being formed, ensuring its further development [2,4].

In recent years, the issue of speech disorders in children has gained particular importance for specialists in various fields—neurologists, speech therapists, psychologists, and educators. This relevance is determined not only by the growing prevalence of this disorder but also by the difficulties in its early diagnosis and timely correction. According to various studies, the prevalence of DSD among children ranges from 5% to 25% [1,6].

Etiologically, DSD may result from both organic and functional factors. Among the organic causes, leading roles are played by perinatal lesions of the central nervous system, brain injuries, neuroinfections, cerebral palsy, epilepsy, neurosensory hearing loss, and other pathological conditions. These factors affect brain structures responsible for the regulation of motor and cognitive processes, thereby slowing down speech development [3,7,8].

In contrast, functional forms of DSD are more often associated with adverse psychoemotional conditions, disturbances in family communication, limited speech environment, and pedagogical neglect [2,5].

2. Purpose of the Research

The purpose of this research was to determine the clinical and neurological characteristics of delayed speech development (DSD) in children, to analyze the relationship between the etiology of speech delay and neurological status, and to identify prognostic markers that differentiate functional from organic forms of speech disorders. The study also aimed to establish clinical criteria that could facilitate early diagnosis and timely therapeutic intervention, thereby improving the overall outcomes of neurodevelopmental rehabilitation in affected children.

Objective is to determine the clinical and neurological features and the relationship between the type of speech disorder and neurological status in children with delayed speech development of various origins.

3. Materials and Methods

The study was conducted at the clinic of Tashkent Pediatric Medical Institute. A total of 90 children aged 3 to 7 years with delayed speech development were examined. All participants were divided into two equal groups: Group I (n = 45; 50%) — children with delayed speech development (general speech underdevelopment, level II) associated with attention deficit hyperactivity disorder (ADHD). Group II (n = 45; 50%) — children with delayed speech development (general speech underdevelopment, level II) due to residual-organic brain lesions (ROL).

A control group of 15 children without any speech impairments was also included, matched for age and sex.

4. Results

To clarify the age and gender composition of the examined children, the distribution of both clinical groups by age and sex was analyzed (Table 1). The obtained data allow assessment of the age periods in which speech delay occurs most frequently and whether differences exist between the ADHD and ROL groups.

Table 1. Distribution of examined children by age

In both groups, boys predominated over girls, which corresponds with literature data indicating a higher incidence of speech disorders in males due to greater vulnerability of immature brain structures during early ontogenesis.

By age distribution, the largest number of cases in both the ADHD and ROL groups was observed at age 5 (40–44%), which corresponds to the period of active development of grammatical and phonetic speech components. At this age, speech defects become most noticeable and can be reliably diagnosed.

Among 3-year-olds, the frequency of DSD was lower (approximately 25–32%), which may be explained by the early detection stage and the absence of clearly formed speech norms. By age 7, the number of children with speech delay decreased, likely due to partial compensation and the effects of corrective therapy.

To assess the degree of speech development, the speech development coefficient was calculated based on expressive and receptive speech indicators, vocabulary, and grammatical skills.

Table 2. Speech Development Coefficient in Children with ADHD and Residual-Organic Lesions

The highest speech development coefficient was observed in children with DSD associated with ADHD (24.9 ± 3.9), indicating a primarily functional nature of speech impairment. In such cases, preserved intellectual and motor potential enables compensation of speech delay when timely corrective interventions are applied.

In children with residual-organic brain lesions, the coefficient was significantly lower (17.7 ± 6.7; p < 0.001), reflecting pronounced neurodynamic disturbances, delayed cortical maturation, and persistent cognitive deficits.

The findings demonstrate that in children with organic CNS damage, speech function develops more slowly and requires long-term, multidisciplinary rehabilitation. In contrast, DSD associated with ADHD is typically of a functional–discoordinative nature and responds well to neuropsychological and speech therapy methods.

5. Discussion

Children with delayed speech development associated with attention deficit hyperactivity disorder exhibit a significantly higher speech development coefficient (mean 24.9 ± 3.9) compared to those with residual-organic brain lesions (17.7 ± 6.7), suggesting a more favorable functional prognosis in functional forms of DSD. Children with organic brain lesions display more pronounced neurological and cognitive impairments, indicating delayed maturation and reduced functional activity of cortical structures. Early diagnosis and timely correctional interventions substantially improve rehabilitation outcomes and prevent the formation of persistent speech and cognitive disorders.

6. Conclusions

The study established that the clinical and neurological profile of delayed speech development in children is largely determined by the underlying etiology. Children with DSD associated with attention deficit hyperactivity disorder (ADHD) demonstrated relatively mild neurological symptoms and higher speech development coefficients, which indicates a functional and reversible nature of their disorder. In contrast, children with residual-organic brain lesions (ROL) exhibited more profound neurological and cognitive impairments, reflecting structural brain dysfunction and delayed cortical maturation.

ACKNOWLEDGEMENTS

The author expresses sincere gratitude to the staff of the Department of Neurology, Pediatric Neurology and Medical Genetics of the Tashkent State Medical University for their valuable guidance, constructive advice, and assistance during the research process. Special thanks are extended to the participating children and their parents for their cooperation and trust, which made this study possible. The author also appreciates the contribution of colleagues from the university clinic for their help in clinical observations and laboratory diagnostics.