Abstract

To study the relationship of N-acetylaspartate (NAA) metabolism and choline (Cl) metabolism in different parts of the brain based on magnetic resonance spectrography (1H-MRS) with clinical manifestations of autism spectrum disorders (ASD). Twenty-two children (16 boys, 6 girls), aged 2-10 years, were studied. Russian-language adapted versions of the Autism Treatment Evaluation Checklist (ATEC) and the Nisonger Child Behavior Rating Form (NCBRF) were administered. The ratio of metabolites NAA/creatine (Cr), Cho/Cr, Cho/NAA in the prefrontal cortex, postcentral gyrus and temporal lobes was studied using 1H-MRS. The following correlations were found: 1) between the NAA/Cr value and the Sensory/Cognitive Awareness scale in the prefrontal cortex on the left (ρ=0.479) and on the right (ρ=0.483); the Health/Physical Behavior scale in the precentral gyrus on the left (ρ=0.572) and on the right (ρ=0.463); the Sociability scale in the temporal lobe on the left (ρ=0.481) and on the right (ρ=0.796); the Speech/Language/Communication scale in the right temporal lobe (ρ=-0.552); 2) between the Cho/Cr value and the Adaptive Social scale in the postcentral gyrus on the left (ρ=-0.466) and on the right (ρ=-0.518); the Compliant/Calm scale in the prefrontal cortex on the right (ρ=0.624) and on the left (ρ=-0.541); 3) between the Cho/NAA ratio and the Speech/Language/Communication scale in the right pre-central (ρ=-0.471) and post-central gyrus (ρ=-0.507); the Self-Isolated/Ritualistic» scale in the left (ρ=-0.486) and right temporal lobe (ρ=-0.596). Thus, the predominant localization of disorders of N-acetylaspartate metabolism in communication disorders (bilaterally in the temporal lobes), cognitive, behavioral and somatic manifestations (bilaterally in the prefrontal regions) was established. Increased CI metabolism has identified deficits in interaction skills in both postcentral gyrus, and reveals bilateral differences in the effect on behavioral control in the prefrontal cortex. The results confirm the previously established numerous patterns between abnormal activation of the prefrontal cortex and neuronal dysfunction in ASD. But unlike other studies, it was possible to trace these relationships within a narrower phenotype of disorders - atypical autism comorbid with psychomotor disinhibition.

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