The absolute quantitative analysis of cingulate cortex metabolites in preschool children with autism spectrum disorder using proton MR spectroscopy / 中华放射学杂志

ABSTRACT

Objective To investigate the metabolite changes in the preschool children with autism spectrum disorder (ASD) using MR spectroscopy (MRS) and explore the associations between image findings and clinical variables, which may provide a noninvasive brain biochemical method for the early diagnosis and prevention of autism. Methods Twenty one cases of preschool ASD children (3-6 years old) and age-and sex-matched 20 preschool healthy controls underwent single voxel short (SVS) short TE (TE=30 ms) MRS. The absolute metabolite concentrations in the anterior cingulate cortex (ACC) , anterior middle anterior cingulate cortex (aMCC) and posterior cingulate (PCC) were quantitatively analyzed using LCModel software. Two independent sample t tests were used for analysis. The relationships between metabolite concentrations and diagnostic and statistical manual of mental disorders (DSM-IV) , childhood autism rating scale (CARS) and autism behavior checklist (ABC) were analyzed by Pearson correlation analysis. Results Compared to control subjects, ASD patients had significantly lower N-acetylaspartate (NAA) values (4.35 ± 0.80, 6.34±0.82, 8.04±0.97 mmol/L respectively) in ACC, aMCC and PCC (t=2.640, P=0.012;t=2.182, P=0.035;t=3.343, P=0.002) , had significantly lower choline (Cho) 1.32±0.22 mmol/L (t=2.905, P=0.006) and glutamine and glutamate complex (Glx) 10.02 ± 0.88 mmol/L (t=2.090, P=0.043) in PCC. Cho, total creatine (tCr) , myo-Inositol (MI) and Glx levels did not differ between groups in other aforementioned regions (P>0.05). Negative correlations between the NAA ualues in the PCC and CARS (r=-0.504, P=0.020) were detected, and no significant correlation among DSM-IV, CARS, ABC and other metabolite values (P>0.05). Condnsions The biochemical changes in the preschool children with ASD in cingulate reflect the neuronal loss, structural or functional damage and cell membrane enzyme metabolic dysfunctions, may reveal the pathological basis of ASD. These results may provide noninvasive and quantitative methods for the diagnosis and prognosis evaluation of ASD child.