Regional brain chemical alterations in young children with autism spectrum disorder
Regional brain chemical alterations in young children with autism spectrum disorder
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DOI：
10.1212/wnl.60.1.100
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发表时间：
2003-01-14
期刊：
影响因子：
9.9
通讯作者：
Dager, SR
中科院分区：
文献类型：
--
作者：
Friedman, SD;Shaw, DW;Dager, SR
目的：作者评价了自闭症患者局部脑化学的证据，神经元堆积密度增加。研究方法：45名3- 4岁自闭症谱系障碍（ASD）儿童，13名典型发育（TD）儿童和15名发育迟缓（DD）儿童使用双回波质子回波平面光谱成像（32 × 32矩阵-1 cm（3）体素）进行了研究，以测量脑化学物质浓度和弛豫时间。根据组织部分体积校正化学定量，并根据成对回波计算化学弛豫的相对测量值（T-2 r）。使用多重比较校正的方差分析比较平均值和单个区域的测量值。结果如下：ASD受试者表现出与TD对照相比降低的N-乙酰天冬氨酸（NAA）（-10%）、肌酸（Cre）（-8%）和肌醇（-13%）浓度，并且相对于TD（7%）和DD（9%）组延长的NAA T-2 r。与DD受试者相比，ASD儿童也表现出胆碱（10%）和Cre（9%）的T-2 r延长。区域分析表明，与TD和DD组相比，ASD中的化学改变具有微妙的模式。结论：ASD患者在3 ~ 4岁时存在脑化学异常。然而，这些异常的方向和广泛分布不支持ASD中弥漫性神经元堆积密度增加的假设。
Objective: The authors evaluated regional brain chemistry for evidence of increased neuronal packing density in autism. Methods: Forty-five 3- to 4-year-old children with autism spectrum disorder (ASD), 13 children with typical development (TD), and 15 children with delayed development (DD) were studied using dual-echo proton echoplanar spectroscopic imaging (32 X 32 matrix-1 cm(3) voxels) to measure brain chemical concentrations and relaxation times. Chemical quantification was corrected for tissue partial volume and relative measures of chemical relaxation (T-2r) were calculated from the paired echoes. Measures from averaged and individual regions were compared using analysis of variance corrected for multiple comparisons. Results: ASD subjects demonstrated reduced N-acetylaspartate (NAA) (-10%), creatine (Cre) (-8%), and myo-inositol (-13%) concentrations compared to TD controls and prolonged NAA T-2r relative to TD (7%) and DD (9%) groups. Compared to DD subjects, children with ASD also demonstrated prolonged T-2r for choline (10%) and Cre (9%). Regional analyses demonstrated subtle patterns of chemical alterations in ASD compared to the TD and DD groups. Conclusions: Brain chemical abnormalities are present in ASD at 3 to 4 years of age. However, the direction and widespread distribution of these abnormalities do not support hypothesis of diffuse increased neuronal packing density in ASD.