Department of Radiology, Medical School of Karadeniz Technical University, Farabi Hospital, 61080 Trabzon, Turkey.
AJR Am J Roentgenol. 2010 Apr;194(4):1110-5. doi: 10.2214/AJR.09.3204.
The aim of this study was to use MR spectroscopy to determine whether the brain metabolism of children with psychomotor delay of unknown cause differs from that of children without psychomotor delay.
Twenty children (10 girls, 10 boys; mean age, 8.65 years; range, 4-15 years) with psychomotor delay and 19 children without psychomotor delay who served as controls (nine girls, 10 boys; mean age, 8.79 years; range, 6-13 years) were evaluated with multivoxel MR spectroscopy of the brain. The Stanford-Binet test and Wechsler Intelligence Scale for Children-Revised were used to evaluate developmental quotient. Psychomotor delay was assessed as severe (developmental quotient, < 50), moderate (developmental quotient, 50-75) and mild (developmental quotient, > 75). The controls had a developmental quotient greater than 95. Spectra were acquired from eight specific voxels at the bilateral parasagittal frontal and parietal gray matter and the bilateral frontal and parietal white matter at the level of the centrum semiovale. The ratios of N-acetylaspartate (NAA) to choline (Cho), NAA to creatine (Cr), and choline to creatine were determined.
Thirteen children had minor and seven children had moderate psychomotor delay. In the psychomotor delay group, the right frontal white matter NAA/Cho, NAA/Cr, and Cho/Cr ratios were 1.45 +/- 0.18, 1.95 +/- 0.33, and 1.36 +/- 0.27; in the control group the ratios were 1.46 +/- 0.23, 2.04 +/- 0.33, and 1.41 +/- 0.19. The ratios for the left frontal lobe white matter were 1.34 +/- 0.21, 2.01 +/- 0.33, and 1.55 +/- 0.26 in the psychomotor delay group and 1.42 +/- 0.15, 2.17 +/- 0.34, and 1.53 +/- 0.25 in the control group. The ratios for the right parietal lobe white matter were 1.80 +/- 0.38, 2.04 +/- 0.43, and 1.18 +/- 0.35 in the psychomotor delay group and 1.89 +/- 0.31, 2.16 +/- 0.30, and 1.17 +/- 0.23 in the control group. The left parietal lobe white matter ratios were 1.66 +/- 0.36, 2.08 +/- 0.35, and 1.35 +/- 0.29 in the psychomotor delay group and 1.81 +/- 0.29, 2.17 +/- 0.35, and 1.22 +/- 0.26 in the control group.
Metabolite distribution varied with brain region in children with and those without psychomotor delay. No significant difference was found between the brain metabolite ratios of children with psychomotor delay of unknown cause and those of age-matched children without psychomotor delay.
本研究旨在使用磁共振波谱技术来确定有原因不明运动发育迟缓的儿童与无运动发育迟缓的儿童之间的脑代谢是否存在差异。
20 名（10 名女孩，10 名男孩；平均年龄 8.65 岁；范围 4-15 岁）有运动发育迟缓的儿童和 19 名作为对照组的无运动发育迟缓的儿童（9 名女孩，10 名男孩；平均年龄 8.79 岁；范围 6-13 岁）接受了脑部多体素磁共振波谱检查。斯坦福-比奈测验和韦氏儿童智力量表修订版用于评估发育商数。运动发育迟缓被评估为严重（发育商数 < 50）、中度（发育商数 50-75）和轻度（发育商数 > 75）。对照组的发育商数大于 95。从双侧矢状位额、顶叶灰质和侧脑室水平的额、顶叶白质的八个特定体素中获取频谱。测定 N-乙酰天冬氨酸（NAA）与胆碱（Cho）、NAA 与肌酸（Cr）以及 Cho 与 Cr 的比值。
13 名儿童有轻度运动发育迟缓，7 名儿童有中度运动发育迟缓。在运动发育迟缓组中，右侧额叶白质 NAA/Cho、NAA/Cr 和 Cho/Cr 比值分别为 1.45 ± 0.18、1.95 ± 0.33 和 1.36 ± 0.27；在对照组中，这些比值分别为 1.46 ± 0.23、2.04 ± 0.33 和 1.41 ± 0.19。左侧额叶白质的比值分别为 1.34 ± 0.21、2.01 ± 0.33 和 1.55 ± 0.26，在运动发育迟缓组和 1.42 ± 0.15、2.17 ± 0.34 和 1.53 ± 0.25，在对照组中。右侧顶叶白质的比值分别为 1.80 ± 0.38、2.04 ± 0.43 和 1.18 ± 0.35，在运动发育迟缓组和 1.89 ± 0.31、2.16 ± 0.30 和 1.17 ± 0.23，在对照组中。左侧顶叶白质的比值分别为 1.66 ± 0.36、2.08 ± 0.35 和 1.35 ± 0.29，在运动发育迟缓组和 1.81 ± 0.29、2.17 ± 0.35 和 1.22 ± 0.26，在对照组中。
有和无运动发育迟缓的儿童的脑区代谢物分布不同。有原因不明运动发育迟缓的儿童与年龄匹配的无运动发育迟缓的儿童之间的脑代谢物比值无显著差异。
