首发偏执型精神分裂症患者胼胝体微结构异常研究

The abnormalities of microstructure in corpus callosum in the first-episode patients with paranoid schizophrenia:A study of DTI and MRS.

目的探讨未用药首发偏执型精神分裂症患者胼胝体纤维束的细微结构改变及其可能的神经生化代谢原因,以期为精神分裂症"神经发育假说"提供依据。方法选取20例首发偏执型精神分裂症患者,应用DTI和MRS技术对脑内胼胝体膝部、压部和体部进行成像检测,并与20名年龄、性别和文化程度与患者相匹配的健康对照者比较。结果(1)患者组胼胝体膝部FA值小于健康对照组(0.731±0.102∶0.815±0.043,t=3.358,P=0.002),胼胝体膝部和体部的ADC值高于健康对照组(8.043±0.462∶7.564±0.470,t=2.645,P=0.012;8.543±0.462∶7.743±0.470,t=3.898,P=0.000)。(2)患者组胼胝体膝部NAA值和体部NNA值、Cho值均低于健康对照组(1.449±0.406∶1.748±0.392,t=2.365,P=0.023;0.911±0.130∶1.164±0.153,t=5.618,P=0.000;1.006±0.869∶1.275±0.367,t=3.190,P=0.003)。结论首发偏执型精神分裂症患者胼胝体膝部纤维束在疾病早期阶段即存在各向异性降低,其可能原因是神经发育不良。

Objective To investigate the fractional anisotropy and the neurochemical metabolites of white matter in corpus callosum in first -episode drug -free patients with paranoid schizophrenia by Diffusion Tenser Image （DTI） and Magnetic Resonance Spectroscopy （MRS）. Methods Twenty first - episode patients with paranoid schizophrenia and twenty health subjects matched with sex, age and education were scanned by DTI and MRS. Fractional anisotropy （FA）, averaged diffusion coefficient （ ADC ） N - acetylasparate （ NAA ） and Choline - containing compound （Cho） were measured in the genu, body and splenium of the corpus callosum. Results （ 1 ） The mean FA in genu of corpus callosum in the patients was significantly lower than that in the health controls （0.731 ± 0.102： 0.815± 0.043, t = 3. 358, P = 0. 002）, while the mean ADC in genu and body of corpus callosum in patients were significandy higher than those of heahh controls （8.043 ±0.462：7.564 ±0.470, t =2.645, P =0.012; 8.543 ±0.462：7.743 ±0.470, t = 3. 898, P =0.000）. （2） The mean NAA in genu,and mean NAA and Cho in body of patients were significantly lower than those of the health controls （ 1. 449 ± 0.406： 1. 748 ± 0.392, t = 2. 365, P = 0.023 ; 0.911±0.130：1.1 64 ±0. 153, t=5.618, P=0.000; 1.006±0.869： 1.275±0.367, t=3.190, P=0.003）.Conclusion The suble abnor- malities in genu of corpus callosum have been developed in the early stages of first - episode paranoid schizophrenia, which may be caused by mal- neurodevelopment.