首页> 中文期刊> 《中华精神科杂志》 >精神分裂症患者及其健康同胞的弥散张量成像研究

精神分裂症患者及其健康同胞的弥散张量成像研究

摘要

目的 探索精神分裂症患者及其健康同胞是否存在类似的脑白质完整性异常.方法 采用弥散张量成像技术扫描精神分裂症患者(患者组)、患者的健康同胞(同胞组)和健康对照(对照组)的全脑,用基于体素的分析方法比较3组的白质纤维分数各向异性(fractional anisotropy,FA)值.结果 在左侧前额叶和海马区,患者组(左侧前额叶:0.303±0.006,海马:0.310±0.O05)和同胞组(左侧前额叶:0.320±0.006,海马:0.318±0.006)的白质FA值显著小于对照组(左侧前额叶:0.338±0.007,海马:0.338±0.005),差异均有统计学意义(P<0.05),患者组与同胞组的差异无统计学意义(P>0.05);在左侧前扣带区,患者组白质FA值(0.391±0.006)显著小于同胞组(0.423±0.006)和对照组(0.412±0.007),差异有统计学意义(P<0.05),同胞组的FA值大于对照组,但差异无统计学意义(P>0.05).结论 精神分裂症患者及其健康同胞存在相似的脑白质完整性异常,左侧前额叶和海马白质FA值降低可能意味着精神分裂症的患病风险,左侧前扣带的白质FA值降低则可能是向该病转换的决定因素.%Objective The objective is to determine whether brain regional pattern of neural disconnectivity is shared by schizophrenic patients and their healthy siblings or only presented in schizophrenic patients.Methods To investigated brain white matter (WM) abnormalities by voxel-based analysis of WM fractional anisotropy (FA) data acquired from diffusion tenor imaging in 34 pairs of schizophrenic patients and their heaithy siblings and 32 healthy controls.Results Both schizophrenic patients and their healthy siblings showed reduced WM FA in the left prefrontal cortex (PFC) ( patients:0.303±0.006 ; siblings:0.320±0.006 ) and hippocampus ( patients:0.310±0.005 ; siblings:0.318±0.006) as compared with healthy controls (PFC:0.338±0.007; hippocampus:0.338±0.005) (P<0.05),without significant difference between patients and siblings (P>0.05).In marked contrast,only schizophrenic patients exhibited reduced WM FA (0.391±0.006) in the left anterior cingulate cortex (ACC) as compared with either siblings (0.423±0.006) (P<0.05) or controls (0.412±0.007) (P<0.05),without significant difference between siblings and controls (P>0.05).Conclusions Schizophrenic patients and their healthy siblings show similar abnormalities of brain WM integrity.Schizophrenic patients and their healthy siblings share neural disconnectivity in the left PFC and hippocampus that may relate to the higher risk of healthy siblings to develop schizophrenia,which may be eventually attributed to additional neural disconnectivity in the left ACC.

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