Goldman M B, Torres I J, Keedy S, Marlow-O'Connor M, Beenken B, Pilla R
Department of Psychiatry, University of Chicago, Chicago, Illinois 60637, USA.
Hippocampus. 2007;17(7):554-62. doi: 10.1002/hipo.20292.
Diminished hippocampal volume occurs in the anterior segment of some schizophrenic patients, and in the posterior segment in others. The significance of hippocampal pathology in general and these segmental differences in specific is not known. Several lines of evidence suggest anterior hippocampal pathology underlies the life-threatening hyponatremia seen in a subgroup of patients with schizophrenia; therefore our goal was to determine if this region was preferentially diminished in hyponatremic patients. We studied seven polydipsic hyponatremic, ten polydipsic normonatremic, and nine nonpolydipsic normonatremic schizophrenic inpatients, as well as 12 healthy controls. All underwent structural scanning on a high resolution (3.0 T) magnetic resonance imaging (MRI) scanner. Hippocampal formation, amygdala, and third ventricle volumes were manually traced in each subject. The hippocampus was divided at the posterior extent of the uncus, and all structural volumes were corrected for whole brain volume and other significant recognized factors (i.e., age, gender, height, parental education). Despite being overhydrated, anterior hippocampal formation volume was diminished in those with polydipsia and hyponatremia relative to each of the other three groups. Third ventricle volume was larger in this group than in healthy controls but similar to the two patient groups. Posterior hippocampal and amygdala volumes did not differ between groups. Other potential confounds (e.g., water imbalance) either had no effect or accentuated these differences. We conclude the anterior hippocampal formation is smaller in hyponatremic schizophrenic patients, thereby linking an important and objective clinical feature of schizophrenia to a neural pathway that can be investigated in animal models. The findings strengthen the hypothesis that anterior hippocampal formation pathology disrupts functional connectivity with other limbic structures in schizophrenia.
部分精神分裂症患者的海马体前部体积减小，而另一些患者的海马体后部体积减小。一般而言，海马体病变的意义以及这些特定节段差异的意义尚不清楚。有几条证据表明，海马体前部病变是部分精神分裂症患者出现危及生命的低钠血症的基础；因此，我们的目标是确定该区域在低钠血症患者中是否优先缩小。我们研究了7例多饮性低钠血症、10例多饮性正常血钠、9例非多饮性正常血钠的精神分裂症住院患者以及12名健康对照者。所有人均在高分辨率（3.0T）磁共振成像（MRI）扫描仪上进行了结构扫描。在每个受试者中手动描绘海马结构、杏仁核和第三脑室的体积。海马体在钩回的后部范围进行划分，所有结构体积均根据全脑体积和其他重要的公认因素（即年龄、性别、身高、父母教育程度）进行校正。尽管存在水分过多的情况，但与其他三组相比，多饮性低钠血症患者的海马体前部结构体积减小。该组的第三脑室体积比健康对照者大，但与两个患者组相似。各组之间的海马体后部和杏仁核体积没有差异。其他潜在的混杂因素（如水分失衡）要么没有影响，要么加剧了这些差异。我们得出结论，低钠血症的精神分裂症患者海马体前部结构较小，从而将精神分裂症的一个重要且客观的临床特征与一个可在动物模型中研究的神经通路联系起来。这些发现强化了这样一种假设，即海马体前部结构病变破坏了精神分裂症中与其他边缘结构的功能连接。
