地方克汀病的病因和发病机制至今仍不十分清楚。根据大量流行病学和临床研究的资料,多数学者认为此病是胚胎期和新生儿期缺碘与甲状激素不足所致。但用单纯缺碘的方法复制地方克汀病动物模型,尚未见成功的报道。本实验自妊娠中期直至哺乳期给Wistar纯系母鼠饲以低碘饮食,造成仔鼠胚眙后期及哺乳期缺碘,得缺碘仔鼠18只。另取妊娠母鼠在同样的时期内饲以充分供碘饮食,得仔鼠22只作对照。用运动防御条件反射、脑电图和形态学方法来检查仔鼠脑功能和形态的变化。仔鼠生后14天检查发现:缺碘仔鼠表现了脑重较轻以及大脑皮质神经细胞密度增加,锥体细胞树突分枝较短较少;小脑皮质外颗粒层消失延 The causes and pathogenesis of local cretinism are still not fully understood. According to a large number of epidemiological and clinical research data, most scholars believe that the disease is caused by lack of iodine and thyroid hormones in the embryonic and neonatal period. However, simply using iodine deficiency method to copy the cretinism animal model has not been successfully reported. This experiment from the second trimester until lactation to Wistar pure system females fed a low iodine diet, resulting in postnatal embryos and lactation iodine deficiency, lack of iodine offspring 18. In addition, pregnant mothers in the same period were fed with sufficient iodine diet, which gave 22 offspring as a control. Changes in brain function and morphology were examined using exercise defensive conditioning, EEG, and morphology. 14 days after birth pups examination found: lack of iodine offspring showed a lighter brain and cerebral cortex nerve cell density increased, pyramidal cell dendritic branches less short; outer layer of cerebellar cortex disappeared