Smith M T, Huntington H W
J Neuropathol Exp Neurol. 1981 Jan;40(1):20-31.
The sequential morphological development of anencephaly was studied in an experimental model. Vitamin A was administered to pregnant rats on gestational days 8, 9, and 10. When the litters were allowed to proceed to term, the treatment resulted in fetuses with anencephalic features. The progressive morphological development of the malformation was then established by histological and gross study of embryos and fetuses of different ages. The earliest lesion identified was a microfocal necrosis located in the head fold epithelium near the anterior neuropore on day 9; it was lateral to the normal position of physiological necrotic foci seen in control embryos. Subsequent to the appearance of the initial lesion, the malformation developed as everted brain folds extending vertically from the diencephalon in the pattern of exencephaly. The neural tube in the region of the malformation never closed, and the exencephaly arose as a progressive development of non-closed neural tube. Finally, the classical anencephalic resulted from the spontaneous necrosis of the exencephalic malformation. This study indicates that anencephaly in an experimental model arises from microscopic foci of necrosis near the anterior neuropore and develops through non-closure of the neural tube.
在一个实验模型中研究了无脑儿的连续形态学发育。在妊娠第8、9和10天给怀孕大鼠施用维生素A。当让这些窝产仔发育至足月时，该处理导致胎儿出现无脑儿特征。然后通过对不同年龄胚胎和胎儿的组织学和大体研究确定了畸形的渐进性形态学发育。最早发现的病变是在第9天位于前神经孔附近头褶上皮的微灶性坏死；它位于对照胚胎中所见生理性坏死灶的正常位置的外侧。在初始病变出现后，畸形发展为从间脑垂直外翻的脑褶，呈露脑畸形的模式。畸形区域的神经管从未闭合，露脑畸形是未闭合神经管的渐进性发展。最后，经典的无脑儿是由露脑畸形的自发性坏死导致的。这项研究表明，实验模型中的无脑儿起源于前神经孔附近的微观坏死灶，并通过神经管未闭合而发展。
