Wood L R, Smith M T
J Neuropathol Exp Neurol. 1984 Nov;43(6):620-33.
An experimental model for anencephaly was used to focus on two important aspects of the development of anencephaly: neurulation and conversion of exencephaly to anencephaly. Vitamin A was administered to pregnant rats on gestational days nine and ten. The animals were killed on successive gestational days to allow study of the development of anencephaly. The scanning electron microscope revealed filopodia and lamellopodia as the predominant mode of initial neural fold contact in the controls. Intertwining and overlapping of filopodia and lamellopodia with fusion of the adjacent cutaneous ectoderm completed neurulation. In embryos developing anencephaly, filopodia and lamellopodia never made contact above the cervical region and exencephaly resulted. The first evidence of the conversion of exencephaly to anencephaly was profound, labyrinthine expansion of the extracellular space of the telencephalic mantle. In spite of normal vascular patency and intact vessel walls, the exencephalic malformation spontaneously disintegrated, converting the lesion to anencephaly. The causes for tissue disintegration other than infarction must be considered in reconstructing the pathogenesis of anencephaly.
神经胚形成以及露脑畸形向无脑儿的转变。在妊娠第9天和第10天给怀孕大鼠施用维生素A。在连续的妊娠天数处死动物，以便研究无脑儿的发育情况。扫描电子显微镜显示，在对照组中丝状伪足和片状伪足是最初神经褶接触的主要方式。丝状伪足和片状伪足相互缠绕、重叠，并与相邻的皮肤外胚层融合，完成神经胚形成。在发育为无脑儿的胚胎中，丝状伪足和片状伪足在颈部以上区域从未接触，导致露脑畸形。露脑畸形向无脑儿转变的首个证据是端脑皮质细胞外空间出现严重的、迷宫样扩张。尽管血管通畅且血管壁完整，但露脑畸形仍自发解体，病变转变为无脑儿。在重建无脑儿的发病机制时，必须考虑除梗死以外的组织解体原因。
