Generation of anencephaly: 1. Aberrant neurulation and 2. Conversion of exencephaly to anencephaly

Abstract

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.