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Histogenesis of experimental open neural defects in the early chick embryo.

The chick embryo is a useful experimental model for investigating neural dysraphism. Windowing at 26 h incubation is by itself teratogenic, resulting in predominantly neural tube defects. A histological study of a regular series of specimens between pre-neurulation and later stages was undertaken. Open brain defects occurred at every stage after the expected closure of the anterior neuropore, suggesting that they arose by non-closure, myeloschisis was preceded by a characteristic triangular shape of the rhomboid sinus. Serial sections revealed regular open defects, with separation between the neural plate and tail-bud sources of neural tissue, but continuity of the neural plate into the caudal region. These findings suggest that myeloschisis arises by nonclosure of the neural folds. The establishment of myeloschisis was followed by local separation of the notochord from an open area of neural tube, but not by overgrowth of neural tissue. Myelodysplasia appeared at about the time of expected closure of the rhomboid sinus. Serial sections revealed irregular open defects, with complete absence of neural plate material and formation of the cord tissue from tailbud material alone. The lesions were accompanied by extensive cystic and hemorrhagic changes in local mesoderm, with reduction in somite volume. There was no associated notochordal separation.