A hypothesis for embryopathogenesis of myeloschisis is described on the basis of experimental studies analyzing the stage specificity and immunohistochemical/histological characteristics of the exposed neural tissue (placode). Myeloschisis developed in six fetuses among 205 chick embryos treated in various stages with teratogens including ethylnitrosourea, and anticonvulsant and antipyretic agents. All but one case (with associated cephalothoracopagus) demonstrated myeloschisis in the thoracic region with a lamina defect of two and three levels. No fetus was exposed to a teratogen prior to or within Hamburger and Hamilton stage 12 (45 to 49 hours postincubation), when the neuropore closes. Immunohistochemical studies of chick myeloschisis clearly indicated that neuron-specific enolase-positive elements were extremely active only in the overgrown placode, corresponding to the histological findings with Kluver-Barrerra's special stain. These findings were compared with observations in a case of myeloschisis in a human neonate. The results of this study imply the possibility of another mechanism for the embryopathogenesis of myeloschisis: namely, the overgrowth and reopening hypothesis.
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