Purpose: Terminal myelocystocele (TMC) is thought to be caused by a misstep during secondary neurulation. However, due to the paucity of data on secondary neurulation and the rarity of TMC, proofs of this pathogenetic mechanism are unavailable. Based on a previous observation that TMC resembles a step of secondary neurulation in chick, a closer look was taken at secondary neurulation of chick embryos focusing on the cerebrospinal fluid-filled distal neural tube (terminal balloon).
Methods: Chick embryos at Hamburger and Hamilton (H-H) stages of 28, 30, 33, 35, 37, and 40 were harvested. Hematoxying-eosin staining, additional immunohistochemistry (laminin, cytokeratin, nestin), and scanning electron microscopy were performed.
Results: In H-H stages 28 to 30, after merging of the lumina of the primary and secondary neural tubes, the caudal end of the confluent tube dilates into a balloon-like structure (terminal balloon). As the proximal tube progressively becomes narrower, the terminal balloon dilates even further, and its wall fuses with the surface ectoderm (H-H stage 33). Later in H-H stages 35 to 40, the terminal balloon shrinks and becomes detached from the surface ectoderm and ultimately disappears, as the proximal lumen of the secondary neural tube continues to collapse.
Conclusion: A dilated balloon doubtlessly exists in the terminal secondary neural tube in chick embryos, and its subsequent disappearance occurs in a variable time course and sequence. Arrest of apoptosis resulting in failure of detachment of the terminal balloon from the surface ectoderm may well be the basis for human TMC.