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Childs Nerv Syst. 2013 Sep;29(9):1683-8. doi: 10.1007/s00381-013-2196-3. Epub 2013 Jun 19.

Pathoembryogenesis of terminal myelocystocele: terminal balloon in secondary neurulation of the chick embryo.

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  • 1Division of Pediatric Neurosurgery, Seoul National University Children's Hospital, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul 110-769, Republic of Korea.



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).


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.


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.


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.

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