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This study reports the smallest human embryos with open myeloschisis, suggesting the condition arises from the neural plate failing to close. Findings challenge existing theories on neural tube defects.
Area of Science:
- Developmental biology
- Embryology
- Teratology
Background:
- Open myeloschisis is a severe neural tube defect.
- Previous research suggested a defective limiting membrane causes neural overgrowth and polarity loss.
Purpose of the Study:
- To report and characterize the earliest human embryos exhibiting open myeloschisis.
- To investigate the developmental origins and cellular characteristics of early myeloschisis.
Main Methods:
- Histological examination of four human embryos (Carnegie stages 12-14) with open myeloschisis.
- Microscopic analysis of neuroectodermal junctions, cellular polarity, and limiting membranes.
Main Results:
- Four human embryos with open myeloschisis, including the smallest reported at Carnegie stage 12.
- No evidence of forced opening; smooth neuroectodermal junctions suggest failure of neural plate closure.
- Well-preserved cellular polarity and limiting membranes despite neural tissue overgrowth.
Conclusions:
- Open myeloschisis likely originates from a failure of neural plate closure, not post-closure defects.
- Findings contradict the hypothesis that a defective limiting membrane causes polarity loss and neural overgrowth in myeloschisis.
Abstract:
Four early human embryos with open myeloschisis are reported. These are a thoracolumbar myeloschisis in Carnegie developmental stage 12, a cervical myeloschisis in stage 13, and two lumbosacral myeloschisis in stage 14. All of them are the smallest human embryos with this type of malformation ever reported. In these embryos, the neuroectodermal junction is smooth and there is no microscopic evidence that the neural tube is forced open after its proper closure. The presence of the lesion in such early embryos, especially in one of stage 12, implies that the lesion evolved from the neural plate which never closed. Cellular polarity and the limiting membrane in the lesion are generally well preserved in spite of apparent overgrowth of the neural tissue. These findings do not support the hypothesis of LEMIRE et al. that the defective external limiting membrane predisposes to a loss of cellular polarity and resultant neural overgrowth.