Background/purpose: Deficiency of motoneuron innervation to the sphincter mechanism has been described in patients with anorectal malformation. Whether this event is primary or secondary remains unclear.
Methods: The authors quantified the motoneuron innervation of the sphincter mechanism by Fluorogold (FG) retrograde tracing experiment in fetal rats with anorectal malformation. Anorectal malformation was induced in rat fetuses by ethylenethiourea (ETU). Serial longitudinal sections encompassing the whole width of lumbosacral spinal cord were examined. The number of FG-labelled motoneurons were scored and compared between male fetuses with or without malformation in the ETU-fed group and normal controls.
Results: The number of FG-labelled motoneurons in the fetuses without defect, with imperforate anus (IA), with neural tube anomalies (NTA), with combined IA and NTA, and normal controls were determined to be (mean +/- SEM) 109.13 +/- 37.88, 55.05 +/- 25.85, 48.20 +/- 30.34, 54.43 +/- 28.55, and 135.22 +/- 28.78, respectively. FG-labelled motoneurons in the fetuses with IA, NTA, and combined IA and NTA are significantly fewer than that in fetuses without defects (P <.05) and in normal controls (P <.005).
Conclusions: These findings suggest that defective motoneuron innervation to the sphincter mechanism is a primary anomaly that coexists with the alimentary tract anomaly in anorectal malformation during fetal development. The intrinsic neural deficiency is an important factor likely to contribute to poor postoperative anorectal function despite surgical correction of anorectal malformation.
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