Postneurulation rapid brain growth represents a critical time for encephalocele formation: a chick model.

Current theory regarding the pathogenesis of encephaloceles suggests that the defect occurs after neurulation is completed in which brain tissue herniates through defective mesodermal elements necessary for skull modeling. To better delineate the mechanisms of encephalocele development, we performed a variety of microsurgical manipulations in the developing cranium of the chick embryo during the postneurulation period of early rapid brain growth. The results of the study revealed that encephaloceles could be induced in 78% of chick embryos manipulated at stage 26 that had evidence of marked decompression of the primitive ventricle. On the other hand, control embryos or embryos manipulated without ventricular decompression at stage 26 did not develop encephaloceles (0 of 32). Embryos with decompression of the primitive ventricle treated at earlier stages (20-24) showed only a 5% incidence of encephaloceles. These findings suggest that there is both a critical time point during postneurulation rapid brain growth when encephaloceles are prone to occur and a mesenchymal defect associated with decompression of the primitive ventricle that must be present to induce encephaloceles.