Animal models have been used to help study the embryopathy and pathophysiology of neurological deterioration in open neural tube defects. Results from studies of lesion induction and defect repair in these animals have become the basis for intrauterine repair in humans. This review attempts to discern the advantages and flaws in animal models that may help us understand why spinal cord function is not preserved to the same degree in humans compared to the animal models.
Copyright 2003 S. Karger AG, Basel