Journal of neurosurgery
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Journal of neurosurgery · Mar 2007
Fetal spina bifida in a mouse model: loss of neural function in utero.
The devastating neurological deficit associated with myelomeningocele has previously been assumed to be a direct and inevitable consequence of the primary malformation-failure of neural tube closure. An alternative view is that secondary damage to the pathologically exposed spinal cord tissue in utero is responsible for the neurological deficiency. If the latter mechanism were shown to be correct, it would provide an objective rationale for the performance of in utero surgery for myelomeningocele, because coverage of the exposed spinal cord could be expected to alleviate or perhaps prevent neurodegeneration. To examine this question, the authors studied the development of neuronal connections and neurological function of mice during fetal and neonatal stages in a genetic model of exposed lumbosacral spina bifida. ⋯ These findings provide support for the hypothesis that neurological deficit in human myelomeningocele arises following secondary neural tissue destruction and loss of function during pregnancy.