ACQUIRED SPINAL-CORD INJURY IN HUMAN FETUSES WITH MYELOMENINGOCELE

Citation
Gm. Hutchins et al., ACQUIRED SPINAL-CORD INJURY IN HUMAN FETUSES WITH MYELOMENINGOCELE, PEDIATRIC PATHOLOGY & LABORATORY MEDICINE, 16(5), 1996, pp. 701-712
Citations number
12
Categorie Soggetti
Pathology,Pediatrics
ISSN journal
10771042
Volume
16
Issue
5
Year of publication
1996
Pages
701 - 712
Database
ISI
SICI code
1077-1042(1996)16:5<701:ASIIHF>2.0.ZU;2-A
Abstract
Experimental studies have shown that there is a potential to attempt i n utero repair of myelomeningocele in human fetuses. To provide a bett er understanding of the pathology of these lesions we prospectively st udied eight stillborn human fetuses with myelomeningocele autopsied at The Johns Hopkins Hospital. The intact vertebral column with surround ing structures was removed, processed as a single block, and prepared as serial histologic sections. Study of the slides showed in all cases that in the center of the myelomeningocele the vertebral arch was ope n, the arrangement of meninges was such that the dura mater was open a nd in continuity with the deep layers of the dermis, and the pia mater was open and in continuity with a layer consisting of the superficial dermis and the epidermis. These meningeal relationships created an ab normally configured arachnoid space containing cerebrospinal fluid ven tral to the spinal cord, which rested on the open pia mater and was ex posed on the dorsal aspect of the sac. At the level of the myelomening ocele the naked cord had undergone varying degrees of injury up to com plete loss of neural tissue. Where ventral remnants of the cord remain ed it was evident that a large degree of normal development of the cor d had occurred. In most instances it appeared that the injury or destr uction of the dorsal spinal cord was recent and consistent with occurr ence during delivery. The results of this study support the concept th at in utero surgery could preserve and protect the exposed spinal cord in a myelomeningocele of a human fetus and thus could reduce the seve rity of the neurologic deficit at birth.