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PubMed1991

[Dysraphism].

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Arnold-Chiari Malformation↗
PubMed1986

Cytochemical localization of acid phosphatase in the hindbrain of dysraphic mice.

The cytochemical localization of acid phosphatase (AP) was studied at the ultrastructural level in the abnormal neuroepithelium of dysraphic loop-tail (Lp/Lp) embryos between 9 and 12 days of gestation. At 9-11 days, normal and abnormal embryos showed a positive AP reaction throughout the thickness of the neuroepithelium, i.e., in apical, intermediate, and basal zones, although many cells were unreactive. The reaction is sensitive to sodium fluoride and occurs in saccules and vesicles associated with the Golgi complex, as well as in vacuoles of varying size containing flocculent and particulate material. Gap-junctional vesicles, which are known to occur in increased numbers in abnormal brains, were AP-negative. By 12 days of gestation, the reaction in normal embryos was localized in the midventral marginal layer, where some cell processes were filled with reaction product; in abnormal embryos, these AP-positive processes were not observed. The results indicate that perturbations in lysosomal activity may not be fundamentally involved in the etiology of dysraphism in this mutant.

Acid Phosphatase↗
PubMed2003

Multiple coexistent dysraphic pathologies.

INTRODUCTION: Four distinct dysraphic anomalies were observed in a single child. While combinations of such anomalies are well recognised, quadruple dysraphic pathology, nevertheless, is extremely uncommon. To our knowledge, no previous cases have been reported in the literature. CASE REPORT: We present the management of a child with a concurrent segmental meningocele, a type-1 split cord malformation (SCM) associated with hemivertebrae, lipomyelomeningoceles in each hemicord of the SCM and a terminal myelocystocele, and we review the literature on potential mechanisms of dysmorphogenesis. DISCUSSION: Existing embryologic hypotheses for the dysraphic spectrum lack experimental evidence and studies in animal models. This case challenges the existing hypotheses and illustrates our incomplete understanding of human terminal spinal cord embryogenesis. Further studies on the morphogenetic basis for these anomalies are required.

Abnormalities, Multiple↗
PubMed1978

Experimental dysraphism in the rat.

An experimental treatment that results in dysraphic lesions in rat embryos was studied to gain insight into the origin of such lesions. Pregnant rats given 100,000 units of vitamin A by gavage tube on gestational Days 8, 9, and 10 produced abnormal litters, and 50% of the embryos had exencephaly and/or spina bifida. Study of these embryonic lesions revealed hyperplesia of neural tube tissue that extended laterally to the edge of an epidermal defect. The epidermal defect consisted of the absence of fetal epidermis over the hyperplastic neural tissue. At no stage in development was embryonic hydrocephalus noted. In fact, the central canals of the embryos with malformations were poorly developed and smaller than those of control embryos. Results with this model indicate that the malformations arise through a process of overgrowth and hyperplasia and not from embryonic hydrocephalus. Continued work with this and other models is required to delineate new mechanisms and to offer alternative postulates for the origin of dysraphic lesions.

Animals↗