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At least 451 records · Page 25Linked to original sources
PubMed1993

New autosomal recessive lethal disorder with polycystic kidneys type Potter I, characteristic face, microcephaly, brachymelia, and congenital heart defects.

We report on 3 pairs of sibs from unrelated families, who present with polycystic kidneys Potter type I claimed to be specific for the ARPKD, and with microbrachycephaly, hypertelorism with telecanthus, large posteriorly angulated fleshy ears and various congenital malformations including congenital heart defects. We suggest that they represent a previously unrecognized autosomal recessive lethal developmental disorder within the group of infantile polycystic kidney disease and Potter sequence.

Abnormalities, Multiple↗
PubMed1980

The cranial base in anencephaly and microcephaly studied histologically.

A histological microradiographical analysis was carried out on the cranial base removed at autopsy from three infants--two with microcephalia, one with anencephalia. The histological findings were compared with those from normal individuals of the same age. It was shown that a reduced size of the brain was accompanied by a change in the remodeling pattern of the internal as well as the external surface of the cranial base, leading to a flattening of the cranial base. The findings further suggest that the development of the brain influences the ossification of the chondrocranium.

Anencephaly↗
PubMed1986

Morphogenesis of isotretinoin-induced microcephaly and micrognathia studied by scanning electron microscopy.

Isotretinoin ingestion during the first trimester of human pregnancy can induce malformations of the skull, ears, face, central nervous system, eyes, palate, lungs, circulatory system, limbs, and digits. A single oral dose of isotretinoin on day 8 of gestation in hamsters induces a similar syndrome of congenital malformation. The present study concerned scanning electron microscopic (SEM) observation of embryonic and fetal hamster craniofacial structures at 4, 8, 12, 24, 48, and 72 hr after administration of an oral dose of 50 mg/kg isotretinoin or an equivalent volume of the vehicle. The variability in development among control embryos recovered 4 hr after treatment precluded objective assessment of pathologic change by SEM at very early time points. Craniofacial damage was obvious within 8-12 hr of isotretinoin treatment, and it included hypoplasia of the maxillary and mandibular processes of the first branchial arch, a rudimentary second arch, and apparent collapse of the forebrain. Equivalent fusion between the lateral nasal process and the maxillary process and between the medial nasal process and the maxillary process in treated and control embryos accounts for the very low incidence of cleft lip observed in fetuses. The terminal microstomia was not associated with excessive merging or overgrowth of the first arch components. Hypoplasia of the first arch can account for retinoid-induced macrostomia and microstomia.

Animals↗
PubMed1992

Repair of giant occipital encephaloceles with microcephaly secondary to massive brain herniation.

Giant occipital encephaloceles rarely contain large amounts of neural tissue that cannot be replaced in the abnormally small calvarium. Resection of neural elements is therefore often necessary in order to accomplish a closure. A technique is described wherein an extracranial compartment is prepared utilizing fine tantalum mesh to enclose the neural contents. The mesh is attached to the periphery of the skull defect providing a rigid extracranial compartment for the encephalocele. As intracranial pressure increases, the calvarium is forced to expand. The tantalum mesh is gradually imbricated into the calvarium by daily digital compression. If ventriculomegaly occurs, an interval ventriculoperitoneal shunt is placed. The encephalocele repair is reopened and the tantalum is surgically imbricated at that time. This allows for a satisfactory cosmetic result with preservation of all neural elements.

Encephalocele↗