Experimental Congenital Hydrocephalus

Abstract

A review was made of experimental methods available to produce congenital hydrocephalus by teratogenic methods. Radiation, infections, trypan blue, hypervitaminosis A, salicylates and nutritional deficiencies were considered. In the course of prenatal zinc deficiency experiments, congenital hydrocephalus was frequently encountered and histologic sections were made of many representative specimens. Details of the findings are described, among them various types of aqueduct stenosis or obliteration. Although these anomalies suggest that occlusion of the aqueduct is the cause of the enlargement of the ventricular system it was noted that there was also ventricular dilatation caudal to the stenotic point of the aqueduct. Hydrocephalus without aqueductal stenosis has also been observed in experimental animals. It seems possible that some cases of congenital hydrocephalus attributed to aqueductal stenosis are examples of hydrocephalus with secondary block of the aqueduct.

On the Pathology of Experimental Hydrocephalus Induced by Artificial Increase in Endoventricular CSF Pulse Pressure

“…One of them is based on the use of teratogenic agents action on fetuses [see the excellent review by Adeloye and Warkany,2]. In this case, the ventricular dilation is often accompanied by important and complex altera tions in the brain development and, therefore, the brain pathology can hardly be compared to that obtained in our experiments.…”

Correlations between Ultrasound and Pathology in Fetal Ventricular System Anomalies

“…Knowledge of the risk factors associated with CH may increase the success of the prenatal ultrasound study. It has been established that a wide range of factors can cause hydrocephalus in animal experiments including alcohol consumption [7], X-ray [8], infections, food disorders, exposure to chemicals [9] and medications taken during pregnancy [10].…”

A family study of hydrocephalus resulting from aqueduct stenosis.

“…His right hand was normal. One index patient (No 4), the blind, severely subnormal, spastic quadriplegic boy who died, unoperated, aged 16, was said to have clasped thumbs from the age of 3. However, at this stage he had marked contractures of the limbs, so it seems reasonable to suppose that his adducted thumbs were secondary to his spasticity.…”