Congenital Hydrocephalus in HTX-rats: Incidence, Pathophysiology, and Developmental Impairment

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The pathophysiology and developmental impairment of congenital hydrocephalus were studied in an albino rat model (HTX). Of 292 newborn HTX rats in a closed colony, 53% were found to have communicating hydrocephalus, which changed to noncommunicating hydrocephalus within 5 days of birth. Three types of hydrocephalus were identified. "Rapidly progressive hydrocephalus" affected 45% of the newborn rats, all of which died from 20 to 49 days (mean, 28 days). In 5%, the progress of the hydrocephalus slowed or ceased ("compensated hydrocephalus"), and these animals survived as long as the nonhydrocephalic rats. The third type of hydrocephalus, which was found in about 14% of adult rats, did not cause head enlargement, although autopsies revealed moderate ventricular dilatation ("normal pressure hydrocephalus"). Comparative histopathological study of 1- and 7-day-old hydrocephalic rats disclosed progressive edema and ultimate destruction of cerebral white matter. Nerve cells in the cerebral cortex proliferated and differentiated, and cortical cell lamination increased from three to six layers during this period. However, as ventricular dilatation progressed, the width of the cerebral mantle gradually decreased, the cortical cell laminae became obscured, and a disturbance in axon formation was evident. In animals with compensated hydrocephalus, extensive disruption of axon and myelin formation was noted in the cerebral cortex, basal ganglia, and thalamus. In normal pressure hydrocephalus, there appeared to be edema of the periventricular white matter and disturbance in myelin formation in the cortical area.
日本脳神経外科学会の論文
1988-10-15

Congenital Hydrocephalus in HTX-rats: Incidence, Pathophysiology, and Developmental Impairment

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