GLIOSIS AND GANGLION-CELL DEATH IN THE DEVELOPING CAT RETINA DURING HYDROCEPHALUS AND AFTER DECOMPRESSION

Even after surgical decompression, infantile hydrocephalus often results in permanent neurological symptoms, including visual deficits. However, little is known about the cellular changes that may be responsible for these effects. The present study was designed to analyze the retinae of normal, mildly hydrocephalic, severely hydrocephalic and surgically decompressed kittens to determine if changes occur in the density and size of retinal ganglion cells. Hydrocephalus was induced in 10 day old kittens by intra-cisternal injection of kaolin. Kittens were allowed to survive from 7 to 28 days after injection. Animals that were decompressed received ventriculoperitoneal shunts 10-15 days after the induction of hydrocephalus and were sacrificed 10-14 days after shunt placement. The density and area of neuronal and glial cells were determined within a sample area in peripheral nasal retina. Total cell density was significantly increased in mildly and severely hydrocephalic animals but returned to normal following decompression. This change represents a significant increase in the glial population. In addition, there was a significant loss of ganglion cells in both the severely hydrocephalic and the shunted groups. Based on these findings, we conclude that gliosis occurs as a result of cell death in the retina following severe hydrocephalus, and decompression is unable to reverse these effects. Furthermore, gliosis occurs in mild cases of hydrocephalus, and may be an early indication that cellular degeneration will follow.