Prenatal methylmercury poisoning of C57BL/6J mice was followed by the development of communicating hydrocephalus in 15% to 25% of surviving offspring. Although examination of the serially sectioned cerebral aqueduct in hydrocephalic animals revealed the presence of stenosis, complete occlusion of the lumen was not observed. The ependymal epithelium of the cerebral aqueduct was preserved, and there was no evidence of periaqueductal inflammation or reactive gliosis. Edema and vacuolar change were, however, observed subependymally. The cerebral white matter, which bore the brunt of the degenerative changes seen in hydrocephalic brains, showed edema, spongy degeneration, gross cystic change and loss of parenchyma. In addition, ependymal cells and choroid plexus epithelial cells in Hg-treated animals contained large amounts of mercury within their cytoplasm, and it is possible that this may have contributed to the development of hydrocephalus by causing disturbances of CSF homeostasis. We believe that the appearance of aqueductal stenosis in Hg-intoxicated animals represents the result rather than the cause of the hydrocephalus.