A model designed to produce chronic communicating hydrocephalus in dogs has been developed in our laboratory. The animals tolerate the procedure well and the yield of animals with communicating hydrocephalus is high. Serial cisternograms show ventricular entry first with "clearing" and later with "stasis". CSF pressures are initially increased, but when the ventricles become enlarged the pressure falls into the normal range. Grossly there is generalized ventricular enlargement and, on histological studies, the ependyma is flattened and denuded. Periventricular edema occurs in the white matter. Autoradiographs show transependymal movement of protein. CSF production appears to be normal despite obstruction to flow of CSF to areas where resorption is greatest. Diversionary shunting probably produces relief of many of the neurological symptoms by providing an efficient pathway for the removal of CSF and thus by lessening edema and ventricular enlargement. A more appropriate treatment would appear to be a noninvasive method of decreasing CSF production. Only when the basic pathophysiological alterations of CSF production and absorption are understood will this be possible. We believe that this animal model affords us the opportunity of studying these mechanisms.