The authors present the results of an investigation of the vasogenic type of brain edema using cold injury in cats as a model. Their findings indicate that bulk flow and not diffusion should be considered the main mechanism for the spread of edema through the white matter. This conclusion is based on: 1) comparison of the distances actually traveled by various substances during edema spread with those calculated theoretically for migration of the substances by diffusion; 2) coincidence in the speed of movement by two substances (sucrose and albumin) with widely different diffusion coefficients; 3) measurement of interstitial fluid pressure (IFP) at various distances from the lesion showing the presence of increased IFP in the lesion area and decreasing pressures along the edema pathway toward the normal tissue; and 4) the fact that spreading of edema can be significantly impeded by inducing before the cold lesion an intracellular type of brain edema that reduces the size of the extracellular space (ECS) and increases the resistance to flow of edema fluid. The pressure-volume curve of the brain ECS, as derived from determinations of IFP and tissue water content, indicates that initial steep slope in IFP probably represents the high resistance to fluid mobility through the small diameter extracellular channels and the counteracting resistance of the intermingled structures of brain parenchyma to be separated. Once the IFP exceeds these opposing forces, the ECS dilates, fluid mobility increases, and the edema front advances.