The possibility that there can be a small but significant net perivascular outflow from the parenchyma of Na+, Cl− and accompanying water may be the resolution of a long-standing difficulty. In non-communicating hydrocephalus, CSF production by the choroid plexuses continues at a nearly normal rate, but the normal route for CSF outflow from the IIIrd ventricle is blocked. Because after an initial period the ventricles do not continue to enlarge at a rate sufficient to accommodate the CSF production, CSF must be escaping via an alternative route (see Sections 4.2.2.1–4.2.2.2 in [41] and Section 4.1 in [4] for discussion and references). The periventricular parenchyma is oedematous which may allow flow of fluid from the ventricles, but the oedema only extends a small distance. In cats with kaolin induced hydrocephalus, Sahar et al. [421] observed penetration of serum albumin only up to about 2.5 mm which they took to mean that the albumin was being absorbed into the blood. There is no known mechanism by which this absorption could have occurred. It would be very interesting to know whether this distance corresponds instead to the distance from the ventricular surface to perivascular pathways that would allow sufficiently rapid removal of albumin to CSF in the subarachnoid spaces and/or to lymph that the concentrations observed deeper in the parenchyma would be small. The importance of fluid escape from the ventricles across the ependyma into the parenchyma in hydrocephalus has recently been given further support by observations of gadobutrol movements in normal pressure hydrocephalus in humans [15].