Cerebral vascular permeability was measured in guinea-pigs developing experimental allergic encephalomyelitis (EAE). A sensitive double radio-isotope method was used which allowed the permeability changes to be measured independently of alterations in cerebral blood volume. The onset of the disease was accompanied by a striking increase in vascular permeability, but there was no evidence that this change preceded the entry of inflammatory cells into the brain and cord. Injection of serum from rabbits with EAE into normal guinea-pigs had no measurable effect on the cerebral vessels.
These findings are consistent with the view that EAE is a cell-mediated lesion and provide no support for the suggestion that the initial damage is due to circulating antibody.