Neurovascular permeability and fibrin deposition in the central neuraxis of Lewis rats with cell-transferred experimental allergic encephalomyelitis in relationship to clinical and histopathological features of the disease.

Abrupt increases in blood-brain barrier (BBB) permeability were detected by the dual-isotope technique, coinciding with evidence of activation of coagulation cascade, occurred 1 day prior to appearance of clinical neurological signs of experimental allergic encephalomyelitis (EAE) and in conjunction with initial detectable cell infiltration. Maximal increase of BBB permeability was observed on the first day of clinical signs, which was 2 days prior to maximum severity of clinical abnormalities and 1 day in advance of the greatest number of central nervous system (CNS) fibrin deposits and perivascular cellular infiltration. Returning of increased BBB permeability and CNS perivascular fibrin deposits to normal levels was demonstrated prior to complete remission of neurological signs. Considerable CNS perivascular cellular infiltrates, however, lasted after complete remission of neurological signs. These findings indicate that increased permeability of the BBB, in association with activation of the coagulation cascade, is the earliest expressions of immune effector activity of experimental allergic EAE.