This study utilized Lewis rats and the cell-transfer form of experimental allergic encephalomyelitis (EAE) to focus on two central nervous system microvascular alterations known to be intimately associated with early clinical neurological signs of the disease, namely increased vascular permeability and deposition of fibrin. The main objective of the work was to define the degree of concordance and the anatomical localization of maximal vascular permeability change and fibrin deposition within the neuraxis of recipient rats during the earliest expression of clinical manifestations of the disease. Recipients were injected with predetermined doses of activated, myelin basic protein (MBP)-reactive syngeneic donor lymphoid cells and killed 6 or 7 days later when they exhibited the first clinical signs of disease. This experimental design allowed assessment of late occurring immune activities of a single population of MBP-reactive effector cells. Increased vascular permeability, expressed as mean extravascular blood equivalents (EVBE), attained maximum change, i.e., 16.04 +/- 5.07, within the lumbosacrococcygeal segment of the spinal cord (LSC). Maximal density of fibrin depositions, i.e., 192 +/- 94 deposits, also occurred within the LSC cord. The concordance of these two histoimmunopathological events, their tight linkage to early clinical signs of disease and the fact that both events attained maximal values within the LSC cord suggest that increased permeability and activation of the coagulation cascade may be prerequisite events for the expression of neurological signs of EAE.