Immune Mediators of Optic Neuritis

The pathophysiology of human optic nerve demyelination is largely undetermined, consequently animal models of demyelination have been utilized in the study of optic nerve and central nervous system (CNS) demyelination. These models include experimental allergic encephalomyelitis (EAE), an autoimmune disorder induced by sensitization of genetically susceptible animals to CNS myelin, viral-induced demyelination and antibody-induced demyelination, The characteristic neurological signs of paralysis, ataxia and visual loss of EAE are similar to patients with MS and have made EAE an extensively utilized animal model for MS. The pathology of inactive EAE lesions shows foci of gliosis without active inflammation that are also seen in MS. The active optic nerve lesions in animals with EAE reveal demyelination, mononuclear cell infiltration and phagocytosis of axons and myelin by effector macrophages. These findings are infrequently seen in MS, due to the scarcity of human pathologic material available during the acute has of this disorder