Abstract Rhesus monkeys were immunized with low doses of encephalitogenic mixture. Twenty two of 24 monkeys developed experimental allergic encephalomyelitis (EAE) lasting from 3 to 252 days. Fifteen of 22 monkeys developed chronic progressive EAE with remissions and relapses. In the early stages of EAE multiple perivascular foci of demyelination and lymphoid histiocytic infiltration were found within the central nervous system (CNS). In advanced disease these foci became confluent, developing foci of plaque type with demyelination and gliofibrosis. Eight affected monkeys received an emulsion of spinal cord with incomplete adjuvant; 6 of them showed a good therapeutic response. In the CNS of those monkeys 514 to 667 days later plaques of demyelination and gliofibrosis and minimal inflammatory lesions were detected. Two monkeys without clinical evidence of EAE had plaques of demyelination and gliofibrosis in the CNS 2 years after immunization. It is suggested that chronic EAE in monkeys may be considered an adequate model for multiple sclerosis (MS).