THE PATHOLOGY OF ACUTE DISSEMINATED ENCEPHALOMYELITIS PRODUCED EXPERIMENTALLY IN THE RHESUS MONKEY AND ITS RESEMBLANCE TO HUMAN DEMYELINATING DISEASE

Abstract

Acute disseminated encephalomyelitis was produced in rhesus monkeys by the admn. of emulsions of homologous and heterologous brain and spinal cord prepared with adjuvants consisting of aquaphor, paraffin oil and heat killed tubercle bacilli. There is rapid and regular development of a syndrome which results from widespread changes in the C. N. S. The clinical picture is marked by the progressive development of a considerable variety of signs, chief among which are paralysis or paresis of one or more limbs, ataxia, nystagmus, diminution of vision or blindness. There may be subsidence and recurrence of this in some animals. Anatomically, the exptl. disease is characterized by wide dissemination of the lesions in the C. N. S., their predilection for the white matter, and their special frequency in the pons, cerebellum and optic pathways. The lesions are perivascular, often perivenular, and are marked by inflammation and myelin destruction with little axonal degeneration. They coalesce into larger discrete or diffuse areas of demyelination. Crops of lesions of different ages can be distinguished in the longest surviving animals. These clinical and pathologic features parallel those in human demyelinating disease (acute disseminated encephalomyelitis and multiple sclerosis). Some striking differences may be due to a species divergence in response to a similar etiologic mechanism or to a dissimilarity in the age of the pathological process as studied in the 2 spp.