Ten inbred strains of mice were tested for their susceptibility to experimental allergic encephalomyelitis (EAE) after sensitization with mouse spinal cord in complete Freund's adjuvant followed by booster injections of Bordetella pertussis. The results extended previous findings in that not all susceptible mice possessed the H-2s haplotype, but mice with an H-2q background (DBA1/J strain) were also susceptible. Neuropathologic examination of experimental allergic encephalomyelitis in the mouse showed that from strain to strain, the condition was similar. The over-all pathologic picture was somewhat midway between that seen in other species sensitized with whole nervous tissue in complex Freund's adjuvant and hyperacute experimental allergic encephalomyelitis in rats similarly sensitized but with the addition of B. pertussis. Perivascular cuffing, though present, was less pronounced than in other species. There was a prominent polymorphonuclear response, and extravasation of fibrin and red cells occurred. Primary demyelination was a transient, early feature of the disease process in mice, but nerve fiber depletion and gliosis occurred as the disease progressed. The observed myelin degradation most commonly involved the ingestion by macrophages of small fragments of dissociated myelin via crypts or infoldings of the cell surface, at the bases of which were pinocytic, coated vesicles. A similar pattern of myelin breakdown has been described in mouse hepatitis virus encephalomyelitis and multiple sclerosis.