The article is devoted to the clinical pathophysiology of two similar autoimmune diseases: multiple sclerosis and optical myelitis (neuromyelitis optica, Devic’s disease). The paper refers to the history of their studies, criteria of diagnosis, specifics of their etiology and pathogenesis and their place among the demyelinating diseases of central nervous system. The multifactorial etiology of these nosological entities is described as determined by the genetic predisposition and epigenetic mechanisms triggered by external factors. Among them, one can distinguish infectious/parasitic agents that play an equivocal role - acting both as initiators and inhibitors of autoaggression. Examples are given showing the possibility of participation in the pathogenesis of multiple sclerosis, mechanisms mediated by T-lymphocytes: molecular mimicry of microorganisms and self antigens and activation of auto-reactive T-lymphocytes under the influence of superantigens. It has been shown that parasitic infections can inhibit auto-aggression in animal models, which can serve as an approach to cure the patients more effectively. The paper summarized current data on the pathophysiologic basis of the differential diagnosis of these similar illnessesand also about main groups of monoclonal antibodies used for the treatment of these demyelinating diseases (in relation to their antigenic specificity and mechanisms of action). The key role of specific marker antibodies to aquaporin-4 for diagnosis of opticomyelitis is emphasized. The pathogenesis of optical myelitis can also depend on various coexisting types of auto-antibodies, probably determining different types of damage to the nervous system. The presence of comorbid autoimmune disorders in one patient shows the complexity of the pathological auto immunity phenomenа, depending both on inherent genetic predisposal and a set of external factors. The quality and time of diagnosis and the disclosure of the etiology of every particular case of disease will determine the therapeutic tactics, results of treatment and prognosis (3 figs, 4 tables, bibliography: 53 refs).