Attentionl has recently been directed toward patients having a polyneuropathy IgM anti‐Myelin‐associated glycoprotein (anti‐MAG) antibody. The possibility of a pathogenetic role for the anti‐MAG antibody in the evolution of the polyneuropathy and in the development of central nervous system signs, including tremor and ataxia, remains unresolved. In 5 patients with this syndrome whose clinical courses were followed closely, in 1 of whom a complete postmortem examination of the nervous system was performed, we made the folowing obsercvations: (1) the anti‐MAG antibody did not localize to the compact layer of the myelin sheath in affected nerves, but did realize to areas of myelin splitting; (2) anti‐MAG antibody present in the sural nerve of an affected individual for 7 years was not associated with progressive pathology; (3) anti‐MAG antibody was not deposited in the central nervous system of an affected individual, although the antibody did bind to these same tissues in vitro; (4) deposition of anti‐MAG antibody observed at postmortem examination did not correlate with the degree of pathological change; and (5) study of the peripheral nervous system favored a primary axonal neuropathy with secondary demyelination.