AN IMMUNOLOGICAL ABNORMALITY COMMON TO BICKERSTAFFS BRAIN-STEM ENCEPHALITIS AND FISHERS SYNDROME

The nosological position of Bickerstaff's brain stem encephalitis (BBE ) has yet to be established, and its etiology is not clear. Because an ti-G(Q1b) antibody frequently occurs in patients with Fisher's syndrom e (FS) and there are clinical similarities between FS and BBE, we inve stigated anti-ganglioside antibodies in sera from 3 BBE patients who h ad transient long tract signs in addition to acute ophthalmoplegia and cerebellar-like ataxia in order to clarify the etiology and nosologic al position of BBE. High IgG anti-G(Q1b) antibody titers were present in all 3 sera samples but decreased with the clinical course of the il lness. In contrast, no anti-G(Q1b) antibody was found in sera from pat ients with other neurologic diseases which were able to produce transi ent brain stem disturbance: multiple sclerosis, neuro-Behcet's disease , brain stem infarction, herpes simplex virus encephalitis, and Wernic ke's encephalopathy. The finding that BBE and FS shared common autoant ibody suggests that autoimmune mechanism common to FS is likely in BBE , and that both conditions represent a distinct disease with a wide sp ectrum of symptoms that include ophthalmoplegia and ataxia.