Autoimmune neuropathies, including Guillain-Barre Β΄syndrome (GBS), may be preceded by certain infections and accompanied by several antiganglioside antibodies. Anti-GM 2 antibodies may contribute to the pathogenesis of GBS following cytomegalovirus (CMV) infections, which usually shows severe neurological deficits. 3,4 We report a patient with facial diplegia but otherwise minor deficits associated with an antecedent CMV infection, and IgM antibodies against GM 2 and GalNAc-GD 1a .
A 33-year-old man developed a sore throat, a cough, and fever which lasted for about 1 week. Two weeks later, he noted bilateral weakness of the facial muscles, and numbness of the hands and feet. Neurological examination revealed marked facial diplegia, numbness of the hands and feet, and diffuse areflexia. Muscle strength was normal except in the facial muscles. He showed no cerebellar ataxia. Routine laboratory tests revealed mild elevation of liver enzymes. Serum level of angiotensinconverting enzyme was normal, and the Paul-Bunnel test was negative. Immunoelectrophoresis of serum revealed no M protein. Serum anti-Borrelia burgdorferi antibodies were negative. Enzyme-linked immunosorbent assay performed as described previously 5 showed that the serum contained high titers of IgM antibodies to GM 2 (1:320) and GalNAc-GD 1a (1:320) (control, <1:40) (Fig. 1). The patient's serum did not bind to GA 2 or GD 2 . The serum IgM-enzyme immunoassay (EIA) cutoff index (CI) and titer of anti-CMV IgG CF antibodies were markedly high (3.5 CI and 1:3600, respectively). Neither IgM nor IgG anti-sulfated glucuronylparagloboside (SGPG) antibody was present. Cerebrospinal fluid showed a normal cell count (2 mononuclear cells/mm 3 ) and slightly increased protein level (43 mg/dL), with a negative IgM-EIA index and a high titer of anti-CMV IgG CF antibodies (1:520). Nerve conduction tests revealed normal values for motor