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Detection of serum antibodies to myelin-associated glycoprotein (MAG) by Western blot (WB) is a valuable assay to diagnose a distinct type of demyelinating polyneuropathy with immunoglobulin M (IgM) monoclonal gammopathy. In this study, the diagnostic accuracy of a new and more practical ELISA to detect these antibodies was validated.

To assess whether human leukocyte antigen (HLA)–DRB1 and HLA-DQB1 alleles confer susceptibility to Guillain–Barré syndrome (GBS) or are related to specific clinical or serologic subgroups of GBS.

This report describes 12 Dutch families of which at least two members have had Guillain-Barré syndrome (GBS). The authors observed an earlier onset of GBS in successive generations. The occurrence of GBS within families suggests a role for genetic factors in the pathogenesis of GBS.

Antibody reactivity to GA1, GM1, GM2, GD1a, GD1b, and GQ1b gangliosides was measured in 87 patients with polyneuropathy associated with monoclonal gammopathy (60 IgM, 25 IgG, 2 IgA) and 42 control patients with monoclonal gammopathy without polyneuropathy (21 IgM, 21 IgG). Of these 87 patients, 30 had anti-myelin-associated glycoprotein antibodies and 15 had antiganglioside antibodies. Antiganglioside antibodies were significantly associated with demyelinating neuropathy and with IgM monoclonal gammopathy. Anti-GD1b and anti-GQ1b antibodies were significantly associated with predominantly sensory ataxic neuropathy.

The number of patients with Guillain–Barré syndrome (GBS) who have been observed in Curaçao, the Netherlands Antilles, may be increasing.

To investigate whether anti-GM2 antibodies in patients with Guillain–Barré syndrome (GBS) are induced by molecular mimicry with cytomegalovirus (CMV).

To investigate the presence of anti-GalNAc-GD1a antibodies in patients with Guillain-Barré syndrome (GBS) and to determine the relation of anti-ganglioside antibodies with clinical features.

To determine which antecedent infections are specifically associated with the Guillain-Barré syndrome (GBS).

Guillain-Barre syndrome (GBS) is usually preceded by infections, in particular cytomegalovirus (CMV) and Campylobacter jejuni infection. We studied the clinical and electrophysiologic features of 20 CMV-associated GBS patients and compared the findings with earlier established data of C. jejuni-related GBS patients (n = 43) and of GBS patients without these infections (n = 71). The patients all participated in the Dutch GBS trial in which we compared the effect of intravenous immune globulins and plasma exchange. We demonstrate that CMV-related GBS patients have a different clinical pattern in comparison with the other two GBS groups. They are significantly younger, initially have a severe course indicated by a high frequency of respiratory insufficiency, and often develop cranial nerve involvement and severe sensory loss. This is in contrast to C. jejuni infection, which is associated with motor GBS. Both infections are associated with delayed recovery compared with the GBS patients without these infections.