Serum antibodies from 8 (13%) of 62 patients with the acute Guillain-B
arre syndrome (GBS) and 1 of 3 patients with the Miller Fisher syndrom
e (MFS) recognized a minor ganglioside in bovine and human brain trisi
aloganglioside fractions. The ganglioside antigen migrated between GD1
a and GD1b on thin-layer chromatograms. The structure of this ganglios
ide was established to be GT1a by thin-layer chromatography blotting a
nd mass spectrometry. GT1a ganglioside was also detected in human and
bovine peripheral nerves by thin-layer chromatogram immunostaining. Se
rum from the GBS patients had IgM. IgG. or IgA antibodies against GT1a
detectable by enzyme-linked immunosorbent assay (ELISA). Serum from t
he MFS patient also had elevated levels of IgG against GT1a. None of t
he sera from 43 patients with other neurological diseases or from 24 h
ealthy controls reacted with GT1a. Sera from 6 of 8 GBS patients with
anti-GT1a antibodies also reacted with GQ1b. There was no difference i
n the incidence of anti-GT1a immunoglobulins in acute GBS patients wit
h or without oculomotor abnormalities. Levels of anti-GT1a antibodies
correlated temporally with clinical symptoms in GBS patients. Although
the incidence of dysphagia was slightly higher in GBS patients with a
nti-GT1a antibodies than in those without, the number of patients stud
ied may have been too small to detect an association between anti-GT1a
antibodies and a specific clinical variant of GBS. Our data demonstra
te that a proportion of CBS patients have antibodies against GT1a gang
lioside and suggest that these antibodies may play a role in the patho
genesis of neuropathy in GBS. (C) 1998 Elsevier Science B.V.