Journal of Neurological Sciences 155 (1998) 186–191 Clinical correlate and fine specificity of anti-GQ1b antibodies in peripheral neuropathy a a b a a Marinella Carpo , Rosetta Pedotti , Francesco Lolli , Anita Pitrola , Silvia Allaria , a a, * Guglielmo Scarlato , Eduardo Nobile-Orazio a ‘ Giorgio Spagnol’ Laboratory of Clinical Neuroimmunology, Institute of Clinical Neurology, Centro Dino Ferrari, University of Milan, IRCCS Ospedale Maggiore Policlinico, Milan, Italy b Department of Neurological and Psychiatric Sciences, USL 10 / D, University of Florence, Florence, Italy Received 18 April 1997; received in revised form 5 August 1997; accepted 2 September 1997 Abstract We studied the frequency, fine specificity and clinical correlate of anti-GQ1b IgG and IgM antibodies in 216 patients with neuropathy ´ including three with Miller Fisher syndrome (MFS), 73 with Guillain–Barre syndrome (GBS), 99 with neuropathy associated with IgM monoclonal gammopathy (PN1IgM) and 41 with other neuropathies, and compared the data with 92 disease or normal controls. We found high ( .1 / 100) anti-GQ1b IgG titers in all three MFS patients and in two GBS patients (2.7%) with ophthalmoplegia and ataxia, while high anti-GQ1b IgM were only found in two patients with a chronic demyelinating sensorimotor neuropathy associated with IgMk monoclonal gammopathy (2%). By overlay HPTLC, IgG antibodies in MFS and GBS either selectively reacted with GQ1b or also bound to GD3, and less intensely to GD1b, while IgM antibodies from both patients with PN1IgM also strongly reacted with GD1b and, in one, with GD3 and GT1b. The constant association of anti-GQ1b antibodies with dysimmune neuropathies and the correlation between their isotype, fine specificity and clinical presentation, support a possible pathogenetic link between these antibodies and the neuropathy.  1998 Elsevier Science B.V. ´ Keywords: Antibodies; Gangliosides; GQ1b; Guillain–Barre syndrome; Miller Fisher syndrome; Neuropathy 1. Introduction paranodal regions of the extramedullary portion of the oculomotor nerves (Chiba et al., 1993) while ataxia in High titers of anti-GQ1b IgG antibodies were reported MFS and GBS has been related to a selective staining of in 80 to 100% of patients with Miller Fisher syndrome the cerebellar molecular layer by IgG from patients with (MFS) (Chiba et al., 1992, 1993; Willison et al., 1993a; high anti-GQ1b IgG (Kornberg et al., 1996). These Yuki et al., 1993a; Yuki, 1996a; Jacobs et al., 1995) as findings together with the decrease of anti-GQ1b anti- ´ well as in some patients with Guillain–Barre Syndrome bodies during clinical improvement (Chiba et al., 1992, (GBS) with ophthalmoplegia (Chiba et al., 1993; Yuki, 1993; Yuki, 1995, 1996b; Yuki et al., 1993c) suggest a 1996a), Bickerstaff’s brain stem encephalitis (Yuki, 1996a; pathogenetic role for these antibodies. Anti-GQ1b anti- Yuki et al., 1993b) or acute ophthalmoparesis (Yuki, bodies were also reported in patients with chronic, pre- 1996a). The frequent association of these antibodies with dominantly sensory neuropathy associated with IgM mono- diseases characterized by oculomotor impairment corre- clonal gammopathy. In these patients anti-GQ1b antibodies lates with the abundant expression of GQ1b in the were of the IgM isotype and also bound to other gan- gliosides containing a disialosyl residue (Yuki et al., 1992; * Daune et al., 1992; Obi et al., 1992; Willison et al., 1993b; Corresponding author. Tel.: 139 2 55033836 / 4; fax. 139 2 55190392; email: spagnol@imiucca.csi.unimi.it Oka et al., 1996). 0022-510X / 98 / $19.00  1998 Elsevier Science B.V. All rights reserved. PII S0022-510X(97)00312-2