Guillain-Barre syndrome with antibody to a ganglioside, N-acetylgalactosaminyl GD1a

Citation
K. Kaida et al., Guillain-Barre syndrome with antibody to a ganglioside, N-acetylgalactosaminyl GD1a, BRAIN, 123, 2000, pp. 116-124
Citations number
33
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
BRAIN
ISSN journal
00068950 → ACNP
Volume
123
Year of publication
2000
Part
1
Pages
116 - 124
Database
ISI
SICI code
0006-8950(200001)123:<116:GSWATA>2.0.ZU;2-6
Abstract
A retrospective case study of 33 Guillain-Barre syndrome (GBS) patients wit h the antibody to the ganglioside N-acetylgalactosaminyl GD1a (Ga1NAc-GD1a) was made to investigate the clinical features of GBS with this antibody. P atients were classified into three groups: (i) 25 with IgG antibody (group G, titre greater than or equal to 1:40); (ii) 16 With high-titre IgG antibo dy (group G-high, titre greater than or equal to 1:320; selected from group G patients), and (iii) eight with IgM antibody but without elevation of Ig G (group M, normal range <1:40 for both IgM and IgG), The control group con sisted of 72 GBS patients without anti-Ga1NAc-GD1a antibody. Compared with the control group, the G-high and G group patients were characterized as ha ving had antecedent gastrointestinal infection (87% and 72% versus 31%, bot h P < 0.001), uncommon cranial nerve involvement (19% and 36% versus 54%, P = 0.02 and 0.2, respectively), distal-dominant weakness (94% and 68% versu s 36%, P < 0.001 and P = 0.01, respectively) and no sensory signs (81 % and 60 % versus 25 %, P < 0.001 and P = 0.003, respectively), Electrophysiolog ical findings indicative of axonal dysfunction were significantly more comm on in the G-high and G group patients (63 % and 52% versus 14%, both P < 0. 001), The pure motor variant that showed neither sensory signs nor abnormal ities in sensory conduction studies was also mort? frequent in these groups (44 % and 32 % versus 9%, both P < 0.001), IgG anti-GalNAc-GD1a antibody m ay be a marker of the pure motor and the axonal variants of GBS, and theref ore it, as well as anti-GM1 antibody, must be investigated in these forms i n order to diagnose and understand the variants, By contrast, mild weakness , frequent facial palsy (75%) and a high incidence of IgM anti-GM2 antibody reactivity (88 %) were characteristic of group M, indicating that the GBS in that group resulted from a different immune mechanism from that in the G group.