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GUILLAIN‐BARRE SYNDROME WITH ANTIBODY TO A GANGLIOSIDE, N‐ACETYLGALACTOSAMINYL GD1A
Author(s) -
Kaida K,
Kusunoki S,
Kamakura K,
Motoyoshi K,
Kanazawa I.
Publication year - 2000
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1111/j.1529-8027.2000.022-6.x
Subject(s) - ganglioside , medicine , antibody , guillain barre syndrome , gastroenterology , titer , weakness , immunology , surgery , biology , biochemistry
A retrospective case study of 33 Guillain‐Barre syndrome (GBS) patients with the antibody to the ganglioside N‐acetylgalactosaminyl GD1a (Ga1NAc‐GD1a) was made to investigate the clinical features of GBS with this antibody. Patients 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 antibody (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 IgG (group M, normal range <1:40 for both IgM and IgG). The control group consisted of 72 GBS patients without anti‐Ga1NAc‐GD1a antibody. Compared with the control group, the G‐high and G group patients were characterized as having had antecedent gastrointestinal infection (87% and 72% versus 31%, both 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% versus 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). Electrophysiological findings indicative of axonal dysfunction were significantly more common 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 abnormalities in sensory conduction studies was also more frequent in these groups (44% and 32% versus 9%, both P < 0.001). IgG anti‐GalNAc‐GD1a antibody may be a marker of the pure motor and the axonal variants of GBS, and therefore it, as well as anti‐GM1 antibody, must be investigated in these forms in 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.