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.