Lh. Visser et al., GUILLAIN-BARRE-SYNDROME WITHOUT SENSORY LOSS (ACUTE MOTOR NEUROPATHY)- A SUBGROUP WITH SPECIFIC CLINICAL, ELECTRODIAGNOSTIC AND LABORATORYFEATURES, Brain, 118, 1995, pp. 841-847
We analysed data obtained from 27 out of a group of 147 patients with
Guillain-Barre syndrome, who did not have sensory loss during a follow
-lip period of 6 months (motor Guillain-Barre syndrome). These patient
s had a distinctive clinical pattern compared with the other 120 Guill
ain-Barre syndrome patients. The clinical course was marked by a more
rapid onset of weakness (3.9 versus 6.1 days, P = 0.002), an earlier n
adir (6.3 versus 9.1 days, P < 0.001), an initially predominant distal
weakness (67% versus 27%, P < 0.001), sparing of the cranial nerves (
26% versus 68%, P < 0.001) and the disease was more often preceded by
a gastro-intestinal illness (41% versus 13%, P = 0.001) often caused b
y a Campylobacter jejuni infection (67% versus 28% in the other Guilla
in-Barre syndrome patients, P < 0.001). High titres of anti-GM1 antibo
dies were also significantly more common in motor Guillain-Barre syndr
ome patients (42% versus 5%, P < 0.001). Electromyographic data of the
motor Guillain-Barre syndrome patients at nadir revealed little or no
evidence for demyelination. Abundant denervation activity was present
in half of the patients. The response to immune globulin treatment wa
s good but with plasma exchange significantly fewer motor Guillain-Bar
re syndrome patients reached the stage of independent locomotion after
a follow-up period of 6 months especially if the acute motor neuropat
hy occurred after a C. jejuni infection. The distinctive clinical, ele
ctrophysiological and laboratory features of motor Guillain-Barre synd
rome patients show that the acute motor neuropathy represents a specif
ic subgroup within the Guillain-Barre syndrome and recognizing these p
atients may have consequences for the choice of therapy.