Table 3

Comparison of patients with Guillain-Barré syndrome (GBS) following SARS-CoV-2 vaccination and previously published European or American patients from the International GBS Outcome Study (IGOS)

GBS after SARS-CoV-2 vaccination (n=70)*IGOS Europe and Americas cohort (n=715)Statistical comparison (p value)
Patient characteristics
Sex at birth
 Female34/70 (49%)297/715 (42%)0.26
 Male36/70 (51%)418/715 (58%)
 Mean (SD)57.84 (±13.05)53 (±22.28)†0.07
 Asian1/70 (1%)NANA
 White69/70 (99%)
Reported antecedent infection (6 weeks prior)
 Yes7/69 (10%)502/652 (77%)<0.0001
Clinical features
Clinical variant
 Sensorimotor55/70 (79%)388/562 (69%) 0.0012
 Pure motor4/70 (6%)78/562 (14%)
 MFS1/70 (1%)62/562 (11%)
 Other‡10/70 (14%)34/562 (6%)
Sensory dysfunction§
 Yes63/68 (93%)408/588 (69%)<0.0001
Oculomotor weakness
 Yes9/66 (14%)84/620 (14%)0.87
Facial weakness
 Yes44/70 (63%)220/620 (36%)<0.0001
Bulbar weakness
 Yes17/65 (26%)136/620 (22%)0.54
Autonomic dysfunction
 Yes16/67 (38%)184/626 (29%)0.34
 Yes29/70 (41%)354/625 (57%)0.0153
Shortness of breath
 Yes14/70 (20%)NA
Time from onset to nadir
 Median (IQR)11 days (7 - 15)NA
Unable to walk independently at nadir
 Yes51/70 (73%)478/626 (76%)0.42
Ventilator dependency
 Yes7/70 (10%)121/715 (17%)0.14
Antiganglioside antibodies¶
 Positive/tested1/49 (2%)NANA
Electrophysiological variant**
 Demyelinating46/54 (85%)312/573 (55%)<0.0001
 Axonal3/54 (6%)33/573 (6%)
 Inexcitable0/54 (0%)10/573 (2%)
 Equivocal1/54 (2%)182/573 (32%)
 Normal4/54 (8%)36/573 (6%)
Initial treatment††
None11/70 (16%)54/715 (7%)0.0180
IVIG50/68 (74%)612/661 (93%)<0.0001
PLEX0/68 (0%)43/661 (6%)
Other7/68 (10%)6/661 (1%)
  • *31 of our patients had chronic comorbidities, including hypertension (n=15), depressive disorder (n=7), chronic respiratory disease, including asthma (n=6), thyroid disease (n=6) and diabetes mellitus (n=5); some patients had more than one comorbidity.

  • †Mean age and its SD for IGOS cohort was derived from median and IQR, as described previously.59

  • ‡Other clinical variants included bilateral facial diplegia with paraesthesias variant in our cohort and pharyngo-cervical-brachial, pure sensory, ataxic or other variants in IGOS cohort.

  • §Sensory dysfunction excludes pain.

  • ¶Antiganglioside antibody testing panel for most patients (40 (82%) of 49) included GM1 IgG, GM2 IgG, GD1a IgG, GD1b IgG, GQ1b IgG, GM1 IgM, GM2 IgM, GD1a IgM, GD1b IgM and GQ1b IgM.

  • **54 patients in our study had nerve conduction studies performed and results available, of whom 32 also had electromyography. The median time to electrophysiological studies was 15 days (IQR 11–25.5; data available for 47 patients patients). Ninety per cent of patients had electrophysiological studies performed at least 1 week from the symptom onset. Like IGOS, we report here the first electrophysiology results, accepting that axonal degeneration may only become manifest at a later time, and that if NCS/EMG is repeated after several weeks some patients need to be reclassified electrophysiologically. The diagnoses for our patients are those given by the reporting clinician, whereas for IGOS, the raw data were analysed centrally according to criteria of Hadden et al.36

  • ††Data on first-line treatment given was available for 68 of the patients who had GBS following SARS-CoV-2 vaccination. The ‘other’ treatment category comprised five patients who initially received corticosteroids and two who had IVIG and corticosteroids together. In the IGOS cohort, ‘other’ included corticosteroids, immunoadsorption and trial medication. Three IVIG recipients in our study had plasma exchange subsequently; two of whom then received a further course of IVIG.

  • IVIG, intravenous immunoglobulin; MFS, Miller Fisher Syndrome; PLEX, plasma exchange.