COVID-19 positive patients with Guillain-Barre syndrome were predominately of demyelinating subtype and appeared more severe than non-COVID-19 patients with Guillain-Barré syndrome.
Results from a study that evaluated the incidence and clinical features of Guillain-Barré syndrome (GBS) across hospitals in northern Italy revealed an increased incidence of the disorder during the COVID-19 outbreak, supporting the hypothesis of a pathogenic link.1
The study consisted of GBS cases diagnosed in 12 referral hospitals in March and April 2020 that were retrospectively collected and compared with a control population of GBS cases diagnosed in March and April 2019 within the same hospitals.
Lead author Massimiliano Filosto, PhD, neurologist, coordinator, Center for Neuromuscular Diseases and Neuropathies, ASST Spedali Civili, and colleagues found the incidence of GBS in March and April 2020 was 0.202 per 100,000/month (estimated rate, 2.43 per 100,000/year) with 34 cases compared to 0.077 per 100,000/month (estimated rate 0.93 per 100,000/year) with 13 cases in the same months of 2019, equating to a 2.6-fold increase.
The 30 COVID-19 positive patients with GBS (88%) represented 0.178 per 100,000 (estimated rate, 2.14 per 100,000/year), while patients who tested negative for COVID-19 with GBS (4 cases) represented 0.024 per 100,000/month (estimated 0.29 per 100,000/year).
A more in-depth evaluation showed an estimated GBS incidence of 47.9 per 100,000 for the total COVID-19 positive population, compared to 236 per 100,000 for patients with COVID-19 who were hospitalized in March and April 2020.
The detailed clinical and laboratory findings of the 30 patients with COVID-19 with GBS revealed a diagnosis of interstitial pneumonia in 28 (93.3%), dysgeusia in 8 patients (26.7%), and anosmia in 6 (20%). Lymphopenia was diagnosed in 20 patients (66.6%).
COVID-19 positive patients with GBS showed a lower Medical Research Council (MRC) sum score (26.3 ±18.3) compared with COVID-19 negative subjects (41.4 ±14.8; P = .006). They also showed a higher frequency of demyelinating subtype (76.6% vs 35.3%; P = .011), more frequent low blood pressure (50% vs 11.8%; P = .017), and higher rate of admission to intensive care unit (66.6% vs 17.6%; P = .002).
Both COVID-19-positive and COVID-19-negative patients with GBS received similar treatment (intravenous immunoglobulin or plasma exchange), and no significant difference in the response was observed. There were no deaths recorded between the 2 groups. Sequential organ failure assessment (SOFA) score, tracked for COVID-19 positive patients, at hospitalization was 4.17 (±4.01), while that at discharge was 2.33 (±1.81).
Creatine kinase (CK) values were available in 22 COVID-19 positive patients with GBS, 3 of which (13.6%) saw increases of at least twice the normal value. Overall, 25 of the 30 patients needed ventilation. Notably, 5 patients developed GBS after the clinical resolution of COVID-19 and were ventilated only during COVID-19 phase.
There were notable limitations to the study, including insufficient findings on antiganglioside antibody titers and spinal magnetic resonance imaging (MRI), as well as a 2-month window which did not fully represent the duration of the pandemic. Lastly, there were likely more patients with GBS outside of the hospitals used in the analysis, which may underestimate the incidence of the disorder.
Filosto et al concluded, “despite these limitations, our results represent the first snapshot of the relationship between COVID-19 and GBS in a large cohort of patients.” The association between the virus and GBS has been observed before, in smaller samples. Two case-based reports describing the neurologic features of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in patients with COVID-19, were published in the New England Journal of Medicine, 1 of which centered around individuals with GBS.2,3