This systematic review shows that SC2-GBS is not due to a direct attack of the virus but rather due to an immunological reaction to the virus. It also shows that the number of reports about SC2-GBS is increasing and that the outcome is worse compared to non-SC2-GBS .
Though the number of cases with SC2-GBS is increasing suggesting that the overall prevalence of GBS has increased since the outbreak of the pandemic, there are conflicting results concerning this matter. In a UK study of 47 SC2-GBS patients, the prevalence of GBS did not increase between March 2020 and May 2020 as compared to the years 2016–2019 . On the contrary, a retrospective, multi-centre study from northern Italy of 34 SC2-GBS patients showed that the estimated incidence of GBS in March 2020 and April 2020 increased from 0.93/100000/year in 2019 to 2.43/100000/year in 2020 . There are several reasons why SC2-GBS may be missed and why the prevalence of GBS in fact increased since onset of the pandemic. First, SC2-GBS may go undetected due to misinterpretation as increased weakness or sensory disturbances of a pre-existing neuropathy. Second, SC2-GBS may be misinterpreted as critical ill neuropathy. Third, work-up for neuropathy may be incomplete due to mild manifestations or due to occurrence during ICU stay.
Before diagnosing SC2-GBS, it is crucial to exclude various differential diagnoses. These include previously existing neuropathy, critical ill myopathy, critical ill neuropathy, toxic neuropathy, or neuropathy or myopathy due to side effects of applied drugs. Lopinavir and tocilizumab have been reported to cause neuropathy [8, 9]. There are also reports indicating that chloroquine may induce neuropathy .
If GBS develops during immobilisation for artificial ventilation, diagnosing SC2-GBS becomes challenging . In patients under artificial ventilation for COVID-19, SC2-GBS should be considered if clinical neurologic exam suggests neuropathy and if patients cannot be weaned from the respirator. In this case, nerve conduction studies and investigations of the CSF should be initiated. Diagnosing SC2-GBS is crucial as appropriate treatment may improve the overall outcome of COVID-19 patients .
In some cases, SC2-GBS develops before classical clinical manifestations of the infection  being explained by subclinical infection with the virus prior to onset of GBS or the incubation time of SARS-CoV-2, which is up to 14 days .
Though there are no prediction models for the outcome or the need of artificial ventilation in SC2-GBS patients available, there are indications that the outcome is poor if there are complications from hypercoagulability (stroke, pulmonary embolism) and if there are superinfections or sepsis.
Most of the studies included in this review did not specify if respiratory failure in SC2-GBS patients resulted from brainstem encephalitis, BFE, involvement of the respiratory muscles in GBS, from pneumonia ending up as acute, respiratory distress syndrome (ARDS), from pulmonary embolism, heart failure, or from mixtures of these conditions. Specifying the cause of respiratory failure however is crucial as treatment and outcome may differ significantly among these conditions.