Letter to the Editor: Pre-Existing Neuropathy Favours SARS-CoV-2 Vaccination Associated Guillain-Barre Syndrome

Dear Editor,

We read with interest the article by Kim et al.1 about two patients with SARS-CoV-2 vaccination associated Guillain Bare syndrome (GBS) (SC2VG). Patient-1 was a 42-year-old male who developed bilateral facial palsy, dysphagia, quadriparesis, and respiratory insufficiency requiring intubation and mechanical ventilation 2 weeks after the first dose of the AstraZeneca vaccine (AZV).1 Upon cerebrospinal fluid (CSF) investigations and nerve conductions studies (NCSs) the patient was diagnosed with GBS received intravenous immunoglobulins, with a beneficial effect.1 Patient-2 was a 48-year-old female with a history of diabetes and arterial hypertension who developed left facial palsy, dysarthria, severe myalgia, numbness, and muscle weakness two weeks after the first dose of the Biontech Pfizer vaccine (BPV).1 SC2VG was suspected and confirmed by CSF and NCSs. 1 IVIG were given with a significant beneficial effect.1 The study is appealing but raises concerns that need to be discussed.

Patient-1 had received tuberculostatic treatment prior to onset of GBS.1 Particularly isoniacid and ethambutol are neurotoxic.2 Though ethambutol predominantly causes optic neuropathy, some cases with neuropathy of peripheral have been reported.3 Also isoniacid can cause polyneuropathy.4 We should be told which tuberculostatics the patient received, how many days prior to onset of GBS, for how long, and which dosages. It is essential to know if patient-1 developed side effects to any of the tuberculostatics, particularly sensory or motor dysfunction. Patients with previous neuropathy seem to be prone to develop GBS. It would be also interesting to know if patient-1 had undergone NCSs prior to onset of SARS-CoV-2 vaccination associated GBS (SC2VG).

Missing is the subclassification of GBS in patient-1. Since sensory functions were described as preserved, and since NCSs revealed an axonal lesion in most of the investigated nerves, GBS should be classified as acute, motor, axonal neuropathy (AMAN).

At onset patient-1 had left-sided facial palsy but on admission to the tertiary unit he had bilateral facial palsy.1 Was this due to progression within a few days or was bilateral facial palsy initially subtle?

We do not agree that the nerve action potential amplitude from the right sural nerve was 42.4 mV respectively 35.0 mV in the left sural nerve as indicated in Table 1.1 Do the authors mean microV?

Patient-2 had diabetes which did not require treatment.1 However, the HbA1c values were not presented to assess if blood glucose levels were in the normal range on the long run. We should also know if patient-2 had any indications for diabetic polyneuropathy on NCSs prior to onset of SC2VG.

Missing is the subclassification of GBS in patient-2. Since nerve conduction velocities were largely normal, since compound muscle action potentials were reduced, and since motor and sensory fibers were affected, the most probable GBS subtype is acute, motor and sensory, axonal neuropathy (AMSAN).

Myalgia in patient-2 remained unexplained. Were there any indications for myositis, which has been previously reported as a neurological complication of SARS-CoV-2 vaccinations.5 Were there any indications for myositis on needle EMG in patient-2? Was the creatine-kinase normal or elevated?

Overall, the interesting study has some limitations and inconsistencies which challenge the results and their interpretation. Addressing these issues would strengthen the conclusions and could increase the status of the study.