With interest we read the article by Shemer et al. about nine patients who developed unilateral, peripheral facial nerve palsy after vaccination with the mRNA vaccine BNT162b2 [1]. It was concluded that a causal relation between vaccination and the neurological compromise could not be established and that the pathophysiological mechanism remains elusive if a causal relation is assumed [1]. The study is appealing but raises the following comment and concerns.

The main shortcoming of the study is that the nine included patients had not undergone neurological investigations [1]. Since there are indications that SARS-CoV-2 triggers the development of Guillain-Barre syndrome (GBS) [2] and that SARS-CoV-2 vaccination may be occasionally complicated by the occurrence of GBS, it is crucial that all 9 patients were seen by a neurologist. Since various subtypes of GBS may be characterised by affection of a single or multiple cranial nerves [3], it is essential that GBS was excluded in all 9 patients. GBS is usually diagnosed according the Brighton criteria by clinical assessment, nerve conduction studies, cerebro-spinal fluid investigations, and eventually MR imaging with contrast medium [3]. Thus, we should be told how many of the 9 patients had involvement of other cranial nerves or even involvement of peripheral nerves, how many had undergone lumbar puncture, and how many nerve conduction studies to confirm or rule out affection of nerves other than the facial nerve. 

There are several arguments against a causal relation between the vaccination and facial palsy. First in two patients the latency between vaccination and development of facial palsy was long (26, respectively 30 days) [1]. Side effects after such a long latency not necessarily can be attributed to the vaccination. Second, nothing is reported about the exclusions or confirmation of alternative causes of the facial palsy. We should know in how many patients was there a malignoma, borreliosis, or varicella zoster virus (VZV) infection. Third, since publication of this report only four further patients have been reported as per the end of March 2021 who developed facial palsy time-linked to a SARS-CoV-2 vaccination [4,5] suggesting that the prevalence of peripheral facial palsy has not increased since introduction of SARS-CoV-2 vaccines. 

Another shortcoming is that it is unknown how many of the 9 included patients had already developed antibodies against SARS-CoV-2 and how many patients were SARS-CoV-2 positive despite having received the vaccination.

A further shortcoming is that nuclear facial palsy was not considered why none of the 9 patients had undergone cerebral imaging to exclude a lesion of the facial nucleus in the pons or affection of the facial tract radiating from the nucleus to the ventral side of the pons.

Patient-2 of the case series obviously had developed facial palsy plus (Ramsey Hunt syndrome) due to a VZV infection [6]. Since the management of Ramsey Hunt syndrome due to VZV infection is challenging and the outcome often worse as compared to Bell’s palsy, we should be informed about the therapeutic management and outcome of patient-2 after her second admission. 

In patient-3 VZV infection occurred prior to the SARS-Co’V-2 vaccination, why it is more likely that VZV was responsible for facial palsy than the vaccination.

Overall, this interesting study has several limitations which challenge the conclusions. GBS and nuclear facial palsy need to be excluded in all patients, results of nerve conduction studies should be provided, and alternative causes of facial palsy should be excluded. Furthermore, it should be mentioned how many of the vaccinated patients were SARS-CoV-2 positive or had developed antibodies against the virus.