Evidence for facial nerve palsy and SARS-CoV-2

Introduction. The World Health Organization (WHO) has recognized a new strain of coronavirus, the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), called Coronavirus Disease 2019 (COVID-19). The mildest and most common symptoms include fever, fatigue and cough; however, more severe cases of the disease can cause breathing difficulties, kidney and heart failure and, eventually, death. However, an increasing number of reports of neurological manifestations have emerged. Objective. Provide a comprehensive review of the neurological manifestations of SARS-CoV-2 and especially the relationship between acute facial nerve palsy and COVID-19, as well as their results in mortality and the implications that this has in clinical practice. Method. The search in seven databases (PubMed, Cochrane Library, Lilacs, Scielo, Web of Science, Scopus and Google Scholar) was carried out by two independent reviewers in search of evidence of Facial Nerve Palsy (VII) and SARS-CoV-2 . After screening, data were collected and discussed. Results. Idiopathic facial palsy is called Bell's palsy and studies have shown that facial palsy increased during the COVID-19 pandemic period. There are many reports on the relationship between COVID-19 and facial paralysis, but little real evidence of their relationship. Conclusion. It is still questionable whether these neuroimmune disorders occur directly from viral infection or as autoimmune sequelae. The pathogenesis of the disease behind this manifestation is not yet fully understood. We believe that more research should be carried out to clarify the association raised by this study.


INTRODUCTION
In an outbreak that broke out in Wuhan in December The titles of all stored publications were read, and, when necessary, the summary, introduction and/or results and discussion sections were carefully investigated to ensure that the publications met the eligibility criteria. After screening, data were collected and discussed. 41 publications were selected to prepare the synthesis of this article after applying the selection method. Duplicates between databases (n=32) were initially excluded, and the electronic search procedure retrieved 5820 publications.
After reading the titles and abstracts, 5388 publications were excluded (they did not directly discuss the evidence between facial paralysis and SARS-CoV-2: n=4322; the terms COVID-19, Facial Paralysis and SARS-CoV-2 were only included in the affiliation of authors or references in the publication: n=1066) and 400 texts were conducted for full reading.

RESULTS AND DISCUSSION
Experimental studies using transgenic mice suggest that SARS-CoV and MERS-COV may enter the central nervous system intranasally through the olfactory nerve.
Once in the brain, they have the potential to spread to the thalamus and brain stem, two regions highly involved in coronaviridae infections 3-5 . It has been suggested that SARS-CoV-2 can enter the central nervous system in two ways: first through systemic vascular dissemination and, second, more locally through the cribiform lamina of the ethmoid bone, which may or may not affect the association with anosmia often described by patients with SARS-CoV-2. Upon entering the systemic circulation, the virus will invade the nervous tissue due to its neurotropism properties. Here, it binds and interacts with angiotensin-converting enzyme 2 (ACE2) receptors in the capillary endothelium 6 .
Studies on the structural integrity of the SARS-CoV-2 peak glycoprotein show that, compared to the SARS-CoV peak protein, the affinity for ACE2 is increased by 10 to 20 times. This can be explained by the fact that although the structure is similar, the two peak glycoproteins are not the Asymptomatic individuals from the randomly selected sample participated in a Spanish study investigating COVID-19 IgG and/or IgM and the prevalence found was 5.47% 24 .
The seroprevalence of the SARS-CoV-2 IgG and/or IgM antibody in asymptomatic individuals was 2.39% in Wuhan 25 .
The highest prevalence of antibodies against SARS-CoV-2 in the literature was found in asymptomatic people in Sergipe, Brazil. SARS-CoV-2 IgG was found to be 8.3% and 11.9% for IgM 26 .
In another study, it was found that facial palsy may be the only symptom of COVID-19, but they emphasize that further studies with larger groups of patients should be done.
The PCR test on patients' first admission could be done to clarify the etiology. The SARS-CoV-2 antibody test to measure IgG and IgM separately can also be performed 16 .
In addition to Bell's palsy, other immune disorders of the nervous system have also been proposed as associated with COVID-19. The involvement of cranial nerves has been described in the context of Guillain-Barré 27 syndrome and its variants [28][29][30] . Descriptions of isolated cranial nerve involvement in the context of COVID-19 are scarce 19 .
In an Italian cohort, Guillain-Barré syndrome was

CONCLUSION
Although it is possible to assert, through scientific evidence, that direct viral neurophysics or an immunological mechanism secondary to elevated pro-inflammatory cytokines can cause facial palsy in COVID-19, it is still necessary to understand the pathogenesis of COVID-19 behind the facial palsy, not yet fully understood. It is known that SARS-CoV can infiltrate the brainstem of mammals through trans-synaptic transfer, which can lead to dysfunction of the cardiorespiratory centers of the brainstem. It is enough to know whether the same occurs with SARS-CoV-2 in the ganglia that emit motor nerve fibers from the facial nerve. We believe that more research needs to be done to clarify the association, correlation or causality between COVID-19 and neuroimmune diseases.