Bell’s palsy is a type of sudden onset, one-sided facial paralysis designated with lower motor neuron dysfunction of the 7th cranial nerve (16). It affects the entire population, regardless of age or gender, and from many populations the incidence has been reported as 11.5–53.3 per 100,000 persons [16]. The most widely accepted causes for Bell’s palsy are inflammatory, traumatic and infectious processes [7]. Although there is a certain link between viral infection and Bell’s palsy, this is frequently associated with members of the Herpesviridae [12]. Studies have reported that HSV-1 DNA was detected around the geniculate nucleus and in the endoneural fluid of the facial nerve in patients with Bell’s palsy [17, 18]. Particularly, HSV and VZV infections are most prominently determined, but many vectors that can cause Bell's palsy have been identified. These are Epstein-Barr virus, Human Herpesvirus 6 (HHV-6), Human Immunodeficiency Virus (HIV), Hepatitis B, Influenza, Adenovirus, Rubella, Mumps and Coxsackievirus, as well as Lyme disease and Mycobacterium tuberculosis [10, 19–24]. Sarcoidosis and neoplasms can also be considered in the non-infectious group [10]. The exact pathogenesis of acute-onset facial nerve paralysis is not known exactly, but in association with neurotropic Herpes viruses (HSV and VZV), it is thought to be associated with axonal spread and viral replication, which leads to inflammation and demyelination in the nerve [11].
In idiopathic facial nerve paralysis, ischemia of vasa nervorum and demyelination induced by an inflammatory process can be supposed as possible mechanisms related to nerve damage [16]. In several postmortem studies, vascular changes and related microthrombi have been consistently reported [25]. As is known, hypercoagulability occurs in some patients with COVID-19 disease, which can result in vascular endothelial damage and related arterial and venous thrombotic complications [26]. This situation appears as a finding that supports the pathogenesis of facial paralysis. Direct viral damage or an autoimmune reaction producing inflammation toward the nerve would be alternative or contributing mechanisms to dysfunction. Increased deterioration of nerve functions can occur with direct viral damage or an autoimmune event that can trigger a boost in inflammation of the nerve [14].
According to recently reported studies, there is increasing information suggesting a neuroinvasive capacity of COVID-19 [27]. SARS- CoV-2 is identical in infectious mechanism to other common coronaviruses (CoV). Neuro-invasive propensity is one of the important features of CoV, and so SARS-CoV-2 is likely to have neurotrophic activities as well [13, 27]. Since this virus has a high affinity for ACE-2 receptors, which are frequently found in the nervous system, it performs neurotropism by directly causing nerve damage [27–29]. The ACE2 receptor is highly expressed in ciliated epithelium and goblet cells, with viral replication being highest in the nasal mucosa, as can be understood from the detection of high viral load by examining nasal cells [30]. SARS-CoV-2 can reach the central nervous system through the olfactory nerve and bulb, which can be directly opened to the central nervous system, or through viremia. A limited number of studies related to neurological complications of COVID-19 have been reported up to now in the literature. Mao et al reported a study on the neurological manifestations of COVID-19 patients. Their findings showed that headache was among the central findings and hyposmia was of the most encountered peripheral nervous system findings. In that study, 36.4% of COVID-19 patients complained of neurological symptoms [31]. In a study by Korkmaz et al., otolaryngological manifestations were examined in COVID-19 patients and a considerable number of neurological findings, such as vertigo / dizziness, headache, and loss of taste and smell, were also mentioned as common symptoms in COVID-19 patients [32]. In milder cases, peripheral nervous system manifestations were predominant, including not only taste and smell disorders but also Guillain-Barré and Miller-Fisher syndromes [33–35]. In the majority of patients with severe COVID-19, encephalopathy, cerebrovascular complications and myelitis were reported as other neurological complications [5, 6].
Some types of vaccines have been developed over the past year to slow down or even end the COVID-19 pandemic. The U.S. Food and Drug Administration (FDA) has approved vaccines developed with mRNA technology and vaccination studies have been initiated. However, in the vaccinated groups during Phase III studies, it was reported that 3 out of 15,185 volunteers in one group and 4 out of 18,801 volunteers in the other group developed peripheral facial paralysis after vaccination. It has been reported that there is no significant difference compared to the total population incidence, and vaccination and facial paralysis cannot be associated at this stage [36]. However, even this situation raises the suspicion that peripheral facial paralysis may be associated with SARS-CoV-2.
In our study, 34 patients were evaluated and 8 of them were evaluated as COVID-19 RT-PCR (+). Peripheral facial paralysis was the first finding in 5 of these 8 patients, and the RT-PCR test performed at the time of first admission was found to be (+), suggesting that peripheral facial palsy could be associated with COVID-19. In a series of 8 cases reported by Lima et al., peripheral facial paralysis was reported as the first symptom in 3 patients included in the study [14]. Similar to our study, although female patients were more common, it is difficult to make a definite assessment that it can be seen more frequently in women due to the small number of cases. Similarly, the facial paralysis severity of the patients with positive SARS-CoV-2 virus was less severe, but in one of the patients we included in our study, no improvement was achieved in the palsy grade despite one month of combined steroid treatment. However, in the study of Lima et al., it was reported that most of the patients fully recovered [14]. The rate of complete recovery was lower in our study group (37.5%). There are also case reports in the literature suggesting that the SARS-CoV-2 virus may cause peripheral facial paralysis. One of the reports is a 6-year-old male patient reported by Theophanous et al [12]. Another case is a pregnant patient reported by Figueiredo et al [13]. Ribeiro and Marchiori also reported a 26-year-old male patient (37). Goh et al. presented a case of peripheral facial paralysis that developed on the sixth day of COVID-19 disease in a 27-year-old male patient [10]. Muras et al. also reported a patient with bilateral facial palsy who presented evidence of SARS-CoV-2 infection and coinfection with Epstein-Barr virus [38]. Zammit et al. and Codeluppi et al. reported that SARS-CoV-2 increased the incidence of peripheral facial paralysis by comparing a certain period of the COVID-19 pandemic with previous years in terms of incidence and emphasized the first presentation symptom of COVID-19 patients may be facial paralysis [39, 40]. In addition to these cases and case series reported in the literature, our study shows that there may be a strong relationship between COVID-19 and peripheral facial paralysis.