A rare case of bilateral Bell' s Palsy in the setting of SARS-CoV-2

ABSTRACT

Objective: To describe a rare case of an AIDP variant with bilateral bell's palsy in the setting of SARS-CoV-2. Background: Bilateral facial paralysis is a rare clinical presentation, usually in the setting of underlying systemic disease. Bilateral Bell 's palsy is defined as facial paresis or paralysis involving both sides of the face with an onset that is either simultaneous or within 30 days of each other and represents less than 2% of all facial palsies. AIDP is a potential cause of bilateral facial palsy, and is prevalent in 24-60% of cases. We report a case of a 62-year-old female who presented with bilateral Bell's palsy with bilateral lower extremity weakness and recently positive for SARS-CoV-2. Patient had appropriate findings to suggest a form of acute inflammatory demyelinating polyneuropathy (AIDP), however hyperreflexia on the exam creates a case of a plausible variant such as Acute Motor Axonal Neuropathy (AMAN). Design/Methods: Case report and literature review. Literature review spanning 2009-2021 was conducted via Pubmed. Search terms were “COVID-19”, “bilateral Bell's Palsy”, “facial diplegia”, “Guillain Barré Syndrome”, “AIDP”, “hyperreflexia” Results: Literature review found 9 nerve conduction studies confirming AIDP cases with bilateral Bell's palsy and SARS-CoV-2. 17 non-SARS-CoV-2 cases were found to have AIDP with hyperreflexia, however nerve conduction studies found an axonal neuropathy, suggesting the diagnosis of AMAN. Since this patient presented with hyperreflexia, AMAN, which is a rare AIDP subtype, could have been a likely diagnosis. Conclusions: SARS-CoV-2 infection has been associated with several neurological manifestations. AIDP, in particular, has increased in incidence with the rise in SARS-CoV-2 infections via unclear immune mediated mechanisms. The patient's bilateral Bell's palsy indicates a rare AIDP variant. Interestingly, this patient had upper motor neuron signs, but with nerve conduction studies consistent with distal demyelinating neuropathy without denervation/motor axonal loss.