Introduction
Starting at the end of 2019 in Wuhan, China, the coronavirus disease 2019 (COVID-19) has been responsible for millions of infections worldwide. Patients commonly present with cough, myalgia, fatigue, and diarrhea [1]. In a retrospective observational case series of 214 cases of COVID-19 in Wuhan, China, 78 patients were found to have neurological manifestations [2]. Neurologic symptoms of COVID-19 ranged from impaired consciousness, dizziness, fever, headache, anosmia, and dysgeusia to acute large vessel cerebrovascular disease, acute disseminated encephalomyelitis, and Guillain Barre syndrome (GBS) [3]. GBS has been reported to have a higher incidence after various epidemics around the world. During the epidemics of the Middle East Respiratory syndrome and Zika Virus in the French Polynesia, the incidence of GBS increased [4,5].
GBS has multiple classifications of autoimmune polyradiculopathies ranging from a spectrum of disease. Complications vary from muscle weakness, sensory abnormalities, dysautonomia, and cranial neuropathies. Variants of GBS include: classical, Miller Fisher syndrome, pharyngeal-cervical-brachial, bifacial weakness with paresthesia of limbs, and paraparetic. The association between these neurologic symptoms in patients with recent COVID-19 is not completely understood. Several proposed mechanisms include multiorgan dysfunction, peripheral nerve damage secondary to a cytokine storm, molecular mimicry, and direct injury from the virus itself. Evidence behind the role of molecular mimicry is controversial. On one hand, there is no homology between any SARS-CoV-2 genetic or linear protein structure and human linear protein structures. On the other hand, there is the possibility of post-translational modification of viral proteins by their host cells leading to the formation of an immunogenic surface. This creates the necessary trigger for the immune system and thus the formation of antibodies against ganglioside components of the peripheral nerves [6]. More thorough research into the characterization of the molecular basis is needed to understand potential causal links. Here, we report a patient with a confirmed GBS diagnosis following a recent COVID-19 diagnosis.