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.