Abstract
Coronavirus disease 2019 (COVID-19) interacts with the nervous system directly and indirectly by affecting the activation of the immune system. Guillain–Barré syndrome (GBS) is triggered by an inappropriate immune system activation that overlaps with the neurotoxic mechanism of an invading pathogen. Here, we discuss the complexity of an abnormal immune system response leading to the generation of autoimmunity in the setting of acute viral infection. A 67-year-old male patient with COVID-19 developed a sensory motor acute polyneuropathy with respiratory failure. Several serum inflammatory and neurodegeneration markers were collected during hospital days 1, 3, 8, and 67 and compared to healthy individuals. Neural cell adhesion molecule 1 (NCAM-1) and neurofilament light chain (NfL) values were highly variable when compared to healthy individuals, but not to the reference COVID-19 group. We focused our attention on NCAM-1 as a possible target for antibodies directed at COVID-19 in silico.
Highlights
Guillain–Barré syndrome (GBS) is a relatively uncommon condition characterized by an acute onset of muscle weakness and/or sensory loss as a result of a disruption in peripheral nerve myelin and axonal function by the body’s immune system [1,2]
What is unclear is if there are specific markers, or inciters, of peripheral nerve damage caused by COVID-19 compared to the those of a viral-induced GBS, or rather a specific cluster for COVID-19-related GBS [16,17]
There is still uncertainty regarding whether the patient had another viral infection that had become symptomatic, if the patient was sensitized secondary to an unknown exposure, or rather if the subsequent worsening of symptoms was secondary to COVID-19 or the worsening respiratory failure from the muscle weakness itself
Summary
Guillain–Barré syndrome (GBS) is a relatively uncommon condition characterized by an acute onset of muscle weakness and/or sensory loss as a result of a disruption in peripheral nerve myelin and axonal function by the body’s immune system [1,2]. The symptoms may progress to respiratory failure, loss of deep tendon reflexes, and dysautonomia. The most common variant is an acute inflammatory demyelinating polyneuropathy, which is characterized by motor weakness, paresthesia and loss of deep tendon reflexes. Less common variants are acute motor and sensory axonal neuropathies, which involve motor and sensory loss, respectively, and characteristic patterns in electromyography and nerve conduction studies (EMG/NCS). EMG demonstrates a pattern of either demyelinating or axonal polyneuropathy and is more sensitive weeks after the acute phase of illness [3,4,5].
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