Facing acute neuromuscular diseases during COVID-19 pandemic: focus on Guillain-Barré syndrome

Abstract

In December 2019, a cluster of cases with 2019 Novel Coronavirus pneumonia from Wuhan, China, aroused worldwide concern due to an escalating outbreak in all the countries in the world. Coronavirus belongs to a family of single-stranded RNA viruses, which includes severe acute respiratory syndrome (SARS-CoV) and Middle East respiratory syndrome (MERS-CoV), that have caused human epidemics with high fatality. The spectrum of the novel coronavirus disease (SARS-Co-2 or COVID-19) ranges from asymptomatic infections to fatal pneumonia, and differs from other viral pulmonary infections. MERS-CoV is known to be potentially neuroinvasive. Extensive reports from China documented central and peripheral nervous system involvement in patients with COVID-19, and identified in angiotensin converting enzyme2 (ACE2), which is present in multiple human organs, the functional receptor for this virus. Guillain-Barré syndrome (GBS) has recently been associated to COVID-19 rising concern among physicians. This review summarizes the current state of knowledge on GBS during or after COVID-19 infection, attempting to clarify the pathophysiology of the associated respiratory dysfunction and failure.

Keywords: Acute axonal; Acute respiratory distress (ARDS); COVID-19; Demyelinating neuropathy; Guillain–Barré syndrome; MERS-CoV; SARS-CoV.

Fig. 1

Example of respiratory pathophysiological changes in a patient with GBS. The upper part of the figure estimate shunt fraction (Q_S) and dead space (VD). The middle represents the pressure–volume relationship of the lung (red line: normal lung, blue line: effect of the supine position and respiratory muscle weakness). The lower part of the figure shows CT scan of the basal areas of the lung. Panel A 62-year-old GBS with intact respiratory muscle function. In supine position, there is a physiological slight decrease in FRC (see lung pressure–volume relationship). CT scan is normal. Panel B The patient develops severe diaphragmatic weakness with appearance of basal atelectasis at CT scan, decrease in compliance and significant increase in shunt fraction (Q_S)