Five patients at 3 hospitals in northern Italy developed Guillain–Barré syndrome after the onset of coronavirus disease 2019 (COVID-19), according to a correspondence published in the New England Journal of Medicine.

Guillain–Barré syndrome is an autoimmune disease that affects peripheral nervous system, and commonly manifests as demyelinating neuropathy with ascending paresthesia and paralysis. Though the exact etiology and pathophysiology are poorly understood, the syndrome is commonly preceded by a respiratory or gastrointestinal infection. Though Campylobacter jejuni, and several viruses including, cytomegalovirus and Epstein-Barr virus, have a recognized association with the development of Guillain–Barré syndrome, the authors of this correspondence highlight that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may warrant a place on this list.

The correspondence authors reported on the cases of 4 patients who had nasopharyngeal samples that tested positive for SARS-CoV-2 and 1 patient who initially had negative swab and bronchoalveolar lavage testing, but later demonstrated positive serology for the infection.

The period between the onset of COVID-19 symptoms and those of Guillain–Barré syndrome was 5 days in 1 patient, 7 days in 2 patients, and 10 days in 2 patients. In 4 patients, the first symptoms indicative of Guillain–Barré syndrome were lower-limb weakness and paresthesia and facial diplegia or weakness; in 1 patient this was followed by ataxia and areflexic paresthesia. The other 4 patients developed generalized, flaccid, areflexic quadraparesis or quadriplegia, over a period ranging from 36 hours to 4 days; this progressed to require mechanical ventilation for 3 patients.


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Cerebrospinal fluid showed a white-cell count of < 5/mm3 in all patients, and a normal protein level in 2. Electromyography demonstrated fibrillation potentials in 3 patients initially, and after 12 days in a fourth patient. The correspondence authors noted that the electromyography findings were consistent with an axonal variant of Guillain–Barré syndrome in 3 patients, whereas 2 patients demonstrated results indicative of a demyelinating process. Gadolinium-enhanced magnetic resonance imaging showed enhancement of the caudal nerve roots in 2 patients, and of the facial nerve in 1 patient; the remaining 2 patients showed no changed on imaging.

All patients received intravenous immune globulin (IVIG). Two patients needed a second round of this treatment and 1 patient received the addition of a plasma exchange after IVIG. At 4 weeks post-treatment, the 2 patients who received a second round of IVIG were still in the intensive care unit, receiving mechanical ventilation; two patients demonstrated improvement, and were undergoing physical therapy to combat flaccid paraplegia, though minimal upper limb movement was noted and one patient was unable to stand 1 month after illness onset; one patient was discharged and was able to walk independently.

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The correspondence authors reported that they were unable to evaluate the effect of reduced vital capacity in these patients as a results of neuromuscular failure due to Guillain–Barré syndrome. They noted, however, that this effect may be considered if chest imaging findings were not proportionate to the clinical severity of respiratory insufficiency.

Guillain–Barré syndrome as a consequence of [COVID]-19 “should be distinguished from critical illness neuropathy and myopathy, which tend to appear later in the course of critical illness than Guillain–Barré syndrome,” concluded the correspondence authors.

Reference

Toscano G, Palmerini F, Ravalgia S, et al. Guillain–Barré syndrome associated with SARS-CoV-2 [published online April 17, 2020]. N Engl J Med. Doi:10.1056/NEJMc2009191