Literature DB >> 32360440

Guillain-Barré syndrome as a complication of SARS-CoV-2 infection.

Matteo Coen1, Grégoire Jeanson2, L Alejandro Culebras Almeida3, Annemarie Hübers3, Florian Stierlin4, Iris Najjar4, Marie Ongaro4, Kelly Moulin4, Maria Makrygianni2, Béatrice Leemann2, Ilona Kronig4, Jérôme Bertrand3, Jean-Luc Reny4, Manuel Schibler5, Jacques Serratrice4.   

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Year:  2020        PMID: 32360440      PMCID: PMC7194931          DOI: 10.1016/j.bbi.2020.04.074

Source DB:  PubMed          Journal:  Brain Behav Immun        ISSN: 0889-1591            Impact factor:   7.217


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A man in his seventies was hospitalized because of paraparesis, distal allodynia, difficulties in voiding and constipation. Ten days before he developed myalgia, fatigue, and a dry cough. He was diagnosed with an oligosymptomatic coronavirus disease 2019 (COVID-19) [positive severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RT-PCR in two nasopharyngeal (NP) swab]. At day 25 from RT-PCR, serum anti-SARS-CoV-2 IgA and IgG ELISA (Euroimmun, Seekamp, Germany) resulted positive. Figure shows a timeline of the main events (Fig. 1 ).
Fig. 1

Timeline indicating the main events of the patient’s illness. Top row: clinical events (before/after patient’s hospitalisation); bottom row: corresponding dates. NP = nasopharyngeal.

Timeline indicating the main events of the patient’s illness. Top row: clinical events (before/after patient’s hospitalisation); bottom row: corresponding dates. NP = nasopharyngeal. The patient had no medical history. Vital signs were normal. Physical examination revealed fine crackles in the left base, bilateral lower limb flaccid paresis, absent deep tendon reflexes of the upper and lower limb and idiomuscular response to percussion of the muscle tibialis anterior, indifferent plantar reflexes. There was no sensory deficit. Blood tests were normal. Cerebrospinal fluid (CSF) analysis showed albuminocytologic dissociation without intrathecal IgG synthesis. FilmArray Meningitis/Encephalitis (ME) Panel testing (BioFire Diagnostics, Salt Lake City, UT) and SARS-CoV-2 RT-PCR were negative; antiganglioside antibodies were not detected. Chest X-ray was normal. Contrast-enhanced MRI excluded myelopathy. Nerve conduction study showed sensorimotor demyelinating polyneuropathy with “sural sparing pattern”; F wave study showed decreased persistence or absent F-waves in tested nerves. Findings were compatible with an acute inflammatory demyelinating polyneuropathy, the most common subtype of Guillain-Barré Syndrome (GBS). On the day following admission the patient was started on intravenous immunoglobulins (IVIg; IgPro10, Privigen®; 0.4 g/kg/day for 5 days). Improvement was rapid. At day eleven from hospitalisation the patient was transferred to the Division of Neurorehabilitation. SARS-CoV-2 is a novel coronavirus first detected in Wuhan, Hubei province, China, in late 2019 and the etiologic agent of COVID-19 (Zhu et al., 2020). It belongs to the genus β-coronavirus, like HCoV-OC43 and HCoV-HKU1 (responsible of mild upper respiratory tract infections), and MERS-CoV and SARS-CoV [the agents of the Middle East Respiratory Syndrome (MERS) and of the SARS, respectively] (Fehr and Perlman, 2015). GBS is an acute, immune-mediated, typically postinfectious polyneuropathy. Its main manifestations are progressive bilateral weakness of arms and legs and hyporeflexia/areflexia in the affected limbs. Dysautonomia (including bowel and bladder dysfunction) is common (Leonhard et al., 2019). Our patient had a classic presentation of GBS. He tested positive for SARS-CoV-2 before the first signs of polyneuropathy, thus supporting a postinfectious GBD phenotype. Before the SARS-CoV-2 pandemic, only two cases of coronavirus-associated GBS were reported in the literature: a man with MERS-CoV who developed Bickerstaff brainstem encephalitis (a variant of GBS) (Kim et al., 2017), and a boy who developed an atypical GBS after a respiratory infections sustained by HCoV-OC43 (Sharma et al., 2019). Up to now, two paper have described a possible association between SARS-CoV-2 and GBS (Zhao et al., 2020, Toscano et al., 2020). We describe one of the first cases of GBS occurring in the context of SARS-CoV-2 infection. In the context of the current pandemic, clinicians should be aware that GBS can complicate SARS-CoV-2 infection an affect patient’s outcomes, thus requiring a prompt intervention. Moreover, physician should remember that that the incidence of GBS during outbreaks of infectious disease can increase (as with the recent Zika virus epidemic) (Leung, 2020). To note, although neurological manifestation in COVID-19 are frequently described (like in the recent case report by Ye et al. (2020), the neuroinvasive potential of SARS-CoV-2 remains hitherto inexplored (Wu et al., 2020).
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Review 3.  Diagnosis and management of Guillain-Barré syndrome in ten steps.

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5.  Potential differences in cleavage of the S protein and type-1 interferon together control human coronavirus infection, propagation, and neuropathology within the central nervous system.

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6.  Guillain Barré syndrome associated with COVID-19- lessons learned about its pathogenesis during the first year of the pandemic, a systematic review.

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Review 8.  Guillain-Barré syndrome associated with Covid-19: A close relationship or just a coincidence? (Review).

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Review 9.  Facing acute neuromuscular diseases during COVID-19 pandemic: focus on Guillain-Barré syndrome.

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Review 10.  Neurological associations of COVID-19.

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