PMC:7309518 / 8354-10168 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7309518","sourcedb":"PMC","sourceid":"7309518","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7309518","text":"GBS in the COVID-19 pandemic\nThese early GBS cases, despite incomplete immunologic workup considering the enormous difficulties in highly stressed in-hospital settings, provide early clues on what to expect in the months ahead regarding the common acute autoimmune neurologic conditions, such as GBS, polyneuritis cranialis, encephalitis, encephalomyelitis, or myositis, which for years we have been casually referring to as postviral if seen after febrile illnesses.\nFirst and foremost, the practicing neurologists in this pandemic should now be aware that a patient who presents with an acute paralytic disease—like GBS, encephalomyelitis, or myositis—even without fever, dyspnea, or any systemic symptoms, may represent the first manifestation of COVID-19. This is compelling, considering that only 43% of COVID-19–positive patients on admission have fever,4–6 and many of the present patients with GBS did not have any COVID-19 symptoms at presentation. These early GBS cases also highlight that 2 clinical and laboratory signs, anosmia/ageusia and lymphocytopenia/thrombocytopenia, are red flags in suspecting COVID-19 in otherwise asymptomatic patients with acute neurologic events. They further confirm what we had feared from other viral pandemics that COVID-19 can trigger neurologic autoimmunity; in contrast to the other postviral neurologic diseases, however, COVID-19 requires high degree of suspicion as a potential hidden trigger to prevent inadvertent viral transmission to health care personnel and patient relatives, as in the Wuhan case.7 The series also highlights that GBS peaks 5–10 days after the first COVID-19 symptoms, which in intensive care unit (ICU) settings helps to distinguish GBS from critical illness neuropathy that usually appears later in the course of very sick ICU 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