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Lower Cranial Nerve Palsies in the COVID-19 Pandemic: A 10-Case Series of Intensive Care Unit Patients
Author(s) -
Pierre Decavel,
Olympe Nahmias,
Carine Petit,
Laurent Tatu
Publication year - 2021
Publication title -
european neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.573
H-Index - 77
eISSN - 1421-9913
pISSN - 0014-3022
DOI - 10.1159/000519226
Subject(s) - pandemic , covid-19 , intensive care unit , medicine , series (stratigraphy) , virology , intensive care medicine , disease , outbreak , biology , infectious disease (medical specialty) , paleontology
A number of neurological complications of COVID-19 have been identified, including cranial nerve paralyses. We present a series of 10 patients with lower cranial nerve involvement after severe COVID-19 infection requiring hospitalization in an intensive care unit. Methods: We conducted a retrospective, observational study of patients admitted to the post-intensive care unit (p-ICU) of Besançon University Hospital (France) between March 16 and May 22, 2020. We included patients with confirmed COVID-19 and cranial neuropathy at admission to the p-ICU. All these patients were treated by orotracheal intubation, and all but one underwent prone-position ventilation therapy. Results: Of the 88 patients admitted to the p-ICU, 10 patients (11%) presented at least 1 cranial nerve palsy. Of these 10 patients, 9 had a hypoglossal nerve palsy and 8 of these also had a deficit in another cranial nerve. The most frequent association was between hypoglossal and vagal palsies (5 patients). None of the patients developed neurological signs related to a global neuropathy. We found no correlation between the intensity of the motor limb weakness and the occurrence of lower cranial nerve palsies. All but 2 of the patients recovered within less than a month. Conclusion: The mechanical compressive hypothesis, linked to the prone-position ventilation therapy, appears to be the major factor. The direct toxicity of SARS-CoV-2 and the context of immune dysfunction induced by the virus may be involved in a multifactorial etiology.

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