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European Journal of Neurology ; 28(SUPPL 1):157, 2021.
Article in English | EMBASE | ID: covidwho-1307711

ABSTRACT

Background and aims: To systematically describe CNS and PNS complications in hospitalized COVID-19 patients. Methods: We conducted a prospective, observational study of adult patients from a tertiary referral center with confirmed COVID-19. All patients were screened daily for neurological and neuropsychiatric symptoms during admission and discharge. Three-month follow-up data were collected using electronic health records. We classified complications as caused by SARS-CoV-2 neurotropism, immune-mediated or critical illness-related. Results: From April-September 2020, we enrolled 61 consecutively admitted COVID-19 patients, 35 (57%) of whom required ICU management for respiratory failure. Forty-one CNS/PNS complications were identified in 28 of 61 patients and were more frequent in ICU compared to non-ICU patients. The most common CNS complication was encephalopathy (n=19, 31.1%), which was severe in 13 patients (GCS 12), including eight with akinetic mutism. Length of ICU admission was independently associated with encephalopathy (OR=1.22). Other CNS complications included ischemic stroke, a biopsy-proven acute necrotizing encephalitis, and transverse myelitis. The most common PNS complication was critical illness polyneuromyopathy (13.1%), with prolonged ICU stay as independent predictor (OR=1.14). Treatment-related PNS complications included meralgia paresthetica. Of 41 complications in total, three were para/post-infectious, 34 were secondary to critical illness or other causes, and four remained unresolved. Cerebrospinal fluid was negative for SARS-CoV-2 RNA in all five patients investigated. Conclusion: CNS/PNS complications were common in hospitalized COVID-19 patients, particularly in the ICU, and often attributable to critical illness. When COVID-19 was the primary cause for neurological disease, no signs of viral neurotropism were detected, but laboratory changes suggested autoimmune-mediated mechanisms.

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