Cross-sectional case-control studies (Blue)
The objective of this prospective, consecutive, observational study was to systematically describe central (CNS) and peripheral (PNS) nervous system complications in hospitalised COVID-19 patients.
Adult patients from a tertiary referral center with confirmed COVID-19 were included. 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. The authors classified complications as caused by SARS-CoV-2 neurotropism, immune-mediated or critical illness-related.
From April to September 2020, 61 consecutively admitted COVID-19 patients were enrolled, 35 (57%) of whom required intensive care (ICU) management for respiratory failure. Forty-one CNS/PNS complications were identified in 28 of 61 (45.9%) 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 8 with akinetic mutism. Length of ICU admission was independently associated with encephalopathy (OR = 1.22). Other CNS complications included ischaemic stroke, a biopsy-proven acute necrotising encephalitis, and transverse myelitis. The most common PNS complication was critical illness polyneuromyopathy (13.1%), with prolonged ICU stay as an independent predictor (OR = 1.14). Treatment-related PNS complications included meralgia paresthetica. Of 41 complications in total, 3 were para/post-infectious, 34 were secondary to critical illness or other causes, and 4 remained unresolved. Cerebrospinal fluid was negative for SARS-CoV-2 RNA in all 5 patients investigated. The authors concluded that CNS and PNS complications were common in hospitalised 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.
DOI: 10.1007/s00415-020-10380-x
