Obstructive sleep apnea: a major risk factor for COVID-19 encephalopathy?


Journal

BMC neurology
ISSN: 1471-2377
Titre abrégé: BMC Neurol
Pays: England
ID NLM: 100968555

Informations de publication

Date de publication:
27 Sep 2023
Historique:
received: 04 04 2023
accepted: 15 09 2023
medline: 20 11 2023
pubmed: 27 9 2023
entrez: 26 9 2023
Statut: epublish

Résumé

This study evaluates the impact of high risk of obstructive sleep apnea (OSA) on coronavirus disease 2019 (COVID-19) acute encephalopathy (AE). Between 3/1/2020 and 11/1/2021, 97 consecutive patients were evaluated at the Geneva University Hospitals with a neurological diagnosis of COVID-19 AE. They were divided in two groups depending on the presence or absence of high risk for OSA based on the modified NOSAS score (mNOSAS, respectively ≥ 8 and < 8). We compared patients' characteristics (clinical, biological, brain MRI, EEG, pulmonary CT). The severity of COVID-19 AE relied on the RASS and CAM scores. Most COVID-19 AE patients presented with a high mNOSAS, suggesting high risk of OSA (> 80%). Patients with a high mNOSAS had a more severe form of COVID-19 AE (84.8% versus 27.8%), longer mean duration of COVID-19 AE (27.9 versus 16.9 days), higher mRS at discharge (≥ 3 in 58.2% versus 16.7%), and increased prevalence of brain vessels enhancement (98.1% versus 20.0%). High risk of OSA was associated with a 14 fold increased risk of developing a severe COVID-19 AE (OR = 14.52). These observations suggest an association between high risk of OSA and COVID-19 AE severity. High risk of OSA could be a predisposing factor leading to severe COVID-19 AE and consecutive long-term sequalae.

Sections du résumé

BACKGROUND BACKGROUND
This study evaluates the impact of high risk of obstructive sleep apnea (OSA) on coronavirus disease 2019 (COVID-19) acute encephalopathy (AE).
METHODS METHODS
Between 3/1/2020 and 11/1/2021, 97 consecutive patients were evaluated at the Geneva University Hospitals with a neurological diagnosis of COVID-19 AE. They were divided in two groups depending on the presence or absence of high risk for OSA based on the modified NOSAS score (mNOSAS, respectively ≥ 8 and < 8). We compared patients' characteristics (clinical, biological, brain MRI, EEG, pulmonary CT). The severity of COVID-19 AE relied on the RASS and CAM scores.
RESULTS RESULTS
Most COVID-19 AE patients presented with a high mNOSAS, suggesting high risk of OSA (> 80%). Patients with a high mNOSAS had a more severe form of COVID-19 AE (84.8% versus 27.8%), longer mean duration of COVID-19 AE (27.9 versus 16.9 days), higher mRS at discharge (≥ 3 in 58.2% versus 16.7%), and increased prevalence of brain vessels enhancement (98.1% versus 20.0%). High risk of OSA was associated with a 14 fold increased risk of developing a severe COVID-19 AE (OR = 14.52).
DISCUSSION CONCLUSIONS
These observations suggest an association between high risk of OSA and COVID-19 AE severity. High risk of OSA could be a predisposing factor leading to severe COVID-19 AE and consecutive long-term sequalae.

Identifiants

pubmed: 37752429
doi: 10.1186/s12883-023-03393-2
pii: 10.1186/s12883-023-03393-2
pmc: PMC10523731
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

340

Informations de copyright

© 2023. The Author(s).

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Auteurs

Gautier Breville (G)

Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, USA. gautier.breville@pennmedicine.upenn.edu.
Department of Neurosciences, Division of Neurology, Geneva University Hospitals, Geneva, Switzerland. gautier.breville@pennmedicine.upenn.edu.

François Herrmann (F)

Department of Rehabilitation and Geriatrics, Division of Geriatrics, Geneva University Hospitals and University of Geneva, Geneva, Switzerland.

Dan Adler (D)

Division of Pneumology, La Tour Hospital, Geneva, Switzerland.

Christine Deffert (C)

Laboratory of Biological Fluids, Laboratory Medicine Division, Diagnostic Department, Geneva University Hospitals, Geneva, Switzerland.
Laboratory Medicine Division, Department of Medical Specialties, Faculty of Medicine, University of Geneva, Geneva, Switzerland.

Giulia Bommarito (G)

Leenaards Memory Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.

Patrick Stancu (P)

Department of Neurosciences, Division of Neurology, Geneva University Hospitals, Geneva, Switzerland.

Alice Accorroni (A)

Department of Neurosciences, Division of Neurology, Geneva University Hospitals, Geneva, Switzerland.

Marjolaine Uginet (M)

Department of Neurosciences, Division of Neurology, Geneva University Hospitals, Geneva, Switzerland.

Frederic Assal (F)

Department of Neurosciences, Division of Neurology, Geneva University Hospitals, Geneva, Switzerland.

Renaud Tamisier (R)

Univ. Grenoble Alpes, INSERM, CHU Grenoble Alpes, HP2, 38000, Grenoble, France.

Patrice H Lalive (PH)

Department of Neurosciences, Division of Neurology, Geneva University Hospitals, Geneva, Switzerland.
Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Diagnostic Department, Division of Laboratory Medicine, Geneva University Hospitals, Geneva, Switzerland.

Jean-Louis Pepin (JL)

Division of Pneumology, La Tour Hospital, Geneva, Switzerland.
Univ. Grenoble Alpes, INSERM, CHU Grenoble Alpes, HP2, 38000, Grenoble, France.

Karl-Olof Lövblad (KO)

Division of Neuroradiology, Geneva University Hospitals and University of Geneva, Geneva, Switzerland.

Gilles Allali (G)

Department of Neurosciences, Division of Neurology, Geneva University Hospitals, Geneva, Switzerland.
Leenaards Memory Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.
Department of Neurology, Division of Cognitive and Motor Aging, Albert Einstein College of Medicine, Yeshiva University, Bronx, NY, USA.

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