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

Background This study evaluates the impact of comorbid obstructive sleep apnea (OSA) on coronavirus disease 2019 (COVID-19) acute encephalopathy (AE). 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 Most COVID-19 AE patients presented with a high mNOSAS, suggesting an underlying 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%). Underlying OSA was associated with a 14 fold increased risk of developing a severe COVID-19 AE (OR=14.52). Discussion These observations suggest an association between comorbid OSA and COVID-19 AE severity. Comorbid OSA could be a predisposing factor leading to severe COVID-19 AE and consecutive long-term sequalae.

Brain functional connectivity alterations associated with neuropsychological post-COVID syndrome (preprint)

Neuropsychological deficits and brain damage following SARS-CoV-2 infection are not well understood. 110 patients, with either severe, moderate or mild disease in the acute phase underwent neuropsychological and olfactory tests, as well as completed psychiatric and respiratory questionnaires at 223 ± 42 days post-infection. Additionally, a subgroup of 50 patients underwent functional magnetic resonance imaging. Patients in the severe group displayed poorer verbal episodic memory performances, and moderate patients had reduced mental flexibility. Neuroimaging revealed patterns of hypo and hyper functional connectivity in severe patients, while only hyperconnectivity patterns were observed for moderate. The default mode, somatosensory, dorsal attention and cerebellar networks were implicated. Partial least squares correlations analysis confirmed specific association between memory performances and brain functional connectivity. The severity of the infection in the acute phase is a predictor of neuropsychological post-COVID syndrome. SARS-CoV-2 infection causes long-term memory and executive dysfunctions, related to largescale functional brain connectivity alterations.

Monocytosis in the Acute Phase of SARS-CoV-2 Infection Predicts the Presence of Anosognosia for Cognitive Deficits in the Chronic Phase (preprint)

Altered awareness of neuropsychological disorders (i.e., anosognosia) is a striking symptom of post-COVID-19 syndrome. Some leukocytes markers in the acute phase might predict the presence of anosognosia in the chronic phase, but they have not been identified yet. This study aims to determine whether patients with anosognosia for their memory deficits in the chronic phase present specific leukocytes distribution in the acute phase, and if so, whether these leukocytes parameters could predict this anosognosia. First, we compare the acute immunological data of the leukocytes distribution of 20 patients infected with SARS-Cov-2 who displayed anosognosia 69 months after SARS-Cov-2 infection (230.25 ± 46.65 days) versus 41 patients infected with SARS-Cov-2 without developing anosognosia. Second, we performed a ROC analysis to evaluate the predictive value of the leukocytes markers that emerged from this comparison. Blood circulating monocytes (%) at the acute phase of SARS-CoV2 infection is associated with long term post-COVID-19 anosognosia. Finally, serology on admission showing a percentage rate of monocytes of 7.35% of the total number of leukocytes, seems to predict the presence of chronic anosognosia for 6–9 months after infection.

Long COVID Neuropsychological Deficits After Severe, Moderate or Mild Infection (preprint)

Background: There is growing awareness that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can include long-term neuropsychological deficits, even in its mild or moderate respiratory forms. Methods: : Standardized neuropsychological, psychiatric, neurological and olfactory tests were administered to 45 patients (categorized according to the severity of their respiratory symptoms during the acute phase) 236.51 ± 22.54 days post-discharge following SARS-CoV-2 infection. Results: : Deficits were found in all the domains of cognition and the prevalence of psychiatric symptoms was also high in the three groups. The severe performed more poorly on long-term episodic memory and exhibited greater anosognosia. The moderate had poorer emotion recognition, which was positively correlated with persistent olfactory dysfunction. The mild were more stressed, anxious and depressed. Conclusion: The data support the hypothesis that the virus targets the central nervous system (and notably the limbic system), and support the notion of different neuropsychological phenotypes.

Long COVID neuropsychological deficits after severe, moderate or mild infection (preprint)

Background: There is growing awareness that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can include long-term neuropsychological deficits, even in its mild or moderate respiratory forms. Methods: Standardized neuropsychological, psychiatric, neurological and olfactory tests were administered to 45 patients (categorized according to the severity of their respiratory symptoms during the acute phase) 236.51 (SD: 22.54) days post-discharge following SARS-CoV-2 infection. Results: Deficits were found in all the domains of cognition and the prevalence of psychiatric symptoms was also high in the three groups. The severe performed more poorly on long-term episodic memory and exhibited greater anosognosia. The moderate had poorer emotion recognition, which was positively correlated with persistent olfactory dysfunction. The mild were more stressed, anxious and depressed. Conclusion: The data support the hypothesis that the virus targets the central nervous system (and notably the limbic system), and support the notion of different neuropsychological phenotypes.