Abstract
Neurologic impairment persisting months after acute severe SARS-CoV-2 infection has been described because of several pathogenic mechanisms, including persistent systemic inflammation. The objective of this study is to analyze the selective involvement of the different cognitive domains and the existence of related biomarkers. Cross-sectional multicentric study of patients who survived severe infection with SARS-CoV-2 consecutively recruited between 90 and 120 days after hospital discharge. All patients underwent an exhaustive study of cognitive functions as well as plasma determination of pro-inflammatory, neurotrophic factors and light-chain neurofilaments. A principal component analysis extracted the main independent characteristics of the syndrome. 152 patients were recruited. The results of our study preferential involvement of episodic and working memory, executive functions, and attention and relatively less affectation of other cortical functions. In addition, anxiety and depression pictures are constant in our cohort. Several plasma chemokines concentrations were elevated compared with both, a non-SARS-Cov2 infected cohort of neurological outpatients or a control healthy general population. Severe Covid-19 patients can develop an amnesic and dysexecutive syndrome with neuropsychiatric manifestations. We do not know if the deficits detected can persist in the long term and if this can trigger or accelerate the onset of neurodegenerative diseases.
Highlights
Elevated compared with both, a non-severe acute respiratory syndrome (SARS)-Cov[2] infected cohort of neurological outpatients or a control healthy general population
Compared with the values obtained during the study visit (90–120 days after hospital discharge), the ferritin values were found in the normal range for our laboratory, while the D-dimer (586.36 ng/ml; SD = 683.75) and C-reactive protein (CRP) (6.47 mg/ml; SD = 16.15) values remained slightly elevated, their values had decreased substantially
The results of our study show a pattern of cognitive impairment with some peculiarities
Summary
Elevated compared with both, a non-SARS-Cov[2] infected cohort of neurological outpatients or a control healthy general population. SARS-CoV-2 spread rapidly throughout the world, and the WHO declared the disease caused by this global virus a pandemic in March 2020. Despite the acute consequences of SARS-CoV-2 infection, patients have described lingering symptomatology after the infection, a condition called Long Covid. Necropsic studies have proven some neuroinvasive capacity of SARS-CoV-27,10,11. This virus may enter the brain through three potential mechanisms: transsynaptic spread from the olfactory bulb following intranasal exposure, migration across the BBB through endothelial cell infection, and migration following disruption of the BBB from resulting inflammation[12–14]. Pathologic studies have found a high prevalence of SARS-CoV2 RNA and surface protein structures in olfactory m ucosa[11]. Further evaluation identifying surface proteins of SARS-CoV2 through electron microscopy documented that endothelial cells in these regions were the primary target of infection[11]. The relationship between viral neuroinvasive infections and neurodegenerative diseases (NDDs) has been described[15–19], with preferent injury to the hippocampus and other regions of the temporal and frontal lobes related to cognition[20,21]
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