Conceptual aspects of public administration of the quality of life in the context of war

Abstract

Introduction: post-COVID syndrome is associated with a wide range of long-term complications, among which neurological manifestations have become increasingly recognized. These complications present diagnostic and therapeutic challenges due to their heterogeneity and the evolving understanding of their pathophysiology. Objective: to investigate the clinical and pathogenetic characteristics of neurological manifestations in patients with post-COVID syndrome, with a focus on identifying patterns and potential underlying mechanisms. Methods: a cohort of 60 patients with confirmed post-COVID syndrome was evaluated. Clinical assessments included neurological examination, neuroimaging (MRI), and neurophysiological studies (EEG, EMG, and evoked potentials). Laboratory markers were also analyzed to assess inflammatory and autoimmune activity. Data were categorized by symptom type and severity. Results: The most frequent neurological symptoms were headaches (48.3%), cognitive impairments (41.6%), sleep disorders (40%), and anxiety-depressive symptoms (38.3%). Neuroimaging revealed structural changes in 35% of patients, while neurophysiological testing showed signs of central and peripheral dysfunction in a significant subset. Laboratory analysis indicated elevated inflammatory markers in patients with more severe neurological presentations. Findings suggest a multifactorial pathogenesis involving neuroinflammation, vascular dysfunction, and possible autoimmune responses. Conclusions: The most frequent neurological symptoms were headaches (48.3%), cognitive impairments (41.6%), sleep disorders (40%), and anxiety-depressive symptoms (38.3%). Neuroimaging revealed structural changes in 35% of patients, while neurophysiological testing showed signs of central and peripheral dysfunction in a significant subset. Laboratory analysis indicated elevated inflammatory markers in patients with more severe neurological presentations. Findings suggest a multifactorial pathogenesis involving neuroinflammation, vascular dysfunction, and possible autoimmune responses.