👤 Yu N Bykov

Post-stroke depression (PSD) is a common and clinically significant stroke complication associated with impaired rehabilitation potential and increased mortality risk. The prevalence of PSD varies from 25% to 59% depending on the duration of observation, reaching a peak in the first years after a stroke. The pathogenesis of PSD results from a complex interplay of biological and psychological factors that extends well beyond monoamine deficiency. Damage to monoaminergic pathways, neuroinflammation, hypothalamic-pituitary-adrenal axis dysfunction, decreased neuroplasticity (including BDNF deficiency), and impaired neural network integrity play a key role. The clinical presentation includes a complex of affective (apathy, anhedonia), cognitive (impaired executive functions), and dyssomnia disorders. While selective serotonin reuptake inhibitors remain the first choice for treatment of PSD, the current therapeutic approach requires targeting all pathogenesis links. A promising direction is the use of antidepressants with a complex mechanism of action, such as the original fluvoxamine, which combines serotonergic effects with anti-inflammatory and neuroprotective properties through sigma-1 receptor agonism. Optimizing PSD treatment is possible through a personalized approach that includes thorough screening and comprehensive correction of identified disorders. Show less

Post-stroke depression (PSD) is a common and clinically significant complication of stroke, associated with worse rehabilitation potential and increased mortality risk. The prevalence of PSD varies from 25% to 59%, depending on the duration of follow-up, peaking in the first years after the stroke event. The pathogenesis of PSD results from a complex interplay of biological and psychological factors, extending far beyond monoamine deficiency. Key roles are played by damage to monoaminergic pathways, neuroinflammation, dysfunction of the hypothalamic-pituitary-adrenal axis, reduced neuroplasticity (including BDNF deficit), and impaired integrity of neuronal networks. The clinical picture is characterized by a complex of affective (apathy, anhedonia), cognitive (executive dysfunction), and dyssomnic disorders. Although selective serotonin reuptake inhibitors remain the first-line treatment, the modern therapeutic approach to PSD requires targeting all components of its pathogenesis. A promising direction is the use of antidepressants with a multimodal mechanism of action, such as the original drug fluvoxamine, which combines serotonergic effects with anti-inflammatory and neuroprotective properties via sigma-1 (σ1) receptor agonism. Optimizing PSD treatment is achievable through the implementation of a personalized approach, including long-term screening and comprehensive management of the identified disorders. Show less