Poststroke depression (PSD) is a significant complication of stroke, affecting a substantial number of patients and contributing to increased disability and mortality. It has been recognized for over a century, but systematic research began in the 1970s. Recent meta-analyses have shown that approximately 31% of stroke patients develop depression within five years of the event. However, these studies often use arbitrary cutoff points on depression rating scales, which may miss important clinical variables such as cognitive impairment. PSD is associated with various neuropsychiatric disorders, including depression, anxiety, apathy, and cognitive dysfunction. The diagnosis of PSD is based on DSM-5 criteria, and vascular depression is a specific form of PSD linked to cerebrovascular disease. Risk factors for PSD include genetic factors, age, gender, medical history, stroke characteristics, and social support. Studies have identified associations between PSD and left frontal or basal ganglia lesions, as well as cognitive impairment and functional disability. The severity of PSD is linked to stroke severity and the degree of physical and cognitive impairment. PSD significantly impacts stroke recovery, with antidepressants showing efficacy in treatment and prevention. Antidepressants may enhance physical and cognitive recovery and improve long-term survival after stroke. PSD is associated with increased mortality, with studies showing that patients with PSD have higher mortality rates compared to those without. Antidepressants have been shown to reduce mortality risk, with a 9-year follow-up study indicating that patients treated with nortriptyline or fluoxetine had higher survival rates than those given placebo. SSRIs may also enhance recovery independent of PSD or its effects on mood. The etiology of PSD involves multiple factors, including psychological, social, and biological mechanisms. Research suggests that alterations in monoamine systems, HPA axis abnormalities, and neuroplasticity may contribute to PSD. Animal studies have provided insights into the neurobiological mechanisms of PSD, including the role of neurotrophic factors and inflammatory cytokines. Treatment of PSD includes antidepressants, which have been shown to be effective in both treatment and prevention. Prevention strategies, such as early antidepressant use, have been demonstrated to reduce the incidence of PSD. Future research should focus on identifying specific mechanisms of PSD and developing targeted interventions. The role of SSRIs in enhancing recovery and the mechanisms underlying increased mortality after PSD are areas of ongoing investigation. Overall, PSD is a complex disorder that requires a bio-psycho-social approach for effective management.Poststroke depression (PSD) is a significant complication of stroke, affecting a substantial number of patients and contributing to increased disability and mortality. It has been recognized for over a century, but systematic research began in the 1970s. Recent meta-analyses have shown that approximately 31% of stroke patients develop depression within five years of the event. However, these studies often use arbitrary cutoff points on depression rating scales, which may miss important clinical variables such as cognitive impairment. PSD is associated with various neuropsychiatric disorders, including depression, anxiety, apathy, and cognitive dysfunction. The diagnosis of PSD is based on DSM-5 criteria, and vascular depression is a specific form of PSD linked to cerebrovascular disease. Risk factors for PSD include genetic factors, age, gender, medical history, stroke characteristics, and social support. Studies have identified associations between PSD and left frontal or basal ganglia lesions, as well as cognitive impairment and functional disability. The severity of PSD is linked to stroke severity and the degree of physical and cognitive impairment. PSD significantly impacts stroke recovery, with antidepressants showing efficacy in treatment and prevention. Antidepressants may enhance physical and cognitive recovery and improve long-term survival after stroke. PSD is associated with increased mortality, with studies showing that patients with PSD have higher mortality rates compared to those without. Antidepressants have been shown to reduce mortality risk, with a 9-year follow-up study indicating that patients treated with nortriptyline or fluoxetine had higher survival rates than those given placebo. SSRIs may also enhance recovery independent of PSD or its effects on mood. The etiology of PSD involves multiple factors, including psychological, social, and biological mechanisms. Research suggests that alterations in monoamine systems, HPA axis abnormalities, and neuroplasticity may contribute to PSD. Animal studies have provided insights into the neurobiological mechanisms of PSD, including the role of neurotrophic factors and inflammatory cytokines. Treatment of PSD includes antidepressants, which have been shown to be effective in both treatment and prevention. Prevention strategies, such as early antidepressant use, have been demonstrated to reduce the incidence of PSD. Future research should focus on identifying specific mechanisms of PSD and developing targeted interventions. The role of SSRIs in enhancing recovery and the mechanisms underlying increased mortality after PSD are areas of ongoing investigation. Overall, PSD is a complex disorder that requires a bio-psycho-social approach for effective management.