The interaction between stroke and depression is exceptionally intricate, and the pathophysiological mechanisms have not as yet been fully explained [14].
Various studies explored prevalence and risk factors for PSD, but inconstant results were reported relying on the studied subjects, assessment tools, and the diagnostic criteria of depression used [15].
The prevalence of PSD in our study was 60.78%, which was higher than previously reported studies [16,17,18], and in line with other studies, which reported that the prevalence of PSD ranged from 5 to 63% [19] and from 25 to 79% [20]. Differences in reported prevalences of previous studies are likely a result of differences in methods of measurement and a function of the timing of the evaluation [13].
Because of the unfavorable impacts of PSD, it is essential to distinguish risk factors to allow for an early diagnosis and management, in this way diminishing the negative impacts in stroke patients [21].
In the current study, there was no relationship between the demographic data (age and sex) and PSD. The results for the relationship between PSD and demographic data are controversial [22]. Some of the earlier reports are in agreement with our results [5, 23], while others are not [21, 24].
Contrary to our results, it was reported that patients under 50 years old occupy a higher percentage of subjects with depression [23]. Also, it was recognized that younger patients appear to be more attentive about the prognosis of the disease [4, 25].
In an Egyptian study, the authors found that male gender, younger age, and frontal lesions were predictors for post-stroke depression [26].
In another Egyptian study, to detect the depression, anxiety, and personality traits in post-stroke patient, there was no significant relation between demographic data and depression in post-stroke patients [27].
Although smoking and hypertension were established risk factors for development of stroke [28], they were not reported as risk factors for development of PSD [13, 29].
Among our subjects, smoking was related to PSD in univariate and multivariate analysis. This is in accord with a study by Ren and colleagues who reported that the frequency of depression in the smoker group was significantly higher than that in the non-smoker group [30]. In addition, Ren and colleagues reported that, the larger proportion of patients with depression in smokers with acute ischemic stroke may be related to lower vitamin D levels induced by smoking [30].
In our study, patients with post-stroke depression had a significant functional disability in (cognition, physical activity) compared to stroke patients without depression, which was consistent with many previous studies that had reported a significant relationship between disability and post-stroke depression [15, 31,32,33,34].
De Ryck and colleagues [13] conducted a prospective, longitudinal epidemiological study in 135 patients who completed follow-up assessments at 3 months post-stroke; they concluded that the most determining features for depression risk after stroke included reduced mobility and cognitive impairment. Leentjens and colleagues [35] assessed 190 consecutively admitted patients for major depressive disorder 1 month after stroke, and at follow-up after 3, 6, 9, and 12 months, they revealed that disability was associated with PSD. Nys and colleagues [36] studied 143 cases within the first 3 weeks post-stroke; they revealed that cognitive impairment and vascular risk factors were significant predictors of long-term depressive symptoms and quality of life after stroke.
Our study had several limitations. The sample size was small which generates imprecision in some estimates. The study population included both ischemic and hemorrhagic strokes. We did not differentiate types of strokes according to TOAST criteria. In addition, we excluded patients with aphasia because this might limit the generalization of our findings. Moreover, the socioeconomic factors and education were not included in the analysis.