Poststroke depression and major depressive disorder: the same or separate disorders?

Poststroke depression is considered one of the most frequent neuropsychiatric consequence of stroke, with up to one-third of stroke survivors experiencing this complication at any one time after stroke (Robinson, 2001a; Gainotti and Marra, 2002; Towfighi et al., 2017). Poststroke depression can have important consequences as it is associated with reduced functional recovery, impaired cognitive function, and increasedmortality (Robinson, 2001a). Poststroke depression appears to be triggered by or linked to the ischemic event, as depression often occurs within 3months of a stroke (Paolucci et al., 2006). The mechanisms explaining how stroke can trigger depression are still debated (Gainotti and Marra, 2002). Two main competing theories have emerged in the literature: (i) a psychological theory suggesting that psychosocial adjustment required by the complications of the disease could lead to the onset of poststroke depression, and (ii) a neurobiological theory hypothesizing that poststroke depression results from specific neurobiological factors related to brain damage, and particularly by lesions affecting the left frontal cortex, left basal ganglia, or brainstem (Robinson and Jorge, 2016). Both major depressive disorder and poststroke depression are currently diagnosed following the same set of criteria. Because major depressive disorder is an heterogeneous brain disorder whose pathophysiology is currently viewed as resulting from variable contributions from both biological and psychosocial factors (Hoertel et al., 2013; Malhi and Mann, 2018; Hoertel et al., 2019), another important issue raised by this debate is whether poststroke depression andmajor depressive disorder should be considered the same or separate disorders. A means of contributing to addressing these issues includes a better knowledge of clinical risk factors of poststroke depression. Perrain et al. (2020) performed a meta-analysis of previously reported putative clinical risk factors of poststroke depression, including gender, social support, marital status, previous history of depression, early depressive symptoms, cognitive impairment, previous history of stroke, disability, aphasia, lesion side, pain, alcohol consumption, and tobacco consumption. Out of these 13 potential risk factors, only five reached statistical significance in random-effects models: previous history of depression (RR= 2.19, 95% CI 1.52–3.15), disability (RR= 2.00, 95% CI 1.58– 2.52), previous history of stroke (RR= 1.68, 95% CI 1.06–2.66), aphasia (RR= 1.47, 95% CI 1.13– 1.91), and female gender (RR= 1.35, 95% CI 1.14– 1.61). Limitations are the limited number of studies included since 2005 (i.e., 18) and the significant variation in depression assessment time across studies (from 2weeks to 6months). The striking result of this meta-analysis is that both known risk factors for major depressive disorder and potential neurologicalrelated risk factors were found to be predictive of poststroke depression, with a tendency toward a greater pooled effect size for depressive-related factors compared to others. These results support an association between functional deficits and poststroke depression, indirectly suggesting that poststroke depressionmay be a psychological reaction to these deficits (Ng et al., 1995). In addition, several risk factors for poststroke depression are also risk factors for major depressive disorder without stroke, such as past psychiatric of depression, disability, and female gender. Finally, the significant relationship between level of impairment and severity of poststroke depression may be underestimated as it has been shown that this relationship is not direct but rather mediated by the patient's perception of the severity of impairment and the meaning that the patient attributes to the deficits (Gainotti, 2003). In contrast, results from the meta-analysis of Perrain et al. (2020) and several prior studies suggest that poststroke depression may not be merely a psychological response to a life-threatening event or physical impairment and may be underpinned by specific neurobiological causes. First, the results of this meta-analysis support that aphasia and prior history of stroke are significant predictors of poststroke depression. Although this result may be compatible with the psychological theory of poststroke depression, it may also be in line with the neuroanatomical model of poststroke depression proposed at the beginning of the 1980s by Robinson et al. (2001b), which postulates that lesions affecting the anterior parts of the left hemisphere (frontal cortex and underlying basal ganglia) could increase the risk of poststroke depression. However, a systematic International Psychogeriatrics (2020), 32:11, 1279–1281 © International Psychogeriatric Association 2020