Post-Stroke Depression

Post-stroke depression (PSD) refers to the onset of unipolar affective disorder after a stroke. Since cerebrovascular disease is common, and a significant proportion of those affected develop PSD (Krishnan, 2000), this disorder is more widespread than one would think from its familiarity. In fact, the pooled frequency over multiple studies revealed a round-about 30 % prevalence of depression after stroke (Hackett, Pickles & Part, 2014; Ayerbe et al., 2013). Depression post stroke is not only accompanied by a higher mortality rate (Bartoli et al., 2018), but the depressive symptoms are also reversely associated with an increased risk of stroke (Krishnan, 2000).

Regarding the causes of post-stroke depression, there are two hypotheses: the biological and psychological hypothesis. The biological hypothesis explains the depressed mood with neurological changes caused by the stroke including lesion location, neurotransmitter changes or cytokines inflammation. The psychological hypothesis refers to the distal effects related to psychosocial stressors such as adaptation to a life situation, reduced mobility or anxiety (Fang & Cheng, 2013). The two hypotheses are not mutually exclusive. Both hypotheses seem reasonable and have been supported in the past, but research on both of them also received contradictory results. Studies on biological causes and risk factors sometimes fail to be replicated, while studies investigating the psychological hypothesis can not explain why silent infarcts with no obvious psychosocial stressors can also cause depressions (Fang & Cheng, 2013).

Since a conclusive explanation for the development of PSD is not yet available, the individual risk factors give insight into the complex pattern of causes. Several variables have been discussed as a potential risk factor (Robinson, Ricardo & Jorge, 2016) with mixed evidence. Typically, one would assume that a specific lesion location is responsible for the disorder, but unfortunately no consensus has been achieved on this to date (Yu et al., 2004), although the same locations – namely the left hemisphere or subcortical regions like basalganglia lesions (Krishnan, 2000) – are usually the focus of the discussion (Sam, Geo, Lekshmi & Kallivayalil, 2020). However, cognitive impairment (Ayerbe et al., 2013; Ayerbe, Ayis, Rudd, Heuschmann & Wolfe, 2011), as well as activities of daily living, dysphagia and urinary incontinence predicted depression (Ayerbe et al., 2011). Of those, activities of daily living are probably the most supported risk factor (Robinson et al., 2016). It is typically assessed with the Barthel Index, which checks 10 everyday skills and its score ranges from 0-100. Patients with depression after their first stroke demonstrated significantly lower scores on the Barthel Index than first-ever stroke patients (Vojtikiv-Samoilovska & Arsovska, 2018).

Although the complex etiology is not completely disentangled, new attempts for therapeutic interventions have been studied. Antidepressant medication demonstrated therapeutic efficiency (Starkstein & Hayhow, 2019; Krishnan, 2000) and are known to reduce mortality significantly (Robinson et al., 2016). In recent studies, repetitive transcranial magnetic stimulation seems to be a functioning therapeutic approach (Medeiros, Roy, Kontos & Beach, 2020).

Share this article

Discover more articles

Validation ki:e SB-C

We are grateful to announce that we will soon be collaborating in a major new decentralized trial, funded by the Alzheimer Drug Discoveries Foundation (ADDF)


ki:e SB-C

Today, clinical research on early Alzheimer’s Disease (AD) dementia relies on invasive procedures and extended cognitive examinations both for screening and within trial usage. With


Listen to Alzheimer

Alzheimer’s disease (AD) affects speech and language (Cummings, Benson, Hill & Read, 1985). This can be caused by the disease affecting language as a neurocognitive