Today, in spite of the abundant literature available on this topic, it is still difficult to define the real prevalence rate of PSD, essentially because of the weak concordance across studies. This relevant variability arises not only from methodological problems of the investigations (differences in study populations and the timing of assessments) but also from the complexity in recognition, assessment, and diagnosis of depression.
In fact, as shown in the , there is a large variability of diagnostic tools used for the detection of PSD. In fact, while most of the studies based the diagnosis on cutoff score in different rating scales, others followed a structured interview and the diagnostic standards defined by DSM (Diagnostic and statistical manual of mental disorders)-III, III-R, and IV, and some studies even based their assessment only on clinical findings.
Prevalence of PSD according to time and setting of evaluation
Moreover, assessment of depression in stroke survivors may be often laborious and the risk of inappropriate diagnosis (under- or overdiagnosing) is high (Fedoroff et al 1991
). In fact, PSD may not only be overdiagnosed because of somatic symptoms caused by medical illness, but also underdiagnosed, particularly in patients with cognitive impairment. Another problem, as observed by Schubert and coworkers (1992)
, may be the inadequacy of physicians without a proper psychiatric training (Schubert et al 1992
). The correct attribution of somatic symptoms (psychomotor retardation, and disturbances in appetite, sleep, and sexual interest) to either PSD or stroke is a very relevant problem, because such symptoms may affect rating scales, as Hamilton Depression Rating Scale (HDRS), Montgomery Asberg Depression Rating Scale (MADRS), or Beck Depression Inventory (BDI), and also because they are among DSM criteria. It is important to remember that rating scales were designed to measure depression severity in primary depressive illness, rather than to diagnose depression, in particular for depression in comorbidity. Furthermore, DSM criteria for classification of disorders, (temporal criteria, in particular)are not always satisfied for dysthymia and major depression. So, we found cases diagnosed as major depression even in reports on PSD in settings characterized by short hospital stay, such as stroke units (Kellermann et al 1999
; Berg et al 2001
). Additionally, other relevant points, as evaluation-time after stroke (acute vs. chronic patients) and variability of the study setting (in-patients, outpatients, patients bedridden in rehabilitation structures, community), minimize the possibility of a generalization. Lastly, the problem of aphasia should be kept in mind. The exclusion of aphasic patients, because of the evident difficulty in evaluating depressive symptoms, reported in several of studies examined, may be an important confounding variable (Carson et al 2000
). However, there is no concordance on frequency of PSD in aphasics, observed either in low (15%) (Damecour and Caplan 1991
), in middle (24%) (Laska et al 2007
) and in high percentage (70% at 3 months and 62% at 12 months after stroke) of cases (Kauhanen et al 2000
A recent meta-analysis, evaluating data from studies conducted between 1977 and 2002, estimated the pooled frequency at 33% (95% confidence interval, 29% to 36%) (Hackett et al 2005b
), even if with relevant differences across studies. In particular, the pooled estimate from the population-based studies was equal in the acute and medium-term phases (33%), with a slight increase to 34% in the long-term phase of recovery after stroke. Moreover, there were only slight differences in the pooled frequencies in the hospital-based (acute 36%, medium-term 32%, and long-term 34%) and rehabilitation-based studies (acute 30%, medium 36%, and long-term 34%) over time.
Studies available after the publication of that report confirmed that PSD is generally observed in nearly one third of cases (Vataja et al 2004
; Verdelho et al 2004
; Paolucci et al 2006
; Linden et al 2007
; Townend et al 2007
). However, a certain degree of variability in the percentages was observed in those reports, too. In particular, the percentage of depression observed in the Sidney Stroke Study was lower than in the previous ones (Brodaty et al 2007
). Moreover, recent longitudinal studies observed not only that frequency PSD increases in prevalence over the initial weeks post-stroke, in particular within three months from stroke, despite an improvement in disability (Andersen et al 1994b
; Aben et al 2003
; Paolucci et al 2006
), but also that patients with early onset PSD were not necessarily affected later and vice versa, indicating the dynamic nature of PSD in the early stages.
Only few epidemiological data on vascular depression are available today. Vascular depression is a new diagnostic concept based on hypothesis that chronic ischemic damage is an important cause of depression in the elderly. This concept initially emerged from the finding that patients with late-onset depression had higher rate of encephalomalacia or hyperintensities observed with magnetic resonance imaging (MRI) compared with patients with early-onset depression (Hickie et al 1995
), and was later formulated by Alexopoulos and coworkers in 1997. These authors hypothesized that cerebrovascular disease can predispose, precipitate, or perpetuate a depressive syndrome in older adults (Alexopoulos et al 1997a
). Affected individuals display more apathy, retardation, and lack of insight, and less agitation and guilt than do elderly individuals who are depressed without vascular risk factors, on one hand, and also greater disability and cognitive impairment, on the other (Alexopoulos et al 1997b
). Mast and coworkers reported vascular depression in nearly 35% (35.2%) of patients with cerebrovascular risk factors admitted in geriatric rehabilitation, but without clinical evidence of stroke (Mast et al 2004
). In that study, a positive association was established between depression and increasing percentage of cerebrovascular risk factors (Mast et al 2004
). Furthermore, patients with depression and subcortical vascular lesions have poor response to antidepressants (Simpson et al 1998
), while might be effective dopamine acting agents or norepinephrine enhancing agents (Alexopoulos 2006
). Thus, should vascular depression be recognized as a separate psychiatric disorder or as a diagnostic subtype of major depressive disorder? Indeed, Alexopoulos refined the notion of vascular depression, proposing a depression executive dysfunction (DED) disorder of late-life, but only on the basis of clinical criteria and regardless the etiology (Alexopoulos 2001
), while Taylor and coworkers (2006)
proposed subcortical ischemic depression as specific entity. On the other hand, while the former may be caused by vascular disease, the latter requires a subcortical vascular impairment. Further researches are needed to clarify these and other doubts.