Psychological impairment is a common result of stroke. In particular, depression following stroke, also known as post-stroke depression (PSD), has the highest prevalence, comprising anxiety, apathy, and emotional liability. About 100 years ago, Kraepelin was the first to describe depression following stroke. Until the late 1970s, PSD did not seem to be the focus of attention, the only work of major interest being an empirical examination by Post. Stroke outcome studies in the 1980s, which showed that the presence or absence of depression significantly influenced recovery, caused PSD to become an item of focus once more. Subsequent epidemiological studies demonstrated the relevance of this problem, with prevalence rates of about 40%. The etiology of PSD is explained by various models. Some authors suggest that the results in damage to serotonergic and/or noradrenergic pathways, which in turn results in depression, while others stress the psychoreactive component and suggest that PSD is an expression of lack of "mental processing" following stroke. Both models are justified. There is, however, evidence to suggest that early PSD (days to weeks following stroke) has an organic cause, while reactive components and lack of coping skills increase the likelihood of late-onset PSD (several weeks to months following stroke).
Different studies have used various criteria for the diagnosis of PSD, which does not require the fulfillment of standardized criteria. Most authors refer to the diagnosis of depression according to the latest Diagnostical and Statistical Manual of Mental Disorders (DSM) from the American Psychiatric Association. In the current fourth edition, there exists a classification of an "affective disorder due to medical illness." Further, DSM-IV allows for subclassification of a "major depressive-like episode" (in which the criteria for major depression must be fulfilled, excluding the general medical condition) and "depressive features" (in the case of incomplete fulfillment of the criteria of major depression). Many authors also diagnose PSD when patients lie outside of the range (cut-off point) of various depression rating scales. There are various instruments required for the diagnosis and determination of severity of PSD, although many have not been validated for a specific population of stroke patients.
Aphasia stroke patients are excluded from most studies concerning PSD, since the impediments of language prevent the precise and safe diagnosis of depression in a significant manner. However, PSD is assumed to be higher in aphasic as opposed to non-aphasic patients. There are significant differences in the subgroups of aphasic patients: 63% of patients with non-fluent aphasia had PSD compared with 16% of patients with fluent aphasia. In order to assess depression in aphasic patients in a standardized fashion, so-called visual analog scales (VAS) and visual analog mood scales (VAMS) are applied, using non-verbal and figurative methods that allow only limited illustration of the total scale of emotional-affective change. Sutcliffe and Lincoln developed a questionnaire for the assessment of depression in aphasic patients.
Various authors have described the phenomenology of PSD. The important questions are whether PSD is an independent entity compared with primary ("endogenous") depression, and how to differentiate between symptoms caused by depression and symptoms caused by stroke. In this context, many authors have commented that symptoms such as loss of appetite, weight loss, or sleeping disorders can occur as a result of stroke without the presence of depression. In 1991, Fedoroff et al. showed that all vegetative symptoms apart from weight loss and early-morning waking are significantly more common in depressed stroke patients, i.e. only the latter are not useful for discrimination of PSD.
Other groups differentiated between PSD and primary ("endogenous") depression. Both forms of depression were distinguished by means of a cluster of symptoms, which varies among studies. Vegetative symptoms, such as lack of energy, sleep disturbances, and vegetative expression of fear, were the center of focus in PSD, whereas sadness, anhedonia, and suicidality were much less common in PSD compared with primary depression.
The median prevalence rates of PSD are 40% (20% major PSD, 20% minor PSD) in an inpatient setting and 23% in community settings. There is a wide range of prevalence between studies, from 6% to 79%. The prevalence rate depends on the following factors: classification of PSD (DSM/ICD versus the cut-off values on various scales), time of assessment, and healthcare setting (acute, rehabilitation, community, institution). Moreover, the sample size and the possible effects of therapy within treatment studies must be borne in mind. There are a number of comprehensive reviews that discuss prevalence in detail.
In terms of the etiology of PSD, there is a traditional division between psychological and biological models, similar to that in hypotheses for other depressive illnesses. It should be noted that these dualistic models are not mutually contradictory. An important question is whether depression is reactive following the psychological stress of severe illness. This is suggested by an approximately 50% rate of spontaneous remission in depression following stroke, as shown by Andersen et al. Persisting depression could then be interpreted as lack of psychological processing of disease. A counterargument is provided by a study published by Folstein et al. in 1977, which showed that the prevalence of depression in stroke patients was four to five times higher than that in orthopedic patients with comparable disability.
Ramasubbu et al. also found that 52% of patients with depression following stroke had no significant functional disability, which argues against the hypothesis of a purely reactive etiology of PSD. Many authors perceive PSD as resulting from a disruption in serotonergic or noradrenergic metabolism, This assumption is based on the concept that serotonergic or noradrenergic pathways are impeded by the lesion, with the disturbance resulting in depression. This theory was supported in a small study by Mayberg et al., and disability was related to the activity of serotonin receptors in PSD patients. Studies showing a reduced proiactin response in patients with PSD also favor the serotonergic dysfunction theory.
Since the 1990s, some authors have suggested that there are at least two forms of PSD. Morris and colleagues formed the hypothesis that the various degrees of severity of PSD (major or minor depression) can be viewed as organic or reactive. It was subsequently suggested that both early and late forms of PSD exist, and that these may differ in pathogenesis. In the case of the early form, PSD begins within days or weeks; in the case of the late-onset form, it arises several months to 1 year following the stroke. A recent study suggests that the early form may have an organic cause, whereas the late form may have a reactive etiology. However, other authors do not support this distinction, and the debate continues.
- Huff, W.; Cooper-Mahkorn, D.; Sitzer, M.. Current Medical Literature: Stroke Review, 2004, Vol. 8 Issue 2, p41-50, 10p
Depression and Stroke
- National Institute of Mental Health. (2011). Depression and Stroke. U.S. Department of Health and Human Services.
Reflection Exercise #4
The preceding section contained information about post-stroke depression. Write three case study examples
regarding how you might use the content of this section in your practice.
What percentage of patients with depression following stroke had no significant functional disability? To select and enter your answer go to Test.