Clinical update • CLINICAL PRACTICE Poststroke depression Fary Khan, MBBS, FAFRM (RACP), is Lecturer, Rehabilitation Studies, Department of Medicine, University of Melbourne, neuro-rehabilitation physician, the Melbourne Extended Care and Rehabilitation Centre, the Royal Melbourne Hospital, and Head, Orthopaedic and Musculoskeletal Unit, Caufield General Medical Centre, Victoria. BACKGROUND Stroke is the leading cause of disability in PSD and functional recovery Poststroke depression (PSD) is common adults and is frequently associated with neu- and often unrecognised. The diagnosis ropsychiatric symptoms such as depressed Poststroke depression is associated with can be difficult due to deficits of stroke mood, generalised anxiety and apathy. The poor functional and psychosocial outcome.8 such as impaired self reporting and prevalence of poststroke depression (PSD) Although there is no long term data on the cognition, poor insight and dysphasia. varies from 25–79% due to the differences in direct effect of PSD on cost of care there are Untreated PSD can interfere with recovery various study diagnostic criteria, selection of reports of: and adversely affect functional and social patients, and the time elapsed since the • prolonged inpatient hospital length of stay4 outcomes. stroke. • greater disability with activities of daily Clinical depression is a common complica- living9 OBJECTIVE tion, and in some long term studies was • severe physical impairment10 This article outlines the diagnosis, shown to persist up to 3 years following • poor cognitive function11 pathophysiology and treatment for PSD. stroke.1,2 Depression decreases patients’ par- • poor participation in rehabilitation11 ticipation in rehabilitation and impairs • reduced social activity1 DISCUSSION functional recovery, community reintegration • poor language function1,2 The natural history of PSD suggests that and long term outcomes.3 It increases the cost • failure to return to work8, and most PSD is not immediate but develops of treatment and burden of care to families. • a higher mortality at 10 years.12 over months with peak prevalence The diagnosis of PSD can be difficult, between 6 and 24 months, and in some and is reported to have been missed in What causes PSD? cases persists up to 3 years following 50–80% of cases by nonpsychiatric physi- The aetiology of PSD is not well understood. stroke. General practitioners and treating cians.4 Longitudinal studies on the natural Different mechanisms for PSD may be specialists need to actively monitor history of PSD progression show that most involved in the aetiology of stroke over time patients for PSD. While antidepressant depression is not immediate but develops and this has implications for treatment. medication is the mainstay of treatment over months with peak prevalence between Depression may be a result of: for PSD, psychotherapeutic interventions 6–24 months poststroke.5 Most major • a biologic effect of brain damage are important. Treatment should include depression remits in the 1–2 years following • a reaction to the losses caused by stroke, patient and family education, re- stroke, either spontaneously having run its or establishment of sleep pattern, addressing course or through treatment – it is rarely • a combination of these factors.13 functional difficulties, increasing chronic.6 Depression also occurs in 40% of Initially PSD may be caused by a neurophysio- community participation, improving diet primary care givers of patients with stroke logic imbalance and depression that develops and regular exercise. and is easily missed.7 later may be caused by psychological factors.1 Reprinted from Australian Family Physician Vol. 33, No. 10, October 2004 831 Clinical practice: Poststroke depression Biological effects of stroke found to be more depressed overall,2 younger be independent of the presence of depres- During the acute brain infarction there is patients tended to be depressed in the acute sion. However, depressed patients perform decreased monoamine synthesis (enzyme early stages following stroke.28 poorly in areas of cognition2 and have poorer inhibition during ischaemia) resulting in verbal abilities.29 Apathy is also seen in stroke decreased 5-HT levels. These have been Diagnosis patients and may coexist with emotional and implicated in altered mood,14 sleep, and The diagnosis of PSD may be difficult due to cognitive poststroke disturbances. appetite.15 The use of serotonergic agents deficits in limited patient self report, impaired Symptoms of depression may be due to has therefore been suggested to augment cognition, poor insight and aphasia. Features an underlying medical condition or cognitive stroke recovery.16 Stroke patients with such as anosognosia, fatigue, emotionalism, deficits rather than an underlying mood disor- depression may also have: apathy and intellectual decline can also limit a der. Differential diagnoses include organic • altered cortical receptor activity17 patient’s ability to express themself. This brain syndrome, side effects of medications, • altered concentration of cerebrospinal may result in discrepancy between self rated sepsis and hypothyroidism. fluid neurotransmitter metabolites18 depression and observer rated depression. A number of standardised tests are used • electrophysiological abnormalities19, and Distinguishing between cognitive decline to screen patients for depression or to • decreased cerebral blood flow.20 due to stroke and poor cognitive function monitor their response to treatment, but Lesions in the left frontal lobe or basal secondary to depression can be difficult in these should not be used for diagnosis in iso- ganglia are reported to cause more PSD than this group of patients. Stroke is followed by lation (Table 1). The Hospital Anxiety and other brain areas.21 There is no clear associa- decline in cognitive function that appears to Depression Scale (HADS) and the General tion between the volume of the lesion22 and cortical/subcortical atrophy23 with the type or Table 1. Screening tools for depression and recommendations33 severity of depressive symptoms. Psychosocial effects of stroke Hospital Anxiety and Depression Scale Seven items each measuring depression and anxiety. Originally used in 100 patients Despite successful rehabilitation for mobility 16–65 years of age in outpatient settings. It has high reliability and validity, and only and self care skills, social reintegration and 1% false positives and negatives. Correlations with psychiatric ratings were 0.79 for depression and 0.54 for anxiety. Recommended by the British Stroke Research group life satisfaction remain an issue for many stroke patients. Stroke is associated with sig- Beck Depression Inventory nificant psychosocial difficulties that can Recommended scale in integrated pathway of PSD. Twenty-one item self report impact on the development of depression instrument with low reliance on somatic items. Respondents are asked how they have been feeling over the past 2 weeks. Each item is rated on a 4 point scale, including: ranging from 0–3. A cut off of 14/15 is indicative of depression. It has good reliability • grief at loss of function, loss of indepen- and validity and has a positive predictive value of 0.54 and negative predictive value dence or loss of employment of 0.99, and few false negatives. It has high internal consistency. Factor analysis can • financial difficulties discriminate between those with cognitive and noncognitive dimensions. The • social isolation advantage in stroke patients is the low demand on memory • poor self esteem, and General Health Questionnaire-28 (GHQ-28) • relationship or sexual difficulties. Uses 28 items for somatic symptoms, anxiety, insomnia, social dysfunction and Early factors predictive of PSD include: severe depression. It is widely used, acceptable for the elderly patients, sensitive to • aphasia at 3–12 months poststroke the effects of intervention and recommended by the British Stroke Research group. It • older age has good reliability and validity. Coefficient correlations between GHQ-28 and interview measures are 0.67 and 0.83 with a median of 0.76. The sensitivity ranged • limited social supports from 0.44–1.0 and specificity ranged from 0.7–0.93 • living alone, and Depression, Anxiety, Stress Scale (DASS) • a previous history of psychiatric This dimensional scale contains 42 questions, with 14 items subdivided into 2–5 problems.24 items. It assesses self reports on depression, hopelessness, anxiety and stress levels. There is conflicting evidence regarding DASS has high internal consistency and yields meaningful discriminations in a gender and PSD. In one study, women were variety of settings found to be more depressed after stroke,25 26 but another found otherwise. When fol- Other depression screening tools include: Hospital Stroke Aphasic Depression lowed up, the male PSD patients had a Questionnaire, Brief Assessment Schedule for Depression Cards, Geriatric Depression poorer prognosis compared with women Scale, Signs of Depression Scale, and Visual Analogue Mood Scale patients.27 Although older patients were 832Reprinted from Australian Family Physician Vol. 33, No. 10, October 2004 Clinical practice: Poststroke depression Health Questionnaire (GHQ) are the best work support; they have not demonstrated coping skills as detailed below. validated scales in patients without commu- any clear benefit on mood state.31 Cognitive Pharmacological management nication problems and are probably the most behaviour therapy (CBT)