Poststroke depression

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					                                                                                                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                                       S  troke 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.
                                                             Hospital Anxiety and Depression Scale
  Psychosocial effects of stroke
                                                             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,
                                                             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
                                                             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
  but another found otherwise. 26 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

832   Reprinted 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
nication problems and are probably the most           behaviour therapy (CBT) results are encour-
                                                                                                             Pharmacological management
useful for screening stroke patients without          aging but these treatments are not always              Selective serotonin reuptake inhibitors
communication difficulties in the rehabilita-         accessible. Language limitations and cogni-            (SSRIs) are the most commonly used drugs
tion or community setting. Those who score            tion issues in stroke patients can interfere           for PSD. Tricyclic antidepressants (TCAs) are
more than eight for depression on the HADS            with psychotherapy interventions including             less commonly used and inhibit the uptake
should be further assessed.                           CBT. In the weeks and months after the                 of both serotonin and noradrenaline. There
    Full history, examination, and patient and        stroke, the residual cognitive and behav-              is no high level evidence to suggest SSRIs
family reports are important. The DSM IV              ioural deficits are common causes for failure          are superior to TCAs. In a double blind,
criteria for major depression are listed in           to return to premorbid levels of interper-             placebo controlled study, fluoxetine was
Table 2. The normal exclusion of symptoms             sonal, vocational and recreational                     compared with nortriptyline – the response
due to an underlying medical condition is             functioning. Patients with behavioural prob-           was adequate with both drugs, but only the
waived in PSD.30 Older patients may experi-           lems that are difficult to manage may be               nortriptyline group improved functional inde-
ence depression without sadness, but they             treated with success in specialised care               pendence. 32 However, SSRIs have a safer
may present with anxiety and a general                where behaviour is monitored, assessed                 side effect profile, a relatively quick onset of
sense of hopelessness.                                and subjected to positive or negative rein-            action of 7–10 days, and good anxiolytic
                                                      forcers. In such patients, giving feedback             effects making them first line antidepres-
Treatment                                             and support assists in engaging the patient            sant, especially in the elderly.
Treatment for PSD involves a combination              in rehabilitation treatment and improves                   Within a class, there is no hard data to
of patient education, antidepressant medica-          compliance.                                            recommend one drug over another for PSD,
tion, behavioural strategies and                         In practice, antidepressants are often the          however, a recent review 32 suggested an
psychotherapy.                                        most pragmatic solution, with more involved            optimum regimen for sertraline with a start-
   A number of psychosocial interventions             psychotherapy reserved for antidepressant              ing dose of 50 mg per day, which can be
have been studied. These interventions                resistant cases or those who are unable to             increased to 100 mg per day in 2 weeks.
included controlled trials of counselling,            tolerate medication. Patients still benefit            There is little benefit from a higher dosage,
occupational therapy for leisure, and social          from pyschoeducation and learning new                  and if there is no benefit after 4–6 weeks on
                                                                                                             100 mg, then it should be discontinued. It
 Table 2. DSM IV criteria for major depression                                                               should be continued for at least 6 months
                                                                                                             and slowly weaned but can continue if
 The American Psychiatric Association Diagnostic and Statistical Manual of Mental                            symptoms recur. Sertraline is also effective
 Disorders (4th edn) (DSM-IV) list the following criteria for diagnosis of depression:                       in the treatment of emotionalism following
 Five or more of the following symptoms persisting over a 2 week period causing                              stroke. Electroconvulsive therapy has been
 clinically important distress or impairing work, social or personal functioning (with                       used to treat refractory severe PSD but is
 depressed mood or decreased interest or pleasure as one of the five):                                       limited due to side effects.
 • depressed mood most of the day, occurring most days (subjective or observed)
                                                                                                             Nonpharmacological treatment
 • markedly diminished interest or pleasure most of the day, nearly every day
                                                                                                             Psychosocial management strategies
 • significant weight or appetite change
 • insomnia or hypersomnia                                                                                   • education about depression to the
 • psychomotor agitation or retardation (observable by others)                                                  patient, carer and family
                                                                                                             • managing sleep-wake cycles
 • fatigue or loss of energy
                                                                                                             • improving nutrition
 • feelings of worthlessness or inappropriate guilt                                                          • anxiety management techniques
 • diminished ability to concentrate or make decisions                                                       • problem solving techniques
 • recurring thoughts of death or suicide plans                                                              • behavioural programs to target specific
                                                                                                                issues (eg. apathy, aggression)
 Note: the normal exclusion of symptoms due to an underlying medical condition is waived in PSD30            • cognitive remediation (Table 1)
                                                                                                             • compensatory rehabilitation strategies
                                                                                                                for specific physical problems (eg. spas-

                                                                                      Reprinted from Australian Family Physician Vol. 33, No. 10, October 2004   833
Clinical practice: Poststroke depression

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834     Reprinted from Australian Family Physician Vol. 33, No. 10, October 2004