Mohammed T. Abou-Saleh

Principles and Practice of Geriatric Psychiatry.Editors: Professor John R. M. Copeland, Dr Mohammed T. Abou-Saleh and Professor Dan G. BlazerCopyright & 2002 John Wiley & Sons LtdPrint ISBN 0-471-98197-4 Online ISBN 0-470-84641-075bDepression after StrokePeter Knapp and Allan HouseUniversity of Leeds, UKIt is now accepted that stroke patients have high rates of all typesof depressive disorder. However, estimates of the prevalence ofdepression within the first month of stroke vary greatly 1,2 ,according to the type of measure used and the way the samplewas derived. The consensus seems to be that 20–25% of patientsafter stroke will suffer a major depressive disorder within the firstmonth 3 . Rates of depression later on after stroke are less certain,because of patient attrition in studies. Depression remits in somepatients, while in others it persists: one study reported that 50% ofthose depressed within 3 weeks of stroke remained depressed 1year later 4 . Depression not only affects quality of life: patientswith depression after stroke may be at greater risk of mortality 5 ,cognitive impairment 6 and poorer functional or social recovery 7,8 .There are claims that post-stroke depression is a distinct subtype9 . There is little unequivocal evidence to support this claim,since psychological and biological symptoms reported by patientsare found in depression seen in non-stroke patients 10 . What doesappear to be distinctive is the increased prevalence of persistentcrying (emotionality) among stroke patients. A small number ofpatients suffer pathological laughing and crying, a syndrome whichis probably neurological in origin, in which emotional expressionarises after minor provocation that often appears meaningless 11 .Amore common syndrome, emotionalism, is also characterized byincreased tearfulness, but is more complex. The emotionalepisodes are provoked by meaningful stimuli, but the crying ischaracterized by a lack of warning and control. There appears tobe a psychological component to its origin 12 . Emotionalism isassociated with an increased risk of depression 13 , but patients withemotionalism may be at greater risk of psychological problemsnot explained by concurrent depression 14 . This syndrome isprobably under-recognized.Reaching a diagnosis of depression after stroke can becomplicated by the presence of problems such as communicativeor cognitive impairment 15 . Patients with expressive communicationproblems can often be assessed by the careful use of closedquestions. The assessment of those with receptive communicationproblems or significant cognitive impairment is much morecomplex: a non-language-based assessment of depression showspromise but is insufficiently reliable in its present form foraccurate diagnosis 16 . The diagnosis of depression might also beconfused by facial palsy and a disturbance of speech prosody(rhythm in speech), both of which are relatively common afterstroke and which give the patient the appearance of a person withdepression 17 . The dexamethasone suppression test is not sufficientlysensitive to be used as a diagnostic tool 18 .The high rate of depression reported in some stroke researchhas led to the suggestion that the neurological damage is a keyfactor in its aetiology 19 . As a result, many studies have attemptedto link depression after stroke with lesion location. A series ofstudies proposed, first, that patients with left hemisphere lesionswere at greater risk of depression 20 , and later, that those with leftanterior lesions were at most risk 21,22 . Other researchers 23–25 havenot replicated these findings, suggesting that patient sampling andthe timing of assessment might explain the differences.Even if lesion location is associated with greater risk ofdepression, the context of this relationship is important. First, itis clear that stroke patients with all sorts of lesions can sufferdepression 9 , so factors other than lesion location must also be atwork. Second, stroke location is extremely varied 26 , so those withany particular lesion (such as left anterior lesions) will be aminority of patients, making the attributable risk due to any onetype of lesion small. Last, although the rate of depression instroke patients is higher than in age-matched non-stroke controls,it is about the same rate as in patients with non-neurologicaldisabling illness 17,27 , suggesting that non-neurological factors areas important. Relevant non-neurological aetiological factors arelikely to include the threat of disability and a sense of loss.That psychosocial factors are likely to be relevant to both theonset and persistence of depression has been illustrated in severalstudies. For example, one study found that depression at 4months after stroke onset was commoner among those withgreater disability, those who were divorced and those with higherpre-stroke alcohol intake 24 . Depression is more likely in thosepatients who perceive their stroke as a greater threat, and in thosewho have fewer psychological resources to deal with that threat.Patients with depression after stroke might be considered forpharmacological or psychological treatments. Two small trialsshowed beneficial effects of antidepressants, although both studieshad high rates of patient dropout 28,29 . The evidence for treatingemotionalism with antidepressants is rather stronger—bothtricyclics and SSRIs have been shown to reduce the frequencyof crying episodes 30–32 . There is no good trial evidence to drawupon in assessing whether psychological interventions are effectivein treating depression after stroke 33 .Some services aim to intervene in an attempt to prevent theonset of depression after stroke. A recent small trial found thatpatients prescribed mianserin as a prophylactic had greaterimprovement in depression scores, but the drug did not reducerates of major depression 6 months after stroke 34 . A variety ofpreventive psychosocial interventions have been evaluated inclinical trials. The interventions, including education, leisuretherapy and specialist stroke nurse visits, have shown no effect inreducing the prevalence of depression. However, many of thetrials are small and imperfectly designed, so the conclusion shouldbe lack of evidence, rather than evidence of no effect 35 .Our own recently completed study suggests that a briefpsychological treatment (problem-solving therapy) may be beneficial36,37 . Patients who received therapy visits from a communityPrinciples and Practice of Geriatric Psychiatry, 2nd edn. Edited by J. R. M. Copeland, M. T. Abou-Saleh and D. G. Blazer&2002 John Wiley & Sons, Ltd