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(Stroke. 2006;37:2854.)
© 2006 American Heart Association, Inc.
Research Reports |
From the National Stroke Research Institute (S.L.P., H.M.D., J.W.S., A.G.T.), Austin Health, Heidelberg Heights, Victoria, Australia; the Department of Medicine (S.L.P., H.M.D., R.A.L.M., A.G.T.), University of Melbourne, Melbourne, Australia; the Neurology Department (H.M.D., R.A.L.M., A.G.T.), Austin Health, Heidelberg, Australia; Gosford Hospital and the University of Newcastle (J.W.S.), Newcastle, Australia; and the Department of Epidemiology and Preventative Medicine (A.G.T.), Monash University, Monash, Australia.
Correspondence to Seana L. Paul, BSc (Hons), National Stroke Research Institute, Level 1, Neurosciences Building, Repatriation Hospital Heidelberg, Austin Health, 300 Waterdale Rd., Heidelberg Heights, Victoria, Australia, 3081. E-mail seana.paul{at}utas.edu.au
| Abstract |
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Methods Five-year survivors from a prospective community-based stroke incidence study were assessed for depression with the Irritability, Depression and Anxiety Scale. Medications indicated primarily for treatment of depression were recorded.
Results At 5-years poststroke, 441 (45%) of 978 incident cases were alive (mean age=74±15 years, 49% female). Seventeen percent of those assessed were depressed. Twenty-two percent with depression were taking an antidepressant medication. Of those taking an antidepressant, 72% were not depressed.
Conclusions Although nearly one-fifth of survivors were depressed, few were taking antidepressants. Further exploration of this low level of treatment is warranted.
Key Words: depression epidemiology psych and behavior treatment
| Introduction |
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Depression is a treatable condition in the general population, yet available data indicate that only a minority of depressed patients with stroke take antidepressants during the first year poststroke.4 There are no longer-term treatment data about poststroke depression.
We aimed to assess the prevalence of depression and antidepressant medication use at 5-years poststroke in a community-based population.
| Methods |
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Depression was assessed using the 5 depression items from the Irritability, Depression and Anxiety (IDA) scale.7 Because depression cannot reliably be assessed by proxy, those with cognitive or communication problems were not assessed. Depression was classified in those with scores
7. The IDA depression subscale has external validity against the Montgomery-Åsberg Depression Rating Scale (Spearman rank correlation, r=0.71) and low false-positive (2%) and false-negative (4%) diagnoses.8 The IDA is advantageous for assessing poststroke mood disorder because it does not include somatic symptoms that might be mimicked by stroke.
All currently prescribed medications were recorded. We assumed that medications were used for their primary indication as listed on the Australian MIMS online medication database.9
Data Analysis
Differences between those assessed and not assessed were determined using Student t test and Fisher exact test. Significance was set at P
0.05 (2-sided).
Ethics
The North East Melbourne Stroke Incidence Study was approved by ethics committees at each participating institution. Informed consent was obtained.
| Results |
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Depression was present in 17% of 5-year survivors (Table). Complete medication data were available for 359 (81%). Of these, 56 (16%) were taking an antidepressant. Among individuals with complete IDA and medication data (n=280), 36 (13%) were taking an antidepressant. Of depressed individuals (n=46), 22% (n=10) were taking an antidepressant. Seventy-two percent (n=26) taking an antidepressant were not depressed. Among those unable to be interviewed because of aphasia or cognitive impairment (n=64), 26% were taking an antidepressant, a significantly greater (P<0.01) proportion than among those able to respond (13%).
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| Discussion |
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Only 22% of 5-year survivors were taking an antidepressant compared with 49% in a recent Swedish study.4 This low figure could indicate reluctance to prescribe antidepressants to patients with stroke because of uncertain efficacy and potential side effects, undiagnosed depression, prescription of nonpharmacologic treatments, or treatment cessation because of poor efficacy or side effects. Future studies would be strengthened by assessment of both pharmacological and nonpharmacologic treatments.
Interestingly, 72% of those taking an antidepressant were not depressed, providing indirect evidence of antidepressants efficacy in many patients. Another possibility is that many were prescribed antidepressants for other indications such as pain. Only 28% of depressed individuals were taking antidepressants similar to 3 months poststroke in Sweden.4 Potential explanations include ineffective treatment possibly attributable to recent treatment initiation, poor compliance, or insufficient dosage. However, this is speculative because treatment duration and dosage were not noted.
Interestingly, those unable to complete the IDA because of dysphasia or cognitive impairment were more often taking antidepressants than those able to respond. The reasons for this finding are uncertain.
Limitations to this study include lack of data on medication doses, duration, and indication. We assumed medications were taken for their primary indication, perhaps overestimating the treatment of depression and its effectiveness. Second, because those requiring a proxy were unable to complete the IDA, the prevalence of depression may be under- or overestimated. Documenting antidepressant use among those requiring a proxy provided some indication of the presence of mood disorders in this group. Furthermore, the IDA is a screening tool for mood disorder. It was impractical to confirm depression with a comprehensive psychiatric interview. Finally, because overseas-born patients were assessed less often, findings may be limited to those whose first language is English.
Conclusions
Depression was present in nearly 20% of all survivors. Use of antidepressants was low. Inadequate detection and treatment of poststroke depression may underlie these findings. Increased awareness of poststroke depression may lead to more effective treatment.
| Acknowledgments |
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Sources of Funding
This work was supported by grants from the National Health and Medical Research Council, the Victorian Health Promotion Foundation, the Foundation for High Blood Pressure Research, and the National Stroke Foundation. S.L.P. was supported by a VicHealth Public Health Post-Graduate Scholarship.
Disclosures
None.
| Footnotes |
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Received June 14, 2006; accepted July 7, 2006.
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