Elsevier

Biological Psychiatry

Volume 54, Issue 3, 1 August 2003, Pages 376-387
Biological Psychiatry

Mood disorders and medical illness
Poststroke depression: prevalence, diagnosis, treatment, and disease progression

https://doi.org/10.1016/S0006-3223(03)00423-2Get rights and content

Abstract

In recent years, poststroke depression has attracted worldwide interest. This review focuses on the major research themes that have emerged. Pooled data from studies conducted throughout the world have found prevalence rates for major depression of 19.3% among hospitalized patients and 23.3% among outpatient samples. The diagnosis of poststroke depression is most appropriately based on a structured mental state exam and DSM-IV criteria for depression due to stroke with major depressive–like episode or depressive features. Rarely, poststroke patients may also develop bipolar mood disorder. The treatment of poststroke depression has been examined in several placebo-controlled randomized clinical trials with both nortriptyline and citalopram showing efficacy. The progression of recovery following stroke can be altered by treating depression, which has been shown to improve recovery in activities of daily living and cognitive impairment and to decrease mortality. In addition, two studies have demonstrated that poststroke depression can be prevented using antidepressant medication, which also decreases the frequency of associated physical illness. Furthermore, two studies have shown that premorbid depression can significantly increase the risk of stroke over the subsequent 10–15 years. The mechanisms underlying the association of cerebrovascular diseases and mood disorder are important areas for future investigation.

Introduction

The World Health Organization (1989) defines stroke as “rapidly developing clinical signs of focal (or global) disturbance of cerebral function, with symptoms lasting more than 24 hours (unless interrupted by surgery or death), with no apparent nonvascular cause.” Stroke is the most common serious neurologic disorder in the world and the third leading cause of mortality among adults. It accounts for half of all the acute hospitalizations for neurologic disease (Hachinski and Norris 1985). The age-specific incidence of stroke varies dramatically over the life course. The annual incidence in developed countries around the world for those aged 55–64 ranges from 10–20 per 10,000, whereas among those over age 85 the annual incidence is almost 200 per 10,000 (Bonita 1992).

Over the past 20 years, there has been a substantial decline in stroke incidence and mortality in most industrial countries Bonita et al 1990, McGovern et al 1992. This decline appears to have been attributable to improved control of hypertension. The association of depression with stroke has been recognized by clinicians for almost 100 years, but it is only within the past 25 years that systematic studies of depression following stroke have been conducted. This review focuses on the major themes that have emerged in the study of poststroke mood disorders.

Section snippets

Controversies related to the diagnosis of poststroke depression

Investigators of depression associated with physical illness have debated the most appropriate method for the diagnosis of depression when some symptoms (e.g., sleep or appetite disturbance) could result from the physical illness (Cohen-Cole and Stoudemire 1987). Cohen-Cole and Stoudemire reported that four approaches have been used to assess depression in the physically ill. These approaches are the inclusive approach in which depressive diagnostic symptoms are counted regardless of whether

Prevalence of poststroke depression

Over the past 10 years, a large number of studies have been published examining the prevalence of poststroke depression. The results of these studies are summarized in Table 2. Compared with prevalence rates for major depression in the general population of 10% over the previous 12 months (Kessler et al 1994), the rates in the stroke patients are significantly higher. The rates are about the same as patients with myocardial infarction (i.e., 18%–20%) Carney et al 1988, Forrester et al 1992,

Pathogenesis of poststroke unipolar and bipolar disorder

The cause of poststroke depression has been associated with left anterior lesion location in numerous independent studies Astrom et al 1993, Herrmann and Walesch 1993, Morris et al 1996, Robinson et al 1984, Vataja et al 2001. Although a meta-analysis by Carson et al (2000) of poststroke depression and lesion location and a subsequent study by Gainotti et al (2001) failed to find a significant association, a subsequent meta analysis examining interhemispheric lesion location and time since

Progression of disease—effect of depression on recovery

Numerous investigators have reported that severity of poststroke depression was associated with severity of impairment in activities of daily living (ADL) Feibel and Springer 1982, Herrmann et al 1998, Ingles et al 1999, Kauhanen et al 1999, Kotila et al 1984, Morris et al 1994, Parikh et al 1987, Pohjasvaara et al 1998, Ramasubbu 1994, Sinyor et al 1986, Wade et al 1987. Several investigators have also studied the effect of poststroke depression on recovery in ADLs Paolucci et al 1999, Parikh

Treatment of poststroke depression

There have been at least five placebo-controlled randomized double-blind treatment studies on the efficacy of single antidepressant treatment of poststroke depression. The first, published by Lipsey et al (1984), examined 14 patients treated with nortriptyline and 20 patients given placebo. The 11 patients treated with nortriptyline who completed the 6-week study showed significantly greater improvement in their scores on the Hamilton Rating Scale for Depression (Ham-D; Hamilton 1960) than did

Prevention of poststroke depression

Based on the significant amount of data demonstrating that poststroke depression is associated with poorer outcome in cognitive function, ADLs, and survival, it is logical to ask whether prevention of depression using antidepressant medication or psychologic therapy might lead to a better outcome than the standard treatment of waiting for depression to occur. There have been three studies thus far that have examined this strategy. The first was by Palomaki et al (1999), who administered

Does depression lead to stroke?

Because this paper has focused on the effect of poststroke depression on recovery and survival from stroke, it is only appropriate to end the discussion with an assessment of whether depression (even preceding a stroke) might lead to the development of a stroke. It is, after all, possible that premorbid depressive disorder might lead to increased frequency of stroke. Two large epidemiologic studies support this hypothesis.

May et al (2002) reported on a prospective study of 2201 men aged 45–59

Future directions

There are numerous areas for future research regarding poststroke depression. Probably the most important is the mechanism by which antidepressants reduce mortality among stroke patients. Similarly, the mechanism of enhanced recovery and the optimal medication to use are also important areas for research. We and other investigators continue to examine the mechanism of poststroke depression and poststroke bipolar disorder. The identification of psychiatric disorder, which profoundly changes the

Acknowledgements

Aspects of this work were presented at the conference, “The Diagnosis and Treatment of Mood Disorders in the Medically Ill,” November 12–13, 2002 in Washington, DC. The conference was sponsored by the Depression and Bipolar Support Alliance through unrestricted educational grants provided by Abbott Laboratories, Bristol-Myers Squibb Company, Cyberonics, Inc., Eli Lilly and Company, Forest Laboratories, Inc., GlaxoSmithKline, Janssen Pharmaceutica Products, Organon Inc., Pfizer Inc, and Wyeth

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