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Medical Comorbidities in Late-Life Depression

Medical Comorbidities in Late-Life Depression

The prevalence of depression is higher in persons with comorbid medical conditions than in those with no comorbidity. Some conditions that are common in older people, such as stroke, cardiac disease, chronic obstructive pulmonary disease (COPD), and diabetes mellitus, are associated with particularly high rates of depression comorbidity.1,2

Late-life depression is both underrecognized and undertreated, and the impact of medical comorbidity may mask depressive symptoms. Depression further complicates the prognosis of medical illness by increasing physical disability and decreasing motivation and adherence to prescribed medications and/or exercise or rehabilitation programs. In addition, chronic disabling disorders can be a contributory factor to suicide attempts and completions in the elderly, but timely, appropriate treatment of depression can reduce this risk.3

This review provides an update of current evidence in relation to late-life depression and its management in the presence of some common medical conditions: stroke, coronary heart disease, diabetes mellitus, Parkinson disease, and COPD. The relatively new concept of vascular depression is also briefly discussed.4,5

STROKE AND MOOD DISORDER
Depression

Because depression and stroke are common in later life, poststroke depression is also common. Depression develops in 20% to 50% of patients within the first year after a stroke: the peak prevalence of major depression occurs at 3 to 6 months poststroke.6-8 However, the risk may continue for up to 2 or 3 years depending on the effects of disability on the patient’s lifestyle. The variability in prevalence is probably the result of clinical heterogeneity of the sample, the timing of the evaluation, and the lack of a valid disease-specific screening questionnaire for poststroke depression.9

A recent systematic review reported that the predisposing factors for poststroke depression include older age, a history of depressive disorder, the size of infarct, female sex, severity of stroke sequelae, and language impairment.10 Poststroke depression has been shown to be a predictor of impaired quality of life and a risk factor for cognitive decline and poorer functional recovery. It is also associated with an elevated risk of morbidity and mortality.9,10

The literature is inconclusive about whether baseline depressive symptoms predict cerebrovascular events in older age. The Framingham Study examined the risk of developing cerebrovascular events in 2 cohorts of patients: one group was 65 years or younger and the other was older than 65 years.11 The study used the Center for Epidemiologic Studies Depression (CES-D) score of greater than 16 as a cutoff for significant depression.12 Those 65 years and younger who had a CES-D score of 16 or greater were 4 times more likely to experience a stroke or transient ischemic attack as the same age-group without depression, after controlling for risk factors such as smoking status and education. There was no significant difference in the rate at which cerebrovascular events occurred in those who were 65 years or older, with or without depression.

In contrast, findings from another study indicate a positive association between the presence of depression and the risk of stroke across the entire adult age range.13 This study also demonstrated a gradient effect (the greater the depression, the greater the risk of stroke), which was most marked among black racial groups. The exact mechanisms of how depressive symptoms predispose to stroke are not fully known, but depression is known to affect autonomic function and platelet activation.

Diagnosing depression after a stroke can be difficult, especially in patients with aphasia. In their review of existing instruments, Bennett and Lincoln14 found the 14-item observer-rated Stroke Aphasic Depression Questionnaire Hospital Version (SADQ-H) to be effective. Difficulty in adjusting to major disability may be sufficient to trigger depression. However, the high rate of depression and the inconsistent relationship between severity of stroke and depression has led to a hypothesis based on the site of the lesion. It has been suggested that a stroke in the left front cerebral hemisphere is a major risk factor for depression, possibly caused by the interruption of the monoaminergic routes that connect the brain stem with the cerebral cortex15,16 However, other researchers disagree with the localization hypothesis.17

Treatment
he principles of treating poststroke depression are the same as the treatment of depression in general. Because spontaneous recovery often occurs within the first 6 weeks, however, watchful waiting may be appropriate. The converse is also true—if a patient remains significantly depressed 6 weeks following a stroke, spontaneous remission is unlikely and somatic treatment should be considered.

A review of the literature provided information on only 10 randomized controlled trials of antidepressants (fluoxetine, citalopram, sertraline, nortriptyline) in poststroke depression.18 These drugs were shown to be efficacious, although the trials were small and of variable quality. Other antidepressants have been less well studied, although there have been controlled studies of psychostimulants such as methylphenidate at doses of 5 to 10 mg daily.18 Of historical interest, stimulants may also effectively target stroke-related apathy.

Antidepressants are preferred over psychotherapeutic interventions such as cognitive-behavioral therapy (CBT) because of a lack of evidence of efficacy of CBT.9,10,19,20 However, such trials are methodologically difficult to conduct. A recent study that examined the benefit of integrated care (liaison with a specialist stroke service, primary care physicians, using a telephone tracking system, management of vascular risk factors, and regular screening for depressive symptoms) in stroke survivors revealed fewer depressive symptoms in the integrated care group than in the control group in a 12-month follow-up.21 The integrated care approach has the potential for detecting and monitoring depressive symptoms in this patient population. It is hoped that future research will clarify the effects of both psychological approaches and stroke rehabilitation in the management of depressed mood.

CORONARY HEART DISEASE
There is a strong link between coronary heart disease and depression. In the United States, coronary heart disease affects more than 16 million people and in about 1 of 5 cases can lead to significant symptoms of depression.22,23 Nicholson and colleagues24 investigated the cause(s) and impact of depression as etiological and prognostic indicators in 54 observational studies. In 21 etiological studies the pooled relative risk (RR) of future coronary heart disease events in patients with depression was 1.81 (95% confidence interval [CI], 1.53 - 2.15)—patients with baseline depression were at 81% higher risk for coronary heart disease than patients without depression.

In 34 prognostic studies (among patient populations with an earlier myocardial infarction or coronary artery surgery), the RR of association of depression and prognosis for coronary heart disease was 1.80 (95% CI, 1.50 - 2.15). Of 804 Canadian patients with stable coronary disease, 7.1% met criteria for major depressive disorder and 5.3% for generalized anxiety disorder; both disorders increased the risk of subsequent adverse cardiac effects.25 This may be a conservative estimate. Depression in patients with acute coronary syndrome is less likely to be recognized (especially in ethnic minorities) in patients with lower educational backgrounds and reduced left ventricular ejection fractions.26

Heart disease progression
The exact mechanism of the link between depression and coronary heart disease is unclear but includes direct biological mechanisms and behavioral factors. The Table lists the variables associated with depression and coronary heart disease.

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