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Recognition and Management of
Late-Life Depression in Primary Care

E. Yusuf Sivrioglu, MD, Yosef A. Berlow, BS, and James M. Ellison, MD, MPH

Primary Psychiatry. 2004;11(1):56-58,61-65

Focus Points

Depressive symptoms in older adults represent a treatable and often overlooked disease state that interferes with functioning, increases medical morbidity and mortality, and elevates the risk for suicide.

The varied presentations of depression among older adults can include symptoms of apathetic withdrawal, depression with psychotic features, depression with concerns about cognitive functioning, depression-executive dysfunction syndrome, and depression as it appears in demented individuals.

In primary care settings, where most depressed older adults can be identified and treated, detection and intervention can be improved through the use of validated screening techniques and differential diagnostic assessment.

Several psychotherapeutic approaches, a variety of antidepressants, and electroconvulsive therapy have been shown to be effective in treating depression in older adults. Specific recommendations can be made on the basis of a literature review and recently published consensus guideline.


Abstract

 

Late-life depressive symptoms place a large burden on affected older adults and their support systems by impairing quality of life, increasing mortality and morbidity rates, and creating serious economic, social, and psychological burdens. Patients with late-life depressive symptoms are more likely to be seen in primary care settings than in specialty mental health settings, yet may go undiagnosed and untreated. This article reviews the common and unique presentations of depression in older adults, with a focus on improving detection. The available treatment options of medications, psychotherapy, and electroconvulsive therapy are reviewed with practical suggestions for their use in primary care settings.

 

Introduction

 

Depressive disorders, increasingly recognized as an important health concern among young and middle-aged adults, also play an important role in the lives of older adults. Late-life depressive symptoms impair quality of life, increase mortality and morbidity rates, and create serious economic, social, and psychological burdens.

 

To date, recognition and treatment of depressive disorders among older adults in primary care have been disappointingly limited. The results of these shortcomings are often a missed diagnosis or inadequate course of treatment. Among the reasons for this are the variant presentations of late-life depression, the reluctance of patients to reveal their symptoms or seek help, and limitations on mental health visits and pharmacy benefits that can interfere with access to treatment. This article reviews the demographics and symptoms of late-life depression and offers suggestions for improving its recognition, performing an appropriate differential diagnostic work up, initiating treatment, and monitoring the patient’s response. Primary care clinicians, who encounter the majority of these individuals, can make use of the suggestions offered here to improve their management of older adults with depressive symptoms or disorders.

 

Demographics

 

Data from large population-based studies indicate, to many clinicians’ surprise, that major depressive disorder (MDD) is less prevalent among older adults than among younger adults. One of the best known of these investigations, the Epidemiological Catchment Area study, estimated the 1-year prevalence of major depression in community-dwelling older adults to be 2.7%, which is lower than the prevalence rates measured in younger cohorts.1 Similarly, the Cache County study reported the prevalence of geriatric MDD to be 4.4% in women and 2.7% in men.2 These low rates reflect the consequences of several unique characteristics of depression in later life.

 

Perhaps the most significant characteristic is that older adults frequently experience depressive symptoms or partial depressive syndromes without meeting full criteria for MDD. Among community-based older people, as many as 15% display symptoms of nonmajor depressive syndromes,3 conditions that, unlike MDD, increase in prevalence with increasing age.4,5 Often, subsyndromal depressive symptoms are mistakenly attributed to concurrent medical problems or stress-related reactions to challenging life circumstances, thereby impeding the possibility of recognizing and treating potentially remediable mood disorders. This can be tragic because nonmajor depressive syndromes, while comprising fewer symptoms, detract from quality of life and increase both functional impairment and mortality.6 Furthermore, the varying manifestations of depressive symptoms in the elderly, including the tendency to under-report or deny experiences of psychological distress, and the limitations of current diagnostic criteria in capturing their significance, may lead to an underestimation of depression’s prevalence.7

 

Some estimates of depression in this older population have been falsely lowered by the exclusion of institutionalized subpopulations. Among residents of long-term care facilities, for example, the prevalence of MDD is as high as 25%.8 This rate increases to 70% when both major and nonmajor depressive syndromes are measured.9,10 In primary care settings, the rate of geriatric depression has been reported to be 17% to 34%, exceeding the rate in the general population.11

 

As medical advances extend life expectancy,12 the population >65 years of age will continue to grow steadily and, by United States Census projections, eventually reach 82 million persons by the year 2050. The medically and mentally ill, two subgroups that are highly susceptible to depression, will share in this trend toward increased longevity, resulting in a greater prevalence of late-life depression. Some data suggest that higher rates of depression among younger adults represent a “cohort effect” that will eventually result in a higher prevalence of late-life depression as these younger cohorts age.13

 

Modifying the diagnostic criteria for depression so as to increase their sensitivity to the manifestations of mood disturbances in older adults, especially those with medical illnesses and/or cognitive impairment, may help to increase the identification of geriatric depressive syndromes. Greater opportunities for intervention and for improvement of quality of life will come with more inclusive categories and the recognition of the great heterogeneity of geriatric depressive symptoms.

 

Consequences of Untreated Depression

 

Untreated depression in later life has been shown to increase both medical morbidity and mortality. Suicide is a well-recognized consequence of depression at all ages and the rate of completed suicide is disproportionately high among older adults. As illustrated in the Figure, white males ?85 years of age constitute a high-risk group, with an annual suicide rate of 59 per 100,000 persons—approximately six times the rate of the general population.14 In many instances, suicide occurs after a first episode of depression. The depressed, older, white widower with access to firearms is of particular concern from an actuarial standpoint.15 The vast majority of older persons who complete suicide have visited their primary care physicians during the final month of their lives, underscoring the critical importance of recognizing and treating depression in primary care settings.16

 

 


 

Mortality among depressed aging adults is also increased through associated medical morbidity from such illnesses as cardiovascular and cerebrovascular disorders. In one study comparing depressed to nondepressed patients suffering from angina, myocardial infarction, or other cardiovascular diseases, the relative risk of cardiac death over the succeeding 4 years was 1.6 for cardiac patients with minor depression and 3.0 for cardiac patients with MDD.17 Depression has also been reported to be a predictive factor for strokes18 and is linked with several associated additional risk factors, including a high preponderance of smoking,19 low levels of physical activity,20 and an increased risk of hypertension.21 Depression, furthermore, affects 30% of stroke victims during the first year after the event and significantly affects the rate of recovery from the stroke.22

 

Functional disability has also been closely associated with geriatric depression in what may be a self-reinforcing interaction. Several studies have found evidence supporting the notion that disability is a significant risk factor for depression, while other studies have found equally compelling support that disability can also be viewed as a consequence of depression.23

 

Untreated depression threatens not only the health and well-being of the patient, but also powerfully impacts the quality of life of the patient’s support system. Caregivers are at increased risk for impaired physical health, depression, anxiety, and even death, possibly as a consequence of increased stress and reduced time for self-care.24,25 Furthermore, when deterioration of a patient’s independence precipitates early placement in long-term care facilities, a huge economic burden may be placed on the support system.

 

Detection of Depression in Late Life

 

Two major diagnostic criteria sets are widely used to identify depression: the Diagnostic and Statistical Manual of Mental Disorders,26 Fourth Edition Text Revision (DSM-IV-TR), and the International Classification of Disease, Tenth Revision.27 Both sets rely upon the presence of specific symptoms and/or symptom clusters to diagnose the disorder.

 

In the DSM-IV-TR, the diagnosis of MDD requires the presence of five or more of the following symptoms: depressive mood, diminished interest or pleasure, weight loss, insomnia or hypersomnia, psychomotor agitation or retardation, fatigue or loss of energy, feelings of worthlessness or inappropriate guilt, diminished ability to think or concentrate, and recurrent thoughts of death or suicidal ideation. These symptoms must all occur during the same 2-week period and cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. When psychotic symptoms such as delusions, hallucinations, or disturbances of motor function are present, the diagnostic phrase “with psychotic features” is added.

 

Unfortunately, these diagnostic criteria do not adequately encompass the range of depressive characteristics seen in older adults, nor do they take into account the diminished reporting of symptoms frequently encountered in older patients. The requirement for five symptoms also reduces the sensitivity of the criteria for this population, especially in regard to individuals who feel uncomfortable reporting psychological symptoms. Such individuals may express their depressive states less directly, by emphasizing secondary behaviors such as social withdrawal or focusing on nonspecific symptoms of anxiety, anorexia, insomnia, anergia, or other somatic complaints. Furthermore, a clinician should be attentive to the influence of cultural factors on patients’ experience of depressive symptoms and willingness or ability to report them.

 

The co-occurrence of depression with somatic disorders is frequent in older persons and makes distinguishing between the somatic symptoms of depression and those arising from a somatic disease more challenging. Medical disorders encompassing psychomotor retardation, apathy, and fatigue; the effects of sedating and mood altering drugs; and nondepressive psychiatric disorders such as anxiety states, adjustment disorders, or psychotic disorders should be differentiated from depression.28 Although some clinicians have questioned whether bereavement should be treated with the same approach applied to MDD, studies have demonstrated that individuals whose functioning is compromised despite adequate opportunity to grieve may benefit significantly from antidepressant treatment and/or psychotherapy.29 Physical examination and basic laboratory screening tests play key roles in this differential diagnostic process.

 

Among patients with geriatric depression, clinical presentation may in part reflect differences related to age of onset. Cases of late-onset depression, with the first depressive episode occurring ?60 years of age, have been associated with a greater prevalence of psychotic symptoms, especially delusions, as compared with cases of early-onset depression.30 Prominent somatic delusions may lead to fruitless physical diagnostic testing. Delusions of persecution, poverty, or nihilism can make depression appear to be a primary psychotic disorder such as schizophrenia. Decreased self-esteem, worthlessness, agitation, ideas of reference (eg, inappropriate personalization of external events), and preoccupations about a particular theme are more prominent with a later onset of depression.

 

Cognitive impairment or complaints of cognitive impairment, which can be associated with depression (especially late-life depression), may lead clinicians to the false diagnosis of dementia. Disturbances in executive function, such as difficulties in planning, sequencing, organizing, and abstracting, are seen in late-onset geriatric depression and have been referred to as the depression-executive dysfunction syndrome. This syndrome is also characterized by psychomotor retardation, limited depressive ideation, and prominent disability.31 The frequent co-occurrence of depressive and cognitive symptoms makes it necessary to screen for dementia in depressed patients with complaints or evidence of cognitive dysfunction. Features that may be helpful in distinguishing depression from dementia are listed in Table 1.

 

Screening for Depression

 

Despite the complexity of diagnosing depression in the elderly, simple screening can be done with brief self-administered or rater-administered questionnaires. Some of these can also be used to track a patient’s response to treatment. A recent review of screening tools for depression reported that brief tests can perform as well as more complicated versions.32 In fact, a positive response to the question, “Have you felt depressed or sad much of the time in the past year?” proved nearly as predictive as a 20-item questionnaire in detecting MDD.33 While screening with subsequent feedback has been shown to reduce the risk of persistent depression,34 the success of any screening method is greatly influenced by patients’ compliance and their ability to provide accurate information.35

 

Several widely used screening scales, including the Hamilton Rating Scale for Depression,36 the Beck Depression Inventory,37 the Zung Self-Rating Depression Scale,38 and the Montgomery-Asberg Depression Rating Scale,39 were not developed specifically for screening depression in the elderly and include items that may be better suited to screen younger populations.35 While these instruments may still have reasonable sensitivity and specificity when applied to geriatric populations, better choices may be the use of geriatric-specific scales such as the Geriatric Depression Scale40 or, for the cognitively impaired, the Cornell Scale for Depression in Dementia.41

 

Treatment of Geriatric Depression

 

A range of interventions, both psychological and somatic, is used to treat depression in older adults. Among the psychotherapies, evidence has supported the efficacy of interpersonal therapy (IPT), problem-solving therapy, cognitive-behavioral therapy, and psychodynamic group approaches. Though it is beyond the scope of this article to discuss the distinctions between these approaches, psychotherapeutic techniques used to target depressive symptoms in older adults tend to focus on a here-and-now orientation, assessment of constructive and counterproductive interpretations of one’s roles and relationships, and a supportive/educative rather than open-ended exploratory approach. In older adults, psychotherapies are considered especially appropriate in treating nonpsychotic depressive states of mild to moderate severity. Psychotherapies may be of particular value in addressing the effects of and reactions to stressful life events, losses, and transitions during life’s later years. Many clinicians recommend concurrent psychotherapeutic and pharmacotherapeutic treatments. The recommendation for this combined approach is also made in a recently published expert consensus guideline on the treatment of depression in older adults.42 A primary care clinician who prescribes and monitors antidepressant therapy may wish to collaborate with a psychotherapist (often a psychologist, social worker, or psychiatrist). This combination approach has also increased medication adherence.43

 

For more severe depression or depression with psychotic features, however, the patient’s capacity to benefit from psychotherapy may be limited; in such cases, pharmacotherapy or electroconvulsive therapy (ECT) would be more indispensable. Pharmacotherapy of depression with psychotic features, moreover, requires an antipsychotic as well as an antidepressant.

 

Somatic therapies of depression are complicated by the effects of aging. Age-related pharmacodynamic factors increase older adults’ vulnerability to side effects, especially those that are anticholinergic. Aging influences pharmacokinetics as well, affecting the absorption, distribution, metabolism, and excretion of drugs. Furthermore, older patients often take multiple medications for comorbid medical conditions, consequently increasing the likelihood of adverse drug-drug interactions. These considerations underlie the axiom “start low and go slow but do not undertreat” with antidepressants. As a general rule, antidepressant treatment of the elderly is characterized by a higher blood level of the medication and a slower elimination
half-life at any given dose.

 

In surveying the antidepressant treatments available to primary care practitioners, it is apparent that the available medications share the property of enhancing neurotransmission of serotonin, norepinephrine, or dopamine. Some antidepressants achieve this effect by blocking the presynaptic reuptake of the neurotransmitters (eg, serotonin reuptake inhibitors [SRIs] and heterocyclic antidepressants [HCAs]) or inhibiting the degradation of neurotransmitters (eg, monoamine oxidase inhibitors [MAOIs]). Other newer non-SRIs may increase neurotransmission by antagonizing presynaptic inhibition of the neurotransmitter’s release (eg, mirtazapine). Each class has its own mechanism of action, as well as additional features that define the associated side effects. Even among drugs with similar mechanisms, distinctions arise as a result of their different pharmacodynamic and pharmacokinetic characteristics. None of these antidepressants has been clearly demonstrated to have greater efficacy, though each has been shown superior to placebo. Some authorities have suggested that the newer antidepressants possess more benign side effects. The following section discusses class-specific issues that relate to these medications’ use and tolerability.

 

Serotonin Reuptake Inhibitors

 

Since 1988, when fluoxetine was introduced in the US as the first selective serotonin reuptake inhibitor (SSRI), the SRIs have become the most frequently prescribed class of antidepressants. The SRI category encompasses six SSRIs, venlafaxine (also termed an SNRI because it blocks both serotonin and norepinephrine presynaptic reuptake), and nefazodone (also termed a serotonin 2A antagonist/reuptake inhibitor [SARI] because of its mix of 5-HT2-receptor selective serotonin antagonist and SRI activities). The preferential SRI selectivity and limited additional receptor-binding effects of the SRIs differentiate this class of antidepressants from HCAs and MAOIs.

 

A recent expert consensus guideline designated SSRIs, along with venlafaxine, as first-line treatment choices for older adults,42 even though meta-analytic studies have not clearly shown them to have superior efficacy or lower discontinuation rates in comparison to HCAs.44,45 These newer agents lack significant antihistaminic properties associated with sedation and weight gain, and (with the exception of paroxetine) the anticholinergic effects associated with constipation, dry mouth, urinary retention, confusion, or delirium. They also lack anti-adrenergic effects, freeing them from unwanted postural hypotension, and are believed to lack cardiac toxicity at therapeutic doses. These properties make them very appropriate choices for patients with cardiac conduction abnormalities or patients with dementia, who are very sensitive to the heterocyclics’ anticholinergic, antihistaminic, and anti-adrenergic properties.

 

The newer antidepressants, however, are by no means free of side effects. Frequently seen secondary results include nausea, vomiting, diarrhea, anxiety, nervousness, dizziness, insomnia, and headache. Sexual dysfunction is also a frequent concomitant with treatment. Bradycardia, with or without hypotension, is rare but can occur, potentially increasing the risk of a fall. Hyponatremia, an infrequent SSRI side effect overall, seems to increase with age, female sex, previous history of hyponatremia, and the concomitant use of other medications known to cause hyponatremia.46

 

In choosing a specific SSRI, the consensus guideline experts suggest citalopram or sertraline as initial first-line agents.42 These SSRIs have relatively low drug-drug interaction risks, an appropriate half-life that allows once-daily dosing, and well-tolerated side effects. The newest SSRI in the US, escitalopram, shares many characteristics with citalopram and possesses a side-effect profile at least as tolerable.47

 

Paroxetine and fluoxetine have nonlinear pharmacokinetics; in addition, paroxetine’s relatively shorter half-life appears to contribute to its more severe discontinuation symptoms. Paroxetine’s significant anticholinergic properties make it a theoretically less desirable choice for patients with Alzheimer’s disease because a cholinergic deficiency with Alzheimer’s increases the vulnerability to anticholinergic side effects. Cytochrome P450 (CYP) interactions mediated by inhibition of the 2D6 enzyme are relative disadvantages of paroxetine and fluoxetine, while inhibition of the 3A4 enzyme characterizes fluvoxamine and nefazodone.

 

Table 2 lists the antidepressants, including SSRIs, currently available in the US with recommendations for starting and target doses in elderly depressed patients. For example, a typical starting dose for citalopram is 10 mg/day with a target dose of 10–40 mg/day, while sertraline can be initiated at 25–50 mg/day and increased every 2–4 weeks to a target of 50–200 mg/day. Escitalopram is initiated at 5–10 mg/day and increased to a target of 10–20 mg/day.48 Doses in the higher range are typically used in treating patients with a treatment resistant depression.

 

Venlafaxine, a highly-ranked treatment choice for older adults, has a side-effect profile similar to that of the SSRIs and a “dual action” effect of blocking both serotonin and norepinephrine presynaptic reuptake. It does not interact as a substrate or inhibitor with CYP enzymes 2D6 or 3A4. In a dose-related manner, it can increase diastolic blood pressure. Its relatively brief elimination half-life increases the likelihood of discontinuation symptoms. If using the less popular immediate release (IR) form, experts suggest initiating treatment with 25 mg/day and aiming for 50–375 mg/day.42 The extended release form can be started at 37.5 mg/day and allows once-daily dosing, with a usual target range of 50–225 mg/day.

 

Nefazodone, perhaps as a result of its postsynaptic 5-HT2 blocking property, appears to be less frequently associated with side effects such as anxiety or sexual dysfunction, as compared to the SSRIs. Some patients find it anxiolytic or even sedating, and it has a benign effect on sleep architecture. Yet because of its inhibition of CYP 3A4 and concern raised by rare but serious or even fatal cases of hepatic damage,49 nefazodone is no longer considered to be a first-line treatment choice for older people. Trazodone, another SARI, which has weak serotonin selectivity, is often used to promote sleep and sedation or to treat agitation in demented patients. It is rarely used as a monotherapy drug in depression because of its significant side effects at doses required for antidepressant effectiveness. Trazodone can produce orthostatic hypotension and is the psychotropic most frequently implicated in drug-induced priapism.

 

Newer Non-SRI Antidepressants

 

Bupropion, classified as a norepinephrine and dopamine reuptake inhibitor, is differentiated from other available agents by its mechanism of action and its lack of serotonergic activity. It is a less sedating antidepressant and is rarely associated with sexual dysfunction. It is also considered potentially anxiogenic for patients primarily suffering from an anxiety disorder or psychotic depression. The IR form of bupropion is associated with a modestly elevated seizure risk, but the increase in seizure risk is low when the sustained release (SR) or extended length (XL) forms are used in patients without pre-existing risk factors and at recommended doses. Bupropion is contraindicated for patients with a history of bulimia or anorexia nervosa. Administration of bupropion SR should not exceed a total of 400 mg/day and individual doses should not exceed 200 mg each. Use of the XL form allows a single dose to be as high as 300 mg/day. In the elderly, the accumulation of a bupropion metabolite, hydroxybupropion,50 is associated with side effects such as headache, somnolence, insomnia, agitation, dizziness, dry mouth, diarrhea, or nausea.

 

Mirtazapine is a noradrenergic presynaptic a2 autoreceptor antagonist that also blocks postsynaptic Histamine1, and serotonin 5-HT2 and 5-HT3 heteroreceptors. The net result of these pharmacodynamic properties is an increase in synaptic norepinephrine and serotonin availability. Clinically, mirtazapine’s antidepressant effects are associated with sedation and appetite increase, but minimal nausea. Studies report its efficacy to be equivalent to amitriptyline, trazodone, and paroxetine.51-53 Though tempting to begin with a low dose such as 7.5 mg/day, this may actually produce greater sedation for some patients than a dose of ≥15 mg/day.

 

Heterocyclic Antidepressants

 

HCAs include the tricyclic and tetracyclic antidepressant agents. These venerable antidepressants, in use since the 1950s, are relatively less selective drugs: they block both serotonin and norepinephrine reuptake and also
possess antagonistic effects on
α1-adrenergic, H1 histaminergic, and Muscarine1 cholinergic receptors. The only tetracyclic marketed in the US is maprotiline. Its elimination half-life and side-effect profile are similar to those of the tricyclics, though it may be associated with a greater risk of seizures, especially when the dose is rapidly increased.

 

Tricyclic antidepressants (TCAs) are traditionally subclassified as tertiary or secondary amines. Available tertiary agents are amitriptyline, imipramine, trimipramine, doxepin, clomipramine, and amoxapine. Because of their high lipid solubility, they tend to achieve high central nervous system levels, which can cause adverse effects. Postural hypotension and sedation are frequently seen and, though this remains disputed, could potentially increase the risk of falls. Anticholinergic properties may promote constipation in older adults and they may facilitate urinary retention, particularly in men with prostatic hypertrophy. Titrating dosage by measuring plasma drug levels can reduce the likelihood of inadequate or excessive dosing of these drugs, but their side-effect profile has led many clinicians to reject them as first-line treatment choices in the elderly. Indeed, some authors recommend that amitriptyline be avoided altogether in depressed elderly patients.54 Amoxapine, which possesses additional postsynaptic dopamine-blocking effects that were initially proposed as a rationale for its use in treating psychotic depression, is characterized by a combination of tricyclic side effects and side effects arising from dopamine receptor blockade. Due to these properties, it is rarely recommended as a first-line drug for the elderly on account of its toxicity.

 

The secondary amine TCAs include nortriptyline, desipramine, and protriptyline. Compared to the tertiary amines, they are better tolerated and are regarded as safer. The most favorably regarded tricyclic for treating older adults is nortriptyline, which has been proven effective in a number of controlled trials. Nortriptyline produces less orthostatic hypotension than other TCAs; furthermore, the relationship between its efficacy and its plasma level is relatively clear. With appropriate monitoring of plasma levels as a basis for guiding dosing, its safety is comparable with that of the SRIs and its effectiveness in the treatment of depressed elderly in long-term care facilities has been demonstrated.55

 

Cardiac toxicity of HCAs remains a concern in treating older adults. These antidepressants can induce arrhythmia by slowing cardiac conduction and can reduce cardiac and cerebrovascular perfusion via postural hypotension. These conduction-slowing properties are one aspect of the great danger associated with overdosing heterocyclics.

 

Four meta-analytic studies have reported that heterocyclics are as effective as other antidepressants, though each investigation noted a statistically nonsignificant trend toward more severe adverse effects.44,45,56,57 Therefore, reserving their first-line use for patients with severe depression is recommended. When HCAs are to be used, nortriptyline is an appropriate drug of choice. An initial dose of 10–25 mg/day is often well tolerated and the target dosage is typically between 25 and 150 mg/day, aiming for the optimal plasma level range of 50–150 ng/mL.

 

Monoamine Oxidase Inhibitors

 

The MAOIs are believed to work by inhibiting the monoamine oxidase (MAO) enzyme in the brain, which degrades catecholamine neurotransmitters. Their side-effect profile, resulting from both MAO inhibition and additional receptor effects, includes weight gain, postural hypotension, dry mouth, constipation, sleep disturbances, fatigue, sexual dysfunction, and elevation of hepatic enzymes. As such, they require constant monitoring. Because MAO is also present in the intestines (where it is responsible for destroying neurotransmitter-like substances in ingested food), nonselective systemic inhibition of MAO renders the brain vulnerable to the effects of neurotransmitter-like food substances or drugs. This vulnerability is the rationale for avoiding specific foods and medications during MAOI treatment. Such prohibitions may be problematic for older adults, particularly those with memory impairment that may facilitate dietary errors. Because of these side effects and necessary restrictions, MAOIs are relegated to second-line treatment in depressed older adults.

 

Electroconvulsive Therapy

 

ECT is a well-studied treatment modality in geriatric depression. It is often recommended for treating psychotic depression and can be a preferred treatment for patients requiring a rapid clinical response, or for those who have previously responded well to ECT. None of the antidepressants has been shown superior to ECT, but the methodologies of these comparisons have been criticized. Relative contraindications to the use of ECT include cardiopulmonary disorders or other risk factors for anesthesia complications, recent cerebral bleeding, increased intracranial pressure, and perhaps some comorbid neurological disorders. The associated memory deficits are generally mild and short term, though patients with pre-existing cognitive impairment can show significant adverse effects.58

 

Trial Duration

 

Achievement of antidepressant response may take longer for older adults than it normally would in younger adults. Many symptoms may show only limited improvement before week 4 and some eventual drug responders may not meet the response criteria until week 10.59 The expert consensus guideline recommendation is to wait at least 2–3 weeks and as long as 7.5 weeks before considering changing the treatment if it is tolerated.

 

Adherence problems are well recognized with antidepressant treatment and may be an even greater problem in primary care settings where patients are seen less frequently (as opposed to mental health settings where a patient is more likely to receive adjunctive psychotherapy and more frequent visits). Scheduling regular follow-up visits, confirming that the patient is taking the antidepressant, inquiring about side effects, and explaining the need to continue pharmacotherapy for a period of time even after remission of symptoms are techniques likely to improve adherence and result in a better outcome.

 

Maintenance Treatment

 

Maintenance treatment is a key factor in sustaining remission. In older adults, there is no clear consensus on optimal maintenance duration, but a sensible current recommendation is to treat depressed patients for at least 1 year beyond remission of a severe first episode, and for 3 years following a third or subsequent episode. A 1999 study showed that IPT may be beneficial in preventing relapse; the study demonstrated a significant reduction in subsequent relapse rates when bereavement-related depression was treated with the combination of nortriptyline and IPT.60

 

Referring Depressed Patients to Specialty Mental Health Care

 

Very often, late-life depression can be successfully treated in primary care settings. Depression with psychotic features, personality disorder, substance abuse, bipolar features (eg, history of mania), or suicidal ideation present unique concerns that are best addressed in a mental health specialty care setting. Patients whose depression has shown treatment resistance, defined as a nonresponse to two adequate antidepressant trials, may also benefit from the more thorough assessment approach and availability of concurrent psychotherapeutic services often found in specialty mental health settings.

 

Conclusion

 

Although depression may appear less prevalent in older adults, the pervasiveness of subsyndromal states, the reduced completeness of symptom reporting, the presence of medical comorbidities, and the effects of normal aging suggest that depression is more widespread than previously imagined. As such, there is a need to fine tune the diagnostic criteria for this special age group. Detection tools are available and can be used for both diagnosis and monitoring to improve treatment outcomes. Pharmacotherapy is often recommended after the detection of depression, but it must be pursued with sufficient vigor to allow adequate treatment while still respecting the metabolic effects of aging that can facilitate adverse reactions among older patients. The combination of biological therapies with psychotherapy is also recommended for mild to moderate depression—sustaining remission is as important as reaching it. Finally, the primary care clinician should consider referral to specialty mental health care for specific, complicated subgroups of older adults with depressive conditions. PP

 

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Dr. Sivrioglu is research fellow at the Geriatric Psychiatry Program at McLean Hospital in Belmont, Massachusetts.

 
 

Mr. Berlow is a research coordinator for the Geriatric Psychiatry Program at McLean Hospital.

 

Dr. Ellison is clinical director of the Geriatric Psychiatry Program at McLean Hospital and associate professor of psychiatry at Harvard Medical School in Boston, Massachusetts.

 

Disclosure: Dr. Sivrioglu is sponsored by the Scientific and Technical Council of Turkey (TUBITAK) NATO B1 scholarship; Dr. Ellison is on the speaker’s bureaus for Eli Lilly, Forest, GlaxoSmithKline, Pfizer, and Wyeth.

 

Please direct all correspondence to: James M. Ellison, MD, MPH, Clinical Director, Geriatric Psychiatry Program, McLean Hospital, 115 Mill St, Belmont, MA 02478; Tel: 617-855-2532; Fax: 617-855-3246; E-mail: ellisonj@mcleanpo.mclean.org.