Depression is common, disabling, and often unrecognized in general medical practice. Even when recognized, physicians frequently do not provide systematic, longitudinal evidence-based management. And from the perspective of the patient, stigma and other psychosocial barriers such as negative expectations often diminish adherence to treatment recommendations. Despite robust documentation that depression is quite treatable and the widespread availability of evidence-based guidelines, overall outcomes remain poor.

This chapter focuses on the core knowledge and skills needed by general medical practitioners to effectively assess and manage major depressive disorder (MDD). We briefly address other related mood disorders: dysthymic disorder, adjustment disorder with depressed mood, depression secondary to general medical conditions, bipolar disorder/bipolar depression, and melancholia. We emphasize the routine use of a brief patient self-assessment tool, the nine-item Patient Health Questionnaire (PHQ-9), for diagnostic and ongoing management purposes. Widespread adoption of this one practice innovation may provide the pivotal leverage needed to improve outcomes for depression.

Major depressive disorder (MDD) is associated with considerable disability, morbidity, and mortality. Epidemiologic studies demonstrate that depression causes more disability and social and role impairment than most other chronic illnesses, such as diabetes, arthritis, hypertension, and coronary artery disease. The World Health Organization has identified major depression as the fourth leading cause of disability worldwide and projects that it will become the second leading cause of worldwide disability by 2020. Major depression is also a well-documented and common comorbidity in many other chronic conditions: for example, heart disease, stroke, diabetes mellitus, cancer, Parkinson disease, arthritis, pulmonary disease, and others. Furthermore, when present as a comorbidity, depression accounts for significant increases in disability, morbidity, and mortality.

The etiologic and sustaining relationships between depression and these other conditions appear to be bidirectional. For example, preexisting depression has been established as a predictor of future atherosclerotic coronary artery disease, cerebrovascular disease, diabetes, and osteoporosis, and conversely, significant physical illness predicts higher prevalence of major depression compared with individuals without physical illness. Depressed patients with heart disease (coronary artery disease, congestive heart failure) have worse medical outcomes including increased risk of reinfarction (after myocardial infarction [MI]) and up to a three-fold increase in all-cause mortality (especially after MI), even after controlling for all other identifiable and measurable cardiac risks (such as overeating, sedentary lifestyle, smoking, and other predictors of poor outcome). Patients with diabetes and depression have worse glycemic control, more microvascular and macrovascular complications and greater all-cause mortality.

Major depression is associated with adverse health habits, such as smoking, poor diet, overeating, and sedentary lifestyle, these in turn contribute to the onset of general medical illness and/or poor outcomes in illness. Conversely, functional impairment stemming from these chronic illnesses predispose to development of new depression. From an etiologic perspective, variables such as genetic vulnerability, childhood adversity (neglect and abuse), and stressful life events all contribute to the development of depression itself as well as to lifestyle risks such as obesity, sedentary behavior, and smoking that themselves predispose to chronic general medical illnesses.

Chronic care of general medical illness requires self-management behaviors to optimize treatment, for example, special diets, exercise regimens, medication changes, daily glucose monitoring, blood pressure checks, and limiting potentially harmful behaviors, such as smoking and risky drinking. Studies show that depression adversely impacts self-management, at least partly due to the fact that depressed patients are more likely to be nonadherent than nondepressed patients. Depressed diabetic patients have decreased adherence to diet and suffer more lapses in refills of oral hypoglycemic medications. Depressed patients with heart disease or stroke show decreased adherence to treatment recommendations such as taking daily aspirin and participating in exercise rehabilitation programs. This nonadherence in post-MI patients predicts increased rehospitalizations and mortality. Major depressive disorder, with or without general medical comorbidity generally is a chronic, recurring illness, with varying cycles of exacerbation and remission. Furthermore, these exacerbations or new episodes of depression tend to occur more frequently and with greater severity as the patient ages.

Dysthymic disorder is a less severe but more chronic form of depressive illness that is also associated with significant disability, and is even more likely to go undiagnosed than major depression. This disorder is diagnosed when depressed mood and at least two other symptoms of depression have been present “more than half the days” during the previous 2 years. Dysthymic disorder has been shown to respond to treatment with antidepressant medication. Patients with dysthymic disorder have an increased risk of experiencing a major depressive episode.

Adjustment disorder with depressed mood involves a reaction to an identifiable stressor, such as divorce or job loss. It presents with a sad or depressed mood, a level of impairment greater than expected for most individuals facing that specific stressor and is diagnosed within the first 6 months after the stressor has occurred. A “normal” reaction to a distressing life event should not be diagnosed as an adjustment disorder. When a stressor precipitates a depressive condition that meets the severity and symptom criteria for major depression, the diagnosis of major depression is made, regardless of the condition’s etiologic relationship to an identifiable stressor.

Mood disorders due to a general medical condition (or substance) refers to psychiatric syndromes judged to result from the direct physiologic consequence of a general medical condition (e.g., hypothyroidism), substance use (e.g., amphetamine withdrawal), or medication (e.g., interferon). Treatment focuses on resolution of the underlying general medical problem or withdrawal of the offending medication, although specific psychiatric treatment may also be useful.

Bipolar disorder is a common and severe mental illness, occurring in about 3–4% of the general population, causing significant disability, and carrying 80–85% genetic heritability. Bipolar I disorder refers to patients with a history of at least one episode meeting full criteria for major depression and at least one other distinct episode meeting criteria for mania. Other bipolar spectrum disorders such as bipolar II disorder (a condition marked by episodes of major depression and at least one documented episode of hypomania, not mania) and cyclothymic disorder (no episodes meeting full criteria for either major depression or mania/hypomania) are probably much more common, thought to occur in approximately 4–6% of the population.

Bipolar depression refers to an episode of illness meeting criteria for major depression in a patient with a history of either mania or hypomania. It can be very difficult for physicians to differentiate an episode of major depression from an episode of bipolar depression because the two conditions are phenotypically identical, that is they present the same signs and symptoms. It is extremely important, however, to distinguish between major depression and bipolar depression because the two conditions, though they present with the same symptoms, should be treated very differently. Studies in primary care indicate approximately 25% of patients presenting with symptoms that suggest the diagnosis of major depression actually suffer from bipolar depression.

Evidence for the best treatment of bipolar depression, however, is still somewhat limited and controversial. Only two medications, quetiapine and a combination product (olanzapine and fluoxetine) have received Food and Drug Administration (FDA) approval for the treatment of bipolar depression. Lamotrigine has FDA approval for maintenance treatment of bipolar depression, but is not yet approved for acute bipolar depression. Many experts recommend treating bipolar depression with a combination of a mood stabilizer (e.g., lithium, valproate, or carbamazepine) plus an antidepressant. Experts agree, however, that bipolar depression should not be treated with an antidepressant alone. Such “unopposed” treatment (i.e., antidepressant without mood stabilizer) increases the likelihood of precipitating an affective switch from depression to mania. Failure to elicit a history of mania or hypomania by the physician can lead, therefore, to potentially serious consequences by (mis)treating the condition with an antidepressant alone, thereby increasing the chances of a “switch” into mania or hypomania, with attendant risks of erratic or irrational behavior, poor judgment in social, occupational, economic, or interpersonal situations, psychosis, and even suicide. The section below on differential diagnosis provides physicians with some guidelines to help them make the diagnosis of bipolar depression in patients presenting with the symptom profile of major depression.

Melancholia is a severe form of major depression, often but not necessarily, associated with psychosis (“psychotic depression”). The symptom profile of melancholia includes lack of mood reactivity to usually pleasurable stimuli, loss of pleasure in all (or almost all) activities, distinct quality of depressed mood, diurnal variation in mood (worse in the morning), early morning awakening, marked psychomotor retardation or agitation, significant weight loss, and excessive or inappropriate guilt. This subtype of major depression is most closely associated with the so-called “biological markers” of depression, that is, nonsuppression of endogenous cortisol after administration of exogenous dexamethasone (DST), blunted thyroid-stimulating hormone (TSH) response to exogenous IV administration of thyrotropin-releasing hormone (TRH), and characteristically abnormal sleep physiology (including prolonged sleep latency, early-onset rapid eye movement [REM], increased total REM, and increased REM density). It appears that presence of melancholic features may predict preferentially better response to tricyclic medications (vs. the selective serotonin reuptake inhibitors [SSRIs]). The presence of melancholic features predicts a positive response to electroconvulsive therapy (ECT).

Epidemiologic studies demonstrate a lifetime prevalence of major depression in 7–12% of men and 20–25% of women. The point prevalence of major depression in a community sample is 2.3–3.2% for men and 4.5–9.3% for women. Reasons for these gender differences have not been fully elucidated, but both biological and sociocultural factors are involved. Numerous studies report a 10–15% prevalence of major depression in ambulatory medical settings with a substantially higher rate (20–40%) in patients with coexisting medical problems, particularly in those with diseases associated with strong biological or psychological predispositions to depression (e.g., stroke, Parkinson disease, traumatic brain injury, diabetes, coronary atherosclerotic disease, pancreatic cancer, and other terminal illnesses).

Prevalence of depression varies among age groups. Recent data point to a cohort effect through which current “baby boomers” experience the highest rates of depression of any previous generation. Although the most current epidemiologic findings show a surprisingly low 1-year prevalence rate of major depression in the elderly (1–2%), the rate of major or minor depression in elderly patients who seek treatment in primary care practices is 5%, with rates ranging from 15% to 25% in nursing home residents. Major depression is often misdiagnosed in elderly primary care patients as signs of aging, and cognitive impairment may also complicate accurate diagnosis. Some medications commonly prescribed in the elderly population may actually precipitate the onset of depression or cause symptoms like fatigue and poor concentration, which may mimic depressive symptoms.

Because the usual age of onset of depression is under the age of 40 years, an apparent first episode of depression in an older patient should prompt a thorough evaluation to exclude other underlying disease and/or medication effects.

Major depressive disorder represents a heterogeneous group of disorders. It is likely that future research will eventually provide diagnostic specificity to these disorders, leading to more targeted and effective treatments. For present purposes, however, the clinical manifestation of a major depressive episode should be considered a final common psychobiological pathway among multiple candidate etiologic determinants. Dramatic advances, however, in genetic, anatomic, physiologic, and immunologic studies already point the way toward a more precise biological understanding of this common and disabling condition.

Recurrent major depression has been shown to have a heritability of 35–40%, and genetic linkage studies have begun to identify specific regions of the genome thought to be candidates for carrying depression susceptibility. One particularly interesting candidate gene is the serotonin transporter gene (5-HTT), which makes functional sense since many antidepressants seem to work through binding to the 5-HTT protein. Recent gene by environment studies have explored the relationship between heterozygous and homozygous states and response to negative life events. While the results are not clear, this type of exploration illustrates the potential impact of genetic and environmental interactions.

Twin studies on depression in women indicate that genetic factors play the strongest etiologic role in depression, followed by recent (as opposed to early environmental) negative life events. Animal studies, on the other hand, demonstrate that early environmental stress predisposes to biological abnormalities associated with depression that may not emerge until adult life.

Postmortem pathologic studies, along with functional and structural imaging studies, converge in locating anatomic loci of depressive illness in the hippocampus, the dorsolateral prefrontal cortex, the anterior cingulate cortex, and the amygdala. Animal and human studies confirm volumetric decreases in the hippocampus in depressive illness in individuals with a history of adverse childhood events. Antidepressant medications appear to induce neurogenesis (increases in volume) in the hippocampus, possibly through increases in brain-derived neurotrophic factor (BDNF).

From the physiologic point of view, a considerable body of emerging evidence now conceptually and experimentally points to dysregulation of distributed brain networks and second messenger abnormalities as the underlying neurobiological abnormalities in recurrent mood disorders. This contrasts with earlier theories postulating that straightforward monoamine neurotransmitter deficits (e.g., decreases in norepinephrine, serotonin, and/or dopamine) serve as the biological substrate of depression. Lastly, immunologic studies have consistently found abnormalities of cytokines associated with depressive illness. Advances in all these biological correlates of depression hold great promise for the development of more specific and more effective treatments of depressive disorders in the not too distant future.

High Stress & Low Support

From a societal perspective, significant life stress, and/or lack of social support predisposes to development of MDD. Life stress that involves loss, for example, death of a parent or spouse, the end of a relationship, and events involving loss of self-esteem, such as termination from a job, create particular vulnerability for depression. Low social support, both independently and in the face of significant stress also predisposes to depressive disorder. Low perceived social support, that is, the extent to which an individual believes himself or herself to lack a supportive social network, creates a higher risk than any absolute or objective measure. (It is worth noting that these same risk factors of high stress and low support tend to increase risk for all illnesses, whether psychiatric or general medical illnesses.)

The stress caused by natural disasters also increases the vulnerability of survivors to depression. While the psychiatric impact of such disasters includes increased prevalence rates of posttraumatic stress disorder (PTSD), substance abuse, and other conditions, the increased rate of depression itself is significant and measurable. For example, children and adults in the tsunami-affected areas of southwestern Thailand showed significantly increased and persistent rates of depression—ranging from 6% to 30% depending upon level of exposure and level of life disruption. Similarly, war has always been a stressor with major mental health consequences. For example, the US ground troops in Iraq have shown an increase in prevalence of depression from 11.4% prior to deployment to 15.2% after deployment.

With increased life expectancy and the aging of the population in the United States, spousal caregiving of persons with disability, including dementia, is increasing. Caregivers (most often the female partner) of spouses with chronic neurodegenerative illnesses (e.g., Alzheimer disease) experience extreme physical and emotional burden. The role of caregiver presents a situation of both high stress and increasingly low support (as the caregiver progressively loses any emotionally meaningful relationship with the patient). Up to 40% of caregivers of patients with progressive dementia suffer from significant depressive symptoms or major depression.

Postpartum “blues” typically occurs in 50–80% of women within 1–5 days of childbirth and lasts up to 1 week. This “normal” reaction should be distinguished from postpartum depression, which occurs in 10–15% of women in the first 3–6 months after childbirth. Postpartum psychosis, which occurs in 0.5–2.0/1000 deliveries and typically begins 2–3 days after delivery, and is most common in individuals with a personal or family history of bipolar disorder. Postpartum psychosis is a highly acute psychiatric illness that usually requires mood stabilizers such as neuroleptic medications or lithium, and psychiatric referral (see Chapter 16).

The criteria for major depression require that five of nine symptoms be present for a 2-week period (Table 25-1). One of these nine symptoms must be either a persistent depressed mood (present most of the day, nearly every day) or pervasive anhedonia (loss of interest or pleasure in living).

Clinicians should realize that a depressed mood is not synonymous with major depression and is neither necessary nor sufficient for a diagnosis of major depression. Sadness (or tearfulness) does not constitute major depression (four other symptoms described in the following paragraph are necessary), and, conversely, major depression can be diagnosed without the presence of depressed mood (if pervasive anhedonia is present), a presentation that is more common in the elderly.

Organizing these nine symptoms into clusters of four hallmarks can facilitate clinical evaluation: (1) depressed mood; (2) anhedonia; (3) physical symptoms (sleep disorder, appetite problem, fatigue, and psychomotor changes); and (4) psychological symptoms (difficulty concentrating or indecisiveness, guilt or low self-esteem, and thoughts of death). Physical symptoms predict a favorable response to biological intervention. For example, when middle insomnia is present (awaking at 3 or 4 a.m. with an inability to return to sleep) and when a diurnal variation in mood is present (feeling more depressed in the morning), patients are more likely to respond to biological interventions.

The Fallacy of “Good Reasons”

Depression is often mistakenly believed to be an “expected” result of stressful life events. Studies of individuals under stress (e.g., terminal cancer or natural disaster) do show rates of major depression above the general population rate, but these rates do not exceed 50%. Although sad or depressed affect is an expected accompaniment of a stressful event, the full syndrome of major depression certainly does not appear in everyone. Thus, life stressors may seem to provide “good reasons” for sadness, but a stressful event, in itself, should not be considered a rationale to withhold depression treatment. If a major depressive syndrome emerges following a stressful life situation, the medical provider should treat it appropriately. This is similar to treating other medical conditions that have a “good reason,” such as hypovolemic shock from a gunshot wound—the etiology is evident but the condition clearly requires treatment.

The term reactive depression has historically suggested a mild syndrome without a biological substrate, resulting from a psychosocial precipitant, and treatable with psychotherapy alone. None of these assumptions is true. Stressful events can precipitate very severe depressions; a biologically predisposed individual may suffer major depression in response to a minor life event; a major depression following a life stressor may develop a biological substrate; and a major depression from a life stress may respond to biological therapy as well as or better than it responds to psychotherapy. Thus, the presence or absence of identifiable precipitants is irrelevant to the diagnosis of major depression, which can be treated pharmacologically whether or not the condition resulted in part from psychological stressors. Depression is a frequent, but not an inevitable consequence of a stressful life event. When major depression is present, it should be treated aggressively.

The Confound of Overlapping Etiology

A comorbid general medical condition (such as cancer or Parkinson disease) may seemingly “cause” many of the physical symptoms of major depression, such as fatigue, anorexia, or psychomotor retardation. These symptoms may lead clinicians to discount their relevance and thus disregard the possibility of a treatable depression. However, a physical symptom may be “caused” by a physical illness (e.g., cancer) or by a major depressive illness or both. It is important to include these symptoms in the initial diagnostic approach to depression in the medically ill, and exclude them only if they are clearly and fully accounted for by the physical illness. Although this “inclusive” approach might seem to result in the overdiagnosis of major depression; studies in stroke, Parkinson disease, hospitalized elderly, and traumatic brain injury indicate that the problem of overdiagnosis is quite low (around 2%) and the underdiagnosis of depression is more of a problem.

Build Trust by Responding to Distress

The medical interview holds the key to the assessment of major depression. Efficient assessment involves attention to data-gathering as well as rapport-building functions of the interview. Physicians should always be alert for nonverbal cues of depression: for example, a sad mood may be communicated by downcast eyes, slow speech, wrinkled brow, or tearful affect. When a depressed mood is detected or emotional distress is suspected, physicians should first respond empathically to this distress, by demonstrating a caring attitude, and using attentive silence or direct reflective and empathic statements, such as “I can see you’re having some trouble,” or “It sounds like you’ve been under a lot of stress lately,” or “You seem pretty down right now.” Responding directly to the patient’s distress in this way builds trust and encourages the patient to more openly share his or her feelings that may underlie a depressive illness.

Use Direct, but Open-Ended Questioning

Use open-ended questions and facilitation techniques to provide patients with the opportunity to discuss the issues that may be troubling (see Chapter 1). In gathering data for assessment, physicians should focus on anhedonia (e.g., “What do you enjoy doing these days?”) and depressed mood (e.g., “How has your mood been the last few weeks?” or “Have you been feeling sad, blue, or down in the dumps?”). These simple questions can effectively uncover an underlying depression in most patients, despite the fact that most depressed patients in the general medical setting initially present with chief complaints more related to physical and bodily symptoms (e.g., headache, fatigue, and insomnia).

Involve the Family

Optimal assessment and management of the depressed patient is enhanced by involvement of one or more significant other(s). A spouse, a partner, a parent, or others can help the physician gather useful information regarding the patient’s mood, activities, behaviors, and history. In fact, because of stigma, denial, and other psychosocial barriers, other persons often provide much more accurate information regarding depressive illness than the self-report of the patient himself or herself.

The Patient Health Questionnaire: Screening, Assessment, Engagement, & Monitoring

The US Preventive Services Task Force (USPSTF) supports screening for depression “in clinical practices that have systems in place to assure accurate diagnosis, effective treatment, and careful follow-up.” Although many tools to screen for depression are available, USPSTF recommends the use of a straightforward two-item (“yes/no”) screener for major depression that is as effective as longer screening instruments. When administered verbally, clinicians can ask:

1. 
   

   “Over the past 2 weeks, have you ever felt down, depressed, or hopeless?” and

   
   
2. 
   

   “Over the past 2 weeks, have you felt little interest or pleasure in doing things?”

A positive answer to either of these two questions requires a full diagnostic assessment for major depression. This screener has over 90% sensitivity but relatively low specificity (many false positives). Alternatively, many experts now advocate administration of the full PHQ-9 (Appendix 25-A) to “red flag” patients, that is, patients likely to be at high risk of major depression. “Red flag” patients generally include those with chronic medical illness (e.g., diabetes), and patients with persistent unexplained medical complaints. This one-step approach, combining screening and assessment, can simplify operational strategies.

The PHQ-9 is an assessment and severity tool that has been validated for use in general medical as well as specialty psychiatric settings. A score of 10 or more has been demonstrated to have 88% sensitivity and 88% specificity for the diagnosis of major depression. Furthermore, the tool can also be used effectively as a severity tool to track patients’ symptom severity and improvement over time. The instrument and scoring key are in Appendices 25-A and 25-B. Pfizer holds the copyright for this tool, but it can be used in the public domain for clinical purposes or research. Readers are also referred to the web site of the MacArthur Foundation Initiative on Depression in Primary Care for materials related to the use of this instrument (www.depression-primarycare.org).

Patient Barriers: Somatic Presentations & Stigma

Patients in general medical practice with major depression typically present with physical complaints, such as pain (headache, backache), fatigue, insomnia, dizziness, or gastrointestinal (GI) problems. Many of these patients are willing to acknowledge feelings of depressed mood and to consider the possibility that biologically mediated depression may also cause or exacerbate their physical problems. There are many somatically preoccupied patients, however, who do not experience any depressed affect at all, and, without this self-appraisal of sadness, they are reluctant to consider the possibility that depression may contribute to their physical problems. In these patients, evaluating both general medical and psychiatric problems simultaneously saves time, expense, and frustration for both the physician and the patient. In addition, many patients and families (particularly in some cultures) are reluctant to accept the diagnosis of depression because of associated social stigma. Physicians can help overcome this barrier by understanding and explaining to patients and families that depression is a common and treatable illness, like other medical illnesses. They may explain that depression represents a chemical imbalance that can, like diabetes and other medical conditions, be corrected or managed with adequate treatment.

Clinician Barriers

Depression is often undetected or is not adequately treated in the medical setting. Some physicians avoid depression diagnoses because they harbor the same stigmatizing attitudes toward depression that many of their patients feel. In addition, inadequate knowledge and skill, lack of time, reluctance to “open up” new domains of emotional distress, and misaligned financial incentives all operate as barriers to physician recognition and treatment. However, early recognition of behavioral and psychiatric disorders is time efficient in the long run while minimizing the cost and risk of extended, unnecessary workups for nonspecific physical complaints.

Suicide risk must be evaluated in all patients with symptoms of depression. It is one of the top 10 causes of death in all age groups, and one of the top 3 causes in young adults and teenagers. Risk factors for completed suicide include gender (elderly white males are at highest risk), alcoholism, psychosis, chronic physical illness, lack of social support, recent humiliation, and use of generally lethal methods (e.g., gun rather than overdose of pills). Increased risk of suicide has also been noted among depressed adolescents and among gay and lesbian patients. Explicit suicidal intent, hopelessness, and a well-formulated plan indicate relatively higher risk. Many patients who eventually commit suicide visit a primary care physician in the weeks before they take their lives.

Physicians are sometimes reluctant to explore suicidal ideation in the mistaken belief that asking about suicide may actually increase a patient’s risk. To the contrary, assessment of suicidal tendencies usually reassures patients, reduces anxiety for both patient and provider, and facilitates partnership in suicide prevention.

The assessment of suicidal ideation is best approached gradually, with general questions like, “Do you sometimes feel that life is not worth living?” and then asking more specifically about a history of suicide attempts, any specific current plans, hopelessness, and any specific current intentions. Once a patient reveals suicidal ideation, the physician must consider psychiatric consultation and hospitalization. If outpatient management is considered, some experts suggest that physicians consider use of a “no suicide contract.” The no suicide contract involves asking the patient to promise that he or she will contact the physician (or other appropriate caregiver) if there is a danger of losing control of a suicidal impulse. In using such a “contract,” however, physicians need to realize that there is no convincing empirical evidence to support its validity. In fact, other experts specifically advise against its use, arguing that a mechanistic pursuit of obtaining a “contract” can functionally undermine an open relationship and provide physicians with a false sense of security. The main utility of the “contract” may be as tool to discuss the strength of the individual’s suicidal ideas.

In all cases, when treating depression, physicians must evaluate suicidality at the initiation of treatment and throughout the treatment program.

Routine use of the PHQ-9 can aid in assessing suicide risk at the initiation of treatment and, of equal importance, can also aid in the recognition of any subsequent or treatment-emergent suicide risk. Because the risk of suicide sometimes increases within the first few weeks of treatment and can emerge at any point in the subsequent treatment, regular and routine use of the PHQ-9 can function as an efficient and effective suicide reassessment tool. The Columbia-Suicide Severity Rating Scale is a useful clinician-administered instrument (http://www.cssrs.columbia.edu/about_cssrs.html).

There are no specific diagnostic signs of depression. A careful medical history and physical examination are required for the evaluation of depression at all ages, but especially in the elderly. Some medical “mimics” of depression (e.g., hypothyroidism and Cushing syndrome) present with classic physical signs.

No laboratory studies can be used to diagnose major depression reliably or specifically. A general laboratory screen (complete blood count, chemistry profile, urinalysis, TSH, and vitamin levels), however, may be useful in selected patients to rule out other conditions that may mimic or exacerbate depression. In treatment-resistant cases, or when indicated, brain imaging, an electroencephalogram (EEG) or lumbar puncture (LP) can be considered, but these studies are not part of the standard work up. Patients over the age 40 years usually require an electrocardiogram (ECG) to rule out conduction disturbances or bradycardia if treatment with a tricyclic antidepressant (TCA) or if citalopram at doses greater than 40 mg/day are being considered since those doses may be associated with prolonged QT intervals and arrhythmias

Mental Disorders

Other mental disorders often present with symptoms similar to depression; in addition, depression often presents in combination with other mental disorders. Thus, knowledge of other mental disorders common in medical practice is essential for adequate assessment and management of depression. In the presence of psychiatric comorbidity, effective treatment of depression may lead to improvement in the other condition as well. Modifications of treatment, however, may be necessary depending on the particular comorbidity present.

Major Depressive Disorder versus Bipolar Depression

One of the most important, yet difficult, differential diagnostic questions facing the physician is to distinguish MDD from bipolar depression (discussed earlier). The clinical signs and symptoms of the two disorders are identical and the differential diagnosis hinges on one and basically only one crucial historical question: Did the patient ever experience clinical mania or hypomania? The symptoms of a manic episode are listed in Table 25-2, the most common of which include an elated or irritable mood, racing thoughts, poor judgment in interpersonal, sexual, or financial situations, and excess energy. Criteria for hypomania are the same, but are less intense and not disruptive of normal functioning. To uncover a possible history of mania/hypomania, the physician should ask about any personal or family history of treatment of mania/hypomania/bipolar disorder and whether the patient has ever experienced any distinct period when he or she experienced racing thoughts, markedly decreased need for sleep, especially high energy or unusually poor judgment, out of character to the patient’s usual behavior. The Mood Disorders Questionnaire (MDQ) can be added to the physician’s diagnostic armamentarium as a guide (Table 25-3), though its sensitivity and specificity are not high enough to rely on as a stand-alone tool. Even if there is no history of mania/hypomania, if the individual has a strong family history of bipolar disorder, the clinician must consider that at least one-third of bipolar patients have depression as their index mood episode. Such a history should help make the clinician alert to potential mood switches with antidepressant treatment. In addition, such patients may also be resistant to antidepressant strategies and require mood stabilizers instead.

Anxiety Disorders

Anxiety and depression commonly co-occur in medical patients. Most patients with depression suffer from anxiety symptoms or a formal anxiety disorder and most patients with an anxiety disorder have depressive symptoms or meet criteria for major depression. The most common anxiety disorders in medical outpatients are PTSD, generalized anxiety disorder (GAD), panic disorder (PD), and obsessive-compulsive disorder (OCD). Central features of these disorders include pervasive and disabling anxiety (e.g., GAD), discrete panic attacks (e.g., PD), or the presence of unreasonable, uncontrollable, and repetitive behaviors (e.g., compulsions such as hand-washing or checking the stove) or the presence of intrusive, uncontrollable, and disturbing thoughts (e.g., sexual and violent obsessions in a patient who has no history or risk of such behaviors) (e.g., OCD). Treatment of the major depression by itself, however, often helps to resolve or improve these other coexisting conditions (see Chapter 26), especially since many antidepressant medications have proven safe and effective for treating some common anxiety disorders.

Somatic Symptom Disorders

Depression often presents with unexplained bodily complaints. It can therefore be challenging to differentiate between a depressive illness and somatic symptom disorder which includes previously used terms such as medically unexplained symptoms (see Chapter 28). Depressive disorders are highly treatable, but somatic symptom disorders can be more chronic and refractory to treatment. Somatic symptom disorders are usually best managed conservatively with a focus on improved functioning, whereas depression should be treated aggressively with the goal of complete recovery. Any of the somatic symptom disorders (formerly diagnosed as conversion, somatization, hypochondriasis, body dysmorphic disorder, and somatoform pain disorder) can present comorbidly with major depression. Approximately 50% of patients with persistent unexplained physical complaints suffer from depression. Effective treatment of major depression usually improves the severity, intensity, and functional impairment of a comorbid somatic symptom disorder.

Related posts:

1: The Medical Interview 8: Global Health and Behavioral Medicine 19: Behavior Change 27: Attention Deficit Hyperactivity Disorder 37: Errors in Medical Practice 40: Palliative Care, Hospice, & Care of the Dying

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