Psychiatric Illness, Depression, Anxiety, and Somatic Symptom Disorder
Joseph Gregory Hobelmann
Mark D. Sullivan
Michael R. Clark
Ajay D. Wasan
Chronic pain and psychiatric illness commonly occur together.1 Yet the high rates of psychiatric illness in patients with chronic cancer and noncancer pain are still poorly understood. Diagnostic hierarchies taught to physicians in medical school and residency, impairment rating strategies used by compensation systems, and the natural scientific method used by medicine that looks for objective causes for clinical symptoms force us into a mind-body dualism. George Engel2 helped develop our modern concept of “psychogenic pain.” Psychogenic pain has been defined as pain due to psychological factors in the absence of an organic basis for pain.3 If we cannot explain pain in terms of objective tissue pathology, Western biomedicine lures us to explain it in terms of patients’ psychopathology.4,5 This is not an evidence-based strategy but rather a reflection of what it means to explain a symptom in modern biomedicine.
The majority of patients with chronic pain and psychiatric illness have a physical basis for pain in the body, whose perception is made worse by overlying psychiatric illness.6 Epidemiologic evidence supports the use of inclusive rather than exclusive models of psychiatric diagnoses in medical settings that allows for the presence of both medical disease and mental disorders (i.e., a comorbidity model). Medical illness in no way excludes the possibility of a clinically important psychiatric illness. Medically ill patients are much more likely to have psychiatric illness than patients without medical illness. Psychiatric illness in no way precludes the possibility of a clinically important medical illness. Psychiatric illness is, in fact, associated with health behaviors and psychophysiologic changes known to promote medical illness.
The structure of our clinical settings makes the integrated delivery of mental and physical health care difficult. Nowhere is this more important than in the care of the patient with chronic pain. Psychotherapeutic interventions for chronic pain are rarely effective in isolation from somatic treatments, and the success of somatic treatments is diminished by co-occurring mental illness. Distress, disuse, and disability are important facets of a chronic pain problem, and all require clinical attention by the pain practitioner. Neglect of one of these components can result in treatment failure even in the presence of excellent care for the other components. Research has indicated that psychiatric comorbidity has an adverse impact on treatments for chronic pain, such as rehabilitation, spinal cord stimulation, or opioid therapy.3,7 Although the details of these interactions are quite relevant to understand, this chapter concentrates on the recognition and diagnosis of psychiatric illness in patients with chronic pain, a sizable task in and of itself. Similarly, psychiatric comorbidity has shown to be particularly prevalent in and salient to the outcomes of a range of noncancer pain disorders (e.g., chronic low back pain,8 fibromyalgia,9 temporomandibular joint disorder,10 chronic daily headache,11 and chronic pelvic pain12). However, the specific role that comorbid psychopathology plays in each of these disorders is beyond the scope of this chapter.
This chapter first outlines an approach to psychiatric diagnosis and to categorizing psychiatric symptoms in patients with chronic pain. Because of the breadth of psychiatric symptoms in pain patients, this section is substantial in order to provide a framework for organizing symptoms into diagnostic and treatment categories. Then, this chapter discusses the main illness categories of depression, anxiety, personality, and somatoform disorders. It is beyond this chapter to discuss to what extent a pain practitioner should evaluate and treat psychiatric problems and when to refer to a psychologist or psychiatrist.
Psychiatric Nosology and Diagnostic and Treatment Approaches
As noted, any discussion of psychiatric disorders in patients with chronic pain is haunted by the concept of psychogenic pain. We are drawn to the concept of psychogenic pain because it fills the gaps left when our attempts fail to explain clinical pain exclusively in terms of tissue pathology. Psychogenic pain, however, is often merely a diagnosis of exclusion made solely on the basis of the inability to identify an objective cause for pain. Positive criteria for the identification of psychogenic pain, mechanisms for the production of psychogenic pain, and specific therapies for psychogenic pain are lacking. Furthermore, neuroimaging studies indicate that anticipated pain, imagined pain, or empathizing with the pain of another are associated with activations of the same brain areas involved in processing a painful stimulus, such as applied noxious heat (the lateral and medial pain systems).13,14 Thus, there is a dynamic interaction between our mental states (mind) and brain function. The dichotomy between mind and body (including brain) underlying the concept of psychogenic pain is hollow. As discussed later in this chapter, it may be more useful to frame the contributions of the mind to pain perception in terms of a process of central sensitization.
Psychiatric diagnosis of many disorders, such as depression, can be helpful to the clinician and patient by pointing to specific effective therapies. The Diagnostic and Statistical Manual of Mental Disorders (5th ed.; DSM-5) lists the current diagnoses treated by psychiatrists and the specific symptoms that serve as descriptive criteria for each condition.15 However, DSM offers only consistency and reliability of symptoms and does not take into consideration course of illness, which is essential in recognizing mental illness.16 This is particularly true of psychiatric disorders in those with medical illness. Most psychiatrists tend to use the DSM as a guide to the major diagnoses, not as a definitive diagnostic method. As a descriptive tool, many of the symptom lists for DSM diagnoses are quite complete and will be referred to throughout this chapter. However, when patients with chronic pain are in need of psychiatric care, they want to know the generative nature of their conditions and how to differentiate them for the sake of receiving prognoses and treatments.17 Multidisciplinary pain treatment functions with the same limitations.18,19 Without the method to determine a set of unique causes and direct specific treatments, the patient receives symptomatic treatments with the expected
“partial” response. Despite the involvement of more disciplines, the approach is clearly dualistic—cures for “organic” problems and management for “functional” problems. Cartesian dualism lives.
“partial” response. Despite the involvement of more disciplines, the approach is clearly dualistic—cures for “organic” problems and management for “functional” problems. Cartesian dualism lives.
The DSM, although it has limitations, provides a taxonomy that serves as the basis for psychiatrists and psychologists to communicate and further study disorders. This has been historically lacking for the classification of chronic pain conditions. However, the Analgesic, Anesthetic, and Addiction Clinical Trial Translations Innovations Opportunities and Networks (ACTTION) has partnered with the U.S. Food and Drug Administration and the American Pain Society (APS) to develop an evidence-based chronic pain classification system called the ACTTION-APS Pain Taxonomy (AAPT).20 This classification incorporates available knowledge regarding both physiologic and biopsychosocial mechanisms contributing to pain conditions. It is important to recognize that psychological and social factors are not solely secondary consequences of chronic pain but rather play a complex role in the persistence and severity of pain conditions. These biopsychosocial factors can be risk factors, protective factors, and process variables within the dynamic system of forces that constitute a chronic pain condition.21 The AAPT classification system provides a framework that incorporates these complicated factors and could be very useful clinically if validated in future outcome studies.
Patients with chronic pain come to or are referred to a psychiatrist because they are ill. In some way, they are considered a diagnostic dilemma.22,23 Despite the utilization of extensive health care resources to perform an exhaustive evaluation, the patients remain ill. A temptation emerges to diagnose them with a psychogenic problem because no “good” cause can be found for their persistent pain and the accompanying disability and suffering.24 The cause for their illness cannot be found until the investigation expands to include the domain of personal meaning.25 This realm contains not only the diseases of the brain (cerebral faculties) but also the disruptions of the motivational rhythms of behavior, the psychological constitution of the individual, and the personal chronicle of desire and relationships. All mental disorders are expressions of life under altered circumstances that affect characteristic mental capacities and generate particular expressions.26,27 These distinctions allow for independently informed perspectives about the nature of mental disorders and what may have happened to generate the disorder.
Four perspectives (diseases, behaviors, dimensions, and life stories) represent classes of disorders that each have a common essence and logical implications for causation and treatment.28,29 In this approach to patient care, diseases are what people have, behaviors are what people do, dimensions are what people are, and life stories are what people encounter. The formulation of a patient with chronic pain should address the contributions from each perspective to the overall presentation and inform the design of a treatment plan that can address each component of the patient’s illness. Although the basis for a mental illness may be dominated by one perspective (i.e., the disease perspective in schizophrenia), generally, each psychiatric diagnosis has contributions from each perspective that are responsible for the onset and maintenance of the disorder.
Diseases of the brain may manifest psychologically. The psychological faculties of the brain include, but are not limited to, consciousness, cognition, memory, language, affect, and executive functions. Abnormalities in the structures or their associated functions of these faculties are expressed in the symptoms typical of common diagnoses such as delirium, dementia, panic disorder, and major depression. However, the patient may describe deficits in these faculties with difficulty and rely on somatic symptoms (e.g., pain) as incomplete proxies for these criteria. The physical symptoms occur because the brain is malfunctioning and suggests pathology in the body. The unifying feature of diseases is a broken part within the individual that is causing the characteristic signs and symptoms typically manifested by the affliction.27 For the patient, only the symptoms and reduction of symptoms are of concern. Finding a cure may repair the broken part, prevent the initial damage from progressing, or compensate for the pathology through secondary compensatory measures.
The perspective of behavior encompasses a wide range of actions and activities. The complex behaviors of human beings are designed with purpose to achieve goals. Human consciousness is characterized by the regular, rhythmic alterations of attention and perception produced by internal drives that increase a person’s motivation toward a particular activity.29,30 The drive pushes the individual into action. Then, after the actions, the drive is satisfied and a state of satiety emerges. Over time, drives reemerge with subsequent effects on the individual’s perceptual attitude toward his setting. In addition, personal assumptions or external opportunities increase the likelihood of certain behaviors. These present a choice to the person who must decide what action to take. After the choice is made and the behavior completed, external consequences emerge from the outcome and influence future actions. The person learns which choices are most effective. When aspects of choice and control over behavior become disrupted, physicians will be asked to address the distorted goals, excessive demands, damaging consequences, and a lack of responsiveness to negative feedback.31,32 Eating disorders and opioid use disorders are examples. Treatment of behavioral disorders begins with regaining temporary control of the situation by stopping the behavior.33 Restricting the patient’s actions and preventing these problematic behaviors eventually limits the chaos of destructive actions. This stable foundation is required for the patient to gain insight about and motivation toward appropriate choices that will result in less distress and more satisfaction.34 This is the basis for the effectiveness of behavioral approaches to chronic pain management as outlined in other chapters.
In contrast, many mental disorders emerge not from a disease of the brain or some form of abnormal illness behavior but a patient’s personal affective or cognitive constitution.29,30 Each individual possesses a set of personal dimensions such as intelligence, extraversion, and neuroticism. These traits describe who a person is, and they are carried into the world as a set of innate capabilities of their psychological makeup. Which traits are relied on and how much of them a person possesses will determine his potential to cope with different situations. Some circumstances are overwhelming and provoke a person’s vulnerability to distress. The patient cannot manage the situation and what is required because of who he is. Borderline personality disorder is an example (Table 31.1). It is probably the most severe personality disorder and generally is evident prior to the onset of pain. Assessment of personality traits is discussed at greater length in the following text. Treatment for disorders of the dimensional type focuses on remediation of specific deficiencies and guidance about overcoming potential vulnerabilities through adaptations such as education about, assistance with, or modification of the particular stressors.19,33
The life story perspective utilizes a narrative composed of a series of events that a person encounters and determines to be personally meaningful.29,30 These self-reflections are the means by which a person judges the value of his life as a whole. They impart a sense of self as the agent of a life plan unfolding in a social setting as well as the reflective subject experiencing and interpreting the outcome of such plans and commitments. If events are occurring as planned, then the person feels on track and successful. However, if the sequence of events results in an unexpected or disappointing outcome, the person will feel a sense of distress about this failure. Life story disorders are interpretive responses to life encounters such as grief from loss or anxiety due to expected threats.31,35,36 In patients with chronic
pain, the demoralization resulting from the inability to work or perform normal duties is a good example. Treatment begins with the expectation to forge a narrative of setting and sequence that suggests some role of the patient in his life, and that illuminates the troubled state of mind as the outcome of that role and course of events.19,33 The effective treatment of life story disorders requires reframing and reinterpretation to remoralize the patient by transforming the story into one with the potential for success and fulfillment.
pain, the demoralization resulting from the inability to work or perform normal duties is a good example. Treatment begins with the expectation to forge a narrative of setting and sequence that suggests some role of the patient in his life, and that illuminates the troubled state of mind as the outcome of that role and course of events.19,33 The effective treatment of life story disorders requires reframing and reinterpretation to remoralize the patient by transforming the story into one with the potential for success and fulfillment.
TABLE 31.1 Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Diagnostic Criteria for Borderline Personality Disorder | ||
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The four perspectives provide a comprehensive yet flexible approach to the evaluation of a patient in distress with chronic pain and other somatic symptoms.29,37 The treatments prescribed are now designed from the individual formulation and relevant perspectives. If a patient’s symptoms and distress continue, the physician must consider other factors that may have been overlooked. Usually, these factors are within one of the perspectives initially thought to be less important. A new combination of therapies is then required to treat the patient successfully. Understanding the relevant contributions from each perspective is important to formulating treatment. In the discussion that follows, categories of psychiatric disorders as defined in the DSM-5 (2013) of the American Psychiatric Association are used as an organizing strategy. The DSM-5 is relatively new, and there are significant changes from the DSM (4th ed., DSM-IV), which was utilized for almost 20 years. As such, there is little research using the new criteria, so this chapter discusses concepts utilizing both DSM-IV and DSM-5.
 FIGURE 31.1 Common psychiatric symptoms in patients with chronic pain. DSM, Diagnostic and Statistical Manual of Mental Disorders; Gen, general; Rx, prescription; SUDs, substance use disorders. (Adapted from Wasan AD, Alpay M. Pain and the psychiatric co-morbidities of pain. In: Stern T, ed. Comprehensive Clinical Psychiatry. Philadelphia: Elsevier; 2008:1067-1080.) |
Framework for Describing Psychiatric Symptoms
Figure 31.1 illustrates common psychiatric symptoms in patients with chronic pain. However, Figure 31.1 does omit substance use disorders, which are beyond the scope of this chapter. It is important to note that substance abuse or addiction in patients with chronic pain is estimated to range from 3% to 48% depending on the population sampled, with most estimates around 15%.38 Psychiatry-based research and health psychology-based research have contributed important insights into characterizing the mental life of patients with chronic pain. The findings from these epistemologies overlap significantly, and although lacking until recently, the new AAPT classification system for pain is a model for integrating these results.39 Common terms to describe the psychological condition in pain patients are heightened emotional distress, high negative affect, and elevated pain-related psychological symptoms (i.e., those that are a direct result of chronic pain, and when the pain is eliminated, the symptoms disappear). These can all be considered forms of psychopathology and psychiatric comorbidity because they represent impairments in mental health and involve maladaptive psychological responses to medical illness. This approach melds methods of classification from psychiatry and behavioral medicine to describe the scope of psychiatric disturbances in patients with chronic pain. Psychiatry is the field of medicine that is concerned with someone’s mental life, such as their emotions, experiences, thoughts, and behaviors. It is focused particularly on disruptive, disordered, or pathologic psychological states. Thus, the constructs from pain psychology are situated in Figure 31.1 as psychiatric symptoms, which in themselves can be at pathologic levels, just as depression symptoms can rise to a level considered abnormal.
In pain patients, the most common manifestations of psychiatric comorbidity involve one or more core psychopathologies
in combination with pain-related psychological symptoms. For instance, poor pain self-efficacy or high levels of pain catastrophizing are most often found in conjunction with high levels of depression or anxiety symptoms.40 These categories interact, and some component of each are part and parcel of other psychopathologies. In other words, “lumping” (a diagnostic approach) and “splitting” (a construct-based approach) are both valid approaches to psychiatric phenomenology. As described in the previous section, not all patients and their psychiatric symptoms fit neatly into DSM categories of illness. This is true not just of those with chronic pain, and hence, looking beyond DSM to broader and more specific methods of illness description and diagnosis is more prudent.
in combination with pain-related psychological symptoms. For instance, poor pain self-efficacy or high levels of pain catastrophizing are most often found in conjunction with high levels of depression or anxiety symptoms.40 These categories interact, and some component of each are part and parcel of other psychopathologies. In other words, “lumping” (a diagnostic approach) and “splitting” (a construct-based approach) are both valid approaches to psychiatric phenomenology. As described in the previous section, not all patients and their psychiatric symptoms fit neatly into DSM categories of illness. This is true not just of those with chronic pain, and hence, looking beyond DSM to broader and more specific methods of illness description and diagnosis is more prudent.
The pain-related psychological symptoms are described at length in other chapters, but it is important to understand how they interact with other psychiatric diagnoses. For example, painrelated anxiety (which includes state and trait anxiety-related to pain) is the form of anxiety most germane to pain.41 Elevated levels of pain-related anxiety (such as fear of pain) also meet DSM-5 criteria for an anxiety disorder due to a general medical condition. Because anxiety straddles both domains of core psychopathology and pain-related psychological symptoms, the assessment of anxiety in a patient with chronic pain (as detailed in the following discussion) must include a review of manifestations of generalized anxiety as well as pain-specific anxiety symptoms (e.g., physiologic changes associated with the anticipation of pain).
As indicated on Figure 31.1, elevated pain-related psychological symptoms have a clear, negative predictive relationship to many outcome areas. Poor coping skills often involve passive responses to chronic pain (e.g., remaining bed-bound and mistakenly assuming that chronic pain is indicative of ongoing tissue damage as a reason for inactivity). Poor copers employ few active self-management strategies (such as using ice, heat, or relaxation strategies for 10 to 20 minutes before resuming activities). Pain catastrophizing (cognitive distortions that are centered around pain) and low self-efficacy (a low estimate by the patient of what he/she is capable of doing) are linked with higher levels of pain and disability and worse quality of life.39 A tendency to catastrophize predicts poor outcome and disability, often independent of other psychopathology, such as major depression. Duration of chronic pain and presence of psychiatric comorbidity are each independent predictors of pain intensity and disability. High levels of anger (which occur more often in men) can also explain significant variance in pain severity.42
Depression
One must begin by distinguishing between depressed mood and the clinical syndrome of major depression. It is important to note, especially when working with chronic pain patients, that depressed mood or dysphoria is not necessary for the diagnosis of major depression. Anhedonia, the inability to enjoy activities or experience pleasure, is an adequate substitute. It is common for patients with chronic pain to deny dysphoria but to acknowledge that enjoyment of all activities has ceased, even those without obvious relation to their pain problem (e.g., watching television for a patient with low back pain).
The DSM-5 criteria for major depressive episodes are listed in Table 31.2. These include psychological symptoms, such as worthlessness, and somatic symptoms, such as insomnia. The three core symptoms of major depression in patients with pain (which also holds true in those without pain) are low mood, impaired self-attitude, and neurovegetative signs.43 It is important to note that somatic symptoms count toward a diagnosis of major depression unless they are caused by “the direct physiologic effects of a general medical condition” or medication. The poor sleep, poor concentration, and lack of enjoyment often experienced by patients with chronic pain are frequently attributed to pain rather than depression. These should generally not be excluded as a direct physiologic effect of pain. Given the high rates of depression in chronic pain patients, in the context of low mood complaints, it is best to attribute these symptoms toward a diagnosis of depression. Indeed, studies of depression in medically ill populations have generally found greater sensitivity and reliability with “inclusive models” of depression diagnosis than with models that try to identify the cause of each symptom.44 Similarly, just as in those without pain, those with depression and pain are very likely to also have high levels of anxiety.45,46
TABLE 31.2 Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Criteria for Major Depressive Episode | ||
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SUICIDAL IDEATION AND BEHAVIOR
Suicide accounts for 1.4% of all deaths in the world, making it the 15th leading cause of death.47 In the United States, 4.6% of the population surveyed had made a suicide attempt, and 13.5% reported a history of suicidal ideation.48 The majority of suicide attempts occur within a year of the onset of suicidal ideation. The risk of suicidality is greatest in patients with affective disorders (e.g., depression and anxiety), personality disorders, substance use disorders, and chronic debilitating physical illnesses.49,50 Depression is the most consistent and strongest predictor of suicidal ideation.51 In one study of patients with major depressive disorder, 58% reported suicidal ideation during a
current episode of illness.52 Suicide was attempted by 15% of these patients with 95% preceded by suicidal ideation. Hopelessness, low levels of function, perceptions of poor social support, and disorders of alcohol use predicted suicidal ideation.
current episode of illness.52 Suicide was attempted by 15% of these patients with 95% preceded by suicidal ideation. Hopelessness, low levels of function, perceptions of poor social support, and disorders of alcohol use predicted suicidal ideation.
Medical illnesses and chronic pain particularly, increase the risk of suicide. In a study of suicide in the elderly, medical conditions such as congestive heart failure, chronic obstructive lung disease, seizure disorder, and urinary incontinence were significantly associated with suicide with treatment for multiple illnesses increasing the risk.53 Yet, except for bipolar disorder, the highest risk of suicide was found in patients with severe pain (odds ratio [OR] = 7.52). Pain has been studied as a contributory factor in episodes of deliberate self-harm involving patients with medical problems admitted to a general hospital.54 Multiple studies have shown that patients with chronic pain are at greater risk for suicidal ideation, suicide attempts, and suicide completions.55
Most clinical diagnoses of pain conditions have been associated with increased risk for suicide.56 A recent comprehensive review notes that the likelihood of death by suicide in patients with chronic pain is 2 to 3 times the rate described in the general population.50 The lifetime prevalence of suicide attempts in patients with chronic pain ranged from 5% to 14%, and the rate of suicide attempts is double that found in the general population. The lifetime prevalence of suicidal ideation associated with chronic pain is approximately 20%. The rate of suicidal ideation in patients with chronic pain is estimated between 5% and 24%. Although a number of methods are used to commit suicide, overdoses with medications are the most common. The relationship between chronic pain and suicidality is complex. Although the associations are consistent, the cause and effect pathways of transition from suicidal ideation to suicide attempt to suicide completion are more difficult to describe. At this time, no successful algorithm exists and only an in-depth and longitudinal evaluation of the patient with chronic pain offers the best strategy for detecting who is considering suicide as a personal option. Although understandable, it is not the norm to be suicidal even in those with severe pain. Most commonly, suicidality in a patient with chronic pain is indicative of an underlying psychiatric disorder.57 Thinking one is better off dead (a passive death wish) is not the same as actively trying or wanting to kill oneself (suicidality). It is important to bear this distinction in mind in evaluating any patient with thoughts about death.
Part of the concern regarding the association between chronic pain and suicidality lies in whether chronic pain is an independent risk factor for suicidal behavior or the presence of depression completely explains this association. A thorough review described the evidence for eight pain-specific risk factors of suicidality, which is defined as suicidal ideation, suicide attempt, or suicide completion.50 The studies available suffer from significant limitations including inadequate assessments, retrospective designs, limited control groups, and the failure to distinguish between the potential risk factors of pain versus pain-related disability. However, the existing pain literature coupled with the general knowledge of suicide supports the following as the strongest predictors of suicidality: family history of suicide, previous suicide attempts, and presence of comorbid depression. Evidence exists for other risk factors including pain characteristics (intensity, location, type, duration), female gender, comorbid insomnia, catastrophizing and avoidance, desire for escape, helplessness and hopelessness, and problem-solving deficits.58,59,60 The prevention of suicide should remain a priority for the care of patients with chronic pain.
WHICH CAME FIRST, DEPRESSION OR PAIN?
Patients with chronic pain often dismiss a depression diagnosis, stating that their depression is a direct reaction to their pain problem. Psychiatry has long debated the value of distinguishing a reactive form of depression caused by adverse life events from an endogenous form of depression caused by biologic and genetic factors.61 Life events are important in many depressive episodes, although they play a less important role in recurrent and severe or melancholic or psychotic depressions.62 Determining whether a depression is a reasonable response to life’s stress may be important to patients seeking to decrease the stigma of a depression diagnosis and has been of interest to pain investigators (for a review, see Fishbain and colleagues6). It is not, however, important in deciding that treatment is necessary and appropriate. Indeed, no clinical benefit is gained from debating whether the depression caused the pain or the pain caused the depression, although such information may be useful in psychotherapy. If patients meet the diagnostic criteria outlined previously, it is likely that they can benefit from appropriate treatment. There is evidence that subsyndromal depression—depression symptoms not quite satisfying the threshold for major depression but debilitating nonetheless—also benefits from treatment and should be treated.63,64,65
Prospective studies of patients with chronic musculoskeletal pain have suggested that chronic pain can cause depression,66 that depression can cause chronic pain,67 and that they exist in a mutually reinforcing relationship.68 One fact raised to support the idea that pain causes depression is that the current depressive episode often began after the onset of the pain problem. The majority of studies appears to support this contention.69 However, it has been documented that many patients with chronic pain (especially those disabled patients seen in pain clinics) have often had episodes of depression that predated their pain problem by years.70 Among patients presenting to chronic pain clinics, one-third to more than one-half meet criteria for current major depression.71 Depression in patients with chronic pain is associated with greater pain intensity, more pain persistence, application for early retirement, and greater interference from pain, including more pain behaviors observed by others.72 This has led some investigators to propose that there may exist a common trait of susceptibility to dysphoric physical symptoms (including pain) and to negative psychological symptoms (including anxiety and depression).73,74 They conclude that “pain and psychological illness should be viewed as having reciprocal psychological and behavioral effects involving both processes of illness expression and adaptation.”
It may be useful when initiating depression treatment to accept that the pain caused the depression because it builds rapport and is consistent with epidemiologic evidence about the current depressive episode. And most frequently, depression follows the onset of chronic pain and is not preceded by it.71
DIFFERENTIAL DIAGNOSIS
When considering the diagnosis of depression in the patient with chronic pain, important alternatives include bipolar disorder, substance-induced mood disorder, and dysthymic disorder (particularly if accompanied by a severe personality disorder, such as borderline personality disorder). Patients with bipolar disorder have extended periods of abnormally elevated as well as abnormally depressed mood. These periods of elevated mood need to last more than one continuous day and include features such as inflated self-esteem, decreased need for sleep, and racing thoughts. A history of manic or hypomanic episodes predicts an atypical response to antidepressant medication and increases the risk of antidepressant-induced mania. Substance-induced mood disorders can also occur in those with pain. Patients with chronic pain may be taking medications such as opioids, corticosteroids, dopamine-blocking agents (including antiemetics), or sedatives (including muscle relaxants) that produce a depressive syndrome. Current medication lists should be scrutinized before additional medications are prescribed for any patient.
BIOLOGIC TESTS FOR DEPRESSION
A variety of biologic tests for depression have been investigated.75 These tests have included the dexamethasone-suppression test, thyrotropin-releasing hormone stimulation test, clonidineinduced growth hormone secretion, and rates of imipramine binding to platelet membrane serotonin transporters. Forty percent to 50% of patients with major depression do not show normal suppression of morning plasma cortisol after receiving dexamethasone the night before. However, high false-positive rates for this dexamethasone-suppression test exist in patients who are pregnant; patients with dementia, alcoholism, anorexia nervosa, and other chronic debilitating diseases; and patients who are taking medications that induce microsomal enzymes, including barbiturates and opioids. This has limited the clinical value of this test.76 The serotonin transport mechanism on platelet membranes is similar to that on serotonergic neurons. 3H-imipramine binding to this platelet receptor is reduced in patients with major depression. It appears to be further reduced in patients who have both pain and depression.77 Lower level of serotonin in the cerebral spinal fluid have found in depressed patients and have been linked to suicidal ideation.78 Although patients show significant differences on these tests, when considered as a group, substantial variation between individual patients limits the usefulness of these tests in the clinical setting. In the future, they may be able to provide a better understanding of the biochemical links between pain and depression.
DYSTHYMIC DISORDER
Dysthymic disorder is a chronic form of depression lasting 2 years or longer. The symptoms are generally less severe than those during an episode of major depression. Individuals with dysthymia can develop major depression as well. This combined syndrome has often been called double depression.79 It is important to note dysthymia because it is frequently invisible in medical settings, often being dismissed as “just the way that patient is.” Dysthymia has been shown to respond to many antidepressants, including the selective serotonin reuptake inhibitors (SSRIs).80 Treatment of double depression can be particularly challenging because of treatment resistance and concurrent personality disorders.81 Psychiatric consultation should be considered when dysthymia or double depression is suspected.
EPIDEMIOLOGY OF DEPRESSION
The prevalence of depression is much higher in medical settings and in patients with chronic illnesses than in the general population. It has been shown in studies using structured psychiatric interviews that a linear increase occurs in the prevalence of major depressive disorder when comparing community, primary care, and inpatient medical populations. Although 2% to 4% have major depression in the community, 5% to 9% of ambulatory medical patients and 15% to 20% of medical inpatients meet diagnostic criteria.82 Primary care patients with major depression have been found to have more severe medical illness than those who are not depressed.83 Even among community samples, the risk for depression appears to increase with worse perceived health status, number of chronic medical conditions, and number of medications taken.84
Depression is the most prevalent mood disorder associated with comorbid chronic pain.85 Prevalence rates of depression among patients in pain clinics have varied widely depending on the method of assessment and the population assessed. Rates as low as 10% and as high as 100% have been reported.86 The reason for the wide variability may be attributable to a number of factors, including the methods used to diagnose depression (e.g., interview, self-report instruments), the criteria used (e.g., DSM-5, cutoff scores on self-report instruments), the set of disorders included in the diagnosis of depression (e.g., presence of depressive symptoms, major depression), and referral bias (e.g., higher reported prevalence of depression in studies conducted in psychiatry clinics compared with rehabilitation clinics). The majority of studies report depression in more than 50% of chronic pain patients sampled.87,88 There is a direct relationship between the duration of pain and the incidence of major depression. Certain chronic painful conditions are associated with higher rates of depression than others. For example, fibromyalgia, chronic daily headache, and chronic pelvic pain, each are associated with higher rates than arthritis.45,89
Studies of primary care populations (in which generalization is less problematic) have revealed a number of other factors that appear to increase the likelihood of depression in patients with chronic pain. Dworkin and colleagues90 reported that patients with two or more pain complaints were much more likely to be depressed than those with a single pain complaint. Number of pain conditions reported was a better predictor of major depression than pain severity or pain persistence.90 Von Korff and colleagues91 developed a four-level scale for grading chronic pain severity based on pain disability and pain intensity: (1) low disability and low intensity; (2) low disability and high intensity; (3) high disability, moderately limiting; and (4) high disability, severely limiting. Depression, use of opioid analgesics, and doctor visits all increased as chronic pain grade increased. Engel and colleagues92 showed that depression was associated with high total health care costs but not high back pain costs among health maintenance organization patients with back pain. When dysfunctional primary care back pain patients are studied for a year, those whose back pain improves also show improvement of depressive symptoms to normal levels.93
These epidemiologic studies provide solid evidence for a strong association between chronic pain and depression but do not address whether chronic pain causes depression or depression causes chronic pain. As indicated previously, this question has more importance in medicolegal contexts than clinical contexts. Overall, in most instances, depression follows the onset of pain.93
PAIN AND DEPRESSION: MECHANISMS OF ASSOCIATION
Beyond documenting the association of chronic pain and depression lies the question concerning mechanisms by which they may interact. Biologic, psychological, and social mechanisms have been proposed to explain the high co-occurrence of chronic pain and depression. There is also substantial evidence (beyond the scope of this chapter to recount) that the following mechanisms underlie the other psychiatric comorbidities of pain, such as anxiety disorders.
Biologic Theories
Pain Sensitivity
It is well documented that patients with major depression, or even depressive symptoms, have more pain complaints than those without depression. Studies have shown that 30% to 60% of depressed patients complain of pain.94 These findings raise the possibility that depressed patients may have a greater sensitivity to noxious stimuli. In other words, depressed patients may have a reduced pain threshold. But many studies have shown that depressed patients and patients with other psychiatric disorders have an elevated, not reduced pain threshold.95,96 Depression appears to elevate pain threshold more for exteroceptive (e.g., cutaneous) stimulation than interoceptive (e.g., ischemic) stimulation, but there is significant heterogeneity in findings among different patient populations and stimulus modalities.97 Psychiatric patients with dissociation such as borderline personality disorder have reliably shown elevated pain thresholds to external noxious stimuli.98,99 Patients with posttraumatic stress disorder (PTSD) show complex responses
with higher pain thresholds and higher pain ratings to noxious stimuli than controls. Elevated pain thresholds were associated with dissociation levels, whereas elevated experimental and clinical pain ratings were associated with anxiety and anxiety sensitivity.100 Thus, there is an unexplained discrepancy between the higher experimental pain thresholds and the higher clinical pain complaints among patients with depression and other psychiatric disorders. But it is clear that the increased pain complaints of patients with psychiatric disorders cannot be explained by changes in pain thresholds.
with higher pain thresholds and higher pain ratings to noxious stimuli than controls. Elevated pain thresholds were associated with dissociation levels, whereas elevated experimental and clinical pain ratings were associated with anxiety and anxiety sensitivity.100 Thus, there is an unexplained discrepancy between the higher experimental pain thresholds and the higher clinical pain complaints among patients with depression and other psychiatric disorders. But it is clear that the increased pain complaints of patients with psychiatric disorders cannot be explained by changes in pain thresholds.
Biogenic Amines, Cytokines, and Neural Pathways
The highly variable relationship between injury severity and pain severity has been known since Beecher’s studies of the soldiers at Anzio beach in World War II. Since the 1970s, great strides have been made in identifying the central nervous system mechanisms of endogenous pain modulation. Opioid and nonopioid branches to this system have been identified. Stimulation of the rostral ventromedial medulla or the dorsolateral pontine tegmentum produces behavioral analgesia in animals and inhibition of spinal pain transmission. The rostral ventromedial medulla is the principal source of serotonergic neurons that project to the spinal dorsal horn. The dorsolateral pontine tegmentum is the major source of noradrenergic neurons that project to the dorsal horn. Both neurotransmitters (serotonin and norepinephrine) inhibit nociceptive dorsal horn neurons when locally applied.101 The descending inhibitory system is modulated by serotonin and norepinephrine, which are also thought to modulate mood. This is perhaps best illustrated by the effects of selective serotonin norepinephrine reuptake inhibitors (SNRIs) on depression and pain. The two drugs approved for use in this class are duloxetine and venlafaxine. Both are FDA-approved antidepressants that have analgesic properties independent of their effects on mood.102,103 These medications enhance serotonergic and noradrenergic neurotransmission. Additional studies indicate that opioid analgesia is enhanced in the presence of antidepressant treatment104 and decreased after serotonin and norepinephrine depletion.105 Therefore, it appears that biogenic amines play a critical role in endogenous pain modulation. To the extent that depletion or impaired function of amines such as serotonin and norepinephrine occurs in depression, this may contribute to the pain experienced and reported by those with major depression. Just as cytokine responses are important to the initiation and maintenance of chronic pain,106 they have also been implicated in the pathogenesis of depression.107 Depressed patients without pain have been found to have higher levels of proinflammatory cytokines and acute phase proteins. Administration of the cytokine interferon-α leads to depression in up to 50% of patients. Proinflammatory cytokines affect neurotransmitter metabolism, neuroendocrine function (particularly the hypothalamic-pituitary-adrenal axis), and synaptic plasticity.
 FIGURE 31.2 Supraspinal pathways of pain perception. ACC, anterior cingulate cortex; Amyg, amygdala; BG, basal ganglia; HT, hypothalamus; PAG, periaqueductal grayPB, parabrachial nucleus; PCC, posterior cingulate cortex; PF, prefrontal cortex; SMA, supplementary motor area. (From Apkarian AV, Bushnell MC, Treede RD, et al. Human brain mechanisms of pain perception and regulation in health and disease. Eur J Pain 2005;9:463-484; Price DD. Psychological and neural mechanisms of the affective dimension of pain. Science 2000;288[5472]:1769-1772.) |
Cortical Substrates for Pain and Affect
Advances in neuroimaging have linked the function of multiple areas in the brain which process pain and mood simultaneously, described at length in a previous chapter. This system is often termed the medial pain system or spinolimbic pain system.108 These cortical areas (e.g., the anterior cingulate cortex [ACC], the insula, amygdala, and the dorsolateral prefrontal cortex [DLPFC]) form functional units through which psychiatric comorbidity may amplify pain and disability (Fig. 31.2). They are also laden with opioid receptors.109 The ACC, insula, and DLPFC are less responsive to endogenous opioids in pain-free subjects with high negative affect (e.g., depression, anxiety, and anger symptoms).110 Thus, high negative affect may diminish the effectiveness of endogenous and exogenous opioids through direct effects on supraspinal opioid binding. The medial pain system runs parallel to the spinothalamic tract and receives direct input from the dorsal horn of the spinal cord. The interactions among the function of these areas, pain perception, and psychiatric illness are still being investigated. But the spinolimbic pathway is involved in descending pain inhibition, whose function may be negatively affected by the presence of psychopathology. This, in turn, could lead to heightened pain perception. Coghill and colleagues111 have shown that differences in pain sensitivity between patients can be correlated with differences in activation patterns in the ACC, the insula, and the DLPFC. The anticipation of pain—a form of anxiety for pain—is also modulated by these areas, suggesting a mechanism by which anxiety about pain can amplify pain perception. Ploghaus and colleagues13 have demonstrated that anticipation for an acute painful stimulus in healthy volunteers is marked by brain activation patterns throughout the medial pain system.
Sleep Disturbance
Depression produces well-documented disturbances to sleep architecture. Polysomnographic recordings have documented reduced slow wave sleep, early onset of the first period of rapid eye movement (REM) sleep, and increased phasic REM sleep in patients with major depression.112 Sleep continuity disturbances and increased phasic REM sleep tend to normalize with depression remission, even with psychotherapeutic treatment. However, reduction of REM latency and decreased slow wave sleep tend to persist despite clinical recovery. In sum, there appear to be state and trait elements to the sleep disturbance associated with depression. Studies have also demonstrated that sleep disturbance may be a result of chronic pain, which, in turn, can make it worse.113 Fibromyalgia patients who were sleep deprived reported worsening pain and were found to be hyperalgesic (beyond their baseline pain) on pressure sensitivity testing.114 Thus, whether depression or pain precipitated or worsened a sleep disturbance, its presence makes pain worse and is an important link between the two conditions.
Psychological Theories
Psychodynamic Theory
In classic psychoanalytic theory,115 depression is postulated to be derived from anger unconsciously turned inward, excessive dependence on others for self-esteem, and feelings of helplessness in achieving one’s goals. Some have suggested that the depression in some chronic pain patients is a manifestation of a personality style that draws from early developmental conflicts of guilt, anger, and masochism.116,117 From this perspective, chronic pain may be a symptom of depressive disorder.118
Psychoanalytic theory stresses the fundamental parallelism between mental and physical pain and the possible displacement from the former to the latter. Intrapsychic links between pain and depression suggest that pain may function as a hysterical or conversion symptom that may prevent the breakthrough of more severe depression. These intrapsychic links largely correspond with the dynamics of pain proneness that were originally described by Engel2 and, in a further elaboration, connected with the concept of masked depression by Blumer and Heilbronn.116
Blumer and Heilbronn116 proposed a new psychological disorder, the “pain-prone” disorder, building on Engel’s2 notion of the pain-prone patient. In this view, pain should be considered as a variant of depressive disease. The central explanation is unconscious core conflicts. Core issues include “strong needs to be accepted and to depend on others as well as marked needs to receive affection and to be cared for.”
Pain in the absence of organic pathology is considered by Blumer and Heilbronn116 to be a depressive spectrum disorder. According to this model, pain and depression are viewed as manifestations of a single, common disease process. Specifically, the pain-prone disorder is viewed as a masked “depressive equivalent … the prime expression of a muted depressive state.” No empiric research has supported the psychoanalytic formulation as presented by Blumer and Heilbronn.116,119,120
A more modern variant of this theory sees chronic pain as an expression of repressed anger and rage toward others. This was initially advanced by John Sarno, MD, a physiatrist practicing in New York City.121,122 This theory has not been thoroughly investigated empirically, but there is preliminary evidence of a significant relationship between forgiveness and pain, anger, and psychological distress in patients with low back pain.123
Behavioral (Operant Conditioning) Theory
The behavioral model of depression concentrates on the most obvious symptom of depression, the motivational deficit characterized by a reduction in active behavior. A central feature of the behavioral model is response-contingent reinforcement (i.e., the responses from significant others to the individual’s behavior). From this perspective, depressive behavior and depression are associated with low rates of positive reinforcement from the environment. Lack of positive reinforcement leads to a decrease in the frequency of the individual engaging in these behaviors, and ultimately, they may be extinguished completely. These low rates of reinforcement may occur because (1) positive reinforcers in the environment may become less available, or aversive events in the environment may have become more prevalent; (2) the positive effect of previous reinforcers may have declined, or the negative impact of aversive events may have increased; or (3) the individual may lack the skills either to attain the available positive reinforcers or to cope with aversive aspects of the environment. When individuals experience low rates of positive reinforcement, they reduce the performance of those behaviors, unless they are self-reinforcing. The reduction of behavior decreases further opportunities to receive positive reinforcement.
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