Why does one patient develop chronic pain and face disability, while another—with seemingly the same injuries, extent of tissue damage, and quality of medical care—recovers and returns to normal activity following a brief convalescence? Arguably, there may be biologic variables between the two that are difficult to discern medically, but a comparison, in most cases, is likely to reveal that the greater portion of the variance consists of psychosocial differences. When pain physicians wonder why a patient fails to respond to procedures and medications that have proven efficacious for many others with the same medical presentation, it is frequently the pain psychologist who can offer the most reasonable and, more importantly, functional set of hypotheses.
Although nociceptive or purely physiologic factors may instigate pain, how it is expressed by the individual, over time, suggests that what might have begun as a simple picture can become considerably more complicated and intricate through the influence of psychological and social factors. Melzack and Wall’s gate control theory emphasizes that pain cannot be fully understood without an assessment of the motivational-affective, sensory-discriminative, and cognitive-evaluative processes of the individual.1 Adherents to the biopsychosocial, mind-body, and behavioral medicine approaches to pain all affirm that, while the origin of pain may not be psychological, how a person responds to it is. Assessing this response expediently and accurately may redirect the focus of a patient’s treatment, highlighting the psychosocial dimension of the patient’s experience as essential to diagnosis and successful outcome. Chronic pain may not lead to adjustment difficulties, mental disorder, and disability, but when it does, psychosocial assessment may offer the only helpful perspective on why, as well as the best hope for recovery.
The principal goal of psychosocial assessment in chronic pain is not, as some patients fear, to determine whether or how much pain can be attributed to psychological sources but rather to identify the emotional, behavioral, and social factors that may be rendering it less tractable to treatment and moving the patient toward physical and psychological disability. The development of a successful plan for treatment often depends on identifying these influences and strategizing how to address them expediently, sensitively, and thoroughly.
It is helpful, early in the assessment process, to have access to the patient’s previous medical records. The records can help in understanding the nature and severity of the underlying medical condition, the suspected peripheral pain generators, the response to previous medical treatments and the rationale for those that are planned, and the expected natural history of the disorder. This background, as it is understood and misunderstood by the patient, becomes highly influential in framing the challenges of treatment. Knowing the biomedical context can be a helpful bridge for conceptualizing and explaining, both to the patient and to other members of the treatment team, what role psychological factors may play. Discrepancies between the medical record and how a patient views his or her pain, as well as between expected and actual outcomes of past treatments, can sometimes indicate areas where psychological factors are central. Discussion with the referral source can be helpful in interpreting the records, hearing observations of the patient that may have been left out of the record, and understanding the concerns and goals behind the referral.
In the interview, we seek to understand in depth the quality, intensity, and patterns of pain; patients’ current coping strategies; their life stories before they ever imagined they would be patients; and their current psychological profiles. It is from the dynamic interplay among pain, current psychological makeup, and life stories that the foundations of treatment arise.
Almost invariably, patients have been referred because of their pain specifically, and so it is here that our interview should begin. A high pain intensity is generally a given in treatment programs, but the patterns can vary widely. Continuous, high-intensity pain imposes a heavier burden than pain that can be relieved temporarily with a certain posture, position, stretch, or form of counterstimulation. The predictability of the pain is likewise important, as is the degree to which the triggers are controllable. Particularly useful for treatment are triggers in the behavioral (such as overactivity), sympathetic nervous system (such as startle), or emotional realms (such as loss, sorrow, or guilt).
Knowing the qualitative characteristics of the pain is helpful, as well. It is an entrance to the subjective world of the patient and hints at how the pain is encoded. The pain may be described in neutral sensory terms (e.g., sharp, squeezing), as an affective experience (e.g., punishing, vicious), as a judgment (e.g., unbearable), or as a vivid description of tissue damage. Changing the encoding may be part of the challenge of treatment. On a purely sensory level, the pain description may hint at the types of imagery that will be most useful for pain control. Moreover, the pain’s qualities and triggers may shed some light on underlying mechanisms. For example, a burning pain that improves with a cool stimulus may turn out to be inflammatory, even if the circumstances of onset did not at first point in this direction.
Patients vary in the range of their vocabularies for pain. It is helpful to have the McGill Pain Questionnaire available (described later in this chapter) for people who have trouble putting their pain into words.
Especially important are those cognitive and affective variables that are likely to influence how the pain is experienced and whether it follows a benign or deteriorating course. Here, we will discuss the most important of these variables, why they matter, and how they are typically assessed. For some patients, psychoeducation—explaining the relevance of the psychological variables to pain—will be necessary at the outset for the interview to make sense to them.
The prevalence of depressive disorders in people with chronic pain is approximately 20% in community samples and 50% in the clinic.2,3 The impact is significant: Depression is not merely noxious to functioning and quality of life; it is intertwined with pain and its outcome on sensory and affective levels.
Thus, major depressive disorder often involves pain, much as does the flu,4 through a lowering of thresholds for pain from within the body.5 Depression increases the probability of the onset,6 chronicity,7 and increasing frequency of pain.8 Moreover, depression is a strong risk factor for poor outcome from lumbar surgery and may interfere with the efficacy of spinal cord stimulation, medial branch nerve blocks, and opiate medications9–11 (although perhaps not cognitive-behavioral pain treatment, in which depression is addressed directly12). In headaches, depression predicts the development of allodynia, a marker of central sensitization and itself a risk factor for migraine chronification.8
In the body, the connections between depression and pain are several and strong: In major depressive disorder, much as in physical illness, blood levels of cortisol and proinflammatory cytokines, particularly interleukin 1-β, are elevated.13 These, in turn, can induce a proinflammatory state in the central nervous system, facilitating pain transmission and presumably contributing over time to pain sensitization.14
Moreover, dysphoria and pain-distress activate overlapping structures: the dorsal anterior cingulate cortex, anterior insula, and the amygdala.15,16 Conversely, pain-distress is modulated by such “reward centers” as the nucleus accumbens and the ventral tegmentum,17 which are generally underactive in depression.18
More generally, depression and pain are inhibited by the same brain regions—dorsolateral, ventral lateral, and orbital prefrontal cortex and rostral anterior cingulate cortex.19,20 Deficient recruitment of these top-down regulatory circuits likely participates in both disorders.21,22
Not only current but also past depression may be relevant: Depression during childhood or adolescence predicts the development of osteoarthritis in adulthood, especially between the ages of 35 and 70, presumably because of the bias toward inflammation.23
While we are always interested in knowing the presence and severity of depression, this is particularly true in cases of poor treatment response to medical interventions and signs of erosion of pain thresholds—localized, regional, or whole-body mechanical allodynia or circumscribed pain and tenderness that have spread over time. The erosion of pain thresholds can have many sources; severe depression, when present, may be among them.
The gold standard for diagnosis of a depressive disorder is a structured clinical interview schedule such as the SCID24,25 or, more briefly, the MINI-Plus.26 However, both of these are likely too lengthy for an interview focused on pain coping.
People are usually, although not invariably, aware of when they are depressed and will report it during the interview. Most often, they describe depression as a consequence of the pain, and an additional burden, but a few report that depression causes an aching or heavy pain or that guilt triggers a migraine. Sometimes, blunted affect, psychomotor slowing, and/or pessimistic and joyless thought content are the only indicators of depression. Inquiring about the DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, 5th ed.) diagnostic criteria, especially the cognitive and affective elements, can be helpful for clarifying whether the severity rises to the level of a clinical disorder. Items that were endorsed on the psychometrics can be a useful starting point.
Psychometrics are used for screening or as measures of severity. The Beck Depression Inventory (BDI),27 Centers for Epidemiological Studies—Depression Scale (CES-D),28 the PHQ-9,29 and the QIDS-SR30 have all been studied psychometrically in chronic pain. Because endorsements of somatic symptoms and performance interference on depression inventories can reflect pain rather than mood, modified cutoff scores have been derived, as given in Table 15-1.
Self-Report Instruments Relevant to Chronic Pain
Construct | Scale | Properties | Comments | References |
Acceptance | Chronic Pain Acceptance Questionnaire | 20 Items, 2 Subscales α≈0.85(full scale)≈0.82(Activity Engagement)≈0.78(Pain Willingness) |
| McCracken et al.197 Nicholas & Asghari198 |
Coping/Catastrophizing | Chronic Pain Coping Inventory | 65 Items, 8 Subscales α≈0.74(Guarding)≈0.75(Resting)≈0.85(Asking for Assistance)≈0.73(Relaxation)≈0.78(Task Persistence)≈0.89(Exercise/Stretch)≈0.87(Coping Self-Statements)≈0.82(Seeking Social Support) Also: α ≈ 0.79 (Pacing) | There is also a 42-item version. The Pacing subscale is available only in the 65-item version. | Ersek et al.276 Jensen et al.277 |
| Coping Strategies Questionnaire | 42 Items, 7 Subscales α≈0.84(Diverting Attention)≈0.89(Reinterpreting Pain Sensations)≈0.82(Coping Self-Statements)≈0.78(Ignoring Pain Sensations)≈0.80(Praying and Hoping)≈0.78(Increasing Activity Level)≈0.74(Catastrophizing) |
| Keefe et al.185 Rosenstiel & Keefe87 |
| Pain Catastrophizing Scale | 13 Items, 3 Factors α≈0.94(full scale)≈0.89(Helplessness)≈0.78(Magnification)≈0.87(Rumination) |
| Chibnall & Tait278 Sullivan et al.88 |
| Vanderbilt Pain Management Inventory | 18 Items, 2 Subscales α≈0.71(Active Coping)α≈0.81(Passive Coping) | An 11-item version is also available (α ≈ 0.71 active coping; α ≈ 0.71 passive coping). | Brown & Nicassio279 Smith et al.280 |
Depression | Beck Depression Inventory (BDI-IA) | 21 Items, 1 Scale α≈0.86(psychiatric samples)≈0.81(non-psychiatric) | Modified cutoff of 12, 15, or 20 has been suggested for pain patients. | Beck et al.27 Geisser et al.281 Love282 Wong et al.283 |
| Beck Depression Inventory-II | 21 Items, 1 Scale α ≈ 0.91 (psychiatric and non-psychiatric) | Modified cutoff of 22 has been suggested for pain patients. Appropriate for ages 13–80. Excellent validity. | Beck et al.233 Dozois & Covin284 Poole et al.285 |
| Center for Epidemiological Studies—Depression Scale (CES-D) | 20 Items, 1 Scale α ≈ 0.87 | Modified cutoff of 26 has been suggested for pain patients. | Geisser et al.281 Radloff28 Wong et al.283 |
| PHQ-9 | Coefficient α = 0.89 Sensitivity ≈ 0.80 Specificity ≈ 0.92 (For cutoff ≥ 10) | Very quick to complete and score. | Gilbody et al.286 Spitzer et al.287 |
| QIDS-SR16 | Coefficient α ≈ 0.87 | Designed as a severity (vs. screening) measure. | Rush et al.288 |
Disability | Oswestry Disability Index | 10 Items α ≈ 0.86 | Designed for low back pain but good psychometric properties for general pain after substituting “pain” for “back pain” in the instructions. | Fairbank et al.289 Wittink et al.290 |
| Pain Disability Index | 7 Items, 2 Subscales α≈0.92(Voluntary Activities)≈0.80(Obligatory Activities) | Validated also for telephone administration. | Tait & Chibnall291 |
Fear of Pain | Fear of Pain Questionnaire – III | 30 Items, 3 Subscales α≈0.92(full scale)≈0.88(Severe Pain)≈0.87(Minor Pain)≈0.92(Medical Pain) | The subscales can be used individually. A 20-item version is also available. | McNeil et al.68 Asmundson et al.292 |
| Pain Anxiety Symptoms Scale (PASS-20) | 20 Items, 4 Subscales α≈0.91(full scale)≈0.86(Cognitive)≈0.75(Escape/Avoidance)≈0.82(Fear)≈0.81(Physiological Anxiety) | A 40-item version is also available and has been extensively studied. | McCracken & Dhingra293 |
Kinesiophobia | Tampa Scale for Kinesiophobia | 17 Items, 2 Subscales α ≈ 0.68 (osteoarthritis) to 0.76 (chronic LBP) | Extensively normed. | Heuts et al.294 |
| Fear Avoidance Beliefs Questionnaire | 16 Items, 2 Subscales α≈0.90(full scale)≈0.72(Physical Activity)≈0.82(Work) | Also in Chinese, French, German, Portugese, Spanish, and Turkish. | Lee, Chiu, & Lam110 Swinkels-Meewisse109 |
Multidimensional | West Haven-Yale Multidimensional Pain Inventory | 52 Items, 12 Subscales α≈0.78(Pain Severity)≈0.92(Life Interference)≈0.78(Life Control)≈0.64(Affective Distress)≈0.84(Support)≈0.82(Punishing Responses)≈0.81(Solicitous Responses)≈0.71(Distracting Responses)≈0.86(Household Chores)≈0.77(Outdoor Work)≈0.70(Activities Away from Home)≈0.74(Social Activities)≈0.87(General Activities) | Three-cluster solution used in treatment matching. Reliabilities here are from Nicholas et al.,188 (first 8 subscales) and Kerns et al.190 (last 4 subscales). Extensive norms are available in Nicholas et al.188 General Activities Scale is a combination of the four preceding subscales. | Kerns et al.190 Nicholas et al.188 Wittink et al.290 |
Pain Quality and Intensity | McGill Pain Questionnaire-Short-Form, Revised (SF-MPQ-2) | 22 Items, 4 Subscales α≈0.95(full scale)≈0.87(Continuous Pain)≈0.87(Intermittent Pain)≈0.83(Neuropathic Pain)≈0.86(Affective Descriptors) |
| Dworkin et al.268 |
| Multidimensional Affect and Pain Survey (101-MAPS) | 101 Items, 30 Subclusters, 3 Superclusters α≈0.97(Somotosensory Pain)≈0.94(Emotional Pain)≈0.94(Well-being) | Interval-level scales Free of ethnic and gender bias. Relatively long. | Clark et al.296 Griswold & Clark297 |
Posttraumatic Stress Disorder | Impact of Events Scale | 15 Items, 2 Components α ≈ 0.80 | Cutoff (≈ 26) does not need adjustment for pain. | Horowitz et al.117 |
| PTSD Symptom Scale – Self-Report | 17 Items, 3 Subscales α≈0.95(full scale)≈0.92(Re-experiencing)≈0.88(Avoidance)≈0.86(Hyperarousal) | Cutoff does not need adjustment for pain. Scale may not distinguish well between PTSD and other anxiety disorders. | Engelhard et al.298 Foa et al.118 |
Self-Efficacy | Pain Self-Efficacy Questionnaire | 10 Items, No Subscales α ≈ 0.93 | Good convergent and divergent validity. Extensive norms are available in Nicholas et al.188 | Nicholas187 Nicholas et al.188 |
Sleep Quality | Chronic Pain Sleep Inventory | 5 Items, 1 Overall Index Score α ≈ 0.93 | Pain-related sleep problems. Only 3 items participate in the index score. | Kosinski et al.174 |
| Insomnia Severity Index | 7 Items, 1 Scale α ≈ 0.91 | Validated in clinical and community samples. Scores ≥ 11 indicate sleep problems. | Bastien et al.299 Morin et al.300 |
| Medical Outcomes Study Sleep Scale | 12 Items, 6 Domains, 1 Overall Index Score α ≈ 0.78 | General sleep scale, validated in pain. Only 9 items participate in the overall index score. | Hays et al.173 Rejas et al.175 |
Stages of Change | Pain Stages of Change Quesionnaire | 30 Items, 4 Subscales α≈0.77(Precontemplation)≈0.82(Contemplation)≈0.86(Action)≈0.86(Maintenance) | Here, the Contemplation subscale subsumes also the preparation stage. | Kerns et al.217 |
Substance Abuse Potential | Opioid Risk Tool | 10 Items PPV ≈ 0.91, NPV ≈ 0.94 Concordance ≈ 0.85 female, 0.82 male | Cutoff < 4 vs. ≥ 8. Low sensitivity in the few attempts to cross-validate. | Webster & Webster238 Moore et al.240 |
| Screener and Opioid Assessment For Patients with Pain—Revised (SOAPP-R) | 24 Items α ≈ 0.88 | For cutoff ≥ 18, sensitivity ≈ 0.81 specificity ≈ 0.68. Local norms will likely be helpful. | Butler et al.237 |
Suicidality | Beck Hopelessness Scale | Sensitivity ≈ 0.80; Specificity ≈ 0.42 | Low specificity reflects low base rate of suicide. | Beck et al.230 McMillan et al.301 |
Trauma History | Childhood Trauma Questionnaire – Short Form | 28 Items, 6 Subscales α≈0.92(Full Scale)≈0.87(Emotional Abuse)≈0.84(Physical Abuse)≈0.94(Sexual Abuse)≈0.88(Emotional Neglect)≈0.69(Physical Neglect)≈0.82(Minimization/Denial) | The five main subscales are highly intercorrelated. | Bernstein et al.54 Gerdner & Allgulander302 |
Values Orientation | Chronic Pain Values Inventory | 12 Items, 2 Subscales α≈0.82(Success)≈0.82(Discrepancy) | Subscales: Success at living in accord with values. Discrepancy between importance of a value and success. | McCracken & Yang201 |