Psychological Strategies for Chronic Pain

Pain Perception: Nervous System Attenuation and Amplification

Back pain is often ascribed to strains, sprains, annular tears, internal disc disruption, facet arthropathy, or bone pathology; however, it is often not explained by examination or imaging. Positive findings on an imaging test may be misleading, since patients with severe symptoms often have normal imaging, and patients with herniations, degenerated discs, bulges, osteophytes, and facet arthropathy are often without symptoms.

To some extent, overreliance on imaging findings derives from the persistence of obsolete concepts concerning nociceptive pain. Essentially, these implied a more or less linear relationship between pain perception and peripheral stimulation; that is, a nociceptor is activated, the signal is transmitted to the dorsal horn (DH) of the spinal cord, and from there via the thalamus to the cortex, where pain is appreciated. Pain was seen as an analog representation of some event; for example, a child stepping on one's toe produces minimal pain, while an adult or an automobile would produce correspondingly greater pains. As a result, when a patient complained of severe pain and no appropriate pathology was found, the validity of the complaints was challenged.

More recent evidence shows that pain is a creation of the nervous system and not just a gauge of nociceptor activation. Nociceptive afferent signals are subject to marked attenuation and amplification by descending facilitatory and inhibitory tracts that have their action at the DH. Further, the presence of prolonged nociceptive stimulation, inflammation, or nerve injury can lead to sensitization of the neurons that relay pain, death of inhibitory cells, loss of tonic inhibition, and structural neuroplastic changes. Perhaps even more interesting, activation of immune cells, including glia that were previously thought of as having only structural roles, produces exaggerated, widespread, and mirror-image pains. DH molecular mechanisms of central sensitization include co-release of substance P and glutamate from afferent neurons, jointly activating N -methyl- d -aspartate receptors and thereby enabling temporal summation which can be reversed with N -methyl- d -aspartate receptor blockade.

Patients with idiopathic chronic low back pain (CLBP) subjected to quantified thumb pressure report more pain and show more functional magnetic resonance imaging (MRI) activation in brain areas likely to reflect pain perception than do controls, suggesting that at least some portion of CLBP is related to central sensitization. Evidence also implicates central sensitization as a significant factor in whiplash-associated pain. Thus, spine pain can result from local tissue pathology, central sensitization, or both. It is therefore unrealistic to expect that reports of chronic spine-related pain will necessarily correlate with the presence of severity of spine pathology. It should be further noted that in addition to such pain sensitization and facilitation, chronic pain syndromes are believed to develop as a result of faulty pain inhibition as well. Pain inhibition involves processing via spinal-supraspinal-spinal loops ; implicated supraspinal structures include the prefrontal cortex, midbrain, and periaqueductal gray. Evidence suggests the activation of healthy or adaptive pain inhibition with the use of exercise, for example, which has been demonstrated in back pain specifically.

The interplay of cognitions and pain modulation is complex and of growing interest. It is known that guarding against the possibility of pain and anticipation of its occurrence activates cells in the rostroventral medulla that function to amplify incoming pain signals at the level of the DH. Animal models suggest that the simple facts of anticipating a pain sensation and expecting it to be important are sufficient to trigger these “on cells,” in essence activating the “amplifiers” before the pain stimulus has even begun.

Increasing evidence points to genetic variability in pain appreciation and in responses to endogenous and exogenous opioids. Furthermore, there is compelling evidence that individual reporting of high/low pain in response to a standard stimulus demonstrates correspondingly high or low activation of the somatosensory cortex, anterior cingulate gyrus (a likely index of affective components of pain), and frontal cortex.

To summarize, at least some forms of chronic back pain are likely secondary to this complex, multifactorial degree of central sensitization, and instruments have been developed and validated for capturing and quantifying central sensitization (i.e., the Central Sensitization Inventory ). Further application of this inventory in both clinical and investigational contexts is warranted before systematic use, yet general consideration of central sensitization in back pain syndromes is certainly critical for any clinician managing this patient population.

Pain and the Psyche

Chronic pain syndrome is a term (not a diagnosis) that has fallen into disfavor with pain specialists but is still often used by others. It describes a condition of severe intractable pain with marked functional impairment and other behavioral changes that have no clear relationship to organic disorder. (Poor concordance between chronic pain and structural pathology does not, as noted earlier, challenge the authenticity of the pain.) Typically, these patients have inordinate use of medications and health care services, which are largely nonproductive. Thus, this is a nonspecific term for patients most typified by abnormal illness behaviors, primarily those of somatic preoccupation and regression into the sick role. The term is useful in that it properly directs therapy toward the reversal of regression and away from an exclusive focus on nociception. It does not, however, substitute for a careful diagnosis of the physiologic, psychological, and environmental factors that produce the syndrome.

Psychosocial vulnerabilities may precede or follow the development of low back pain, both proving to substantially contribute to overall outcomes. Carragee et al. followed 100 patients with mild CLBP and no prior spine-related disability for 5 years. Moderate or severe Modic changes (degenerative changes noted on spine MRI) of the vertebral endplate were the only structural variable that weakly predicted adverse outcome. Provocative discography and baseline MRI predicted no outcome variables, but were weakly associated with pain episodes. Psychosocial variables strongly predicted long- and short-term disability and health care visits for low back pain. A model based on scores on the Modified Zung Depression Test, Modified Somatic Pain Questionnaire, Fear Avoidance Beliefs Questionnaire (physical activity subscale), and smoking status identified 100% of long-term disability subjects, 88% of all disability subjects, and 75% of subjects having a remission.

It is reasonable to posit a stress-diathesis model in which the degree of disability from a given degree of organic pathology will vary with the psychological reserves of the individual, the stresses of the workplace, and incentives/disincentives for recovery. Clearly, these variables overlap—the person with poor coping skills and limited education is unlikely to obtain the most desirable work situation.

Psychiatric Comorbidities

The most frequent psychiatric illnesses (excluding somatic symptom disorders) in pain center patients are anxiety disorders, depression, and substance abuse. In 200 CLBP patients entering a functional restoration program, Polatin et al. found that 77% of patients met lifetime diagnostic criteria and 59% demonstrated current symptoms for at least one psychiatric diagnosis. The most common were those listed. A total of 51% met criteria for personality disorder. Substance abuse and anxiety disorders appeared to precede CLBP, while major depression could either precede or follow it. Studies vary as to the prevalence of psychiatric disorder; however, they tend to agree about those that are most common.

The prevalence of depression in chronic pain patients ranges from 10% to 83%. This extreme variance reflects variable settings, populations, and diagnostic criteria. In a Canadian general population survey of 118,533 people, CLBP was present in 9%. Major depression was present in 5.9% of those without pain and in 19.8% of those with CLBP. The rate of major depression increased in a linear fashion with pain severity. It is likely that the arrow of causality can point in either direction, as there is evidence that pain predicts depression and depression predicts pain, and to similar degrees.

In a probability sample of 5692 US adults, 35% of those with CLBP had comorbid mental disorders. Major depression was present in 12.6%, dysthymia in 5.6%, any anxiety disorder in 26.5%, and any substance use disorder in 4.8%. There was no increased prevalence of (nonalcohol) drug abuse.

Major affective disorder can present with pain, in which case treatment of the mood disorder often provides relief. More commonly, however, depression appears as a consequence of pain, though not necessarily a direct result of it. Rudy et al. showed that the link between pain and depression could be mediated by perceived life interference (loss of gratifying activities) and loss of self-control. Moreover, Strigo et al., in a study of the association of major depressive disorder and experimental pain, observed that anticipation of pain was associated with increased activity in the amygdala, anterior insula, and anterior cingulate cortex in patients with major depressive disorder when compared with normals. This suggests that depressed patients experienced an affective response even before they experienced the painful stimulus. This was also associated with greater perceived helplessness. They posit that patients with major depressive disorder have an altered functional response within specific neural networks during the anticipation of pain that may lead to an impaired ability to modulate the painful experience as well as their emotional response to the pain.

There seems to be a vicious cycle in which pain behavior, loneliness, inactivity, helplessness, depression, withdrawal, loss of reinforcers and distractions, and pain are mutually reinforcing. Improving one element in this series often benefits the others. These issues, of course, are not resolved by pharmacotherapy, but do respond to successful rehabilitation.

Other Psychological Contributors to Chronic Pain

Anxiety adversely affects pain through a number of mechanisms, and it can be the major reason for failure of rehabilitation from CLBP. Phobic processes can promote a cycle of unnecessary self-protection and avoidance. Ultimately, this can lead to deconditioning in the individual with chronic pain. When people become afraid to move, disability and dysfunction can result as much from unwarranted fear as from the pain itself. Anxiety can also lead to muscle guarding and tension that lead to muscle shortening and other physiologic responses that worsen pain. Nociceptors that are normally unaffected by norepinephrine become sensitive to it following injury so that neuropathic pains are often exacerbated by anxiety as well as fear, anger, or excitement.

Pain catastrophizing is a cognitive–affective response to anticipated or actual pain, comprised of three domains (helplessness, magnification, and rumination). It has been shown to markedly amplify pain and is associated with poorer outcome, heightened pain sensitivity, and impaired functioning. This is the case for both acute and chronic pain.

Anger is associated with exacerbation of both acute and chronic pain. A number of authors have found associations between anger regulation, both expression and suppression, and severity of chronic pain. In a study examining the effects of anger suppression in pain severity, Burns et al. found that patients with CLBP who were told to suppress their anger toward a study confederate exhibited more pain behaviors and reported more pain than those who did not suppress their anger.

Recent research has looked at other psychological contributors to pain, such as guilt and various aspects of mood—including reactivity and positive affect—among those with CLBP. Serbic and colleagues explored the relations between pain-related guilt, lack of diagnostic certainty, and disability through structural equation modeling in CLBP patients. They found that pain-related guilt (especially social guilt) and diagnostic uncertainty contributed substantially to disability and mood. While this study does not attribute causality to the associations, it does underscore the potential importance of addressing guilt through psychological strategies. Furthermore, low levels of positive affect combined with high negative affect among individuals with CLBP may increase the odds of comorbid fibromyalgia and worse functioning overall. Individuals with high levels of reactivity (high negative affect and high positive affect) have shown similar levels of pain, mood, and disability as those who are considered having a “healthy” balance of affect (high positive affect and low affect).

Psychogenic Pain/Somatization: Diagnostic Considerations

Psychogenic pain is a concept whose existence is disputed and whose use has decreased with more modern understandings of the role of the nervous system in chronic pain. It was previously used when a medical explanation for pain was not identified. Similarly, the term somatization is used to refer to the presentation of physical symptoms with psychological underpinnings or influence. Clinically, patients may demonstrate behaviors that are incompatible with the degree of impairment that they describe. A plethora of complaints and marked functional impairment may coexist with well-preserved muscle definition. It may be that the term is used for several unrelated conditions, given that some diagnosed with psychogenic pain appear euthymic, animated, and sleep well, while others appear to suffer severely, cannot sleep, and even contemplate suicide. One clue to the presence of somatization is apparent reluctance to discuss nonsomatic issues. If asked about family, work, or politics, the response inevitably and rapidly diverges to talk about doctors, symptoms, and treatments. This is not typically seen even in severe physical illness. Another clue is the sense of immediacy in the recounting of the traumatic event—a minor remote event is described as though it occurred yesterday.

The American Psychiatric Association has historically grouped these disorders under the framework of “somatoform disorders,” including diagnoses such as hypochondriasis, pain disorder, factitious disorder, and conversion disorder. The diagnostic terminology has changed multiple times, with the most recent revisions from the Diagnostic and Statistical Manual of Mental Disorders, 5th edition ( DSM-5 ) being the “somatic symptom disorders.” This new classification system allows for a specifier, “with predominant pain,” to account for those with pain symptoms. A diagnosis of somatic symptom disorder requires the presence of one or more somatic symptoms that cause distress or disruption in daily life, accompanied by an “excessive” psychological response (thoughts, feelings, behaviors), such as high levels of anxiety or preoccupation with symptoms for at least 6 months. Alternatively, if it is determined that psychological or behavioral factors contribute to adverse outcomes associated with the condition, a diagnosis of “psychological factors affecting pain condition” may be used.

There is evidence of a continuum between symptoms of posttraumatic stress disorder, dissociation, somatization, and affect dysregulation. These interrelated symptoms commonly follow major trauma, and there seems to be a hierarchy of traumas, such that natural disasters lead to fewer symptoms than do adult interpersonal traumas, with childhood trauma causing the most severe symptoms. Rome and Rome hypothesized that a process akin to kindling follows psychic trauma, leading to symptom amplification, spontaneous symptoms, anatomic spreading, and cross-sensitization. These are processes that also characterize pain following neurologic trauma. They noted a melding of sensory and affective symptoms and a “polymodal allodynia” that rendered these people sensitized to both physical and emotional stressors. Most studies linking adult-onset chronic pain with childhood trauma have been retrospective. However, a study by Jones et al. looking prospectively at a 1958 British cohort of 7571 subjects found that, although adult onset of chronic pain was not associated with childhood surgery, it was associated with hospitalization for a motor vehicle accident, institutional care, maternal death, and familial financial hardship. Strengthening directionality of their findings, they also found that the association was not explained by adult psychological distress or social class. Von Korff et al. also examined the effects of childhood psychosocial stressors and the onset of adult arthritis in a prospective study of 18,309 subjects from 10 countries participating in a World Mental Health Survey in the Americas, Europe, and Asia. They found that, controlling for age, sex, and early onset of psychological disorders, subjects with significant childhood stressors had an increased risk of adult arthritis. Early-age onset of symptoms of depression and/or anxiety were associated with an increased risk of adult arthritis even after controlling for childhood stressors.

Other psychiatric conditions that may present with pain include hypochondriasis, dementia, psychosis, and factitious disorder. Experience suggests that new onset of conversion/somatization in the elderly is rare, and when present it may herald dementia. Malingering is by definition not a psychiatric illness. While thought to be uncommon in chronic pain (based on no data), it does occur.

Psychogenic Pain/Somatization: Pain Amplifiers

Multiple psychological factors affect both the perception of pain and ability to cope with it. Chronic stress increases both the perception of pain and disability. Distraction reduces pain awareness, while isolation and inactivity increases it and fosters self-preoccupation. Perhaps the major psychological factors that affect chronic pain are cognitions and incentives.

Cognitive theories of depression, anxiety, and pain hold that thoughts and beliefs are major determinants of affect, that is, how a person feels is less determined by events than by the person's interpretation of them. The individual who concludes from an unsuccessful job interview that the company has no openings reacts differently than the one who infers that he or she is undesirable and unlikely to find work. The terminal cancer patient who believes that “the surgeon got it all” will be more content than the healthy person who believes one's intractable pain is due to severe but undetected pathology. Maladaptive cognitions tend to be automatic and habitual; thus, they are rarely examined for validity. They are simply accepted.

Cognitive factors have an impact on pain in several ways. First, the adverse quality of pain is modified by its interpretation. Such “catastrophic” interpretations of pain as “the nerves are being crushed” or “the exercises feel like they're tearing something loose” impede coping. The situation can be worsened by health care providers who attribute the pain to incidental findings on imaging that may bear only a modest relationship to the pain. Chronic back pain, which is the leading cause of disability and absenteeism from the workplace, lacks a specific structural explanation in over 80% of cases. Additionally, it is often strongly driven by such psychosocial factors as fear of pain/reinjury, “catastrophizing,” depression, and anxiety. Failure to address these issues in treatment of chronic back pain often leads to continued disability. Pain tolerance is reduced by thoughts emphasizing the averseness of the situation, the inadequacy of the person to bear it, or the physical harm that could occur. Such beliefs as “I will have a life again only after I am cured,” “I can't go out to dinner if I am in pain,” and “I shouldn't exercise if it hurts” have obvious impacts on adaptation.

Self-appraisal may be as important as appraisal of the pain itself. Those who feel unable to influence events eventually give up. Belief in personal helplessness fosters pain and disability; alternatively, a sense of self-efficacy promotes efforts to cope. Thus, perceptions of helplessness lead to depression, resignation, and passivity, which, in turn, increase disability and pain. Self-efficacy, the opposite of helplessness, has been repeatedly correlated with pain outcomes among a variety of chronic pain conditions, including CLBP. “Locus of control” is a psychological construct that refers to one's sense of the determinants of future events. The perception that events are a consequence of the individual's own behavior (internal locus of control) is associated with better mood and function. Those with external locus of control tend to see future events as contingent on other people or “fate.” People with chronic pain who have an external locus of control report depression and anxiety, feel helpless to deal with their pain, and often rely on maladaptive coping strategies such as excessive rest and eating. Decreased perception of self-control may explain much of the relationship between depression and pain.