Psychosocial Factors in Chronic Pain in the Dysvascular and Diabetic Patient

Dysvascular and diabetic patients are faced with high rates of chronic pain as a consequence of numerous secondary sequelae, including diabetic neuropathy and limb loss. Researchers and scientists have put forth a tremendous amount of effort to understand the complex nature of pain in this population of individuals, as well as others with chronic pain secondary to illness and injury. The emergent understanding of anatomy and sensory physiology within the past century has fueled an initial focus of understanding pain from a purely neurologic and biochemical perspective. Over the past few decades, the field has moved toward an understanding of pain as a process involving the dynamic interaction of biologic, psychological, behavioral, and social variables. This article provides a brief overview of several psychosocial processes, cognitive, affective, and behavioral, that have emerged as influential to the experience, impact, and treatment of pain.

Pain in dysvascular and diabetic patients

Dysvascular and diabetic patients are faced with high rates of chronic pain as a consequence of numerous secondary sequelae, such as diabetic neuropathy and limb loss, to name 2 of the most common. Diabetic peripheral neuropathy (DPN) accounts for the most common of all of the diabetic neuropathies, explaining approximately 78% of those with any type of diabetic neuropathy. The rates of those with painful DPN are as high as 12% to 15%, with this pain usually described as having burning, electric, sharp, shooting, tingling, and lancinating qualities. There is no cure for DPN, but treatment may include maintaining glycemic control and use of certain antidepressants, antiepileptics, and opioids. Unfortunately, medication often must be dosed at lower than optimum levels to minimize the unpleasant side effects of these drugs, limiting the effectiveness of these medications to treat pain.

In a recent study, Ziegler-Graham and colleagues found that in 2005, about 38% of all 1.6 million persons living with a limb loss had an amputation secondary to dysvascular disease with a comorbid diagnosis of diabetes mellitus. Numerous studies have shown that chronic pain in multiple sites is common for persons with an acquired amputation, with phantom limb pain (PLP), residual limb pain (RLP), and back pain reflecting 3 of the most common areas of difficulty. In another recent survey, Ephraim and colleagues found that, of 914 persons with amputation sampled, 80% reported PLP, 68% reported RLP, and 62% reported back pain, compared with the 12% to 45% rate of back pain for the general population. Moreover, 39% and 30% of their sample rated PLP and RLP as severe (ie, having an average intensity of 7 or more on a 0–10 scale), respectively. Unfortunately, similar to DPN, PLP and RLP are often refractory to treatment.

Taken together, the prevalence of common types of chronic pain in dysvascular and diabetic patients coupled with the refractory nature of this pain calls for an approach to chronic pain management that also considers psychological and social factors that impact pain and related dysfunction; that is, a biopsychosocial approach.

Psychosocial factors in chronic pain

Researchers and scientists have put forth a tremendous amount of effort to understand the complex nature of pain. The emergent understanding of anatomy and sensory physiology within the past century has fueled an initial focus of understanding pain from a neurologic and biochemical perspective. This approach, the biomedical model, has centered our attention on the processing of peripheral noxious sensory input in the central nervous system. Under the tenets of this model, reports of pain sensations lead to a search for pathology or physical injury and to the development of treatments geared toward symptom reduction. Although the biologic underpinnings of pain are an important piece of the puzzle, restrictive biomedical models have been unable to adequately explain all aspects of pain, including differential outcomes to similar pain treatments, the variable association between impairment, reported pain intensity and disability, and the development and maintenance of chronic pain in the absence of identifiable pathology. In consequence, our attempt to understand pain has broadened beyond the scope of a purely biologic model. Over the past few decades, the field has moved toward an understanding of pain as a process involving the dynamic interaction of biologic, psychological, behavioral, and social variables. This article provides a brief overview of several psychosocial processes, cognitive, affective, and behavioral, that have emerged as influential to the experience, impact, and treatment of pain.

Psychosocial factors in chronic pain

Appraisals and coping

Of particular interest in the conceptualization of pain as a multidimensional process are the effects of cognitive and behavioral processes on pain and adjustment to pain. An increasing body of research has established the important role that these entities play in the expression of pain and disability. This section systematically discusses appraisals and coping repertoires that have emerged as particularly important with regard to their influence on pain behavior, functional limitations, mental health, and adjustment to and perception of pain.

Fear of Movement/Reinjury

Several models have been developed in an attempt to explain why some individuals develop a chronic pain syndrome long after tissue damage or pathology has healed. Lethem and colleagues proposed the Fear-Avoidance Model of Exaggerated Pain to understand why some persons with musculoskeletal pain have an “exaggerated” pain perception that they hypothesized ultimately contributes to functional limitations, development and maintenance of chronic pain, and poorer psychological health. More recently, Vlaeyen and colleagues proposed a “cognitive model of fear of movement/(re)injury” that is an adaptation of Lethem and colleagues’ model. The central tenet of both theories is “fear of pain.” Two very different possible responses to this fear are “confrontation” and “avoidance,” which are thought to result in a reduction of fear or a maintenance and exacerbation of fear over time, respectively. “Confrontation” was hypothesized to contribute to the reintroduction of social and physical activities as the organic etiology of the pain resolves, whereas “avoidance” serves to limit mobility through an avoidance of activities and an exaggerated perception of pain.

Pain-related fear has been examined mostly in persons with acute low back pain, and has been associated with impaired physical performance and increased self-reported disability beyond that predicted by pain severity and biomedical findings. Pain-related fear has also been examined more recently in persons with sickle-cell disease, with reported rates comparable to those with acute low back pain and persons with pathologic shoulder pain. Pain-related fear has been linked with disability, depressed mood, pain severity, and lower treadmill performance in persons with fibromyalgia syndrome. Finally, the impact of pain-related fear has been found also to contribute significantly to outcomes from delayed-onset shoulder soreness in healthy persons.

Vlaeyen and Linton proposed several pathways by which pain-related fear can lead to disability, decreased activity, and consequent chronic pain in persons with musculoskeletal pain. They synthesized several models, including the aforementioned cognitive model of fear of movement/(re)injury, as well as those of Lethem and colleagues, Philips (1987), and Wadell and colleagues. First, it is possible that negative appraisals or beliefs about pain (eg, pain is an indication of injury; expectancies of suffering) precipitate the development of pain-related fear. These indices have the potential to contribute disproportionately to disability and adjustment. For example, the belief that one’s pain is an ongoing indication of tissue damage or illness, versus that of a stable problem that may improve, can contribute to the avoidance of painful activities. In turn, according to operant models of conditioning (see section on Operant model of pain and illness behaviors), avoidance behaviors are reinforced by repeatedly averting potential opportunities to experience pain. There is little opportunity to challenge the belief that pain is an indication of danger to physical health or of acute damage, thus providing no opportunities to reinforce more adaptive beliefs. Over time, maladaptive beliefs can be reinforced and are hypothesized to lead to increased disability. Second, long-standing avoidance of behavior can have a detrimental impact on musculoskeletal and cardiovascular integrity, possibly resulting in “disuse syndrome.” So the perpetuation of avoidance behavior beyond normal healing time can lead to physical deconditioning, thus introducing further obstacles to regaining functional capabilities. Finally, pain-related fear, similar to other types of anxiety, can interfere with cognitive processes and distract from active and adaptive coping. In other words, persons with greater fear avoidance may show heightened awareness to signals of threat and thus pay greater attention to pain-related information, to the detriment of active coping (see section on Pain-Related Coping).

Treatment studies further corroborate the relationship between pain-related fear and disability. Recent treatments have been successful at reducing pain-related fear and improving functional abilities. For example, Boersma and colleagues evaluated the effectiveness of in vivo exposure to reduce maladaptive beliefs and expectations and increase functioning in persons with back pain. Through graded exposure to ordinary movements and activities, they recorded a decrease in fear and avoidance beliefs and subsequent increase in overall functioning. Moreover, in the context of a multidisciplinary pain treatment program, Jensen and colleagues found that decreases in the belief that pain signals damage was associated with decreases in patient disability. Taken together, these treatment studies substantiate the potential detrimental impact of pain-related fear and lend support for the utility of targeting this factor in treatment.

Pain-Related Coping

Pain-related coping strategies, including cognitive and behavioral efforts to deal with and attempt to reduce or minimize pain, play a central role in predicting disability and adjustment to pain. A myriad of coping strategies have been shown to influence the perception of pain intensity, the ability to manage or endure pain, and one’s ability to persist with activities of daily living. Coping strategies that have been examined include praying/hoping, ignoring pain, distraction, resting, task persistence, guarding, asking for assistance, relaxation, positive coping self-statements, exercise/strength, seeking social support, and pacing, to name only a few. It is outside the scope of this article to review the body of research that has examined each of these coping responses, thus the authors focus on a few that seem to be particularly influential in the prediction of adjustment in persons with pain.

Broadly speaking, coping strategies can be divided between those that are active versus those that are passive. Active coping strategies (eg, exercise, distraction, ignoring pain) are more consistently associated with better psychological and functional outcomes, whereas passive coping strategies (eg, withdrawal, resting, guarding, medication use) generally predict inferior outcomes. The passive coping responses that seem to be most detrimental are resting in response to pain and guarding painful body parts, both of which have been linked with poor adjustment and disability in persons with chronic pain, as well as PLP. In a recent longitudinal study, Steultjens and colleagues found that resting predicted disability 3 months later for persons with knee osteoarthritis. Alternatively, active coping strategies, including pacing and exercise, seem to be associated with better psychological and functional outcomes. Because of the correlational nature of these studies, it is not possible to draw conclusions regarding the extent to which coping plays a causal role in the adjustment to pain. To identify the mechanisms that promote changes in strategies of coping, studies are needed that focus on changing specific coping strategies and observe subsequent changes in outcome.

Of note is the finding that the relationship between detrimental coping strategies (eg, resting) and poor outcomes (eg, functional limitations) is stronger than the relationships between adaptive coping responses and positive outcomes. Maladaptive coping may thus pose a far greater threat to outcome than do adaptive coping strategies in producing positive outcomes. Therefore, interventions that discourage the use of maladaptive coping strategies (eg, discouraging resting and guarding in response to pain, promoting activity) may prove more effective in buffering against disability and functional limitations than interventions that teach and encourage adaptive coping responses.

Catastrophizing

Of particular interest in the domain of appraisals and coping, and the focus of considerable research, is catastrophizing. Catastrophizing can best be characterized as the use of excessive and unrealistic negative self-statements in response to pain, such as, “This pain is awful and I believe that it overwhelms me,” or “I can’t stand this.”

Some investigators have argued that catastrophizing is a type of appraisal, whereas others characterize it as a particular type of (maladaptive) coping. No matter how catastrophizing is conceptualized, however, all agree that it is strongly linked to adjustment for persons with chronic pain. For example, catastrophizing has been consistently associated with increased pain intensity, greater disability and pain-related interference, and poor mental health in a wide variety of pain populations, as well as greater use of analgesics and health care services. Moreover, catastrophizing responses show consistently strong relationships with distress and physical disability of persons with equivalent levels of pain intensity. Turner and colleagues found that among 174 community residents with spinal cord injury and chronic pain, catastrophizing was independently and significantly predictive of psychological distress and pain-related disability above and beyond other coping indices and behavioral responses to pain. Finally, longitudinal research has shown that catastrophizing is able to predict greater pain intensity, functional impairment, and depression 6 months later. In a more recent longitudinal study, catastrophizing has been shown to predict the development of PLP 6 months after amputation in patients with dysvascular disease.

Unfortunately, much of the research on catastrophizing is correlational in nature; the extent to which catastrophizing merely mirrors dysfunction, as opposed to causing dysfunction, is not entirely clear. However, in a recent study catastrophizing was shown to partially mediate the relationship between life stress and depression in a sample of workers’ compensation patients with chronic pain, and to be a risk factor for the development of depression following injury.

Another issue concerning catastrophizing is the extent to which it can be differentiated from depression. However, the current consensus is that catastrophizing responses are closely linked with, but conceptually distinct from, depression. In sum, catastrophizing seems to be one of the strongest predictors of adjustment, experience, and disability related to chronic pain. Whether this strong link is due to a causal impact of catastrophizing on functioning has not yet been determined, and requires causal research.

Depression and pain

A large body of research has noted and sought to understand the close link between pain, pain interference, and depression. One review identified studies with the most stringent criteria for depression, using Diagnostic and Statistical Manual of Mental Disorders criteria for Major Depressive Disorder (MDD), and found that between 30% and 54% of persons with chronic pain also meet criteria for MDD. In contrast, the population prevalence rates for current and lifetime major depression are about 5% and 17%, respectively. Fishbain and colleagues sited higher prevalence of suicidal ideation, as well as more suicide attempts in a community sample of patients with pain versus those without. Moreover, depression in persons with chronic pain seems to occur more frequently than in other illness populations, including patients with cardiac disease, cancer, diabetes, and neurologic disorders.

The additive impact that concurrent depression has on clinical outcomes of persons with pain has been well documented. Several correlational studies have shown a positive relationship between depression and levels of pain. In one review, Bair and colleagues evaluated the outcomes of persons with and without depression treated for pain in managed care and primary care settings. These investigators found across studies that patients with pain and comorbid depression expressed more complaints of pain, greater pain intensity, longer pain duration, and higher rates of persistent pain. In addition, the presence of depression predicted future episodes of pain, including low back, chest, headache, and musculoskeletal pain. Patients with both pain and depression reported greater functional limitations, (eg, mobility, activity restrictions), subsequent days ill in bed, and number of hospitalizations. Finally, Bair and colleagues cited several studies documenting higher unemployment rates and lowered patient satisfaction for those with comorbid pain and depression. Linton, in a review of factors associated with back and neck pain, suggested that psychological factors, including depression, play a more important role in the development of chronic pain problems and disability than biomedical or biochemical factors.

The high rates of depression in persons with chronic pain, as well as the additive detriment of comorbid depression and pain on outcome, has inspired an investigation of the exact nature of this relationship. Although the pain-depression relationship is likely not direct, nor consistently unidirectional, recent progress has been made to understand their temporal relationship, suggesting that depression is a common (but not necessarily universal) consequence of chronic pain. Banks and Kerns proposed a diathesis-stress model of a temporal relationship between pain and depression. According to their model the diathesis may be psychological in nature, and include maladaptive schemas or a depressive attributional style that, when combined with the stress associated with the experience of chronic pain, can result in depression. Fishbain and colleagues reviewed 40 studies addressing the relationship between pain and depression, and concluded that a diathesis-stress model is appropriate to explain the relationship. They found support for 3 hypotheses, including (1) depression can be a consequence of pain, (2) certain cognitions (eg, catastrophizing) mediate the relationship between pain and depression, and (3) previous history of depression can predispose an individual with chronic pain to develop depression.

It is outside the scope of this article to explore all of the factors that likely contribute to the development of depression in the context of chronic pain (eg, previous history of depression). Rather, the remainder of this section focuses on a select number of psychosocial mediators that have been most consistently associated with the onset of depression in the context of chronic pain. These mediators include catastrophizing, social support, and pain-related self-efficacy.

As discussed earlier, catastrophizing (eg, an excessive and unrealistically negative appraisals of pain; see previous section) has emerged as a particularly potent cognitive error linked consistently with functional and psychological outcomes in persons with chronic pain and is believed specifically to be a possible mediator between pain and depression. In correlational studies, greater catastrophizing has been associated with depression in persons with chronic low back pain and rheumatoid arthritis beyond clinical indices. Moreover, in a longitudinal study Keefe and colleagues examined the relationship between catastrophizing and adjustment to chronic pain in persons with rheumatoid arthritis. Greater initial pain-related catastrophizing scores were related with depression, pain intensity, and physical disability 6 months later, after controlling for demographic variables and duration of pain. Smith and colleagues replicated this in a 4-year study of rheumatoid arthritis patients, predicting depression from initial levels of cognitive distortion. Further implicating the mediating role of catastrophic thinking is the success of cognitive behavioral therapy, targeting maladaptive thinking (eg, catastrophizing) in reducing pain and depression in patients with chronic pain.

Pain-related low self-efficacy (eg, lack of confidence in one’s own ability to manage, cope with, and function despite persistent pain) has also emerged as a possible mediator between pain, pain interference, and depression. Rudy and colleagues used structural equation modeling with latent variables to examine loss of control and interference in activities as mediators between pain and the development of depression. Their model provided evidence for the mediation of these factors, and suggested that depression is secondary not to pain but to appraisals about pain. In another cross-sectional study of patients with chronic pain without a prior history of depression, Arnstein and colleagues found support for a mediating role for self-efficacy in predicting depression as well as disability.

The quality and quantity of social support has also been identified as a factor related to depression in persons with chronic pain. In general, a lack of social support has been associated with the occurrence and severity of depression in physical disorders such as chronic pain. Romano and colleagues found that persons in families characterized by low cohesion and high conflict reported higher levels of depression. Marital conflict and dissatisfaction have also been linked with depression and adaptation to pain. For example, rheumatoid arthritis patients who report critical responses from spouses also report higher levels of depression. Again, treatment outcome studies lend further evidence to this relationship, as those interventions including spouses and caregivers of persons with pain have been effective in reducing psychological distress and pain.

It is well accepted that depression is disproportionately prevalent in persons with chronic pain compared with other medical populations and in the general public. What is equivocal is the nature and direction of this relationship. The aforementioned mediators, taken together, support the hypothesis that depression is more often a consequence than an antecedent of pain. However, the direction of the pain-depression relationship is unlikely consistently unidirectional, nor is this relationship influenced by psychosocial factors alone (see Bair and colleagues for a review, eg, of common biologic pathways for pain and depression). However, the findings from research highlight the potential importance of psychological factors when considering approaches to the treatment or prevention of depression in the context of pain (see Campbell and colleagues for a review of psychosocial and pharmacologic treatments of depression in persons with pain).

Only gold members can continue reading. Log In or Register to continue