, Robbie Haggard1, Christina Thomas1 and Krista J. Howard1
(1)
Department of Psychology, College of Science at The University of Texas at Arlington, Arlington, TX, USA
Abstract
At the beginning of the twenty-first century, pain began to be identified in clinical research and medical settings as a fifth vital sign (in addition to pulse, blood pressure, temperature, and respiration). Pain has become such a common medical problem in the USA that an estimated 10% of doctor visits result from pain being reported as the chief complaint (Woodwell, D. A. (2000). National Ambulatory Medical Survey: 1998 Summary Advanced Data from Vital and Health Statistics No. 315. Hyattsville, MO, National Center for Health Statistics.), and more than 50 million Americans are impacted by pain annually, with costs exceeding $70 billion annually in healthcare costs and lost productivity according to experts (Gatchel, R. J. & Mayer, T. G. (2000) Occupational musculoskeletal disorders: Introduction and overview of the problem. In T. G. Mayer, R. J. Gatchel, & P. B. Polatin (Eds.), Occupational musculoskeletal disorders: function, outcomes, and evidence (pp. 3–8). Philadelphia: Lippincott Williams & Wilkins). This chapter will introduce and review in some detail the current understanding of the biopsychosocial (BPS) perspective of pain. This more inclusive approach to understanding and helping people manage their pain has proven to be the most heuristic method when considering issues of pain etiology, assessment, and treatment. In order to understand how clinicians and researchers arrived at this perspective, it is first important to have some understanding of what theories came before and led up to the BPS perspective.
Early Theories of Pain
Two definitions are of primary importance in order to comprehend some of the prior theories of pain. While pain is a subjective experience, resulting from the transduction, transmission, and modulation of sensory information, nociception is a more objective phenomenon resulting from the stimulation of nerves that convey information about potential tissue damage to the brain. The traditional biomedical model of nociceptive processing dominated the medical views of the nineteenth and twentieth centuries, and considered pain processes within a model of disease processes. These early models were informed by Cartesian views of an isomorphic relationship between reported pain and visible or measurable tissue injury. These early models consist primarily of two schools of thought. The first of these, termed the specificity theory required unique receptors and specific pathways in order to transmit painful information from the periphery to the spinal cord and, finally, to the brain. This particular point of view may date back as far as the ancient Greeks, who understood pain transmission as part of a direct transmission line. The work of von Frey (an early modern specificity theorist) involved identification and description of mechanical and thermal receptive fields on the skin (Gatchel et al. 2007).
An early twentieth-century theory termed the “pattern response” described nociceptive information as resulting from the particular pattern of responses in afferent systems, instead of activation of specific receptors and pathways, as in specificity theory (Gatchel et al. 2007). According to this theory, the response to pain resulted from stimulus intensity and the processing of the pattern of responses, which in turn determined the perceptual response to the nociceptive trigger. While these preceding theories successfully explained much of the phenomena reported in the literature and prompted a wealth of further scientific publication, they had some serious limitations, lacking specifically in explanations for the relationship between pain and the concept of suffering. A third perspective, popular through the early twentieth century, actually has its origins in concepts associated with the Greek philosopher Aristotle. Instead of a purely sensory model, as with the preceding theories, Aristotle viewed pain as an emotional concept, termed “quality of the soul.” Drawing from these ideas, Livingston was one of the first to argue for pain as a subjective experience, resulting from activation of aversive networks in the brain. In exposing the weaknesses of specificity theory, Livingston described certain “appetites,” which included pleasure and pain as motivating factors (Gatchel et al. 2007). These earlier models fell short, in that observations derived in clinical and experimental settings could not be fully explained by purely sensory and affective models (Beecher 1956). A more complex set of integrative models was eventually proposed in response to the largely ineffective treatments that had been constructed around these earlier theories. These more encompassing models are discussed in the next section, with a specific focus on the gate control theory of pain (Melzack and Wall 1965; Melzack and Casey 1968).
The Gate-Control Theory of Pain
The gate control theory of pain introduced by Melzack and Wall (1965) emphasized the close interaction between psychosocial and physiological processes affecting the perception of pain. The primary contribution of gate control theory to the scientific community was the idea that the central nervous system interacts with various psychosocial factors in the pain perception process. Psychosocial factors in the perception of pain thus took on a more important meaning in the assessment, treatment, and understanding of pain (Melzack 1993). Because scientific understanding is itself a self-correcting process, other researchers contributed to our understanding by pointing out the flaws and unexplained phenomena still to be answered by this model (Schmidt 1972; Nathan 1976). These contributions further strengthened the model by responding to these criticisms with revisions and reformulations of gate control theory (Wall 1989). But due to its versatility and simplicity, the gate control model of pain has withstood the rigor of changing scientific data and theoretical challenges, and continues to provide a heuristic conceptualization for a wide array of pain symptomatology encountered in clinical and experimental settings. Still, our understanding of pain phenomena becomes more refined over time by scientific contributions, particularly due to technological advances that allow us to better assess underlying pain neurophysiology, neurotransmission, and opioid receptor processes.
This more complex view was followed up during the next decade by Engel (1977), who first introduced the concept of the biopsychosocial (BPS) approach to medicine. Prior to this development, the term psychogenic pain was used to suggest that pain that could not at the time be physiologically measured was a result of underlying psychological etiology. It was often implied, and even outright stated in many cases, that this was not “authentic” pain because it could not be objectively measured. The ideology resulting from this model effectively stunted the development of treatment modalities necessary to address comorbid psychiatric and pain conditions. Fortunately, psychogenic pain is no longer classified as a diagnostic disorder in modern psychiatry thanks to the work of the researchers like Melzack, Engel, and others (DSM–IV; American Psychiatric Association 1994). However, this does not preclude the dynamic relationship that psychosocial factors and pain can play for any particular patient. Pain disorder is instead used to more accurately define and describe various subtypes of conditions, as well as the degree of relationship between physiological and psychosocial factors. More detail pertaining to the BPS perspective is discussed in an upcoming section but, before this, another contributing model of pain based upon neurological factors is described in detail – the neuromatrix model of pain.
The Neuromatrix Model of Pain
Melzack (1999, 2005), in building on his prior work with the gate-control theory of pain, has proposed a neuromatrix model of pain which integrates models of stress along with a great deal of physiological and psychological factors associated with pain. Specifically, this theory proposes that pain is an elaborate process resulting from the distinctive neurosignature of a widely disbursed neural network in the brain, which Melzack labeled the body – self neuromatrix (Melzack 1999). The body – self neuromatrix is responsible for the integration of cognitive – evaluative, sensory – discriminative, and motivational – affective functions originally proposed by Melzack and Casey (1968). According to this model, the output patterns of the neuromatrix are what activate specific perceptual, behavioral, and homeostatic systems in response to injury and chronic stress. Of particular importance in distinguishing neuromatrix theory from other pain models is the identification of pain as subsequent to neural network output, as opposed to pain being thought of as a direct antecedent to injury or inflammation (Melzack 2005).
Chronic Pain and Stress
While it is proposed that this neuromatrix is to some degree genetically derived, sensory experience and learning also affect it (Gatchel et al. 2007). Therefore, according to this model, when a person is injured, homeostatic regulation is disrupted or altered. A complex hypothalamic–pituitary–adrenal (HPA) axis response is initiated due to this disruption, in order to restore homeostasis. The effect on this system due to chronic stress can result in a suppressed or compromised immune response and the limbic system. The limbic system is a keystone element in this dynamic interaction because it is responsible for much of human emotion, motivation, and cognitive processes (Gatchel et al. 2007).
As a result of all the aforementioned complex interactions, the neuromatrix is shaped by learning history, cognitive interpretation, and individual physio-behavioral response patterns. This interactive process, in which predisposed factors interact with an acute stressor, is referred to as a diathesis-stress model. Pain is a discrete stressor in this process as the body attempts to achieve homeostasis. Chronic pain is therefore an ongoing stressor that continually makes demands on the body’s defense systems. A combined threat of fear, anxiety, and cognitive interpretation of the pain then contributes to the ongoing stress, thereby producing a feedback loop of sorts which, without intervention, is likely to maintain an ongoing pain-stress process (Gatchel et al. 2007).
The basis of the neuromatrix model comes from research with patients who have spinal cord injuries and in patients who experience phantom limb syndrome and phantom limb pain (see also Foell and Flor 2011). Findings have demonstrated that a significant number of people who have lost a limb or sensation in another body region, also continue to experience the sensation of the limb or other area. While it is thought that phantom limb phenomena might occur in some cases due to altered peripheral nerve activity in the region of the stump (Gatchel et al. 2007), the available evidence does not fully account for all of the observed phenomena (Katz and Melzack 1990). While traditional sensory-based theories of pain cannot adequately address these phenomena, the neuromatrix theory may be able to, as no actual sensory input is required to produce sensation experiences.
The Biopsychosocial Perspective of Pain
The BPS model of pain, introduced earlier in this chapter, is widely recognized in modern clinical and research settings as the most heuristic approach for conceptualizing and treating pain disorders. Physical disorders (such as pain) often are likely the result of dynamic interactions between physiological and psychosocial factors. As with the neuromatrix model, these interactions perpetuate and contribute to the overall pain experience. While each person experiences pain uniquely, a range of psychosocial and socioeconomic factors also interact with physical symptoms to create the clinical presentation. In a very brief period of time, the BPS perspective has produced a large evidence-based repository of information that has contributed to improved patient care, pain prevention, and clinical understanding of persons with pain conditions (Gatchel and Maddrey 2004).
Turk and Monarch (2002) discussed, in a review of literature regarding the BPS perspective on chronic pain, how individuals differ significantly in the frequency with which physical symptoms are reported, in their likelihood to visit physician, and treatment response. It was observed that, often, treatment response is not directly related to objective physical symptoms. Observations like this have been reported for some time, as with findings by White et al. (1961) that less than one-third of all persons with clinically significant symptoms ever actually consulted a physician. Conversely, Dworkin and Massoth (1994) reported that approximately 30–50% of patients who seek treatment in primary care do not have specific diagnosable disorders. For emphasis, this means that many people with identifiable symptoms do not seek treatment, while many patients who do seek treatment and report pain do not have clinically identifiable or diagnosable ailments.
The terms disease and illness are further distinguished in the pain literature (Turk and Monarch 2002). Disease typically refers to a process that interferes with the functions of an organ or organ system, resulting from infection, injury, genetics, or other precursors. Illness, however, primarily refers to an individual’s experience of that disease, resulting in a range of physical, behavioral, and psychosocial stressors. Similar differences are noted in nociceptive versus pain processes. Two individuals may have similar injuries that, in turn, transmit information regarding nerve and tissue damage to the brain, as an example of nociception. Subjectively, though, they may experience entirely different pain processes. Pain, similar to illness, refers to how physical and psychosocial experiences are subjectively interpreted through the transduction, transmission, and modulation of sensory input. Pain can therefore only be evaluated and fully described from the perspective of the person who has endured the nociceptive process. Illness is the primary focus of assessment and treatment within the BPS model. While patterns and similarities between experiences emerge from this perspective, the biological, psychological, and social factors interact in such a complex manner that no two people are likely to bring the same pain experience to the fore. This diversity of pain experiences requires an empathic clinical understanding of pain, along with the patient’s perception and response to that process. It has been demonstrated repeatedly throughout clinical and research literature that any assessment and treatment approach with neglect in these constructs is incomplete. To further emphasize this point, the success of the BPS treatment modality has been consistently demonstrated (Turk and Monarch 2002).
Comorbidity of Chronic Pain and Mental Health Disorders
Identifying comorbid mental health disorders is a vital component in treating pain from the BPS perspective, because subjective experiences of pain may be intensified by comorbid psychopathology, thus perpetuating any associated disability (Dersh et al. 2002; See also Donovan et al. 2011). Patients experiencing chronic pain are at increased risk for depression, suicide, and sleep disorders, and these factors become more significant in the maintenance of dysfunction and suffering as pain becomes more chronic in nature (Gatchel 1996). The three major psychiatric concomitants of chronic pain are mood disorders, anxiety disorders, and substance abuse disorders (Dersh et al. 2002).
Several relationships have been demonstrated between mental health disorders and pain. As evaluated through the multiaxial classification system of the DSM-IV-TR (American Psychiatric Association 2000), mental health disorders are defined and categorized as part of a five axis domain that encompasses more transient states, consistent traits, medical conditions, social factors, and global functioning. The more acute clinical disorders that are often focused on clinically are coded on Axis I, while the more persistent trait disorders (personality disorders (PDs) and mental retardation (MR)) are reported on Axis II. Major depressive disorder (MDD), an Axis I disorder, has a particularly high prevalence among patients being treated for chronic pain symptoms (Kinney et al. 1993; Polatin et al. 1993). Also within the Axis I diagnostic categories, Anxiety disorders (Burton et al. 1997; Fishbain et al. 1986; Polatin et al. 1993) and substance use disorders (Fishbain et al. 1986; Katon et al. 1985; Polatin et al. 1993; Reich et al. 1983) have high prevalence rates among persons being treated for pain symptoms.
In the literature, depression has been defined as a mood, symptom, or syndrome, and assessed by multiple methods that make it difficult to compare results across study designs, further complicating accurate diagnosis and treatment for pain and depression in clinical settings (Dersh et al. 2002). Several researchers (Kinney et al. 1993) have identified high rates of MDD in patients with chronic pain. Prevalence rates for MDD from these studies were reported as current rates of about 45% and lifetime rates of approximately 65%. In a comprehensive meta-analysis of 14 studies that identified MDD in patients with chronic pain, nine studies reported current prevalence of MDD between 30 and 54% (Banks and Kerns 1996). During this time period, estimates of MDD in the US population were reported as 5% for current major depression and 17% for lifetime major depression (Blazer et al. 1994). It is most likely that the high prevalence rate of MDD in patients with chronic pain accounts for much of the research investigating the association between the two.
As mentioned earlier, high prevalence rates of anxiety disorders have also been documented among patients with chronic pain (Fishbain et al. 1986; Polatin et al. 1993; Burton et al. 1997). Within the larger domain of anxiety disorders, panic disorder and generalized anxiety disorder tend to be the most commonly diagnosed of the specific anxiety disorders. These also include agoraphobia, specific phobia, social phobia, posttraumatic stress disorder (PTSD), and obsessive compulsive disorder (OCD) (Dersh et al. 2002). In contrast to findings with MDD, in studies that relied upon DSM diagnostic criteria, the overall prevalence for anxiety disorders was similar to those estimated in the general population. Follow-up findings suggest, however, that anxiety disorders are more often associated with chronic pain than has been previously reported (Dersh et al. 2002). Researchers have reported lifetime prevalence rates similar to the general population, while current prevalence rates of other mental health disorders in patients with chronic pain are significantly higher (Polatin et al. 1993; Burton et al. 1997).
While anxiety disorders have been frequently identified in both acute and chronic pain populations, higher prevalence rates of other mental health disorders have also been indicated in patients with chronic pain (Kinney et al. 1993; Gatchel et al. 1996). It might simply be that, while anxiety is a common reaction to acute pain, other conditions such as MDD develops over time along with chronic pain. This would seem to support a model of progression from acute pain to chronic pain disability (Gatchel 1991a, b). Some patients may have genetic markers that would predispose them to a mental health disorder that, in turn, is then activated by the stress of a chronic pain experience. Following this logic, chronic pain might be exacerbated by physiological mechanisms that “follow on the heels” of an anxiety response. Avoidance of activities that might actually help to reduce pain symptoms, in turn, contributes to the maintenance of pain by avoidance of activities like exercise, primarily due to fear of re-injury. In addition to this, some patients with pain disorders might have unwanted responsibilities and social obligations that they may avoid which, in turn, leads to lowered self-esteem and reinforces their belief that exertion might increase pain. Such a cognitive-behavioral mediation cycle may actually occur with patients who are anxiety-sensitive, and who catastrophically misinterpret physical sensations of arousal as pain related.
Brown et al. (1996) found rates of current substance use disorders ranging from 15 to 28%, while lifetime substance use disorders ranged from 23 to 41%, among patients with chronic pain disorders. It should also be noted that these rates were higher among male patients than female patients in the chronic pain population, similar to findings within the general population. In contrast to the general population, however, the prevalence rates of both lifetime and current substance use disorders were significantly higher for male and female patient in the chronic pain population (Dersh et al. 2002). While chronic pain may not induce substance use disorders as once believed, it was demonstrated by one study that 94% of chronic pain patients have experienced lifetime substance use disorders prior to the onset of a chronic pain disorder (Polatin et al. 1993). While these statistics can be intimidating from a treatment perspective, Brown et al. (1996) found that patients with chronic pain were no more likely than other patients in a medical setting to have current substance use disorders. So, while there is not a unique risk for substance abuse within the chronic pain population, these patients do seem to be at an increased risk for new substance use disorders during the 5 years following the onset of chronic pain (Brown et al. 1996). It may even be that iatrogenic factors (conditions induced inadvertently by a physician or as a result of medical treatment) are at least partly responsible for this increased risk.
One measure to prevent or reduce this risk is for the treatment provider to conduct a comprehensive history and physical during their initial intake with a pain patient. During this exam and interview process, specific issues should be addressed, including opiate use patterns, the pain condition itself, previous treatments utilized and their outcomes, how the patient obtains and utilizes his or her opiate medications, evidence of drug-seeking behaviors or loss of control, and the current level of relief (Bernstein et al. 2007). One important note of caution is that patients habituated to chronic pain are more likely to underestimate medication use and in some circumstances may attempt to hide illicit drug use. For this reason, a comprehensive screening for these issues must include a combination of experienced clinical observation confirmed by physiological testing such as urinalysis. While pain medications can be effective and safe, treatment providers must also balance the risk of prescription drug abuse with the needs of patients in need of effective relief (Bernstein et al. 2007).
A Conceptual Model of How Acute Pain Develops into Chronic Pain
All chronic pain conditions arise from acute occurrences, yet not all acute injuries result in chronic pain situations. Understanding the factors that contribute to the development of chronic pain conditions has been a primary goal in pain research. It is understood that individuals experience acute pain in reaction to noxious stimuli often associated with physical injury (Basbaum and Jessell 2000). In most cases, as the disease state heals, the perception of pain, at this acute level, fades. Most individuals who have sustained injuries report some level of anxiety; yet, this psychosocial response is viewed as an adaptive emotion in that it promotes behaviors associated with healing, such as focusing on the injury and seeking appropriate medical care. Individuals for whom the pain state does not cease with the healing of the injury have been seen to enter an intermediate phase that can last several months following the injury. This secondary phase is marked with prolonged psychosocial distress, which can include emotions such as increased anxiety, fear, or anger, and can lead to behaviors involving learned helplessness. Furthermore, during this phase, secondary symptoms not associated with the original injury are often reported. The increased levels of stress can be associated with other physiological disturbances, such as in the respiratory and digestive systems, that qualify as somatization disorders (Gatchel 2001).
Within 6 months following an injury, the natural healing process should have restored the body back to the original condition. However, some individuals continue to experience pain following the sufficient period of biological repair (Gatchel 1991a, b) (see also Short and Vetter 2011). In fact, long-term pain conditions are repeatedly found to occur in conjunction with psychosocial issues, primarily depression (Gatchel and Maddrey 2004). Physical deconditioning often occurs with chronic pain conditions, in that exercise neglect results in the deterioration of the muscles and skeletal regions associated with the injured site (Mayer and Gatchel 1988). Oftentimes, chronic pain patients also exhibit “deconditioning” of their psychosocial state, such that daily activities are often abandoned and personal relationships can collapse (McMahon et al. 1997). Motivation can become a major factor for the chronic pain patient. Many times, individuals with chronic pain lose interest in normal responsibilities which can have direct negative effects on their family and with their work. In fact, if this lack of motivation becomes problematic with their work, patients with chronic pain can incur financial difficulties that can also contribute to their psychosocial distress. Once the individual has developed a chronic pain condition, it is essential to attend to the patient from a holistic, or BPS approach, to accommodate the biological, psychological, and social needs. Moreover, because each patient’s circumstances are unique, it is vital to mold the treatment to match the needs of each individual (Gatchel and Maddrey 2004).
The Biopsychosocial Approach to Pain Assessment and Management
Chronic Pain Assessment
The concept of pain cannot be separated into discrete physical or psychosocial elements (Gatchel and Maddrey 2004). The BPS approach to understanding pain has been identified as the most successful model to date, in that the interactions among the biological, psychological, and social components unique to each individual are taken into account. The complexity of pain manifests not only within the range of psychological, social, and physical attributes, but also with respect to chronicity, such that these intertwined components are seen to modulate the patient’s perception of pain and disability. The BPS model, therefore, uses physical, psychological, social, cognitive, affective, and behavioral measures, along with their interactions, to best assess the individual’s unique pain condition (Gatchel and Maddrey 2004).
A recent expansion of this model shows a better understanding of how the neuroendocrine system affects the chronic pain condition (Gatchel 2004, 2005). In addition to the impact of general emotional distress, elevations of stress hormones produced by the hypothalamic-pituitary-adrenocortical (HPA) system, such as cortisol, have been shown to exacerbate pain conditions. McEwen (1998) had highlighted the importance of evaluating cortisol dysregulation under condition of allostatic load increases due to stress. Underlying mechanisms related to the HPS axis may therefore help to explain individual differences in stress and pain. Cogntive-behavioral therapy may be helpful in preventing and reducing the physiological and behavioral toll of this stress module (Turner et al. 2006; Gatchel and Rollings 2008).
Furthermore, growing technologies have allowed for a better understanding of the pain experience through various modalities, such as functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) (see also Naylor et al. 2011). These types of imaging techniques focus on the displacement of blood flow within specified regions of the brain. Although there is some controversy regarding the implications derived from imaging procedures, these noninvasive technologies have provided knowledge about the anatomy and pathways related to the central nervous system (Gatchel et al. 2007). In addition to the brain imaging techniques, other developments in pain research have been found in areas of genetics, electrophysiology, molecular biology, and pharmacology (Gatchel et al. 2007). The unification of disciplines focused on pain provides the most effective methods to understanding pain because it gives a comprehensive and holistic view of how the nervous system perceives, interprets, and responds to pain (Gatchel 1999, 2007).
When attempting to assess an individual’s pain condition, there are two essential “traps” to avoid. First, although there are numerous pain assessments available, the practitioner cannot assume that any one assessment will have more validity or reliability than another measure in a given pain patient. Secondly, while physical measures of pain are more objective than self-report instruments, both must be taken into consideration in the evaluation of the pain condition. Regardless of the level of accuracy in the objective analysis of pain, the interpretation on the part of the health care professional must be considered for an adequate diagnosis to be made. Furthermore, the individual’s psychosocial state can influence the performance on a physical assessment, such that fear of re-injury and lack of motivation may adversely affect the outcome measures (Gatchel 2001).
When considering the types of assessments to use, the measure is only valid if it is aligned with the purpose at hand. Assessments used in chronic pain populations that focus solely on biological and physiological aspects may not be valid in predicting impairment or disability (Gatchel and Maddrey 2004). Not only is it important to consider how each measure will be used but, moreover, it is essential to be able to identify how the various tools assimilate into a complete portrait and analysis of the individual’s pain condition (see also Hjermstad et al. 2011; See also Dy and Seow (2011); see also Palermo 2011). A step-wise approach to assessment has been advocated, beginning with a general evaluation of the factors under consideration, leading up to a more definitive diagnosis (Gatchel 2000). By taking this multidimensional view, the BPS approach to assessment will lead not only to a better understanding of the patient’s pain condition, but ultimately will lead to a comprehensive treatment protocol customized to the individual’s unique situation.
Related posts:
Educating Patients and Caregivers About Pain Management: What Clinicians Need to Know
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Chronic Low Back Pain
Hope in the Context of Pain and Palliative Care
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