Biobehavioral Model of Pain

A comprehensive understanding of pain and its treatment requires a multidimensional approach that goes beyond nociceptive activity associated with the disease. A model that acknowledges this complexity of pain is needed as a foundation for development of effective pharmacological and nonpharmacological treatments. The most widely accepted definition of pain (“an unpleasant sensory and emotional experience associated with actual or potential tissue damage”) views it as simultaneously a physiological and psychological experience. Beginning with the gate control theory of pain, researchers have advanced a biobehavioral model focused on the unique and interactive components of nociceptive activity, emotions, cognitions, and behavior.

Nociceptive Activity. Nociception describes the physiological, anatomical, and chemical properties of the nervous system that contribute to the perception of pain. Noxious mechanical, thermal, or chemical stimuli generate neuronal impulses conducted along peripheral (afferent) nerve fibers that synapse in the dorsal horn circuitry of the spinal cord and project to the thalamus and cortex via the spinothalamic tract. Neural projections also descend from the brain and synapse with neurons in the spinal cord ( Fig. 8-1 ). The dorsal horn circuitry is an important site within the central nervous system, where modulation (excitatory or inhibitory) of neuronal impulses takes place. The inhibition of spinal nociceptive transmission can diminish the experience of pain, as when endogenous opioids (such as endorphins) are released during stress and produce analgesic effects. This descending pain modulation system, first proposed in the gate control theory of pain, provides a neurochemical and anatomical basis for considering the pain-enhancing or pain-inhibiting effects of psychological factors, such as cognitions and emotions. Nociceptors may be modality specific or polymodal (respond to multiple types of stimuli). Activation occurs only with intense, potentially damaging stimuli, and generally there is no spontaneous activity. The cell bodies of the afferent nociceptive fibers are in the dorsal root ganglia and terminate over several spinal segments in the dorsal horn of the spinal cord.

Diagram showing overview of pain pathways from the peripheral sensory nerves to the cerebral cortex. CRH , corticotropin-releasing hormone; NOR , norepinephrine.

The thalamus is the center of integrations of nociceptive information and plays a dominant role in pain modulation. In addition, there are four cortical areas identified as important in the pain experience: (1) the prefrontal cortex, (2) anterior cingulate cortex (ACC), (3) sensory cortex (both primary and secondary), and (4) the insula. The prefrontal cortex is thought to be site of executive function, cognitive aspects of pain, and such beneficial skills as coping. The ACC is part of the limbic system and considered the site of activity related to affective/emotional and motivational aspects of pain. The sensory cortex is where sensory information is processed and the secondary area neurons are some of the first to receive nociceptive input. The insula is another part of the limbic system and possibly functions as a sensory component regarding the body’s overall sense of physical well-being as it related to pain.

In rheumatic disease–related pain, nociceptive afferents in the joint are located in the joint capsule and ligaments, bone, periosteum, articular fat pads, and perivascular sites. They are activated by joint motion or any noxious movement or stimuli such as inflammation or injury. Two nociceptive neuropeptide neurons dominate: the isolectin-positive and the calcitonin gene-related peptide-containing neurons. Both spatial and temporal summation in a population of nerve fibers results in the sensation of pain and correlates with the magnitude. The enhanced pain associated with arthritis is probably due to the response of joint afferents to the mechanical and heat stimulation present during inflammation, and chemical mediators of joint inflammation such as prostaglandins, which sensitize joint afferent fibers. This inflammation-induced sensitization of articular afferents likely contributes to hyperalgesia (an increased sensitivity or response to painful stimuli), and allodynia (pain due to stimuli that do not typically provoke pain). Also, studies of experimentally induced pain found reduced pain threshold in inflamed and noninflamed joints of children with active arthritis and to a lesser degree in the joints of children in remission. A recent study showed significantly lower pain threshold among children with JIA, leading the authors to conclude JIA alters pain perception, leading to a continued lower pain threshold. The persistence of a lowered pain threshold, even after nociceptive input to the joint might be expected to cease, suggests a role for long-lasting structural and functional changes or “neuroplastic alterations” due to “central sensitization.” Thus, peripheral and central sensitization mechanisms may be operative in arthritis-related pain.

Emotions . Pain is an emotional, as well as a sensory, experience. There is strong correlational support for the link between negative emotions, particularly anxiety and depression, and increased pain intensity and interference in the lives of children with JRA. Also, daily stressful events and negative mood have been linked to increased pain, stiffness, and fatigue in children with polyarticular JRA. In addition, pain often varies throughout the day, especially in children with more severe disease, leading to a lower quality of life. Although causality studies examining the link between emotional distress and pain have yet to be conducted, emotional distress and pain may share common etiological factors; they are reciprocally linked and can occur concurrently. Increased anxiety can induce muscle tension, thereby directly inducing or exacerbating musculoskeletal pain, or increased pain can induce anxiety about future prognosis or interference with life activities. Also, substance P, a neuropeptide, has been implicated in the pathophysiology of inflammatory disease, depression and anxiety, and pain, thus possibly sharing a common mediating factor.

Cognitions . Cognitive factors refer to how people attend (or not) to pain and how they evaluate their pain experience. The focus in the pain literature has been on maladaptive rather than adaptive thinking. Cognitive processing of pain can be maladaptive in at least two ways: (1) people can fail to attend to information or fail to generate self-talk that might be helpful in coping with pain, or (2) people can engage in dysfunctional thinking that leads to maladaptive coping and greater pain (such as wishful or catastrophic thinking). Catastrophizing may be the most “toxic” type of dysfunctional thinking related to pain. Catastrophizing is thought to include three components: (1) rumination (preoccupation with pain-related thoughts); (2) magnification (exaggeration of the threat value of pain); and (3) helplessness (adopting a helpless orientation to cope with pain).

Several studies have investigated cognitive coping strategies in children with arthritis. Studies in Denmark have found that catastrophizing is associated with higher pain intensity during a cold pressor paradigm and clinically over a 3-week period. Reid and colleagues found that “emotion-focused avoidance” coping (catastrophizing and expressing negative emotions) was associated with greater pain intensity, pain duration, and anxiety. Varni and colleagues found that “cognitive self-instruction” (primarily wishful thinking) was related to greater emotional distress and that “cognitive refocusing” (engaging in activities as a distraction from pain) was related to less pain intensity and emotional distress. Another study found that “pain control and rational thinking” (controlling and decreasing pain while avoiding catastrophizing) predicted lower pain intensity.

Behaviors . When children are in pain, they exhibit a wide variety of pain behaviors, such as limping, grimacing, crying, resting, or asking for medication. How others respond to these pain behaviors can be adaptive or maladaptive for the child experiencing pain. Pain behaviors such as guarding and malpositioning of affected joints may be maladaptive for children with arthritis. Caregivers’ responses to children’s pain-related behaviors may also be maladaptive, such as when parents allow children to avoid attending school, which results in low academic performance and missed opportunities for social interactions. Conversely, if children engage in “well” behaviors (e.g., positive coping strategies) and parents reinforce adaptive behaviors, children would be expected to experience less pain and disability from pain. This operant behavioral perspective is well supported in the pediatric pain literature, mostly with respect to chronic abdominal pain or headache. For instance, one study found that children with JRA who reported resting more and withdrawing from activities showed higher levels of pain and emotional distress. Another study found that children with JRA who engaged in “approach” coping (which included talking to a friend or family member about how they felt) showed less functional disability. There is some evidence that mothers of children with more severe arthritis engage in overprotective behaviors that can impede children’s autonomy and management of their pain and other symptoms.

Treatment Implications . A biobehavioral model of pain would suggest a number of treatment options. Early identification and aggressive pharmacological treatment of chronic arthritis could lead to enhanced pain relief and improved function, both in the short term and long term, via a reduction in peripheral and central sensitization mechanisms. Adequate control of the inflammatory disease is of utmost importance in the overall approach to pain management. Adherence to effective pharmacological therapies (see Chapters 12 and 13 ) can be less than optimal, and strategies for improving and maintaining adherence need to be routinely implemented in pediatric rheumatology practice.

There are neurochemical mechanisms that suggest the value of nonpharmacological therapies in the treatment of arthritis-related pain, such as cooling and resting inflamed joints (to control nociceptive inputs and avoid peripheral sensitization) and relaxation or other psychological treatments to control pain by influencing “central” mechanisms.

Psychological interventions that reduce negative emotional states would be expected to directly or indirectly reduce pain intensity and pain interference. Helping children to manage disease-related stressors (e.g., relaxation and problem-solving techniques) should result in concomitant reductions in negative emotions and pain. Enlisting the social support and reinforcement of family and friends should foster greater participation in social and recreational activities by patients, thereby reducing emotional distress and preoccupation with pain and suffering. Psychopharmacological agents (such as the serotonin-specific reuptake inhibitors, or SSRIs) could help reduce depression and pain through common biological pathways.

For children who are not “mindful” or fail to attend to their thoughts about pain, increasing their awareness of these thoughts (by using “thought diaries” to record thoughts when their pain is bothersome) may be a useful first step in learning to cope with their pain. However, without additional coping strategies, just making children mindful of their pain-related thoughts could lead to nonadaptive thinking.

Cognitive “restructuring” may be helpful in countering nonadaptive thinking about pain. This involves having children identify negative thoughts (e.g., “I can’t do anything to make my pain better”), challenge or question these thoughts, and substitute more helpful thoughts (e.g., “I can distract myself or do relaxation exercises to reduce my pain”). There may be a role for distraction in the management of pain, such as encouraging children to engage in behaviors that divert their attention from their pain. Imagery techniques (e.g., vividly imagining a relaxing place or experience) combined with relaxation exercises are often helpful in diverting attention from pain and reducing muscle tension, thereby reducing pain.

Parents are important role models for their children and need to be made aware of how they cope with their own pain (such as headaches) and thereby influence how their children cope with pain. One may need to directly assist parents in learning more adaptive strategies for coping with pain so they can model these strategies for their children (e.g., not avoid responsibilities because of pain and use effective medical or psychological therapies to control pain). Providers also need to teach family members (especially parents) and friends to respond in adaptive ways to children’s pain behaviors. This would include not being overly solicitous and attentive to pain behaviors and, instead, reinforcing alternative and adaptive coping strategies. Children require assistance in finding ways (in spite of their pain) to do what they want and need to do. Also, cautioning parents to avoid being overly protective will help their children develop autonomy and self-management skills. Pain beliefs are influential on the longitudinal course of pain in JIA, and parents’ pain beliefs obviously have an impact on the child’s. Dysfunctional health beliefs in patients with high pain persist over time.

Cognitive-Behavioral Treatments for Pain

Cognitive-behavioral therapy (CBT) approaches to chronic pediatric pain typically involve teaching children to use deep breathing, guided imagery, and relaxation, and to replace maladaptive thinking (such as catastrophizing) with adaptive thinking (such as focusing on what can be done to control pain and encouraging oneself to engage in more effective coping). Parents are taught to encourage their children to stay as active as possible and to engage in positive coping. Parents are also taught to avoid reinforcing pain behaviors (such as allowing children to avoid school or other responsibilities). A CBT approach, in conjunction with standard pharmacological treatments, is consistent with the biobehavioral model of pain and is empirically supported as a treatment for chronic pediatric pain. A recent meta-analysis of CBT interventions for chronic pediatric pain (mostly on chronic headaches) found large positive effects on pain reduction and that self-administered versus therapist-administered programs showed similar benefits in pain reduction.

Two published studies have tested CBT for children with JRA. Lavine and colleagues used a multiple baseline design with eight children with JRA to evaluate a six-session treatment that included relaxation and biofeedback training. They showed significant reductions in pain intensity and pain-related behaviors at follow-up. Walco and colleagues used a single-group pretest-posttest design with 13 children with JRA to evaluate an eight-session treatment that included progressive muscle relaxation, deep breathing, and guided imagery. Parents were seen for two sessions to review how they could reinforce “well” behaviors and avoid reinforcing pain behaviors. There were significant reductions in pain intensity at immediate follow-up as well as maintenance of gains at 6-month and 12-month follow-ups. Although these studies are promising, they involved small samples and no control or alternative treatment comparison groups. There is a need for well-controlled, multisite pain intervention trials for children and adolescents with arthritis.

There is one study that has shown the benefits of daily massage for children with juvenile rheumatoid arthritis. Children who were massaged 15 minutes a day for 30 days by a trained parent experienced less pain (frequency and severity) and pain-limiting activities relative to a control group. However, the sample size was small (N = 20) and the children were not randomized to conditions. More studies are needed to demonstrated the efficacy of this adjunctive mode of treatment for pain, as well as other complementary and alternative medicine approaches patients and their caregivers use without informing their pediatric rheumatologist.