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11 Articles in Volume 11, Issue #8
Pain Following Combat Trauma In the 21st Century: A New Look at an Old Problem
Part 2: Fibromyalgia: Practical Approaches To Diagnosis and Treatment
Advances in Regenerative Medicine: High-density Platelet-rich Plasma and Stem Cell Prolotherapy For Musculoskeletal Pain
Implant Technologies for Severe Pain: Why, When, and the Outcomes
Value of EMG in Patients With Non-Migrainous, Persistent Head Pain
Drug Interactions Among HIV Patients Receiving Concurrent Antiretroviral and Pain Therapy
Etiology of Chronic Pain and Mental Illness: The Biopsychosocial Component
Insights Into Patients’ Views About Topical Opioids: Observations From a Small Clinical Study
Teenage Boy With Multiple Pain Disorders
The Bench Delivers and It Matters
Renewing Opioid Prescriptions Over the Phone

Etiology of Chronic Pain and Mental Illness: The Biopsychosocial Component

Part 1 of a three-part series examining the comorbidity of chronic pain and mental health disorders.

It has been well established that there are high levels of comorbidity between chronic pain conditions and mental health disorders.1,2 Moreover, psychiatric conditions, such as depression, anxiety, substance abuse, personality disorders, and post-traumatic stress disorder (PTSD), occur more frequently in patients with chronic pain than in the general population.3-11 Many clinical researchers have proposed explanations for the co-occurrence of pain conditions and mental health disorders. The strongest evidence has been found in support of biopsychosocial models, which simultaneously incorporate both biological and psychosocial components. This article will address the biological process involved in mental illness and pain. Future articles in the series will address assessment of mental illness and treatment of the comorbid patient.

Neurotransmitter Activity
One of the most widely studied mechanisms for comorbid pain and mental health disorders is the effect of neurotransmitters. Many of the same neurotransmitters are implicated in both pain and psychosocial disorders, including serotonin, norepinephrine, and dopamine.12-15 Low levels of serotonin have been associated with migraine, cluster, and analgesic abuse headaches, as well as fibromyalgia (FM).16-18 Antidepressants that inhibit serotonin reuptake have been shown to improve symptoms in temporomandibular disorders (TMD), tension-type headaches, FM, and certain neuropathic pain conditions.19-22 Klauenberg et al found that in an experimental pain task, depressed patients failed to inhibit the summation of pain signals.23 The investigators hypothesized that dysfunction of the serotonin system may be responsible for the failure to modulate sensory inputs, leading to greater vulnerability to chronic pain conditions. Numerous other clinical trials have also been conducted that revealed a correlation between decreased serotonin functioning and lowered pain thresholds.17,24,25

Neuroendocrine Function
The relationship of the neuroendocrine system, especially the hypothalamic–pituitary–adrenal (HPA) axis, to both psychosocial and pain disorders has been well established. The HPA axis is the body’s primary stress pathway, and it is activated by corticotropin-releasing factors from the hypothalamus, which stimulate the release of cortisol from the adrenal glands. Cortisol modulates the metabolism of serotonin, norepinephrine, and dopamine.26 Melzack proposed that cortisol might have a cumulative destructive effect on bone, muscle, and neural tissue.27 The dysregulation of cortisol has been associated with a number of pain conditions, such as TMD, FM, and chronic daily headaches.18,28,29 Additionally, mental health disorders, such as anxiety, depression, PTSD, and substance abuse, are associated with abnormal HPA axis functioning.15,30-32 Several clinical studies have concluded that evidence of cortisol dysfunction is particularly strong in patients with comorbid pain conditions and major depressive disorders (MDD).33-35

fMRI Brain Imaging
Functional magnetic resonance imaging (fMRI) technology can provide a real-time view of brain area activity. Few studies have examined the combination of chronic pain and mental health disorders; however, several brain areas have been identified as important in the processing of both pain and mood state. Reduced cerebral blood flow to the thalamus, a region of the brain responsible for relaying signals to the cortex, has been found in both chronic pain and depression.15,36 Similarly, the dorsal anterior cingulate cortex, anterior insula, and amygdala are involved in both depression and the emotional appraisal of painful sensations.35 Giesecke et al found that the presence of MDD and chronic pain was associated with activation of the amygdala and anterior insula (brain areas that process the emotional and motivational aspects of pain) in response to experimental pain.14 Numerous researchers have proposed that both chronic pain and MDD involve abnormal anticipatory processing and hypervigilance.14,37,38

Peripheral Pain-Processing Mechanisms
Differences in peripheral pain processing have been documented in patients with comorbid pain and mental health disorders.23,39,40 Klauenberg et al found that patients with both chronic pain and MDD failed to inhibit pain under conditions of repetitive stimulation, with repetitive noxious stimuli leading to a decompensation of the patients’ pain suppression mechanisms.23

Several psychosocial mechanisms to account for the comorbidity of pain and mental health disorders have been proposed. Learning and conditioning mechanisms have been implicated in both chronic pain and mental health disorders.1,14,35 Giesecke et al proposed that the association of sadness with pain was common to both chronic pain and depression, as was learned helplessness, a condition in which a person who has been unable to control a noxious stimulus eventually stops trying and responds with depressive symptomatology.14

Cognitive mechanisms also have shown an association with both pain and psychosocial conditions. Catastrophizing, which refers to responding to negative events with overwhelming helplessness and by seriously overestimating the likely negative consequences, is associated with pain, depression, and anxiety.35 Several researchers have found support for the hypothesis that catastrophizing and other negative appraisals of pain alter the effects of depression on the affective and evaluative experience of pain.40,41 Personality traits also have been linked to both pain and mental health disorders. Neuroticism, a tendency to experience negative emotional states, has been associated with psychosocial disorders, including PTSD, anxiety, and depression, as well as pain conditions such as TMD, low back pain (LBP), and migraine headache.42-46 Another personality trait linked to chronic pain and psychosocial disorders is anxiety sensitivity, which increases risk for panic and anxiety disorders and is associated with chronic musculoskeletal pain and recurrent headache.47-50

Other psychosocial factors that influence chronic pain and psychopathology include self-regulation and coping strategies. Self-regulation often is lacking in personality disorders.35,51 Sansone et al proposed that in some patients with borderline personality disorders, chronic pain is related to a failure to regulate the experience of pain and the emotional reactions associated with pain.51 Coping strategies that are passive (such as hoping) or avoidant (such as reducing activity or isolation) also are associated with comorbid chronic pain and depression.52

Biopsychosocial Explanations
Although there is much evidence for the roles of both biological and psychosocial factors in the comorbidity of pain and mental health disorders, the most promising explanations involve processes that combine the two. This model emphasizes the interactions among biological, mental health, and social factors in the development and maintenance of chronic pain and mental health disorders.

Transition From Acute to Chronic Pain
Gatchel described the role of biopsychosocial processes in the transition from acute to chronic pain (Figure).53 In stage 1 (acute pain), the physical painful stimulus evokes emotional reactions of fear, anxiety, and worry. These reactions are adaptive in prompting the organism to avoid physical harm and seek treatment for injuries; however, if pain symptoms persist beyond the normal healing period of 2 to 4 months, the patients progress into stage 2 (subacute pain).

In this stage, greater variations in emotional reactions are seen. The stress of unrelieved pain will tend to exacerbate preexisting personality characteristics and psychosocial characteristics. The emotional reactions of stage 2 also are affected by social and economic conditions. Patients who receive secondary gains from pain conditions, such as financial compensation or sympathy, may be more likely to experience symptom magnification and somatization. If pain symptoms are not resolved by the fourth month, the patient progresses into stage 3 (deconditioning).

In this stage, the person becomes habituated to the sick role and accustomed to exemption from normal social and occupational responsibilities and obligations, which may trigger depressive symptoms and maladaptive coping strategies that can progress into diagnosable conditions such as MDD or personality disorders.

The entire process of transition from acute to chronic pain also is affected by physical factors.53 If the person responds to pain sensations with activity avoidance or abnormal movement patterns, physical deconditioning may develop. Physical deconditioning and psychosocial distress may exacerbate each other, forming a feedback loop in which poor physical conditioning decreases the person’s emotional well-being and negative emotions encourage avoidance of activity through isolative behavior and decreased motivation. However, it should be noted that this model does not claim that psychosocial factors cause chronic pain. Instead, the form of mental health disorders that co-occur with chronic pain depends on preexisting personality traits and psychosocial characteristics.

The Diathesis–Stress Model
The original conceptualization of the diathesis–stress model was developed as a description of schizophrenia. The diathesis–stress model proposes that psychopathology develops from an interaction of genetic predisposition and environmental triggers.54 This model has been adapted to explain the comorbidity of pain and psychosocial disorders. Turk et al proposed that premorbid physical characteristics (diathesis) interact with intense or recurrent stressors (stress) and inadequate coping mechanisms to produce chronic LBP.55

In contrast, researchers also have claimed that chronic pain is the stressor that activates preexisting depressive tendencies. The stress may result from the physical sensation of pain, as well as the secondary losses (financial, physical ability, self-esteem, etc.) associated with pain.11,56 Other diatheses that may result in psychopathology when activated by chronic pain include genetic predisposition to anxiety or panic, anxiety sensitivity, somatization, maladaptive personality traits, and poor coping mechanisms.1

The Biopsychosocial Model
The biopsychosocial model of chronic pain is a comprehensive perspective that encompasses all the aspects of the pain experience. It has four primary components: biological, physical functioning, mental health, and social function.57 Pain is most complex when it persists over time, with mental health, social, and economic factors interacting with physical pathology to modulate the experience of pain and the development of subsequent disability.2 The effectiveness of biopsychosocial treatment programs has been well established for the treatment of chronic pain and for psychiatric disorders.58-63

Temporal Relationships Between Chronic Pain and Psychosocial Disorders
Studies on the temporal relationship between the onset of pain and the onset of diagnosable psychopathology have revealed that certain psychiatric disorders precede chronic pain (substance abuse, anxiety disorder), whereas others (MDD) develop either before or after the onset of pain.64 The prevalence of most Axis I disorders were also found to be elevated only after onset of injuries.1 Other studies on the prevalence of psychiatric disorders in acute versus chronic pain found higher rates of psychopathology in the chronic pain group.65,66 The question of whether mental health disorders cause chronic pain, or whether chronic pain causes mental health disorders, has been examined by many clinical researchers. Some of the explanations offered include the antecedent hypothesis, the consequence hypothesis, the cognitive-behavioral mediation hypothesis, and common pathogenic mechanisms for both psychosocial and pain disorders.67 Various studies have provided support for all these explanations.64,68

Although mental health disorders are frequently comorbid with chronic pain conditions, the combination of pain and psychopathology does not necessarily translate to poor response to treatment, particularly if a biopsychosocial treatment model is used.69-71 Owen-Salters et al found that rates of affective disorders in patients with chronic LBP were significantly reduced following treatment with interdisciplinary biopsychosocial rehabilitation.69

It is not surprising that there have been certain attempts in recent years to develop the most effective assessment and management techniques for chronic pain. The past decade has produced an abundance of scientific literature supporting a major paradigm shift from the outdated biomedical model to the much more integrative biopsychosocial one to address this problem. The importance of this shift is highlighted, not only by the successful treatment of chronic pain patients, but also its success for patients with comorbid mental health disorders as well.

The next installment in this series will address the importance of assessment tools in identifying patients with comorbid mental illness and pain.

Last updated on: December 15, 2014
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