The Relationship of Chronic Pain and Major Depression
Struggles of the human condition often involve strife and suffering. Human history provides volumes of evidence supporting that the human condition involves a variety of forms of obstacles. Mental challenges of depression, anxiety, or psychosis are common themes of psychological strife. Physical afflictions, such as illness, injury, or handicaps, are also considered part of the ordinary challenges most individuals face. However, often it is forgotten that these groups are not mutually exclusive and often coexist together. Some even mutually sustain each other, such as pain and depression. Chronic pain and major depression have a reciprocal relationship, in which each can increase intensity/proclivity for the other through various psychological and physical factors.
The link between chronic pain and depression has been well established in scientific literature. Though various definitions exist, pain is considered chronic when it continues for more than one month after healing of an injury and occurs repeatedly. Meaning that the original cause of the pain should be healed, yet the pain continues. Depression also has many definitions and classifications. When using the common term depression, people are usually referring to ‘major depression’, where extensive depressive symptoms interfere with an individual’s daily life for a minimum period of time. According to the DSM-IV, the individual must have depressive symptoms (negative mood, loss of interest, loss of pleasure in life, etc.) that interfere with normal functioning for a minimum of two weeks (2000). In addition to being thoroughly defined, both chronic pain and depression have been extensively covered in psychiatric and medical research. Analyzed in independent and related studies, research has attempted to establish and explain the link between the two phenomenon.
The relationship that has been established between the chronic pain and depression is well supported empirically. Research has shown that about 75% of patients with depression experience chronic/reoccurring pain (Lepine & Briley, 2004) and 60% of chronic pain patients report significant depressive symptoms (Bair & Robinson, 2003). Researchers often disagree on the causes of this relationship. For example, opinions differ on the direction of the relationship and whether it is a moderating or direct relationship. Despite such conflicts, there is a consensus that a correlation exists (Banks & Kerns, 1996; Bair, Jinwei, Damush, Sutherland & Kroenke, 2008). However, identifying the correlation does little to explain the factors leading to it or causative direction of it.
Explanations for the relationship of chronic pain and depression are found in numerous areas of psychology. The link is thought to be sustained/supported by a variety factors. For example, the emotional state of an individual is one of these factors. An individual’s emotional state can be influenced by and can influence both physical and psychological experiences. Meaning various events affect emotions and emotions influence perceptions of events. This reciprocal relationship is well illustrated by the phenomenon of negative attribution. Individuals feeling frustrated/stressed are more likely to have negative anticipatory biases. These individuals attach disproportionate negative feelings to events. Meaning that if individuals are in a negative emotional state, they will be more likely to expect/confirm unpleasant sensations with events. Such biases increase the development and maintenance of depression and chronic pain disorders (Boersma, 2006). Individuals perceive bad events (both pain and emotion based) as more negative and damaging than they would normally seem. And this continued enhancement of depressive/chronic pain symptoms gradually leads to more negative emotional states. This sinking of emotional state can further intensify later negative anticipatory biases, perpetuating them into a causative loop.
Social consequences also factor into the bi-directional relationship of chronic pain and depression. Social dysfunction is a consequence of both pain and depression. Attending social functions, keeping commitments, and staying active in a community can all be threatened by chronic pain and depression. Maintaining interpersonal connections and mutual support between friends and family members can consequently be impaired because of the isolation chronic pain and depression can create (Peveler, Edwards, Daddow, & Thomas, 1996). Unfortunately, that loss of social support can increase feelings of depression, further limiting social activity and intensifying pain. The cycle essentially continues and pushes the suffering individual into a state of relative isolation. Cut off from social support, the cycle will merely continue to worsen.
Behavioral effects also factor into the relationship between pain and depression. Learned helplessness heavily factors into the onset of major depression. When an individual feels incapable of changing/influencing his/her situation, he/she will slowly come to feel helpless and hopeless. Seeing any positive action as ineffective, they descend into a slump of helplessness that ends with depression (Abramson, Seligman, & Teasdale, 1978). This sense of helplessness is easily created by chronic pain. Not only does the individual feel incapable of stopping the pain, but the pain will restrict them from performing normal activities. Many activities, such as outdoor play, exercise, walking, cooking, and driving, can be interfered with or completely halted by chronic pain. When a person is stopped from doing activities they love or rendered incapable of fully caring for themselves, they see themselves in a hopeless situation where they are helpless to change anything. With such a set up, it is easy to see why behavioral disruptions, brought on by pain, can trigger the beginnings of depression and help maintain that depression.
Depression and chronic pain are physically interrelated largely because of how the human nervous system is wired. For example, it is hypothesized that sensory pain pathways are tightly intertwined with emotion pathways in the brain. This relationship is supported by studies that suggest that both pain and emotion regulation involves some of the same neurotransmitters and brain locales/pathways (Basbaum & Fields, 1978). Research denotes that neurotransmitters such as serotonin and norepinephrine play critical roles in both depressive illnesses and pain perception. When one system is overtaxed beyond its capacity to self-limit, the other system may also be impaired. Meaning that if one of the interconnected systems falls into a state where it cannot modulate neural responses, both systems will be unable to modulate neural responses. Because intensity of pain/emotion experiences somewhat rely on stable regulation of their systems, perception of either will spike when either system has been overtaxed. Overtaxing can result from extensive periods of above normal strain, such as prolonged physical pain or emotional suffering.
Another important physical link between chronic pain and depression is signaled by the common use of anti-depressants to treat chronic pain. Anti-depressants are commonly prescribed to depressed and non-depressed patients of pain management clinics, for analgesic effects. The doses are lower than those for depression and show positive benefits in lowering pain (Ryder & Stannard, 2005). These benefits are thought to stem from the related monoamines in both pain sensation and major depression: serotonin and/or norepinephrine. They are also thought to interact with share receptors. Although the exact mechanisms of this benefit are poorly understood, the shared benefits strengthen the theory of their relationship.
When these related brain mechanisms malfunction, an individual will experience higher sensitivity to pain and mood changes. This is due to higher magnitudes of neuronal activation in the associated brain regions. It has been suggested that this alteration in functional responses may be due to faulty anticipatory processing, impairing the brain’s ability to modulate processing of pain and negative affective states (Strigo, Simmons, Matthews, Craig, & Paulus, 2008). Extended periods of attaching negative bias to events will force the brain into a physical response pattern of increased sensitivity. Essentially, because an individual has perceived something as negative for so long, the brain will increasingly automatically attach heightened sensitivity to the negative qualities of that experience. Some pathways are more vulnerable to this alteration in activity than others. Relevant response pathways that are easily given this attachment of heightened sensitivity are feelings of pain and negative emotion.
Somatosensory amplification is another concept that helps illustrate the neurological relationship between chronic pain and depression. Somatosensory amplification includes a hypervigilance to unpleasant sensations and a tendency to overanalyze sensations (Barsky, 1992. Individuals experiencing prolonged periods of psychological distress (such as major depression) will be more likely to experience intensifying trends of somatosensory amplification. This amplification refers to both psychological processing and nerves experiencing stronger reactions to normal stimuli. When this happens, an individual will perceive sensory events as more intense than they normally would (Barsky & Wyshak, 1990). The connotation here is that neural pathway responses are amplified due to psychological stress. Thus a normal signal of pain is amplified into a more painful experience (the perception of pain increases without an actual increase in the stimulus of that pain).
The physical and psychological interrelationship of chronic pain and major depression is complex and has many facets. However, despite the confusing mechanisms, each factor that contributes to this relationship also functions as empirical evidence further supporting it. The evidence today shows that there are many individual factors that connect chronic pain and major depression. They contribute to and sustain one another, binding them into a strong interrelated cycle. To find out the details, more research is necessary, and someday the inner mechanisms of these factors will be revealed.
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