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Additional Somatic Presentations and Chronic Pain Conditions
Abnormal Psychology · Chapter 14: Somatic Symptom and Related DisordersSection 14.4 · lesson 54 of 9715 min · free with a free account
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In this lesson
Pain is always real - and it is processed, not simply transmitted.
- Describe the remaining conditions in this family
- Explain why tissue findings and pain correlate poorly
- Explain the biopsychosocial model of chronic pain
- Describe the psychological approaches in pain management
Transcript
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Somatic Symptom and Related Disorders
Additional Somatic Presentations and Chronic Pain
This final section of the chapter completes the family of somatic conditions, and then turns to chronic pain. Pain is where the ideas of this chapter matter most, and where they are most often misunderstood. We look at why tissue findings and pain match so poorly, how pain is processed, and what the biopsychosocial model really claims. And we finish with how chronic pain is managed, and how to explain it without dismissing anyone.
Read This First
Pain Is Never Imaginary
One statement comes first, and it will be repeated. Pain is always a real experience. It is never imaginary. Some of the material ahead, especially the poor match between tissue damage and pain intensity, is routinely misread as evidence that someone is exaggerating. It is not. It is a finding about how pain works. This material is educational, and it is not a basis for changing any pain treatment you receive. Medication is described by class only, and every medication decision rests with a prescriber. And rehabilitation and pacing are described as clinician-led principles, not a program anyone should follow on their own.
The Rest of the Family
3 Remaining Categories
Three remaining categories complete this diagnostic family. The first is psychological factors affecting other medical conditions. Here, a medical condition is documented and established. What is recorded is that psychological or behavioral factors are making it worse. They might affect its course, interfere with treatment, or worsen its symptoms. For example, diabetes affected by difficulty engaging with treatment, or asthma that worsens during periods of high demand. The physical condition is real and primary. The second is the residual categories, other specified and unspecified presentations. They cover presentations that resemble this family without fitting any one description. They are criticized as unreliable, and they attract little research. But without them, clinicians must record a poor fit or nothing at all, which in many systems means no access to care. The third is pseudocyesis, a false belief of being pregnant, with genuine physical changes. It was historically prominent in writing about this area, but it is rare today. And the person is not pretending.
What Pain Is
An Experience, Not a Signal
The modern definition of pain describes it as an unpleasant sensory and emotional experience. It is associated with, or resembles that associated with, actual or potential tissue damage. Three features of that definition do a great deal of work. First, pain is an experience, not a signal. It cannot be measured from the outside, which is why self-report remains the primary evidence. Second, it is sensory and emotional together. The unpleasantness is part of the pain, not a reaction to it. Third, the words or resembling were chosen deliberately. They explicitly allow that pain can occur without tissue damage. So, stated once more. Pain reported without an identified structural cause is not less real, not imagined, and not exaggerated. The experience is the pain. There is no more authentic version of it located somewhere in the tissues.
Tissue and Pain
A Poor Correlation - and What It Doesn't Mean
Two well-established findings show something important about how pain works. First, imaging studies of people with no pain at all repeatedly find degenerative changes, disc abnormalities, and joint changes. They become more common with age. To a large extent, these are ordinary features of ageing tissue, not reliable causes of pain. Second, many people experience severe, disabling pain, with no structural abnormality found on investigation. Together, these establish that pain intensity is not read directly off the state of the tissues. The relationship runs through processing. What they do not establish is that anyone is exaggerating. The inference that the scan does not explain this much pain, so the pain must be overstated, assumes that pain should track tissue damage. That is exactly the assumption these findings refute. Making that inference misreads the evidence in the direction that does the most harm.
Acute vs. Chronic
Not Just Acute Pain That Lasted Longer
Chronic pain is not simply acute pain that has gone on longer. The two differ in mechanism, in meaning, and in what should be done. Acute pain signals actual or threatened tissue damage. It is a useful warning. Chronic pain often signals nothing about the current state of the tissue. The alarm keeps sounding after the danger has gone. Acute pain resolves as tissue heals. Chronic pain persists beyond the expected healing time. In acute pain, rest, protection, and avoiding load are adaptive. In chronic pain, those same responses become maintaining factors, producing deconditioning and disability. Acute pain usually comes from a peripheral source. Chronic pain frequently involves amplified processing in the central nervous system. And the useful outcome differs. For acute pain, it is intensity, which is expected to fall. For chronic pain, it is function and quality of life. So hurt equals harm is a sensible rule for acute pain. For chronic pain, it is a harmful one.
Figure 14.4.1
Pain Is Processed, Not Transmitted
This figure shows pain processing in functional terms. It begins with a tissue event. Or, importantly, with no event at all. A nociceptive signal travels toward the brain. But it is not simply transmitted. It passes through modulation, where it can be amplified or damped before it reaches awareness. The psychological inputs, attention, mood, beliefs, sleep, and expectation, act here, on the processing of the signal. The result is the pain experience. That is why psychological contribution to pain is not psychological causation. And the diagram works even with an empty first box and a full last one.
Modulation
Gate Control and Central Sensitization
Two terms need keeping apart. Nociception is the detection and signaling of potentially damaging stimuli. It is not pain. Nociception can happen without pain, as with an injury noticed only afterward. And pain can happen without nociception. Descending pathways run from the brain toward the periphery, and modulate incoming signals, amplifying or damping them. The gate control model proposed a spinal mechanism that acts as a gate on incoming signals, influenced from above as well as below. Its historical importance is hard to overstate. It made psychological influence on pain a physiological claim, rather than a metaphor. Its specific spinal mechanism has been superseded. But its central insight, that signals are modulated rather than simply transmitted, survives. Central sensitization is a documented mechanism, not a hypothesis. The central nervous system becomes more responsive, and amplifies the input it receives. So ordinary stimuli can produce pain, and painful stimuli can produce more pain, with nothing changed in the tissue. It explains physiologically how severe pain can persist after healing, with no appeal to exaggeration at all.
Biopsychosocial Model
Contribution Is Not Causation
The biopsychosocial model is the framework for understanding chronic pain. And it is most often misread in one particular way. Psychological contribution to pain is not psychological causation. Saying that attention, mood, and belief influence pain processing describes a mechanism that operates in everyone. Including people with clear structural disease, and people in acute pain from obvious injury. The model is not a way of moving someone's pain from the physical column to the psychological one. It states that all three domains contribute to every pain experience. Biological contributors include tissue pathology where it exists, central sensitization, sleep disruption, deconditioning, and medication effects. Psychological contributors include attention to pain, catastrophizing, fear of movement, low self-efficacy, and mood. And social contributors include work conditions, compensation systems, family responses, and isolation. Notice that the biological domain is fully populated. A biopsychosocial formulation is not a way of avoiding the physical.
Psychological Contributors
Catastrophizing and Fear of Movement
Among psychological contributors, catastrophizing is the most consistently supported. It combines magnifying the threat the pain represents, ruminating about it, and feeling helpless in the face of it. It predicts pain intensity, disability, and treatment outcome more consistently than most other psychological factors. Two cautions. The name sounds like an accusation of overreacting, and it is not. It is an understandable pattern in someone in persistent pain, who has never been given an explanation. And it is not a personality trait. It responds to treatment, and it changes when understanding changes. Fear of movement leads to avoidance. When movement is expected to cause damage, it is avoided, and avoidance produces deconditioning and further disability. The alternative pathway is maintained activity with guidance. Not pushing through. Along that path, disability falls even while the pain itself may not change. And low self-efficacy, believing one cannot manage or influence the pain, strongly predicts disability. Raising it is one of the more reliable achievements of pain programs.
Operant and Social Factors
Effects Nobody Chose
Operant principles apply to pain as well. Behaviors associated with pain happen in a social world that responds to them. And those responses can inadvertently increase the behaviors they follow. A partner taking over household tasks, reduced obligations, or care that depends on demonstrating severity can all work this way. This must never be used to imply that a person wants their pain, or is keeping it for what it brings. Operant processes operate without awareness or intention. That is exactly what makes them operant, rather than choices. The people responding kindly are doing what any decent person would do. And where a benefits system requires demonstrated incapacity, no individual chose that contingency. The related idea of secondary gain is contested, and casual use of it causes documented harm. It ignores the far larger secondary losses of chronic pain. Income, career, relationships, identity, and independence. And once recorded, it follows a person through their notes, and cannot be disproved. It has no place in ordinary clinical reasoning about someone in pain.
Management
Multidisciplinary, Measured in Function
Multidisciplinary pain management is the standard model, with the strongest evidence. Medical, psychological, physiotherapy, and occupational input work together to one formulation, with shared functional goals, and with psychology present from the start. Cognitive-behavioral approaches target catastrophizing, fear of movement, avoidance, and self-efficacy. They improve function and mood, with smaller effects on pain intensity, as the model predicts. Acceptance-based approaches aim instead at engagement in valued activity while pain is present. Where pain does not resolve, a goal of pain reduction guarantees failure. A goal of living the life one wants does not. Pacing and graded activity are clinician-led principles. And sleep and mood are treated in their own right, since they are among the more tractable parts of the picture. Medication is described here by class only. The harms of long-term opioid prescribing for chronic non-cancer pain are well documented, and have reshaped prescribing guidance. Every medication decision, including any change, rests with a prescriber. And outcomes are measured in function and quality of life, not pain elimination. Stating that honestly at the outset is part of the treatment.
In the Clinic
Explaining the Model Without Dismissing the Pain
Explaining the biopsychosocial model goes wrong more often than any other explanation in pain medicine. There are four principles for getting it right. Lead with the mechanism, not the psychology. Central sensitization explains persistent pain physiologically, and can be described first. A person who has been given a physiological account, is far more able to hear about a psychological contribution afterward. Say what the model applies to. All three domains contribute to every pain experience, in everyone. It is not a claim that their pain is different. Use the imaging findings carefully. These findings don't doom you is reassuring. Your scan doesn't justify this is an accusation. And never use the word just. It's just how your nervous system is processing it carries the dismissal, whatever the rest of the sentence says.
2 Composite Cases
Wesley and Priscilla
Two composite cases close the chapter. They describe no real people. Wesley, forty-six, has had back pain for three years after a lifting injury. His imaging shows changes consistent with his age. At eighteen months, he was told his scan did not explain this level of pain. He heard that he was not believed. His formulation contains nothing implying exaggeration. Central sensitization, deconditioning, poor sleep, fear of movement, low mood, and a compensation process are each a target, not an accusation. The aim is a return to activity, work, and social contact. His pain intensity may not change much, and that is not failure. Priscilla, fifty-two, has type two diabetes, with worsening control and the start of a complication. She has missed appointments and avoided reviews, finding the whole subject frightening. Assessment identifies a year-long depression. This is psychological factors affecting a medical condition. Her condition is real and explained, and she is avoiding it rather than preoccupied with it. So treating her depression may do more for her diabetes than anything aimed at the diabetes alone.
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