L02 Psychological Medicine The psychology of pain

Overview

This lecture introduces pain as a biopsychosocial phenomenon rather than a purely physical one. It covers the scale and impact of persistent pain in New Zealand, terminology and classification of acute versus persistent pain, the physiological ascending/descending pain network, how acute pain can become persistent (nociceptive vs nociplastic mechanisms), the factors that make pain subjective (including cultural inequity and the fear-avoidance model), and how to assess, measure and manage patients with pain.

The burden and impact of persistent pain

• Public understanding of pain is poor: 68% of people have slight/no understanding of pain, and 65% often/sometimes doubt the reality and impact of pain.
• Economic cost in NZ: NZD 15 billion (2016), projected to rise to NZD 24 billion by 2048.
• Prevalence: 20.2% of the NZ population experiences persistent pain.
• Activities persistent pain “greatly affects” (approximate proportions): playing sports ~57%, ability to sleep ~53%, enjoying social activities ~25%, holding down a job ~24%, managing household ~18%, studying ~15%, raising children ~7%. [flag: bar chart values are visually estimated from the chart, no exact figures were labelled]
• Ongoing (unresolved) pain can cascade into wider effects on the person:
  • Identity and mood: regret, changes to sense of self, anxiety, stress, low mood.
  • Distrust of the medical system and feeling invalidated (e.g. “it’s all in my head”).
  • Occupational and social consequences: loss of employment, changes in role, limited social interactions.
  • Can also create caregiver stress, giving the patient a sense of being a burden.

Pain terminology and classification

• Pain (definition): an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.
• Acute pain: recent onset/limited duration; acts as a warning sign of danger; facilitates healing through immobilisation (encourages not moving); involves less complex psychological processing and is more socially accepted.
• Persistent (chronic) pain (> 6 months): pain persisting beyond the expected healing time of an injury; often has no identifiable cause; involves more complicated psychological processing and social acceptance.
• Persistent (chronic) pain sits under the broader umbrella term Persistent Somatic Symptoms (PSS), alongside functional neurological disorders (FND), somatisation, somatic symptom disorder (SSD), and bodily stress syndrome (BSS). [flag: this slide’s text was not captured by text extraction and was transcribed from the rendered image]
• PSS can involve any body system, and symptoms may be atypical or not confined to a single system, e.g.:
  • Neurological: weakness, tremor, dystonia, paralysis, tics, sensory/speech disturbance, functional seizures, chronic fatigue syndrome/ME-CFS.
  • Gynaecological: chronic pelvic pain (CPP).
  • Gastrointestinal: non-specific abdominal pain, irritable bowel syndrome (IBS), tension and migraine headache.
  • Musculoskeletal: fibromyalgia, complex regional pain syndrome (CRPS), back pain.
  • Dermatological: rash, eczema.
  • Cardiovascular: non-cardiac chest discomfort, dyspnoea, dizziness, fainting, vocal cord dysfunction (VCD).
  • Respiratory: recurring throat/urinary symptoms without infection.

Pain physiology: the ascending and descending pain network

• Historically (16th-century model), pain was understood as a single, bottom-up ascending signal from a noxious stimulus straight to the brain.
• The modern (21st-century) model recognises pain as bidirectional: an ascending pathway carries the signal to a “pain experience” in the brain, while a descending, top-down pathway modulates it. Descending modulation is shaped by prior experiences, attention/expectation, mood (anxiety, depression), neurochemical and structural changes, genetics, and peripheral/central sensitisation.
• Key definitions:
  • Noxious stimulus: a stimulus that is damaging or threatens damage to normal tissues.
  • Nociception: the neural process of encoding a noxious stimulus.
  • Nociceptor: a high-threshold sensory receptor of the peripheral somatosensory nervous system, capable of transducing and encoding noxious stimuli.
• Ascending pathway, in order:
  1. Receptor (nociceptor) at the site of injury: signal transduction. Local mediators released include bradykinin, prostaglandins and substance P, carried centrally by slow unmyelinated C-fibres and fast myelinated A-delta fibres.
  2. Primary afferent neuron: carries the signal from the periphery to the ipsilateral spinal cord (dorsal horn/dorsal root ganglion/substantia gelatinosa).
  3. Ascending spinothalamic tract carries the signal further up the cord.
  4. Second-order neuron: the integrative centres in the thalamus.
  5. Third-order neuron: thalamus onward to higher centres (cortex, limbic system, brainstem/reticular formation).
• Descending pathway (endogenous pain control): runs from the brainstem back down to the spinal cord, inhibiting (“-ve”) incoming pain signals at the dorsal horn.

How persistent pain develops

• Nociception ≠ pain: nociception is how pain signals travel from the site of injury to the brain; pain is the (subjective) unpleasant sensory and emotional experience itself.
• Two mechanisms of pain:
  • Nociceptive: arises from actual/potential tissue damage detected by nociceptors.
  • Nociplastic: altered nociception with no clear evidence of ongoing actual or threatened tissue damage causing activation of peripheral nociceptors. This is the mechanism underlying persistent pain.
• Repeated and ongoing noxious stimulation may enhance pain sensitivity (Hyperalgesia) and drive neuroplastic changes such as gene induction and synaptic strengthening.
• Injury shifts the pain sensation-vs-stimulus intensity curve leftward/upward relative to the normal curve, producing:
  • Allodynia: pain triggered by a normally non-painful, low-intensity stimulus.
  • Hyperalgesia: an exaggerated pain response to a given stimulus.

What shapes the pain experience (subjectivity and biopsychosocial factors)

• Pain is subjective. Factors that influence/modulate an individual’s pain experience: source of injury (e.g. accident, self-infliction, abuse, treatment), beliefs/concerns (e.g. “no pain no gain”), cultural issues (language, expectations, expressions, health inequity), other illnesses and body sensitivity, coping strategies, social factors (family, work), and psychological factors (anxiety, anger).
• Cultural issues in NZ:
  • NZ Europeans (22%) and Māori (23%) are the ethnic groups most affected by persistent pain.
  • Reporting: cross-cultural comparisons show Māori patients report the highest pain levels, highest number of pain sites, pain interference, psychological distress, depression, stress and anxiety. Māori, Pasifika and Asian populations are under-represented in tertiary pain services, and Pasifika and Asian populations are less likely to report pain than Europeans.
  • Inequity: perceived racial discrimination leads to hopelessness, which leads to worse pain management and lower quality of life (Ezenwa et al., 2012).
  • Culture can be harnessed for better treatment, e.g. incorporating family and spiritual beliefs alongside psychological and physical approaches. [flag: this line appeared cut off at the bottom of the slide, so the list of examples may be incomplete]

The fear-avoidance model

Fear-avoidance is the key biopsychosocial mechanism linking pain appraisal to disability: how a patient interprets pain, not just its intensity, drives whether they recover or become disabled by it.

• Flow: nociception leads to pain, which then branches depending on whether the pain is appraised as high threat or low threat.
• High-threat/negative cycle: threat thoughts/beliefs (“going to get hurt”, “not going to get better”, “I cannot manage”) → negative affect/harm representation → priority given to pain control (worrying thoughts, staying focused on the body) → fear → avoidance (reduced activities) → interference (no work, sleep difficulties, reduced appetite) → negative affect, which loops back and reinforces the pain. This is a maladaptive avoidance cycle.
• Low-threat/positive cycle: positive affect/optimism → priority given to valued life goals → approach behaviour → recovery. This is an adaptive cycle.

Assessing, measuring and managing pain patients

• Assessment: build rapport, actively listen, validate and normalise first. Then establish frequency (F), intensity (I) and duration (D) of pain; area of pain/injury; description of the pain (e.g. tingling, sharp, needles); what makes it better/worse; and its impact on quality of life/lifestyle. Also assess the same subjectivity factors as above: coping strategies, beliefs/concerns, other illnesses, cultural issues, psychological factors, social factors.
• Measurement tools:
  • Body charts (e.g. Body Pain Locator, Head and Hand Pain Locator).
  • Self-report scales (e.g. a Wong-Baker-style faces scale from 0-10, “No Pain” to “Unimaginable/Unspeakable”, with functional-impact descriptors at each level; numerical rating/visual analogue scales).
  • Self-report inventory (e.g. Brief Pain Inventory, short form).
• Common myths about chronic pain to address directly: “it’s all in my head”; “I can’t live with this label of ‘chronic’ pain, meaning no options”; “just tell me what’s wrong and fix it.” The response to all of these is to build rapport, actively listen, validate and normalise.
• Treatment approach: education (provide information, shared language, correct factual errors); provide models of pain and what may/may not be helpful; pain medication; explain and make a referral to the pain management team.
• Chronic pain management is multidisciplinary, with a team including: physician, psychologist, occupational therapist, physical therapist, nurse.

Self-test

1. Define pain (as used in this lecture), and distinguish it from nociception.
2. Describe the scale of the persistent pain problem in NZ (public understanding, economic cost, prevalence).
3. List the ways ongoing, unresolved pain can impact a person’s identity, relationships, and social/occupational life.
4. Distinguish acute pain from persistent (chronic) pain, giving the defining features of each.
5. Where does persistent (chronic) pain sit within the classification of persistent somatic symptoms, and name three other conditions grouped under this umbrella.
6. Describe the steps of the ascending pain pathway from the site of injury to the brain, naming the order of neurons/tracts involved at each stage.
7. What chemical mediators are released at the site of injury, and which nerve fibre types carry the signal centrally?
8. Describe the descending pain pathway and explain its function.
9. Distinguish the nociceptive and nociplastic mechanisms of pain.
10. Explain how repeated, ongoing noxious stimulation can lead to persistent pain.
11. Distinguish allodynia from hyperalgesia.
12. List the factors that shape the subjectivity of an individual’s pain experience.
13. Describe how culture and perceived racial discrimination affect the reporting and outcomes of persistent pain in NZ.
14. Describe the fear-avoidance model, contrasting the high-threat/avoidance cycle with the low-threat/approach-recovery cycle.
15. A patient with persistent low back pain tells you “the doctors keep saying it’s all in my head.” Describe how you would respond to this in your assessment and initial management.
16. List the three categories of pain measurement tool used in clinical assessment, with an example of each.
17. Name the members of a multidisciplinary chronic pain management team.

Answers

Reveal answers

1. Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage; it is subjective. Nociception is distinct: it is the neural process/mechanism by which pain signals travel from the site of injury to the brain. Nociception can occur without pain being experienced, and vice versa.
2. 68% of people have slight/no understanding of pain and 65% often/sometimes doubt the reality and impact of pain; the economic cost in NZ was NZD 15 billion in 2016, projected to rise to NZD 24 billion by 2048; 20.2% of the NZ population experiences persistent pain.
3. It can affect identity and mood (regret, anxiety, stress, sense of self), cause distrust of the medical system and feelings of invalidation (“it’s all in my head”), lead to loss of employment and changes in role, limit social interactions, and create caregiver stress/a sense of being a burden.
4. Acute pain: recent onset/limited duration, acts as a warning sign, facilitated healing via immobilisation, less complex psychological processing and more social acceptance. Persistent (chronic) pain (>6 months): persists beyond expected healing, often has no identifiable cause, and involves more complicated psychological processing and social acceptance.
5. It sits under the umbrella of Persistent Somatic Symptoms (PSS). Other conditions under this umbrella include functional neurological disorders (FND), somatisation, somatic symptom disorder (SSD), and bodily stress syndrome (BSS).
6. (1) Receptor (nociceptor) at the injury site: signal transduction; (2) primary afferent neuron: periphery to ipsilateral spinal cord; (3) ascending spinothalamic tract; (4) second-order neuron: integrative centres in the thalamus; (5) third-order neuron: thalamus to higher centres (cortex, limbic system, brainstem).
7. Bradykinin, prostaglandins and substance P are released at the injury site; the signal is carried by slow unmyelinated C-fibres and fast myelinated A-delta fibres.
8. It runs from the brainstem down to the spinal cord and inhibits (“-ve”) incoming pain signals at the dorsal horn, providing endogenous pain control.
9. Nociceptive pain arises from actual/potential tissue damage detected by nociceptors. Nociplastic pain is altered nociception with no clear evidence of ongoing actual or threatened tissue damage activating peripheral nociceptors; it underlies persistent pain.
10. Repeated/ongoing noxious stimulation can enhance pain sensitivity (hyperalgesia) and cause neuroplastic changes such as gene induction and synaptic strengthening, shifting the pain-sensation-vs-stimulus curve leftward/upward so lower-intensity stimuli produce greater pain.
11. Allodynia is pain triggered by a normally non-painful, low-intensity stimulus. Hyperalgesia is an exaggerated pain response to a stimulus that would normally be painful.
12. Source of injury, beliefs/concerns, cultural issues, other illnesses and body sensitivity, coping strategies, social factors, and psychological factors.
13. NZ Europeans (22%) and Māori (23%) are the groups most affected. Māori patients report the highest pain levels, most pain sites, greatest interference, and highest psychological distress/depression/stress/anxiety; Māori, Pasifika and Asian populations are under-represented in tertiary pain services, and Pasifika/Asian populations are less likely to report pain than Europeans. Perceived racial discrimination leads to hopelessness, which leads to worse pain management and lower quality of life (Ezenwa et al., 2012).
14. Both start from nociception leading to pain, then diverge by threat appraisal. High threat: threat thoughts/beliefs → negative affect/harm representation → priority to pain control → fear → avoidance/reduced activity → interference (no work, sleep difficulties, reduced appetite) → negative affect, looping back to reinforce pain (maladaptive). Low threat: positive affect/optimism → priority to valued life goals → approach → recovery (adaptive).
15. Build rapport, actively listen, validate and normalise the patient’s experience rather than dismissing it. Provide education to give shared language and correct factual errors (e.g. clarify that “chronic” does not mean no options), offer a model of what pain is and what may/may not help, consider pain medication, and explain and make a referral to the multidisciplinary pain management team.
16. Body charts (e.g. Body Pain Locator); self-report scales (e.g. faces pain scale or numerical/visual analogue scale); self-report inventories (e.g. Brief Pain Inventory).
17. Physician, psychologist, occupational therapist, physical therapist, and nurse.