Mednotes

L17 MSK Pain

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aliasesL17 MSK Pain

14 min read

Overview

This lecture introduces pain as a biopsychosocial phenomenon rather than a simple nociceptive signal. It covers the epidemiology and definitions of pain, contrasts the historical “straight-through” pathway model with the modern view that ascending nociceptive input is shaped by descending brain modulation, and introduces the three mechanistic pain phenotypes (nociceptive, neuropathic, nociplastic). It then covers persistent/chronic pain and its underlying mechanisms, brain reorganisation and the pain input/inhibition imbalance model, common myths about pain and natural pain inhibition, pain assessment, the case formulation approach, and multimodal (pharmacological and non-pharmacological) management.

Epidemiology of pain

  • Pain is the most common reason people seek medical attention.
  • Globally, 1 in 5 adults suffer from pain; 1 in 10 adults are diagnosed with chronic pain each year.
  • In New Zealand, 1 in 5 adults suffers from chronic pain, and no two people are affected in the same way; a single solution to the problem has not yet been identified (Dominick, Blyth & Nicholas, 2011).
  • NZ chronic pain affects about 770,000 people, projected to rise to around 1.26 million by 2048 as the population ages, pushing cost above $24 billion (Australian and New Zealand College of Anaesthetists, 2019).

Chart data approximate

NZ chronic pain diagnosis rates by gender and ethnic group (year ended June 2022) showed Māori and European/Other groups with the highest rates (roughly mid-to-high 20%), Pacific Peoples intermediate (roughly mid-teens%), and Asian groups the lowest (roughly low-to-mid teens%). The source chart carried no printed data labels, so these figures are visual estimates only.

Definitions of pain and the shift away from a straight-through model

  • Epicurus (341-270 BC): pursuit of pleasure and absence of pain is the purpose of life, without excess (drawing on Plato and Aristotle). Jeremy Bentham: “Nature has placed mankind under the governance of two sovereign masters, pain and pleasure.”
  • Nociception: the neural process of encoding noxious stimuli.
  • Pain (IASP definition, Raja et al., 2020): “An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.”
    • Pain is always a personal experience, influenced to varying degrees by biological, psychological and social factors.
    • Pain and nociception are different phenomena.
    • A person’s report of an experience as pain should be respected.
  • Historical model (Descartes, 1644; “16th century” diagram): a single, straight-through ascending pathway from a noxious stimulus to the brain — now rejected as too simplistic.
  • 21st-century model: an ascending (bottom-up) noxious-input pathway plus a separate descending (top-down) modulation pathway. The brain integrates prior experiences, attention/expectation, mood (anxiety, depression), neurochemical and structural changes, genetics, and peripheral/central sensitisation to shape the pain that is perceived.
  • “Through their life experiences, individuals learn the concept of pain” (Raja et al., 2020) — illustrated by fire-walkers, who show altered affective and physiological responses during an extreme collective ritual (Fischer et al., 2014).

Pain as a dynamic, individual, context-dependent experience

  • Pain is a dynamic process and pain experiences are unique to each individual; there is a difference between contributing factors and causes of pain.
  • “Pain is not a static experience — it changes over time as symptoms ebb and flow and as a person’s adjustment to it evolves” (Adams & Turk, 2018).
  • Biopsychosocial model of pain: the pain experience sits at the centre of three interacting domains:
    • Biological: genetics, physiology, neurochemistry, tissue health.
    • Psychological: perceived control, self-efficacy, catastrophic thinking, hypervigilance, depression, anxiety, anger.
    • Social: socioeconomic status, social scepticism, social support, social learning, operant factors.
  • Sequential pathway (Costa, 2022): peripheral nociceptors detect a noxious stimulus -> the signal travels along a peripheral nerve -> it synapses at the dorsal horn of the spinal cord -> ascending input reaches the brain, generating the conscious experience of “pain” -> pain in turn can produce “suffering”, its emotional component.
  • Brain involvement does not make pain imaginary: the brain-mind is genuinely involved in the experience of pain, but this can be misread as implying “it’s all in the mind”, when sufferers experience the pain as real and physical. Unpleasantness of pain is itself an emotion.
  • Context can shape the experience of any event — e.g. the thought “it could be worse” can improve feelings about a present misfortune. Pain, despite being unpleasant, can have positive consequences: providing contrast for pleasurable experience, increasing self-regulation through cognitive control, and promoting affiliation via empathy and group formation (Bastian et al., 2014). [flag: only the header, authors and opening lines of the accompanying journal excerpt on pain’s (un)pleasantness were legible]
  • Culture and social practice can shape whether an intense stimulus is experienced as pain or pleasure, e.g. Thaipusam ritual practices (hook suspension, kavadi piercing). Pain and pleasure share overlapping neurobiology, including a role for opioid and dopamine systems in modulating both (Leknes & Tracey, 2008).

Mechanistic pain phenotypes

Three descriptor/phenotype categories, defined by IASP terminology:

  • Nociceptive pain: arises from actual or threatened damage to non-neural tissue, due to activation of nociceptors.
  • Neuropathic pain: caused by a lesion or disease of the somatosensory (nerve) nervous system; history of nerve injury, pathology or mechanical compromise. Characteristic features: unusual sensations, pain from light touch (allodynia), burning, numbness, tingling, balance problems.
  • Nociplastic pain: arises from altered nociception despite no clear evidence of actual or threatened tissue damage activating peripheral nociceptors, and no evidence of disease or lesion of the somatosensory system. Examples: fibromyalgia, chronic low back pain of unknown cause (non-specific low back pain).

Persistent (chronic) pain

  • Definition (Treede et al., 2015): pain which persists roughly 3-6 months; present almost every day, though intensity may vary; has lasted, or is expected to last, more than 3-6 months; persists past normal healing/recovery time; involves complex biological, psychological and behavioural factors.
  • Trajectory: pain spikes sharply at the moment of injury, within an initial inflammation/scarring/remodelling phase. Nociceptive pain due to injury normally resolves as tissue heals, but pain can instead stay elevated and fluctuate, developing into subacute/chronic pain through any combination of ongoing overuse, inflammation, neuropathic pain and nociplastic pain.
  • Six changes seen in chronic pain (Brown et al., 2021):
    1. Unhelpful psychological states (beliefs, stress).
    2. Increased sensitivity of peripheral nerve endings (Peripheral sensitisation).
    3. Increased activation of spinal cord neurons (Central sensitisation).
    4. Altered immune response (systemic inflammation).
    5. Decreased descending modulation of nociceptive processing at dorsal horn neurons.
    6. Altered brain activity (neuroplasticity) and altered communication between brain regions linked to the pain experience.

Brain changes and the pain-balance model in chronic pain

  • Chronic pain is associated with brain reorganisation across peripheral, spinal and cortical levels (Neurosynth meta-analysis of 516 fMRI studies from chronic pain patients).
  • Abnormal activity is seen across three functional systems:
    • Sensory-discriminative (“pain sensory”) — lateral pathway: somatosensory cortex (SSC/S2) and thalamus.
    • Motivational-affective (“suffering”) — medial pathway: dorsal anterior cingulate cortex (dACC), anterior insula (AI), thalamus.
    • Anti-nociceptive (“pain inhibition”) — descending pathway: pregenual anterior cingulate cortex (pgACC), dorsolateral and medial prefrontal cortex (dlPFC, mPFC), periaqueductal grey (PAG), rostral ventromedial medulla (RVM).
  • Imbalance concept of chronic pain (Neurosynth meta-analysis of 420 fMRI studies; De Ridder, 2020): when pain input and pain inhibition are balanced, there is no pain. When pain input increases and/or pain inhibition decreases, the system becomes imbalanced and chronic pain results.
  • Functional connectivity: the similarity between, and interaction/communication of, brain signals from two regions. Functional connectivity between the pain sensory, suffering and pain inhibition regions decreases in chronic pain (Lancaster et al., 2007; De Ridder, 2022).

Myths about pain and natural pain inhibition

  • Myths identified: pain is caused by injury signals travelling a straight-through pathway to the brain for perception; sensory systems are straight-through pathways; pain is purely “biological”; hurt = harm. The hurt = harm myth leads to fear-avoidance behaviour.
  • The Descartes (1644) straight-through model is the historical origin of these myths and is now rejected.
  • Gate control theory (Melzack & Wall, 1965) underlies natural pain inhibition:
    • A-δ and C fibres are activated by noxious stimuli (pain, temperature).
    • A-β fibres are activated by non-noxious stimuli (light touch, pressure, hair movement) and can inhibit pain transmission.
    • Inactivity negates this natural inhibitory mechanism — hence the advice: Move, Move, MOVE!
    • Clinical correlates: exercise produces exercise-induced hypoalgesia, and pleasant touch has an analgesic effect in people with chronic pain.

Pain assessment

Domains assessed (Dworkin et al., 2005):

  • Pain severity (average, worst, least and current pain).
  • Pain interference.
  • Pain unpleasantness.
  • Pain bothersomeness.
  • Physical function.
  • Physical activity.
  • Psychological wellbeing.
  • Sleep and quality of life.
  • A 0-10 numeric pain scale is used, from No Pain to Worst Pain Possible; “worst pain possible” is different for everyone.

Case formulation approach

  • Case formulation integrates the multidimensional contributors of persistent pain: “Case formulation aims to describe a person’s presenting problems and use theory to make explanatory inferences about causes and maintaining factors that can inform interventions” (Thompson, 2017).
  • Mechanism categories — nociplastic/CNS sensitisation, neuropathic, and nociceptive mechanisms — all feed into chronic pain.
  • Chronic pain interacts bidirectionally with maintaining factors: altered activity patterns, physical changes, unhelpful thoughts/beliefs, repeated treatment failures, depression/helplessness/irritability/poor sleep, long-term use of analgesic/sedative medication, side effects, and loss of job/financial difficulty/family stress — all of which feed into suffering and disability.
  • Family, employer and other healthcare providers also feed into the chronic pain picture.

Management of chronic pain

  • “One size does not fit all”: know who has the pain and what happens in their life normally, know the nature of the condition(s) (they are not all the same), and consider co-morbidities.
  • Multimodal principle: inform (dispel myths, reduce fear-avoidance), give specific or modifying treatments when available, control pain symptoms (many medicines used off-label), and address lifestyle (reactivation, relaxation imagery, exercise/physical activity).
  • Three components of multimodal management: pharmacological, non-pharmacological, and interdisciplinary approach.
  • Pharmacological options:
    • Opioids (e.g. fentanyl, methadone, morphine, oxycodone, tramadol).
    • NSAIDs (e.g. diclofenac, ibuprofen).
    • Antidepressants (e.g. bupropion, duloxetine, imipramine).
    • Antiepileptic drugs (e.g. gabapentin, lamotrigine, pregabalin).
    • Cannabinoids (e.g. ajulemic acid, cannabis, cannabidiol).
    • Local anaesthetics (e.g. levobupivacaine, lidocaine).
    • Others (e.g. clonidine, neostigmine, paracetamol/acetaminophen).
    • Many pain-altering medications (e.g. antidepressants, antiepileptics) are not registered as analgesics and so are used “off-label”.
    • Multiple factors influence drug choice (Guindon, 2007): cultural belief, personal experience, medical history, pain intensity, interference with meaningful activity, other diseases interacting, drug-drug interactions, toxicity, cost, patient acceptance/compliance, and patient expectations/beliefs about the cause of pain.
  • Non-pharmacological options:
    • Psychological approaches: cognitive-behavioural therapy, pain coping skills training, mind-body interventions.
    • Neuromodulation: neurofeedback, repetitive transcranial magnetic stimulation, transcranial electrical stimulation, transcranial direct current stimulation.
    • Exercise and physical activity.

Self-test

  1. Define nociception and distinguish it from pain.
  2. State the IASP definition of pain, along with its three accompanying principles.
  3. Describe how the 21st-century model of pain differs from the historical straight-through (Descartes) model.
  4. List the three domains of the biopsychosocial model of pain, with one example factor from each.
  5. Describe the steps of the pathway from a noxious stimulus to the conscious experience of “suffering”.
  6. Distinguish nociceptive, neuropathic and nociplastic pain, giving a defining feature of each.
  7. List two characteristic clinical features of neuropathic pain, and one example condition of nociplastic pain.
  8. Define persistent (chronic) pain, including a timeframe.
  9. List the six changes that occur in chronic pain.
  10. Describe the three brain systems affected in chronic pain and the region(s) associated with each.
  11. Explain the “imbalance concept” of chronic pain in terms of pain input and pain inhibition.
  12. What happens to functional connectivity between pain-related brain regions in chronic pain?
  13. List two myths about pain identified in the lecture, and explain the clinical consequence of the “hurt = harm” myth.
  14. Describe gate control theory, naming the fibre types involved and what activates each.
  15. Why does the lecture advise people with pain to “Move, Move, MOVE”?
  16. List the domains assessed in a comprehensive pain assessment.
  17. What is the purpose of the case formulation approach to chronic pain?
  18. Describe the three components of multimodal pain management, and the three factors that should be known about the patient before treating.
  19. List the pharmacological drug classes used for chronic pain, giving one example drug per class.
  20. Distinguish psychological, neuromodulation and physical non-pharmacological approaches to chronic pain, giving one example of each.
  21. Using the gate control and imbalance concepts together, explain how exercise could help reduce chronic pain.

Answers

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