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Understanding Pain

Last updated 1 Jun 2026 Β· Pain & analgesia

πŸ“‹ Key Information Summary

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  • Pain is subjective: The International Association for the Study of Pain (IASP) defines pain as "an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage" (2020 revision).
  • Pain β‰  nociception: Nociception is the neural process of encoding noxious stimuli; pain is the conscious experience that may occur with or without nociception, and nociception may occur without pain.
  • Four phases of nociception: Transduction, transmission, modulation, and perception β€” each a potential therapeutic target.
  • Nociceptors detect tissue threat: AΞ΄ fibres transmit sharp, well-localised acute pain; C fibres transmit dull, burning, poorly-localised pain.
  • Ascending and descending pathways modulate pain: The spinothalamic tract carries nociceptive signals rostrally; descending serotonergic and noradrenergic pathways from the periaqueductal grey and rostral ventromedial medulla inhibit or facilitate spinal transmission.
  • Peripheral sensitisation lowers activation thresholds of nociceptors at the site of injury via inflammatory mediators (prostaglandins, bradykinin, substance P, NGF).
  • Central sensitisation amplifies pain signalling in the dorsal horn through wind-up, long-term potentiation (LTP), and loss of inhibitory interneurons β€” contributing to hyperalgesia, allodynia, and chronic pain states.
  • NMDA receptor activation is a key mediator of central sensitisation; ketamine (an NMDA antagonist) is used therapeutically to "reset" central sensitisation in refractory pain.
  • The biopsychosocial model recognises that pain is shaped by biological factors, psychological states (anxiety, depression, catastrophising, fear-avoidance), and social determinants (work, family, culture, socioeconomic status).
  • Chronic pain affects ~3.4 million Australians (AIHW, 2023), is the leading cause of early retirement, and costs the Australian economy an estimated 9 billion annually.
  • Aboriginal and Torres Strait Islander Australians experience chronic pain at approximately 1.5–2 times the rate of non-Indigenous Australians, with significant barriers to culturally safe pain management.
  • Effective pain management is multimodal: combining pharmacological (simple analgesics, adjuvants, opioids when indicated), physical, psychological, and interventional strategies β€” aligned with the biopsychosocial framework.
  • Pain assessment must be individualised: use validated tools (NRS, BPI, DN4 for neuropathic pain, COMFORT-B for paediatrics) and consider functional impact, not just intensity.

Introduction & Australian Epidemiology

Pain is the most common reason Australians seek medical attention. It is a complex, multidimensional experience that serves as a crucial protective mechanism β€” alerting the individual to actual or potential tissue damage β€” but can become a debilitating disease state when it persists beyond normal healing timeframes. Understanding the neurobiology of pain, the distinction between nociception and the pain experience, the mechanisms of sensitisation, and the influence of psychological and social factors is fundamental to delivering effective, patient-centred pain care.

The International Association for the Study of Pain (IASP) revised its definition of pain in 2020 to emphasise that pain is always a subjective experience, that it is learned through early life experiences, that it is distinct from (but often associated with) nociception, and that it cannot be inferred solely from activity in sensory neurons. Verbal description is only one of several behaviours used to express pain; inability to communicate does not negate the possibility of pain.

Australian Burden of Pain

According to the Australian Institute of Health and Welfare (AIHW, 2023):

  • Approximately 3.4 million Australians (16% of the population) live with chronic pain.
  • Chronic pain prevalence increases with age: approximately 30% of adults aged β‰₯65 years report chronic pain.
  • Musculoskeletal conditions (back pain, osteoarthritis) are the leading causes of chronic pain burden.
  • Neuropathic pain affects approximately 5–8% of the general population and is present in up to 40% of people with chronic pain presentations.
  • Chronic pain is the leading cause of disability in Australia and a major contributor to early workforce exit.
  • The economic cost of chronic pain in Australia was estimated at 9.3 billion in 2018 (including direct healthcare costs, productivity losses, and carer costs), projected to rise to 5.6 billion by 2050 (Painaustralia, 2019).
  • Opioid-related harm remains a significant concern: Australia recorded 1,244 opioid-induced deaths in 2022, with pharmaceutical opioids implicated in approximately 70% of cases (Penington Institute, 2023).
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Clinical pearl: Pain intensity scores alone do not capture the full clinical picture. Always assess functional impact, sleep disturbance, mood, and psychosocial contributors. A pain score of 7/10 with maintained function may require a different management approach than 7/10 with complete functional collapse.

Definition of Pain

The IASP (2020) defines pain as:

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"An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage."

Six key notes accompany this definition:

  1. Pain is always a personal experience influenced to varying degrees by biological, psychological, and social factors.
  2. Pain and nociception are different phenomena. Pain cannot be inferred solely from activity in sensory neurones.
  3. A person's report of pain should be respected, even in the absence of identifiable tissue pathology.
  4. Although pain usually serves an adaptive role, it can have adverse effects on function and well-being.
  5. Verbal description is only one of several behaviours used to express pain; inability to communicate does not negate the possibility of pain.
  6. Pain is learned through life experiences; the biological substrate for pain is genetically determined and modified by experience.

Classification of Pain by Duration

Type Duration Characteristics Common Examples
Acute pain <3 months (typically resolves with tissue healing) Proportional to nociceptive stimulus; serves protective function; associated with sympathetic activation (tachycardia, diaphoresis) Post-surgical, fracture, acute infection, renal colic
Subacute pain 1–3 months (transitional phase) May represent normal healing or early transition to persistent pain; critical window for intervention Post-whiplash, subacute low back pain
Chronic (persistent) pain β‰₯3 months (beyond normal tissue healing) Often disproportionate to identifiable pathology; central sensitisation frequently present; associated with functional impairment, mood disturbance, sleep disruption Chronic low back pain, fibromyalgia, osteoarthritis, neuropathic pain

Classification of Pain by Mechanism

Mechanism Source Quality Examples
Nociceptive Tissue damage or inflammation activating peripheral nociceptors Aching, throbbing, localised, worse with movement Osteoarthritis, post-operative pain, fracture, visceral colic
Neuropathic Lesion or disease of the somatosensory nervous system Burning, shooting, electric, tingling, numbness; often with allodynia or hyperalgesia Diabetic peripheral neuropathy, post-herpetic neuralgia, trigeminal neuralgia, spinal cord injury pain
Nociplastic Altered nociception without clear evidence of tissue damage or somatosensory lesion (central sensitisation) Diffuse, widespread; fatigue, cognitive disturbance, sleep dysfunction common Fibromyalgia, irritable bowel syndrome, non-specific chronic low back pain, chronic tension-type headache
Mixed Combination of mechanisms Varied β€” features of more than one mechanism Lumbar radiculopathy with muscle spasm, cancer pain, chronic post-surgical pain
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IASP 2020 update β€” Nociplastic pain: The recognition of "nociplastic pain" as a third mechanistic category (alongside nociceptive and neuropathic) was a landmark revision. It accounts for conditions where pain arises from altered nociception despite no clear tissue or nerve damage, and is central to understanding conditions such as fibromyalgia and functional pain syndromes.

Nociception

Nociception is the neural process of encoding and processing noxious stimuli (those that threaten or cause tissue damage). It is a neurophysiological process that can occur without conscious awareness and is distinct from pain, which is the subjective experience. Nociception comprises four sequential phases: transduction, transmission, modulation, and perception.

Phase 1: Transduction β€” Detection of Noxious Stimuli

Transduction is the conversion of a noxious stimulus (thermal, mechanical, or chemical) into an electrical signal at the peripheral nerve ending. This occurs at specialised receptors called nociceptors.

Receptor / Channel Stimulus Location
TRPV1 (transient receptor potential vanilloid 1) Heat (>43°C), capsaicin, acid (H⁺) Free nerve endings in skin, viscera, joints
TRPA1 Cold, chemical irritants (mustard oil, formalin) Free nerve endings
TRPM8 Cool temperatures (<25Β°C), menthol Free nerve endings
Piezo2 Mechanical force (light touch and proprioception β€” not nociceptive) Mechanoreceptors
ASICs (acid-sensing ion channels) Extracellular acidosis (pH <5.9) Free nerve endings; particularly important in inflammatory and ischaemic pain
P2X3 ATP released from damaged cells C-fibre nociceptors

Nerve Fibre Types

Fibre Type Myelination Diameter Conduction Velocity Pain Quality
AΞ΄ fibres Thinly myelinated 2–5 ΞΌm 5–30 m/s Sharp, pricking, well-localised ("first pain")
C fibres Unmyelinated 0.4–1.2 ΞΌm 0.5–2 m/s Burning, aching, diffuse, poorly-localised ("second pain")
AΞ² fibres Heavily myelinated 6–12 ΞΌm 30–70 m/s Touch, vibration, pressure (normally non-nociceptive; can become involved in allodynia after sensitisation)

Phase 2: Transmission β€” Central Relay of Nociceptive Signals

Nociceptive signals travel from the periphery to the spinal cord and then ascend to the brain via well-defined pathways.

Peripheral to spinal cord: AΞ΄ and C fibre cell bodies reside in the dorsal root ganglia (DRG). Their central axons enter the spinal cord dorsal horn (laminae I, II, and V for AΞ΄; laminae I and II for C fibres). Here they synapse on second-order neurones.

Key neurotransmitters at the first synapse:

  • Glutamate β€” primary excitatory transmitter acting on AMPA and NMDA receptors on second-order neurones (fast transmission)
  • Substance P β€” co-released with glutamate from C fibres; acts on NK1 receptors; slower, modulates prolonged excitation
  • CGRP (calcitonin gene-related peptide) β€” vasodilator and neuromodulator; key in migraine pathophysiology

Ascending pathways:

Pathway Origin Termination Function
Spinothalamic tract (anterolateral system) Dorsal horn (laminae I, V) VPL thalamus β†’ somatosensory cortex (S1, S2); medial thalamus β†’ anterior cingulate cortex, insula Discriminative (location, intensity) and affective-motivational components of pain
Spinoreticular tract Dorsal horn Reticular formation β†’ intralaminar thalamus Arousal, autonomic responses to pain
Spinoparabrachial tract Lamina I Parabrachial nucleus β†’ amygdala, hypothalamus Affective-emotional, fear, autonomic, and endocrine responses to pain
Spinomesencephalic tract Dorsal horn Periaqueductal grey (PAG), superior colliculus Activates descending modulatory circuits; visual orientation toward pain source

Phase 3: Modulation β€” The Descending System

Pain transmission at the spinal cord level is not passive β€” it is subject to powerful facilitatory and inhibitory modulation from supraspinal centres. This is clinically important as it explains why identical nociceptive input can produce very different pain experiences depending on context.

Gate Control Theory (Melzack & Wall, 1965): A foundational concept proposing that non-nociceptive input (AΞ² fibre activity, e.g. rubbing the skin) can "close the gate" to nociceptive transmission at the spinal cord level by activating inhibitory interneurons in the substantia gelatinosa (lamina II). This theory explained why massage, TENS, and acupuncture can modulate pain.

Descending inhibitory pathway (the "pain brake"):

  • Periaqueductal grey (PAG) in the midbrain receives input from the prefrontal cortex, amygdala, and hypothalamus.
  • PAG projects to the rostral ventromedial medulla (RVM), which contains "ON-cells" (facilitate pain) and "OFF-cells" (inhibit pain).
  • RVM projects to the spinal cord dorsal horn via the dorsolateral funiculus.
  • Key neurotransmitters: serotonin (5-HT) and noradrenaline (NA) β€” these activate inhibitory interneurons in the dorsal horn that release endorphins (enkephalins, Ξ²-endorphin), GABA, and glycine, suppressing nociceptive transmission.
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Pharmacological relevance: Many analgesics work by enhancing descending inhibition. SNRIs (duloxetine, venlafaxine) increase synaptic serotonin and noradrenaline. Tricyclic antidepressants (amitriptyline, nortriptyline) also enhance descending inhibition. Tapentadol combines ΞΌ-opioid agonism with noradrenaline reuptake inhibition. Opioids activate ΞΌ-receptors in the PAG and RVM to enhance descending inhibition.

Phase 4: Perception β€” Conscious Pain Experience

Pain perception involves the integration of nociceptive signals across multiple cortical and subcortical regions, collectively termed the "pain matrix" (now more accurately referred to as the pain neuromatrix):

  • Primary somatosensory cortex (S1): Localisation and discrimination of stimulus intensity.
  • Secondary somatosensory cortex (S2): Pain recognition and integration with other sensory modalities.
  • Anterior cingulate cortex (ACC): Affective-motivational dimension β€” the "unpleasantness" of pain.
  • Insular cortex: Interoception, integration of body state with emotional context; critical for pain chronification.
  • Prefrontal cortex: Cognitive evaluation, anticipation, catastrophising, pain-related decision-making.
  • Amygdala: Fear conditioning, emotional memory of pain.
  • Thalamus: Key relay station; VPL nucleus β†’ S1/S2 (discriminative); medial/intralaminar β†’ ACC, insula (affective).
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Clinical significance: The multi-dimensional nature of pain perception explains why psychological interventions (CBT, ACT, mindfulness-based stress reduction) are evidence-based treatments β€” they modulate activity in prefrontal cortex, ACC, insula, and amygdala, thereby altering the pain experience without changing peripheral nociceptive input.

Sensitisation

Sensitisation refers to an increased responsiveness of nociceptive neurones to their normal input and/or recruitment of a response to normally subthreshold inputs. It occurs at both the peripheral and central levels and is a key mechanism underlying hyperalgesia, allodynia, and the transition from acute to chronic pain.

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Key definitions:
Hyperalgesia: Increased pain from a stimulus that normally provokes pain (an exaggerated response to a painful stimulus).
Allodynia: Pain due to a stimulus that does not normally provoke pain (e.g. light touch causing pain).
Primary hyperalgesia: Occurs at the site of injury (peripheral sensitisation).
Secondary hyperalgesia: Occurs in surrounding uninjured tissue (central sensitisation).

Peripheral Sensitisation

Tissue injury triggers an inflammatory response that releases a "soup" of inflammatory mediators at the site of injury, collectively called the "inflammatory milieu". These mediators lower the activation threshold of nociceptors and increase their firing rate, a process known as peripheral sensitisation.

Key inflammatory mediators:

Mediator Source Mechanism Clinical Relevance
Prostaglandins (PGEβ‚‚, PGIβ‚‚) COX-1/COX-2 in damaged tissue Sensitise nociceptors to bradykinin and other mediators; lower threshold of TRPV1 Target of NSAIDs (COX inhibition reduces PGEβ‚‚)
Bradykinin Plasma kinin cascade Direct activation of B1/B2 receptors on nociceptors; potent pain-producing substance ACE inhibitors may reduce bradykinin degradation β†’ associated with cough and occasionally angioedema
Histamine Mast cell degranulation H1 receptor activation on nociceptors; contributes to itch and pain Anti-histamines partially modulate inflammatory pain
Substance P C fibre terminals (antidromic release) Neurogenic inflammation: vasodilation, plasma extravasation, mast cell activation (axon reflex) NK1 receptor antagonists have been disappointing as analgesics in clinical trials
NGF (nerve growth factor) Keratinocytes, immune cells Upregulates TRPV1 and sodium channels; promotes C fibre sprouting; key in chronic pain states Anti-NGF antibodies (tanezumab) in clinical development for osteoarthritis and chronic low back pain
TNF-Ξ±, IL-1Ξ², IL-6 Macrophages, Schwann cells Pro-inflammatory cytokines that directly sensitize nociceptors; upregulate sodium channels Target of biologics in inflammatory arthropathies (TNF inhibitors reduce pain partly through this mechanism)
H⁺ (protons) Tissue acidosis (anaerobic metabolism) Activation of ASICs and TRPV1; contributes to ischaemic pain Why ischaemic conditions (e.g. peripheral vascular disease) are painful

Clinical consequence: Primary hyperalgesia (increased sensitivity at the site of injury). Peripherally sensitised nociceptors fire spontaneously (causing resting pain) and respond more vigorously to stimuli.

Central Sensitisation

Central sensitisation is an amplification of neural signalling within the central nervous system that elicits pain hypersensitivity. It is defined by the IASP as "increased responsiveness of nociceptive neurones in the central nervous system to their normal or subthreshold afferent input." Central sensitisation is a major contributor to the persistence of pain, the spread of pain beyond the original site of injury, and the development of chronic pain states.

Key mechanisms of central sensitisation:

1. Wind-Up

Repeated C-fibre stimulation at frequencies >0.5 Hz causes a progressive increase in the firing of dorsal horn neurones. This is a form of activity-dependent synaptic plasticity at the spinal cord level. Wind-up depends on the removal of the Mg²⁺ block from NMDA receptors by sustained depolarisation, allowing Ca²⁺ influx and enhanced synaptic transmission.

2. NMDA Receptor-Mediated Long-Term Potentiation (LTP)

Sustained nociceptive input activates NMDA receptors on second-order neurones in the dorsal horn, triggering intracellular signalling cascades (Ca²⁺ β†’ CaMKII β†’ CREB) that produce long-lasting changes in synaptic efficacy. This LTP in pain pathways is analogous to LTP in hippocampal memory circuits β€” in a sense, the spinal cord "learns" pain.

3. Loss of Inhibitory Interneurons

Persistent nociceptive input can cause apoptosis or functional impairment of GABAergic and glycinergic inhibitory interneurons in the dorsal horn (lamina II). This loss of inhibition ("disinhibition") permits unopposed excitatory transmission. Morphological studies have shown loss of GABAergic neurones in animal models of chronic pain.

4. Microglial Activation

Peripheral nerve injury activates spinal cord microglia (the CNS-resident immune cells), which release pro-inflammatory mediators (TNF-Ξ±, IL-1Ξ², IL-6, BDNF, reactive oxygen species) that enhance excitatory synaptic transmission and suppress inhibitory transmission. This "neuroinflammation" in the dorsal horn is a critical driver of chronic neuropathic pain.

5. Descending Facilitation

In chronic pain states, the RVM shifts from predominantly inhibitory to facilitatory output. "ON-cells" in the RVM become hyperactive, sending facilitatory signals to the dorsal horn via the dorsolateral funiculus, further amplifying nociceptive transmission. This maladaptive descending facilitation is mediated by brain-derived neurotrophic factor (BDNF) and serotonin acting on 5-HT3 receptors.

Clinical Features Suggesting Central Sensitisation

Early Indicators
Peripheral Dominance
Pain remains localised to the site of injury or innervation territory; proportional to nociceptive input; responsive to peripherally-acting analgesics (NSAIDs, local anaesthetics).
Setting: Primary care / acute pain
Transitional
Mixed Peripheral + Central
Pain spreading beyond original injury site; secondary hyperalgesia; decreasing response to peripheral analgesics; sleep and mood disturbance emerging; functional decline.
Setting: Persistent pain β€” consider multidisciplinary input
Established
Central Sensitisation Dominant
Widespread pain; marked allodynia (light touch painful); disproportionate pain response; poor sleep, significant mood disturbance; minimal response to peripherally-acting analgesics; may respond to centrally-acting agents (duloxetine, amitriptyline, pregabalin) and non-pharmacological strategies.
Setting: Persistent pain β€” multidisciplinary pain service referral indicated
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Why this matters clinically: Escalating opioid doses for pain driven by central sensitisation is generally ineffective and hazardous. Opioids themselves can paradoxically induce central sensitisation through opioid-induced hyperalgesia (OIH). When central sensitisation is suspected, the focus should shift to centrally-acting adjuvant analgesics (duloxetine, amitriptyline, pregabalin/gabapentin), NMDA antagonists (ketamine infusions in specialist settings), and evidence-based non-pharmacological therapies (CBT, graded motor imagery, exercise therapy).

Summary of Key Sensitisation Mechanisms

Feature Peripheral Sensitisation Central Sensitisation
Location Site of injury (peripheral nociceptors) Dorsal horn, brainstem, brain
Key mediators PGEβ‚‚, bradykinin, NGF, H⁺, TNF-Ξ± Glutamate (NMDA), BDNF, CGRP, microglial cytokines
Clinical sign Primary hyperalgesia (at injury site) Secondary hyperalgesia, allodynia, widespread pain
Reversibility Generally reversible with resolution of inflammation Partially reversible; may become self-sustaining
Effective treatments NSAIDs, local anaesthetics, corticosteroids, ice Duloxetine, amitriptyline, pregabalin, ketamine, CBT, exercise

Biopsychosocial Model

The biopsychosocial model, first proposed by George Engel in 1977 and now endorsed by the IASP, the Royal Australian College of General Practitioners (RACGP), and the Australian Pain Society, recognises that pain is not simply a product of tissue damage but is the result of dynamic interactions between biological, psychological, and social factors. This model has supplanted the reductionist biomedical model as the framework for understanding and managing chronic pain.

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The biopsychosocial model is not "just psychological": It does not imply that pain is "in the head." Rather, it acknowledges that all pain has biological underpinnings, but that the experience of pain β€” its intensity, its impact on function, and its trajectory toward chronicity β€” is modulated by psychological and social factors. These factors are real, measurable, and therapeutically modifiable.

Biological Factors

  • Tissue pathology: Structural damage, inflammation, degeneration (e.g. osteoarthritis, disc herniation).
  • Nerve injury or dysfunction: Peripheral neuropathy, radiculopathy, central post-stroke pain.
  • Central sensitisation: Amplified CNS processing (as detailed above).
  • Genetic factors: Polymorphisms in COMT, SCN9A (sodium channel Nav1.7), OPRM1 (ΞΌ-opioid receptor), and GCH1 influence individual pain sensitivity and analgesic response.
  • Neuroendocrine dysfunction: HPA axis dysregulation, cortisol dysregulation in chronic stress.
  • Sleep disturbance: Bidirectional relationship β€” poor sleep amplifies pain sensitivity; pain disrupts sleep.
  • Comorbidities: Obesity, metabolic syndrome, autoimmune conditions, depression β€” all independently associated with increased pain burden.

Psychological Factors

Factor Definition Impact on Pain Therapeutic Approach
Pain catastrophising Exaggerated negative cognitive and emotional orientation toward pain β€” rumination, magnification, helplessness Strongest psychological predictor of pain chronification and disability; amplifies pain perception via ACC and insular cortex CBT, pain neuroscience education, graded exposure
Fear-avoidance Avoidance of physical activity due to fear of (re)injury Deconditioning, disability, social withdrawal; creates a vicious cycle of escalating pain and declining function Graded activity, graded exposure, physiotherapy, CBT
Self-efficacy An individual's belief in their ability to manage their pain and function despite it Higher self-efficacy predicts better outcomes; lower self-efficacy predicts disability and opioid use Motivational interviewing, goal-setting, self-management programs
Anxiety and depression Comorbid mood disorders are present in 30–50% of chronic pain patients Bidirectional: depression amplifies pain perception and reduces coping; chronic pain causes depression via shared neurocircuitry (serotonin, noradrenaline deficiency) Pharmacotherapy (SNRIs, TCAs β€” dual benefit), CBT, mindfulness-based stress reduction (MBSR), acceptance and commitment therapy (ACT)
Attention and hypervigilance Selective attention toward pain-related stimuli Amplifies pain perception; perpetuates the pain cycle Distraction techniques, mindfulness, attention retraining

Social and Environmental Factors

  • Socioeconomic status: Lower SES associated with higher chronic pain prevalence, reduced access to multidisciplinary pain management, and poorer outcomes.
  • Workplace factors: Job dissatisfaction, physical demands, lack of workplace support, compensation/insurance processes β€” all independently predict chronicity after acute injury.
  • Social support: Strong social networks are protective; social isolation exacerbates pain and disability.
  • Cultural factors: Cultural norms influence pain expression, help-seeking behaviour, and treatment expectations. Culturally safe pain care requires awareness of these differences.
  • Health literacy: Understanding of pain neurobiology improves engagement with self-management strategies and reduces catastrophising.
  • Trauma history: Adverse childhood experiences (ACEs) and history of trauma are significantly associated with chronic pain in adulthood, likely mediated by HPA axis dysregulation and central sensitisation.

Australian Pain Management Frameworks

Australia has several key frameworks and guidelines that embed the biopsychosocial model:

  • PainAustralia National Strategic Action Plan for Pain Management (2019): Endorses a whole-of-system, biopsychosocial approach; calls for improved access to multidisciplinary pain services, particularly in rural and remote areas.
  • RACGP Guideline for the Management of Knee and Hip Osteoarthritis (2018): First-line management is education, exercise, and weight management β€” not pharmacotherapy.
  • RACGP Prescribing Drugs of Dependence in General Practice (2022): Emphasises the biopsychosocial assessment before initiating opioids, dose limits, regular review, and multimodal non-opioid strategies.
  • Faculty of Pain Medicine, ANZCA β€” ANZCA PS01 (2020): Recommends that all patients with persistent pain have access to psychological and physical therapies alongside pharmacological management.
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Key message for clinicians: Effective chronic pain management requires addressing all three domains simultaneously. A pharmacological-only approach will fail in most patients with chronic pain. Conversely, purely psychological or physical interventions may be insufficient without appropriate analgesia. Multidisciplinary pain programs (combining medical, physiotherapy, psychology, and occupational therapy) produce the best outcomes and are cost-effective β€” yet fewer than 10% of Australians with chronic pain have access to them (Painaustralia, 2019).

Pain Neuroscience Education (PNE)

Pain neuroscience education (PNE), also known as "explaining pain," is a therapeutic intervention that teaches patients about the neurobiology of their pain experience. It aims to reconceptualise pain from a signal of tissue damage to an output of the brain and nervous system modulated by multiple factors. PNE has been shown to:

  • Reduce pain catastrophising (moderate-quality evidence).
  • Improve pain knowledge and self-efficacy.
  • Reduce pain intensity and disability when combined with exercise therapy.
  • Decrease healthcare utilisation and opioid use in some populations.

PNE should be delivered by trained clinicians (GPs, physiotherapists, psychologists) and should be individualised to the patient's educational level, cultural background, and readiness to engage with the concepts.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Australians experience a significantly higher burden of chronic pain compared with non-Indigenous Australians, yet face disproportionate barriers to culturally safe, evidence-based pain management. Understanding the unique biological, psychological, and social determinants of pain in First Nations communities is essential for equitable care.

Epidemiology

  • Chronic pain prevalence in Aboriginal and Torres Strait Islander adults is estimated at 25–30% β€” approximately 1.5–2 times the rate in non-Indigenous Australians (AIHW, 2023).
  • Musculoskeletal conditions (particularly back pain and osteoarthritis), headaches, dental pain, and neuropathic pain are among the most commonly reported types.
  • Chronic pain in First Nations Australians is associated with earlier onset and greater severity, contributing to significant disability at younger ages.
  • Opioid use for chronic pain is higher in Aboriginal and Torres Strait Islander populations, with associated risks of dependence and harm.

Unique Biopsychosocial Determinants

Intergenerational trauma
The lasting impacts of colonisation, the Stolen Generations, and ongoing systemic disadvantage profoundly influence pain experience and health behaviour. Trauma-informed care is essential in all pain management for First Nations patients.
Connection to Country and Culture
Disconnection from Country, language, family, and cultural practices is a significant psychosocial stressor that can amplify pain. Conversely, cultural strengthening programs (on-Country healing, cultural camps, yarning circles) are emerging as effective adjuncts to pain management.
Remote and rural access
Approximately 35% of Aboriginal and Torres Strait Islander people live in remote or very remote areas where specialist pain services, multidisciplinary teams, and allied health professionals are scarce or absent. Telehealth has expanded access but digital literacy and connectivity remain barriers.
Communication and health literacy
English may be a second, third, or fourth language for some patients. Pain neuroscience education materials must be culturally and linguistically adapted. Use of Aboriginal health workers and practitioners, and use of visual and yarning-based educational approaches, improves engagement.
Stigma and racism
Previous experiences of racism in healthcare settings reduce trust and help-seeking. Some patients may under-report pain to avoid being perceived as "drug-seeking." Culturally safe, non-judgmental care and Aboriginal health worker involvement are critical to building trust.
Polypharmacy and comorbidity
Higher rates of diabetes, renal disease, cardiovascular disease, and mental health conditions mean pain management must account for complex comorbidities and polypharmacy. Renal impairment is common and influences analgesic choice and dosing.

Practical Strategies for Culturally Safe Pain Management

  • Involve Aboriginal health workers and practitioners (AHW/Ps) in pain assessment, education, and management planning from the outset.
  • Use yarning-based approaches to explore the patient's pain story, beliefs, and goals β€” avoid purely biomedical questioning.
  • Employ trauma-informed care principles: safety, trustworthiness, choice, collaboration, and empowerment.
  • Incorporate holistic and cultural healing alongside biomedical management where desired by the patient (e.g. on-Country activities, traditional healing practices, connection with Elders).
  • Ensure multidisciplinary care is accessible: advocate for expanded allied health and specialist pain services in regional and remote areas; utilise telehealth for specialist outreach.
  • Screen for and address psychosocial contributors sensitively β€” including intergenerational trauma, grief and loss, social determinants of health, and substance use.
  • Use locally relevant pain education resources β€” Painaustralia and various Aboriginal Community Controlled Health Organisations (ACCHOs) have developed culturally adapted materials.
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Opioid prescribing caution: Aboriginal and Torres Strait Islander Australians are disproportionately affected by opioid-related harm. Prescribers should ensure opioids are used at the lowest effective dose for the shortest duration, with regular review. Non-pharmacological strategies and adjuvant analgesics should be prioritised. Always assess for and address psychosocial contributors to pain before escalating pharmacotherapy.

πŸ“š References

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  13. 13. Lin I, Wiles L, Waller R, et al. What does best practice care for musculoskeletal pain look like? Eleven consistent recommendations from high-quality clinical practice guidelines. Br J Sports Med. 2020;54(2):79–86.
  14. 14. Gatchel RJ, Peng YB, Peters ML, Fuchs PN, Turk DC. The biopsychosocial approach to chronic pain: scientific advances and future directions. Psychol Bull. 2007;133(4):581–624.
  15. 15. Australian Institute of Health and Welfare (AIHW). The health and welfare of Australia's Aboriginal and Torres Strait Islander peoples 2015. Cat. no. IHW 147. Canberra: AIHW; 2015.
  16. 16. Yong RJ, Mullins PM, Bhattacharyya N. Prevalence of chronic pain among adults in the United States. Pain. 2022;163(2):e328–e332.
  17. 17. Finnerup NB, Kuner R, Jensen TS. Neuropathic pain: from mechanisms to treatment. Physiol Rev. 2021;101(1):259–301.
  18. 18. Institute of Medicine (US) Committee on Advancing Pain Research, Care, and Education. Relieving pain in America: a blueprint for transforming prevention, care, education, and research. Washington (DC): National Academies Press; 2011.
for PBS scripts. Utilise ACCHS pharmacies and Remote Area Aboriginal Health Worker programs for medication supply in remote areas. Avoid initiating benzodiazepines; support holistic pain management including community-based exercise programs.
Preventive health
Promote bone health: encourage vitamin D supplementation (1000 IU daily in deficient individuals), smoking cessation support, reduction of alcohol intake, and weight-bearing exercise. MBS Item 715 health checks provide a structured opportunity to assess bone health, screen for osteoporosis risk factors, and discuss musculoskeletal health in a culturally safe context.

Quick Reference: Differential Diagnosis at a Glance

Costovertebral dysfunction
Paracetamol Β± NSAID; manual therapy
2–6 weeks
Provocable on palpation; no red flags
Thoracic compression fracture
Paracetamol; Β± calcitonin; DXA + osteoporosis Rx
6–12 weeks healing
Elderly; osteoporosis; acute onset
ACS (posterior MI)
Aspirin 300 mg, GTN, heparin; urgent PCI
Time-critical
ECG, troponin; CV risk factors
Aortic dissection
IV labetalol; urgent CT aortogram; surgery (Type A)
Time-critical
Tearing pain; BP differential >20 mmHg
Vertebral osteomyelitis
IV antibiotics (vancomycin + ceftriaxone initially); ID consult
6 weeks IV antibiotics
Fever, elevated CRP, IV drug use
Biliary colic / cholecystitis
Paracetamol Β± morphine; lap cholecystectomy
Surgical within 72 h (cholecystitis)
RUQ/infrascapular; post-prandial; RUQ US

πŸ“š References

  1. 1. Briggs AM, Smith AJ, Straker LM, Bragge P. Thoracic spine pain in the general population: prevalence, incidence and associated factors in children, adolescents and adults. A systematic review. BMC Musculoskelet Disord. 2009;10:77.
  2. 2. National Health and Medical Research Council (NHMRC). Evidence-based management of acute musculoskeletal pain. Canberra: NHMRC; 2003 (updated 2020).
  3. 3. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Summary report 2023. Canberra: AIHW; 2023.
  4. 4. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760–765.
  5. 5. Stochkendahl MJ, Kjaer P, Hartvigsen J, et al. National Clinical Guidelines for non-surgical treatment of patients with recent onset low back pain or lumbar radiculopathy. Europ Spine J. 2018;27(1):60–75.
  6. 6. Erwin WM, Jackson PC, Homonko DA. Innervation of the human costovertebral joint: implications for clinical back pain syndromes. J Manipulative Physiol Ther. 2000;23(6):395–403.
  7. 7. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice. 9th edn. Melbourne: RACGP; 2018 (updated 2023).
  8. 8. Hirsch JA, Singh V, Falco FJE, et al. Thoracic facet joint interventions. Pain Physician. 2016;19(4):E581–E593.
  9. 9. Erwin WM, Jackson PC. The costovertebral joint: anatomy, biomechanics, and clinical significance in thoracic back pain syndromes. J Can Chiropr Assoc. 2003;47(2):112–120.
  10. 10. Strayer RJ, Gunnerson JM, Brown LH, et al. Aortic dissection: clinical features, diagnosis, and management. Aust Crit Care. 2019;32(2):144–153.
  11. 11. Ombregt L. A system of orthopaedic medicine. 3rd edn. Edinburgh: Churchill Livingstone Elsevier; 2013. Chapter 18: Thoracic spine.
  12. 12. Lin CC, Chen KH, Li DM, et al. Characteristics and outcomes of patients presenting with thoracic back pain to the emergency department. Emerg Med Australas. 2020;32(5):805–811.
for PBS-listed medicines at participating pharmacies.
Cultural safety
Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.
Medication adherence
Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.
Specific conditions
Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.
Referral pathways
Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

πŸ“š References

  1. 1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
  2. 2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
  3. 3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
  4. 4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
  5. 5. Smolen JS, LandewΓ© RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
  6. 6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
  7. 7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
  8. 8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
  9. 9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
  10. 10. Pisetsky DS. Antinuclear antibody testing β€” misunderstood or misused? Clin Immunol. 2023;255:109717.
  11. 11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
  12. 12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFΞ± blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
  13. 13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).
for PBS-listed medicines at participating pharmacies.
Cultural safety
Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.
Medication adherence
Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.
Specific conditions
Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.
Referral pathways
Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

πŸ“š References

  1. 1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
  2. 2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
  3. 3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
  4. 4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
  5. 5. Smolen JS, LandewΓ© RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
  6. 6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
  7. 7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
  8. 8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
  9. 9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
  10. 10. Pisetsky DS. Antinuclear antibody testing β€” misunderstood or misused? Clin Immunol. 2023;255:109717.
  11. 11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
  12. 12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFΞ± blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
  13. 13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).