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Human Physiology · Nervous system and exercise

Pain

Pain protects us, but it is not a simple measure of tissue damage. This page explains nociception, how signals are modulated in the spinal cord and brain, how sensitisation develops, and what the evidence says about education and exercise for chronic pain.

12Sections
5Figures
3Tables
10Questions

Part 9 · Nervous System and Exercise · Chapter 41 of 47

Learning objectives

By the end of this page you should be able to:

  • State the current definition of pain and distinguish pain from nociception.
  • Describe transduction, transmission, modulation and perception.
  • Explain gate control and descending modulation.
  • Explain peripheral and central sensitisation.
  • Distinguish acute, chronic, nociceptive, neuropathic and nociplastic pain.
  • Summarise the evidence for pain education and exercise.

Why it matters

Pain is the commonest reason people see a physiotherapist. Explaining it well and loading tissues confidently are central skills.

Misunderstanding pain leads to fear, avoidance and overtreatment.

Defining pain

In 2020 the international pain association revised its definition. Pain is “an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage” [1].

This replaced the 1979 definition after a two-year review by a 14-member task force [1].

Figure 1 · From stimulus to pain

Four steps of nociception: transduction, transmission, modulation and perception Nociceptors transduce damaging stimuli into signals; A-delta and C fibres transmit them to the dorsal horn and up the spinothalamic tract; signals are modulated in the dorsal horn and by descending pathways; the brain constructs pain using context, mood, memory and meaning. 1. Transductionnociceptor convertsheat, pressure orchemicals to signals2. TransmissionAδ and C fibresto dorsal horn, thenspinothalamic tract3. Modulationdorsal horn signal isamplified or damped,incl. from the brain4. Perceptionbrain constructs painusing context, mood,memory and meaningNociception is the neural process; pain is the experience. Each can occur without the other.
Pain is not a direct readout of damage. It is defined as an experience associated with, or resembling that associated with, actual or potential tissue damage [1].

Nociceptors and fibres

FeatureAδ fibresC fibres
MyelinThinNone
SpeedAbout 5–30 m/sAbout 0.5–2 m/s
SensationFirst, sharp, well-localised painSecond, dull, burning, poorly localised pain
Main transmitter in dorsal hornGlutamateGlutamate and substance P

Nociceptors respond to intense heat, pressure and chemicals. Inflammatory chemicals such as prostaglandins, bradykinin and nerve growth factor lower their threshold.

Modulation

Figure 2 · Gating in the dorsal horn

Touch fibres and descending pathways modulating nociceptive transmission in the dorsal horn Nociceptor input excites a projection neuron in the dorsal horn that sends signals to the brain. Large touch fibres excite an inhibitory interneuron that dampens the projection neuron. Descending brainstem pathways using opioids, serotonin and noradrenaline can inhibit or facilitate transmission. Dorsal hornINinhibitoryinterneuronTprojectionneuronAβ touch fibre (rubbing, TENS)C / Aδ nociceptorto brainDescending control from brainstem(PAG, RVM): opioids, serotonin,noradrenaline; can inhibit or facilitate
Why rubbing helps and stress hurts. Touch input and descending control change how much nociceptive signal reaches the brain. Schematic.

Gate control describes how large-fibre touch input reduces nociceptive transmission in the dorsal horn. Descending pathways from the periaqueductal grey and rostral ventromedial medulla can inhibit or enhance transmission.

Exercise, expectation and attention engage these pathways. Fear, poor sleep and stress can tip them towards facilitation.

Sensitisation

Figure 3 · Sensitisation shifts the curve

Stimulus-response curves for normal and sensitised states showing allodynia and hyperalgesia In a sensitised state the stimulus-response curve shifts left. Normally innocuous stimuli become painful, called allodynia, and noxious stimuli produce more pain than usual, called hyperalgesia. pain thresholdallodynia:touch now hurtshyperalgesia:more pain for thesame stimulusStimulus intensity (innocuous to noxious)Pain reportedNormalSensitised
Peripheral and central. Inflammation sensitises nociceptors; prolonged input can increase dorsal horn and brain responsiveness. Schematic.
TypeMechanismTypical clues
NociceptiveActivation of nociceptors by tissue damage or threatProportionate, mechanical pattern, localised
NeuropathicLesion or disease of the somatosensory nervous systemBurning, shooting, dermatomal, sensory loss
NociplasticAltered nociception without clear tissue or nerve damageWidespread, disproportionate, sensitive to many stimuli

Acute and chronic pain

Figure 4 · Pain is biopsychosocial

Biological, psychological and social factors overlapping to produce the pain experience Three overlapping circles labelled biological, psychological and social, with pain at the centre. Acute pain is a protective warning linked to injury; chronic pain lasts beyond normal healing time, usually over three months. Biologicaltissue, nerves,immune systemPsychologicalbeliefs, fear,mood, attentionSocialwork, family,culture, financesPAINAcute painprotective warningclosely linked to injuryChronic painlasts beyond healing,usually over 3 months [3]
Pain is a sensory and emotional experience [1]. Biological, psychological and social factors all shape it, to different degrees in different people.

Chronic pain lasts beyond normal tissue healing time, generally taken as 12 weeks [3]. It affects about one in five adults [3].

Education and exercise

Pain neuroscience education explains the biology of pain to patients. Louw and colleagues reviewed 13 randomised trials in chronic musculoskeletal pain [2].

Education reduced pain and disability and improved function, movement, psychosocial factors and healthcare use [2].

Figure 5 · Exercise for chronic pain

Summary of an overview of reviews of exercise for chronic pain Twenty-one reviews of 381 studies with 37,143 participants. Physical function improved in 14 reviews with small to moderate effects; pain results were favourable but inconsistent; dropout was similar; adverse events were mainly short-lived muscle soreness. Reviews / studies21 / 381Participants37,143Function improved14 reviews, small–moderatePain severityfavourable but inconsistentDropout per 100082.8 vs 81 (no difference)Adverse eventsmainly short-lived sorenessExercise versus no or minimal intervention across many chronic pain conditions [3]
Safe and useful, if modest. Exercise has few adverse events and may improve pain and function; evidence quality was low [3].

Geneen and colleagues summarised 21 Cochrane reviews of exercise for chronic pain [3]. Function improved most consistently, with few adverse events [3].

Practical skill · explaining pain

Use simple metaphors, such as an alarm system that has become too sensitive. Link the explanation to a graded activity plan. Reassure without dismissing the pain.

Clinical relevance for the physiotherapist

  • Listen and believe. Pain is an experience, not just a signal [1].
  • Educate. Pain neuroscience education helps in chronic musculoskeletal pain [2].
  • Move. Graded exercise is safe and improves function [3].
  • Classify. Recognise neuropathic and nociplastic features.
  • Expect soreness. Warn that early soreness is common and settles [3].

Assessment and application

SituationInterpretationAction
Acute ankle sprain, swollen, painful to loadNociceptive, inflammatoryProtect, then progressive loading
Back pain for one year, fearful of bendingChronic pain with fearPain education and graded exposure [2]
Burning pain in a dermatome with numbnessPossible neuropathic painNeurological exam; refer if progressive
Widespread pain, poor sleep, sensitive to touchPossible nociplastic painEducation, graded aerobic exercise [3]

Common mistakes

  • Equating pain intensity with tissue damage [1].
  • Advising rest for chronic pain [3].
  • Explaining pain with only structural findings.
  • Ignoring sleep, mood and work.
  • Stopping exercise at the first soreness [3].

Exam preparation

Long answer

Describe the pain pathway and the mechanisms of pain modulation.

  • Definition [1].
  • Four steps (Figure 1).
  • Fibres and transmitters (table).
  • Gate control and descending control (Figure 2).
  • Sensitisation (Figure 3).

Short notes

  • Gate control theory.
  • Referred pain.
  • Central sensitisation.
  • Pain neuroscience education [2].

Viva and practical

  • “Which fibres carry burning pain?” — C fibres.
  • “What is allodynia?” — pain from a normally non-painful stimulus.
  • “Does exercise help chronic pain?” — it improves function with few harms [3].
  • OSCE: explain chronic back pain to a patient in two minutes.

Current evidence

Exam and traditional teaching

Pain reflects injury; rest until pain settles.

What the evidence adds

Pain is defined as an experience, not a damage signal [1].

Education and exercise help people with chronic pain [2, 3].

What the student should understand

Treat the person in pain, not only the tissue. Explain, then move.

Check yourself

10 questions on this page. Tap one to see the answer and the reasoning.

Q1. The revised 2020 definition describes pain as an unpleasant sensory and emotional experience associated with:
  1. (A) Only actual tissue damage
  2. (B) Or resembling that associated with actual or potential tissue damage
  3. (C) Only nerve injury
  4. (D) Only inflammation

Answer: (B) The definition reads “associated with, or resembling that associated with, actual or potential tissue damage” [1].

Q2. The previous definition of pain had been adopted in:
  1. (A) 1959
  2. (B) 1979
  3. (C) 1999
  4. (D) 2015

Answer: (B) The earlier definition was adopted in 1979 [1].

Q3. Pain neuroscience education for chronic musculoskeletal pain was supported for:
  1. (A) Pain, function, disability, psychosocial factors, movement and healthcare use
  2. (B) Only knowledge, not pain
  3. (C) Nothing
  4. (D) Acute fractures only

Answer: (A) The review supported benefits across all these outcomes [2].

Q4. How many randomised trials were in the pain neuroscience education review?
  1. (A) 3
  2. (B) 13
  3. (C) 130
  4. (D) 1,300

Answer: (B) Thirteen RCTs were included [2].

Q5. Chronic pain is generally defined as pain lasting longer than:
  1. (A) 1 week
  2. (B) 12 weeks
  3. (C) 1 year
  4. (D) 5 years

Answer: (B) Beyond normal healing time, generally 12 weeks [3].

Q6. The weighted mean prevalence of chronic pain in adults is about:
  1. (A) 2%
  2. (B) 20%
  3. (C) 60%
  4. (D) 90%

Answer: (B) About 20% [3].

Q7. In the Cochrane overview, the most consistently improved outcome with exercise was:
  1. (A) Death
  2. (B) Physical function
  3. (C) Healthcare use
  4. (D) Adherence

Answer: (B) Physical function improved in 14 reviews [3].

Q8. The main adverse event with exercise for chronic pain was:
  1. (A) Fracture
  2. (B) Increased soreness or muscle pain that settled within weeks
  3. (C) Heart attack
  4. (D) None were ever reported

Answer: (B) Most adverse events were soreness that subsided after a few weeks [3].

Q9. Dropout from exercise groups compared with control was:
  1. (A) Much higher
  2. (B) Slightly higher, not significantly
  3. (C) Zero
  4. (D) Double

Answer: (B) 82.8 versus 81 per 1000, not significant [3].

Q10. The main reason the exercise evidence was rated low quality was:
  1. (A) Exercise is harmful
  2. (B) Small sample sizes and short follow-up
  3. (C) Fraud
  4. (D) No trials existed

Answer: (B) Most studies had fewer than 50 participants and short follow-up [3].

Quick review

Key takeaways

  • Pain is an unpleasant sensory and emotional experience [1].
  • Nociception: transduction, transmission, modulation, perception.
  • Touch input and descending pathways modulate the dorsal horn.
  • Sensitisation causes allodynia and hyperalgesia.
  • Pain education improves pain, function and disability [2].
  • Exercise is safe and improves function in chronic pain [3].

Further reading

SourceWhy it earns its place
Raja SN et al. — Pain, 2020Revised definition of pain [1]
Louw A et al. — Physiother Theory Pract, 2016Pain neuroscience education [2]
Geneen LJ et al. — Cochrane, 2017Exercise for chronic pain [3]

References

  1. Raja SN, Carr DB, Cohen M, et al. The revised International Association for the Study of Pain definition of pain: concepts, challenges, and compromises. Pain. 2020;161(9):1976–1982. doi:10.1097/j.pain.0000000000001939 PMID 32694387 Consensus review
  2. Louw A, Zimney K, Puentedura EJ, Diener I. The efficacy of pain neuroscience education on musculoskeletal pain: a systematic review of the literature. Physiotherapy Theory and Practice. 2016;32(5):332–355. doi:10.1080/09593985.2016.1194646 PMID 27351541 Systematic review
  3. Geneen LJ, Moore RA, Clarke C, et al. Physical activity and exercise for chronic pain in adults: an overview of Cochrane Reviews. Cochrane Database of Systematic Reviews. 2017;4(4):CD011279. doi:10.1002/14651858.CD011279.pub3 PMID 28436583 Overview of systematic reviews

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Reviewed by the Physiotherapist India Team. · Human Physiology contents