Physiology chapters
Pain and temperature
How pain and temperature are detected and carried to the brain, the difference between fast and slow pain, referred pain, and how the body blocks pain through the gate control and opioid systems.
- Pain is detected by free nerve endings (nociceptors), which adapt very little.
- Fast pain travels in Aδ fibres (glutamate) and is sharp and well localised; slow pain travels in C fibres (substance P) and is burning and poorly localised.
- Both cross in the cord and ascend in the spinothalamic tract; the brain can block pain through the gate control and opioid systems.
On this page
Overview
Pain is a protective sense. It warns that tissue is being damaged and makes us move away from the cause.
Pain and temperature are detected by free nerve endings in the skin and deeper tissues. They are carried by thin, slow fibres in the spinothalamic tract, which crosses in the spinal cord.
Pain receptors (nociceptors)
All pain receptors are free nerve endings. They respond to three kinds of stimulus:
- Mechanical: cutting, crushing, stretching.
- Thermal: extreme heat or cold.
- Chemical: substances released from damaged tissue.
Chemicals that excite pain endings include bradykinin, histamine, serotonin, acids, potassium, acetylcholine and protein-digesting enzymes. Prostaglandins and substance P make the endings more sensitive.
Bradykinin is thought to be the most powerful pain-producing chemical released by damaged tissue.
Pain receptors adapt very little. Some even become more sensitive with ongoing stimulation (hyperalgesia), so pain keeps warning us while damage lasts.
Fast pain and slow pain
| Feature | Fast pain | Slow pain |
|---|---|---|
| Felt within | About 0.1 second | 1 second or more, rising over time |
| Quality | Sharp, pricking | Burning, aching, throbbing |
| Localisation | Precise | Poor |
| Fibres | Aδ (thin, myelinated) | C (unmyelinated) |
| Speed | 6–30 m/s | 0.5–2 m/s |
| Transmitter in the cord | Glutamate | Substance P (and glutamate) |
| Pathway | Neospinothalamic tract | Paleospinothalamic tract |
| Stimuli | Mechanical and thermal | All types, especially chemical |
This is why a stubbed toe gives a sharp pain at once, followed by a slower, burning ache.
Pain pathways
Neospinothalamic tract (fast pain)
Aδ fibres end mainly in lamina I of the dorsal horn. The second-order neurons cross in the anterior white commissure and ascend in the lateral spinothalamic tract to the ventrobasal complex (VPL) of the thalamus, and then to the somatosensory cortex. This allows fast pain to be localised well.
Paleospinothalamic tract (slow pain)
C fibres end in laminae II and III, the substantia gelatinosa. After one or more short neurons, the signals cross and ascend. Most fibres end in the reticular formation of the brainstem and in the intralaminar nuclei of the thalamus. This explains why slow pain is poorly localised but strongly arousing and unpleasant.
Fast pain is well localised because it reaches the somatosensory cortex via the VPL. Slow pain is poorly localised because it ends mainly in the reticular formation.
Because spinothalamic fibres cross within one or two segments, a cord lesion causes loss of pain and temperature on the opposite side of the body below the lesion.
Referred pain
Pain from an internal organ is often felt on the skin at a distance from the organ. This is referred pain.
How it happens: pain fibres from the organ and from the skin enter the same spinal segment and synapse on the same second-order neurons. The brain, used to pain from the skin, wrongly places the pain there.
| Organ | Pain felt in |
|---|---|
| Heart | Left chest, inner left arm, neck, jaw |
| Diaphragm | Tip of the shoulder |
| Appendix (early) | Around the umbilicus |
| Gallbladder | Right upper abdomen, right shoulder tip |
| Ureter | Loin to groin |
The body's pain control systems
Gate control
Large Aβ touch fibres send branches to the dorsal horn. When they fire, they activate inhibitory interneurons that reduce the passage of pain signals.
This explains why rubbing a painful area, or applying a TENS unit, can ease pain.
The analgesia (descending) system
The brain can switch off pain signals at the cord.
- Periaqueductal grey of the midbrain and around the third ventricle.
- → Nucleus raphe magnus in the lower pons and upper medulla (uses serotonin).
- → Dorsal horn, where local interneurons release enkephalin.
- Enkephalin blocks calcium channels on the pain fibre endings, so less transmitter is released (presynaptic inhibition).
The body's own opioids are β-endorphin, met-enkephalin, leu-enkephalin and dynorphin. Opioid drugs act on the same receptors.
Electrical stimulation of the periaqueductal grey can almost completely suppress severe pain.
Temperature sensation
There are separate cold and warmth receptors, plus pain receptors that fire only at extreme temperatures.
- Cold receptors are far more numerous than warmth receptors. Signals travel in Aδ fibres (and some C fibres).
- Warmth signals travel in C fibres.
- Below about 10–15°C and above about 45°C, pain fibres are stimulated, so extreme heat or cold feels painful.
Temperature receptors adapt a lot but not completely. Getting into a hot bath feels very hot at first and then less so.
Temperature signals travel with pain in the lateral spinothalamic tract.
Clinical relevance
Hyperalgesia
How it happens: damaged tissue releases prostaglandins and other chemicals that sensitise pain endings (primary hyperalgesia); changes in the cord make it more responsive (secondary).
What you see: normal touch feels painful near an injury. NSAIDs reduce pain partly by blocking prostaglandin synthesis.
Syringomyelia
How it happens: a cavity in the centre of the cervical cord damages the crossing spinothalamic fibres.
What you see: loss of pain and temperature in a cape over the shoulders and arms, with touch preserved, and painless burns on the hands.
Thalamic pain syndrome
How it happens: a stroke in the ventrobasal thalamus.
What you see: loss of sensation on the opposite side at first, then severe, burning pain on that side.
Herpes zoster
How it happens: the virus reactivates in a dorsal root ganglion.
What you see: pain and a rash along one dermatome.
Expect: Aδ vs C fibres and their transmitters, fast vs slow pain pathways, why slow pain is poorly localised, the mechanism of referred pain, gate control, the descending analgesia system (periaqueductal grey, raphe magnus, enkephalin) and the most potent pain chemical (bradykinin).
Quick revision
- Nociceptors: free nerve endings; adapt very little.
- Fast pain: Aδ, glutamate, sharp, localised, neospinothalamic.
- Slow pain: C, substance P, burning, poorly localised, paleospinothalamic.
- Spinothalamic fibres cross within 1–2 segments.
- Referred pain: organ and skin share the same spinal segment.
- Gate control: Aβ touch fibres inhibit pain at the dorsal horn.
- Analgesia: periaqueductal grey → raphe magnus → enkephalin in the dorsal horn.
Written by The House Job from standard physiology references (Guyton and Hall Textbook of Medical Physiology; BRS Physiology).
FAQ
What is the difference between fast and slow pain?
Fast pain is sharp and well localised and travels in Aδ fibres. Slow pain is burning and poorly localised and travels in C fibres.
Which neurotransmitter is released by slow pain fibres?
Substance P, along with glutamate.
Why does rubbing a painful area help?
Touch fibres activate inhibitory interneurons in the dorsal horn that reduce pain transmission (gate control).
What causes referred pain?
Pain fibres from an organ and from an area of skin enter the same spinal segment, so the brain misplaces visceral pain to the skin.