Pain Physiology and Gate Control
On this page
Direct answer
Pain reaches the cord by two parallel routes: fast pain in thinly myelinated A-delta fibres conducting at 6–30 m/s — sharp, well-localised, the first stab — and slow pain in unmyelinated C fibres at 0.5–2 m/s — burning, aching, poorly localised. Both synapse on dorsal horn neurons, but before they can, the substantia gelatinosa (lamina II) acts as a gate: activity in large non-nociceptive A-beta fibres activates inhibitory interneurons that close the gate to C-fibre traffic, which is why rubbing a knock eases it — the core of Melzack and Wall's 1965 gate control theory. Above the gate sits a descending analgesic system from periaqueductal grey through nucleus raphe magnus to the dorsal horn, running on endogenous opioids.
What you must remember
- Nociceptors are free nerve endings, many polymodal, sensitised by bradykinin, potassium, hydrogen ions and prostaglandins; substance P and glutamate are the primary transmitters at the cord.
- Fast A-delta pathway: neospinothalamic, lateral, to VPL thalamus and somatosensory cortex — discrimination and localisation.
- Slow C pathway: paleospinothalamic, medial, to brainstem and medial thalamus — the suffering component, with autonomic and emotional responses.
- Gate control (Melzack and Wall, 1965): substantia gelatinosa inhibitory interneurons are opened by C-fibre activity and closed by A-beta activity; descending fibres also close it.
- Descending analgesia: periaqueductal grey stimulation releases endogenous opioids, activating serotonergic neurons of nucleus raphe magnus, which excite enkephalinergic dorsal horn interneurons that inhibit nociceptive transmission both pre- and post-synaptically.
- Endogenous opioids: beta-endorphin (from POMC), met- and leu-enkephalin, dynorphin; receptors mu (morphine's target, also miosis, respiratory depression, dependence), kappa and delta; naloxone reverses all.
- Referred pain by convergence-projection: heart to T1–T5 dermatomes (left arm and medial forearm), diaphragm to C3–C5 shoulder tip, ureter to T10–L2 groin, appendix initially periumbilical (T10) until parietal peritoneum localises it to the right iliac fossa.
- Hyperalgesia (primary at the injury, secondary in surrounding skin) and allodynia (pain from innocuous touch) define sensitisation; phantom limb pain affects most amputees.
Why rubbing a knocked elbow works
Hit your elbow on a door and instinctively rub it — the manoeuvre is gate control made visible. The rub floods the segment with A-beta input from touch and proprioceptive receptors; these large fibres synapse on inhibitory interneurons in the substantia gelatinosa, which release inhibitory transmitter onto the C-fibre terminals and projection neurons, closing the gate through which the slow burning message would pass. The pain is not removed at its source — the bradykinin and prostaglandins are still there — it is gated at the door. Transcutaneous electrical nerve stimulation uses exactly this mechanism, and dorsal column stimulation extends it centrally.
Now move up a level. The brain does not merely receive pain; it grades it. Stimulating the periaqueductal grey of a rat produces analgesia deep enough for surgery — the discovery of the descending system. Opioids act at every station: morphine in the PAG, raphe and dorsal horn, which is why intrathecal opioids work and why naloxone reverses not just morphine but placebo analgesia too. The military and sporting observation that severe injury can go unnoticed in the heat of the moment is this system discharging under stress and emotion.
Where students slip
Numbers first: A-delta conducts at 6–30 m/s and C fibres at 0.5–2 m/s — swap them and every MCQ on "first pain" is lost. Mechanistic slips follow. Referred pain is not radiation: the cardiac impulse enters T1–T5 segments shared with the left arm, and the cortex, trained by a lifetime of somatic input, attributes the visceral signal to the skin dermatome — convergence-projection, learned misattribution. Visceral pain characteristics deserve precise wording: poorly localised, accompanied by autonomic responses (sweating, nausea, bradycardia), and often midline because of bilateral innervation. Finally, gate theory does not explain phantom limb or neuropathic pain, which persist with no gate left to close — the theory was a beginning, not an end.
Frequently asked questions
What are the differences between fast and slow pain fibres?
Fast pain travels in myelinated A-delta fibres at 6–30 m/s to the lateral thalamus for sharp localised sensation; slow pain travels in unmyelinated C fibres at 0.5–2 m/s medially, producing dull burning suffering.
What is the gate control theory of Melzack and Wall?
Transmission of nociceptive signals through the dorsal horn is modulated by substantia gelatinosa interneurons, which large-diameter A-beta activity inhibits and C-fibre activity facilitates.
Why is cardiac pain felt in the left arm?
Visceral afferents from the heart enter the T1–T5 spinal segments along with somatic afferents from the left arm and chest, and the cortex misattributes the shared-segment signal to the somatic dermatome.
Which pathway mediates descending pain inhibition?
Periaqueductal grey to serotonergic nucleus raphe magnus to enkephalinergic dorsal horn interneurons, suppressing nociceptive transmission presynaptically and postsynaptically.
What is allodynia, and how does it differ from hyperalgesia?
Allodynia is pain from a normally innocuous stimulus such as light touch; hyperalgesia is an exaggerated response to a painful one, from sensitised nociceptors or dorsal horn neurons.