🦴 Chronic Pain Central Sensitization Simulator

Normal Pain Processing

Injury signals travel proportionally from nerve to brain.

• ~1M: Dorsal horn neurons (per spinal segment)
• 1:1: Signal fidelity (stimulus matches response)
• C-fiber: Nociceptor type (slow unmyelinated pain fibers)
• ~100 ms: Reflex latency (withdrawal arc speed)

What triggers a pain signal

Tissue injury activates peripheral nociceptor nerve endings.

Spinal relay in the dorsal horn

Dorsal horn neurons pass signals up to the brain.

A proportional response

Firing rate closely matches actual injury severity.

Repeated Nociceptive Input

Persistent low back pain floods the spinal cord.

• 12 wks: Chronic pain threshold (defines chronic pain)
• ~20%: Adult prevalence (live with chronic pain)
• Elevated: Signal frequency (sustained nociceptive barrage)
• Early: Peripheral sensitization (nerve endings grow reactive)

Chronic back pain as a driver

Ongoing signals keep dorsal horn neurons repeatedly firing.

Peripheral sensitization begins

Injured tissue nerve endings become easier to trigger.

A barrage reaches the cord

Constant input primes neurons for lasting change.

Synaptic Strengthening (Wind-Up)

Repeated firing progressively strengthens dorsal horn synapses.

• NMDA: Wind-up mechanism (receptor unblocking)
• Staircase: Response growth (each pulse bigger)
• >0.5 Hz: Trigger frequency (repeated C-fiber firing)
• Rising: Synaptic strength (long-term potentiation)

NMDA receptors unblock

Repeated glutamate release removes the magnesium block on NMDA.

Wind-up amplifies each pulse

The same stimulus produces progressively larger responses.

Potentiation locks the change in

Synapses strengthen, remembering the repeated pain pattern.

Central Sensitization Established

Dorsal horn neurons now fire without proportional cause.

• High: Neuron excitability (lowered firing threshold)
• Expanded: Receptive field (spreads beyond injury site)
• Present: Spontaneous activity (fires without new input)
• Emerges: Allodynia (light touch feels painful)

Hyperexcitability sets in

Neurons fire spontaneously, even without fresh signals.

Receptive fields expand

Nearby healthy tissue now triggers pain responses.

Non-painful input turns painful

Ordinary touch and pressure now register as pain.

Amplified, Persistent Pain

Perceived pain stays severe despite minimal tissue damage.

• Severe: Perceived pain (reported 7-9 of 10)
• Minimal: Actual tissue damage (often near baseline)
• Up to 9×: Amplification factor (signal gain)
• CNS: Treatment target (not just injury site)

Pain outlives the injury

Tissue heals, but pain signaling stays amplified.

The damage-pain gap widens

Perceived pain diverges sharply from actual injury.

Treatment implications

Therapy must target the spinal cord, not just tissue.