Mechanisms involved
This condition is explained through the mechanisms below. Each one is taught as ordinary physiology first.
Primary
Secondary / contributing
Immune cells involvedWho is actually in the tissue
Sensitization is a nervous system state, maintained in part by immune cells inside the nervous system.
Selected cell
Macrophage
Clears debris and old blood. When clearance is incomplete it switches to a repair-and-inflame phenotype that feeds fibrosis and new nerve growth.
Microglia — the resident macrophages of the cord and brain — shift to a reactive state that keeps pain circuits amplified.
Schematic drawings, not micrographs. Immune findings here describe mechanism and association; none of them are diagnostic tests.
What it is
A state, not a disease: the spinal cord and brain amplify nociceptive input, so pain spreads beyond the original site, ordinary pressure hurts, and pain persists after the initial driver is treated. It can sit on top of any of the other conditions here, which is why it belongs in its own place.
How the mechanisms produce this
- Repeated input increases synaptic efficiency in the dorsal horn, and descending inhibition weakens.
- Receptive fields widen, which is why one pelvic organ becomes a whole lower quadrant.
- Sleep loss, threat and disbelief each measurably increase gain, which is why the clinical encounter itself is part of the mechanism.
- Because the amplification is central, imaging of the original site stays unremarkable while pain worsens.
What tends to help
- Name it explicitly — explanation itself reduces pain in trials.
- The Central Sensitization Inventory as a documentable measure to bring to appointments.
- Treat peripheral drivers and central gain simultaneously.
- Sleep, graded predictable movement, and medications that act centrally rather than anti-inflammatories alone.
Where the evidence is thin
No test confirms it; the construct is inferred from pattern, which is both its clinical usefulness and its main criticism.