Learned Pain
Updated 2026-08-09
INTRODUCTION
English translation pending.
CORE DEFINITION
A clinical framing drawn from pain neuroscience, especially research on central sensitization by Clifford Woolf and others. Prolonged noxious input can lower pain thresholds and strengthen synaptic connections in the central nervous system, so nociceptive circuits fire more readily and with less provocation. The core claim is that pain has a learned, memory-like component and can persist as disease rather than symptom. It is qualified by the fact that tissue pathology may still coexist and must not be dismissed.
SCAFFOLDING EFFECT
Reduce cognitive load
- Use Symptom Triage: Separate current tissue damage from sensitized central signaling before choosing treatment. - Use Loop Breaking: Interrupt the cycle where pain expectancy amplifies the next pain episode. - Use Gradual Exposure: Reintroduce movement in graded doses to retrain the nervous system's threat estimate.
Anchor fast decisions
Repeated noxious input strengthens synaptic transmission in spinal and brain circuits, a process called central sensitization. Thresholds fall, receptive fields widen, and normally innocuous stimuli start to provoke pain. Expectation and catastrophizing add descending signals that further amplify the response, so each episode confirms the brain's prediction of threat. Because the pattern is stored rather than merely triggered, the pain persists after the original tissue insult resolves.
MINIMUM ACTION
In progress 0/1Practice this model in one real situation:
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Source support: Explicit
- en.wikipedia.orghttps://en.wikipedia.org/wiki/Nociplastic_painverified
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