THE GATE THEORY OF PAIN II: Early vs. delayed neural reactions
This is the second article in a series on the Gate Control Theory of Pain — a cornerstone theory published in the 1960s that still plays a crucial role in how we understand pain processing. It rests on an idea that seems counterintuitive at first: sensation (as picked up by receptors in the skin) and the experience of pain (constructed by the central nervous system) are independent processes.
In this part, we'll take a closer look at the timing of the pain signal’s journey. In part one we explored the multimodal journey from sensation to pain. In part three, we'll dig into the neuropsychology behind the experience.
In the previous article we learned how pain is not a simple reaction, but a multimodal sensory experience. But it gets even a little more complex, because pain unfolds in phases, and each has its own neural circuitry and thus time reaction.
What happens when you twist your ankle? First comes a vague, general sense that “something is wrong”, followed by an immediate motor response to prevent further damage, i.e. you’ll support yourself. After a few minutes passes, the pain becomes more localized and defined - you can relatively clearly feel where it hurts. The experience of pain changes too - it becomes less sharp and more dull. The pain experience unfolds over time.
This sequence involves two types of nerve fibers:
A-delta fibers (the “first pain system”: Fast, myelinated neurons that deliver a sharp, immediate signal to alert the brain - this is your “first responder” system. It serves to protect the integrity of the body, i.e. you re-balance to avoid falling - all for the purpose of increasing the chances of survival.
C-fibers (“the second pain system”): Slower, unmyelinated neurons that transmit a duller, longer-lasting signal. These also communicate with the brain to initiate the release of pain-mitigating neuropeptides like endorphins, endocanabioids and opioids, among others. Yes, this is what we want in impact play.
Because A-delta fibers fire first and C-fibers take longer to engage, sessions that move too fast or hit too hard early on tend to stay stuck in "first pain" — sharp, alarming, and not much else. Give the C-fiber system time to catch up, and the body's own pain-relief chemistry has a chance to kick in instead. (We cover exactly how fast that chemistry moves — endorphins, dopamine, oxytocin — in Neurochemistry of Pain II.)
But timing doesn't just affect which fibers are active — it also changes the gate itself.
The dorsal horn's "gate" isn't a fixed switch; it's a threshold that shifts with repetition. Repeated, unpredictable, or too-rapid C-fiber input can lower that threshold over time — a phenomenon called temporal summation or amplification. If you rush the hits, it will feel exponentially sharper and more distressing with time, because the nervous system is amplifying rather than adapting.
Rhythm and predictability push the gate the other way. Steady, expected input — especially combined with touch (which travels on the large A-beta fibers, the ones that actively help close the gate) — allows the gate's threshold to rise instead. This is also when descending inhibitory pathways from the brain to the skin fully engage — a top-down "volume control" that takes a little time to switch on. This gate mechanism ultimately does more to shape the experience than the raw intensity of the strikes themselves.
Part 3 of this article explains the curious paradox of why mitigating pain actually leads to a deeper altered state of consciousness and not the end of the pleasure.