How do you define pain? You could ask a thousand people and probably get a thousand different
answers. It’s both physiological and psychological. It’s emotional and cultural. According
to the Association for the Study of Pain in 1979, pain is “an unpleasant sensory and
emotional experience associated with actual or potential tissue damage, or described in
terms of tissue damage.” But how did we arrive at this maybe-not-so-crystal-clear
definition? And what does pain theory teach us about our own bodies?
This question has been the subject of scientific and philosophical debate since Ancient Greece, but in the last
few centuries, it hinged on one question: where does pain come from physiologically?
Is there a specific set of nerves for pain? And if not, how do our regular nerves
know when something is painful or not painful? And is this even happening at the nerve level,
or is the brain more involved? Well, in 1811 a surgeon named Charles Bell attempted to
answer that question. His idea was that specific nerve fibers send pain signals back to the
brain, just like how any other sensory fibers like vision or smell send signals to the brain.
We call this specificity theory today. And experiments by physiologists in the years
afterwards seemed to back him up. Scientists identified specific receptors for all kinds
of different sensations — including loads of different touch receptors embedded in your
skin. Like Meissner’s corpuscles are stimulated when something textured moves over our fingertips.
And those are different than Pacinian corpuscles which only sense signals for fine textures
and high frequency vibration. Or how Merkel’s discs help us determine things like pressure
while Ruffini corpuscles are probably responsible for sensing stretching in your skin. These
four types of receptors all sense mechanical touch, so we call them mechanoreceptors. Likewise,
the receptors for pain were named nociceptors — noci- for noxious, or painful. Then in
the early twentieth century, the main competing theory was pattern theory,
and it was pretty much the opposite. According to pattern theory, our nerves send signals
to the brain, and if the brain detects a familiar pattern of pain stimuli, the signals will
be interpreted as pain. As anatomists kept discovering new sensory receptors, pattern
theory fell out of favor and specificity theory was more accepted. But specificity theory
still had some issues. The most important was that pain isn’t just the result of physical
injury. It’s a complex experience involving emotional, psychological, and cognitive factors.
So in 1965, two scientists published a paper describing what they called the gate control
theory, which is the most popular model of pain physiology used today. This theory says
that signals from the peripheral nerves first have to travel to three areas of the spinal
cord before traveling to the brain — the substantia gelatinosa, the fibers of the dorsal
column of the spinal cord, and specialized cells called transmission cells in the dorsal
horn as well. Those nerves from the mechanoreceptors and nociceptors all converge at this gate,
the substantia gelatinosa. If a signal from a nociceptor reaches a certain intensity,
the gate will open and that signal will be sent to the brain where it’s interpreted
as pain. But if the gate is closed, the signal never makes it farther than the spinal cord.
So it wasn’t a straight route from skin to brain after all, pain had to pass through
a gate first. Those researchers in 1965 suggested a few ways that the central nervous system
could close that gate, including moderation from the brain itself. This was an important
step in pain theory that demonstrated how the brain and peripheral nerves both influenced
how we feel pain. These days, we’ve added a few more details that give us a more complete
model of pain perception. We now know that not all nociceptors signal for the same types
of pain. We have receptors for high intensity mechanical pain, like getting punched, but
different ones for high temperature, like stepping on a George Foreman grill.
"I clamped down on my foot. That's it. I don't see what's so hard to believe about that."
And these nociceptors aren’t just in your skin. They’re found in joints, muscles, and around organs.
Most of those receptors are attached to one of two major nerve types, either a Type A-delta
fiber or a Type C fiber. More of those Type A Delta fibers are wider and covered in a
substance called myelin that lets them send signals faster than the unmyelinated Type
C fibers. And this lends itself to a cool physiology hack. Type A Delta fibers send
signals to the spinal cord faster, they’re responsible for the first perception of pain,
while the slow Type C fibers convey pain intensity. But the mechanoreceptors are myelinated too,
so if you stimulate any of the non-painful touch receptors, that signal arrives at the
substantia gelatinosa first, closing the gate. That’s why rubbing a banged up elbow works.
You’re taking advantage of the gate control theory. Then again it might all be in vain.
Life is pain, and anyone who says otherwise is selling something. Did I write this entire
episode so I could sneak in a Princess Bride quote? You bet I did! Thanks for watching
this episode of Seeker Human. We’ve got more episodes like this one coming, so make
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