Being Skeptical of Your Brain, Part One: Introducing the Model

I’ve decided I’m going to try to put together some ideas that might eventually end up as a conference talk. I have some ideas in my head for a basic outline, but they’re not very organized, so my plan is to write about them until they organize themselves.

The talk is going to be about how to be skeptical of your own brain, and is going to mainly center around a model for thinking about our experiences that helps with this. I want to do more research on the model, because while I know there is good science backing it up when it comes to the perception of pain, I haven’t done as much research on it with respect to other forms of perception. At present I feel completely comfortable calling it a “useful” model, but I’m hoping to get to the point where I can call it both “useful” and “pretty well substantiated by research” with respect to all of the ways I apply it.

This post is going to be what I presume will end up being the beginning of the talk. It is an outline of my basic mental model for how tactile sensory experiences (pain in particular) occur and how they can be inaccurate or be misinterpreted.

Here we go:

I think of any experience of pain as a three-step process: trigger, feeling, and explanation. In the first step, the trigger, something activates danger sensors in the skin called “nociceptors” that respond to heat, pressure, or acidity, and those signals are sent to the brain*. For example, when you sprain your ankle, the resulting tissue damage will activate nociceptors in your ankle.

The second step is the translation of those signals into a sensory experience — the feeling: the brain receives nociceptive signals, and makes a decision about whether or not you should feel anything as a result. That decision is based on putting the signals in historical context — has the brain gotten signals like this before? Have they generally been dangerous? Not dangerous? Is it likely they are dangerous now? — essentially, the brain takes your whole life, all of your lived experiences, into consideration and makes a decision about whether or not to produce the conscious experience of pain. When you sprain your ankle, your brain should, if everything is working correctly, decide to produce some intense ankle pain in response to the triggered nociceptors.

The third step is the explanation. A person has a sensory experience and comes up with an explanation for it (e.g. “My ankle hurts therefore I injured it in some way.”).

If everything goes perfectly, then the way that the system works is: the trigger occurs, the brain interprets the significance of the trigger correctly and causes an appropriate and proportionate sensory experience, and then the explanation for that sensory experience correctly identifies the trigger. When you sprain your ankle, your brain should translate the resulting nociception input into a painful sensory experience, and your ideal conscious response is, “Shit, I sprained my ankle!”

In the real world, however, the system does not always work so perfectly. In reality, the first step isn’t even necessarily required. The activation of physical sensors in the skin is neither necessary nor sufficient to produce an experience of pain. Pain can be produced in completely healthy people solely by creating a context in which their brain interprets a situation as dangerous — for example, if you hook someone up to a device and tell them it’s running electrical shocks through their brain, they will experience more pain the more you turn a dial higher, even if the device and the dial do not actually do anything.

Pain research rockstar Lorimer Moseley tells a fantastic story from his own life about how this system can go terribly wrong: he was hiking with some friends one day and felt a mild twinge on his leg, thought nothing of it, and ended up in a hospital having been bitten by an incredibly poisonous snake. One of the effects of snake venom is that it locks nociceptors into an activated position, so the amount of danger signals sent to the brain would have been massive, and yet when those signals got to the brain, the brain had no historical context to indicate such signals were dangerous, and so did not create a correspondingly massive pain experience. In fact, it created almost no sensory experience at all. As a result, Lorimer nearly died. About six months later, however, Lorimer was hiking again and experienced a sudden, massive pain on his leg in the same place as before, and very nearly ended up taking a trip to the hospital until one of his friends took a glance at the leg and discovered that it was only a tiny scratch from a twig.

In both of those cases, the system failed. When the trigger was a snake bite, the brain did not produce a sensory experience that felt anything like a snake bite. As a result, the explanation for the sensory experience did not correctly identify the trigger, and that mistake was nearly fatal. Later, when the trigger was only a twig, the brain interpreted it, mistakenly, as incredibly dangerous, presumably because it then had the context of the near-fatal snakebite informing the sensory interpretation. In both cases, neither the sensory experience nor the resulting conscious explanation of that experience usefully corresponded to the event that triggered the nociception in the first place.

In dealing with chronic pain, the lesson I have needed to learn is this: sometimes my pain has nothing to do with the state of my tissues. Sometimes my experience of pain happens solely because my brain has decided, mistakenly, that something threatening is going on. Sometimes, I need to be skeptical of my own lived experience of pain. Sometimes my pain is a lie.

Additionally, even when my sensory experience is a proportionate response to the state of my tissues, I can get the explanation wrong. For example, the experience of repetitive stress injury often manifests for me as an itching sensation. Occasionally, I will get an itching sensation in an arm and assume it’s RSI symptoms, and then later discover a bug bite. The sensations of mild RSI and bug bites are completely indistinguishable to me.

So, to review, the experience of pain is a three-step process: first, there is the trigger that activates nociceptors (e.g. an ankle sprain, a snake bite, a repetitive stress injury, etc.), then there is the feeling – the physical sensation your brain decides to produce in response to the trigger (e.g. a twinge, a sharp pain, itching, etc.) — and then there is the explanation — your brain’s assumption about what the trigger was (e.g. an ankle sprain, a snake bite, a repetitive stress injury, etc.). If the system works correctly, then the physical sensation corresponds well to the trigger, and the explanation thus implicates the trigger successfully (e.g. “It feels like I hurt my ankle, which probably means I hurt my ankle.”). The system fails when the trigger is not accurately identified. This can happen either because the physical sensation is not sufficiently specific to the trigger to make a reliable determination (e.g. when an itching feeling could be either RSI symptoms or a bug bite), or because the physical sensation does not correspond well to the trigger at all (e.g. a snakebite that feels like a scratch from a twig or vice versa).

This is the mental model that I used to think critically about my experiences of pain. It helps me to make a determination, when I am experiencing pain, about whether that pain represents a trigger that is worth my doing something about (e.g. I actually injured my back and should stop exercising), or I should be skeptical of it (e.g. I have chronic back pain and should probably assume nothing is wrong with the tissues and keep exercising). In the next post, I’ll talk about how I apply this same rough model to other experiences.

If anyone has any thoughts or questions on any of the above, I’m interested in refining it as far as possible, so any input is appreciated.

* Actually, there are some modulation steps between the sensor and the brain, and some other steps in the overall process, but I’m simplifying for the sake of brevity.


2 comments on “Being Skeptical of Your Brain, Part One: Introducing the Model

  1. Pingback: Reconceptualizing the Placebo Effect | Research to be Done

  2. Pingback: Gender, Gender Identity, Pain, and Snakebites | Research to be Done

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