Spatial perception of pain (II)

Where does it hurt? A common answer to this question is: it hurts at the location of the pain receptors in the body. I will discuss three counter-arguments to this proposition, starting with the simple one. The simple argument is that there is a discrete set of pain receptors on the skin, but the spatial perception of pain is not discrete (the same argument applies to touch): we do not feel pain at discrete locations on our skin. It seems that the phenomenal space of pain is continuous, and this observation does not match anatomy. Then there are the anecdotical arguments: we have headaches but there is no pain receptor in the head; when you lose a limb (say a hand), the non-existent limb can hurt (phantom limb pain); there are systematic mislocalizations of the causes of pain, for example heart pains are felt in the arm. Finally there is a more sophisticated argument. Let us assume that we do feel pain at the location of our pain receptors. But then how do you know where your pain receptors are? One answer would be: we know it because it is somehow encoded in our genes. The “somehow” would deserve some precise explanation, but this is not necessary for this argument. This proposition requires that there is a systematic mapping between our genes and our body at a fine level of detail. That is, the precise location of pain receptors should depend only on our genes. But we know that this is not true. For example the size of our body depends on the diet we had when we were kids, and therefore so does the location of nerves. Therefore, even if we felt pain at the location of the receptors, we would still need to find out where these receptors are.

Another common answer to the question “where does it hurt?” is the objectivist answer: it hurts where the cause of the pain is, or where the injury is. An important difference with the previous one is that it does not imply discrete spatial perception. From our experience, this proposition seems to be correct most of the time but a simple objection is that there are cases of mislocalizations of pain (e.g. heart pains). The same argument as above leads us to the same question: how do you know where the injury or cause of pain is?

If genes are not sufficient, then it must be based on experience. Let us imagine that you hit your knee against a wall. You can see the knee hitting the wall; you also have a tactile experience; you feel an intense pain at the moment of contact, which perhaps gradually fades out. I start with proposition A: there are two independent channels, one that provides pain information (intensity of pain, through pain receptors) and another one that provides spatial information (through tactile receptors or vision). The same question now applies to the spatial channel: how do you know where something touches you? This is simpler to answer because you can touch yourself: you can associate your movements with activation patterns of tactile receptors when you touch your skin. You know where a tactile stimulus is in the sense that you know how to make movements to touch it. An objection to proposition A is: what if there is no external stimulus that activates the tactile receptors? For example, your stomach could hurt because of acidity or a tooth could hurt because of bacteria. There is nothing you can see, and all the tactile receptors are on the skin, so there is no independent source of spatial information, and yet the pain feels precisely localized. The only way to save proposition A is to assume that there actually is another source of spatial information. For example, in the case of tooth pain, maybe tactile receptors (or the nerves) are actually activated. In the case of stomach ache, it is harder to imagine that these receptors on the skin are activated (but I leave it as an open question), and in this case you would need to hypothesize that there are other types of receptors, perhaps acidity receptors, that carry spatial information. But then we are back to the same problem as before: how do these receptors get to carry any spatial information at all? (how do you know where these neurons are?) You would then need to assume that these receptors inside your body can also be activated with your own movements. I leave this as an open possibility. There is still one difficulty, which I will address later because it is shared with other propositions: how can pain be localized inside the body?

I will now discuss two other related propositions. Proposition B is purely sensorimotor: you feel pain at a particular location because specific movements that you make produce that pain. This explanation only requires pain receptors, but these receptors must be activated in a way that is spatially specific (i.e., which varies systematically with the location of the pain stimulus). For example, by pinching yourself, you associate the pattern of pain receptor activation with the location of the skin where you pinched yourself. This proposition implies that you cannot feel any localized pain unless you have previously produced it yourself. But what about when a tooth aches? It seems that you could feel tooth ache without having hurt your tooth yourself before. To save proposition B, it seems necessary to assume that the pain receptors can be activated at a “subthreshold” level that does not produce pain. In this case, to feel pain at a particular location requires previously producing specific movements that produce a similar (but possibly less intense) pattern of activation of the pain receptors.

There is a variation of B, which I will call proposition B2, which goes as follows. You feel the pain at a particular location because whenever this particular activation pattern of pain receptors is present, you can manipulate this pattern or the intensity of pain by specific movements or actions. For example, you hurt your knee and then you know you will feel a bit better if you put your hand on it, maybe because of the heat. Proposition B2 is slightly different from B by the fact that it is how you can manipulate pain, rather than how you can cause pain, that provides spatial information. The example of the tooth would then be: your tooth aches, and you know where it aches because by moving your tongue on your teeth you alter the intensity of pain.

Proposition C is learned association: the localization of pain is inferred from the activation pattern of pain receptors (which must be spatially selective), by association with another channel that carries spatial information (e.g. tactile receptors). For example: you hit your knee against the wall, the tactile receptors carry information about the location of pain, which you associate with the activation pattern of pain receptors. Later, you knee hurts but there is no mechanical contact with anything: you still feel the pain in the knee because it is the same activation pattern as when it was hit by the wall. In proposition C, you could not experience the location of a pain unless you have previously experienced the same pain in conjunction with an independent cue of location. So we have the same problem as in proposition A: what if a tooth aches for the first time? The proposition can be saved in the same way by assuming that pain receptors can be activated at a subthreshold level that does not induce pain.

There are now two questions I want to address: 1) How can we feel pain inside the body? 2) Why do we make systematic errors in localizing pain?

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