Laurenz Casser

A persistent claim throughout the history of modern medicine has been that human beings differ in their sensitivity to pain: that, when afflicted with comparable conditions, certain individuals, and especially certain groups of individuals, ‘hurt more’ than others. While opinions about which groups hurt more and which groups hurt less have varied over time, special emphasis has always been placed on the sensitivity of people of colour, women, and other socially significant groups. However, contrary to widespread medical opinion, this paper argues that claims about biosocial differences in pain sensitivity, past or present, have never been supported by compelling evidence. More specifically, I argue that (i) evidence for systematic differences in prominent measures of pain sensitivity—such as pain thresholds and pain tolerance—has been spurious and inconsistent, and that (ii) even if it was not, such differences still wouldn’t imply a gap in people’s sensitivity to pain. The reason for this, I argue, is that the experimental results are equally well explicable in terms of differences in response biases—a possibility which prevalent pain measurement methodologies typically do not (and possibly could not) adequately control for. While the arguments presented in this paper aren’t intended to rule out variations in pain sensitivity altogether, they cast serious doubt on the incessant search for differences in sensitivity at the level of racial and gender groups.

(Commentary on target article "Core Perception: Re-imagining Precocious Reasoning as Sophisticated Perceiving" by Dawei Bai, Alon Hafri, Véronique Izard, Chaz Firestone, & Brent Strickland) The target article makes a compelling case for “core perception”. However, it is striking that this view is supported almost exclusively by visual evidence alone. We question whether visual evidence is sufficient to motivate core perception (as opposed to “core vision”) and speculate about candidate core representations in non-visual modalities, with a special focus on the bodily senses.

A foundational assumption of contemporary cognitive science is that perceptual processing involves inferential transitions between representational states. However, it remains controversial whether accounts of this kind extend to modalities whose perceptual status is a matter of debate. In particular, it remains controversial whether we should attribute inferential mechanisms to the sensory processing underpinning (human) pain experiences. This paper argues that, contrary to recent proposals in the philosophy and science of pain, pain processing is not mediated by inferential transitions. To this end, I show that standard motivations for inferentialism—including appeal to underdetermination, illusion, cue combination, cognitive penetration, perceptual constancy, and invariance—do not carry over to pain. Instead, I suggest that pain's sensory processing may be better characterised as an idiosyncratic form of transduction, distinguishing it both from paradigmatic perceptual modalities and canonical transducers.

The following argument is widely assumed to be invalid: there is a pain in my finger; my finger is in my mouth; therefore, there is a pain in my mouth. The apparent invalidity of this argument has recently been used to motivate the conclusion that pains are not spatial entities. We argue that this is a mistake. We do so by drawing attention to the metaphysics of pains and holes and provide a framework for their location which both vindicates the argument's validity and explains why it appears invalid. To this end, we show that previously proposed explanations for the apparent invalidity of the argument fail. Moreover, we show that our account accommodates and explains seemingly opposing linguistic data. We conclude that the ‘pain-in-mouth argument’ does not undermine the view that pains are spatial entities.

We suggest that pain processing has a modular architecture. We begin by motivating the (widely assumed but seldom defended) conjecture that pain processing comprises inferential mechanisms. We then note that pain exhibits a characteristic form of judgement independence. On the assumption that pain processing is inferential, we argue that its judgement independence is indicative of modular (encapsulated) mechanisms. Indeed, we go further, suggesting that it renders the modularity of pain mechanisms a default hypothesis to be embraced pending convincing counterevidence. Finally, we consider what a modular pain architecture might look like, and question alleged counterevidence to our proposal.

Various prominent theories of pain assume that it is pain’s biological function to inform organisms about damage to their bodies. I argue that this is a mistake. First, there is no biological evidence to support the notion that pain was originally selected for its informative capacities, nor that it currently contributes to the fitness of organisms in this specific capacity. Second, neurological evidence indicates that modulating mechanisms in the nociceptive system systematically prevent pain from serving a primarily informative role. These considerations threaten to undermine standard perceptual and representational accounts of pain.