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Commentary
Representation and Regulation in Emotional Theory
Philip Gerrans
University of Adelaide, AU
Gerrans, Philip. 2024. “Representation and Regulation in Emotional Theory.”
Journal of Philosophy of Emotion 5, no. 2: 36-43. https://doi.org/10.33497/2024.Winter.5.
Abstract: The case of pain asymbolia is a case study that provides evidence of the mechanisms underlying the relationship between bodily experience, affective experience, and self-awareness. On one account pain asymbolia is the result of an affective deficit. Sensory signals of bodily damage are not associated with characteristic negative affect. Cochrane endorses this account as part of his version of a “conceptual act” theory of affective experience. In contrast, I propose an active inference account of affect in general and pain asymbolia in particular. In the active inference framework the self is inferred as the endogenous cause of bodily and affective experience in the process of organismic regulation. This preserves Cochranes ambition to ground affect in bodily regulation but avoids the problem for affective deficit accounts of asymbolia that cannot do justice to the neural correlates.
Keywords: pain asymbolia, affect, emotion, self awareness
Like Cochrane, I endorse what we can call an approach to the mind/brain that treats it as fundamentally a device of regulation rather than representation. The two approaches are not incompatible (after all regulation requires representation), but they do have different emphases. In general, regulatory approaches focus on mechanisms that regulate adaptive behaviour (Pezzulo et al. 2015; Seth and Friston 2016; Huebner and Schulkin 2022). On such views, representation emerges to enable regulation. Representational theories start with representational content of a system and treat mechanisms as implementation of a representational/ computational system. The regulative approach fits well with what has recently been called active inference approaches to the mind, and my aim here is to finesse some of Cochrane’s ideas using that framework. One advantage is that the active inference framework fills out Cochrane’s ambition “to give a detailed mechanistic account of the generation of affect” (Cochrane 2018, 42).
Another thing I agree with is that the best way to think of emotional experience is as “taking us beyond the immediate impact upon our bodies and representing the subject’s own agentive powers, emotional bodily feelings constitute a basic form of self-consciousness” (2018, 111). This is part of his theory of the dual intentionality of emotional experience. It informs us about the state of the body and the relevance of the eliciting object or
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situation to our concerns. This conception is shared by somatic and cognitivist (appraisal) theories, but it creates a different explanatory problem for each (Sander et al. 2005). As Cochrane says, “The bodily feelings we have when undergoing emotions are not simply patterns of bodily sensations” (2018, 89). So, a somatic theorist needs to explain how a bodily experience can represent emotional content that is the relevance of something to our concerns. As Cochrane says, “Without some conceptual framework to deliver representational meaning, bodily feelings only present a certain degree of arousal in themselves” (2018, 108). Cognitivist theories face the inverse version of the problem. On those theories, the emotion of fear, for example, implicitly or explicitly represents the danger to me (the “formal object” of emotion, as it is known). But why should such a representation be felt as a bodily sensation? In general there is no intrinsic connection between applying a concept and a distinctive phenomenology (pace Goldie 2002; Scherer 2004).
Cochrane’s solution is that emotional experiences have “dual intentional content.” They represent the body and the conceptual aspects of emotion (its relevance to the subject along dimensions familiar to conceptual act and appraisal theorists). Interestingly, although Cochrane is a regulatory theorist of emotion, he deals with this problem as it is posed in the representational framework, and the structure of his solution reflects this. He says,
x is an emotional bodily feeling when: (1) the individual conceptualises (implicitly or explicitly) bodily feelings as emotional and (2) the individual is in a bodily condition that matches the typical condition of their body when undergoing an emotion about a particular situation. (2018, 107)
This explanation requires that the relevant bodily state be “conceptualised” as emotional, an approach which is very close to the conceptual act view of emotions that treats them as bodily experiences interpreted or conceptualised in emotional terms. He explains conceptualisation as follows:
Our feelings tell us something about our current ‘state of self’– as solid and secure or weak and contingent, enduring or transient. Although this content is represented intuitively by means of anon-literal sense of one’s bodily condition in relation to an ‘emotional space’, the status represented can be entirely warranted. It is to be analysed as an awareness of the disposition of the body towards interacting with the environment in a certain way. (114)
So far, we have a detailed conceptual analysis that does justice to the phenomenology of affective experience as (i) being grounded in the body, (ii) informing us about the subjective relevance of elicitors, and (iii) being a form of self-awareness. As stated, this account lies more at the conceptual end of “a continuum of mechanism schemata that abstract away to a greater or lesser extent from the gory details,” to quote Gualtiero Piccinini and Carl Craver, paraphrasing Philip Kitcher (Piccinini and Craver 2011). At one end we have useful phenomenal models and mechanism sketches, and at the other complete descriptions of mechanisms. These provide the “gory details” that, as Piccinini and Craver say, are fully explanatory. Clearly Cochrane’s aim is not just a mechanism sketch in Craver’s terms, but a mechanistic explanation. This is why he discusses the condition known as pain asymbolia to support the idea that affective experience is not reducible to sensory experience. It provides empirical support for a model/sketch that distinguishes sensory and affective components of experience.
However, the account on which he relies, that of Nikola Grahek (2007), does not do justice to the phenomenology of pain, suffering, and asymbolia or its mechanistic bases. The active inference account by contrast explains the complex phenomenology of pain, suffering, and self-awareness in a range of conditions in mechanistic terms (Von Mohr and Fotopoulou 2018; Gerrans 2020; Kiverstein et al. 2022). In that respect, it helps realise Cochrane’s ambition for a “detailed mechanistic account.”
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The more detailed picture does suggest that one ambition of Cochrane’s theory cannot be met. That ambition is to preserve the idea that emotions are natural psychological kinds. A control or regulatory theory that focuses on mechanisms should abandon this ambition. The natural kind view of emotion comports better with the representational view of psychological processes. When, for example, we look at perception in primates, there is a clear decomposition from the computational level of description, via representation and algorithm, to implementation in a perceptual system. There are some specialised mechanisms that perform the representational task of vision initially defined independently of its mechanistic substrate. This is true on any theory of vision: Marrian, enactive, inferential, and hierarchical predictive processing. However, there is no clear analogy with emotional experience. When we try and explain how it is that bodily experiences can do double duty as carrying information about bodily states and of formal objects of emotion, we do not find anything analogous to a visual system. There is no specialised system whose role is to transform feelings of bodily arousal to feelings of danger. This does not mean that emotional episodes cannot be the object of scientific investigation, just that that investigation does not disclose the operations of a specialised emotional processing system that meets the criteria for being a natural kind. So, to sum up, the regulatory/control approach is more radical than Cochrane suggests.
One way to see this is via his discussion of pain asymbolia, a condition in which the subject is aware of sensory aspects of pain (nociceptive pathways are intact), but reports that the pain does not matter, is not “painful,” or in some cases, feels like it is happening to someone else. For example:
When a part of my body hurts, I feel so detached from the pain that it feels as if it were somebody else’s pain. (Sierra 2009)
This rare condition is associated with damage to the posterior insula cortex, which is a convergence zone for interoceptive and basic bodily signaling. It is important to the understanding of the condition that the subject is aware of actual or potential injury but does not feel it to be distressing and is not motivated to avoid the painful stimulus. So, a key issue to be explained is why and how damage to the posterior insula causes the phenomenology of “pain without suffering.”
The condition is thus a test case for theories about the relationship between bodily experience, which is intact in pain asymbolia (PA), and the emotional experience of suffering. A standard view in the early literature was that PA is evidence that pain has sensory and emotional/affective components that can dissociate. The dissociation is then explained in terms of distinct neural processing systems. This invites the idea that the experience of pain has a sensori-motor and an emotional/affective aspect with the latter being provided by an emotional processing system. This comports well with Cochrane’s characterisation of the relationship between sensory processing and affective experience: “[alongside the sensory qualities of an experience] we should recognise a distinct affective aspect that is directly responsible for the intrinsically pleasant or unpleasant aspects of the experience” (2018, 42-43). And Cochrane uses pain asymbolia as a case to “distinguish unpleasant affect from the sensory components of pain” (45).
So, on a straightforward interpretation of pain asymbolia, it is a case of pain sensation without affect. This suggests that the affective aspect of an experience is something that is added by a discrete system that interprets and enriches the bodily signal, allowing its emotional significance as well as sensory information to be felt.
Philosophers such as Nikola Grahek who endorse this conception can point to classic neuroscientific studies of pain processing that posit a modular architecture with sensori-motor and affective components. This idea localises the sensori-motor aspect of pain experience to the integration of nociceptive signals in the posterior insula (PI) and the affective aspect of pain to a network whose hub is an anterior insula-anterior cingulate circuit
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(AI-ACC). The idea that the affective aspect of a pain experience is based in activity in this AI-ACC circuit was part of the first wave of pain theorising (Danziger 2006; Klein 2015).
As a theory of pain asymbolia, this faces two problems. The first is that asymbolia is a product of damage to posterior insula, not anterior (the hypothesised basis of suffering). This is not a decisive problem because inactivity in PI will compromise activity in the AI it afferents, and that could explain the lack of affect. However, even if pain asymbolia is associated with lack of affect, it is not that lack that explains the lack of aversive response. Patients with frontal lobotomy have absent or reduced affect but exaggerated aversive response to noxious stimuli. It is also interesting that Roger, a patient with widespread insula and limbic damage has exaggerated aversive responses to painful stimuli (Philippi et al. 2012; Feinstein et al. 2015). Does this matter to Cochrane’s account? It does not undermine it decisively, but it suggests that it does not yet provide a satisfactory account of underlying mechanisms if that account posits a modular architecture for pain processing.
In fact, another aspect of Cochrane’s account can come to the rescue here. And that is the idea that affective feelings are a form of self-awareness that locates the subject in a space of possibilities for regulatory action. To show how this explains pain asymbolia, and affect in general, we have to treat pain processing as a species of active inference implemented in essentially amodal circuitry. So, the control/regulatory ambition is supported, but the idea that emotions are natural kinds is not.
In general, the science of pain processing has moved away from a modular conception, with dissociable sensory and affective components, to the idea that pain is processed by a distributed matrix of interconnected circuits (Melzack 1990; Betti and Aglioti 2016). The other salient feature of the matrix conception is that outside initial nociceptive processing, there is no circuitry specialised for pain. Pain experience involves a coordinated suite of neuroendocrine, immune/inflammatory, and autonomic responses mobilised by the brain to respond to a threat to bodily integrity. It also involves sensori-motor and cognitive processes that are not intrinsically specialised for pain. It turns out that pain processing is not really a case of activity in a specialised system with modular architecture, but the coordination by the mind of a suite of essentially amodal resources to respond to nociceptive signals. What we see in an episode of pain is a characteristic pattern of activity across a distributed matrix, most of whose elements are not specialised for nociceptive processing (Bushnell et al. 2013; Corns 2014; Betti and Aglioti 2016; Corns 2018).
This is consistent with the active inference conception of the mind, which treats cognition as the mobilisation of the mind’s resources to enable adaptive action. Such actions include internal regulatory activity as well as overt action. Of course, regulation takes many forms: cytokine cascade, inflammatory response, appraisal (using cognitive systems that are not specialised for emotion), attention, memory, and executive functioning. The result of this coordinated activity is the affective feeling that signals success or failure of regulatory activity (Velasco and Loev 2021). In the case of pain, it signals suffering or its reduction. Recall that for Cochrane, affective feeling tells the subject whether to act to increase or reduce a form of experience by focussing attention adaptively.
Within active inference, representation arises as an aspect of regulation. Crucial to this conception is the idea that in order to anchor and integrate activity the mind represents systemic functioning as the activity of a unified entity: the source and target of regulation. The result of this integrative process is the feeling of basic, bodily self-awareness, one of whose primary substrates is activity in the posterior insula (Frot et al. 2014; Moayedi 2014). This integrative role for the PI is the reason why the nociceptive signal is felt to belong to me qua something I need to regulate. However, as a variety of conditions show, activity in the posterior insula is not sufficient to produce affective experience. That requires the integration of bodily self-representation with information that enables adaptive response that is mediated according to the subjective relevance of the eliciting situation.
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AI is a crucial integrative hub or relay station between bodily self-representation (whose hub is the PI) and the other systems whose coordination is necessary to determine and monitor adaptive response. It thus anchors activity across the mind, ensuring that it optimises organismic function at all levels from basic bodily regulation to explicit social and personal-level cognition. In virtue of this integrative regulatory function, activity in the AI allows bodily experience to be felt affectively. This also explains the functional promiscuity of the AI, involved in almost every self-referential form of processing, and the fact that it is not intrinsically specialised for anything. Rather, it is an integrative hub for the adaptive coordination of basic bodily and higher order processing. In virtue of playing that role, it sustains affective experience understood as “a basic form of self-consciousness” (Cochrane 2018, 111); because, as Cochrane says, “At every level of representational sophistication, affect will evaluate the success or failure of our concern-regulating projects” (2018, 65).
The key point is that projects are felt as ours, giving rise to a sense of basic bodily awareness and the sense of the self as the subject of affective experience. The relationship between bodily awareness, affect, and self-awareness is explained by the coordinating role of the AI. It ensures that regulatory activity is taken to optimise the functioning of the entity whose subsystemic functioning it represents as aspects of a unified self (Craig 2009; Eckert et al. 2009; Cauda et al. 2011; Terasawa et al. 2012).
This is why, as Klein says, asymbolia is best explained, not as loss of affect per se, but as a change in self-awareness. The nociceptive signal is not modelled as belonging to the subject, qua target of regulation due to damage to the PI. As a result, the signal is not felt to require an adaptive response and does not initiate the cascade of higher order signalling coordinated by the AI. The system is not trying to regulate the nociceptive signal using affective experience as an index of success or failure. Asymbolia arises not because the subject has lost affective response to pain (although she has), but because she does not feel as though the pain is her’s because the sensory signal is not processed as one that matters to her concerns. They recognise it as pain, but in some important sense it has ceased to be something worth caring about. It thus has the feel of a sensation which they can no longer identify with as their own (Klein 2015).
As I say, I don’t think any of this undermines Cochrane’s account of affect or pain asymbolia since, despite the reductive ambition, they are pitched at a level of mechanism sketch, not at the level of explanation. The gory details in fact reinforce a lot of his account. At the same time, since those mechanisms are largely amodal and not specialised for emotional processing, the regulatory approach should lead to abandonment of the idea that emotions are natural kinds.
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Philip Gerrans © 2024
Author email: philip.gerrans[at]adelaide.edu.au
