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During the course of this lecture, I will present the relationship between philosophical and scientific research of human pain experience. According to the traditional philosophical view – which concords with our commonsensical intuitions – pain is essentially an unpleasant sensation that motivates us to react to damaging or potentially damaging stimuli. This traditional view faced a seriouschallenge in 1928, with the discovery of a rare syndrome, known as pain asymbolia. By considering the results of neuroscientific research of this unusual syndrome, as well as the contemporary philosophical interpretation of these results, I intend to show that the relationship between science and philosophy is much more complex than is typically assumed, and that it is by no means one-sided, but rather that these research areas are closely interconnected on their path to a better understanding of our conscious experiences and the world around us.

Pain is often used as the paradigmatic example of a phenomenal kind with a phenomenal quality common and unique to its instantiations. Philosophers have intensely discussed the relation between the subjective feeling, which unites pains and distinguishes them from other experiences, and the phenomenal properties of sensory, affective, and evaluative character along which pains typically vary. At the center of this discussion is the question whether the phenomenal properties prove necessary and/or sufficient for pain. In the empirical literature, sensory, affective, and evaluative properties have played a decisive role in the investigation of psychophysical correspondence and clinical diagnostics. This paper addresses the outlined philosophical and empirical issues from a new perspective by constructing a multidimensional phenomenal space for pain. First, the paper will construe the phenomenal properties of pains in terms of a property space whose structure reflects phenomenal similarities and dissimilarities by means of spatial distance. Second, philosophical debates on necessary and sufficient properties are reconsidered in terms of whether there is a phenomenal space formed of dimensions along which all and only pains vary. It is concluded that there is no space of this kind and, thus, that pain constitutes a primitive phenomenal kind that cannot be analyzed entirely in terms of its varying phenomenal properties. Third, the paper addresses the utility of continued reference to pain and its phenomenal properties in philosophical and scientific discourses. It is argued that numerous insights into the phenomenal structure of pain can be gained that have thus far received insufficient attention.

Why is pain bad? The most straightforward theory of pain's badness,dolorism, appeals to the phenomenal quality of displeasure. In spite of its explanatory appeal, the view is too straightforward to capture two central puzzles, namely pain that is enjoyed and pain that is not painful (e.g. pain asymbolia). These cases can be captured byconditionalism, which makes the badness of displeasure conditional on an agent's attitude. But conditionalism fails where dolorism succeeds with explanatory appeal. A new approach is proposed,reverse conditionalism, which maintains the explanatory appeal of dolorism, but gives attitudes a value-defeating role. It is argued that this view does best in fulfilling the desiderata and capturing the cases.

Frederique de Vignemont argues on the basis of several empirical counterexamples that Bain and Klein are wrong about the relationship between pain and bodily care. I argue that the force of the putative counterexamples is weak. Properly understood, the association between pain and care is preserved in a way that is consistent with both de Vignemont's own views and the empirical facts.

Pain asymbolics feel pain, but act as if they are indifferent to it. Nikola Grahek argues that such patients present a clear counterexample to motivationalism about pain. I argue that Grahek has mischaracterized pain asymbolia. Properly understood, asymbolics have lost a general capacity to care about their bodily integrity. Asymbolics� indifference to pain thus does not show something about the intrinsic nature of pain; it shows something about the relationship between pains and subjects, and how that relationship might break down. I explore the consequences of such a view for both motivationalism and the categorization of pain asymbolia as a syndrome, arguing for a close link between asymbolia and various forms of depersonalization.

Sometimes the philosophical armchair gets bumped by empirical facts. So it is when thinking about pain. For good or ill (good, actually, as we shall see) most of us are intimately acquainted with physical pain, the kind you feel when you stand on a nail or burn your hand. And, from the armchair, it can seem blindingly obvious that pain is essentially unpleasant. There are of course unpleasant experiences that aren’t pains – nausea or itches, for example – but surely there aren’t pains that don’t hurt, pains that are neutral or even pleasurable rather than unpleasant. Surely, indeed, there couldn’t be. For it is part of the very concept of a pain that a pain be unpleasant. Or so it has seemed to many. Yet over recent decades philosophers’ confidence in these putative truisms has been shaken by some fascinating cases from the clinic, the lab, and life.

Pain asymbolia is a rare condition caused by brain damage, usually in adulthood. Asymbolics feel pain but appear indifferent to it, and indifferent also to visual and verbal threats. How should we make sense of this? Nikola Grahek thinks asymbolics’ pains are abnormal, lacking a component that make normal pains unpleasant and motivating. Colin Klein thinks that what is abnormal is not asymbolics’ pains, but asymbolics: they have a psychological deficit making them unresponsive to unpleasant pain. I argue that an illuminating account requires elements of both views. Asymbolic pains are indeed abnormal, but they are abnormal because asymbolics are. I agree with Klein that asymbolics are incapable of caring about their bodily integrity; but I argue against him that, if this is to explain not only their indifference to visual and verbal threat, but also their indifference to pain, we must do the following: (i) take asymbolics’ lack of bodily care not as an alternative to, but as an explanation of their pains’ missing a component, and (ii) claim that the missing component consists in evaluative content. Asymbolia, I conclude, reveals not only that unpleasant pain is composite, but that its ‘hedomotive component’ is evaluative.

This paper addresses the oldest controversy in the phenomenology of pain, which concerns the intentional nature of pain experience. First, I present the central reasons that underlie the view that originates in Carl Stumpf’s writings, which suggests that pain is a non-intentional feeling-sensation. Second, I present the evidence that underlies the Brentanian perspective, which suggests that pain is an irreducibly intentional experience. Third, I argue that Edmund Husserl’s schema, “apprehension—content of apprehension,” enables one to reconcile these positions. In this regard, I argue that this schema provides the conceptual basis for defending two claims: (1) pain is an irreducibly stratified phenomenon; (2) while some of its strata are non-intentional, others are marked by intentionality. Fourth, with the aim of demonstrating the philosophical significance of this schema in the framework of phenomenological pain research, I open a brief dialogue between phenomenology and cognitive science. I show how this schema can clarify the experiential structures of lobotomized, cingulotomized as well as morphinized patients as well as how it can shed light on such syndromes as threat hypersymbolia, pain asymbolia and congenital analgesia.

It is widely thought that functionalism and the qualia theory are better positioned to accommodate the ‘affective’ aspect (i.e., the hurtfulness) of pain phenomenology than representationalism. In this paper, we attempt to overturn this opinion by raising problems for both functionalism and the qualia theory on this score. With regard to functionalism, we argue that it gets the order of explanation wrong: pain experience gives rise to the effects it does because it hurts, and not the other way around. With regard to the qualia theory, we argue that it fails to capture the sense in which pain's affective phenomenology rationalises various bodily-directed beliefs, desires, and behaviours. Representationalism, in contrast, escapes both of these problems: it gets the order of explanation right and it explains how pain's affective phenomenology can rationalise bodily-directed beliefs, desires, and behaviours. For this reason, we argue that representationalism has a significant advantage in the debates about pain's affective phenomenology. We end the paper by examining objections, including the question of what representationalists should say about so-called ‘disassociation cases’, such as pain asymbolia.

Background: Depersonalization (DP) is characterized by persistent or recurrent episodes of detachment from one’s self with reduced pain perception being a common feature. Alterations in the body schema similar to the cortico-limbic disconnection syndrome of pain asymbolia are suggested to be responsible for DP. In this study we used hypnosis to induce DP in healthy subjects and to examine neural patterns of pain perception in the state of DP by means of functional magnetic resonance imaging (fMRI). Methods: Pain perception was investigated in 7 healthy subjects with high susceptibility to hypnosis in three different mental states: waking state (N-W), hypnotic relaxation (H-R) and hypnotic DP (H-DP). Pain was induced with electrical stimulation to the median nerve at the right wrist. fMRI measurements were performed during all states. Results: Nociceptive stimuli led to an activation of the well described pain network including somatosensory and insular regions and the cerebellum. Activation was markedly reduced in the contralateral somatosensory cortex, parietal cortex (Brodmann area 40, BA40), prefrontal cortex (BA9), putamen and the ipsilateral amygdala during H-DP. Subjects also reported a significant decrease in pain intensity from N-W to H-DP. Conclusion: Pain response during H-DP was reduced in sensory and affective pain-related areas, reflecting the diminished intensity of the perceived pain. Moreover, a network of cortical and subcortical areas that have been implicated in the perception of the own body was less responsive during DP, which might point to a specific neural mechanism underlying the ‘out-of-body’ experience. Although the small number of subjects does not allow a generalization of our findings, H-DP seems to be a promising tool for the investigation of psychological and biological mechanisms of self-inflicted injuries as well as the mind-body interplay within the realm of psychosomatic disorders.

Feeling pain is in the same time a sensory and an affective experience. Pain asymbolia and prefrontal lobotomy, two distinct neurological pictures, help to better understand the cerebral basis of the emotional dimension of pain. In pain asymbolia, the selective alteration of the affective dimension of pain is associated with a loss of the sense of threat and danger. Following prefrontal lobotomy, the emotional impact of chronic pain is dramatically reduced, while affective responses to acute pain are paradoxically increased. Such clinical observations allow to make a clear distinction between immediate pain unpleasantness on the one hand, and secondary pain affect, linked to the significance of the pain experience in terms of the self and of the future, on the other hand. Moreover, recent functional neuroimaging data allow to better define the neural substrates of the affective dimension of pain and to highlight the shared neuro-anatomical networks between physical and psychic suffering.

The insular cortex is an important region of brain involved in the processing of pain and emotion. Recent studies indicate that lesions in the insular cortex induce pain asymbolia and reverse neuropathic pain. Endogenous cannabinoids (endocannabinoids), which have been shown to attenuate pain, are simultaneously degraded by fatty acid amide hydrolase (FAAH) that halts the mechanisms of action. Selective inhibitor URB597 suppresses FAAH activity by conserving endocannabinoids, which reduces pain. The present study examined the analgesic effects of URB597 treatment in the insular cortex of an animal model of neuropathic pain. Under pentobarbital anesthesia, male Sprague–Dawley rats were subjected to nerve injury and cannula implantation. On postoperative day 14, rodents received microinjection of URB597 into the insular cortex. In order to verify the analgesic mechanisms of URB597, cannabinoid 1 receptor (CB1R) antagonist AM251, peroxisome proliferator-activated receptor alpha (PPAR alpha) antagonist GW6471, and transient receptor potential vanilloid 1 (TRPV1) antagonist Iodoresiniferatoxin (I-RTX) were microinjected 15 min prior to URB597 injection. Changes in mechanical allodynia were measured using the von-Frey test. Expressions of CB1R, N-acyl phosphatidylethanolamine phospholipase D (NAPE-PLD), and TRPV1 significantly increased in the neuropathic pain group compared to the sham-operated control group. Mechanical threshold and expression of NAPE-PLD significantly increased in groups treated with 2 nM and 4 nM URB597 compared with the vehicle-injected group. Blockages of CB1R and PPAR alpha diminished the analgesic effects of URB597. Inhibition of TRPV1 did not effectively reduce the effects of URB597 but attenuated expression of NAPE-PLD compared with the URB597-injected group. In addition, optical imaging demonstrated that neuronal activity of the insular cortex was reduced following URB597 treatment. Our results suggest that microinjection of FAAH inhibitor into the insular cortex causes analgesic effects by decreasing neural excitability and increasing signals related to the endogenous cannabinoid pathway in the insular cortex.

Pain is unpleasant. It is something that one avoids as much as possible. One might then claim that one wants to avoid pain because one cares about one's body. On this view, individuals who do not experience pain as unpleasant and to be avoided, like patients with pain asymbolia, do not care about their body. This conception of pain has been recently defended by Bain [2014] and Klein [forthcoming]. In their view, one needs to care about one's body for pain to have motivational force. But does one need to care about one's body qua one's own? Or does one merely need to care about the body that happens to be one's own? In this paper, I will consider various interpretations of the notion of bodily care, in light of a series of pathological cases in which patients report pain in a body part that they do not experience as their own. These cases are problematic if one adopts a first-personal interpretation of bodily care, according to which pain requires one to care about what is represented as one's own body. Th...

The argument from moral psychology is one of the strongest arguments that non-cognitivists use against cognitivism-the metaethical position according to which our moral judgements express beliefs. According to this argument, once we put together the Humean theory of motivation and motivational internalism, we yield the conclusion that cognitivism cannot represent the correct view about the semantic function of moral discourse. I will first attempt to show that a neurological syndrome, called pain asymbolia (a rare condition caused by lesions to the posterior insula that produces complete, thoroughgoing indifference to pain), can be used in order to formulate a persuasive defence of the Humean theory of motivation. After that, I will consider motivational internalism and argue that, without additional empirical evidence, neither internalism nor externalism can provide a plausible explanation of the connection between moral judgements and motivation. In conclusion, I intend to defend the claim that, until more persuasive arguments in favour of internalism are presented, non-cognitivists should not rely on the argument from moral psychology in their attempts to refute cognitivism.

Words such as ‘consciousness’ and ‘self’ actually encompass a number of distinct phenomena that are loosely lumped together. The study of neurological syndromes allows us to explore the neural mechanisms that might underlie different aspects of self, such as body image and emotional responses to sensory stimuli, and perhaps even laughter and humour. Mapping the ‘functional logic’ of the many different attributes of human nature on to specific neural circuits in the brain offers the best hope of understanding how the activity of neurons gives rise to conscious experience. We consider three neurological syndromes (phantom limbs, Capgras delusion and pain asymbolia) to illustrate this idea.

We describe the behavioral and neuroanatomical features of asymbolia for pain occurring in 6 patients following unilateral hemispheric damage secondary to ischemic lesions in 5 and traumatic hematoma in 1. In the absence of primary sensory deficits, these 6 patients showed a lack of withdrawal and absent or inadequate emotional responses to painful stimuli applied over the entire body, as well as to threatening gestures. Five patients also failed to react to verbal menaces. Patients appeared unconcerned about the defect and seemed unable to learn appropriate escape or protective responses. Common associated abnormalities were rapidly resolving hemiparesis, cortical-type sensory loss, unilateral neglect, and body-schema disorders. Neuroradiological examination disclosed left hemispheric lesions in 4 patients and right hemispheric involvement in 2. Although lesion extension differed, the insular cortex was invariably damaged in all 6 patients. These findings suggest that insular damage may play a critical role in the development of the syndrome by interrupting connections between sensory cortices and the limbic system.