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Evolution of mechanisms and behaviour important for pain

Scientific meeting

Location

Kavli Royal Society Centre, Chicheley Hall, Newport Pagnell, Buckinghamshire, MK16 9JJ

Overview

Theo Murphy international scientific meeting organised by Dr Amanda Williams and Professor Edgar Terry Walters.

Image: layer 5 pyramidal neurons in the infralimbic prefrontal cortex of mice with neuropathic pain. Credit: Stephanie Shiers

This meeting will be the first to convene scientists from diverse fields studying mechanisms and behaviour important for pain together with experts in evolutionary medicine. The goals are to encourage the application of an evolutionary perspective to pain research, to identify pain-related questions having important evolutionary considerations, and to highlight advances in our understanding of the evolution of pain.

More information on the schedule of talks will be available soon. Recorded audio of the presentations will be available on this page after the meeting has taken place. Meeting papers will be published in a future issue of Philosophical Transactions B.

Poster session

There will be a poster session at 16:20 on Monday 11 February. If you would like to apply to present a poster please submit your proposed title, abstract (not more than 200 words and in third person), author list, name of the proposed presenter and institution to the Scientific Programmes team no later than Friday 11 January 2018. Please note that places are limited and posters are selected at the scientific organiser's discretion. Poster abstracts will only be considered if the presenter is registered to attend the meeting.

Attending this event

This is a residential conference, which allows for greater discussion and networking.

  • Free to attend
  • Advance registration essential
  • Catering and accommodation available to purchase during registration

Enquiries: contact the Scientific Programmes team.

Event organisers

Select an organiser for more information

Schedule of talks

11 February

09:00-12:30

Session 1: Evolutionary context of injury, illness and pain

5 talks Show detail Hide detail

Chairs

Dr Amanda Williams, University College London, UK

09:00-09:05 Welcome by the Royal Society and lead organiser

09:05-09:30 Evolutionary medicine and pain

Dr Randolph Nesse, Arizona State University, USA

Abstract

Evolutionary medicine has encouraged recognising the utility of aversive responses, distinguishing them carefully from diseases, and using the smoke detector principle to understand normal but unnecessarily aversive responses. In recent years, recognition has also been growing that natural selection has shaped mechanisms that adjust defensive responses as a function of experience. Repeated elicitation of a defensive response often indicates that prior responses have been inadequate to provide protection or that the environment is extremely dangerous; in such situations, the utility of more rapid or intense responses can shape mechanisms that adjust thresholds and response strength. However, such mechanisms are intrinsically prone to dysregulation from positive feedback, offering a possible evolutionary explanation for vulnerability to chronic pain. Evolutionary thinking has also increasingly considered connections between physical pain and mental pain. They share common phylogenetic origins, functions, regulation mechanisms, and vulnerability to dysregulation. Both evolve to subtypes for coping with different kinds of situations. For physical pain the situations are different kinds of tissue damage. For mental pain, the relevant situations are social dangers, losses, and efforts in pursuit of unreachable goals. Further exploration of these connections offers major opportunities for understanding the utility of low mood and anxiety, and their pathological counterparts in depression and anxiety disorders. This perspective also has implications for prevention and treatment, especially in light of the shared neural modulators and pathways that regulate physical and mental pain.

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09:30-09:40 Discussion

09:40-10:05 Adaptive mechanisms contributing to maladaptive pain

Professor Edgar Terry Walters, University of Texas Health Science Center, USA

Abstract

Because chronic pain is maladaptive for patients, pain researchers often assume that its underlying mechanisms are mainly pathological. For example, chronic neuropathic pain has been attributed to death of inhibitory interneurons, to aberrant re-expression in pain pathways of Na+ channels that normally function embryonically, and to "ectopic" generation of action potentials in the cell bodies of primary nociceptors. However, some forms of clinically maladaptive pain might result from evolutionarily adaptive responses. This might occur, for example, after traumatic injury severe enough to leave damaged tissue chronically weakened and without adequate sensory reinnervation. Continuing protective attention to a severely injured region (eg, post-amputation pain) may be achieved by persistently increased responsiveness of surviving sensory neurons and by spontaneous activity in intact and axotomized nociceptors representing that region. In several phyla, peripheral injury induces persistent nociceptor hyperexcitability and behavioral hypersensitivity. Experimentally preventing nociceptive sensitization (and nociceptor hyperactivity) induced by peripheral injury has been shown to decrease survival of squid during attacks by predators. In mammals, painful consequences of both peripheral and central neural injury result from induction of persistent nociceptor hyperactivity. Mechanisms underlying persistent hyperactive states in nociceptors that can drive clinically maladaptive pain under various conditions may have been selected during evolution to enhance survival after severe traumatic injury.

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10:05-10:15 Discussion

10:15-10:40 Immune activation influences nociception in the caterpillar Manduca sexta: An evolutionary perspective on its functional significance

Dr Shelley Adamo, Dalhousie University, Canada

Abstract

Attacks by predators or pathogens are fitness-reducing events. Selection will favour animals that can reconfigure their physiology to mitigate the present threat and reduce future losses. For example, a mock predator attack activates nociceptors and leads to a reconfiguration of the immune system in the caterpillar Manduca sexta. These changes appear to enhance wound protection. Similarly, activation of an immune response alters nociceptor sensitivity. As in vertebrates, this enhancement occurs in response to systemic infection (injection of heat-killed pathogens into the hemolymph), local infections (small amounts of heat-killed pathogens injected locally), and to gut immune reactions (produced by feeding heat-killed bacteria to caterpillars). Exposure of caterpillars to heat-killed pathogens induces expression of plasmatocyte spreading peptide (PSP, an insect cytokine), in caterpillar fat body. PSP injected locally into the caterpillar’s head capsule also results in increased nociceptor sensitivity in the abdomen, as well as inducing other aspects of sickness behaviour such as illness-induced anorexia. Changes in nociception may be part of the sickness behaviour syndrome, reducing the risk of further exposure to potential pathogens.

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10:40-10:50 Discussion

10:50-11:20 Coffee

11:20-11:45 Immune responses and pain in mammals

Dr Stephen McMahon, King’s College London, UK

Abstract

What is the purpose of pain? A standard answer is that it serves a protective function to alert an organism to potential or actual damage. A standard example is the effect of touching a dangerously hot object which activates peripheral nociceptors, that in turn can drive flexion reflexes. These reactions are essentially all neuronal and pain has become associated with purely neuronal phenomena. But there are other recognised functions of pain. One is to promote recovery and repair after injury and a standard example here is the prolonged reduced motility and rest associated with, say, a broken leg. Another recognised function of pain is promoting learning about the dangers of the world and this too often takes place over a prolonged time course. It is now clear that these prolonged pain states are inevitably associated with the recruitment of another defence system of the body – and that is the immune system. There are almost no circumstances where repetitive and maintained activation of the nociceptive system does not also lead to activation of the innate or adaptive immune system. There is growing evidence, which will be reviewed in this lecture, that these two systems do not operate independently but are closely co-ordinated in their actions. Thus, there is ample evidence that a major activator of the nociceptive system is the immune system and we have many example of immune mediators acting as pain mediators (eg NGF). Some of these mediators are closely associated with reparative functions. For instance, there is growing evidence that the fatigue associated with many chronic pain states is driven by immune factors like IL6 acting on the nervous system. Perhaps more surprisingly, there is also a growing body of evidence that the sensitivity of the immune system is also regulated by activity in the nervous system, sometimes with dramatic functional consequences. These too will be reviewed in this lecture.

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11:45-11:55 Discussion

11:55-12:20 Biology of nociception and pain in fish

Dr Lynne Sneddon, University of Liverpool, UK

Abstract

In order to survive animals must avoid injury and be able to detect potentially damaging stimuli via nociceptive mechanisms. If the injury was accompanied by a negative affective component future behaviour should be altered and one can conclude the animal experienced the discomfort associated with pain. Fishes are the most successful vertebrate group when considering the number of species that have filled a variety of aquatic niches. The empirical evidence for nociception in fishes shall be discussed from the underlying molecular biology, neurobiology and anatomy of nociceptors through to whole animal behavioural responses to demonstrate the evolutionary conservancy of nociception and pain. Studies in fish have shown that the biology of the nociceptive system is strikingly similar to that found in mammals. Further, potentially painful events result in behavioural and physiological changes such as reduced activity, guarding behaviour, suspension of normal behaviour, increased ventilation rate and abnormal behaviours that are all prevented by the use of pain-relieving drugs. Fish also perform other tasks less well when painfully treated and are willing to pay a cost to accessing pain-relief. Therefore, there is ample evidence to demonstrate that it is highly likely that fish experience pain which has important implications for the treatment of fish in a variety of contexts.

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12:30-13:30

Lunch

13:30-17:00

Session 2: Conserved and convergent nociceptive mechanisms found in invertebrates

4 talks Show detail Hide detail

Chairs

Professor Edgar Terry Walters, University of Texas Health Science Center, USA

13:30-13:55 Fitness effects of nociception sensitization in cephalopods

Dr Robyn Crook, San Francisco State University, USA

Abstract

Sublethal injury triggers long-lasting sensitization of defensive responses in many species, suggesting that powerful evolutionary selection pressures have driven this widespread pattern. In humans, persistent nociceptive sensitization is often accompanied by heightened sensations of pain and anxiety. While considerable experimental and clinical evidence supports the adaptive value of immediate nociception during injury, identifying the function of long-lasting sensitization after injury in mammalian models has been challenging. Cephalopod molluscs have the largest and most complex brains of all the invertebrates, and are promising comparative models of neurobiology and behavior. Previous work has shown that cephalopods express short- and long-term behavioral and neural sensitization after minor injury, expressed as decreased response thresholds and escalated defensive behaviors. In recent experiments that place injured cephalopods into naturalistic experimental settings with predators, those that expressed nociceptive sensitization after injury survived predatory encounters at higher rates that those for which nociceptive sensitization was blocked. Ongoing studies examining adaptive functions for nociceptive sensitization are focusing on foraging, cognition and mate choice, to identify fitness benefits that extend both across behavioral domains and across the lifetime of the injured animal.

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13:55-14:05 Discussion

14:05-14:30 Using annelids to understand synaptic plasticity in nociceptive circuits

Professor Brian D Burrell, University of South Dakota, USA

Abstract

In the medicinal leech, Hirudo verbana, it is possible to identify and record from polymodal and mechanical nociceptors, non-nociceptive touch- and pressure-sensitive neurons, and many of the postsynaptic neurons these afferents target. This makes Hirudo a useful species for studying synaptic modulation within nociceptive circuits and the functional relevance of such neuromodulation at the behavioral level. In this presentation, I will discuss three examples of synaptic plasticity and their potential behavioral significance not just to Hirudo, but to animals in general. First, we have shown that repetitive stimulation of non-nociceptive afferents elicits persistent depression in nociceptive synapses that is endocannabinoid-dependent. This endocannabinoid-mediated mechanism may provide an alternative explanation for how repetitive, non-painful stimulation can have persistent anti-nociceptive effects. Second, we have found that noxious stimuli potentiates non-nociceptive synapses via a mechanism that is also endocannabinoid-dependent and involves a disinhibitory mechanism. This contributes to understanding how endocannabinoids can have both pro- and anti-nociceptive effects. Finally, we have observed a potential interaction between NMDA receptor mediated long-term potentiation in nociceptive synapses and endocannabinoid-mediated depression that points to crosstalk between pro- and anti-nociceptive modulatory mechanisms. Together these studies demonstrate the strength of using comparative approaches to understand nociceptive mechanism from the cellular to behavioral level.

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14:30-14:40 Discussion

14:40-15:10 Tea

15:10-15:35 Loss of Central Inhibition Leads to Neuropathic Pain in Drosophila

Dr Greg Neely, University of Sydney, Australia

Abstract

Nerve injury can lead to devastating pain that is difficult to treat, in part because we have an incomplete understanding of the biology driving disease. To identify core disease mechanisms we investigated neuropathic pain in Drosophila. We show that peripheral injury triggers a loss of central inhibition which was necessary and sufficient to develop neuropathic sensitization. Similar changes in central inhibitory tone have been described in mammalian pain and this may represent a core disease pathology that is amenable to therapy. To this end, we generated inhibitory neurons derived from human induced pluripotent stem cells (hiPSC) and transplanted these neurons into the spinal cord of neuropathic mice. Remarkably, hiPSC-derived inhibitory transplants survive long-term, show integration, and promoted lasting pain relief without side effects. Together, these data highlight that central disinhibition is a core mechanism driving neuropathic pain, and argue that hiPSC-derived transplants may be an effective and non-addictive pain therapy.

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15:35-15:45 Discussion

15:45-16:10 Conserved nociceptive sensitization mechanisms in insects and mammals

Dr Michael Galko, University of Texas MDAnderson Cancer Center, USA

Abstract

The Galko laboratory is interested in how tissue damage and other stimuli sensitize peripheral nociceptors. Historically, this topic has been studied in vertebrate systems. The approach of this laboratory is to use the genetically tractable model organism, Drosophila melanogaster (a fruit fly) to interrogate the molecular/genetic basis of injury-induced changes in nociceptive responsiveness. To do this they combine tissue damage assays with behavioral tests of nociceptive responsiveness. An overview of the lab’s work identifying conserved signaling pathways that are required for acute injury-induced thermal nociceptive sensitization will be presented. Ongoing efforts to establish nociception assays for all sensory modalities (heat, cold, touch, chemical) will be reviewed. A goal of having assays for all sensory modalities is so that one can fully understand how different types of injury (UV irradiation, physical wounding), disease states (diabetes or cancer) and disease treatment (chemotherapy) impact the ability of an animal to perceive and properly respond to noxious stimuli. Progress recently identifying signaling pathways (insulin signaling) that regulate the duration or persistence of nociceptive sensitization will be presented as will data connecting this finding to the etiology of nociceptive sensory changes that accompany diabetes. Finally, recent progress using mouse genetics approaches to test whether some of the conserved pathways identified in flies act in similar ways during nociceptive sensitization in vertebrates will be covered.

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16:10-16:20 Discussion

16:20-17:00 Poster session

12 February

09:00-12:30

Session 3: Evolutionary perspectives on pain-related mechanisms in mammals

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Chairs

Dr Stephen McMahon, King’s College London, UK

09:00-09:05 Welcome by chair

09:05-09:30 Evolutionary adaptations of nociceptors in mammals

Dr Ewan St John Smith, University of Cambridge, UK

Abstract

Utilising comparative biology, single-cell transcriptome analysis, human tissue and the study of variation in human nociception, the Smith lab and collaborators have identified a variety of evolutionary adaptations in mammalian nociceptors. Unusually among animals, it was found that naked mole-rats lacked a behavioural response to capsaicin or acid, even though receptors for detecting both substances are expressed by naked mole-rat nociceptors. However, an absence of nociceptor neuropeptides alongside altered spinal cord connectivity underpins the capsaicin insensitivity, whereas acid-insensitivity largely results from an amino acid variation in the voltage-gated sodium channel 1.7 such that acid switches it off. It was further demonstrated that naked mole-rats lack nerve-growth factor (NGF) induced hyperalgesia due to hypofunctionality of the NGF receptor TrkA. Using transcriptomic analysis of identified sensory neurones in mice, the Smith lab have recently discovered sensory neurone subsets that have likely evolved for specific functional purposes, ie subsets subserving pain and subsets mediating mechanosensation, using human tissue to validate findings. In further studies, altered pain phenotypes have been identified in humans and tracked back to changes in ion channel function, demonstrating a shared sensory pathway in mice. Overall, this research highlights a variety of evolutionary adaptations in mammalian nociceptors across species.

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09:30-09:40 Discussion

09:40-10:05 Primitive and recently evolved mechanisms driving persistent pain in mammals

Dr Theodore Price, University of Texas, USA

Abstract

Damaging stimuli change the excitability of nociceptors in species where experiments have been conducted to examine such changes. In many cases this plasticity, which leads to a lowering of action potential threshold and increased excitability upon depolarization, is long-lasting, outliving the duration of the plasticity-inducing stimulus. This plasticity also sometimes leads to the development of spontaneous activity in nociceptors, which is believed to be a key driver of chronic pain. Dr Price will argue that this form of intrinsic neuronal plasticity is ancient, perhaps the first form of neuronal plasticity, and is critically dependent on changes in gene expression within the sensitized neuron. Interestingly, this plasticity is not dependent on transcription but is reliant on translation and the existing evidence strongly supports the conclusion that the signaling mechanism is conserved across evolution. In Aplysia, mice, rats, and humans, persistent nociceptor plasticity requires activation of the mechanistic target of rapamycin (mTOR) and mitogen activated protein kinase (MAPK) pathways. Emerging evidence suggests that this translational event may be mediated by a single phosphorylation event at a site on a protein that binds the 5’ cap structure of mRNAs called eukaryotic translation initiation factor 4E (eIF4E) in vertebrates and invertebrates. Despite the striking conservation of this signaling event, translational events that occur downstream of eIF4E are likely divergent across species and point to the importance of degeneracy in signaling in nociceptor plasticity. This degeneracy is likely to be a key challenge in developing chronic pain medicines that can target this form of sensitization.

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10:05-10:15 Discussion

10:15-10:40 Epigenetics and mechanisms of chronic pain

Dr Sandrine Géranton, University College London, UK

Abstract

Two factors influence animal behaviors: the genes we inherit and environmental experiences. For example, in both rats and humans, stressful early life events such as being reared by an inattentive mother can leave a lasting trace and affect stress response in adult life. This is due to a chemical trace left on the chromatin, the combination of DNA and proteins that make up chromosomes. This trace has been attributed to so called epigenetic mechanisms and can have long-term consequences of the functioning of our genes. In other words, epigenetic processes provide a bridge between the genes and the environment by imprinting experiences such as social interactions onto the genome, thereby allowing individuals to adapt to their environment within their lifetime.

This talk will focus on the role of the stress axis in the development of persistent pain and will describe how past experience, such as injury, can be imprinted onto our chromatin by epigenetic mechanisms and could therefore be a major determinant not only of the pain experience but also, perhaps, of the susceptibility to chronic pain. Dr Géranton will also discuss the likelihood that these epigenetic mechanisms are evolutionarily conserved across phyla, like other sensization mechanisms that drive long-lasting pain states. Finally, the possibility that epigenetic effects of stress can be transmitted across generations and therefore might modulate the pain experience across generations will be debated with the audience.

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10:40-10:50 Discussion

10:50-11:20 Coffee

11:20-11:45 Emotional and cognitive processes related to chronic pain in mammals revealed by brain imaging

Dr Catherine Bushnell, National Institutes of Health, USA

Abstract

Chronic pain in humans can lead to many co-morbidities, including anxiety, depression and cognitive deficits. On the reverse side, emotional and cognitive factors, including attention and mood state, alter pain perception. Studies in rats, rhesus monkeys and humans show a preservation of the relationship between pain, emotions and cognitions across mammalian species. Almost half of people who experience chronic pain have associated anxiety, depression and/or cognitive changes. We have examined the development of similar co-morbidities in rats and mice and found that after a neuropathic injury causing long-term pain behaviours, the rodents develop memory deficits, anxiety-like behaviour and anhedonia, a cardinal sign of depression. In both rodents and humans, structural changes in brain areas, including in pain-modulatory brain circuitry, develop along with the pain co-morbidities. In humans, descending pain-modulatory circuitry involved in attentional and emotional modulation of pain has been identified using brain imaging methodology. In rhesus monkeys, we have examined the activity of single neurons in afferent pain pathways and shown that nociceptive activity is reduced when the monkey’s attention is diverted away from the noxious stimulus, similar to what is shown in humans using functional MRI. Finally, in both humans and rodents, there is evidence that chronic pain leads to reductions in the availability of opioid receptors within pain-modulatory brain regions. Together, these findings suggest that the brain circuitry underlying pain perception and modulation by psychological factors is preserved across mammalian species.

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11:45-11:55 Discussion

11:55-12:20 Mice are people too: social modulation of and by pain in mice and undergraduates

Dr Jeffrey Mogil, McGill University, Canada

Abstract

Many believe social phenomena such as empathy and helping behaviours to be the sole province of humans. However, evidence of these abilities are starting to be demonstrated in non-human animals, and even in rodents. The speaker will discuss recent experiments in my lab and others' showing the effect of social communication on pain behaviour, and the effect of pain on social interactions. The group have found that mice are capable of empathy (emotional contagion) and apparent helping behaviour, that pain status is communicated by facial expression, and that intriguing mouse-mouse and mouse-human interactions can importantly affect laboratory studies of pain. Many of these phenomena can be translated to human beings in a surprisingly direct manner. The ease of such translation has direct implications for evolutionary theories of pain communication.

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12:20-12:30 Discussion

12:30-13:30

Lunch

13:30-17:00

Session 4: Evolutionary perspectives on cognitive and social aspects of pain

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Chairs

Dr Catherine Bushnell, National Institutes of Health, USA

13:30-13:55 Pain communication behaviour in diverse mammals

Dr Matthew Leach, Newcastle University, UK

Abstract

The considerable scientific debate and inquiry around pain in mammals has predominantly focused on whether they truly experience pain (ie have an emotional reaction) and whether pain can be effectively assessed. However, there remains an often posed but unanswered question: ‘Why do animals exhibit overt signs of pain?’. One hypothesis is that such reactions to pain are a form of social communication that benefits the individual exhibiting pain by recruiting assistance from conspecifics.

The universal applicability of this hypothesis across such a diverse class as mammals is fraught with at least two potential problems. Firstly, it is easy to recognize that this strategy would benefit group-living social species and so be evolutionarily conserved. However solitary species still exhibit overt indices of pain, and it would be reasonable to assume that such traits would not offer an evolutionary advantage, and therefore would not be conserved. Secondly, many animal species are thought to ‘hide’ their pain as a survival enhancing strategy, which is likely to increase the selection of animals that do not exhibit overt signs of pain. This presentation will focus on these problem questions.

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13:55-14:05 Discussion

14:05-14:30 Pain as an evolved sensation to guide action, like any other

Professor Barbara L Finlay, Cornell University, USA

Abstract

Understanding pain as a sensation and motivational state has failed to keep pace with our understanding of more tractable targets like vision, speech perception or the perception and satisfaction of thirst, for reasons neither hard to understand nor blameworthy. Computational, ecological and evolutionary approaches to such subjects currently emphasize the statistical, predictive, and jointly ecological- and species-specific contingencies of every modality. Two examples will be explored. The first, termed the “pain of altruism”, concerns the alteration in primary perception of pain, in an evolutionary time frame, when expressions of pain reliably elicit help in the minimal forms of protection and provisioning, such as humans and our domesticated species experience. The second concerns the contingent and prediction interpretation of complex sensations, and which may span such diverse domains as cosmetic hair removal, “runner’s high”, deep tissue massage and self-harm. Both examples spring from an evolutionary account where the functional role of pain to guide behavior is paramount.

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14:30-14:40 Discussion

14:40-15:10 Tea

15:10-15:35 Clinical aspects of human pain in an evolutionary context

Dr Judith Kappesser, Giessen University, Germany

Abstract

There is little disagreement that acute pain is an essential survival mechanism. Of the varied behaviors by which humans communicate their pain, facial expression plays a predominant role. Evolutionary psychologists propose that all communication systems require rules on whether to transmit information. For pain, it is likely more beneficial to share information with closer cooperators than with potential competitors. This is supported by results of studies showing that the expression of pain is disadvantageous for people being exploited and that people facially express less (or suppress more) pain in the presence of others whom they perceive to be socially threatening. Facial expressions necessarily co-evolve with attention to it and comprehension of its meaning, providing relevant information for the observer. Accordingly, observers were found to recognize facial pain displays above chance. Situations in which patients’ pain has to be estimated could be regarded as social exchange situations in which health care professionals are a source of help for patients in genuine pain. In such situations a cheater detection device may be activated leading to more conservative pain judgements in observers. This is supported by results of several studies showing that the device’s activation affected pain judgements leading to pain underestimation.

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15:35-15:45 Discussion

15:45-16:10 Persistence of pain and pain behaviour in humans and other animals

Dr Amanda Williams, University College London, UK

Abstract

Evolutionary models have been largely overlooked in the study of pain and pain-related behaviours. The widespread view is that acute pain has clear survival value, while chronic pain (outlasting healing) is an inevitable if rare malfunction of acute pain mechanisms. The neurophysiology of acute pain is extraordinarily conserved across animal phyla, and nociception is recognised across invertebrates and vertebrates, although the existence of pain experience is disputed: the emotional component of pain experience, particularly prominent and problematic in humans, is often denied in all but a few mammals.

Chronic pain models exist in laboratory animals, mostly rodents, and chronic pain is observed in farm and companion animals in veterinary medicine. If chronic pain is an inevitable by-product of acute pain, it would be expected in at least some animals that survive acute injury, even if at a very low rate. Survival of acute injury, including breaks to long bones, is evident in various large wild mammals, but behaviour indicating chronic pain is not recorded.

If the development of acute into chronic pain differs according to living conditions - captive versus free - then assumptions about chronic pain need re-examination. This talk will explore several questions: (1) Do demands of survival counteract persistence of acute pain neuroplastic changes? (2) Does anxiety about future pain and disability, or overgeneral learning of cues associated with pain, occur uniquely in humans? (3) Is behaviour communicating pain suppressed where disadvantages outweigh possible benefits?

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16:10-16:20 Discussion

16:20-16:50 General discussion

Dr Amanda Williams, University College London, UK
Professor Edgar Terry Walters, University of Texas Health Science Center, USA

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16:50-17:00 Summary and closing remarks

Evolution of mechanisms and behaviour important for pain

Theo Murphy international scientific meeting organised by Dr Amanda Williams and Professor Edgar Terry Walters

Kavli Royal Society Centre, Chicheley Hall Newport Pagnell Buckinghamshire MK16 9JJ
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