Persistence of pain in humans and other mammals

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Abstract

Evolutionary models of chronic pain are relatively undeveloped, but mainly concern dysregulation of an efficient acute defence, or false alarm. Here, a third possibility, mismatch with the modern environment, is examined. In ancestral human and free-living animal environments, survival needs urge a return to activity during recovery, despite pain, but modern environments allow humans and domesticated animals prolonged inactivity after injury. This review uses the research literature to compare humans and other mammals, who share pain neurophysiology, on risk factors for pain persistence, behaviours associated with pain, and responses of conspecifics to behaviours. The mammal populations studied are mainly laboratory rodents in pain research, and farm and companion animals in veterinary research, with observations of captive and free-living primates. Beyond farm animals and rodent models, there is virtually no evidence of chronic pain in other mammals. Since evidence is sparse, it is hard to conclude that it does not occur, but its apparent absence is compatible with the mismatch hypothesis.

This article is part of the Theo Murphy meeting issue ‘Evolution of mechanisms and behaviour important for pain’.

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Synaptic plasticity in the anterior cingulate cortex in acute and chronic pain.

Tim Bliss, Graham L. Collingridge, Bong-Kiun Kaang … (2016)

The anterior cingulate cortex (ACC) is activated in both acute and chronic pain. In this Review, we discuss increasing evidence from rodent studies that ACC activation contributes to chronic pain states and describe several forms of synaptic plasticity that may underlie this effect. In particular, one form of long-term potentiation (LTP) in the ACC, which is triggered by the activation of NMDA receptors and expressed by an increase in AMPA-receptor function, sustains the affective component of the pain state. Another form of LTP in the ACC, which is triggered by the activation of kainate receptors and expressed by an increase in glutamate release, may contribute to pain-related anxiety.

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Geert Crombez, Christopher Eccleston, Stefaan Van Damme … (2012)

The fear-avoidance (FA) model of chronic pain describes how individuals experiencing acute pain may become trapped into a vicious circle of chronic disability and suffering. We propose to extend the FA model by adopting a motivational perspective on chronic pain and disability. A narrative review. There is ample evidence to support the validity of the FA model as originally formulated. There are, however, some key challenges that call for a next generation of the FA model. First, the FA model has its roots in psychopathology, and investigators will have to find a way to account for findings that do not easily fit within such framework. Second, the FA model needs to address the dynamics and complexities of disability and functional recovery. Third, the FA model should incorporate the idea that pain-related fear and avoidance occurs in a context of multiple and often competing personal goals. To address these 3 key challenges, we argue that the next generation of the FA model needs to more explicitly adopt a motivational perspective, one that is built around the organizing powers of goals and self-regulatory processes. Using this framework, the FA model is recast as capturing the persistent but futile attempts to solve pain-related problems to protect and restore life goals.

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Grooming is a widespread activity throughout the animal kingdom, but in primates (including humans) social grooming, or allo-grooming (the grooming of others), plays a particularly important role in social bonding which, in turn, has a major impact on an individual's lifetime reproductive fitness. New evidence from comparative brain analyses suggests that primates have social relationships of a qualitatively different kind to those found in other animal species, and I suggest that, in primates, social grooming has acquired a new function of supporting these. I review the evidence for a neuropeptide basis for social bonding, and draw attention to the fact that the neuroendrocrine pathways involved are quite unresolved. Despite recent claims for the central importance of oxytocin, there is equally good, but invariably ignored, evidence for a role for endorphins. I suggest that these two neuropeptide families may play different roles in the processes of social bonding in primates and non-primates, and that more experimental work will be needed to tease them apart.