Neuroscience of Pain, Stress, and Emotion

Psychological and Clinical Implications

Magne Arve Flaten, Mustafa al'Absi

• Publisher: Academic Press
• Year: 2015
• Print ISBN: 9780128005385
• eBook ISBN: 9780128006665
• Topic: Psychology
• Subtopic: Cognitive Psychology & Cognition
• Index: Psychology

Neuroscience of Pain, Stress, and Emotion: Psychological and Clinical Implications presents updated research on stress, pain, and emotion, all key research areas within both basic and clinical neuroscience. Improved research understanding of their interaction is ultimately necessary if clinicians and those working in the field of psychosomatic medicine are to alleviate patient suffering.This volume offers broad coverage of that interaction, with chapters written by major researchers in the field. After reviewing the neuroscience of pain and stress, the contents go on to address the interaction between stress and chronic/acute pain, the role of different emotions in pain, neurobiological mechanisms mediating these various interactions, individual differences in both stress and pain, the role of patient expectations during treatment (placebo and nocebo responses), and how those relate to stress modulation.While there are books on the market which discuss pain, stress, and emotion separately, this volume is the first to tackle their nexus, thus appealing to both researchers and clinicians.- Represents the only comprehensive reference detailing the link between pain, stress and emotion, covering the neuroscientific underpinnings, related psychological processes, and clinical implications- Compiles, in one place, research which promises to improve the methodology of clinical trials and the use of knowledge of pain-stress-emotion effects in order to reduce patients' suffering- Provides comprehensive chapters authored by global leaders in the field, the broadest, most expert coverage available

Part 1

Introduction and Background on Pain and Stress

Outline

Chapter 1. Neuroscience of Pain and Emotion

Chapter 2. The Neurobiology of Stress

Chapter 3. Emotional Modulation of Pain

Chapter 4. Sex Differences in Pain and Stress

Chapter 1

Neuroscience of Pain and Emotion

Matthias J. Wieser, and Paul Pauli Department of Psychology, Biological Psychology, Clinical Psychology and Psychotherapy, University of Würzburg, Würzburg, Germany

Abstract

In this chapter, we summarize the neurocognitive processes underlying acute pain and the impact of emotions on these processes. First, we briefly introduce the neural substrates of nociception and pain, as well as emotions, and potential shared networks. Then, we focus on the emotional modulation of experimentally induced acute pain by affective visual stimuli, both affective scenes and emotional faces. Thus we review literature investigating the influence of emotions on subjective, peripheral, and cerebral correlates of pain perception. A special section thereby deals with the effect of facial expressions of pain perception and on the mutual influences. Overall, a viewpoint emerges that emotions can exert their effects at multiple levels of pain processing (supraspinal and spinal). However, it also becomes clear that pain reversely influences emotion perception, although future research needs to probe the effects of pain at various levels of emotion processing by using different psychophysiological methods. Furthermore, the emotion–pain interactions and their neural substrates, which potentially are characterized by multiple feedback mechanisms, still need to be clarified more precisely.

Keywords

Affective picture stimuli; Emotion; Emotion networks; Emotion–paininteraction; Emotional faces; Neurological pain signature; Nociception; Pain; Pain faces; Pain networks

Neuroanatomy of Pain and Emotion

The International Association for the Study of Pain defines pain as an “unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (International Association for the Study of Pain, 1994, pp. 209–214). This definition implies that pain and nociception have to be differentiated, with the latter referring to the physiological processes triggered by tissue damage. Although nociception normally results in pain, this is not mandatory, and vice versa, pain may be experienced without nociception. This definition also clarifies that negative emotions are a constituent of the pain experience, and therefore a close interaction or overlap between brain processes related to pain and emotions has to be expected. As a matter of fact, it may be argued that pain is an emotion, an emotion that requires the presence of a bodily sensation with qualities like those reported during tissue-damaging stimulation (Price, 1999).

The pain–emotion interaction is also emphasized by the fact that both pain and emotions are adaptive responses to survival-relevant challenges in the environment. Whereas pain's main functional significance is to alert the organism that its body integrity is threatened in order to attend to the source of pain and possibly avoid it, emotion's functional significance lies in the detection of motivationally relevant stimuli that may trigger avoidance or approach behavior. Both pain and emotions thus have an adaptive value that ensures the survival of the organism.

Nociceptive Pathways

Human nociception is the process of encoding specific somatosensory information in the periphery and its transduction to the brain. Nociceptors are peripheral neurons that respond to noxious stimulation and detect potentially damaging stimuli (Basbaum & Jessell, 2000). Nociceptors can be specific to a particular type of stimulus (e.g., mechanical, chemical, or temperature) or can respond to a variety of noxious stimulations. The latter nociceptive neurons are referred to as polymodal nociceptors and are more abundant in the human body in comparison to the stimulation-specific nociceptors (Ringkamp & Meyer, 2008). The nociceptive signal is transduced to the central nervous system (CNS) by two main types of nociceptive fibers constituting the starting point of the nociceptive signal cascade and found throughout the body tissue: the thinly myelinated Aδ neurons, which transmit information about acute and localized pain at fast conduction speed, and the unmyelinated C fibers, which signal more widespread pain with slower conduction speeds (Campbell & Meyer, 2006).

After nociceptive stimulation, the Aδ and C fibers transmit the nociceptive signals to the CNS. The peripheral Aδ and C fibers terminate in the dorsal horn of the spinal cord. In turn, second-order neurons are activated, and the axons of these neurons cross the midline of the spinal cord directly to the ventral surface of the spinal cord. Ascending pain signals are then sent to the brain via the spinothalamic tract, whose fibers project to the intralaminar and ventroposterior nuclei of the thalamus (Ringkamp & Meyer, 2008). Then two supraspinal neuronal systems can be differentiated with regard to their primary role within the processing of nociceptive information: the lateral system, mainly encoding sensory discriminative components of pain, and the medial system encoding the affective, motivational component of the resulting pain percept (Apkarian, 2013; Price, 2000).

It is important to note that these ascending nociceptive pathways can be modulated by descending pathways starting in the brain. These mainly alter the transmission of nociceptive inputs at the spinal dorsal horn (Kwon, Altin, Duenas, & Alev, 2014). The periaqueductal gray (PAG) and the rostroventral medulla (RVM) are two regions known to play a role in the endogenous control of pain via the inhibitory PAG–RVM–dorsal horn pathway (Fields & Basbaum, 1994). Receiving inputs from frontal and insular cortices, hypothalamus, and amygdala, the PAG has a critical role in the descending modulation of pain by interacting with the RVM and the dorsolateral pontine tegmentum (Fields & Basbaum, 1994). The PAG, parabrachial nucleus, and nucleus tractus solitaries provide input to the RVM, which has direct connections to the laminae of the dorsal horn (Millan, 1999, 2002).

Central Representation of Pain

In the brain, pain is represented in neuronal networks that encompass a number of subcortical and cortical structures that code various aspects of pain (Apkarian, Bushnell, Treede, & Zubieta, 2005; Peyron, Laurent, & Garcia-Larrea, 2000). Functional imaging studies most consistently revealed the following main brain areas constituting the brain network for acute pain (see Figure 1): primary and secondary somatosensory cortices, insular cortex (INS), anterior cingulate cortex (ACC), prefrontal cortex (PFC), and thalamus (Th) (Apkarian et al., 2005; Price, 2000). The somatosensory cortex receives input from the lateral nuclei of the Th, whereas the ACC receives input mainly from the medial portions of the Th via the INS and further provides the PFC with nociceptive information. The cerebellum receives direct input from the spinothalamic tract and is one of the subcortical pain-coding structures together with the caudate putamen, amygdala, and PAG. Accordingly, sensory and discriminatory aspects of pain are encoded in somatosensory, lateral thalamic, and cerebellar portions of the brain, whereas affective and cognitive components of pain are represented dominantly in the cingulate, insular, and prefrontal areas (Apkarian et al., 2005; Bushnell, Čeko, & Low, 2013).

Figure 1 The brain network for acute pain. ACC, anterior cingulate cortex; AMY, amygdala; BG, basal ganglia; PAG, periaqueductal gray; PB, parabrachial nucleus; PFC, prefrontal cortex; S1 and S2, primary and secondary somatosensory cortices. Adapted from Bushnell et al. (2013).

This network, which has been referred to as the “pain matrix” (e.g., Tracey & Mantyh, 2007) and was inspired by the so-called neuromatrix of pain (Melzack, 1999, 2001), proposes a specific neuroanatomical representation of pain (as mentioned above). However, this concept has been challenged with regard to its pain specificity (Iannetti & Mouraux, 2010; Legrain, Iannetti, Plaghki, & Mouraux, 2011), concluding that various somatosensory and emotional states have common neural representations. Yet, a series of functional magnetic resonance imaging (fMRI) studies encompassing a large data set (more than 100 participants) and incorporating various experimental pain approaches revealed activity in the ventrolateral Th, S2, and dorsal posterior INS to be specific for pain and distinguishable from other salient events such as social rejection. These findings identified—at least to some degree—a brain signature that specifically corresponds to the sensory and affective representation of pain (Wager et al., 2013).

Given the unbeatable time resolution of electroencephalography (EEG) and magnetoencephalography (MEG), it is no surprise that studies employing these techniques were able to disentangle the dual pain sensation that is typically elicited by a single brief painful stimulus and which is based on the difference of about 1 sec in conduction times of Aδ and C fibers (see above). These studies found two sequential brain activations in EEG and MEG recordings from S1 versus S2 and ACC (e.g., Bromm & Treede, 1987; Iannetti, Zambreanu, Cruccu, & Tracey, 2005; Ploner, Gross, Timmermann, & Schnitzler, 2002; Ploner, Holthusen, Noetges, & Schnitzler, 2002; Timmermann et al., 2001;...

Table of contents

• Cover image
• Title page
• Table of Contents
• Copyright
• Contributors
• Foreword
• Part 1. Introduction and Background on Pain and Stress
• Part 2. Psychological Processes Related to Pain and Stress
• Part 3. Clinical Implications
• Index