Examining the Neurobiological Overlap Between Social and Physical Pain:
All of us have, at one time or another, experienced negative social events that threaten our sense of social connection: divorce and breakups, exclusion from attractive groups, the deaths of loved ones. Interestingly, our descriptions of these experiences borrow heavily from the language of physical pain. We say, for example, that being left by a romantic partner causes ‘heartache,’ an insult is like a ‘slap in the face,’ and criticism from someone we admire is ‘crushing.’ This linguistic pattern is not peculiar to English;MacDonald and Leary (2005) observed that cultures around the world rely exclusively on physical pain terms to convey the emotional distress of being devalued by other people (i.e., what English speakers refer to as hurt feelings).
Research suggests that the reason these metaphors come so easily to us may be that social pain – the profound distress experienced when social ties are absent, threatened, damaged, or lost – is elaborated by the same neural and neurochemical substrates involved in processing physical pain (Eisenberger, 2012,Eisenberger and Lieberman, 2004, MacDonald and Leary, 2005 and Panksepp, 1998). In other words, social disconnection (and the threat thereof) hurts in a very real way because it recruits some of the same neural mechanisms that respond to physical injury. Here, we explore this proposition by discussing the evolutionary value of social pain, reviewing evidence for the neurochemical and neural overlap between social and physical pain, and exploring some consequences of this overlap.
The Evolution of Social Pain:
Humans are a deeply social species whose most joyful and despondent moments arise from the gratification and frustration of social belongingness needs (Jaremka, Gabriel, & Carvallo, 2011). Our motivation to maintain stable and meaningful social relationships is rooted in evolutionary history (Baumeister & Leary, 1995). For our ancestors, group living was the primary survival tool that facilitated predator defense, hunting, foraging, mating, as well as childrearing (Baumeister and Leary, 1995 and Brewer and Caporael, 1990), and provided a life-sustaining source of care during illness, injury (Hublin, 2009), and the utter dependency of childhood (Bowlby, 1969/1982).
As solitary individuals were ill-equipped to face the daunting challenges of their environment, the survival of our ancestors depended as much on the integrity of their social network as on the integrity of their physical body. Consequently, the evolutionarily ancient pain signal, which serves to limit damage to the body, may have been co-opted to alert humans and other social mammals to the possibility of damage to one’s social relationships (Eisenberger and Lieberman, 2004, MacDonald and Leary, 2005 and Panksepp, 1998). Just as physical pain protects animals by drawing attention to the site of the physical injury and motivating appropriate restorative action, social pain may signal potential estrangement from one’s social network and motivate restoration of belongingness. In the next section, this idea is further explored, with the delineation of some of the neurochemical and neural systems that subserve both physical and social pain.
Neurochemical Evidence for an Overlap Between Physical and Social Pain:
I must give due praise to the man who first extracted morphine from poppyheads. The pain stopped seven minutes after the injection … and I forgot completely about the woman who deceived me. (Bulgakov, 1975, p. 125)
As in the semi-autobiographical account presented here, writers have long suggested that opioid drugs, a class of potent painkillers, also alleviate the ache of social loss. Indeed, the endogenous opioid system appears to play a key role in modulating both physical pain (Fields, 2007) and social affect (Panksepp, 1998). Morphine, whose pain-relieving effects are primarily mediated through the μ-opioid receptor subclass (Matthes et al., 1996), attenuates social separation distress (as indexed by a characteristic call termed a distress vocalization) in a variety of animal species (Carden et al., 1996, Carden and Hofer, 1990,Herman and Panksepp, 1978, Kalin et al., 1988, Kehoe and Blass, 1986, Panksepp et al., 1978, Panksepp et al., 1978 and Sufka et al., 1994). Importantly, this effect is observed with low, nonsedative doses of morphine that do not affect other behavioral responses. Conversely, opioid receptor antagonists, which are known to aggravate physical pain (Anderson et al., 2002 and Levine et al., 1978), increase distress vocalizations in isolated animals (Herman and Panksepp, 1978, Kehoe and Blass, 1986 and Sufka et al., 1994) and slow the reduction in distress vocalizations typically seen when animals are reunited with their companions (Carden and Hofer, 1990, Carden et al., 1996, Herman and Panksepp, 1978, Martel et al., 1995 and Panksepp et al., 1980).
These findings suggest that the endogenous opioid system, a primary neurochemical system for regulating physical pain, also mediates social attachments (Panksepp, 1998 and Panksepp et al., 1985). Specifically, it is postulated that social separation causes a painful, low-opioid state that motivates social proximity seeking and is terminated once social contact is resumed, which prompts the release of endogenous opioids. Consistent with this view, elimination of the μ-opioid receptor through genetic engineering causes deficits in attachment, including lack of distress vocalizing (Moles, Kieffer, & D’Amato, 2004). In addition to suggesting a specific point of overlap between the physical and social pain systems, research on endogenous opioids also demonstrates that the elaboration of social attachment is contingent on the ability to experience social distress.
Neural Evidence for an Overlap Between Physical and Social Pain:
Neural Substrates of Physical Pain
The experience of physical pain can be dissociated into two constituent components: the sensory-discriminative and the affective-motivational (Treede, Kenshalo, Gracely, & Jones, 1999). The sensory component provides information about the intensity, quality, and spatiotemporal characteristics of the pain stimulus, whereas the affective component is associated with the perceived unpleasantness of the stimulus, promotes focus on the pain stimulus, and provides the motivation to terminate the painful experience (Rainville et al., 1999 and Treede et al., 1999).
These two pain elements are subserved by different neural mechanisms (Craig, 2002, Price, 2000, Tölle et al., 1999 and Treede et al., 1999). Pain sensation is processed in the primary and secondary somatosensory cortices (SI and SII) and the posterior insula (PI), whereas pain affect relies on the dorsal anterior cingulate cortex (dACC) and the anterior insula (AI) (see Figure 1). Although highly correlated, the dissociability of the two components of pain is evident in the fact that individuals with lesions to the dACC (Cohen et al., 2001) and the AI (Berthier, Starkstein, & Leiguarda, 1988) can still identify the presence of pain, but find it less bothersome and distracting. Given that social exclusion does not involve tissue damage but does require an efficient mechanism for capturing attention and motivating pain-terminating behavior, it is probable that the affective component of physical pain is more directly involved in social pain experience, although the sensory component has been shown to play a role in certain types of social pain as well (Kross, Berman, Mischel, Smith, & Wager, 2011).
The Evolution of Social Pain:
Humans are a deeply social species whose most joyful and despondent moments arise from the gratification and frustration of social belongingness needs (Jaremka, Gabriel, & Carvallo, 2011). Our motivation to maintain stable and meaningful social relationships is rooted in evolutionary history (Baumeister & Leary, 1995). For our ancestors, group living was the primary survival tool that facilitated predator defense, hunting, foraging, mating, as well as childrearing (Baumeister and Leary, 1995 and Brewer and Caporael, 1990), and provided a life-sustaining source of care during illness, injury (Hublin, 2009), and the utter dependency of childhood (Bowlby, 1969/1982).
As solitary individuals were ill-equipped to face the daunting challenges of their environment, the survival of our ancestors depended as much on the integrity of their social network as on the integrity of their physical body. Consequently, the evolutionarily ancient pain signal, which serves to limit damage to the body, may have been co-opted to alert humans and other social mammals to the possibility of damage to one’s social relationships (Eisenberger and Lieberman, 2004, MacDonald and Leary, 2005 and Panksepp, 1998). Just as physical pain protects animals by drawing attention to the site of the physical injury and motivating appropriate restorative action, social pain may signal potential estrangement from one’s social network and motivate restoration of belongingness. In the next section, this idea is further explored, with the delineation of some of the neurochemical and neural systems that subserve both physical and social pain.
Neurochemical Evidence for an Overlap Between Physical and Social Pain:
I must give due praise to the man who first extracted morphine from poppyheads. The pain stopped seven minutes after the injection … and I forgot completely about the woman who deceived me. (Bulgakov, 1975, p. 125)
As in the semi-autobiographical account presented here, writers have long suggested that opioid drugs, a class of potent painkillers, also alleviate the ache of social loss. Indeed, the endogenous opioid system appears to play a key role in modulating both physical pain (Fields, 2007) and social affect (Panksepp, 1998). Morphine, whose pain-relieving effects are primarily mediated through the μ-opioid receptor subclass (Matthes et al., 1996), attenuates social separation distress (as indexed by a characteristic call termed a distress vocalization) in a variety of animal species (Carden et al., 1996, Carden and Hofer, 1990,Herman and Panksepp, 1978, Kalin et al., 1988, Kehoe and Blass, 1986, Panksepp et al., 1978, Panksepp et al., 1978 and Sufka et al., 1994). Importantly, this effect is observed with low, nonsedative doses of morphine that do not affect other behavioral responses. Conversely, opioid receptor antagonists, which are known to aggravate physical pain (Anderson et al., 2002 and Levine et al., 1978), increase distress vocalizations in isolated animals (Herman and Panksepp, 1978, Kehoe and Blass, 1986 and Sufka et al., 1994) and slow the reduction in distress vocalizations typically seen when animals are reunited with their companions (Carden and Hofer, 1990, Carden et al., 1996, Herman and Panksepp, 1978, Martel et al., 1995 and Panksepp et al., 1980).
These findings suggest that the endogenous opioid system, a primary neurochemical system for regulating physical pain, also mediates social attachments (Panksepp, 1998 and Panksepp et al., 1985). Specifically, it is postulated that social separation causes a painful, low-opioid state that motivates social proximity seeking and is terminated once social contact is resumed, which prompts the release of endogenous opioids. Consistent with this view, elimination of the μ-opioid receptor through genetic engineering causes deficits in attachment, including lack of distress vocalizing (Moles, Kieffer, & D’Amato, 2004). In addition to suggesting a specific point of overlap between the physical and social pain systems, research on endogenous opioids also demonstrates that the elaboration of social attachment is contingent on the ability to experience social distress.
Neural Evidence for an Overlap Between Physical and Social Pain:
Neural Substrates of Physical Pain
The experience of physical pain can be dissociated into two constituent components: the sensory-discriminative and the affective-motivational (Treede, Kenshalo, Gracely, & Jones, 1999). The sensory component provides information about the intensity, quality, and spatiotemporal characteristics of the pain stimulus, whereas the affective component is associated with the perceived unpleasantness of the stimulus, promotes focus on the pain stimulus, and provides the motivation to terminate the painful experience (Rainville et al., 1999 and Treede et al., 1999).
These two pain elements are subserved by different neural mechanisms (Craig, 2002, Price, 2000, Tölle et al., 1999 and Treede et al., 1999). Pain sensation is processed in the primary and secondary somatosensory cortices (SI and SII) and the posterior insula (PI), whereas pain affect relies on the dorsal anterior cingulate cortex (dACC) and the anterior insula (AI) (see Figure 1). Although highly correlated, the dissociability of the two components of pain is evident in the fact that individuals with lesions to the dACC (Cohen et al., 2001) and the AI (Berthier, Starkstein, & Leiguarda, 1988) can still identify the presence of pain, but find it less bothersome and distracting. Given that social exclusion does not involve tissue damage but does require an efficient mechanism for capturing attention and motivating pain-terminating behavior, it is probable that the affective component of physical pain is more directly involved in social pain experience, although the sensory component has been shown to play a role in certain types of social pain as well (Kross, Berman, Mischel, Smith, & Wager, 2011).
Figure 1: Cortical substrates of the affective and sensory components of pain. Regions displayed in red are hypothesized to be more strongly involved in the affective component of pain while regions displayed in yellow are hypothesized to be more strongly involved in the sensory component of pain. The medial view (on the left) shows the dorsal anterior cingulate cortex (dACC). The lateral view (on the right) shows the anterior insula (AI), posterior insula (PI), primary somatosensory cortex (SI), and secondary somatosensory cortex (SII).
Image Courtesy: Huffington Post
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