“Me seeing you seeing my pain”

Meanings of Pain (Springer International Publishing, 2016) was created to advance understanding of pain experience as a bearer of meaning. Progress in modern biomedicine is necessary to explain pain and to aid in its treatment; yet, preference for biomedical explanation of pain in the field has meant that research and clinical attention to the experience of pain and to common factors of pain, such as meaning, as both a clinical topic and a research method, mostly remains a blind spot in knowledge.

Meaningful changes that we notice in others are often subtle and small changes in facial expression, and are similar to features of clinicians that patients find meaningful, such as aspects of clinician demeanour (enthusiasm, positive personality, attentiveness), which are often embodied in subtle facial expressions, gestures, or particular tones of voice (e.g., Gracely et al. 1985). Pain is a personal experience, not an action; yet it displays itself in those actions in which a human person in pain is revealed to observation (Craig et al. 2010). Body-parts are subject to involuntary changes during pain, such as reflexive withdrawal, but in the social transaction of pain, the involuntary changes revealed in the face are more meaningful than in other body-parts (Prkachin et al. 1983; Craig, 2009). This is because body-parts do not have the individuating meaning of the face: the meaning of revealing me, here, now. The expression on a human person’s face is largely determined by involuntary facial actions; yet, it is the living picture of the person that “peers” from it, and hence a concentrated symbol of the “self”. In facial expressions of pain, the face is not a mere bodily part, but the whole person: the self is spread across its surface, and there displayed.

Intentional control of pain through facial actions is normally judged by observers to be an insincere expression of pain, and open to doubt (Hill & Craig, 2002). The controlled pain face is perceived as a mask, which conceals the person lying “behind” it. The expressions on the human face are not always transparent effects of the personal experiences that elicit them, as perhaps they are in nonhuman mammals. Human beings can deceive through their faces, and children and adults can use the face to fake, as well as exaggerate, or suppress, pain (Williams, 2002). It is possible that deception is possible because we do not distinguish a human person from his or her face. Protective acts such as withdrawal reflexes, guarded postures, and disabled behaviour, can communicate pain to sensitive observers (Sullivan, 2008). But when I observe another’s pain face, I am not meeting a physical part of him, as I am when I notice his injured arm or leg. I am meeting him, a real person, who reveals himself in the face as one like me. There are deceiving faces, but not deceiving arms or legs.

Facial expressions of pain call on you to respond to me. As soon as I notice pain in another person, my responsibilities are engaged. I am held to account for it. The face has this meaning for us because it is the boundary at which the other in pain appears, offering “this person” as one in need of help. This feature is perhaps at the heart of what it means to treat pain. Care of persons in pain would be impossible without the assumption that we can commit ourselves through promises, take responsibility now for some event in the future or the past, and enter into obligations that we hold as not transferable to other persons—all of which are perceived in the face.

We may separate pain from its social meaning, and assign to it an impersonal, “bodily” meaning. However, an observation of pain which, whether or not intentionally, focuses exclusively upon the body-parts of another, but which neglects the preliminary changes in the face, as well as in the voice, hands and posture, perhaps is unethical. The failure to recognise the personal existence of the other in pain is therefore an affront, both to him and to oneself. In separating pain from its social meaning, we remove it from the interpersonal world of social relations, which compels us to recognise human beings as persons and sometimes to compromise or risk ourselves for them.

The most meaningful feature in displays of pain is the eyes, followed by brows, eyelids, mouth, head, forehead, and then other body-parts (Prkachin et al. 1983). Although glances are normally voluntary, they participate in the pattern of involuntary social communication where one person in painful distress is “revealed” in his body to the one who observes him. To turn my eyes to you is a voluntary act; but what I receive from you is not anything I voluntarily do. The eye enables the human person in pain to be displayed to another in his body, and in the act of display to call on the observer to intervene on their behalf. The complex transaction of pain involves the voluntary and the involuntary to co-mingle on the surface of the human body. The joining of minds that begins when an expression of pain is answered with a reciprocated response is partly fulfilled in “me seeing you seeing my pain”, which is not the reciprocity of normal cooperation, but of meaning. I believe many patients with pain desire to experience first-hand this more concentrated form of social recognition.

References

Craig KD. A social communications model of pain. Canadian Psychology/Psychologie Canadienne 2009; 50:22-32.

Craig KD et al. Perceiving pain in others: automatic and controlled mechanisms. J Pain 2010; 11(2):101-8.

Gracely RH et al. Clinicians’ Expectations Influence Placebo Analgesia. Lancet 1985; 1(8419):43.

Hill ML, Craig KD. Detecting deception in pain expressions: The structure of genuine and deceptive facial displays. Pain 2002; 98:135-144.

Prkachin KM et al. Judging nonverbal expressions of pain. Canadian Journal of Behavioural Science/Revue canadienne des sciences du comportement. 1983; 15(4):409.

Sullivan MJL. Toward a biopsychomotor conceptualization of pain. Clin J Pain 2008; 24:281-290.

van Rysewyk S (ed). Meanings of Pain. Springer International Publishing: Switzerland, 2016.

Williams AC. Facial expression of pain: An evolutionary account. Behav Brain Scien 2002; 25:439-488.

A neurobehavioral-polyvagal theory of pain facial expression

The personal experience of pain produces a reliable effect on facial behavior in humans and in nonhuman mammals. Why should pain have a face? What is it for? I will attempt to head towards answering this question by invoking a theoretical framework: polyvagal theory (Porges, 2001, 2006).

1 Polyvagal Theory

According to polyvagal theory (Porges, 2001, 2006), evolution of neural control within the autonomic nervous system (ANS) has tracked three stages, each revealing a specific behavior, and a specific function:

In the first stage, the ancient unmyelinated visceral vagus nerve that enables digestion could respond to danger and pain only by reducing metabolic output and producing immobilization behaviors.

In the second stage, the sympathetic nervous system (SNS) made it possible to increase metabolic activity and inhibit the visceral vagus nerve, thus allowing fight/flight behaviors following perceived threat or pain.

The third stage, which is uniquely mammalian, involves a myelinated vagus that can rapidly control cardiac and bronchi output to enable spontaneous interaction (i.e., engagement or disengagement) with the environment. The interaction of the autonomic nervous system (ANS) with the hypothalamo-pituitary-adrenal (HPA) axis, nervous and immune systems change to maximize response to stressors such as nociception. During nociception, the ANS operates together with nervous, endocrine and immune systems to produce stress (Chapman et al. 2008; Porges, 2001, 2006). In terms of polyvagal theory, pain facial expression is a dynamic autonomic response caused by noxious signaling. In terms of polyvagal-type identity mechanistic theory pain facial expression is a type of behavior that is identical to a type of neurophysiological mechanism; namely, the phylogenetically recent brain-heart-face mechanism.

The expansion of cortex in the third stage increased innervation and neural control of the mammalian face: upper face innervation is bilateral and arises from the supplementary motor area (M2) and the rostral cingulate motor area (M3). Lower face innervation is contralateral and arises from primary motor cortex (M1), ventral lateral premotor cortex, and the caudal cingulate motor cortex (M4) (Morecraft et al. 2004). Human pain facial movements of the eyebrows and upper lip are type identical with negative emotional aspects of pain and activation of M1, M2, M3, whereas facial movements around the eyes are type identical with somatosensory aspects of pain, and activation of M2 and M3 (Kunz et al. 2011). Thus, evolution of cranial anatomy enabled a highly integrated facial representation of the multidimensional experience of pain.

2 Why Pain Should Have a Face

In clinical and experimental settings, the pain face is observed to rapidly appear following noxious stimulation, and diminish concurrent with cessation of the noxious stimulus, or when analgesics are administered (e.g., Craig & Patrick, 1985). The brain-heart-face mechanism is an integrated system with both a somatomotor part controlling the striated facial muscles and a visceromotor part controlling the heart through a myelinated vagus nerve (Porges, 2001, 2006). When the vagal tone to the cardiac pacemaker is high, the myelinated vagus acts as a brake or restraint limiting heart rate. Rapid inhibition and disinhibition of vagal tone to the heart supports the rapid mobilization of facial muscles and formation of the pain face concurrent with pain onset. In humans and nonhuman mammals, the main vagal inhibitory pathways in the myelinated vagus originate in the nucleus ambiguus.

The vagal brake supports the low-metabolic requirements involved in the rapidly appearing and disappearing pain face. Withdrawal of the vagal brake is strongly correlated with the rapid appearance of the pain face; reinstatement of the vagal brake is strongly correlated with the rapid diminishing of the pain face. These correlations are not unique to pain facial expression; similar relationships hold with regard to the vagal brake and the timing and duration of aversive, but non-noxious emotional facial expressions (e.g., Pu et al. 2010), and positive emotional facial expressions (e.g., Kok & Fredrickson, 2010).

In terms of the function of rapid pain face onset and offset, the vagal brake makes it possible for the individual in pain to quickly disengage from source of wounding and pain, concurrent with the rapid appearance or diminishing of pain facial expression, which may offer temporary access to additional metabolic resources to aid healing, recovery and self-soothing behaviors, with likely involvement from care givers.

Concerning aid from others, the vagal brake reliably maps onto specific interaction types observed in mammalian pain events. In pain events comprising the individual in pain and care givers, mammalian behavior is typed according to interpersonal communication through facial expressions, vocalizations, head and hand gestures (Hadjistavropoulos et al. 2011; Porges, 2001, 2006; Williams, 2002). A relevant feature is the rapid ‘switching’ of temporary engagement to temporary disengagement behaviors between the individual in pain and care givers. This interaction type may involve care givers speaking to the one in pain, and then quickly switching to listening; for the one in pain, looking into the face of the care giver, and then quickly switching to vocalizing (Craig et al. 2011; Hadjistavropoulos et al. 2011; Porges, 2001, 2006; Williams, 2002). The brain-heart-face mechanism thus allows the one in pain and the care giver to get the timing right. Some philosophers and neuroscientists claim that evolutionary neurobehavioral solutions to timing problems such as these are implicated in the origin of empathy and ultimately consciousness itself (Churchland, 2002; Cole, 1998; Engen & Singer, 2012; van Rysewyk, 2011).

However, if pain is severe or chronic and the vagal brake is withdrawn (or dysfunctional), the concurrency of increased pain facial expression, cardiac output, and other mobilization behaviors (i.e., increased SNS and HPA output), means that, if care giving is to succeed in promoting healing and recovery, the care giver’s vagal brake must be dynamically reinstated. By applying their own vagal brake, care givers may regulate their own visceral distress and thereby succeed in allocating valuable metabolic resources to communicate safety to the one in pain (and themselves) through calming facial and head behaviors, eye gaze, and prosodic vocalizations (i.e., increasing the vagal brake decreases SNS and HPA output). Since the vagal brake of the person in pain has been provisionally withdrawn, the care giver is effectively an integrated external brain-heart-face mechanism (cf. Tantam, 2009, the ‘interbrain’).

Thus, the pain facial muscles function as neural timekeepers detecting and expressing features of safety and danger that cue the one in pain to quickly disengage from the source of wounding and pain, simultaneous with the rapid appearance or attenuation of pain facial activity, and also cue others who can help.

References

Chapman, C. R., Tuckett, R. P., & Song, C. W. (2008). Pain and stress in a systems perspective: reciprocal neural, endocrine, and immune interactions. Journal of Pain, 9(2), 122-145.

Churchland, P. S. (1989). Neurophilosophy: Toward a Unified Science of the Mind-Brain. Cambridge, Mass.: MIT Press.

Cole, J. (1998) About face. Cambridge, Mass.: The MIT Press.

Craig, K. D., & Patrick, C. J. (1985). Facial expression during induced pain. Journal of Personality and Social Psychology, 48(4), 1080-1091.

Craig, K. D., Prkachin, K. M., & Grunau, R. E. (2011). .The facial expression of pain. In D. C. Turk, & R. Melzack, Handbook of Pain Assessment, 2nd Edition (pp. 117-133). New York: The Guilford Press.

Engen, H. G., & Singer, T. (2012). Empathy circuits. Current Opinion in Neurobiology, 23, 1-8.

Hadjistavropoulos, T., Craig, K. D., Duck, S., Cano, A., Goubert, L., Jackson, P. L., Mogil, J. S., Rainville, P., Sullivan, M. J. L., de C. Williams, Amanda C., Vervoort, T., & Fitzgerald, T. D. (2011). A biopsychosocial formulation of pain communication. Psychological Bulletin, 137(6), 910-939.

Kok, B. E., & Fredrickson, B. L. (2010). Upward spirals of the heart: Autonomic flexibility, as indexed by vagal tone, reciprocally and prospectively predicts positive emotions and social connectedness. Biological Psychology, 85(3), 432-436.

Kunz, M., Lautenbacher, S., LeBlanc, N., & Rainville, P. (2011). Are both the sensory and the affective dimensions of pain encoded in the face? Pain, 153(2), 350-358.

Morecraft, R. J., Stilwell-Morecraft, K. S., & Rossing, W. R. (2004). The Motor Cortex and Facial Expression: New Insights From Neuroscience. The Neurologist, 10(5), 235-249.

Porges, S. W. (2001). The polyvagal theory: phylogenetic substrates of a social nervous system. International Journal of Psychophysiology, 42(2), 123-146.

Porges, S. W. (2006). Emotion: An Evolutionary By‐Product of the Neural Regulation of the Autonomic Nervous System. Annals of the New York Academy of Sciences, 807(1), 62-77.

Pu, J., Schmeichel, B. J., & Demaree, H. A. (2010). Cardiac vagal control predicts spontaneous regulation of negative emotional expression and subsequent cognitive performance. Biological Psychology, 84(3), 531-540.

van Rysewyk, S. (2011). Beyond faces: The relevance of Moebius Syndrome to emotion recognition and empathy. In: A. Freitas-Magalhães (Ed.), ‘Emotional Expression: The Brain and the Face’ (V. III, Second Series), University of Fernando Pessoa Press, Oporto: pp. 75-97.

Williams, A. C. D. C. (2002). Facial expression of pain: an evolutionary account. Behavioral and Brain Sciences, 25(4), 439-455.