Efectos en relación a los herederos llamados a

Pain facial expression is uniform across experimental pain submodalities including cold, electric shock, pressure, and ischaemic pain (Craig et al. 2011; Prkachin, 1992, 2009; Williams, 2002). Prkachin (1992) observed that lowered brow, tightened eyelids, raised cheeks, wrinkled nose, raised upper lip and pulled up lip corner actions were present across all tested pain stimuli (see Figure 6 for prototypical pain face across time). Other reliably observed pain facial actions across pain submodalities are oblique lip pull, jaw drop, mouth opening, and horizontal mouth stretch (Botvinick et al. 2005; LeResche & Dworkin, 1988; LeResche et al. 1992; Prkachin, 1992). Acute exacerbation of chronic musculoskeletal pain shows a reliable pain face expression (Craig et al. 1991; LeResche & Dworkin, 1988; Prkachin & Mercer, 1989; Prkachin et al. 1994). Moderate correlations have been reported between facial expression measures and self-reported chronic disability (Prkachin & Mercer, 1989), and verbal self-report chronic pain assessments (Craig et al. 1991). Currently, it is not known whether these relationships exist in other chronic pain subtypes, such as fibromyalgia or neuropathic pain (Williams, 2002).

In a cognitive behavioural study, Kunz et al. (2011b) used a reliable psychological strategy (suggestions) to differentially alter the somatosensory and emotional features of pain. The authors found that suggestions for either increased pain unpleasantness or pain sensation evoked specific changes in facial expression, irrespective of pain submodality. Facial actions around the eyes were closely correlated with pain somatosensation, whereas facial actions of the nose, upper lip and also eyebrows were closely correlated with the unpleasantness or aversiveness of pain. Pain facial actions are under tight neural control through the

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somatomotor component of the brain-heart-face mechanism: 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). Thus, human pain facial movements of the nose, 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. Evolution of cranial anatomy enabled a highly integrated facial representation of the multidimensional experience of pain. These identity claims are heuristic to emphasize that they are assumptions that then guide subsequent empirical investigation (McCauley & Bechtel, 2001).

The unique integration of pain in the mammalian face appears paralleled within cortical targets in the paleospinothalamic tract. In an fMRI study, Kunz et al. (2011a) found strong activation in M1, S1, AINS, and ACC in the within-subject analyses comparing trials with and without facial expression in facial expressive subjects. Differences in verbal pain self-report did not explain the variability in pain facial expressions and the corresponding cortical activation because verbal pain self-report was not associated with pain facial

expressiveness and did not differ between painful trials with and without facial expressions. Based on the type identity I claimed between pain unpleasantness and specific parts of the paleospinothalamic tract, the results of Kunz et al. (2011a) suggest that facial expression uniquely represents pain emotion compared to verbal pain self-report (Craig et al. 2011; Prkachin, 2009; Williams, 2002). Electrocortical evidence for preferential processing of dynamic pain expressions compared to other emotional expressions adds further support to this hypothesis (González-Roldan et al. 2011; Reicherts et al. 2012).

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Pain through dynamic facial expression is characterized by mobilization. Thus, pain facial expression is type identified with the defensive fight-flight behaviours the NEIM that functionally increases metabolic output by increasing sympathetic, HPA and immune excitation. Simultaneous with these changes is a withdrawal of the myelinated vagal

pathways in the brain-heart-face mechanism that is the vagal brake. Pain is always personal, but it is also social: it invariably is expressed in complex social environments, and manifest pain that leads to caregiving requires an ability to restrain facial and bodily mobilizations (Craig et al. 2011; Hadjistavropoulos et al. 2011; Williams, 2002; Wittgenstein, 2009). For example, during mammalian play, a playmate may sustain a wound. In full-contact sports, one player may be hit with an elbow or knee in the face. A fight may occur if the player who accidentally hits another in the face walks away without mitigating the pain through a face- to-face display of care and empathy. Similarly, when puppies play, one playmate may accidentally bite too hard and cause pain in the other. Play will likely stop if the puppies do not make face-to-face contact after this event. Face-to-face contact alerts the individuals involved that the intentionality of the behaviour is benign, and facial muscle activity influences the neural mechanisms that regulate visceral qualia (e.g., Gellhorn, 1964;

Levenson et al. 1990). Thus, the mammalian face is necessary in understanding mobilization as play and not aggression (Porges, 2001, 2006; Porges & Furman, 2011). Although pain facial expression shares parts of the NEIM involved in fight-flight behaviours, expressed pain is social and requires dynamic neural regulation of state to expedite safe interactions and recovery. Hence, both sympathetic activation to increase metabolic output to enable pain behaviours and the vagal brake to restrain mobilization and to support caregiving are

recruited to ultimately restore allostasis and homeostasis. Section 3.3 below links these ideas in relation to pain modulation.

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The compromised brain-heart-face mechanism is correlated with a change in

autonomic regulation type identified as a reduction in the influence of the myelinated vagus on the heart (Porges, 2001, 2006). This results in difficulties in behavioral state control with a loss of neural control to facial muscles regulating the comparatively flat negative emotional expressions often seen in clinical disorders (Porges, 2001, 2006; Porges & Furman, 2011). Since pain is part negative emotion, I would anticipate similar type identity relationships between autonomic state during pain and facial control in psychiatric populations, though this hypothesis has yet to be experimentally tested.