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Le bâillement, du réflexe à la pathologie
Le bâillement : de l'éthologie à la médecine clinique
Le bâillement : phylogenèse, éthologie, nosogénie
 Le bâillement : un comportement universel
La parakinésie brachiale oscitante
Yawning: its cycle, its role
Warum gähnen wir ?
Fetal yawning assessed by 3D and 4D sonography
Le bâillement foetal
Le bâillement, du réflexe à la pathologie
Le bâillement : de l'éthologie à la médecine clinique
Le bâillement : phylogenèse, éthologie, nosogénie
 Le bâillement : un comportement universel
La parakinésie brachiale oscitante
Yawning: its cycle, its role
Warum gähnen wir ?
Fetal yawning assessed by 3D and 4D sonography
Le bâillement foetal

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16 mai 2010
Philosophical Pyschology
Content and Contagion in Yawning
John Sarnecky
Professor of philosophy University of Toledo USA


Yawning has a well documented contagious effect: viewing or hearing a yawn&emdash;as well as talking or thinking about yawns&emdash;causes human subjects to yawn. While comparative ethological and neurological accounts suggest that yawning is a function of primitive biological structures in the brain stem, these analyses do not account for infectious yawning caused by representational and semantic states.
Investigating the relationship between perceptual and cognitive avenues of yawn induction affords a unique opportunity to examine how higher level cognitive faculties interact with involuntary or automated processing systems. In this paper, I examine three distinct attempts to reconcile the cognitive properties of contagious yawning with its physiological basis&emdash;one neurological, one philosophical, and one functional. None of these accounts are unproblematic, and the most plausible hypothesis for the evolution of contagious yawning does not satisfactorily explain the cognitive iterations of the phenomenon.
I argue that the most likely explanation of the contagion links perceptual elements of witnessed yawns to conceptual representations. More centrally, this kind of integrated account has repercussions for general theories of human thought and rationality, and suggests that higher level representational states engage neurophysiological structures in determining human behavior.

Standard ethological accounts of innate releasing mechanisms suggest a system of stimulus feature detectors that are responsive to a narrow range of behavioral signals. In contrast to learned behaviors, which can be tuned to a variety of features in the environment, these mechanisms are rigidly connected to specific perceptual cues. In contagious yawning, these cues appear limited to particular features of the auditory and visual profile of witnessed yawns. However, the fixed and inflexible nature of the stimuli feature detectors that lead to contagious yawns stand in stark contrast to the relative plasticity of yawning contagion in thought. Discussing or even thinking or reading about yawns also yields bouts of contagious yawning. Moreover, these episodes are not attributable to innate signal releasing mechanisms in perception. There are many ways one could come to think about yawning, none of them rigidly tied to tell-tale behavioral signals. As a consequence, it would be difficult to account for the cognitive causes of yawning in terms of innate signal detection mechanisms. The signals are too variable across time and different populations to function as a trigger for this behavior.
The dual perceptual and cognitive aetiology of infectious yawning speaks to the larger difficulties in characterizing the neurological and behavioral qualities of the act itself. Yawning is common in the animal world, suggesting a ''phylogenic antiquity'' (Provine, 1996) that comports well with neurological studies that place yawning triggers in the lower brain stem. However, the conceptual or representational form of contagious yawning indicates a social and cognitive role for yawning that appears incompatible with a purely noncognitive account of their causes. Even if the proximate causes of yawning are ultimately identified in the lower brain stem, the fact that infectious yawning is responsive not merely to perceptual cues but also to the content of what we think and communicate suggests that the causal profile of yawning is not limited to lower level responses. This is an unexpected detour for what appears at first to be a simple reflex.
Consider, for example, how infectious yawning compares with other involuntary or reflexive behaviors. Inhaling pepper can cause a sneeze, but the idea of pepper does not. Chopping or slicing onions can cause tears, but thinking about or describing chopped onions does not. The difference lies with the nature of the stimuli itself. Ideas of pepper and onions lack the chemical properties (in these cases, piperine and propanthial S-oxide respectively) that underlie our characteristic physical responses to both substances (see Sloop, 1995 for pepper and Imai et al., 2002 for onions). But it does not come down to simple chemistry. Other examples of infectious behavior do not rely on chemical irritants. Being around an anxious person can lead to heightened arousal or anxiety amongst those who perceive that person's discomfort. However, it is doubtful that reading a clinical account of anxiety will similarly increase the reader's blood pressure or pulse rate. Studies of mood induction (see Martin, 1985) show that individuals can acquire moods not only from observing behavioral (particularly facial) expressions of those moods, but also from considering the circumstances that typically elicit them (sad stories can evoke sadness, for example). However, the same is not true for infectious yawning. One is not required to imagine the circumstances of yawning to experience this phenomenon.
A consideration of the concept itself, as opposed to instances of boredom or fatigue, is often sufficient to trigger episodes of contagious yawning. The mere idea of anxiety (as opposed to considering potential reasons for it) appears decidedly less infectious than the visual or perceptual awareness of its presence. This shouldn't be surprising. The idea of anxiety and its display are very different things. However, this distinction dissolves in the causes of infectious yawning. Whatever property of the perception of yawns that is responsible for its contagion effects, the same or similar property appears to be present in symbolic representations of the yawn itself. What makes yawning unusual is not simply that it is an involuntary physical response to the content of a thought. Anxiety and other moods can be generated this way, as well as laughter. What is surprising in this case is the suggestion that both the perceptual and conceptual variations of this contagion result in the same behavioral responses.
This parallel response between reflex and representation is not the norm: thinking about a punch doesn't trigger our blink reflex when ducking an actual one does. Blinking to avoid a punch (or minimize its impact) makes a kind of sense with actual punches that doesn't carry over to notional ones. This functional dissimilarity is augmented by the fact that the processes involved, in terms of perceptual and cognitive processing, are physiologically and functionally distinct. However, something similar might be said about the two causes of contagious yawning. A perceptual input that causes an involuntary response can be likened to a reflex, a simple unthinking (and hence lower brain stem) response to immediate input. Perceptual reflexes like shivering in response to cold, or puckering in response to sourness largely if not entirely bypass conscious awareness or cognitive appraisal. Tickling may cause laughter in a subject, but rarely does thinking of tickling generate the same response. Catching yawns from reading about them, on the other hand, seems to involve a set of processes distinct from those used in perceptual input and reflex processing. Interpreting a symbol or contemplating ideas engages higher level processes located not in the brain stem, but the cortex itself.
The apparent tension between these two causes of contagious yawning suggests a promising avenue for research into the relation between the innate feature detectors that subserve the perceptual component of infectious yawning and the cognitive or intentional features that trigger it in communication and thought. Since analyses of perceptual reflexes typically proceed independently of functional analyses of mental representation and cognition, they often fail to address links between innate feature detectors and the determinants of voluntary behavior. Recent studies (see, e.g., Gallese, Fadiga, Fogassi, & Rizzolatti, 1996) that link the perception and performance of particular behaviors to brain activation within what has been called the ''mirror'' neuron system have emphasized voluntary responses without addressing the most mirror-like of human responses, contagious behaviors.1 Hence, contagious yawning offers a valuable opportunity to examine the neurological and perceptual models of involuntary and contagious behaviors in the context of these discoveries and against the background of causal/functional models of mental content, with the potential to shed light on both. As Robert Provine writes, ''in studying contagious yawning . . . we move seamlessly from the neural to the social level of analysis'' (1996, p. 180). The bridge is a psychological one.
Yawning ......
Achitectural approaches to yawning ......
It is a curious feature of infectious yawning that despite the robust relationship between depictions and discussions of yawning and increased yawning in subjects, many individuals are relatively unresponsive to the presence of any yawning stimulus. A theory of yawning contagion should explain not merely why yawns are contagious, but also why, for some people, they are not. Recent studies by Steven Platek and his colleagues (2005) suggest that this variation can best be explained in terms of differing levels of empathetic response amongst distinct individuals: the more empathetic a person is, the more likely she will respond to the yawning stimulus. Platek found that the better subjects were able to recognize and attribute (as well as make inferences about) mental states, the more likely they were to experience infectious yawning. Conversely, subjects who scored highly on a schizotypal personality index and thus show decreased mind-reading abilities were less likely to exhibit contagious yawning than those who did not. Platek hypothesizes that contagious yawning depends on one's capacity to engage with and imagine the mental states of another. This empathetic identification leads to the reproduction of another individual's yawns in oneself
Platek's theory presupposes a strong connection between empathetic response and a theory of mind. A theory of mind is the mechanism by which individuals read and attribute mental states to others. On this view, empathy requires the ability not merely to take on the feelings of another, but also to be able to predict and explain other people's behavior. Empathetic identification would thus break down in cases where an individual's theory of mind is diminished or absent. Platek's model suggests that in those cases we would likewise encounter an absence of contagious yawning. Recent studies with autistic children and in animal ethology seem to confirm this point. Autism has long been associated with decreased capacities to predict and explain the behavior of others. Simon Baron-Cohen (1997) has characterized this condition as a sort of mind blindness. In accordance with Platek's findings, we would expect autism to effectively immunize affected individuals from infectious yawning. Senju et al. (2007) offer compelling evidence that this is indeed the case. They found that children with autistic spectrum disorder were significantly less likely to yawn when viewing video presentations of yawning adults than developmentally normal children (even though they are equally likely to yawn at a neutral stimulus).
The theoretical connection between contagious yawning and the theory of mind could also be questioned if we could find an example of contagious yawning in some species with a doubtful claim to a theory of mind.6 However, as Anderson, Myowa- Yamakoshhi, and Matsuzawa (2004) have shown, there is very little evidence for contagious yawning outside of the higher primates. Whether in fact higher nonhuman primates have a theory of mind remains contentious, but there have been significant experimental results to suggest that they do.7 Even so, it would be difficult to draw strong conclusions from the spotty evidence we currently possess. A recent study by Paukner and Anderson (2006) suggests that yawning contagion can also be found in stumptail macaques, which would complicate any straightforward equation of theory of mind with contagious yawning. A full resolution of these issues will ultimately depend on further empirical data on yawning in the animal world as well as a more complete account of theories of mind among monkeys and other animals.
Platek has also uncovered a new source of evidence for the empathetic nature of contagious yawning in fMRI studies of the brain. This research suggests that the neural substrates involved in contagious yawning are the same as those that have been connected to ''identifying words that describe oneself, retrieval of autobiographical events/memories, engaging in self-generated actions and selfmonitoring, and discriminating between theory of mind stories and 'physical' stories'' (Platek et al., 2005, p. 450). However, Platek did not find activation in other areas associated with self-reference or conscious self-recognition in the forebrain. He suggests that this allows us to draw a line between the conscious (and intermittent) processing of self-awareness and empathy with what he calls ''a primitive form of empathetic modeling'' (2005, p. 450). Contagious yawning finds its home in the latter.
The differences between the two are instructive. In contagious yawning, the bilateral thalamic and parahippocampal gyrus are also activated (Platek, 2005, p. 451). These substrates have been tied to visual and facial sensory processing. The strong (and as Provine has pointed out, profoundly specific) perceptual sensitivity of contagious yawning suggests a sensory link between visual encounters with yawns and the production, in a primitive level empathetic response system, of a yawning reflex.8 Noticeably absent from this account, however, is the involvement of higher level processing mechanisms. In distinguishing between two levels of empathetic response, one higher level and more theoretical, and another primitive, lower level system, Platek risks offering a split account of the causes of contagious yawning. The epidemiology of perceptual encounters with yawns falls under the lower level response system, while conceptual precursors of the contagion are processed outside the primitive response system. As a consequence, Platek's model cannot explain how higher level representations can engage the response system implicated in perceptual instances of yawning. This problem is exacerbated by the fact that Platek's experiments exclusively employ visual presentations of yawns as triggering stimuli for the contagion. Understanding the activation of neural substrates during the semantic variant of the contagion could help shed some light on how or whether the two releasing mechanisms for contagious yawning are related. The connection Platek and his colleagues have discovered between yawning and primitive empathetic processing suggests a social role for contagious yawning. Since contagious yawning appears to require some rudimentary theory of mind, neurological structures that subserve this system are central to Platek's account.
Surprisingly, the structures most often implicated in the formation and development of empathy, mirror neurons (see Gallese & Goldman, 1998), do not appear to play a role in the empathetic response that governs episodes of contagious yawning. Platek's (2005) fMRI studies identify little or no activation in the cortical regions associated with mirror neurons during episodes of contagious yawning. What role mirror neurons play in mind-reading and empathy remains obscure, but these results suggest that contagious yawning might not share their primarily imitative function.
Platek's studies indicate a link between empathy and the perceptual exemplars of yawning contagion.....
Yawning and Adaptive Purposes
While contagious yawning appears connected to one's capacity to read or empathize with others, Platek's accounts offers little insight into the adaptive purpose of yawns. That is, contagious yawning might depend on empathy, but this gives us little clue about why. This problem is made more difficult by the fact that yawns might be used to play different roles in different species. Yawning has been associated, particularly in primate species, with aggression and dominance displays (Deputte, 1994; van Lawick-Goodall, 1968). Male patas monkeys use yawns to bare their canine teeth in facing down perceived threats (see Trois, Aureli, Schino, Rinaldi, & De Angeli, 1990 on male threat displays)&emdash;a pointless act for humans without similarly large canine teeth.12 This role in aggression might help explain both the predominance of male yawners in the animal world (though there is no gender discrimination in human yawning, see Schino & Aureli, 1989) and its connection to sexuality. Researchers have found that in rats chemicals that induce yawns also induce erections (see Melis, Stancamiano, Lai, & Argiolas, 1995), while testosterone injections in female rhesus monkeys elicits increased yawning. Interestingly, even though anti-depressants typically suppress sexual desire and receptivity in humans, some have been known to cause orgasms in human subjects during yawns (Provine, 2005). Yawning has also been linked to increased stretching and abrupt changes in levels of attention or arousal (Provine & Hamernik, 1986; Provine, Hamernik, & Curchack, 1987).
These links hardly point to a definitive purpose for yawning, but together they are suggestive of the most plausible adaptive account of their function. Building on a suggestion made by Arthur Myrberg (1972) and Provine, Hamernik, and Curchack's (1987) pioneering studies, Ronald Baenninger (1987) argues that yawning plays a role in transitioning between different states of wakefulness or arousal. In particular, he contends that the purpose of yawning is to help individuals remain alert in poor or weak stimulus conditions. The connection between yawning and arousal is well-documented. Yawning is most common in the hours immediately after waking and in those immediately preceding sleep (Provine et al., 1987). Studies have shown that individuals yawn more frequently in the hour before they go to bed than they do while lying in bed waiting to fall asleep (Greco, Baenninger, & Govern, 1993). If yawning were simply an indicator of fatigue, one would expect yawning to continue to increase as one approaches sleep. In Greco's (1992) study, she found that subjects who were discouraged from yawning during a simulated driving task made more mistakes than those that were not (even though many subjects actively suppressed yawns). This suggests that active yawning helps maintain higher levels of awareness and function in fatigued or stimulus deprived individuals (Baenninger, 1997, p. 201; Provine, Hamernik, & Curchack, 1987).
Similar results can be obtained in the animal world. Zoo animals yawn more frequently while waiting for feedings than they do afterwards (Baenninger, 1987). Baenninger also notes that carnivores, for whom the cycle of daily activity and arousal is typically more varied, tend to yawn more than herbivores (1997, p. 200). In these cases yawning appears to function primarily as a noncognitive mechanism for increasing an individual's level of attention or arousal in contexts where actionpreparedness is important but difficult to sustain.
While we might be able to make a plausible case that arousal is the adaptive purpose of yawning, it is difficult to establish this claim in the absence of an account of how yawns serve this function. That is, it is hard to say that this is what yawning is for if we don't know the mechanism used to sustain or increase levels of awareness in individuals who yawn. However, there are some theories of the physical structure of yawning that seem congenial to this view. If yawning really did increase oxygen uptake, then it might as a consequence lead to more alert individuals. Though this theory has been largely discredited, other so far unsubstantiated accounts fit the same mold. Askenasy (1989) argues, for example, that yawning may dilate arteries in the brain, thus increasing cerebral blood flow. This process may yield increasing levels of awareness. Neither theory, however, explains the contagion effect of yawns. If yawns are primarily a means of regulating oxygen uptake or cerebral blood flow, then why are yawns any more contagious than liver function? Why should my need to increase cerebral blood flow have any influence on yours?
The answer might lie in the social nature of animal communities. There are situations in which maintaining group arousal can accrue a significant evolutionary advantage to members of the group. Consider, for example, the advantage of maintaining high levels of alertness against predators in feeding situations. The population is more secure in circumstances in which each of its members is in a position to issue an alarm call. As one group member begins to succumb to fatigue or boredom, the ensuing yawn might help other members of the group maintain their vigilance against attack. Similarly, a sensitivity to yawning stimuli might help arouse or awaken a group in the early morning or after a rest. Yawning might be used, in these contexts, to co-ordinate the timing and vigor of activities within a community.
Whether in fact yawning plays a similar role in human communities is unclear. Robert Provine (2005) tells the story of the Bakairi people of central Brazil who signal the end of their evening conversations with a yawn that passes through each member of the group. This is perhaps a more explicitly cultural adaptation of the yawning reflex or contagion that might serve a similar purpose in other groups. Provine evidently thinks so: ''the chain reaction of contagious yawning synchronizes the behavioral as well as the physiological state of our tribe'' (2005, p. 532). The contagious nature of yawning in human (and other animal) communities might have emerged, then, as a prelinguistic attempt to harness an arousal mechanism to engage and manipulate group activities.
This model fits well with Platek's data. In supposing that yawning plays a social role in coordinating group behavior, the connection between contagion and empathy suggests an avenue by which this coordination could be achieved. By hardwiring the response to perceived yawns into our theory of mind, signals can be easily and reliably transmitted throughout a population. However, this account shares the limitations of Platek's account. While actual yawns are elicited in circumstances in which group arousal falls below optimum levels, talking about yawning is only intermittently associated with fatigue or boredom. While actually yawning might lead us to consider and think about yawns, such a connection would be redundant as a social signal designed to increase awareness. Presumably the yawn that started us thinking about yawning will have already served that purpose. However, as any researcher of yawning knows all too well, any consideration of yawning can lead to the increased production of yawns whether they are situationally appropriate or not. Moreover, it is not clear that circumstances of fatigue or boredom are causally related to thoughts about yawning in the same way that they are related to yawns themselves&emdash;being tired doesn't make one think about yawns in the same way that it appears to induce actual yawns. As a consequence, many of the regulatory benefits we might associate with the production of yawns do not apply to thoughts about yawns. In fact, thinking about yawning might lead one to engage arousal mechanisms when they are a hindrance to sleep or other biologically necessary functions.
The social arousal model of contagious yawning, that the propagation of yawns through an animal community can function to regulate and synchronize patterns of activity in animal populations, is currently the best candidate to explain why yawns cause others to yawn. Such an explanation is limited, however. It does not extend to the semantic or cognitive forms of the contagion. Since the semantic form of the contagion does not generate situationally appropriate regulative interactions, it seems unlikely to play any significant social role within a community. These considerations do not suggest that the social theory is false, but rather that the best avenue to explore semantic contagion will come not from an understanding of what yawning is for, but rather from a theory that connects conceptual understanding to the perceptual precursors of contagion. On this view, the semantic element of yawning contagion is best seen as a side effect or carryover from the perceptual cases.
Accepting this link between perception and higher level representational states does not, however, resign us to the details of the Prinz/Barsalou account. On this view, the relation between the conceptual elements of contagion and their root perceptual causes is not necessarily constitutive. Instead, a weaker relation between perceptual and semantic components could be imagined. This suggestion is supported by evidence that the perceptual form of contagion is more robust than its cognitive counterpart. This gives us reason to suppose that cognitive contagion emerges from an echo chamber effect that is ultimately triggered by perceptual exemplars of the contagion's cause.
Robert Provine has suggested a hybrid releasing mechanism that tunes higher level cognitive functions to more basic or lower level cognitive/behavioral responses. He suggests that contagious laughter conforms to this model: ''Humour and joking are modern cognitive and linguistic triggers of laughter, recently evolved cortical bells and whistles superimposed on laughter's ancient neurological core'' (2000, p. 190). The semantic form of contagion, Provine suggests, may reflect a similar reprogramming of innate feature detectors towards a more flexible set of releasing mechanisms. Unlike the radically empiricist account, the connection between perceptual and semantic forms is not a by-product of other cognitive processes, but would have been modeled to perform a particular task. Nevertheless, it remains unclear why or how the new signaling mechanism became grafted onto the older or more basic action pattern. Further study into this area would benefit from a consideration of the priming literature both on yawning and other involuntary behaviors like blinking or coughing and their influence on contagious behaviors. Tracing out the path of this contagion can thus begin to uncover the representational structures at the heart of cognition.
The links between perception and cognition that lead to the production of both forms of contagious yawning offer an opportunity to better understand the mechanisms that underlie all representational states. In pursuing an account of the semantic version of yawning contagion, we can gain a unique perspective on the connection between lower levels of cognition and their relation to higher level representational states. In so doing, we can begin to develop an account of cognition that takes into account not merely higher level cognitive processes, but also their relations to basic level neurobehavioral responses.
As a consequence, we have the opportunity to develop an account of mental representations that is neither top heavy nor structurally uninformed. I hope these considerations show not merely that yawning contagion requires further empirical research, but that the study of borderline cognitive states can illuminate more general theories of human thought and rationality.