mystery of yawning
 
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mise à jour le
8 septembre 2014
Scholarpedia
 
Vidéo d'un bâillement typique
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In english
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Revue des théories d'Hippocrate à nos jours
Walusinski O 2014
 
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Le bâillement est un comportement physiolgique banal, décrit dès l'antiquité par Hippocrate qui pensait que le bâillement permettait l'évacuation de la fièvre, comme une cheminée évacue la fumée. Oublié après les publications de JM Charcot , la médecine de XX° siècle n'y a pas attaché beaucoup d'intérêt jusqu'aux années 80, marquées par les progrès de la neurophysiologie et de la neuropharmacologie qui lui redonnent sens.
 
Les organismes vivants, en particulier les vertébrés, exhibent des comportements variés, essentiels à leur survie, caractérisés par leur récurrence cyclique. Il en va ainsi pour les trois comportements fondamentaux de la vie et de sa transmission: la vigilance (être apte à survivre face aux prédateurs alors que le sommeil est indispensable à l'homéostasie du cerveau), la satiété (capter de l'énergie), la sexualité (transmettre la vie). Les bâillements et les pandiculations, en restant morphologiquement identiques, apparaissent associés à chaque état transitionnel des rythmes infradiens, circadiens, ultradiens qui caractérisent ces comportements.
 
Le bâillement est un comportement, phylogénétiquement ancien (présent chez les reptiles), stéréotypé mais modulable, physiologiquement contemporain des étirements musculaires lors de l'éveil, isolé lors du besoin de sommeil, associé ou non à une érection, présent chez l'homme et les animaux, des reptiles, aux poissons et aux oiseaux, donc probablement presque chez tous les vertébrés. L'embryologie et l'ontogénèse (la précocité ontogénique est correlée avec la phylogénèse ancienne) montre le parallélisme entre succion et bâillement, entre sommeil paradoxal et bâillement.
 
Le bâillement se déroule en trois phases suivies d'une sensation de bien-être et de détente: une longue inspiration, une acmé, une expiration rapide, associée ou non à des étirements. Sa fonction n'est qu'incomplètement élucidée. Sans améliorer l'oxygénation cérébrale, comme cela fut répété pendant des siècles, le bâillement apparaît comme une stimulation de notre vigilance; il joue un rôle dans la communication non-verbale en particulier chez les primates non humains, chez qui il est, pour certains comme les macaques, testostérone dépendant.
 
Alors que le bâillement disparait dans certains syndromes parkinsonniens, les salves de bâillements répétés sont pathologiques et peuvent révélées de multiples pathologies, cérébrales neurologiques ou neuropsychologiques. Les causes de bâillements iatrogènes sont les plus fréquentes.
 
Bâillements et pandiculations extériorisent l'activité des centres moteurs du tronc cérébral (V, VII, IX, X, XI, XII) et de la moelle cervicale (C1-C4), sous la commande du noyau paraventriculaire de l'hypothalamus (PVN). Le PVN est un centre d'intégration entre les systèmes autonomes central et périphérique. Il intervient, notamment, dans la balance métabolique (osmolarité, énergie), la pression artérielle et la fréquence cardiaque, la sexualité.
 
Bâillements et pandiculations peuvent être déclenchés par des injections (apomorphine, hypocrétine, etc) ou disparaître après électrolésion dans la zone parvo-cellulaire du PVN. Un groupe de neurones ocytocinergiques, situés dans cette zone du PVN, projetant vers l'hippocampe, le tronc cérébral (locus coeruleus) et la moelle, contrôlent les bâillements et l'érection. La stimulation de ces neurones par la dopamine ou ses agonistes, des acides aminés excitateurs (NMDA), l'ocytocine elle-même, déclenche des bâillements et des érections, alors que le GABA ou les opioïdes inhibent. Ce schéma trop simplificateur omet d'autres molécules également impliquées telles NO, glutamate, GABA, sérotonine, ACTH, MSH, hormones sexuelles, hypocrétine et autres neuro-petides. Cette richesse neurophysiologique explique l'intérêt de l'observation du bâillement pour des tests pharmacologiques des nouveaux psychotropes. Les multiples projections du noyau paraventriculaire sur le locus coeruleus et la réticulé du tronc cérébral sont les déterminants de l'effet de stimulation de la vigilance attribué actuellement au bâillement.
 
Le curieux phénomène de la contagion (mieux vaut dire réplication ou échokinésie) du bâillement, propre à l'Homme et aux grands singes, implique la mise en jeu de circuits neuronaux superposables à ceux activés au cours des processus de l'empathie, comme l'imagerie fonctionnelle cérébrale contemporaine l'a montrée.
 
De notre premier à notre dernier souffle nous bâillons environ 250 000 fois !
et n'oubliez pas le slogan: trainaillez plus pour bâillez plus !
 yawning inside story
Animaux endormis. Le bâillement. Hediger H 1955
 
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
http://www.baillement.com
 
Voulez-vous répondre à un questionnaire sur vos bâillements ?
 
Le bâillement raconté aux enfants d'après une émission télévisée
 
S'inscrire à la lettre d'information sur le bâillement 
 
 Le premier Holter pour les bâillements
 
 Bâillements du foetus: la naissance d'un comportement révélé par l'échographie 4D
 
L'examen clinique du bâilleur excessif
 
Questionnaire estimant les bâillements
 
Le bâillement: son histoire interne
 
Echokinésie du bâillement, théorie de l'esprit et empathie
 
Le bâillement : de l'éthologie à la médecine clinique
 
Illustrations de la thèse de Wolter Seuntjens  
 
yawning
 
Les vertébrés exhibent des comportements variés, essentiels à leur survie, caractérisés par leur récurrence cyclique : se nourrir, se reproduire, dormir. Leur apparition correspond à une transition comportementale qui ne résulte pas d'une adaptation passive aux conditions d'environnement, mais obéit à des stimuli internes caractérisant des adaptations homéostatiques générées, en particulier, par l'hypothalamus. Des horloges biologiques internes autorisent une adéquation précise entre besoins métaboliques (satiété), survie de l'espèce (accouplement) et conditions d'environnement (rythme veille - sommeil et alternance jour - nuit).
 
Les bâillements et les pandiculations sont associés aux transitions entre des états d'éveil et de sommeil, lors de l'installation de la faim ou de la satiété, lors de l'installation ou de la disparition d'états émotionnels secondaires à une vie en groupes sociaux hiérarchisés et dans certaines espèces (rats, macaques, hippopotames) à la sexualité. Présents chez les reptiles donc phylogénétiquement anciens, ils apparaissent chez le fœtus dès la 12 semaine de grossesse, donc ontogénétiquement précoces. Toutes ces observations et des mesures de gaz du sang ou d'air exhalé ont prouvé que le bâillement ne modifie en rien l'oxygénation cérébrale, mais que la puissante activité musculaire qu'il engendre, stimule, par un mécanisme de rétrocontrôle, les structures responsables de l'éveil au niveau du tronc cérébral. Bâillements et pandiculations activent le retour de la circulation veineuse et l'écoulement du liquide céphalo-rachidien, ouvrent les trompes d'Eustache, optimisent l'étalement du surfactant dans les alvéoles pulmonaires et enfin créent un bref agréable bien-être, acutisant l'image de notre schéma corporel.
 
Forme de langage non verbal, il permet à des animaux vivants en groupe de synchroniser leurs activités (lions, hippopotames, autruches). Bien différente, la contagion ou, à mieux dire, la réplication ou échokinésie du bâillement ne semblent exister que chez l'Homme et quelques grands singes capables de se représenter l'état mental de l'autre et de se reconnaître dans un miroir. Les mécanismes neurobiologiques qui la sous-tendent sont communs au comportement d'empathie. Plusieurs données confortent cette théorie. L'enfant n'est sensible à cette échokinésie qu'entre 4 et 5 ans, âge d'acquisition de cette faculté. Les tests de personnalité montrent que les personnes empathiques y sont très sensibles alors qu'à l'inverse les personnalités schizoïdes ne le sont pas. De même, l'échokinésie est très restreinte en cas d'autisme. Les neurones miroirs de l'aire motrice gauche, sollicités au cours de l'imitation, ne s'activent pas au cours de l'échokinésie mais les techniques d'imagerie fonctionnelle cérébrale indiquent que ceux des aires pariéto-temporales droites et d'autres régions, actifs lors du décodage de la vue d'une émotion ressentie par autrui, sont bien stimulés lors de ce comportement.
 
Le bâillement a l'unique qualité d'être physiologique et donc d'avoir sa pathologie, mais aussi d'en déclencher certaines et d'en soulager d'autres. Raréfié au cours de la maladie de Parkinson ou lors de la prise de morphine, il peut être exagérément fréquent après la prise de certains antidépressifs, en cas d'hypertension intracrânienne, de certaines pathologies de l'hypophyse et la migraine. Le bâillement est la cause la plus fréquente de la luxation de la mâchoire et peut déclencher des névralgies ou des dystonies. Lors de variations de pression (vol aérien, plongée sous-marine), le bâillement aide à recouvrer l'audition et soulage les douleurs d'oreille. Sa pratique en relaxation procure une détente édénique.
 
Scholarpedia
 
Why do people yawn ?
The Yawn is a stereotyped and often repetitive motor act characterized by gaping of the mouth accompanied by a long inspiration of breath, a brief acme, and then a short expiration of breath.
 
==Introduction==
 
Stretching and yawning (known as ''pandiculation'' when they occur together) are under-researched features of behavior. Ethologists agree that almost all vertebrates yawn (Deputte, 1974). Yawning is morphologically similar in reptiles, birds, mammals and fish. These behaviors may be ancestral vestiges maintained throughout evolution with little variation (phylogenetic old origins). Systematic and coordinated pandiculations occur in a similar pattern and form across all animals, and consistently occur during behaviors associated with cyclic life rhythms: sleep-arousal, feeding and reproduction. Pandiculation appears as one undirected response to an inner stimulation, underlying the homeostasis of these three behaviors (Provine, 2005; Walusinski & Deputte, 2004).
 
Relatively sedentary species that sleep very little, such as many herbivores, yawn infrequently; species that sleep 8 or 12 h and alternate between active and inactive periods (e.g., predatory carnivores and primates) yawn much more frequently following a circadian rhythm. In humans, daily frequency of yawning varies between 5 and 15 times per day. The diurnal distribution of yawning frequency is illustrated by higher frequency upon waking and before sleep (Baenninger et al., 1996).
 
In his 1755 book De perspiratione insensibili, Johan de Gorter was the first to describe yawning as accelerating blood flow, supposedly to improve the oxygenation of the brain, in response to cerebral anaemia. Well into the 20th century, there were regular references to this notion, even though it had never been demonstrated. The inaccuracy of this hypothesis was formally shown by Provine, Tate and Geldmacher in 1987. They had their subjects inhale air with higher than normal levels of CO2 (3-5% vs. <0.5%). In response, the subjects' breathing rates increased, but they did not yawn. Likewise, when the subjects inhaled pure oxygen, there was no inhibition of spontaneous yawning at normal rates. Hence yawning is not a physiological reflex to improve cerebral oxygenation.
 
== Neurophysiology==
 
A good number of clinical and pharmacological arguments indicate that yawning involves the hypothalamus (particularly the paraventricular nucleus, PVN), the bulbous and pontic regions of the brainstem, with frontal region connections in primates and to the cervical medulla (Argiolas & Melis, 1998). The PVN is an integration centre between the central and peripheral autonomic nervous systems. It is involved in a number of functions ranging from feeding, metabolic balance, blood pressure and heart rate, to sexual behavior and yawning. In particular, a group of oxytocinergic neurons originating in this nucleus and projecting to extra-hypothalamic brain areas (e.g., hippocampus, medulla oblongata and spinal cord) controls both yawning and penile erection (Kita et al., 2006).
 
Activation of these neurons by dopamine and its agonists, excitatory amino acids (N-methyl-D-aspartic acid), oxytocin itself, or by electrical stimulation leads to yawning; conversely their inhibition by gamma-amino-butyric acid (GABA) and its agonists or by opioid peptides and opiate-like drugs inhibits both yawning and sexual response. The activation of these neurons is secondary to the activation of nitric oxide synthase, which produces nitric oxide. Nitric oxide in turn causes, by a mechanism that is as yet unidentified, the release of oxytocin in extra-hypothalamic brain areas (Sato-Suzuki, 1998). Other compounds modulate yawning by activating central oxytocinergic neurons: sexual hormones, serotonin, hypocretine and endogenous peptides (adrenocorticotropin-melanocyte-stimulating hormone). Oxytocin activates cholinergic neurotransmission in the hippocampus and the reticular formation of the brainstem. Acetylcholine induces yawning via the muscarinic receptors of effectors from which the respiratory neurons in the medulla, the motor nuclei of the Vth,VIIth, IXth, Xth, and XIIth cranial nerves, the phrenic nerves (C1-C4) and the motor supply to the intercostal muscles. An arousal response accompanied by yawning behavior can be evoked by electrical and chemical stimulation of the hypothalamic paraventricular nucleus (PVN) in rats, although the mechanism responsible for the arousal response accompanied by yawning evoked by PVN stimulation is still unknown.
 
 
==Development in humans==
 
Yawn is present in fetuses as shown by this 3D sonography. Fetal yawning indicates a harmonious progress in the development of both the brainstem and the peripheral neuromuscular function (Walusinski et al., 2005b).]]
 
At the beginning of the third month, the embryo becomes a fetus with the occurrence of the first oral and pharyngal motor sequences under the control of the neurological development of the brainstem which coordinates the respiratory, cardiac and digestive regulations. Circuits that generate organized and repetitive motor patterns, such as those underlying feeding, locomotion and respiration belong to the Central Pattern Generators in the medulla (CPG) which are genetically determined, subserving innate motor behaviors essential for survival. As an example, yawning occurs as early as 12 weeks after conception and remains relatively unchanged throughout life (Walusinski, 2005). Its survival without evolutionary variations postulates a particular importance in terms of developmental needs. The ability to initiate motor behavior generated centrally and linked to arousal and respiratory function is a property of the brainstem reticular formation, which has been remarkably conserved during the phylogeny of vertebrates including agnathans, fishes, amphibians, reptiles, and birds. Thus, yawning and stretching have the traits of related phylogenetic old origins.
 
==Yawning and thermoregulation (the latest and debatable hypothesis)==
 
As reviewer, Gallup adds his new theory: consistent with the role of the hypothalamus and the PVN, evidence from diverse sources suggests that yawning may be a thermoregulatory mechanism (Gallup & Gallup, in press). Multiple sclerosis, epilepsy, schizophrenia, treatment for opiate withdrawal, sleep deprivation, migraine headaches, stress and anxiety, and central nervous system damage are all related to thermoregulatory dysfunction and each of these conditions is associated with atypical yawning. Excessive yawning appears to be symptomatic of conditions that increase brain and/or core temperature, such as central nervous system damage, sleep deprivation, and specific serotonin reuptake inhibitors. Drugs that lead to hypothermia (e.g., opioids) inhibit yawning. Nasal breathing and forehead cooling, which have been identified as specific brain cooling mechanisms, diminish the incidence of yawning (Gallup & Gallup, 2007).
 
There is no work indicating that cerebral activity modifies the internal temperature of the brain in a variable way according to the level of attention. Parmeggiani (2007) has reported changes in brain temperature during the ultradian sleep cycle in several mammalian species. The temperature decrease in NREM sleep appears as a normal effect of thermoregulation operating at a lower set point temperature than in wakefulness. In contrast, the increase in brain temperature related to REM sleep appears paradoxical from the viewpoint of normal thermoregulation. The problem of the physiologic mechanisms underlying this temperature change remains unresolved. Changes in brain temperature are in general relevant to both the energy metabolism of the brain and the function of the preoptic-hypothalamic thermostat. It is obvious that brain homeothermy is altered essentially by quantitative imbalances between metabolic heat production and heat loss. Heat loss from systemic heat exchangers, affecting carotid blood temperature through the systemic venous return to the heart (systemic brain cooling), is the most important determinant of brain temperature in primates. Concerning humans, in particular, there is no consensus as to whether a mechanism for selective brain cooling plays a significant role. The arguments advanced by Gallup & Gallup appear quite slight and little demonstrated.
 
Altough, the origine and function of yawning have been subject to speculations for centuries, the first complete review of the experimental evidences for each of this hypotheses can only now be read (Guggisberg , Mathis et al, 2010).
 
 
==Contagiousness of yawning==
 
Although yawning often procures a sense of well-being for the yawner, attempting to mask this behavior is standard practice. Many worldwide cultural beliefs and myths portray it as socially and singly offensive (Meenakshisundaram, 2008 in press). Hominids have the unique capacity to be receptive to the contagiousness of yawning (echokinesis would be a more accurate term). Yawning appears to trigger a sort of social coordination function (arousal synchrony) and reflects the capacity to unconsciously, automatically be influenced by the behavior of others, supporting the hypothesis that contagious yawning shares the neural networks involved in empathy. Echokinesis only occurs in situations of minimal mental stimulation (public transport, for example); people are not susceptible to this phenomenon during prolonged intellectual effort.
 
Using functional magnetic resonance imaging (fMRI), Schürmann ''et al.'' confirmed that whilst observation of facial gestures in another person caused activation of [[mirror neurons]] in motor areas of the human brain (left posterior inferior frontal cortex), there was no such activation during echokinetic yawning. These ethological and neurophysiological elements demonstrate that, strictly speaking, echokinetic yawning is ''not'' simply motor imitation.
 
Recognition of human faces involves specific dedicated neurons in the temporal lobe. The inferior temporal region (IT) allows immediate overall recognition of faces, both their identity and their expression, apparently through its own autonomous, non-hippocampal memory. As for the superior temporal sulcus (STS), it is specifically activated during perception of eye and mouth movements, which suggests its implication in the visual perception of emotions, once again by the activation of mirror neurons. These neurons mime the expression perceived, helping the observer to understand it. Schürmann et al. demonstrated that the STS is activated during echokinetic yawning. This activation, automatic and involuntarily, is transmitted to the left amygdala, the posterior cingulate cortex and the precuneus. These structures are thought to play a role in differentiating emotions expressed by the human face and, especially, in evaluating the sincerity of the sentiment expressed.
 
Using fMRI, Platek ''et al.'' found a correlation between personality traits and the activation of neuronal circuits beyond the STS. « In contrast to those that were unaffected by seeing someone yawn, people who showed contagions yawing identified their own faces faster, did better at making inferences about mental states, and exhibited fewer schizotypal personality characteristics. These results suggest that contagious yawning might be related to self-awareness and empathic processing». Subjects considered empathetic, who were very susceptible to echokinetic yawning, activated the amygdala and the cingulate cortex, whereas schizotypal subjects, who were not susceptible to this type of yawning, did not activate these structures. Neurophysiological studies of empathy show similar zones of activation (STS, insula, amygdala, cingulate cortex). These data imply that contagious yawning may reside in brain substrates which have been implicated in self-recognition and mental state attribulion, namely the right prefrontal cortex (Platek, 2003, 2005; Schürmann, 2005). Consistent with this view, autistic children who are characterized by impaired mental state attribution do not show contagious yawning (Senju et al., 2007). Giganti and Ziello (2009) support the hypothesis of a link between contagious yawning and social abilities and the existence of different processes underlying spontaneous and contagious yawning.
 
In the interpersonal contact with individuals with schizophrenia we can often experience impaired empathic resonance. Haker H, and Rössler W (2009) try to determine differences in empathic resonance-in terms of contagion by yawning and laughing-in individuals with schizophrenia and healthy controls in the context of psychopathology and social functioning. They conclude Individuals with schizophrenia showed lower contagion rates for yawning and laughing but it may be argued that the treatment by neuroleptic drugs reduce drastically spontaneous and contagious yawning by themselves.
 
==Pathology==
 
On Tuesday, Oct.23, 1888, Jean-Martin Charcot presented, during one of his celebrated Tuesday gatherings at La Salpêtrière, the case of a young woman inconvenienced by 8 yawns a minute, that is 480 per hour! He qualified this as a form of hysteria, despite his examination revealing binasal hemianopsia, right-side cheirobrachial skin insensitivity to all stimuli and loss of smell. Given our contemporary knowledge, this points to a pituitary adenoma.
 
The disappearance of yawning may be due to an extrapyramidal syndrome, to the use of opioid drugs or high doses of caffeine, but is rarely a cause for complaint. The family-medicine practice shows that excessive yawning is a source of embarrassment in social circles. There are multiple causes of excessive yawning, that is, a cluster of 10 to 30 yawns, many times a day. Of short duration, they may predict a vasovagal reaction or neurovegetative disorders (dyspepsia, migraine-like syndromes). All insults to the intra-cranial central nervous system or the hypothalamo-hypophyseal region may be involved: tumors with intracranial hypertension, infections, temporal epilepsy, strokes, etc. For example, we coined the term "parakinesia brachialis oscitans" to describe cases of hemiplegia where the onset of yawning coincides with involuntary raising of the paralysed arm. We argued that a lesion in the internal capsule affecting an inhibitory pathway liberates certain subcortical structures that coordinate the massive inspiration of yawning and the motor control associated with quadrupedal locomotion (Walusinski, 2005).
 
The development of psychotropic drugs has given rise to a rich iatrogenic pathology: serotoninergic agents, apomorphine, acetylcholinesterase inhibitors, sismotherapy and, opiate withdrawal are triggers of yawn clusters. Excessive sleepiness with excessive yawning should suggest examination for an obstructive sleep apnea syndrome. Finally, after after ruling out all other causes, some patients may be suffering from a type of chronic motor tic disorder, associated with yawn clusters, and treated with haloperidol (Walusinski, 2009).
 
Selective serotonin reuptake inhibitors (SSRI) have significant side effects from stimulation of 5-HT2A, 5-HT2C and 5-HT3, from noradrenergic receptor stimulation, as well as from interactions at other receptors including muscarinic, histaminergic, and postsynaptic alpha1-adrenergic. Complex neurotransmitter systems make pin-pointing an exact mechanism of yawning induction difficult and conflicting data exist regarding the role of specific neurotransmitters. Yawning as side effect was described with paroxetine, escitalopram, duloxetine. The excessive yawning was not accompanied with drowsiness. The error would be to believe in the aggravation of the depression and to increase doses of SSRI treatment. This side effect disappeared completely once treatment was terminated (Gutiérrez-Álvarez, 2007).
 
==Conclusion==
 
Yawning and pandiculation are a universal behaviour amongst vertebrates, closer to an emotional stereotypy than a reflex. Phylogenetically ancient and ontogenetically primitive, they exteriorize homeostatic processes of systems controlling wakefulness, satiety and sexuality in the diencephalon. An arousal response accompanied by yawning behavior can be evoked (Baenninger, 1997; Walusinski, 2006).
 
==References==
 
* Argiolas A, Melis MR. The neuropharmacology of yawning. ''Eur J Pharmacol''. 1998;343(1):1-16.
 
* Baenninger R. On yawning and its functions. ''Psychonomic Bul Rev''. 1997;4(2):198-207.
 
* Baenninger R., Binkley S., et al. Field observations of yawning and activity in humans. ''Physiol Behav''. 1996; 59:421-425.
 
* Deputte BL. Revue sur le comportement de bâillement chez les vertébrés. Bull Int Soc Fr Etud Comport Anim. 1974;1:26-35.
 
* Giganti F, Ziello ME. Contagious and spontaneous yawning in autistic and typically developing children. Current Psychology Letter 2009;25(1)
 
* Gallup AC, Gallup GG Jr. Yawning as a brain cooling mechanism: Nasal breathing and forehead cooling diminish the incidence of contagious yawning. ''Evol Psychol''. 2007;5:92-101.
 
* Gallup AC, Gallup GG Jr. Yawning and thermoregulation. ''Physiol Behav''. 2008;95:10-16
 
* Guggisberg AG, Mathis J, Schnider A, Hess CW. Why do we yawn ? ''Neurosci Biobehav Rev. 2010;34:1267-1276.
 
* Gutiérrez-Álvarez ÁM. Do your patients suffer from excessive yawning? Acta Psychiatrica Scandinavica 2007;115(1):80-81.
 
* Haker H, Rössler W. Empathy in schizophrenia: impaired resonance. Eur Arch Psychiatry Clin Neurosci. 2009, in press.
 
* Kita I, Yoshida Y, Nishino S. An activation of parvocellular oxytocinergic neurons in the paraventricular nucleus in oxytocin-induced yawning and penile erection. ''Neurosci Res''. 2006;54(4):269-275.
 
* Meenakshisundaram R, Walusinski O, et al. Yawning, comparative study of knowledge and beliefs popular and medical. "J Ethnobiology Ethnomedicine". 2008 Submitted
 
*Parmeggiani PL. REM sleep related increase in brain temperature: a physiologic problem Archives italiennes de biologie 2007;145(1):13-21 .
 
* Platek SM, Critton SR, Myers TE, Gallup GG Jr. Contagious yawning: the role of self-awareness and mental state attribution. ''Brain Res Cogn Brain Res''. 2003;17(2):223-227.
 
* Platek SM, Mohamed FB, Gallup GG Jr. Contagious yawning and the brain. ''Brain Res Cogn Brain Res''. 2005;23(2-3):448-452.
 
* Provine R.R., Tate B.C., Geldmacher L.L. Yawning: no effect of 3-5% CO2, 100% O2, and exercise. ''Behav Neural Biol''. 1987;48:382-393.
 
* Provine RR. Yawning. ''American Scientist''. 2005;93(6): 532-539.
 
* Sato-Suzuki I, Kita I, Oguri M, Arita H. Stereotyped yawning responses induced by electrical and chemical stimulation of paraventricular nucleus of the rat. ''J Neurophysiol''. 1998;80(5):2765-2775.
 
* Schürmann M, Hesse MD, Stephan KE, Saarela M, Zilles K, Hari R, Fink GR. Yearning to yawn: the neural basis of contagious yawning. ''Neuroimage''. 2005;24(4):1260-1264.
 
* Seuntjens W. On yawning or the hidden sexuality of the human yawn. ''Thesis. Vrije Universiteit''. 464p. Amsterdam. Oct 2004.
 
* Senju, A, Maeda, M, Kikuchi, Y, Hasegawa, T, Tojo, Y, Osanai, H. Absence of contagious yawning in children with autism spectrum disorder. ''Biology Letters''. 2007;3: 706-708.
 
* Walusinski O, Deputte BL. Le bâillement: phylogenèse, éthologie, nosogénie. ''Rev Neurol (Paris)''. 2004;160(11):1011-1021.
 
* Walusinski O, Quoirin E, Neau JP. Parakinesia brachialis oscitans. ''Rev Neurol (Paris)''. 2005a;161(2):193-200.
 
* Walusinski O, Kurjak A, Andonotopo W, Azumendi G. Fetal yawning assessed by 3D and 4D sonography. ''The Ultrasound Rev Obs Gyncecol''. 2005b;5(3):210-217.
 
* Walusinski O. Yawning: Unsuspected avenue for a better understanding of arousal and interoception. ''Med Hypotheses''. 2006;67(1):6-14.
 
* Walusinski O. Yawning in Diseases. Eur Neurol. 2009;62(3):180-187.