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
!
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.
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).
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