The facial bone structure and the brain
become distinct starting from a common
embryonic structure, the ectoblast. The
cephalic pole comprises an original
embryological encephalo-facial and
encephalo-cervical segmentation with a strict
topographical correspondence: the
naso-frontal and premaxillary structures are
joined to the anterior brain; the
maxillo-mandibular and anterior cervical
structures are joined to the brainstem and
its nerves. 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:
development
of the suction-deglutition and yawning
activity. Therefore, suction and yawning
have the same embryological origin, which
shows the importance of the brain stem in the
neurophysiological development of the
oropharyngeal activity coordinated with the
respiratory, cardiac and digestive
regulations which have the same
neuroanatomical localisation. Starting at the
12th week of pregnancy, echography reveals
yawning and suction activities, at a
developmental stage when the brain stem is
already individualised and the pituitary
gland has become functional, whereas the
extension of the temporal and frontal
neocortex takes up to 22-24 weeks to reach
completion.
Until now, no specific cerebral structure
has been identified as a yawning centre. A
good number of clinical and pharmacological
arguments indicate that yawning involves the
hypothalamus (particularly the
paraventricular nucleus), the bulbus and
pontic regions, with frontal region
connections in primates and to the cervical
medulla. Muscles which contract during a yawn
are controlled by cranial nerves
5,7,9,10,11,12, cervical nerves C1-C4
(phrenic nerve) and dorsal nerves innervating
the intercostals, or accessory breathing
muscles. During the few hours of life of
anencephalous babies, it has been noted that
they yawn and stretch, a sign of the
mammalian syndrome of awakening activity or
« Rekel
Syndrom ». Patients afflicted with
the locked-in syndrome, still yawn, despite
being paralysed. This shows that yawning
originates in the brain's archaic structures
common to all vertebrates.
The central nervous system is based on a
common overall organisational plan and
reveals, from the most ancient to the most
recent vertebrates, a gradual increase in
complexity corresponding to life levels that
are increasingly independent and functionally
developed. Yawning helps understand the
phylogenesis of the encephalon by inferring a
functional organisational pattern of the
nervous system similar to that advanced by
Paul MacLean
with the superposition of :
- an ancestral "reptilian" brain (brain
stem and central gray nuclei), where yawning
originates,
- a "paleomammalian" brain (limbic system)
common to all mammifers, functioning as a
synaptic and humoral interface, in fact the
seat of the monkeys' emotivity yawn,
- a "neomammalian" brain characterised by
human's cortical development, particularly
the frontal lobes, seat of the "contagious"
yawn.
Vigilance and yawning
Let's forget about the old theories
disproved by contemporary explorations.
Yawning does not oxygenate the brain (a
marathoner would have to yawn at each
stride!), does not alter the thyroid's
activity. Ample inspiration hinders the
venous return to the heart, thus increasing
the peripheral venous pressure; this
contributes indirectly to the flow of
cephalo-rachidian fluid, but without any
identifiable consequence (5,6).
Sleep and awakening regulation is
controlled by some 15 different and redundant
circuits, mainly located in the pons
(adrenergic), the peduncle (dopaminergic),
the hypothalamus (histaminergic), the Meynert
basifrontal region (cholinergic). There are
two permissive networks controlling awakening
that must be inhibited for sleep to occur.
Experiences realised on rodents and non-human
primates confirm the role of each of these
neurotransmitters in triggering yawning.
How is a yawn triggered?
At the moment there is no definite and
irrefutable data on this. Here are some of
the proposed mecanisms.
Vegetative data: the controls
exercised by the autonomous nervous system
(or vegetative) on the major vital functions
are modulated by states of vigilance. The
balance between sympathetic and
parasympathetic activity is modified
depending on the state of vigilance at play.
There is a tendency to a progressive increase
in vagal (parasympathetic) activity from
waking to slow sleep with a peak during tonic
paradoxical sleep, while sympathetic activity
decreases almost proportionally. During
sleep, this leads to a clear reduction of
muscle activity in the upper respiratory
airways. It reaches its maximum during
paradoxical sleep, which is of longer
duration at the end of the night, and
combines overall peripheral muscular
hypotonia with a tendency to collapsus of the
upper respiratory airways. At awakening, the
yawning and stretching open the
pharyngo-larynx to its maximum and activate
the return of muscle tone, which increases
cardiac frequency, blood pressure, muscle
metabolism, all associated with a loosening
up of articulations. Repeated stress
experiments trigger the suppression of
paradoxical sleep in association with the
disappearance of yawning. This seems to
confirm the close link between paradoxical
sleep and yawning, which does not mean that
the effect of stress does not count.
Reflex data: fatigue, boredom, lack
of sleep, etc, have an impact on muscle tone,
which is perceived by the nervous system
(deep sensibility). The control of muscle
tone in the nape of neck (trapezius) and of
the masseters is one of the elements
contributing to the triggering of our
awakening. The modification of this tone
would be the triggering event of the yawning
reflex. During the powerful contraction
caused by yawning, the spindles of the
masticatory muscles (masseters, temporal,
inner and outer pterygoid), which have
receptors that respond to stretching, send
influxes via afferent fibres of the Ia
category, which are located in the
mesencephalic root of the trifacial nerve.
With the motoneurons of the same muscles
these fibres form a monosynaptic link. This
is the basis of the masseteric reflex. These
fibres have projections on the reticular
formation and the locus cruleus (two
structures involved in the awakening
mechanisms) which are anatomically close to
the nucleus of the trifacial nerve (motor
nucleus of the mastication muscles). Through
the massive contraction of the masseteric
muscles, yawning stimulates those structures
responsible for cortical activation. The fact
that the amplitude of the masseteric reflex
varies in parallel with the level of
vigilance constitutes another argument.
Under this perspective, yawning is
triggered by the stimulation of reticular
activity and of the locus cruleus, thus
acting as a vigilance reflex, as confirmed by
the nature of neurotransmitting
secretions.