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- mise à jour
du
- 20 janvier
2026
- Dent
Med Probl.
- 2026;63(1):5-7
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- Yawning
as a clinical clue?
- Revisiting
COMISA phenotypes
- in
sleep-disordered breathing
- Meira E Cruz
- Sleep Unit, Cardiovascular
Center of the University of Lisbon, Lisbon
School of Medicine, Portugal
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- Abstract
- Nocturnal yawning may represent a subtle
clinical marker of arousal instability in
patients with sleep-disordered breathing (SDB),
potentially unveiling latent comorbid insomnia
and sleep apnea (COMISA) phenotypes, and
expanding the interpretative scope of
sleep-related behaviors.
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- Les bâillements nocturnes peuvent
constituer un marqueur clinique subtil de
l'instabilité de l'éveil chez les
patients souffrant de troubles respiratoires du
sommeil (TRS), révélant
potentiellement des phénotypes latents
d'insomnie et d'apnée du sommeil
comorbides (COMISA) et élargissant le
champ d'interprétation des comportements
liés au sommeil.
Importance
of yawning in the evaluation
of excessive daytime
sleepiness
- The recent case
report by Michalek et al. describes a rare
and intriguing cooccurrence of yawning during
sleep in a patient with obstructive sleep apnea
(OSA) and sleep bruxism (SB). The researchers'
hypothesis of a hypoxiatriggered arousal
mechanism is compelling and well-grounded in the
observed polysomnographic patterns. Nonetheless,
it would be interesting to integrate further
reflections that may expand and enrich the
interpretation of this complex behavioral
constellation.
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- One critical angle that deserves
consideration is the possible presence of
insomnia-related physiology, particularly within
the framework of comorbid insomnia and sleep
apnea (COMISA). Although this diagnosis has not
been formally addressed, some reported features,
such as marked sleep fragmentation,
microarousals and low adherence to positive
airway pressure (PAP) therapy, are often part of
some COMISA phenotypes and may reflect a
background of sleep-state hyperarousal, which is
frequently observed in those patients.
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- Indeed, it has been recently proposed that
COMISA encompasses a heterogeneous spectrum,
with emerging interest in identifying clinical
phenotypes. While such phenotypic models are
still in the hypothesis-building stage and
require stronger empirical validation, the
existence of subclinical insomnia manifested
through subtle neurophysiological and behavioral
mechanisms, even in the absence of subjective
complaints, is increasingly recognized as a
relevant issue in both clinical practice and
sleep research.
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- In this context, the observed nocturnal
yawning might be not only a direct response to
hypoxia, but also a behavioral expression of the
underlying arousal instability, which could
reflect a latent insomniac phenotype with
challenging aspects from the clinical point of
view. This possibility highlights an
often-overlooked dimension in sleep medicine -
the presence of non-overt insomnia traits that
nonetheless modulate sleep architecture,
treatment adherence and the emergence of
sleep-related motor behaviors.
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- Moreover, COMISA patients frequently show
the dysregulation of sleep-wake transitions, a
state that can facilitate the intrusion of
transitional behaviors, such as yawning, into
otherwise consolidated sleep. Also, recent
evidence suggests that SB may play a mechanistic
and phenotypic role in COMISA, potentially
reflecting a hyperarousaldriven motor expression
that is intensified in the presence of
overlapping insomnia and OSA. In a
polysomnographic study by Blaszczyk et al.,
patients with COMISA presented a significantly
higher frequency of rhythmic masticatory muscle
activity (RMMA) and bruxism-related arousals as
compared to patients with OSA alone.
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- These findings support the idea that SB may
serve as a physiological link between cortical
arousal and autonomic dysregulation, helping to
explain the heightened motor instability
observed in COMISA cases. Yawning, traditionally
associated with sleep onset or state
transitions, may in these cases re-emerge
inappropriately due to an incomplete inhibition
of wake-promoting networks, possibly exacerbated
by the repeated respiratory-related arousals of
OSA, eventually associated with motor
exacerbations. Similar mechanisms were described
in clinical reports of unusual yawning patterns
associated with SB and OSA.
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- This proposal is further strengthened by
neurobiological insights. As Blaszczyk et al.
noted, yawning, bruxism and sleep fragmentation
share overlapping neurochemical pathways,
particularly those involving dopaminergic
modulation. The hypothesis that bruxism and
yawning share common subcortical circuitries,
particularly within the basal ganglia and
hypothalamus, could reflect a broader state of
central disinhibition, where motor pattern
generators are more likely to get activated in
the presence of disturbed arousal
regulation.?& These considerations align
with recent data on the etiological mechanisms
and metabolic consequences of OSA, including
inflammation, oxidative stress and insulin
resistance.?,10 From a clinical perspective,
raising awareness about such subclinical or
latent forms of insomnia embedded in OSA
presentations is vital. These forms often go
unrecognized due to the absence of explicit
complaints, but may substantially influence
treatment outcomes, including tolerance to PAP
therapy, symptom persistence and behavioral
adherence. Recognizing this overlap,
particularly through unusual motor or autonomic
markers, such as nocturnal yawning, may open new
diagnostic and therapeutic pathways.
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- As illustrated in Fig. 1, yawning may emerge
at the intersection of OSA, subclinical insomnia
and SB, reflecting shared arousal-related
mechanisms. Nocturnal yawning might serve as a
clinical clue, albeit subtle and unspecific, of
latent COMISA physiology, especially in patients
who otherwise present a predominantly
respiratory sleep disorder phenotype. Such
behavioral markers may reflect deeper layers of
arousal instability and neurochemical
dysregulation that are not easily captured by
conventional sleep diagnostics.
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- In conclusion, the unusual case reported by
Micha_ek et al.! provides fertile ground for
reflection. While the hypoxiaarousal mechanism
is essential, the integration of additional
domains, namely subclinical insomnia expression,
COMISA-related hyperarousal, neurochemical
overlap, and behavioral arousal markers, may
offer a broader, more integrative understanding
of these phenomena. On the other hand, framing
yawning as a potential clinical clue, rather
than a mere physiological reflex, invites us to
revisit the complexity of COMISA phenotypes and
rethink how subtle behaviors during sleep can
guide us toward more precise diagnostic and
therapeutic strategies.
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