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- mise à jour
du
- 1 octobre
2025
- Cranio
- 2025
Sep4:1-5
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- Yawning-induced
alternobaric facial palsy
- in a
healthy young adult:
- A case
report and review of the
pathophysiology
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- Cammalleri M, Zatta E, Sala G, Fusetti S,
Salmini Sturli A, Favero V
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- Abstract
- Alternobaric facial palsy (AFP) is a rare
peripheral facial nerve palsy resulting from
transient neurapraxia when sudden
ambient-pressure changes disrupt middle-ear
equilibrium. Common precipitants include scuba
diving, air travel, and altitude. AFP triggered
by routine activities is exceedingly
uncommon.
-
- A healthy 27 year old man developed acute
right facial paresis after a prolonged yawn,
while in the car. He reported ear fullness,
cheek and tongue numbness, and inability to
close the right eye, without other neurological
sympthoms. Examination revealed a right
peripheral facial palsy (House - Brackmann Grade
IV), positive Bell's sign, and otherwise normal
findings. CT and MRI of the brain and temporal
bones showed no lesions. Other causes were
ruled-out. Given the abrupt onset, absence of
structural pathology, exclusion of other
etiologies, AFP was diagnosed.
-
- Prednisone (50 mg, tapered over 3 weeks),
eye care, and close follow-up led to full
recovery within three weeks. No recurrence
occurred at 3, 6, or 12 months.
-
- This case highlights an atypical AFP trigger
- a simple yawn - and underscores the importance
of considering alternobaric mechanisms in acute
peripheral facial palsy, even in everyday
settings.
-
- Résumé
Une paralysie
barotraumatique déclenchée par un
bâillement
- La paralysie faciale barotraumatique est une
paralysie rare du nerf facial
périphérique résultant
d'une neurapraxie transitoire lorsque des
changements soudains de pression ambiante
perturbent l'équilibre de l'oreille
moyenne. Les facteurs déclenchants
courants sont la plongée sous-marine, les
voyages en avion et l'altitude. La paralysie
faciale barotraumatique déclenchée
par des activités courantes est
extrêmement rare.
-
- Un homme de 27 ans en bonne santé a
développé une parésie
faciale aiguë du côté droit
après un bâillement
prolongé, alors qu'il se trouvait dans
une voiture. Il a signalé une sensation
de plénitude dans l'oreille, un
engourdissement de la joue et de la langue, et
une incapacité à fermer l'œil
droit, sans autres symptômes
neurologiques. L'examen a
révélé une paralysie
faciale périphérique droite
(degré IV de House-Brackmann), un signe
de Bell positif et des résultats par
ailleurs normaux. Le scanner et l'IRM du cerveau
et des os temporaux n'ont montré aucune
lésion. D'autres causes ont
été exclues. Compte tenu de
l'apparition soudaine, de l'absence de
pathologie structurelle et de l'exclusion
d'autres étiologies, un diagnostic de
paralysie faciale barotraumatique a
été posé.
-
- La prednisone (50 mg, à dose
dégressive sur 3 semaines), des soins
oculaires et un suivi étroit ont permis
une guérison complète en trois
semaines. Aucune récidive n'est survenue
à 3, 6 ou 12 mois.
-
- Ce cas met en évidence un
déclencheur atypique de la paralysie
faciale barotraumatique - un simple
bâillement - et souligne l'importance de
prendre en compte les mécanismes de
variations de pression dans la paralysie faciale
périphérique aiguë,
même dans des situations quotidiennes
- Introduction
- Facial paralysis can arise from numerous
central or peripheral aetiologies (1,2,3).
Peripheral facial nerve injuries stem from a
variety of causes, including congenital
anomalies, idiopathic disorders (notably Bell's
palsy), infections, iatrogenic injury, and
metabolic conditions (4), with Bell's palsy
being the predominant etiology [5]. A
less common yet clinically relevant cause is
barotrauma, whose typical triggers include scuba
diving, air travel, or high-altitude exposure
[6). Barotrauma can cause dysfunction of the
Eustachian tube leading to middle-ear pressure
dysregulation, and the resulting overpressure
can impinge on the facial nerve, producing what
is termed facial baroparesis [7). Facial
baroparesis typically presents suddenly and is
often self-limiting, making it likely to be
underrecognized and underreported in clinical
practice. Its propensity for rapid spontaneous
recovery - frequently without medical
intervention - contributes to this
underreporting [8,9]. Pathophysiology of
facial baroparesis remains unclear; however,
studies suggest a combination of Eustachian tube
dysfunction and dehiscence of facial nerve
canal, that can cause the facial nerve to be
directly subjected to elevated middleear
pressures, resulting in a temporary ischemic
neuropraxia [1,10,11]. Literature on
facial canal dehiscence (FCD) shows a wide range
of prevalence: clinical series of middle-ear
surgeries report rates from 6% to 33.3%
[12,13], whereas anatomical (cadaver)
studies find even higher frequencies, between
25% and 57% [14,15]. Most dehiscences
are located in the tympanic segment of the
facial canal, immediately adjacent to the oval
window [16].
-
- We present a unique case of AFP induced by a
simple yawn in an otherwise healthy young adult.
Yet no prior report has identified yawning as an
inciting event and given the complete absence of
yawning-induced facial palsy in the literature,
presenting this case is justified to fill this
observational void and to broaden clinicians'
differential diagnoses for acute facial
paralysis.
-
- Case presentation
-
- A 27-year-old man presented to the Emergency
Department of Azienda Ospedaliera Universitaria
Integrata di Verona with acute right-sided
facial paresis developed immediately after a
long yawn while seated in a car. The episode
started approximately 2 h before his arrival at
the hospital, with the sensation of sudden
fullness in his right ear, numbness of the right
tongue and cheek, and inability to close his
right eye. No other symptoms such as dysphagia,
diplopia, vertigo, or tinnitus were reported by
the patient.
-
- Physical examination revealed a young man in
good general condition, vital signs were within
normal limits and pupillary reflex was normal in
response to light stimulation on both sides.
Cranial nerves examination revealed a right
peripheral facial palsy involving the forehead,
inability to raise the right eyebrow and
drooping of the right corner of the mouth. The
patients showed inability to close the right
eyelid with positive Bell's sign. Facial nerve
palsy was assessed with House-Brackmann Grading
Scale (HBGS), and the patient was scored with
Grade IV (moderate functional impairment, with
significant facial muscle weakness or evident
facial deformity, resulting in pronounced
asymmetry at the corners of the mouth).
-
- Neurological examination yielded otherwise
normal findings, without impairment of speech or
motor functions. Otolaryngology examination
showed normal auditory canals on both sides,
without signs of hemotympanum, abnormalities of
tympanic membrane or presence of lesions.
Routine laboratory tests were within normal
limits.
-
- His past medical history was notable only
for seasonal allergic rhinitis causing nasal
congestion and rhinorrhea. No history of herpes
simplex or herpes zoster, recent rashes,
arthralgias, or fevers were reported. History of
peripheral nerve palsy was negative as well as
history of recent traumas, altitude exposure or
barotrauma. Medications prior to the present
diagnosis included oral antihistamines and nasal
decongestants. The patient underwent a CT scan
of the brain and skull base, as well as an MRI
during the acute phase. The CT scan of the skull
base revealed a dehiscence of the facial nerve
canal. The MRI, particularly the postcontrast
fat-saturated Tl-weighted turbo spin-echo
sequence (Tl TSE FS), demonstrated increased
enhancement of the facial nerve along both its
intralabyrinthine and intramastoid segments.
These imaging findings, while suggestive, are
not pathognomonic for alternobaric palsy, and
the current literature does not unanimously
agree on their diagnostic significance.
- Discussion of differential diagnoses led to
the exclusion of infectious causes such as
Ramsay Hunt syndrome or Lyme disease (absence of
pain or systemic prodromes, absence of vesicular
eruption in ear canal, no tick exposure or
cutaneous rush); polyneuropathies such as
Guillain-Barré syndrome or sarcoidosis
were excluded for their usual affection of both
facial nerves; intracranial masses were excluded
by CT/RMN and others central causes, such as
stroke and multiple sclerosis, were ruled out
(no additional neurological symptoms or
radiological findings).
- In view of the sudden onset, lack of
structural pathology, exclusion of others
possible causes, and presence of possible
Eustachian tube dysfunction from allergic
rhinitis, AFP was diagnosed.
- Treatment was started within 72 h hours from
onset of the symptoms. Oral corticosteroids were
administered (Prednisone 50 mg daily for 7 days,
then tapered over 2 weeks) in accordance with
literature recommendations (17,18), in order to
reduce the risk of unsatisfactory facial nerve
recover and to help reduce inflammation.
Ophthalmic care was made with artificial tears
and overnight eye patching. No indication for
antivirals medications was considered given that
the potential cause of the infectious nature of
the disease had been eliminated.
-
- The patient was dismissed from hospital
after 6 h of observation.
-
- The patient was seen again at our outpatient
clinic 3 days after starting cortisone therapy
and then once a week for the following month. We
reported the improvement of facial movements at
every appointment using HBGS. Facial nerve
function was completely restored after 3 weeks,
without sequelae ore adverse effects from the
corticosteroid therapy. Follow-up was continued
at 3-, 6-, and 12-month without recurrence of
facial palsy.
-
- Discussion acial nerve palsy from barotrauma
results when abrupt hanges in ambient pressure
transmit through the middle ear and mastoid air
cells to a dehiscent portion of the facial
canal, mechanically stretching or compressing
the nerve fibers [19]. Anatomical
studies demonstrate complete facial canal
dehiscence in approximately 12-26% of temporal
bones at the tympanic segment, with up to 55%
showing areas of marked thinning or focal
defects, thereby providing a plausible substrate
for pressureinduced neuropraxia [12,13,20).
The rapid yawning maneuver in our patient likely
created a transient but significant negative
middleear pressure against an unnoticed
dehiscence, precipitating acute nerve
dysfunction.
- A rigorous differential diagnosis is
crucial. Central lesions such as brainstem
stroke typically present with corticofacial
signs and forehead sparing and would be excluded
by normal MRI. Idiopathic Bell's palsy, while
common, usually evolves over hours to days
without an identifiable trigger (21,22). Ramsay
Hunt syndrome involves reactivation of
varicellazoster virus, classically with painful
vesicles in the ear canal and sometimes hearing
loss or vertigo (22,23]. Lyme
neuroborreliosis often has systemic symptoms
(fever, arthralgias), erythema migrans, and
positive serologies (24). Our patient's normal
imaging, lack of prodromal viral symptoms or
rash, negative Lyme titres, and the immediate
temporal correlation with yawning support a
barotraumatic mechanism.
-
- Some authors have reported that narrowing of
the facial nerve canal, particularly at the
labyrinthine segment, may predispose the nerve
to compression and ischemia in Bell's palsy,
suggesting a potential anatomical vulnerability
(25). Others have highlighted that contrast
enhancement of the facial nerve - especially at
the geniculate ganglion and labyrinthine segment
- is frequently observed in affected patients,
though such findings are also seen in other
inflammatory or infectious etiologies
[26]. Additionally, Celik et al.
[27) found a significant increase in facial
nerve width at the labyrinthine, geniculate, and
tympanic segments on the affected side, despite
no significant difference in the canal diameter,
suggesting that nerve swelling within a
relatively fixed bony canal may contribute to
clinical symptoms. Overall, while these
radiological features are commonly described in
Bell's palsy, they have also been described in
the literature in cases of barotrauma-induced
facial palsy.
-
- Despite this convincing clinical picture,
our report has limitations. We did not perform
baseline audiometric or vestibular testing to
assess preexisting subclinical nerve compromise.
Furthermore, electromyography (EMG) performed
later might not distinguish neuropraxia from
axonotmesis in its acute phase. Future cases
should include these evaluations to better
characterize severity and recovery
potential.
-
- Patient-specific factors may have heightened
susceptibility: her history of allergic rhinitis
and chronic Eustachian tube dysfunction would
predispose to middleear pressure dysregulation
and negative pressure events. In addition,
age-related microvascular changes could lower
the threshold for ischemic injury under
mechanical stress. These considerations
emphasize the need to assess individual anatomic
and physiologic vulnerabilities when evaluating
atypical facial palsy.
- A review of published barotraumatic facial
palsy cases - mostly in scuba divers,
freedivers, and airplane passengers during rapid
cabinpressure changes - yields fewer than two
dozen reports worldwide, none implicating
yawning as the sole precipitant [28-31].
To our knowledge, this is the first description
of yawning-induced barotraumatic facial nerve
palsy, marking it as a novel clinical entity.
Its documentation expands the spectrum of
recognized triggers and alerts clinicians to
consider even innocuous Valsalvalike maneuvers
in the etiologic workup.
-
- Conclusion
- This first reported case of yawning-induced
barotraumatic facial nerve palsy highlights a
rare but plausible mechanism of acute facial
paralysis, expanding the spectrum of recognized
triggers. Clinicians should maintain diagnostic
vigilance when evaluating sudden facial palsy,
especially in the absence of typical viral,
vascular, or traumatic causes. Awareness of
potential anatomical predispositions - such as
facial canal dehiscence or Eustachian tube
dysfunction - may aid in early recognition and
appropriate management.
-
- Clinical take-home messages include the
importance of considering even minor barometric
events (like yawning) in the differential
diagnosis and the utility of correlating symptom
onset with potential pressure changes. Future
research should focus on evaluating anatomical
risk factors through high-resolution imaging and
exploring the true prevalence of barotraumatic
facial palsy in non-diving populations.
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