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                     mise à jour
                     du1 octobre
                     2025Cranio2025
                     Sep4:1-5 | 
                     Yawning-induced
                     alternobaric facial palsyin a
                     healthy young adult:A case
                     report and review of the
                     pathophysiology Cammalleri M, Zatta E, Sala G, Fusetti S,
                     Salmini Sturli A, Favero V | 
                     
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                     AbstractAlternobaric 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
                     bâillementLa 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'il
                     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
                     
                     
IntroductionFacial 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. ConclusionThis 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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