Case Report: Flight-related facial baroparesis and third-window lesion

Introduction

Transient peripheral facial nerve palsy related to air travel is a rare clinical entity that has received relatively little attention in the otologic and neurotologic literature. AFP has historically been attributed to barometric changes acting at the level of the middle ear, particularly during ascent and descent, when rapid pressure differentials across the tympanic membrane may produce localized facial nerve compression (Bloch et al., 2023; Alwan and Gordan, 2021; Mikuš, 2020). This mechanism presumes some degree of Eustachian tube dysfunction, allowing negative or positive middle-ear pressure to develop.

More recent case reports, however, suggest that temporal bone anatomy may play a critical role in susceptibility. High-resolution temporal bone CT has revealed thinning or dehiscence of the tympanic segment of the facial canal in selected patients with recurrent AFP (Ah-See et al., 2012; Motamed et al., 2000). These anatomic variations may provide a direct path for pressure transmission from aerated spaces to the facial nerve.

In parallel, the otologic literature has identified third-window lesions—areas of bony dehiscence within the otic capsule that can alter labyrinthine fluid mechanics (Garaycochea et al., 2018; Gianoli, 2022; Merchant and Rosowski, 2002; Thomson and Madani, 2014). These include classic superior semicircular canal dehiscence, but also less common variants such as cochleo-facial dehiscence (CFD) (Garaycochea et al., 2018). CFD describes focal loss of bone between the second cochlear turn and the labyrinthine segment of the facial nerve canal, potentially increasing labyrinthine compliance and modifying sound or pressure transmission to inner-ear structures (Merchant and Rosowski, 2002; Thomson and Madani, 2014). Although CFD has been associated with vestibular migraine, autophony, and atypical auditory symptoms, it has not been clearly linked to AFP.

An additional factor rarely discussed is mastoid and petrous hyper pneumatization. Extensive air-cell development may modify the distribution and propagation of pressure within the temporal bone (Hussein et al., 2019; Ben-Ari et al., 2024). In the presence of focal dehiscence, these pneumatized cells could enable micro pressure gradients capable of stressing vulnerable neural segments.

Here we present a case of recurrent, transient right-sided peripheral facial palsy occurring exclusively at cruising altitude. Unlike previously reported cases, our patient had

• normal tympanometry and audiometry,
• abnormal cVEMP suggestive of third-window physiology,
• multiple focal bony dehiscences on HRCT, and
• marked petrosal bone hyper pneumatization.

To our knowledge, this is the first case integrating neurophysiologic evidence, thin-cut CT imaging, and real-time in-flight video documentation to support a barometric facial nerve neuropraxia mechanism independent of middle-ear dysfunction.

Case description

A *25 years-old*woman presented with episodes of sudden-onset right-sided facial weakness occurring only during commercial flight and exclusively at cruising altitude. Each episode began abruptly once the aircraft had reached a stable flight ceiling, without associated pain, otalgia, or ear fullness, and resolved spontaneously within approximately 20–30 min. The patient reported a *total of five episodes*of transient facial weakness occurring during separate commercial flights, consistently when the aircraft reached cruising altitude. Each episode lasted less than 30 min but was sufficiently prolonged to allow clear visual observation of facial asymmetry. She had **no prior history of middle-ear disease, otologic surgery, or chronic ear symptoms**. Outside the flight environment, she did not report classical third-window manifestations such as sound-induced vertigo, pressure-induced dizziness, bone-conduction hyperacusis, or voice autophony. During the in-flight episodes only, besides autophony she occasionally perceived a transient aural sensation described as a brief click associated with ipsilateral auricular numbness.

There were no symptoms during ascent, descent, or landing, and no associated hearing loss, tinnitus, vertigo, diplopia, limb weakness, or dysarthria.

Self-recorded smartphone videos captured during episodes documented a visible, peripheral-type facial palsy on the right, predominantly affecting the lower and middle facial thirds. *A retrospective assessment performed by a senior otolaryngologist was consistent with a House–Brackmann grade III–IV peripheral facial palsy* (House and Brackmann, 1985).

Between episodes, otologic and neurologic examinations were normal. There were no spontaneous or positional nystagmus and no gaze-holding abnormalities. Cranial nerve function was otherwise intact.

Audio vestibular evaluation

Pure-tone audiometry showed normal thresholds bilaterally. Speech audiometry was within normal limits (Figure 1A). Tympanometry demonstrated type A curves bilaterally with normal middle-ear pressure and compliance. Stapedial reflexes were present bilaterally (Figure 1B). Cervical vestibular evoked myogenic potentials *(cVEMPs)were performed using a Biologic Navigator Pro system (Natus Medical Inc., Pleasanton, CA, USA) withair-conducted 500-Hz tone bursts delivered through insert earphones*. Surface electromyographic activity was recorded over the sternocleidomastoid muscles according to standard methodology. Although suprathreshold amplitudes were higher on the left side, the most relevant physiologic finding was a lower response threshold on the symptomatic right side (~80 dB nHL) compared with the contralateral ear (~90 dB nHL) (Figure 1C). This asymmetric threshold pattern was interpreted as increased labyrinthine compliance, consistent with *a possiblethird-window pathophysiology. The *cVEMPs profile did not suggest alternative vestibular pathology such as Ménière disease or vestibular migraine, particularly given the patient's young age and absence of fluctuating auditory symptoms.**

Radiological evaluation

A dedicated high-resolution CT (HRCT) of the temporal bone with 0.5–0.6 mm slices was therefore obtained in axial, coronal, and sagittal planes.

The HRCT demonstrated:

• Extensive hyper pneumatization of the mastoid and petrous portions of the temporal bone, with confluent and well-developed air cells (Figures 2, 3A, B).
• On the right side, a focal bony dehiscence of the inferior aspect of the lateral semicircular canal, directly facing the tympanic segment of the facial nerve canal (Figures 3A, B).
• A right cochleo-facial dehiscence, with millimetric contact between the labyrinthine segment of the facial canal and the posterosuperior surface of the second cochlear turn (Figures 4A, B).
• Normal configuration and density of the remaining cochlea, vestibule, and other semicircular canals.
• Normal internal auditory canals, carotid canals, jugular bulbs, vestibular and/or cochlear aqueducts, and bony otic capsule outside the dehiscent regions.

No mass lesions, inflammatory changes, or abnormal enhancing processes were identified on additional MRI of the posterior fossa and cerebellopontine angles, which was performed to exclude central causes or a neurovascular conflict involving the facial nerve. *Imaging was independently reviewed by senior otolaryngologists involved in patient care and discussed with an experienced neuroradiologist specialized in temporal bone *imaging.**

In-flight documentation

One of the episodes was captured on a self-recorded smartphone video obtained in-flight at cruising altitude. The video clearly demonstrated right-sided lower facial paresis, with asymmetry of the oral commissure and malar depression, without altered consciousness, dysarthria, or ocular dysmotility (Supplementary Video 1).

Management and outcome

Considering the recurrent nature, the clear temporal association with cruising altitude, and the anatomical vulnerabilities identified on HRCT, the case was interpreted as a barometric neuropraxia of the facial nerve facilitated by two ipsilateral otic capsule dehiscences and mastoid hyper pneumatization.

After discussion with the patient, a long-term transtympanic ventilation tube was placed in the right ear. The rationale was to provide more stable pressure equilibration and to reduce localized barometric stress in the region of the dehiscent segments. *Following the *procedure, the patient traveled by airplane without recurrence of facial symptoms.** At last follow-up, she remained asymptomatic and was highly satisfied with the outcome.

Discussion

Most reports of AFP describe symptoms occurring during ascent or descent and attribute them to barometric stress generated by rapid pressure variations within the temporal bone air spaces rather (Bloch et al., 2023; Alwan and Gordan, 2021; Mikuš, 2020; Ah-See et al., 2012; Motamed et al., 2000). During ascent, changes in ambient pressure and air density may lead to transient hyperpressure within the mastoid pneumatic system, resulting in mechanical stress on an exposed or dehiscent segment of the facial nerve within the fallopian canal, particularly along its tympanic portion.

In contrast, our patient had normal tympanic membrane mobility, normal tympanometry, and normal acoustic reflexes on multiple tests. Therefore, middle-ear pressure dysfunction was unlikely to be a primary mechanism.

Instead, we propose that temporal bone anatomy, particularly multiple focal bony dehiscences combined with petrosal bone hyper pneumatization, would facilitate barometric stress reaching some fragile portions of the facial nerve at cruising altitude.

Third-window pathophysiology

The lower cVEMP threshold (~80 dB nHL) on the symptomatic side supports an atypical third-window phenomenon, as third-window lesions typically reduce impedance and increase sensitivity to pressure stimuli (Gianoli, 2022; Merchant and Rosowski, 2002; Thomson and Madani, 2014; Hussein et al., 2019). *Classical third-window lesions often demonstrate markedly reduced cVEMP thresholds *(<65–70 dB nHL). In the present case, threshold reduction was more moderate. This may be explained by the small surface area and biomechanical orientation of the micro-dehiscence, resulting in limited acoustic energy shunting toward the endolymphatic system, particularly at 500-Hz stimulation frequencies.**

The patient's cochleo-facial (Garaycochea et al., 2018) and lateral semicircular canal–facial dehiscence (Gianoli, 2022) are radiologic substrates capable of producing abnormal labyrinthine compliance. Beyond isolated defects, the existing anatomo-clinical classification emphasized that otic capsule dehiscences (Reynard et al., 2022) behave as three functional categories of third-window abnormalities depending on their biomechanical expression which might be slightly different.

Within this framework, our patient most closely aligns with a multi-window phenotype, in which coexisting third-window interfaces—namely the lateral semicircular canal–facial canal dehiscence and the cochleo-facial micro-dehiscence—may act synergistically. Notably, this configuration did not produce the classic audiometric signature typically associated with third-window lesions, such as bone-conduction hyperacusis or an apparent air–bone gap. Instead, functional evidence of altered labyrinthine mechanics was provided by cervical vestibular evoked myogenic potentials, which demonstrated a lower response threshold on the side harboring the micro-dehiscences. This neurophysiological finding closely mirrors the anatomical abnormalities identified on high-resolution CT and supports the presence of clinically relevant third-window-like physiology despite the absence of overt audiometric manifestations.

Mastoid hyperpneumatization as a pressure amplifier

The extensive petrosal bone air-cell system seen in this case may have provided a large pneumatic reservoir capable of amplifying subtle intracavitary pressure changes during prolonged cabin hypobaria (Hussein et al., 2019; Ben-Ari et al., 2024). Under cruising-altitude conditions, the relatively reduced ambient pressure does not merely create a passive hypobaric environment but may instead induce a relative hyperpressure within the hyperpneumatized mastoid air-cell system, acting as a large volumetric reservoir. This compartmental hyperpressure can generate micropressure vectors directed toward zones of minimal mechanical resistance, particularly at dehiscent interfaces involving the facial nerve course. Such focused stress may result in transient conduction block and facial nerve neuropraxia.

A similar hyperpressure phenomenon might theoretically occur at the onset of descent, when ambient pressure begins to increase. However, in the present case, no symptoms were reported during descent. This paradoxical absence of symptoms may be explained by a possible more efficient pressure equilibration mechanism, likely mediated by passive opening of the Eustachian tube during increasing ambient pressure, allowing more effective venting of mastoid air spaces compared with the stabilized hypobaric conditions encountered at cruising altitude.

Cruising altitude specificity

A distinguishing feature of this case is the exclusive occurrence of symptoms at cruising altitude rather than during ascent/descent. Previous AFP cases emphasize rapid barometric shift as the trigger (Bloch et al., 2023; Alwan and Gordan, 2021; Mikuš, 2020; Ah-See et al., 2012; Motamed et al., 2000). Here, a steady-state hypobaric environment appears sufficient to induce focal neural dysfunction, likely through slow pressure drift within hyper pneumatized temporal bone compartments.

Therapeutic implications

The successful resolution of symptoms following insertion of a transtympanic ventilation tube suggests that providing continuous pressure equilibration within the middle ear and mastoid reduces barometric stress at dehiscent sites. Ventilation tube placement may thus represent a simple and effective intervention in selected patients.

Strengths and limitations

A major strength of this case lies in the multimodal correlation between clinical findings, high-resolution temporal bone imaging, cervical vestibular evoked myogenic potentials, and in-flight video documentation, supporting barometric neuropraxia involving third window micro-dehiscences. The convergence of anatomical and functional data strengthens the proposed interpretation. However, this report is limited by its single-case nature and by the absence of direct middle-ear pressure measurements. In addition, the clinical presentation did not exhibit classic symptoms typically associated with otic capsule dehiscence, which limits the extent to which the identified anatomical defects alone can be considered causative. It should also be noted that the CT acquisition slice thickness (0.5–0.6 mm) may introduce partial-volume effects, potentially overestimating the presence of a true bony dehiscence. The observed findings may therefore correspond to extremely thin bone rather than complete absence of the osseous barrier. Higher-resolution imaging modalities, such as photon-counting CT or flat-panel systems with sub millimetric resolution, could provide more definitive anatomical characterization. However, given the complete clinical resolution following tympanostomy tube placement and the absence of recurrence, additional imaging was not considered clinically necessary. Should symptoms recur, higher-resolution imaging would be considered.

Conclusion

This case suggests that APF palsy can alternatively arise from intratemporal pressure transmission mediated by temporal bone dehiscence and mastoid hyperpneumatization, not only by middle-ear barotrauma. High-resolution CT and cVEMPs are valuable diagnostic tools. As in other similar conditions, transtympanic ventilation tube placement may prevent recurrence in susceptible patients.

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Supplementary material

The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fauot.2026.1767522/full#supplementary-material

Supplementary material Supplementary material at the source

Footnotes

Edited by: Bryan Kevin Ward, Johns Hopkins University, United States

Reviewed by: Gerald Fritz Schusser, Leipzig University, Germany

Batoul Berri, University of Michigan, United States