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Alternobaric Facial Paresis

Editor: Eric J. Hexdall Updated: 2/25/2024 7:43:31 PM


Alternobaric facial paresis (AFP), also known as facial baroparesis, baroparesis facialis, or alternobaric facial nerve palsy, is a rare and usually transient neurapraxia affecting the seventh cranial nerve (CNVII, the facial nerve) due to pressure-related effects in the tympanic cavity.[1][2][3] AFP arises when pressure in the middle ear compresses the facial nerve against the cochlear promontory in the medial wall of the tympanic cavity, resulting in symptoms resembling Bell palsy. Symptoms can include the inability to wrinkle the forehead, to close the eye, to smile symmetrically, and sometimes to taste on the back of the tongue. Sparing of the forehead should suggest a central rather than peripheral cause, like stroke, and is inconsistent with AFP. 

The diagnosis of AFP is based on history and findings consistent with peripheral facial nerve palsy in the setting of appropriate exposure to situations that can impede pressure equilibrium in the middle ear (usually diving or flying). AFP most commonly occurs on ascent during air travel or when surfacing with diving. Equalization of the middle ear pressure (yawning, swallowing, or Toynbee or Valsalva maneuver) can make it disappear. This pressure disequilibrium may also cause alternobaric vertigo. Misdiagnosis as neurologic decompression sickness or air embolism results in unnecessary recompression treatment and restriction of diving activities.

A causative relationship between middle-ear over-pressure and AFP is suggested by the palsy's marked on/off responses to changes in ambient pressure. AFP demonstrates rapid onset with drops in ambient pressure, and it disappears when ambient pressure increases or the middle ear over-pressure releases.

Generally, AFP is transient and resolves with equalizing pressure in the middle ear. If that pressure is not relieved, permanent facial nerve palsy can ensue, similar to the spectrum of deficit seen in Bell palsy. 


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Caused by a changing pressure gradient across the tympanic membrane in the presence of a combination of Eustachian tube dysfunction and a dehiscent facial canal, AFP occurs most commonly with underwater diving but has also been reported with high-altitude airplane travel.

Although human tissue can withstand significant pressure, tissue injury can occur when a gas-filled space cannot equilibrate to an increase or decrease in environmental pressure. This phenomenon is called barotrauma. For barotrauma to occur, 2 conditions must be present: a change in ambient pressure and a transfer of pressure to a gas-filled space. Failure of the Eustachian tube to equalize pressure between the middle ear and external ear canal due to mucosal edema from irritation, infection, or allergy can lead to elevated middle ear pressure (compared to ambient pressure) on ascent, whether in the water for a diver or ascending or descending during air travel. A pressure increase in the middle ear of as little as a few feet of seawater (66 cm H2O) can impede capillary blood flow to the facial nerve traversing the area, causing compressive ischemic neuropathy.[1][4]  Generally, these cases are seen in scuba diving, free diving, and flying, although cases have been reported from traveling to altitudes, including hiking.[5]  


Any rapid decrease in ambient pressure may be responsible for peripheral facial paralysis due to alternobaric trauma. AFP typically occurs in an ascent in diving (SCUBA or surface supplied) or flying. Cases have also occurred during mountain climbing ascents. AFP is undoubtedly underreported, given that many cases are brief—lasting from only a few minutes to a few hours—and do not recur.[6] Interestingly, this condition is not reported with helium-breathing scuba diving gas mixtures but has been reported during breath-hold diving. [2]

Eustachian tube dysfunction plays a role in alternobaric facial paresis, as described above. The incidence of Eustachian tube dysfunction in the United States was estimated at 4.6% based on NHANES data collected between 2001 and 2006 and 2009 and 2012.[7] There is a male predominance of about 2:1. Eustachian tube dysfunction is almost always unilateral.[5] 

Even though the facial nerve lies in a bony canal as it traverses the middle ear, it is frequently exposed due to bony defects, known as dehiscences. Interestingly, the predisposing defect of facial canal dehiscence anywhere along the canal is a common anatomic variant: one study found dehiscence occurring in more than 50% of the otherwise healthy study sample; another study reported dehiscence rates as high as 29%, with a third of those being bilateral.[8][9] More commonly, studies report dehiscence rates between 18% to 33%.[10][11][12]


The facial nerve follows a complex path, making it vulnerable to compressive ischemic injury at some points on its lengthy pathway from the brainstem to the periphery. The middle part of the facial nerve travels along the medial wall of the tympanic cavity, where its anterior portion is deeply embedded; in its posterior portion, it lies superficially, bulging in the tympanic cavity and constituting the prominence of the facial canal (the portion of the temporal bone connecting the internal auditory canal to the stylomastoid foramen).[2] The tympanic portion of the nerve's pathway lies above the vestibule window's dimple. At this level, the wall of the facial canal is thin and can expose the facial nerve. Without pressure equalization of the middle ear, a descent of just 4 feet underwater yields a 90-mmHg pressure differential. This pressure is sufficient to impinge the facial nerve if it is exposed within the facial canal.

At present, consensus supports the hypothesis that AFP results from an ischemic neuropraxia caused by compression of the vasa nervorum, the capillary blood supply to the nerve.[5] A recent report supports the association of hyperpneumatization of the temporal bone as an etiologic factor in developing AFP: most of the imaging reviewed revealed at least one area of temporal bone hyperpneumatization.[13]  Some cases have been reported as associated with predisposing ear surgeries, eg, transmastoid decompression for a facial nerve Schwannoma.[5]

History and Physical

Patients with AFP may report a sensation of "plugged ear" or "fullness of the ear," along with acute pain and hearing loss. Occasionally, there is face and tongue numbness and paresthesia. Headache has been reported.[5] Sometimes, hemotympanum occurs (with or without tympanic membrane perforation). Other occasional symptoms arise, such as acute onset otalgia and hearing loss. [14]  Alternobaric vertigo can occur concomitantly: a unilateral overpressure in the tympanic chamber stimulates the labyrinthine system, causing vertigo. Peripheral facial paralysis can occur in water (near the surface) or soon after emergence.

Examination shows unilateral lower motor neuron facial paralysis, sometimes accompanied by altered taste sensation. The otoscopic examination may find a bulge of the tympanum. Recall that peripheral facial nerve palsy should affect the entire ipsilateral side of the face with no "central sparing" of the forehead muscles. Sparing of the forehead should suggest a central rather than peripheral cause, like stroke, and is inconsistent with AFP.  


The diagnosis of AFP is based on history and findings consistent with peripheral facial nerve palsy in the setting of appropriate exposure to situations that can impede pressure equilibrium in the middle ear (usually diving or flying).

MRI can be used to image the inner ear and to exclude stroke or underlying mass lesion. High-resolution CT scanning of the temporal bone has poor (66%) sensitivity for finding the facial canal defect, which predisposes to AFP. However, high-resolution CT is the study of choice for imaging the course of the nerve within the fallopian canal to the stylomastoid foramen.[15][16] There may be utility for this test to exclude other potential etiologies, such as neoplasm, in the setting of repeated occurrences of AFP.[16][15] Further testing is unlikely to be of use.

Treatment / Management

In AFP, rapid management within 3 hours of symptom onset is essential to avoid permanent injury to the facial nerve.   

Simple maneuvers should be tried to reduce pressure in the eardrum. Yawning and swallowing may open the Eustachian tube. The Toynbee (nose pinch followed by swallowing) and Valsalva (exhaling against a closed mouth and pinched nose) maneuvers work similarly. Chewing gum or food can likewise open the Eustachian tube. The use of local decongestants has the same goal: to reduce the edema of the Eustachian tube and its meatus in the nasopharynx to allow the air in the tympanic cavity to escape. As a last resort, a simple myringotomy may be used.[14]

In the airplane, the pressure variation in the eardrum is typically resolved upon landing. Another therapeutic measure is to ensure sufficient local oxygenation. The increase in blood oxygen content by high-rate oxygen inhalation opposes the effects of ischemia; the air contained in the middle ear is gradually eliminated by ventilation of the Eustachian tube or resorbed locally.

Hyperbaric oxygen therapy, generally with a low-pressure setting of about 1.2 ATA (absolute technical atmosphere) with pure oxygen respiration, has been used to treat this type of barotrauma. This therapy combines the actions of oxygenation and the increase of ambient pressure. Recovery under hyperbaric oxygen therapy was observed in less than 2 minutes, and under normobaric oxygen therapy at high flow within 15 minutes. A recent study in rats demonstrated facial nerve regeneration with hyperbaric oxygen therapy, a promising area for future research.[17](B3)

Prophylactic use of topical inhaled decongestants is anecdotally helpful, although it is unlikely to be unnecessary given rare recurrences. Oral decongestants may be efficacious as well. For example, a study of pseudoephedrine for middle ear discomfort during flight showed a statistically significant decrease in symptoms from 62% to 32%.[18] Although treatment with both oral and intranasal decongestants can be done, there is evidence that oral decongestants may be more effective than topical for the prevention of otic barotrauma (and therefore for the prevention of AFP), eg, oxymetazoline nasal spray appeared to be a little better than placebo.[19]  (A1)

In the setting of recurrent AFP episodes related to flying, venting myringotomy tubes can prevent the pressure differential causing the problem.[8][20] However, this would present a contraindication for diving. (B3)

Differential Diagnosis

Cerebral air embolism or decompression sickness, which occurs when inert gas comes out of solution and forms bubbles as the surrounding pressure decreases during ascent to the surface, is a serious potential sequelae of diving that must be considered whenever a diver returns to the surface exhibiting a neurological deficit. However, in AFP, the precipitating scenario and lack of symptoms (other than occasional vertigo due to alternobaric vertigo) strongly suggest baroparesis. 

Other rare transient unilateral facial paresis occurrences have been reported, including subarachnoid bleed, transient ischemic attack, high altitude cerebral edema, and tumor.[21][22][23] History of diving, flying, or other changes in ambient pressure helps exclude these issues.  


Generally, AFP is a transient condition and resolves with equalization of pressure in the middle ear.  If that pressure is not relieved, permanent facial nerve palsy can ensue, similar to the spectrum of deficit seen in Bell's palsy.  AFP can be a recurrent issue for divers and flyers alike. Permanent facial nerve damage results if treatment is not initiated promptly. Grommet myringotomy can be used for recurrent AFP from flying, but deliberately perforating the tympanic membrane would be a poor solution, given exposure to open water, in divers.  


There is limited understanding of AFP in the literature, which creates the possibility of under- and over-diagnosis of AFP. Misdiagnosis of central facial palsy (forehead sparing is the hallmark of this) as AFP could delay the diagnosis of stroke or another intracranial issue. On the other hand, a case of AFP mistaken as a stroke can lead to excessive reactions, such as the emergency landing of a commercial aircraft, followed by emergent hospital stroke evaluation, extensive neuroimaging, and an overnight stay.[24]

Likewise, failure to recognize the nature of AFP, particularly in the high altitude setting, can lead to misdiagnosis and inappropriate management.[5] Recompression treatment and advanced imaging are expensive and time-consuming. If AFP is mistaken in a diver as an air embolism, this will lead to unnecessary recompression treatment, restricted diving, and additional testing and treatment.  

Until the AFP is resolved, the most significant risk is corneal damage due to keratitis from an inability to blink fully. This can be alleviated with eye lubricant and eye patching.

Deterrence and Patient Education

Patients who have had only a single episode of AFP and are without known Eustachian tube dysfunction can usually be managed conservatively. Such patients should understand how AFP occurs and that it is not synonymous with other causes of facial nerve paresis. 

All patients with a history of AFP should be counseled to avoid air travel if they have an upper respiratory tract infection. They should also be instructed correctly to conduct maneuvers to equalize middle ear pressure. They should be warned about the risk of permanent facial nerve injury should prolonged ischemia occur in a future episode of AFP. 

Pearls and Other Issues

"Alternobaric" is defined as something resulting from differences or alternations of air pressure.

Misdiagnosing alternobaric facial palsy as decompression illness may lead to an unnecessary transfer to a hyperbaric facility and expensive, time-consuming, and contraindicated therapy.  

Enhancing Healthcare Team Outcomes

AFP is a rare neurological condition involving transient facial paralysis due to changes in ambient pressure. Typically associated with scuba diving or air travel, AFP manifests as unilateral facial weakness during pressure variations. Clinicians must recognize the distinct features of AFP, differentiate it from other causes of facial palsy, and consider the patient's recent activities. The condition is generally self-limiting, but monitoring for complications and providing reassurance are essential. This summary emphasizes prompt recognition and differentiation, enabling clinicians to offer appropriate management and guidance for individuals experiencing AFP.

Neurologists, emergency medicine physicians, critical care physicians, advanced practitioners, nurses, and other health professionals involved in the care of patients with AFP should possess the essential clinical skills and knowledge to diagnose and manage it accurately. This includes expertise in recognizing the varied clinical presentations of facial nerve paresis and the ability to distinguish AFP from upper motor neuron (ie, "central") presentations along with understanding the approach to AFP-specific evaluation and management. Patient and caregiver education about triggering factors and maneuvers to equilibrate middle ear pressure is essential to prevent morbidity from AFP.



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