Alternobaric facial paresis, facial baroparesis, baroparesis facialis, or alternobaric facial nerve palsy is a neurapraxia of the seventh cranial nerve due to pressure effects.
The pressure in the middle ear can cause compression of the facial (seventh cranial) nerve against the tympanic promontory (cochlear promontory). Symptoms are similar to Bell's palsy. It occurs on ascent during airplane trips or with diving. Equalization of the middle ear pressure can make it disappear (yawning, swallowing, or a Toynbee maneuver). This pressure issue may also cause alternobaric vertigo. A causative relationship between middle-ear overpressure and facial palsy may be supported by the palsy's rapid onset when ambient pressure is reduced, as well as, its quick disappearance when ambient pressure increases or the middle ear overpressure releases. Divers experience a similar palsy, ischemic neurapraxia of the fifth cranial nerve, from compression in the maxillary sinus. Misdiagnosis as neurologic DCS or air embolism results in unnecessary recompression treatment and restriction of diving.
Although human tissue can withstand significant pressure, tissue injury can occur when a gas-filled space is unable to equilibrate to environmental pressure. This can be an increase or decrease in pressure. This phenomenon is called barotrauma. Two conditions must be present for barotrauma to occur: a change in ambient pressure and 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 (as compared to ambient pressure) on ascent whether in the water or air. A pressure increase in the middle ear of as little as a few feet of seawater (66 cmH2O) can impede capillary blood flow to the facial nerve traversing the area producing ischemic neuropathy.
Any rapid decrease in ambient pressure may be responsible for peripheral facial paralysis. This typically occurs either in an ascent in diving (SCUBA or surface supplied) and in flying. Cases have occurred from ascent in the mountains as well. It is a rare condition and undoubtedly under-reported as it is usually quite transient, lasting from only a few minutes to a few hours. Interestingly, this condition is not reported with helium-breathing mixtures but has been reported during breath-hold diving.
The facial nerve follows a complex path. The middle part of the facial nerve runs along the medial wall of the tympanic cavity. It is deeply embedded in its anterior portion, but superficial in its posterior portion, bulging in the tympanic cavity and constituting the prominence of the facial canal. The tympanic portion is located above the dimple of the vestibule window. At this level, the wall of the facial canal is thin exposing 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 in the facial canal.
Even though the facial nerve lies in a bony canal as it traverses the middle ear, the nerve is not uncommonly exposed due to bony defects or dehiscences. One study found an incidence of this occurring in over 50% of the otherwise normal population.
Patients may report a sensation of "plugged ear" or "fullness of the ear" often acute pain and hearing loss. Sometimes hemotympanum occurs (with or without tympanic membrane perforation). 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 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 and is not consistent with alternobaric facial palsy.
Testing is unlikely to be of use. The diagnosis is based on history and findings consistent with a peripheral facial nerve palsy. MRI can be used to exclude stroke as well as to image the inner ear.
Rapid management within 3 hours is important 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. Toynbee maneuver (nose pinch followed by swallowing) and Valsalva (exhale against a closed mouth and pinched nose) maneuver 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 contained in the tympanic cavity to escape. As a last resort, myringotomy may be used.
In the airplane, the pressure variation in the eardrum is resolved upon landing.
Another therapeutic means 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 the ambient pressure. Recovery under hyperbaric oxygen therapy was observed in less than 2 minutes, under normobaric oxygen therapy at high flow within 15 minutes.
Prophylactic use of topical nasal decongestants is also considered helpful although given rare recurrences it is unlikely to be unnecessary.
Until the palsy is resolved, the most significant risk is of corneal damage due to keratitis from an inability to fully blink. This can be ameliorated with eye lubricant and eye patching.
Obviously, decompression sickness affecting the brain (type II) or cerebral gas embolism must be considered when a diver returns to surface and exhibits a neurological deficit. However, the scenario and lack of other symptoms (other than vertigo on occasion sue to alternobaric vertigo) strongly suggest baroparesis.