Otogenic facial paralysis is peripheral facial paralysis caused by conditions such as otitis media or middle ear cholesteatoma.
Pathology
Otitis media can destroy the bony facial nerve canal, allowing the inflammation to invade the facial nerve tissue. The inflammation may spread into the facial nerve canal through fissures, vascular connections, or other pathways, leading to nerve edema, inflammatory cell infiltration, hemorrhage in the nerve sheath, and venous thrombosis. These changes result in swelling of the endoneurium, venous congestion, compression of arterial blood supply, ischemia, nerve dysfunction, and even nerve degeneration. This inflammatory swelling differs from the edema seen in viral or traumatic facial paralysis.
Cholesteatomas can compress the tympanic, geniculate (geniculate ganglion), or mastoid segments of the facial nerve canal.
Figure 1 Bony wall defect of the geniculate segment of the facial nerve canal
Congenital cholesteatomas often destroy the labyrinthine segment of the facial nerve and further compress the nerve tissue. The thick outer sheath of the facial nerve in the mastoid and geniculate segments makes these areas particularly susceptible to increased pressure, leading to nerve degeneration and facial nerve paralysis.
Clinical manifestations
The clinical features of facial paralysis caused by otitis media or cholesteatoma can be seen in peripheral facial paralysis.
Treatment
During the acute phase of otitis media, antibiotics should be used to control the infection. Corticosteroids are administered to reduce facial nerve edema.
The underlying disease, such as cholesteatoma or infection, should be eliminated. Facial nerve decompression can be performed. The bony facial nerve canal can be opened and the outer sheath of the nerve can be incised to relieve swelling.
Neurotrophic drugs can be used to support nerve recovery. Facial massage can be applied to prevent facial muscle atrophy.