Histopathology of Facial Nerve Disorders
The normal histology of the facial nerve needs defining before discussing the histopathology. The facial nerve is composed of ∼10,000 neurons, 7,000 of which are myelinated and innervate the nerves of facial expression. Three thousand of the nerve fibers are somatosensory and secretomotor and make up the nervus intermedius. The nerve fibers, containing microfilaments and microtubules, are surrounded by a multilayered myelin sheath. The fibers are in turn surrounded by endoneurium that encompasses each fiber but also surrounds groups of fibers to form fascicles. In the temporal bone, a tough perineurium surrounds the entire nerve and is cushioned from surrounding tissues and structures by the epineurium ( Fig. 3.1a, b ).
Sitting atop the nerve at the external genu where the nerve makes a sharp turn posteriorly, at the junction of the meatal and tympanic segments, is the geniculate ganglion that carries autonomic fibers from the greater superficial petrosal nerve.
The chorda tympani nerve, which carries taste and glandular secretory fibers, is an integral part of the facial nerve extending from the geniculate ganglion area to the descending mastoid segment, where it leaves the facial nerve to cross the middle ear. The fibers are not recognizable within the nerve unless it has been divided proximal to the geniculate ganglion. In this case, they can be seen as a discrete bundle of fibers near their exit from the tympanic segment ( Fig. 3.2 ).
A congenital dehiscence of the tympanic segment of the fallopian canal containing the nerve may occur in 30% of ears, per Shea as quoted by Kaplan ( Fig. 3.3 ).1 The dehiscence may be large enough to allow a prolapse of the nerve so that it appears to be a middle ear tumor.
Histopathology
A variety of exogenous circumstances can affect the facial nerve. These can generally be classified as idiopathic, inflammatory, and neoplastic. We describe the various pathologies in each of these categories and provide histopathological examples.
Idiopathic
Bell palsy or idiopathic facial paralysis is a unilateral, sometimes recurrent facial nerve paralysis that usually spontaneously recovers. In a few cases, it may become permanent or result in partial impairment or synkinesis. Although referred to as “idiopathic,” there is some suggestion that the etiology may be viral. Inflammatory cells have been seen early in the course of the paralysis, and there is clinical evidence that the paralysis is due to a herpes simplex infection.2 When the nerve is surgically decompressed at the time of paralysis, there is often evidence of an inflammatory swelling of the nerve. The narrowest area of the facial nerve canal is the labyrinthine segment, and this is believed by many to be the primary site of nerve compression by inflammatory edema ( Fig. 3.4 ).
No residual histologic abnormalities are found in the nerves of patients who have been left without residual paralysis. However, in those cases with incomplete recovery, there are varying amounts of residual degenerative changes manifested by areas of the nerve that stain poorly with hematoxylin and eosin, and may exhibit some edema and residual round cell accumulations ( Fig. 3.5 ).
Inflammation
Viral
Herpes zoster refers to a reactivation of the latent chicken pox virus. When the process affects the temporal bone, it causes facial nerve paralysis as well as inner ear disturbances (Ramsay Hunt syndrome). The acute phase is manifested by an infiltration of the geniculate ganglion, atop the facial nerve, by lymphocytes and plasma cells.3 Recovery of the nerve and function is variable. The number of adjacent fibers that are poorly stained depends on the degree of residual function. Fig. 3.6a, b shows the partially degenerated nerve of an 83-year-old woman who suffered a total facial paralysis, concha rash, vertigo, and hearing loss 7 years prior to death. Recovery of facial function was to House-Brackmann facial nerve grade II. The vertigo subsided, but a 35 dB hearing deficit remained.
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