The meatal ganglion in neoplasia and inflammation of the facial nerve.
In the vast majority of facial nerves (88%), the geniculate ganglion is the major component of facial nerve sensory input; in 4% of facial nerves, the number of cells in the geniculate and meatal ganglia are approximately equal, and in 8%, the meatal ganglion is larger than the geniculate ganglion. In rare cases when the geniculate ganglion fails to develop; a large meatal ganglion represents the entire sensory component of the facial nerve. The variable proportions of the facial nerve ganglionic mass reflect genetically programmed levels of different neurotrophic substances that guide the formation of neural systems during their development. (2,3) Although the geniculate ganglion has been implicated in the neoplastic and inflammatory causes of facial paralysis, it is important to recognize the role of the meatal ganglion in similar disorders of the facial nerve.
The most common location of hemangiomas in the temporal bone is the geniculate ganglion (4-6) (figure 2), and the second most common location is the meatal segment of the facial nerve. (6) Since it is generally accepted that the capillary and small-vessel network in sensory ganglia are precursors of capillary hemangioma, the presence of a large meatal ganglion in 12% of temporal bones may be responsible for the development of facial nerve hemangioma within the internal auditory canal.
[FIGURE 1 OMITTED]
[FIGURE 2 OMITTED]
The most common cause of idiopathic facial paralysis (Bell palsy) is now believed to be the reactivation of a latent neurotrophic virus (herpesvirus family) in the sensory neurons of the facial nerve. (7) Although it was first assumed that the geniculate ganglion is the location of this latent viral infection, recent neuroimaging and histopathologic evidence (8,9) places the earliest enhancement (on magnetic resonance imaging [MRI]) in the fundus of the internal auditory canal (figure 3). Most of the radiologic, (8,9) surgical, (10) and histopathologic (11) observations in Bell palsy point to the meatal ganglion as the location of this virus.
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(3.) Farinas I, Jones KR, Backus C, et al. Severe sensory and sympathetic deficits in mice lacking neurotrophin-3. Nature 1994;369 (6482):658-61.
(4.) Lo WW, Horn KL, Carberry IN, et al. Intratemporal vascular tumors: Evaluation with CT. Radiology 1986; 159(1): 181-5.
(5.) Mangham CA, Carberry JN, Brackmann DE. Management of intratemporal vascular tumors. Laryngoscope 1981;91 (6):867-76.
(6.) Fisch U, Ruttner J. Pathology of intratemporal tumors involving the facial nerve. In: Fisch U, ed. Facial Nerve Surgery. Birmingham, Ala.: Aesculapius Publishing; 1977:488-96.
(7.) Adour KK, Bell DN, Hilsinger RL Jr. Herpes simplex virus in idiopathic facial paralysis (Bell palsy). JAMA 1975;233(6):527-30.
(8.) Kohsyu H, Aoyagi M, Tojima H, et al. Facial nerve enhancement in Gd-MRI in patients with Bell's palsy. Acta Otolaryngol Suppl 1994;511:165-9.
(9.) Engstrom M, Abdsaleh S, Ahlstrom H, et al. Serial gadoliniumenhanced magnetic resonance imaging and assessment of facial nerve function in Bell's palsy. Otolaryngol Head Neck Surg 1997; 117(5):559-66.
(10.) Fisch U, Esslen E. Total intratemporal exposure of the facial nerve. Pathologic findings in Bell's palsy. Arch Otolaryngol 1972; 95(4):335-41.
(11.) Gacek RR, Gacek MR. Meatal ganglionitis: Clinical pathologic correlation in idiopathic facial paralysis (Bell's Palsy). Otorhinolaryngol Nova 1999;9:229-38.
Richard R. Gacek, MD
From the Department of Otolaryngology-Head and Neck Surgery, University of Massachusetts Medical School, Worcester.
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|Title Annotation:||CLINICAL NUGGETS|
|Author:||Gacek, Richard R.|
|Publication:||Ear, Nose and Throat Journal|
|Date:||Aug 1, 2008|
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