Intensity of MR contrast enhancement does not correspond to clinical and electroneurographic findings in acute inflammatory facial nerve palsy.

PURPOSE: To determine the value of MR contrast enhancement in predicting the course of acute inflammatory facial nerve palsy and in selecting patients for surgical decompression. METHODS: Six patients with an acute inflammatory incomplete or complete peripheral facial nerve palsy (five idiopathic and one herpetic in origin) had repeated MR imaging studies with and without contrast enhancement, electroneurography, and clinical examinations to establish a connection between the intensity of contrast enhancement on MR images, the clinical condition, and the electrophysiological data. The examinations were performed every second day starting on the first day of admission until clinical recovery was proved by clinical deblockage (spontaneous clinical improvement). The last examination was performed 3 months after the onset of the facial nerve palsy. RESULTS: An abnormal, very intense contrast enhancement of the facial nerve was always present in the distal intrameatal and proximal tympanic segments and in the geniculate ganglion. The labyrinthine segment exhibited a mild to moderate enhancement, and the distal tympanic and mastoid segments showed a moderate to intense enhancement. The intensity of contrast enhancement did not correspond to the severity, duration, or course of the facial nerve palsy, and the electroneurographic data had no predictive value in indicating the severity of the inflammatory process. Three months after clinical recovery, a persistent and more or less unchanged or even slightly more intense contrast enhancement was observed. CONCLUSION: The long-lasting intense contrast enhancement seen in the facial nerve segments of patients who have acute peripheral inflammatory facial nerve palsy is explained by a two-phase breakdown of the blood-nerve barrier.

Correlation of MRI, clinical, and electroneuronographic findings in acute facial nerve palsy.

Intratemporal enhancement of (Gd-DTPA) was investigated by an interleaved-overlapping magnetic resonance imaging (MRI) technique in 35 cases of acute facial palsy. In a reference group (normal facial function), enhancement was localized from the ganglion geniculi to the stylomastoid foramen. In cases of acute palsy, the facial nerve enhanced in the meatal fundus independent of etiology (idiopathic, herpetic, or traumatic). In 70% of those with Ramsay-Hunt syndrome, the vestibular and cochlear nerves, the labyrinth, and the sheets of the internal and external auditory canal additionally enhanced. No correlation was found between intensity, extension, and duration of the enhancement and the clinical, intraoperative, or electroneuronographic degree of the facial palsy. The pathogenesis of the Gd-DTPA enhancement of the facial nerve appears to be closely connected with the vascular supply of the fallopian canal and the permeability of the neural sheets.

Ototoxicity of ear drops: a clinical perspective.

Although experimental data confirm the presence of ototoxicity due to topical ear drops, the clinical relevance still remains debatable. Only few case reports document sensorineural hearing loss (SNHL) attributable to ototopical preparations in patients with chronic otitis media. A careful review of 134 patients charts evaluated between 1953 and 1995 for possible antibiotic related ototoxicity revealed two patients with bilateral profound SNHL attributable to excessive administration of framycetin- and polymyxin-containing ear drops in the presence of tympanic membrane perforation. Although ototopical preparations are widely used, they rarely induce SNHL. The authors emphasize patient education, application of topical ear drops using soaked gauze strips, and documentation of the patients hearing status at the beginning of the treatment regimen.