Our data, in conjunction with that of others, suggest that Meniere's disease may predispose patients to intractable BPPV. Hydropically induced damage to the maculae of the utricle and saccule or partial obstruction of the membranous labyrinth may be possible mechanisms that explain the coexistence of Meniere's disease and BPPV.
To develop an objective, fast, and simply performed screening protocol for cis -platinum (CP) ototoxicity, we compared the efficacy of screening with distortion-product otoacoustic emissions (DPOAEs) with the outcome of both conventional and ultra-high-frequency (UHF) audiometry. Baseline audiometric and DPOAE testing was performed in 66 patients, 33 of whom met criteria for inclusion in the final database. Comparisons were made between baseline measurements and those recorded before subsequent CP infusions. Outcomes were analyzed clinically and with paired repeated-measures analysis of variance. Results indicated that DPOAEs and UHF were better measures than conventional audiometry. Further, DPOAEs may be better suited for screening older patients receiving CP chemotherapy because DPOAEs are as sensitive as UHF and are present in a greater number of these patients. Screening with DPOAEs may be enhanced by testing only in the 3- to 5.2-kHz range, thus decreasing testing time. Higher time averages to increase the signal-to-noise ratio and use of this narrower bandwidth might also allow for accurate bedside testing.
Congenital cholesteatoma may originate in various locations within the temporal bone, including the petrous apex, the area of the geniculate ganglion, the jugular foramen, the middle ear, the mastoid process, and the squamous portion of the temporal bone. According to Nager, 1 the mastoid process is the least frequent. We report an unusual case of congenital cholesteatoma that originated in and was restricted to the mastoid process and presented as an expansile mass that compressed the cerebellum. CASE REPORTA 54-year-old woman presented at the University of Miami Ear Institute in 1993 with right neck pain and persistent instability. She had no previous ear surgery. The findings on physical examination were unremarkable, and a hearing test showed a symmetric sloping high-tone sensorineural hearing loss.High-resolution computed tomography (CT) of the temporal bones revealed an expansile lytic lesion in the right mastoid (Fig 1 ). Her mastoid pneumatization was well developed bilaterally. The middle ear, inner ear, attic, aditus ad antrum, and antrum were within normal limits. Magnetic resonance imaging (MRI) of the brain revealed a nonenhancing expansile lesion of the right mastoid, involving the mastoid tip and the posterior aspect of the mastoid air cells (Fig 2). The lesion had compressed the adjacent right cerebellar hemisphere and caused narrowing of the right transverse sinus. On T2-weighted images it was hyperintense, and on Tl-weighted images, moderately hypointense. The signal characteristics were those of a semisolid mass, not of a simple cyst.The patient was lost to follow-up until 1 year later, when she presented with similar symptoms. A subsequent CT without contrast showed no significant differences from the original findings.At surgery the mastoid was found to be filled by the cholesteatoma, which had almost completely destroyed the tegmen mastoideum, the posterior fossa bony plate, and the bony plate covering the sigmoid sinus. The sinodural angle had been invaded and the superior petrosal sinus had been exposed. However, Fig 1. Erosion and expansion of right mastoid. Axial computed tomogram ( 1 -mm-thick section, with gray scale adjusted for bone imaging) at level of epitympanum and internal auditory canal demonstrates erosion and expansion of mastoid, especially at medial margin (arrows), as well as destruction of normal bony septations between mastoid air cells. Internal auditory canal, bony labyrinth, and tympanic cavity are normal.
Azithromycin, an azalide antibiotic, rarely causes ototoxicity. According to the few reports in existence, azithromycin-induced ototoxicity occurred following prolonged high-dose therapy in patients with acquired immunodeficiency syndrome and resulted in a reversible sensorineural hearing loss. We present a case of irreversible sensorineural hearing loss due to azithromycin ototoxicity in an otherwise healthy woman following low-dose exposure to azithromycin.
In a retrospective review of seven patients with AIDS who were diagnosed with necrotizing external otitis between 1990 and 1995, it was found that the presentation of necrotizing external otitis in patients with AIDS differed from the classic description of malignant external otitis in several respects. The patient population was significantly younger and nondiabetic. Granulation tissue was usually absent from the external auditory canal and Pseudomonas aeruginosa was not the predominant pathologic organism. Also, outcome was found to be significantly worse. Thus a high index of suspicion must be entertained and vigorous local and systemic treatment initiated early in the course of disease to achieve a satisfactory outcome.
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