Richard A. Chole

Role of electrode placement as a contributor to variability in cochlear implant outcomes.

Suboptimal cochlear implant (CI) electrode array placement may reduce presentation of coded information to the central nervous system and, consequently, limit speech recognition. Background: Generally, mean speech reception scores for CI recipients are similar across different CI systems, yet large outcome variation is observed among recipients implanted with the same device. These observations suggest significant recipient-dependent factors influence speech reception performance. This study examines electrode array insertion depth and scalar placement as recipient-dependent factors affecting outcome. Methods: Scalar location and depth of insertion of intracochlear electrodes were measured in 14 patients implanted with Advanced Bionics electrode arrays and whose word recognition scores varied broadly. Electrode position was measured using computed tomographic images of the cochlea and correlated with stable monosyllabic word recognition scores. Results: Electrode placement, primarily in terms of depth of insertion and scala tympani versus scala vestibuli location, varies widely across subjects. Lower outcome scores are associated with greater insertion depth and greater number of contacts being located in scala vestibuli. Three patterns of scalar placement are observed suggesting variability in insertion dynamics arising from surgical technique. Conclusion: A significant portion of variability in word recognition scores across a broad range of performance levels of CI subjects is explained by variability in scalar location and insertion depth of the electrode array. We suggest that this variability in electrode placement can be reduced and average speech reception improved by better selection of cochleostomy sites, revised insertion approaches, and control of insertion depth during surgical placement of the array.

Genotypic Differences in Behavioral, Physiological and Anatomical Expressions of Age-Related Hearing Loss in the Laboratory Mouse: Original Papers Travaux originaux

The auditory nerve isoelectric thresholds, in response to tone pigs ranging from 5 to 20 kHz, are similar in the young C57BL/6 and CBA/J mice, although the latter genotype has somewhat more sensitive responses from 30 to 80 kHz. But their behavioral audiograms, obtained by the classical conditioning technique of Ehret, are very discrepant. Even though the behavioral audiogram of the CBA/J mouse can be predicted by measurements from its auditory nerve, the behavioral thresholds of the young C57BL/6 mouse are approximately 40 dB less sensitive than its electrophysiological measurements. Cochlear hair cell loss was not evident in young mice of either genotype. As the CBA/J approaches the end of its predicted life span, its auditory anatomy, physiology and behavior are not significantly altered; but those rare individuals, who exceed their predicted life span by 40% finally develop hearing loss of a mixed nature. By contrast, the C57BL/6 mouse shows a relatively rapid decline of hearing as it ages. By 200 days of age, its auditory nerve responses are 30 dB less sensitive at 5 kHz, and 55 dB less sensitive at 30 kHz, than similar measures taken at adolescence. Over this same age span, its behavioral sensitivity has only declined by 15 and 25 dB at these two frequencies. Hair cell counts correlated poorly with both behavioral and electrophysiological auditory measures in the C57BL/6 mouse.

Pathophysiology of otosclerosis.

Objective To review current knowledge of the pathophysiology of otosclerosis and to review hypotheses for the amelioration of this disease. Data Sources Review of the literature and experimental observations by the authors. Conclusions Otosclerosis is a localized disease of bone remodeling within the otic capsule of the human temporal bone. Unlike other similar bone diseases, it does not occur outside of the temporal bone. These lesions seem to begin by resorption of stable otic capsule bone in adults, followed by a reparative phase with bone deposition. There are clearly genetic factors that lead to this disease, but measles virus infection and autoimmunity also may play contributing roles. Surgical correction of the conductive hearing loss is highly effective, but nonsurgical intervention has not yet been shown to prevent or slow the disease. Of the factors that may inhibit this process, fluorides, cytokine inhibitors, and bisphosphonates, third-generation bisphosphonates appear to hold the most promise.

Tinnitus, vertigo, and temporomandibular disorders

Although tinnitus and vertigo have been reported as associated with temporomandibular disorders (TMD) for many years, no control studies have been reported. This study was designed to include two large control populations, as well as a large TMD sample. The null hypothesis was tested. The results revealed that tinnitus and vertigo were significantly more prevalent in the TMD group than in either control group. Reasons for the association of TMD and these otologic symptoms have been proposed and they are discussed. Presently the cause is unknown.

Petrous Apicitis Clinical Considerations

Although petrous apicitis was a frequent occurrence in the first half of this century, it has become an uncommon disease because of the widespread use of antibiotics for otitis media. In this series of eight cases of petrous apicitis it is evident that petrositis cannot be equated with Gradenigos triad (otitis, abducens paralysis, and deep pain) since none of the cases manifested with the classical syndrome. Abducens paralysis was seen in only two of the eight cases. Deep facial or ear pain was present in four of the eight cases and appeared to be the most useful symptom in the diagnosis of petrositis. Four of the eight cases were discovered only after previous, unsuccessful surgical procedures. Chronic petrous apicitis may be occult and manifest only after failure to control suppuration by conventional tympanomastoid surgery. When petrositis is suspected, conventional x-ray study may show bone erosion and asymmetric clouding of the petrous tip. Computed tomographic scanning was most useful in the delineation of bone destruction and opacification of the apex. When the diagnosis of petrous apicitis is made, aggressive surgical drainage is indicated.

Experimental retraction pocket cholesteatoma.

An animal model for retraction pocket (primary acquired) cholesteatoma is presented. Bilateral eustachian tube obstruction by electrocauterization of the nasopharyngeal portion was performed in 16 Mongolian gerbils. Animals were killed at 2, 4, 8, and 16 weeks. At 2 weeks all animals had bilateral serous effusions and retracted tympanic membranes. At 4 weeks, four of eight ears had middle ear fluid, retractions, and cholesteatomas. After 8 weeks, five of eight ears had middle ear effusions, and four of these had cholesteatomas; one ear had total atelectasis with a cholesteatoma filling the bulla. By 16 weeks, six of eight ears had developed cholesteatomas. Some animals did not develop effusion or retraction because of failure or recanalization of eustachian tube obstruction. This study provides experimental evidence that aural cholesteatomas may arise by retraction of the tympanic membrane.

Anatomical studies of the posterior petrous apex with regard to hearing preservation in acoustic neuroma removal

Some surgeons have shown that tumors of the internal auditory canal and cerebello‐pontine angle may be removed with preservation of hearing through the suboccipital approach. If hearing is to be conserved, the cochlear division of the VIIIth cranial nerve and blood supply of the labyrinth must be preserved. In addition, surgical entry into the labyrinth, upon removal of the posterior wall of the internal auditory canal, must be avoided since it is likely to result in permanent sensorineural hearing loss.

Cholesteatoma: Experimental Induction in the Mongolian Gerbil, Meriones Unguiculaus

Surgical ligation of the external auditory canal of the Mongolian gerbil produces aural cholesteatomas that are similar to the spontaneous gerbilline cholesteatoma. Some 6-9 months after ligation of the external auditory canal, these cholesteatomas are in contact with the bone of the middle ear. These induced cholesteatomas were seen to erode bone and displace soft tissue structures, as is typical of human aural cholesteatomas. The induced gerbilline cholesteatoma is an ideal experimental model for the study of the osteolytic characteristics of cholesteatoma.

Optimal cochlear implant insertion vectors.

Hypothesis: An optimal insertion trajectory during cochlear implantation may be determined from the anatomic relationship between the facial nerve and round window. Background: Cochlear implantation functional outcomes improve with insertion of the implant into the scala tympani. This depends on creating a cochleostomy in the proper position and inserting the electrode along a trajectory coaxial with the centerline of the scala tympani. The anatomic landmarks for this insertion trajectory have not been described. Methods: Clinical computed tomography and micro-computed tomographic analysis of 8 cadaveric temporal bones. Results: Appropriate insertion vectors pass inferior or anteroinferior to the round window membrane. In many individuals, the facial nerve interrupts all or most of the insertion vectors coaxial to the centerline of the scala tympani. Conclusion: A cochleostomy placed inferior or anteroinferior to the round window membrane may facilitate atraumatic insertion of a cochlear implant along the centerline of the scala tympani. The lateral and anterior wall of the fallopian canal must be adequately thinned to achieve an optimal insertion trajectory. This is particularly true when inserting through cochleostomies placed away from the round window along the basal turn of the cochlea.

A mechanism for sympathectomy-induced bone resorption in the middle ear.

BACKGROUND Recent investigations have demonstrated a link between sympathectomy and osteoclast-mediated bone resorption. The exact nature of this link, however, is unknown. We hypothesize that substance P, a potent vasoconstrictive neuropeptide found in peripheral sensory fibers, including those innervating bone, is the mediator of this phenomenon. To test this theory, the effects of substance P on in vitro calcium release from cultured neonatal mouse calvaria were assessed. In addition, an in vivo study was conducted whereby gerbils were injected with capsaicin to eliminate substance P-containing fibers before sympathectomy with 6-hydroxydopamine. If the effects of 6-hydroxydopamine were eliminated by prior administration of capsaicin, the role of sensory nerves in sympathectomy-induced resorption would be strongly implicated. IN VITRO STUDY Substance P at 10(-8) mol/L was incubated with eight newborn Swiss-Webster mouse hemicalvarial explants and compared with explants incubated in control media alone. The neonatal mice were euthanized at day 3, and their hemicalvaria were preincubated in 2 ml of stock media without treatment for 24 hours at 36.5 degrees C as a stabilization period. After the stabilization period, the stock media were replaced with 2 ml of fresh control media or media containing substance P at 10(-8) mol/L. A similar experiment was performed with the addition of indomethacin at 5 x 10(-7). The explants were then incubated for 72 hours with gassing every 12 hours with a mixture of O2, N2, and CO2. At the end of the 72-hour period, the media were analyzed for calcium content by atomic absorption spectrophotometry and compared by one-way analysis of variance with Bonferroni-corrected post hoc tests. IN VIVO STUDY Forty-eight Mongolian gerbils were placed into four groups: group 1 received intraperitoneal injections of 6-hydroxydopamine at 75 micrograms/gm body weight on days 1, 2, 6, 7, and 8; group 2 received identical injections of hydroxydopamine, but 12 hours after receiving subdermal injections of capsaicin at 50 micrograms/gm body weight; group 3 received only subdermal injections of capsaicin; and group 4 received only saline injections to serve as controls. Seven days after treatment, the animals were euthanized, and the ventral wall of each animals right bulla was resected and quantified for osteoclast number and surface with a computer-based histomorphometry system. Analysis was then made by one-way analysis of variance with Bonferroni-corrected post hoc tests. RESULTS The results of the in vitro study revealed that substance P at 10(-8) mol/L (11.05 +/- 3.37 micrograms/ml) induced significant calcium release from cultured neonatal mouse calvaria when compared with control bone incubated in base media alone (0.92 +/- 2.85 micrograms/ml, p < 0.01). The process was completely inhibited by 5.0 x 10(-7) indomethacin. The results of the in vivo study showed 6-hydroxydopamine treatment significantly increased both the osteoclast number (NOc/TL = 3.14 +/- 1.33/mm) and the osteoclast surface (OcS/BS = 16.04% +/- 6.95%) of bone when compared with bone from saline-treated controls (NOc/TL = 1.77 +/- 0.79/mm, p < 0.01; OcS/BS = 8.88% +/- 4.15%, p < 0.01). These 6-hydroxydopamine-induced increases were eliminated, however, in animals pretreated with capsaicin before sympathectomy (NOc/TL = 1.86 +/- 0.68/mm, p > 0.05; OcS/BS = 9.92 +/- 3.73, p > 0.05), whereas treatment with capsaicin alone had no effect when compared with bone from saline-treated controls (NOc/TL = 2.02 +/- 0.50/mm, p > 0.05; OcS/BS = 10.28% +/- 2.62%, p > 0.05). Substance P has thus been shown to induce calcium release from membranous bone in vitro, whereas capsaicin, a substance P-specific sensory neurolytic chemical, eliminates the in vivo osteoclast-inductive effects of 6-hydroxydopamine when given 12 hours before treatment. The results indicate that substance P is capable of inducing resorption and that substance P-containing sensory ne