The Triological Society 106Th Annual Meeting Program Sunday, May 4, 2003 Delta Ballroom C
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THE TRIOLOGICAL SOCIETY 106TH ANNUAL MEETING PROGRAM SUNDAY, MAY 4, 2003 DELTA BALLROOM C 7:00 Reception for New Fellows 7:30 Business Meeting (Members Only) 8:00 Welcome and Presidential Address - Roger L. Crumley, MD*, Irvine, CA 8:15 Introduction of Guest of Honor - Brian F. McCabe, MD*, Iowa City, IA 8:20 Presidential Citations Richard L. Goode, MD*, Stanford, CA Charles J. Krause, MD*, Marco Island, FL W. Fred McGuirt, Sr., MD*, Winston-Salem, NC Ernest A. Weymuller, Jr., MD*, Seattle, WA JOINT SESSION WITH AMERICAN NEUROTOLOGY SOCIETY 8:30 Invited Presidential Speaker - Mr. Richard Teske, Arlington, VA When the Chip Marries the Cell MODERATOR: C. PHILLIP DASPIT, MD*, PHOENIX, AZ 9:00 MOSHER AWARD WINNER - TRIOLOGICAL SOCIETY THESIS The Mechanism of Hearing Loss in Paget’s Disease of Bone Edwin M. Monsell, MD PhD, Detroit, MI EDUCATIONAL OBJECTIVE: At the conclusion of this presentation, the participants will be able to identify, diagnose, and manage hearing loss in Paget's dis- ease of bone in accordance with a new understanding of the mechanism of hearing loss. OBJECTIVES: The mechanism of hearing loss in Paget’s disease of bone was investigated. The present study was a systematic, prospective, controlled set of clinical investigations to test the hypothesis that there is a general underlying mechanism of hearing loss in Paget’s disease of bone and to gain additional insights into the auditory and otologic dynamics of this disease. Specific questions were: 1) whether the mechanism is cochlear or retrocochlear, and 2) whether the bone mineral density of the cochlear capsule is related to hearing levels. STUDY DESIGN: Several double-blinded, cross-sectional, prospective, correlational studies were conducted in a population of elderly human subjects with skull involvement with Paget’s disease versus a control population of eld- erly subjects free of Paget’s disease. Demographic and clinical data were recorded. Longitudinal observations were made in subjects under treatment. METHODS: Subjects were recruited from a Paget’s disease clinic. Pure tone auditory thresholds, word recognition, and ABRs were recorded. The dimensions of the internal auditory canals were measured using CT images and digital image analysis. The precision, accuracy, and temporal stability of methods to meas- ure the bone mineral density of the cochlear capsule and an adjacent area of non-otic capsule bone were validated and applied. Correlations were sought between hearing levels and cochlear capsule bone mineral density. RESULTS: Auditory brainstem responses (ABRs) were recorded in 64 ears with radiograph- ically confirmed Paget’s disease involving the skull. Responses were absent in 8 ears, all of which had elevated high pure tone thresholds. ABRs were inter- preted as normal in 56 ears; none were abnormal. The mid-length diameter and minimum diameter of the internal auditory canal of 68 temporal bones from subjects with Paget’s disease were found to have no statistically significant relationship to hearing thresholds. The Pearson product-moment correlation coef- ficients (age- and sex- adjusted) in the group with Paget’s disease involving the temporal bone were -0.63 for left ears and -0.73 for right ears for high-fre- quency air conduction pure-tone thresholds (mean of 1, 2, and 4 kHz) versus cochlear capsule density. Correlation coefficients (age- and sex- adjusted) between cochlear capsule density and air-bone gap (mean at 0.5 and 1 kHz) for the affected group were -0.67 for left ears and -0.63 for right ears. All corre- lations between hearing thresholds and cochlear capsule density in pagetic subjects were significant at p < 0.001. The regressions were consistent through- out the ranges of hearing level. There were no significant correlations between cochlear capsule mean density and hearing level in the volunteer subjects. CONCLUSIONS: The evidence supports the existence of a general, underlying, cochlear mechanism of pagetic hearing loss that is closely related to loss of bone mineral density in the cochlear capsule. This mechanism accounts well for both the high-frequency sensorineural hearing loss and the air-bone gap. Early identification, radiographic diagnosis of temporal bone involvement, and vigorous treatment with third generation bisphosponates are important to limit the development and progression of pagetic hearing loss. 9:12 FOWLER AWARD WINNER - TRIOLOGICAL SOCIETY THESIS Platelet-Activating Factor-Induced Hearing Loss Medicated by Nitric Oxide Chung-Ku Rhee, MD PhD, Cheonan, Choongnam, Korea EDUCATIONAL OBJECTIVE: At the conclusion of this presentation, the participants will be able to recognize the hearing loss induced by platelet-activating fac- tor in otitis media is mediated by nitric oxide and its blocker can block the hearing loss. The purpose of this study is to investigate the role of nitric oxide (NO) in the mechanism of PAF-induced hearing loss in otitis media. Guinea pigs were divid- ed into 3 groups: PBS, PAF, and L-NAME. The PBS group received phosphate buffered saline (PBS) and the PAF groups received 10, 20, and 40 µg of PAF on the round window membrane (RWM). NG-nitro-L-arginine-methylester (L-NAME) were injected intraperitoneally prior to PAF 20 µg application on the RWM. Hearing was tested with an auditory brainstem response (ABR) test, cochlear hair cells were examined by scanning electron microscopy (SEM), and immunohistochemistry was carried out on the cochlea to test the expression of inducible nitric oxide (iNOS). The PAF groups developed significant eleva- tion of ABR threshold and cochlear hair cell damage in SEM. The L-NAME group did not show significant elevation of ABR threshold and cochlear hair cell damage. Strong expression of iNOS on cochlea was observed in the PAF group while lighter expression was seen in PBS and L-NAME groups. These findings suggest that the PAF-induced hearing loss caused by cochlear hair cell damage may have been mediated by NO. The L-NAME may have future ther- apeutic implications in preventing sensorineural hearing loss associated with chronic otitis media. The results of this study have significant potential clinical application. -1- 9:24 Relationship Between Middle Ear Pressure Changes Following Nitrous Oxide Anesthesia and Its Effect on Postoperative Nausea and Vomiting (PONV) Nader D. Nader, MD, PhD, Buffalo, NY George T. Simpson, MD, MPH, Buffalo, NY (Presenter) Roberta R. Reedy, CRNA, Buffalo, NY EDUCATIONAL OBJECTIVE: At the conclusion of this presentation, the participants should be able to understand and explain how nitrous oxide anesthesia con- tributes to postoperative nausea and vomiting (PONV) through its effects on middle ear pressure changes. OBJECTIVES: To establish a relationship between middle ear pressure changes following nitrous oxide anesthesia and its effect on postoperative nausea and vomiting (PONV). STUDY DESIGN: Prospective blind randomized study of adult patients receiving general anesthesia for arthroscopy. All received identical isoflurane inhalant anesthesia but were randomized into a group receiving inhaled Nitrous oxide and a control group receiving inhaled air. METHODS: Middle ear pressures were measured bilaterally with tympanometry before the surgery and every 15 minutes during the surgery and in the recovery room by recov- ery room nurses, blinded for the study, who recorded symptoms of nausea and episodes of vomiting. Pearson regression analysis was used to analyze the data. The incidence of PONV associated with nitrous oxide was analyzed using Fisher’s exact test and Chi Square values were obtained to check the significance. RESULTS: Patients in both groups were comparable with regard to age, weight, and duration of anesthesia. A positive correlation between the maximum pos- itive pressure (MPP) to maximum negative pressure (MNP) gradient and PONV was demonstrated. The incidence of PONV in the nitrous oxide group was 5/11 patients, while only 2/10 patients in the control group developed vestibular symptoms. This signifies a 50% increase in the incidence of PONV in the treatment group. Those patients that did not experience PONV demonstrated a median MPP of 155 with a MNP of -59. The patients that experienced PONV exhibited a median MPP of 199 with a median MNP of -183. In nitrous oxide group, P value was 0.04, which was statistically significant. CONCLUSIONS: We conclude that barometric changes in the middle ear contribute to the incidence of PONV induced by N2O. 9:32 Hearing Results: Vestibular Nerve Section vs. Intratympanic Gentamicin for Meniere’s Disease Todd A. Hillman, MD, Pittsburgh, PA Douglass A. Chen, MD, Pittsburgh, PA Moises A. Arriaga, MD, Pittsburgh, PA EDUCATIONAL OBJECTIVE: At the conclusion of this presentation, the participants should be able to compare the hearing loss produced by vestibular nerve section or intratympanic gentamicin when used for vertigo control in Meniere’s disease. OBJECTIVES: Vestibular nerve section and transtympanic gentamicin administration are procedures with proven efficacy in the treatment of vertigo associat- ed with Meniere’s disease refractory to medical management. Hearing loss is a known complication of each of both procedures; however there has not been a report of hearing results of both treatments from a single institution. STUDY DESIGN: Retrospective review. METHODS: Review of 25 patients undergoing gentamicin injection and 39 patients undergoing vestibular nerve section for Meniere’s disease. Rate of vertigo control, pre- and post-procedure pure tone averages (PTA), and speech discrimination scores (SDS) are reported. RESULTS: The mean preoperative PTA for nerve section patients was 47.2 dB with an SDS of 75.4%. The postoperative PTA was 49.1 dB and the SDS 75%. Patients undergoing gentamicin injection had a mean pre-procedure PTA of 55.9 dB and a SDS of 62%. The post-procedure PTA and SDS for the gentamicin group was 68.8 dB and 49.3%. Four out of 25 patients (16%) in the gentamicin group and 2/39 (5%) in the nerve section group had a > 20 dB increase in nerve threshold. The amount of post-procedure hearing loss was significantly greater in the gentamicin group (p=0.006).