The goals of this two-part series on children with histories of early recurrent otitis media with effusion (OME) were to assess the risk for speech disorder with and without hearing loss and to develop a preliminary descriptive-explanatory model for the findings. Recently available speech analysis programs, lifespan reference data, and statistical techniques were implemented with three cohorts of children with OME and their controls originally assessed in the 1980s: 35 typically developing 3-year-old children followed since infancy in a university-affiliated pediatrics clinic, 50 typically developing children of Native American background followed since infancy in a tribal health clinic, and (in the second paper) 70 children followed prospectively from 2 months of age to 3 years of age and older. Dependent variables included information from a suite of 10 metrics of speech production (Shriberg, Austin, Lewis, McSweeny, & Wilson, 1997a, 1 997b). Constraints on available sociodemographic and hearing status information limit generalizations from the comparative findings for each database, particularly data from the two retrospective studies. The present paper reports findings from risk analysis of conversational speech data from the first two cohorts, each of which included retrospective study of children for whom data on hearing loss were not available. Early recurrent OME was not associated with increased risk for speech disorder in the pediatrics sample but was associated with approximately 4.6 (CI = 1.10-20.20) increased risk for subclinical or clinical speech disorder in the children of Native American background. Discussion underscores the appropriateness of multifactorial risk models for this subtype of child speech disorder.

A data base of acoustic-immittance measures in normal adults is presented. The subject pool consisted of 127 adults with normal hearing and a negative otologic history. Norms are presented for hearing thresholds, ipsilateral and contralateral acoustic-reflex thresholds, tympanometry, static acoustic-admittance measures, and middle-ear (tympanogram peak) pressure.

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To develop an objective statistic for quantifying acoustic-reflex magnitude, a computer sampled baseline and perstimulatory conductance and susceptance. For each component, the difference between baseline and perstimulatory means was divided by the pooled standard deviation of the samples yielding a statistic similar to d′. Component d′’s were combined by taking the square root of the sum of the squared d′s. The resultant d′ was used to represent acoustic-reflex magnitude in an objective, statistically based format. Stimulus level required to elicit reflexes of specific magnitudes was estimated using the PEST adaptive procedure. Magnitude-intensity functions were determined for a 1-kHz tone, 50- and 300-Hz wide noise bands, and white noise. Stimuli at estimated levels were then used as references in loudness balances among all stimulus pairs, yielding four equal-loudness contours. Equal-loudness and equal-reflex contours had similar shapes, suggesting a relationship between loudness and the acoustic reflex. The magnitude-intensity functions were quite steep, indicating that small intensity changes produced large changes in reflex magnitude. We concluded that the data do not permit rejection of the hypothesis that stimuli eliciting equal reflexes are equally loud. However, the quantification technique has value in that the notion of reflex ’’threshold’’ can be replaced with a mathematically rigorous measure of reflex magnitude. Experiments to refine this technique are in progress.