In the evaluation of suspected occupational hearing losses, an expanding part of current otologic practice, the otologist is expected to differentiate noise sequelae from other types of ear pathology and to estimate the extent to which each abnormality contributes to the total hearing disability. The audiometric identification of acoustic trauma is possible only in early cases. When the noise effects are more advanced and when they are combined with aging, the pure tone curves are nonspecific. The standard battery of audiologic tests does not help in the quantitative separation of acoustic trauma from presbycusis. Most authorities consider that when acoustic trauma and presbycusis are concomitant, the effects of each are independent and that the influences of each upon auditory acuity are simply additive.
There are significant individual differences in susceptibility to acoustic trauma and in the degree of hearing deterioration which occurs with aging. While it is not yet possible to make retrospective determinations of these variances, it is feasible to make age corrections of noise‐induced hypoacusis if one averages acoustic vulnerability and aging effects. Such averaging results in some inequalities in individual cases, but the validity of this approach in large numbers of cases is justifiable because of the absence of alternatives.
The authors have modified the prebycusic data of Spoor (which combine several important hearing surveys conducted in the United States and in western Europe) by changing the calibration from ASA‐1954 to ANSI‐1969 and have prepared curves which demonstrate mean aggregate hearing levels at specified frequencies according to age and sex.
Two formulae for age correction are presented along with examples of each formula and the authors' evaluation.
The electronystagmogram (ENG) was abnormal in 94 percent of 88 consecutive patients with motor neuron disease (MND). The most common ENG abnormalities were dysrhythmic caloric responses (64 percent), active random eye movements with eyes closed (25 percent), caloric directional preponderance (24 percent), and caloric vestibular preponderance (20 percent). Torsional preponderance, poor fixation suppression (of induced vestibular nystagmus), spontaneous nystagmus, square waves, tracking and optokinetic abnormalities were also frequent. Most of these ENG findings are considered to be of central nervous system origin. Although these findings are not considered specific for MND, they appear to have clinical significance.
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