picked up on the midfrequency hearing loss, or paid any particular attention to them and therefore have not reported the cases. These accidents may easily be misdiagnosed as beginning Menière’s disease or sudden deafness due to viral infection.
The typical acoustic trauma notch in the 3- to 6-kHz range is not a common finding in this group of patients. This unfortunate experience with human subjects illustrates the findings of many experimental studies documenting the relation between maximum stimulation and maximum damage positions along the organ of Corti [6–8] by using pure tones or narrow band noises as stimuli. The morphological substrate underlying temporary threshold shifts (TTS) has been extensively studied with some controversial results. TTS may be detected without any significant ultrastructural change suggesting a metabolic disturbance; more intense stimulations result in temporary swelling of dendrites to inner hair cells. The resulting TTS lasts for several hours . Vascular disturbances in the pathogenic sequences after an acute noise exposure have also been reported [10–13]. Changes in microcirculation may still be present 3 weeks after short-term and mild noise exposure . In the light of the most recent studies, at the electron microscopy level, more subtle and consistent changes have been described. The most common finding observed in several different animal models [14–16] is depolymerization of the actin filaments at the base of the hair cells stereocilia reducing their stiffness which returned to normal within 6 weeks after exposure .
It is imperative that physicians and audiologists become aware of the potential hazard that telephones may produce under certain circumstances. The greatest danger results from telephones (cordless or not) in which the ringing device is located in the ear receiver. For this reason, these telephones should be prohibited. Unlike the patients of Singleton et al.  or Orchick et al. , our 2 patients have fortunately recovered normal hearing; however, such a favorable outcome is not always predictable and, at the present time, no treatment is known for reestablishing normal hearing after acoustic trauma.
1 Singleton, G.T.; Whitaker, D.L.; Keim, R.J.; Kemker, F.J.: Cordless telephones: a threat to hearing. Ann. Oto-Lar. 93:565–568 (1984).
2 Orchik, D.J.; Schmaier, D.R.; Shea, J.J., Jr.; Emmett, J.R.; Moretz, W.H.; Shea, J.J., III: Sensorineural hearing loss in cordless telephone injury. Otolaryngology 96:30–33 (1987).
3 Gerling, I.J.; Jerger, J.F.: Cordless telephones and acoustic trauma: a case study. Ear Hearing 6:203– 205 (1985).
4 Constitution Fédérale, article 36, 29 mai 1874.
5 Vertes, D.; Axelsson, A.; Hornstrand, C.; Nilsson, P.: The effect of impulse noise on cochlear vessels. Archs Otolar. 110:111–115 (1984).
6 Stockwell, C.W.; Ades, H.W.; Engström, H.: Patterns of hair cell damage after intense auditory stimulation. Ann. Otol. Rhinol. Lar. 78:1144– 1168 (1969).
7 Elliot, D.N.; McGee, T.M.: Effects of cochlear lesions upon audiograms and intensities discriminations in cats. Ann. Otol. Rhinol. Lar. 74:386– 408 (1965).
8 Clark, W.W.; Bohne, B.A.: Animal model for the 4-kHz tonal dip. Ann. Otol. Rhinol Lar. 87: suppl. 51 (1978).
9 Spoendlin, H.: Primary structural changes in the organ of Corti after acoustic overstimulation. Acta oto-lar. 71:166–176 (1971).
10 Kellerhals, B.: Pathogenesis of inner ear lesions in acute acoustic trauma. Acta oto-lar. 73:249–253 (1972).