Comprehensive Physiology Wiley Online Library
For Librarians For Authors Editors About

Pathophysiological Responses of the Auditory Organ to Excessive Sound

Stephen A. Falk

10.1002/cphy.cp090102

Source: Supplement 26: Handbook of Physiology, Reactions to Environmental Agents

Originally published: 1977

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Morphology and Physiology of Normal Auditory Organ
2 Noise‐Induced Hearing Loss
2.1 Distinguished from Blast Trauma
2.2 Characteristics of Exposure
2.3 Pathogenesis of 4‐kHz Dip
2.4 Pathology of Permanent Threshold Shift
2.5 Pathology of Temporary Threshold Shift
2.6 Ionic and Biochemical Changes
2.7 Vascular Changes
2.8 Age Dependency
2.9 Potentiation by Ototoxic Drugs
3 Blast Trauma
3.1 Pathogenesis and Pathology
3.2 Audiometric Changes
Figure 1.

Transverse section of one turn of a guinea pig cochlea.

From Hawkins 35
Figure 2.

Surface preparation of a normal organ of Corti. Outer hair cells (OHC) are arranged in a regular array of three rows: outer (O), middle (M), and inner (I). Between OHCs are phalangeal processes (arrows) of Deiter's cells. Inner hair cells (IHC) are arranged in a single row. Between IHC and OHC are outer (OP) and inner (IP) rows of pillar cells. Phase‐contrast microscopy; OsO4; × 400.
Figure 3.

Scanning electron micrograph of a normal guinea pig organ of Corti. The stereocilia of the outer hair cells are arranged in a W‐shaped pattern, whereas those on the inner hair cells line up in parallel rows.

Courtesy of D. Lim
Figure 4.

The outer hair with its cytoplasmic organelles. The stereocilia are attached to the cuticular plate. The smooth endoplasmic reticulum (ER) complex consists of Hensen's body (ER surrounded by mitochondria) and subsurface and subsynaptic cisternae. The smooth ER is continuous with the outer nuclear membrane. The afferent (hair cell to cochlear nucleus) and efferent (superior olivary complex to hair cell) nerve endings join the outer hair cell at its base.

From Lim & Melnick 57
Figure 5.

Temporary threshold shifts (○ — ○) occurring 2-4 min after exposure to pure tones of 1, 2, 3, and 4 kHz simultaneously (110 dB sound pressure level, duration 15 min). A, B, C, and D represent temporary threshold shifts (TTS) occurring after exposure to the same pure tones individually. The thick curve represents the absolute threshold of hearing. The TTS after exposure to the 4 tones simultaneously corresponds to the superimposition of the individual TTS's.

From Lehnhardt 55
Figure 6.

Surface preparation of a noise‐damaged organ of Corti. Collapsed cells (small arrow) and phalangeal scars (large arrow) indicate hair cell necrosis. Phase‐contrast microscopy; OsO4; × 250.
Figure 7. Figure 7.

Cochleograms showing the distribution of cellular damage in a guinea pig cochlea exposed to white noise at 113 dB for 2 h on each of 3 consecutive days. (•, damaged hair cell; ○, normal hair cell.) The dots in toto comprise a cochleogram that is an exact cell‐for‐cell diagram of the pathology. Greatest damage occurs at 1/2 and 1 1/2 turns from the base.

From Engström & Ades 21
Figure 8.

Transmission electronmicrograph of vacuolated (OH2) and moderately vesiculated (OH3) outer hair cells of the second turn. Animal was exposed to noise of 117 dB sound pressure level with octave bandwidth of 300-600 Hz for 4 h.

[From Lim & Melnick 57.]
Figure 9.

Transmission electronmicrograph of base of noise‐damaged outer hair cell showing vacuole (V2) formed by a dilated outer nuclear membrane (ONM), vacuoles (V2) formed by dilated subsynaptic cisternae, and vacuole (V1) formed by dilated subsurface cisternae. Afferent nerve ending (A) contains swollen mitochondria compared to efferent (E) endings. The supporting (Deiter, D.) cell also is vacuolated.

From Lim & Melnick 57


Figure 1.

Transverse section of one turn of a guinea pig cochlea.

From Hawkins 35


Figure 2.

Surface preparation of a normal organ of Corti. Outer hair cells (OHC) are arranged in a regular array of three rows: outer (O), middle (M), and inner (I). Between OHCs are phalangeal processes (arrows) of Deiter's cells. Inner hair cells (IHC) are arranged in a single row. Between IHC and OHC are outer (OP) and inner (IP) rows of pillar cells. Phase‐contrast microscopy; OsO4; × 400.



Figure 3.

Scanning electron micrograph of a normal guinea pig organ of Corti. The stereocilia of the outer hair cells are arranged in a W‐shaped pattern, whereas those on the inner hair cells line up in parallel rows.

Courtesy of D. Lim


Figure 4.

The outer hair with its cytoplasmic organelles. The stereocilia are attached to the cuticular plate. The smooth endoplasmic reticulum (ER) complex consists of Hensen's body (ER surrounded by mitochondria) and subsurface and subsynaptic cisternae. The smooth ER is continuous with the outer nuclear membrane. The afferent (hair cell to cochlear nucleus) and efferent (superior olivary complex to hair cell) nerve endings join the outer hair cell at its base.

From Lim & Melnick 57


Figure 5.

Temporary threshold shifts (○ — ○) occurring 2-4 min after exposure to pure tones of 1, 2, 3, and 4 kHz simultaneously (110 dB sound pressure level, duration 15 min). A, B, C, and D represent temporary threshold shifts (TTS) occurring after exposure to the same pure tones individually. The thick curve represents the absolute threshold of hearing. The TTS after exposure to the 4 tones simultaneously corresponds to the superimposition of the individual TTS's.

From Lehnhardt 55


Figure 6.

Surface preparation of a noise‐damaged organ of Corti. Collapsed cells (small arrow) and phalangeal scars (large arrow) indicate hair cell necrosis. Phase‐contrast microscopy; OsO4; × 250.



Figure 7.

Cochleograms showing the distribution of cellular damage in a guinea pig cochlea exposed to white noise at 113 dB for 2 h on each of 3 consecutive days. (•, damaged hair cell; ○, normal hair cell.) The dots in toto comprise a cochleogram that is an exact cell‐for‐cell diagram of the pathology. Greatest damage occurs at 1/2 and 1 1/2 turns from the base.

From Engström & Ades 21


Figure 8.

Transmission electronmicrograph of vacuolated (OH2) and moderately vesiculated (OH3) outer hair cells of the second turn. Animal was exposed to noise of 117 dB sound pressure level with octave bandwidth of 300-600 Hz for 4 h.

[From Lim & Melnick 57.]


Figure 9.

Transmission electronmicrograph of base of noise‐damaged outer hair cell showing vacuole (V2) formed by a dilated outer nuclear membrane (ONM), vacuoles (V2) formed by dilated subsynaptic cisternae, and vacuole (V1) formed by dilated subsurface cisternae. Afferent nerve ending (A) contains swollen mitochondria compared to efferent (E) endings. The supporting (Deiter, D.) cell also is vacuolated.

From Lim & Melnick 57
References
 1. Akiyoshi, M., A. Ambmiya, K. Sato, T. Takeda, and T. Hoji. On the pathogenesis of acoustic trauma of the cochlea from air blasts of .50 to 1.02 kg/cm2 in rabbits and guinea pigs due to explosion. Int. Audiol. 5: 270-271, 1966.
 2. Babel, J., A. Bischoff, and H. Spoendlin. Ultrastructure of the Peripheral Nervous System and Sense Organs. St. Louis: Mosby, 1970, p. 232-251.
 3. Beagley, H. A. Acoustic trauma in the guinea pig. II. Electron microscopy including the morphology of cell junctions in the organ of Corti. Acta Oto‐Laryngol. 60: 479-495, 1965.
 4. Bess, F. H., and R. E. Poynor. Snowmobile engine noise and hearing. Arch. Otolaryngol. 95: 164-168, 1972.
 5. Bohne, B. A. Anatomical correlates of a temporary shift in the threshold of hearing. J. Acoust. Soc. Am. 53: 292, 1973.
 6. Bohne, G. A., D. H. Eldredge, and J. H. Mills. Cochlear potentials and electron microscopy applied to the study of small cochlear lesions. Ann. Otol. Rhinol. Laryngol. 82: 595-608, 1973.
 7. Bredberg, G., H. W. Ades, and H. Engstrom. Scanning electron microscopy of the normal and pathologically altered organ of Corti. Acta Oto‐Laryngol. Suppl. 301: 3-48, 1972.
 8. Burns, W. Noise and Man. Philadelphia: Lippincott, 1968.
 9. Cohn, E., E. Gordes, and S. Brusilow. Ethacrynic acid effect on the composition of cochlear fluids. Science 171: 910-911, 1971.
 10. Committee on Conservation of Hearing. Guide for Conservation of Hearing in Noise. Rochester, Minnesota: American Academy of Ophthalmology and Otolaryngology, 1969.
 11. Craig, D. H. Blast injuries. J. Laryngol. Otol. 59: 443-456, 1944.
 12. Darrouzet, J., and E. D. L. Sobrinho. Inner ear, kanamycin, and acoustic trauma, experimental study. Rev. Brasil Cirurg. 46: 120-134, 1963.
 13. Davis, H. Acoustic trauma in the guinea pig. J. Acoust. Soc. Am. 25: 1180-1189, 1953.
 14. Davis, H., H. O. Parrock, and D. H. Eldredge. Hazards of intense sound and ultrasound. Ann. Otol. Rhinol. Laryngol. 58: 732-738, 1949.
 15. Davis, H., and S. R. Silverman. Hearing and Deafness. New York: Holt, Rinehart and Winston, 1970.
 16. Dayal, V. S., A. Kokshanian, and D. P. Mitchell. Combined effects of noise and kanamycin. Ann. Otol. 80: 897-902, 1971.
 17. Duggan, D. E., and R. M. Noll. Effect of ethacrynic acid and cardiac glycosides upon a membrane adenosine triphosphatase of the renal cortex. Arch. Biochem. 109: 388-396, 1965.
 18. Eames, B. L., R. P. Hamernik, and D. Henderson. The role of the middle ear in acoustic trauma from impulses (Abstract). Proc. Acoustical Soc. Am., 85th, Boston, 1973.
 19. Eldredge, D. H. Noise‐induced hearing loss—pathological effects. Presented at AMA Congress on Environmental Health, 6th, Chicago, Ill. 1969.
 20. Engström, H., and H. W. Ades. Effect of high‐intensity noise on inner ear sensory epithelia. Acta Oto‐Laryngol. Suppl. 158: 219-229, 1960.
 21. Engstrom, H., H. W. Ades, and A. Andersson. Structural Pattern of Organ of Corti. Stockholm: Almquist & Wiksell, 1966.
 22. Engstrom, H., and J. Wersall. The ultrastructural organization of the organ of Corti and of the vestibular sensory epithelia. Exptl. Cell. Res. Suppl. 5: 460-492, 1958.
 23. Falk, S. A. Combined Effects of Noise and ototoxic drugs. Environ. Health Perspect. 2: 5-22, 1972.
 24. Falk, S. A., R. O. Cook, J. K. Haseman, G M. Sanders. Noise‐induced inner ear damage in newborn and adult guinea pigs. Laryngoscope 84: 444-453, 1974.
 25. Finegold, S. M. Toxicity of kanamycin in adults. Ann. NY Acad. Sci. 132: 942-956, 1966.
 26. Finegold, S. M., and E. A. Kantor. Long‐term follow‐up on ototoxicity and nephrotoxicity of kanamycin. Clin. Res. Proc. 7: 73-74, 1959.
 27. Flugrath, J. M. Modern‐day rock and roll music and damage risk criteria. J. Acoust. Soc. Am. 45: 704-711, 1969.
 28. Friedman, O. Blast injuries. Arch. Otolaryngol. 47: 471-484, 1948.
 29. Frost, J. O., J. E. Hawkins, Jr., and J. F. Daly. Kanamycin. II. Ototoxicity. Am. Rev. Respirat. Diseases 82: 23-30, 1960.
 30. Gannon, R. P., and S. S. Tso. The occult effect of kanamycin on the cochlea. Excerpta Med. 18 (9): 98, 1969.
 31. Glorig, A. Noise and Your Ear. New York: Grune & Stratton Co., 1958.
 32. Gravendeel, D. W., and R. Plomp. Micro‐noise trauma? Arch. Otolaryngol. 71: 656-663, 1960.
 33. Guild, S. R. Ear lesions caused by acoustic trauma. AMA Arch. Indust. Hyg. 5: 121, 1952.
 34. Hanzelik, I., and M. Peppercorn. Deafness after ethacrynic acid. Lancet 1: 416, 1969.
 35. Hawkins, J. E., Jr. Hearing: anatomy and acoustics. In: The Physiological Basis of Medical Practice (8th ed.), edited by C. H. Best and N. B. Taylor. Baltimore: Williams & Wilkins, 1966, chapt. 17, p. 375-394.
 36. Hawkins, J. E., Jr. Hearing: biomechanics and neurophysiology. In: The Physiological Basis of Medical Practice (8th ed.), edited by C. H. Best and N. B. Taylor. Baltimore: Williams & Wilkins, 1966, chapt. 18, p. 395-408.
 37. Hawkins, J. E., Jr. Iatrogenic Toxic Deafness in Children. In: Deafness in Childhood edited by F. McConnell and P. H. Ward. Nashville Tenn.: Vanderbilt University Press, 1967.
 38. Hawkins, J. W., Jr. The role of vasoconstriction in noise‐induced hearing loss. Ann. Otol. 80: 903-913, 1971.
 39. Henry, G. A. Blast injuries. Laryngoscope 55: 663-672, 1945.
 40. Homer, M. J. Deafness after Ethacrynic Acid. New Engl. J. Med. 285: 1152, 1971.
 41. Hough, J. V. D. Otologic trauma. In: Otolaryngology, edited by M. M. Paparella and D. A. Shumrick. Philadelphia: Saunders., 1973, vol. II, p. 260-261.
 42. Igarashi, M., H. F. Schuknecht, and E. N. Myers. Cochlear pathology in humans with stimulation deafness. J. Laryngol. Otol. 78: 115-123, 1964.
 43. Ireland, P. E. Traumatic perforations due to blast injury. Can. Med. Assoc. J. 54: 256-258, 1946.
 44. Jauhiainen, T., A. Kohonen, and M. Jauhiainen. Combined effect of noise and neomycin on the cochlea. Acta Oto‐Laryngol 73: 387-390, 1972.
 45. Jerger, J., and S. Jerger. Temporary threshold shift in rock and roll musicians. J. Speech Hearing Res. 13: 221-224, 1970.
 46. Johnstone, B. M. Genesis of the cochlear endolymphatic potential. In: Current Topics in Bioenergetics, edited by D. R. Sanadi. New York: Academic, 1967.
 47. Keller, A. P., Jr. A study of the relationship of air pressure to myringopuncture. Laryngoscope 68: 2015-2027, 1958.
 48. Klahr, S., J. J. Bourgoignie, and J. Yates. Inhibition of glycolysis by ethacrynic acid and furosemide. Federation Proc. 30: 608, 1971.
 49. Koide, Y., M. Konno, and J. Yoshikawa. Some aspects of the biochemistry of acoustic trauma. Ann. Otol. 69: 661-697, 1960.
 50. Korkis, F. B. Rupture of the tympanic membrane of blast origin. J. Laryngol. 61: 367-390, 1946.
 51. Korkis, F. B. Blast injuries of the ear. J. Laryngol. Otol. 66: 95-103, 1952.
 52. Kretchmer, J. House Congressional Record, H 2176, March 30, 1971. Washington, D.C.: U.S. Govt. Printing Office, 1971.
 53. Kryter, K. D., W. D. Ward, and J. D. Miller. Hazardous exposure to intermittent and steady‐state noise. J. Acoust. Soc. Am. 39: 451-464, 1966.
 54. Lawrence, M. Effects of interference with terminal blood supply on organ of Corti. Laryngoscope 76: 1318-1337, 1966.
 55. Lehnhardt, E. The C5 dip: its interpretation in the light of generally known physiological concepts, Internat. Audiol. 6: 86-95, 1967.
 56. Leonard, J. E., T. Nakashima, and J. B. Snow, Jr. The effects of damage to the organ of Corti and the stria vascularis on endolymphatic cationic changes. Arch. Otolaryngol. 94: 541-547, 1971.
 57. Lim, D. J., and W. Melnick. Acoustic damage of the cochlea. Arch. Otolaryngol. 94: 294-305, 1971.
 58. Lim, D. J., and W. Melnick. Morphological correlates of asymptotic temporary threshold shifts in chinchilla. J. Acoust. Soc. Am. 53: 292, 1973.
 59. Lipscomb, D. M., and R. L. Roettger. Capillary constriction in cochlear and vestibular tissues during intense noise stimulation. Laryngoscope 83: 259-263, 1973.
 60. Lutovats, M. Age in the occurrence and evolution of acoustic trauma. Srpski Archiv. Celokupno Lekar. 97: 869-873, 1969.
 61. Matz, G. J., D. D. Beal, L. Krames. Ototoxicity of Ethacrynic Acid. Arch. Otolaryngol. 90: 152-155, 1969.
 62. McCabe, P. A., and F. L. Day. The Effect of Aspirin upon Auditory Sensitivity. Ann. Otol. 74: 312-324, 1965.
 63. McReynolds, G. S., F. Guilford, and G. Chase. Blast injuries to ear; Texas City Disaster. Arch. Otolaryngol. 50: 1-8, 1949.
 64. Meyers, E. N., J. M. Bernstein, and G. Fostiropoulos. Salicylate Ototoxicity: a clinical study. New Engl. J. Med. 273: 587-590, 1965.
 65. Miller, J. D., C. S. Watson, and W. E. Covell. Deafening effects of noise on the cat. Acta Oto‐Laryngol. Suppl. 176, 1963.
 66. Misrahy, G. A., K. H. Hildreth, E. W. Shinabarger, and W. J. Gannon. Electrical Properties of wall of endolymphatic space of the cochlea (guinea pig). Am. J. Physiol. 194: 396-402, 1958.
 67. Misrahy, G. A., W. E. Shinabarger, and J. E. Arnold. Changes in cochlear endolymphatic oxygen availability, action potential and microphonics during and following asphyxia, hypoxia and exposure to loud sounds. J. Acoust. Soc. Am. 30: 701-704, 1958.
 68. Nakashima, T., M. J. Sullivan, J. B. Snow, Jr., and F. Suga. Sodium and potassium changes in inner ear fluids: an in vivo study with glass microelectrodes. Arch. Otolaryngol. 92: 1-6, 1970.
 69. Ng, P. S. Y., C. E. Conley, and T. S. Ing. Deafness after Ethacrynic acid. Lancet 1: 673-674, 1969.
 70. Perlman, H. B., and R. Kimura. Cochlear blood flow in acoustic trauma. Acta Oto‐Laryngol. 54: 99-110, 1962.
 71. Pillay, V. K. G., F. D. Schwartz, and K. Aimi. Transient and Permanent Deafness following Treatment with Ethacrynic Acid in Renal Failure. Lancet 1: 77-79, 1969.
 72. Poche, L. B., Jr., C. W. Stockwell, and H. W. Ades. Cochlear hair‐cell damage in guinea pigs after exposure to impulse noise. J. Acoust. Soc. Am. 46: 947-951, 1969.
 73. Prazma, J., W. G. Thomas, N. D. Fisher, and M. J. Preslar. Ototoxicity of Ethacrynic Acid. Arch. Otolaryngol. 95: 448-456, 1972.
 74. Quante, M., H. Stupp, and J. P. Brun. Ototoxikosen unter Larmbelastung. Arch. Klin. Exptl. Ohren‐, Nasen‐, und Kehikopfheilkunde. 196: 233-237, 1970.
 75. Rauch, S. Biochemie des Hörorgans. Stuttgart: Georg Thieme, 1964.
 76. Ruggles, R. L., and R. Votypka. Blast injuries of the ear. Laryngoscope. 83: 974-976, 1973.
 77. Seaman, R. W., and R. C. Newell. Another etiology of middle ear chlesteatoma. Arch. Otolaryngol. 94: 440-442, 1971.
 78. Schneider, W. J., and E. L. Becker. Acute transient hearing loss after ethacrynic acid therapy. Arch. Internal Med. 117: 715-717, 1966.
 79. Schuknecht, H. F. Neuroanatomical correlates of auditory sensitivity and pitch discrimination in the cat. In: Neural Mechanisms of the Auditory and Vestibular Systems, edited by Rasmussen, G. L. and W. F. Windle. Springfield Ill.: Thomas, 1960, chapt. 6, p. 76-90.
 80. Schuknecht, H. F. Techniques for study of cochlear function and pathology in experimental animals. Arch. Otolaryngol. 58: 377-397, 1953.
 81. Schwartz, G. H., D. S. David, R. R. Riggio, K. H. Stenzel, and A. L. Rubin. Ototoxicity induced by furosemide. New Engl. J. Med. 282: 1413-1414, 1970.
 82. Silverstein, H., J. M. Bernstein, and D. G. Davies. Salicylate ototoxicity: a biochemical and electrophysiological study. Ann. Otol. 76: 118-126, 1967.
 83. Singh, D., and K. J. S. Ahulwalia. Blast injuries of the ear. J. Laryngol. Otol. 82: 1017-1028, 1968.
 84. Snow, J. B., T. Nakashima, F. Suga, J. E. Leonard, M. J. Sullivan, and N. L. Meiring. Pathophysiologic responses of the inner ear to intense sound. Ann. Otol. 80: 871-880, 1971.
 85. Speaks, C., D. Nelson, and W. D. Ward. Hearing loss in rock and roll musicians. J. Occupational Med. 12: 216-219, 1970.
 86. Spoendlin, H. H. Ultrastructural features of organ of Corti in normal and acoustically stimulated animals. Ann. Otol. 71: 657-677, 1962.
 87. Taylor, G. House Congressional Record, H 2173, March 30, 1971. Washington, D.C.: U.S. Govt. Printing Office, 1971.
 88. Teter, D. L., R. C. Newell, and K. B. Aspinall. Audiometric configurations associated with blast trauma. Laryngoscope. 80: 1122-1132, 1970.
 89. von Bekesy, G. Experiments in Hearing, edited and translated by E. G. Wever. New York: McGraw‐Hill, 1960.
 90. Ward, W. D. Biochemical Implications in Auditory Fatigue and Noise‐induced Hearing Loss. In: Biochemical Mechanisms in Hearing and Deafness, edited by M. M. Paparella. Springfield, Ill: Thomas, 1970.
 91. Ward, W. D., A. Glorig, and D. L. Sklar. Temporary threshold shift from octave‐band noise: applications to damage‐risk criteria. J. Acoust. Soc. Am. 31: 522-528, 1959.
 92. Weiner, F. M., and D. A. Ross. The pressure distribution in the auditory canal in a progressive sound field. J. Acoust. Soc. Am. 18: 401-408, 1946.
 93. Wever, E. G., and M. Lawrence. Physiological Acoustics. Princeton, New Jersey: Princeton University Press, 1954.
 94. Whitfield, I. C. The Auditory Pathway. London: Edward Arnold Ltd., 1967.

Contact Editor

Submit a note to the editor about this article by filling in the form below.

* Required Field

Article Title: Pathophysiological Responses of the Auditory Organ to Excessive Sound
 

How to Cite

Stephen A. Falk. Pathophysiological Responses of the Auditory Organ to Excessive Sound. Compr Physiol 2011, Supplement 26: Handbook of Physiology, Reactions to Environmental Agents: 17-30. First published in print 1977. doi: 10.1002/cphy.cp090102