- Email: [email protected]
Inner Ear Disorders Caused by Barotrauma in Guinea Pigs
Auris·Nasus·Larynx (Tokyo) 19 (Suppl. I) SI-S11,1992
INNER EAR DISORDERS CAUSED BY BAROTRAUMA IN GUINEA PIGS Noriyuki YANAGITA, M.D., Shigeji FUKUTA, M.D., Hisashi YOKOI, M.D., Kazuya ISHIDA, M.D., and Tsutomu NAKASHIMA, M.D. Department of Otorhinolaryngology, Nagoya University School of Medicine, Nagoya, Japan
'To determine the mechanism of hair cell damage caused by barotrauma to the inner ear, we investigated morphological changes in the organ of Corti and stria vascularis using transmission electron microscopy (TEM) and scanning electron microscopy (SEM). Fractures of the stereocilia with minimal intracellular changes were observed immediately after trauma. One day later, there was marked degeneration of outer hair cells and expansion of supporting cells. The damage to stereocilia clearly preceded morphological alterations within the hair cell bodies. Most outer hair cells eventually disappeared and were replaced by supporting cells. Inner hair cells degenerated slowly: some were almost intact 1 month after the trauma despite the disappearance of stereocilia. The continuity of reticular lamina was maintained throughout the period of hair cell degeneration, preventing leakage of endolymph into the organ of Corti. Reversible dendritic swelling of inner hair cells occurred immediately after trauma. No change in the stria vascularis was observed over time. Our results suggest that the mechanism of hair cell damage caused by inner ear barotrauma is related to a deformity of the organ of Corti caused by a pressure discrepancy between the perilymph and endolymph, resulting in injury to stereocilia. Sudden changes in atmospheric pressure damage the acoustic organs, with the middle ear being especially susceptible. Barotrauma of the inner ear has a low incidence compared with barotrauma of the middle ear. However, when barotrauma occurs in the inner ear, the resulting damage is severe, and can lead to acute sensorineural hearing loss. We induced inner ear barotrauma in guinea pigs exposing them to rapid compression and decompression in a high pressure chamber and investigated morphological changes in the cochlea using scanning electron microscopy (SEM) and transmission electron microscopy (TEM). Received for publication September 1, 1992 SI
S2
N. YANAGITA et al
METHODS AND MATERIALS
White guinea pigs weighing 200 to 300 g with normal Preyer's reflex were exposed to changes in atmospheric pressure in a pressure chamber in which a pressurized oxygen infusion elevated the atmospheric pressure up to 2 absolute atmosphric pressure (AT A) within 10 min, that pressure was maintained for 10 min. The chamber gas outlet was then opened to reduce the atmospheric pressure from 2 ATA to 1 ATA within 30 to 60 sec. After this pressure loading, Preyer's reflex disappeared bilaterally or unilaterally in about one-fifth of animals. We examined the organ of Corti and stria vascularis in the basal turn and the third turn in cochlea in the side in which Preyer's reflex disappeared immediately, 1 day, 1 week, and 1 month after pressure loading in cochlea using TEM and SEM. We observed either the organ of Corti or stria vascularis in one cochlea. The organ of Corti was observed in 7 cochleas at each period after the pressure loading. To prepare the specimens for TEM investigation, the animals were decapitated after the intraperitoneal injection of 10% urethan (0.02 mljg). The cochlea were exposed and perfused with phosphate buffer containing 2.5% glutalaldehyde and 2% paraformaldehyde through a hole made in the bony cochlear wall. The cochlea were removed, fixed with the same fluid and osmium acid phosphate buffer, dehydrated in a series of alcohols, and embedded in Epon 812. After thin sections had been cut and stained twice with uranyl acetate and lead citrate, the specimens were examined, with a Hitachi H-300 electron microscope. Specimens for examination by SEM were fixed as described above for TEM. Cochlea were subjected to ethanol dehydration, microdissection, critical point drying, and gold metallization, according to the method of Handoh et al. 1 Specimens were then observed under a SEM (JSM-SI5), with special attention to the organ of Corti and surface structure of the stria vascularis of the luminal side. RESULTS
A)
The organ of Corti SEM immediately after pressure loading showed that sensory hairs of the organ of Corti were disarranged and bent in various directions (Fig. 1). Random disappearance of the hairs was detected especially in the outer hair cells. TEM showed that stereocilia were bent at their bases. Though structural distortions were observed under the cuticular plate, no laceration was observed in the cuticular plate or cell junctions and continuity of the reticular lamina was maintained. No significant changes were observed inside the cell bodies except for a slight increase in the number of vacuoles (Fig. 2). Inner hair cells were less damaged than outer hair cells, but swelling of afferent nerve endings was observed in about half of the specimens (Fig. 3).
INNER EAR BAROTRAUMA
S3
Fig. I. SEM . Immediately after pressure loading of the third turn. Sensory hairs were disarranged and bent in va rious directions.
Fig.
2. Immediately after pressure loading of third turn. Stereocilia of outer hair cells (OHCs) were bent at the base. No significant changes were observed inside the cell bodies.
One day after pressure loading, severe disarrangement of stereocilia of the outer hair cells was apparent. Fusion of stereocilia was occasionally observed and the degeneration of cell bodies was detected (Fig. 4). Nuel's space was almost completely replaced by supporting cells in sites with severely damaged stereocilia, but no tears were detected in the reticular lamina. Fusion of stereocilia of inner
N. YANAGITA et al
S4
.'
Fig. 3. Immediately after pressure loading of basal turn. Swelling of afferent nerve endings of inner hair cell (IHC) was observed.
Fig. 4.
One day after trauma of basal turn. Degeneration of OHC bodies was detected.
INNER EAR BAROTRAUMA
Fig. 5.
S5
One day after trauma of basal tum. Degeneration inside IHC was slight.
Fig. 6. SEM. One week after trauma of basal tum. Disappearance and fusion of stereocilia of OHCs were observed.
hair cells was also observed, but there was less degeneration inside the inner hair cells than inside the outer hair cells (Fig. 5). Slight swelling of afferent nerve endings was observed in only a small number of specimens. One week after pressure loading, disappearance of stereocilia progressed, and fusion of the remaining stereocilia was observed (Fig. 6). Inside the outer hair cells, the number of lysosomes increased, and cytoplasmic inequalities and signifi-
S6
N. YANAGITA et al
Fig. 7. One week after trauma. Significant progression of degeneration of OHC bodies was observed.
cant degeneration were observed (Fig. 7). In some specimens, the remains of organelles were identified in the endolymphatic space, although the continuity of the reticular lamina was maintained by supporting cells that proliferated upwards (Fig. 8). In most inner hair cells, no significant degeneration was observed in cell bodies except for the formation of small vacuoles. One month after pressure loading, most of the outer hair cells had disappeared, being replaced by supporting cells (Fig. 9). The damaged inner hair cells were also replaced by supporting cells in some places, but the extent of the replacement and degeneration inside the cell bodies was minimal compared with the outer hair cells. The degree of impairment did not differ significantly between the basal turn and the third turn. B)
Stria vascularis In one cochlea examined 1 week after pressure loading, a slight increase of the intercellular gap and the accumulation of a homogeneous substance between the intermediate cells were observed at the basal turn. However, no abnormalities were observed at the third turn. No abnormalities such as degeneration or atrophy were
INNER EAR BAROTRAUMA
S7
Fig. 8. One week after trauma of basal turn. Remains of organelles of ORC were identified in the endolymphatic space.
Fig. 9. SEM. Two weeks after trauma of second turn. Most ORCs had disappeared and had been replaced by supporting cells.
observed in other specimens at any of the examination periods (Fig. 10). DISCUSSION
In this experiment, we induced inner ear barotrauma by the method described
S8
N. YANAGITA et al
Fig. 10. Stria vascularis. No abnormalities were observed. SEM. One month after trauma.
A) One day after trauma. B)
by Handoh et al. 1 Disarrangement of stereocilia, fracture of stereocilia at the basal end, and distortion of outer hair cells beneath the cuticular plate were observed immediately after pressure loading, suggesting that displacement occurred between the tectorial membrane and reticular lamina and between the reticular lamina and basilar membrane. Only slight damage to the hair cell body was observed immediately after pressure loading, but degeneration of the hair cells occurred one day after pressure loading. The outer hair cells sustained severe degeneration, especially when stereocilia were damaged significantly. No intracellular degeneration was observed in the absence of damage to stereocilia. These results suggested
INNER EAR BAROTRAUMA
S9
that damage to the stereocilia preceded the intracellular degeneration that such is necessary for hair cell degeneration to occur. Thome et al and Fredelius reported that damage to stereocilia preceded secondary degeneration of hair cells in acoustic trauma. 2,3 Hair cell damage appears to be similar in acoustic trauma and barotrauma because in both conditions the inner ear is subjected to a mechanical load over a short period. We did not observe laceration of the reticular lamina either in the period immediately after pressure loading or later. Beagley also found no tears at cell junctions in the organ of Corti following acoustic trauma. 4 These findings suggest that the reticular lamina is resistant to mechanical stimuli. In studies by Spoendlin of acoustic trauma5 and Forge of the degenerative process of outer hair cells following gentamicin administration, 6 continuity of the reticular lamina was maintained after destruction of the hair cells because supporting cells covered the areas where hair cells disappeared. The continuity of the reticular lamina was also maintained during the degenerative process that followed barotrauma in our study, suggesting that direct contact between the endolymph and perilymph was not a likely cause of degeneration. Outer hair cells sustained greater damage and exhibited more rapid degeneration compared with inner hair cells following barotrauma. This difference in susceptibility has been described in studies in aminoglycoside intoxication by Duvall and WersaC and Engstrom and Kohonen 8 and in acoustic trauma by Spoendlin. 5 The swelling of afferent nerve endings observed immediately after pressure loading appeared to be transient and disappeared one day after pressure loading. Similar findings have been reported in acoustic trauma. 3,5,9,1Q No significant damage to the stria vascularis was observed, indicating that degeneration of hair cells was not caused by changes in the composition of inner ear fluid produced by the disruption of the stria vascularis. These findings, together with an earlier reports, 1l,15 suggest that the stria vascularis is resistant to mechanical stimuli. Goodhill has suggested that inner ear barotrauma can be induced through the implosive route.12 Pressure transmission via the inner ear window may cause perilymphatic pressure elevation, leading to a pressure difference between the endolymph and perilymph. This pressure difference may cause displacement of the basilar membrane and Reissner's membrane, leading to alteration in the shape of the organ of Corti and subsequent impairment of stereocilia and hair cell degeneration. Pressure is transmitted equally to different places as long as it follows Pascal's principle. Damage to the organ of Corti caused by pressure loading can occur anywhere from the basal tum to the apical tum. We observed no significant difference in damage between the basal tum and the third tum. In contrast, acoustic trauma usually causes characteristic localizable damage according to frequency of the sound. When blast injury was induced, pressure transmission occurred extraordinarily fast,13 and there was greater damage to the stereocilia of
SIO
N. YANAGITA et al
the basal and the second turns than to those of the upper turns. Several authors have reported varying degrees of damage among cochlear turns in studies of barotrauma. l3· tS The pattern of the damage is believed to be related to the experimental condition of pressure loading. CONCLUSION
Immediately after pressure loading in guinea pigs, bending of sensory hairs of the outer and inner hair cells was observed, but changes inside the hair cells were slight. One day after pressure loading, degeneration inside the hair cells was observed. The severity of stereocilia damage was correlated with degeneration of hair cells. Greater damage and more rapid degeneration occurred in outer hair cells than in inner hair cells. No siginificant changes of the stria vascularis were observed. Inner ear barotrauma appears to be induced primarily by a difference between the endolymphatic and perilymphatic pressures, resulting in movement of the organ of Corti and damage to the stereocilia of the hair cells. This work was supported by a grant from the Ministry of Health and Welfare of Japan. REFERENCES I.
2. 3. 4. 5. 6. 7. 8. 9. 10. 11.
Handoh M, Yanagita N, Yokoi H: Scanning electron microscopic studies on inner ear barotrauma. Mainly on the damage of cochlear sensory hairs. Jpn J Otol (Tokyo) 85:941-950, 1981. Thorne PR, Duncan CE, Gavin JB: The pathogenesis of stereocilia abnormalities in acoustic trauma. Hear Res 21 :41-49, 1986. Fredelius L: Time sequence of degeneration pattern of the organ of Corti after acoustic overstimulation: A transmission electron microscopy study. Acta Otolarygol 106:373-385, 1988. Beagley HA: Acoustic trauma in the guinea pig: II. Electron microscopy including the morphology of cell junctions in the organ of Corti. Acta Otolaryngol 60:479-495, 1965. Spoendlin H: Primary structural changes in the organ of Corti after acoustic overstimulation. Acta OtolaryngoI71:166-176, 1971. Forge A: Outer hair cell loss and supporting cell expansion following chronic gentamicin treatment. Hear Res 19:171-182, 1985. Duvall AJ, Wersiill J: Site of action of streptomycin upon inner ear sensory cells. Acta Otolaryngol 57:581 -598, 1964. Engstrom H, Kohonen A: Cochlear damage from ototoxic antibiotics. Acta Otolaryngol 59 :171178, 1965. Robertson D: Functional significance of dendric swelling after loud sound in the guinea pig cochlea. Hear Res 9:263-278, 1983. Liberman MC, Dodds LW: Acute ultrastructural changes in acoustic trauma: Serial-section reconstruction of stereocilia and cuticular plate. Hear Res 26:45-64, 1987. Duvall AJ, Ward WD, Lauhala KE: Stria ultrastructure and vessel transport in acoustic trauma.
INNER EAR BAROTRAUMA
Sl1
Ann Otol Rhinol Laryngol 83:498-515, 1974. 12. Goodhill V: Sudden deafness and round window rupture. Laryngoscope 81:1462-1472, 1971. 13. Yokoi H, Yanagita N: Blast injury to sensory hairs: A study in the guinea pig using scanning electron microscopy. Arch Otorhinolaryngol 240:263-270, 1984. 14. Hiraide F, Kakoi H, Tabe T, et al: Light microscopic observation on experimental inner ear barotrauma. Oto-Rhino-Laryngol Tokyo 29:391-396, 1986. 15. Lamkin R, Axelsson A, McPherson 0, et al: Experimental aural barotrauma: Electrophysiological and morphological findings. Acta Otolaryngol (Suppl 335):1-24, 1975.
Request reprints to:
Dr. N. Yanagita, Department of Otorhinolaryngology, Nagoya University School of Medicine, Nagoya 466, Japan
INNER EAR DISORDERS CAUSED BY BAROTRAUMA IN GUINEA PIGS Noriyuki YANAGITA, M.D., Shigeji FUKUTA, M.D., Hisashi YOKOI, M.D., Kazuya ISHIDA, M.D., and Tsutomu NAKASHIMA, M.D. Department of Otorhinolaryngology, Nagoya University School of Medicine, Nagoya, Japan
'To determine the mechanism of hair cell damage caused by barotrauma to the inner ear, we investigated morphological changes in the organ of Corti and stria vascularis using transmission electron microscopy (TEM) and scanning electron microscopy (SEM). Fractures of the stereocilia with minimal intracellular changes were observed immediately after trauma. One day later, there was marked degeneration of outer hair cells and expansion of supporting cells. The damage to stereocilia clearly preceded morphological alterations within the hair cell bodies. Most outer hair cells eventually disappeared and were replaced by supporting cells. Inner hair cells degenerated slowly: some were almost intact 1 month after the trauma despite the disappearance of stereocilia. The continuity of reticular lamina was maintained throughout the period of hair cell degeneration, preventing leakage of endolymph into the organ of Corti. Reversible dendritic swelling of inner hair cells occurred immediately after trauma. No change in the stria vascularis was observed over time. Our results suggest that the mechanism of hair cell damage caused by inner ear barotrauma is related to a deformity of the organ of Corti caused by a pressure discrepancy between the perilymph and endolymph, resulting in injury to stereocilia. Sudden changes in atmospheric pressure damage the acoustic organs, with the middle ear being especially susceptible. Barotrauma of the inner ear has a low incidence compared with barotrauma of the middle ear. However, when barotrauma occurs in the inner ear, the resulting damage is severe, and can lead to acute sensorineural hearing loss. We induced inner ear barotrauma in guinea pigs exposing them to rapid compression and decompression in a high pressure chamber and investigated morphological changes in the cochlea using scanning electron microscopy (SEM) and transmission electron microscopy (TEM). Received for publication September 1, 1992 SI
S2
N. YANAGITA et al
METHODS AND MATERIALS
White guinea pigs weighing 200 to 300 g with normal Preyer's reflex were exposed to changes in atmospheric pressure in a pressure chamber in which a pressurized oxygen infusion elevated the atmospheric pressure up to 2 absolute atmosphric pressure (AT A) within 10 min, that pressure was maintained for 10 min. The chamber gas outlet was then opened to reduce the atmospheric pressure from 2 ATA to 1 ATA within 30 to 60 sec. After this pressure loading, Preyer's reflex disappeared bilaterally or unilaterally in about one-fifth of animals. We examined the organ of Corti and stria vascularis in the basal turn and the third turn in cochlea in the side in which Preyer's reflex disappeared immediately, 1 day, 1 week, and 1 month after pressure loading in cochlea using TEM and SEM. We observed either the organ of Corti or stria vascularis in one cochlea. The organ of Corti was observed in 7 cochleas at each period after the pressure loading. To prepare the specimens for TEM investigation, the animals were decapitated after the intraperitoneal injection of 10% urethan (0.02 mljg). The cochlea were exposed and perfused with phosphate buffer containing 2.5% glutalaldehyde and 2% paraformaldehyde through a hole made in the bony cochlear wall. The cochlea were removed, fixed with the same fluid and osmium acid phosphate buffer, dehydrated in a series of alcohols, and embedded in Epon 812. After thin sections had been cut and stained twice with uranyl acetate and lead citrate, the specimens were examined, with a Hitachi H-300 electron microscope. Specimens for examination by SEM were fixed as described above for TEM. Cochlea were subjected to ethanol dehydration, microdissection, critical point drying, and gold metallization, according to the method of Handoh et al. 1 Specimens were then observed under a SEM (JSM-SI5), with special attention to the organ of Corti and surface structure of the stria vascularis of the luminal side. RESULTS
A)
The organ of Corti SEM immediately after pressure loading showed that sensory hairs of the organ of Corti were disarranged and bent in various directions (Fig. 1). Random disappearance of the hairs was detected especially in the outer hair cells. TEM showed that stereocilia were bent at their bases. Though structural distortions were observed under the cuticular plate, no laceration was observed in the cuticular plate or cell junctions and continuity of the reticular lamina was maintained. No significant changes were observed inside the cell bodies except for a slight increase in the number of vacuoles (Fig. 2). Inner hair cells were less damaged than outer hair cells, but swelling of afferent nerve endings was observed in about half of the specimens (Fig. 3).
INNER EAR BAROTRAUMA
S3
Fig. I. SEM . Immediately after pressure loading of the third turn. Sensory hairs were disarranged and bent in va rious directions.
Fig.
2. Immediately after pressure loading of third turn. Stereocilia of outer hair cells (OHCs) were bent at the base. No significant changes were observed inside the cell bodies.
One day after pressure loading, severe disarrangement of stereocilia of the outer hair cells was apparent. Fusion of stereocilia was occasionally observed and the degeneration of cell bodies was detected (Fig. 4). Nuel's space was almost completely replaced by supporting cells in sites with severely damaged stereocilia, but no tears were detected in the reticular lamina. Fusion of stereocilia of inner
N. YANAGITA et al
S4
.'
Fig. 3. Immediately after pressure loading of basal turn. Swelling of afferent nerve endings of inner hair cell (IHC) was observed.
Fig. 4.
One day after trauma of basal turn. Degeneration of OHC bodies was detected.
INNER EAR BAROTRAUMA
Fig. 5.
S5
One day after trauma of basal tum. Degeneration inside IHC was slight.
Fig. 6. SEM. One week after trauma of basal tum. Disappearance and fusion of stereocilia of OHCs were observed.
hair cells was also observed, but there was less degeneration inside the inner hair cells than inside the outer hair cells (Fig. 5). Slight swelling of afferent nerve endings was observed in only a small number of specimens. One week after pressure loading, disappearance of stereocilia progressed, and fusion of the remaining stereocilia was observed (Fig. 6). Inside the outer hair cells, the number of lysosomes increased, and cytoplasmic inequalities and signifi-
S6
N. YANAGITA et al
Fig. 7. One week after trauma. Significant progression of degeneration of OHC bodies was observed.
cant degeneration were observed (Fig. 7). In some specimens, the remains of organelles were identified in the endolymphatic space, although the continuity of the reticular lamina was maintained by supporting cells that proliferated upwards (Fig. 8). In most inner hair cells, no significant degeneration was observed in cell bodies except for the formation of small vacuoles. One month after pressure loading, most of the outer hair cells had disappeared, being replaced by supporting cells (Fig. 9). The damaged inner hair cells were also replaced by supporting cells in some places, but the extent of the replacement and degeneration inside the cell bodies was minimal compared with the outer hair cells. The degree of impairment did not differ significantly between the basal turn and the third turn. B)
Stria vascularis In one cochlea examined 1 week after pressure loading, a slight increase of the intercellular gap and the accumulation of a homogeneous substance between the intermediate cells were observed at the basal turn. However, no abnormalities were observed at the third turn. No abnormalities such as degeneration or atrophy were
INNER EAR BAROTRAUMA
S7
Fig. 8. One week after trauma of basal turn. Remains of organelles of ORC were identified in the endolymphatic space.
Fig. 9. SEM. Two weeks after trauma of second turn. Most ORCs had disappeared and had been replaced by supporting cells.
observed in other specimens at any of the examination periods (Fig. 10). DISCUSSION
In this experiment, we induced inner ear barotrauma by the method described
S8
N. YANAGITA et al
Fig. 10. Stria vascularis. No abnormalities were observed. SEM. One month after trauma.
A) One day after trauma. B)
by Handoh et al. 1 Disarrangement of stereocilia, fracture of stereocilia at the basal end, and distortion of outer hair cells beneath the cuticular plate were observed immediately after pressure loading, suggesting that displacement occurred between the tectorial membrane and reticular lamina and between the reticular lamina and basilar membrane. Only slight damage to the hair cell body was observed immediately after pressure loading, but degeneration of the hair cells occurred one day after pressure loading. The outer hair cells sustained severe degeneration, especially when stereocilia were damaged significantly. No intracellular degeneration was observed in the absence of damage to stereocilia. These results suggested
INNER EAR BAROTRAUMA
S9
that damage to the stereocilia preceded the intracellular degeneration that such is necessary for hair cell degeneration to occur. Thome et al and Fredelius reported that damage to stereocilia preceded secondary degeneration of hair cells in acoustic trauma. 2,3 Hair cell damage appears to be similar in acoustic trauma and barotrauma because in both conditions the inner ear is subjected to a mechanical load over a short period. We did not observe laceration of the reticular lamina either in the period immediately after pressure loading or later. Beagley also found no tears at cell junctions in the organ of Corti following acoustic trauma. 4 These findings suggest that the reticular lamina is resistant to mechanical stimuli. In studies by Spoendlin of acoustic trauma5 and Forge of the degenerative process of outer hair cells following gentamicin administration, 6 continuity of the reticular lamina was maintained after destruction of the hair cells because supporting cells covered the areas where hair cells disappeared. The continuity of the reticular lamina was also maintained during the degenerative process that followed barotrauma in our study, suggesting that direct contact between the endolymph and perilymph was not a likely cause of degeneration. Outer hair cells sustained greater damage and exhibited more rapid degeneration compared with inner hair cells following barotrauma. This difference in susceptibility has been described in studies in aminoglycoside intoxication by Duvall and WersaC and Engstrom and Kohonen 8 and in acoustic trauma by Spoendlin. 5 The swelling of afferent nerve endings observed immediately after pressure loading appeared to be transient and disappeared one day after pressure loading. Similar findings have been reported in acoustic trauma. 3,5,9,1Q No significant damage to the stria vascularis was observed, indicating that degeneration of hair cells was not caused by changes in the composition of inner ear fluid produced by the disruption of the stria vascularis. These findings, together with an earlier reports, 1l,15 suggest that the stria vascularis is resistant to mechanical stimuli. Goodhill has suggested that inner ear barotrauma can be induced through the implosive route.12 Pressure transmission via the inner ear window may cause perilymphatic pressure elevation, leading to a pressure difference between the endolymph and perilymph. This pressure difference may cause displacement of the basilar membrane and Reissner's membrane, leading to alteration in the shape of the organ of Corti and subsequent impairment of stereocilia and hair cell degeneration. Pressure is transmitted equally to different places as long as it follows Pascal's principle. Damage to the organ of Corti caused by pressure loading can occur anywhere from the basal tum to the apical tum. We observed no significant difference in damage between the basal tum and the third tum. In contrast, acoustic trauma usually causes characteristic localizable damage according to frequency of the sound. When blast injury was induced, pressure transmission occurred extraordinarily fast,13 and there was greater damage to the stereocilia of
SIO
N. YANAGITA et al
the basal and the second turns than to those of the upper turns. Several authors have reported varying degrees of damage among cochlear turns in studies of barotrauma. l3· tS The pattern of the damage is believed to be related to the experimental condition of pressure loading. CONCLUSION
Immediately after pressure loading in guinea pigs, bending of sensory hairs of the outer and inner hair cells was observed, but changes inside the hair cells were slight. One day after pressure loading, degeneration inside the hair cells was observed. The severity of stereocilia damage was correlated with degeneration of hair cells. Greater damage and more rapid degeneration occurred in outer hair cells than in inner hair cells. No siginificant changes of the stria vascularis were observed. Inner ear barotrauma appears to be induced primarily by a difference between the endolymphatic and perilymphatic pressures, resulting in movement of the organ of Corti and damage to the stereocilia of the hair cells. This work was supported by a grant from the Ministry of Health and Welfare of Japan. REFERENCES I.
2. 3. 4. 5. 6. 7. 8. 9. 10. 11.
Handoh M, Yanagita N, Yokoi H: Scanning electron microscopic studies on inner ear barotrauma. Mainly on the damage of cochlear sensory hairs. Jpn J Otol (Tokyo) 85:941-950, 1981. Thorne PR, Duncan CE, Gavin JB: The pathogenesis of stereocilia abnormalities in acoustic trauma. Hear Res 21 :41-49, 1986. Fredelius L: Time sequence of degeneration pattern of the organ of Corti after acoustic overstimulation: A transmission electron microscopy study. Acta Otolarygol 106:373-385, 1988. Beagley HA: Acoustic trauma in the guinea pig: II. Electron microscopy including the morphology of cell junctions in the organ of Corti. Acta Otolaryngol 60:479-495, 1965. Spoendlin H: Primary structural changes in the organ of Corti after acoustic overstimulation. Acta OtolaryngoI71:166-176, 1971. Forge A: Outer hair cell loss and supporting cell expansion following chronic gentamicin treatment. Hear Res 19:171-182, 1985. Duvall AJ, Wersiill J: Site of action of streptomycin upon inner ear sensory cells. Acta Otolaryngol 57:581 -598, 1964. Engstrom H, Kohonen A: Cochlear damage from ototoxic antibiotics. Acta Otolaryngol 59 :171178, 1965. Robertson D: Functional significance of dendric swelling after loud sound in the guinea pig cochlea. Hear Res 9:263-278, 1983. Liberman MC, Dodds LW: Acute ultrastructural changes in acoustic trauma: Serial-section reconstruction of stereocilia and cuticular plate. Hear Res 26:45-64, 1987. Duvall AJ, Ward WD, Lauhala KE: Stria ultrastructure and vessel transport in acoustic trauma.
INNER EAR BAROTRAUMA
Sl1
Ann Otol Rhinol Laryngol 83:498-515, 1974. 12. Goodhill V: Sudden deafness and round window rupture. Laryngoscope 81:1462-1472, 1971. 13. Yokoi H, Yanagita N: Blast injury to sensory hairs: A study in the guinea pig using scanning electron microscopy. Arch Otorhinolaryngol 240:263-270, 1984. 14. Hiraide F, Kakoi H, Tabe T, et al: Light microscopic observation on experimental inner ear barotrauma. Oto-Rhino-Laryngol Tokyo 29:391-396, 1986. 15. Lamkin R, Axelsson A, McPherson 0, et al: Experimental aural barotrauma: Electrophysiological and morphological findings. Acta Otolaryngol (Suppl 335):1-24, 1975.
Request reprints to:
Dr. N. Yanagita, Department of Otorhinolaryngology, Nagoya University School of Medicine, Nagoya 466, Japan