Auris·Nasus·Larynx (Tokyo) 19, 95-104 (1992)
ENDOLYMPHATIC HYDROPS INDUCED BY NOISE EXPOSURE Hidetaka KUMAGAMI, M.D. Department of Otolaryngology, Nagasaki University, Nagasaki, Japan
In animal with cochlear deafness induced by firecracker explosion, fibrous degeneration of the endolymphatic sac was observed 4 months after the disappearance of Preyer's reflex. Endolymphatic hydrops induced by noise exposure may develop as the results of degeneration of the endolymphatic sac due to cochlear deafness by acoustic trauma after the lapse of a long period of time. It is well known that endolymphatic hydrops develops after obliteration of the endolymphatic sac (ES) (KIMURA and ScHUKNECHT, 1965). In clinic, a syndrome that occurs in patients who have sustained a profound hearing loss in one ear, usually from middle ear infection or head trauma, and then develops after a prolonged period of time into either episodic vertigo in the same ear or fluctuating hearing loss in the opposite ear is called delayed endolymphatic hydrops (ScHuKNECHT and GUL YA, 1983). Histopathologically, severe endolymphatic hydrops has also been shown in the temporal bone of delayed endolymphatic hydrops by ScHUKNECHT, SuzuKA, and ZIMMERMANN (1990). Histopathological findings of the ES which were caused by experimental cochlear deafness in animal were studied in order to elucidate why endolymphatic hydrops is caused by cochlear deafness.
SUBJECTS AND METHODS Albino guinea pigs weighing approximately 250 g were used for this experimental study. Each of the guinea pigs having lost the Preyer's reflex by the explosion of a firecracker (made in China) was examined after the lapse of 4, 5, and 6 months, respectively. Two such animals were examined after the lapse of 1 year. Guinea pigs were placed in a cage which was covered by an 80 X 80 em wooden box Received for publication September 9, 1991 This paper was presented at the 38th Annual Meeting of the Ear Research Japan, held in Sendai on February 15, 1991. 95
96
H.
KUMAGAMI
and then a firecracker was fired. The noise level of one firecracker explosion was 130dB or more at the distance of 50cm as measured by a sound level meter (NA61, Lion). Frequency analysis of explosion sound showed a flat energy below 3 kHz. Auditory nerve action potential ( AP) was recorded using a click of one cycle and cochlear microphonics (CM) at 0.5 and 4kHz were recorded using pure tone. AP and CM were recorded from the round window. In normal guinea pigs, the detection threshold of AP is 30 dB SPL and the output potential at 120dB SPL is 503± 110 ,uV. The detection threshold of CM at 0.5 and 4kHz is 50 dB SPL. The output potential at 120dB SPL of 4kHz is 343± 151 ,uV and that at 120dB SPL of 0.5 kHz is 820±220 ,uV. The method used for measurement was reported previously (KUMAGAMI, NISHIDA, and MoRIUCHI, 1981 ). Animals showed no abnormal posture and walking for 1 year. Animals were sacrificed by intraperitoneal injection of pentobarbital sodium after the AP and CM recording. The otic bulla was fixed in 10% neutral buffered formaldehyde, and decalcified for 4 days in 10% EDT A solution, and then part of the cochlea and part of semicircular canals (posterior part) were transsectioned. The medial bony wall of the ES was removed as a SEM specimen. The specimen was washed in phosphate buffer solution (PBS) and fixed in 2% tannic acid containing 1% glutaraldehyde for 2 hr, then immersed in 2% osmium oxide for 3 hr, washed thoroughly in PBS and dehydrated in serial ethanol, replaced by isoamyl, critical point dried, and coated by AU. A JSM-35 scanning electron microscope was used for observation. The cochlear part was further decalcified in 10% trichloroacetic acid, embedded in celloidin, sectioned in 20 ,urn at modiolar horizontal plane, and stained with hematoxylin-eosin. As a control, a 1-year-old guinea pig (n = 1) without any treatment was used. RESULTS As a preliminary examination, one guinea pig having lost the Preyer's reflex was examined under SEM after the lapse of 1 month in order to know how cochlear hair cells are damaged by a firecracker explosion. The outer hair cells were severely damaged from the basal turn to the upper middle turn (Fig. 1).
Cochlear pathology In the month 4 animal, no endolymphatic hydrops was seen. In the rrionth 5 animal, a slight degree of endolymphatic hydrops at the apical turn was seen. In the month 6 animal, slight endolymphatic hydrops was seen in all turns, and no atrophy of the stria vascularis was found. In the year 1 animals, endolymphatic hydrops increased in intensive degree varying from moderate to extensive extending to all turns (Fig. 2). No atrophy of the stria vascularis nor abnormal findings of the spiral ganglion cells were found except in the left year of the year 1 animal No.5, showing
ENDOLYMPHATIC HYDROPS
Fig. I. SEM showing severe damage of the hair cells in the middle tum. AP output potential as 120dB SPL showed 108 t.tV (X 1,000).
Fig. 2. Animal No. 5, year I, the left ear. Photomicrograph showing extensive endolymphatic hydrops.
97
98
H. KUMAGAMI
Fig. 3. Animal No. 5, year 1, the right ear. Photomicrograph showing a few floating cells and precipitates stained with eosin in the ES.
the disappearance of spiral ganglion cells in the basal turn. In the vestibule and semicircular canals from month 6 to year 1 animals, slight to moderate endolymphatic hydrops of the saccule was found, but not so intensive as to extend to the footplate. No abnormal findings were found in the sensory epithelia of the otolith maculae and semicircular canal. In the month 4 animal (No. 1), the ES of the left ear showed many floating cells and precipitates stained with eosin in the lumen of the vestibular aqueduct and rugose portion. In the month 5 animal (No. 2), the ES of the right ear also showed the same findings as in animal No. 1. In the month 12 animals (Nos. 4 and 5), the left ear and the right ear, respectively, still disclosed a few floating cells and precipitates stained with eosin covering the epithelial layer in the vestibular aqueduct and rugose portion (Fig. 3). SEM findings of the ES In the month 4 animal, the ES of the right ear already revealed degeneration of epithelial cells with remarkable proliferation of collagen fibers on the cell surface. Floating cells were found scatteringly among the epithelial cells (Fig. 4). In the month 5 animal, epithelial cells disappeared in some portion of the ES of the left ear, particles measuring 1 f.Lm in size were adhered to the surface of the preserved epithelial cells, and the proliferation of fibrils was observed on the surface of some of the cells (Fig. 5). In the month 6 animal, the ES of the left ear showed no great difference from that in the month 5 animal. However, the proliferation of fibrils covering the epithelial cells was more intensive. In the year 1 animal (No. 5), epithelial cells of the ES of the left ear showed deposit substances covering the surface of sac cells as in animal No.4 (Fig. 6).
ENDOLYMPHATIC HYDROPS
Fig. 4. A: Normal control. Note well arranged epithelial cells in the rugose portion (X 1,300). B: Animal No. 1, month 4, the right ear. Note fibrous change of the epithelial cells (X 1,500).
99
100
H. KUMAGAMI
Fig. 5. Animal No. 2, month 5, the left ear. SEM showing a remarkable change of the sac cells in the rugose portion (X 2,000). AP and CM responses in the month 4 animal showed a low output potential, but the responses in the year I animals were absent or extremely low (Table 1). In Table 1, blank space without D (degeneration) for SEM, sac means that SEM examination was not done because the whole inner ear was observed using the celloidin specimen. A control guinea pig showed normal findings in both cochlea andES. DISCUSSION Endolymphatic hydrops divided by SCHUKNECHT and GULYA (1983) into symptomatic and asymptomatic, each being subdivided into embryopathic, acquired, and idiopathic endolymphatic. The acquired group was further divided into postinftammatory and posttraumatic. Delayed endolymphatic hydrops belongs to the symptomatic acquired group. Acquired endolymphatic hydrops is caused by syphilitic labyrinthitis, virus infection, and bacterial infection. Cases of posttraumatic endolymphatic hydrops accompanied with Meniere's disease-like attack have been reported (CLARK and REES, 1977; PAPARELLA and MANCINI, 1983) and acoustic trauma-induced Meniere's syndrome also has been reported (RoiTMAN, TALMI, FINKELSTEIN, SILVER, SADOV, and ZOHAR, 1989).
ENDOL YMPHATIC HYDROPS
101
Fig. 6. Animal No. 5, year I, the left ear. SEM showing the deposit substances covering the surface of sac cells (A, X 1,000; B, X 6,600).
H. KUMAGAMI
102
Table I. Endolymphatic hydrops induced by noise exposure. Animal Lapsed No. month 4
Hydrops
SEM, Sac
AP (J.tV)
R
R
R
L
R
L
R
L
125
120
10
15
10
50
L
D
L
4kHz CM (J.tV) 0.5 kHz CM (J.tV)
110 120 20 20 20 50 D + + D 85 50 10 5 8 0 6 3 + + 0 0 D 0 0 0 0 4 12 ++ ++ 10 D 50 0 10 0 0 5 12 ++ +++ +, slight; + +, moderate; + + +, extensive; D, degeneration; AP, CM, output potential at 120
2
5
dB SPL.
It is also known that vertiginous attack is caused by unilateral total deafness of unknown etiology (EVERBERG, 1960; KAMEl, NORO, YABE, and MAKINO, 1971; WOLFSON and LEIBERMAN, 1975; OLIVEIRA and SCHUKNECHT, 1990). There is a long time lag from inner ear damage to the development of endolymphatic hydrops or to the appearance of vestibular and cochlear symptoms. For this reason, SCHUKNECHT, NORTHROP, and IGARASHI (1965, 1968) stated that there is a great difference among animal species in time requirement before the completion of endolymphatic hydrops after the disturbance of endolymphatic resorptive function. The time required is a few weeks in guinea pigs, 3 years in cats, and a longer period in human. It is said that 1 year of guinea pig corresponds to approximately 10 years of human life considering from a viewpoint of the average life span (SUTHERLAND and FESTING, 1987). In animal experiments, review was made on endolymphatic hydrops upon inducing cochlear deafness by acute noise exposure. It was considered that endolymphatic hydrops begins to develop 5 months after the disappearance of the Preyer's reflex and gradually increases thereafter. Degeneration and fibrous changes in both intradural portion of the ES and rugose portion were already observed in the month 5 animal in which the development of endolymphatic hydrops was minimal. It is considered that fibrous changes may advance with time and endolymphatic hydrops may increase as endolymphatic resorptive function in the rugose portion is disturbed. The severity of degeneration of the epithelial cells in the rugose portion and the degree of endolymphatic hydrops seem to be proportional to the severity of cochlear damage. Previously, we reported a case of a 30-year-old male with delayed endolymphatic hydrops (KUMAGAMI and SASANO, 1992). In this case, the ES showed fibrous degeneration and disappearance of the epithelial cells. In our experiments of inner ear damage due to firecracker explosion, AP and CM showed a remarkable low output potential compared with normal guinea pigs, suggesting that a severe damage was caused to the cochlea. In the same firecracker explosion induced cochlear damage, AP and CM responses seemed to decrease with time. On the other hand, the shape of the vestibule and semicircular canals was well preserved light microscopically. This may be due to
ENDOLYMPHATIC HYDROPS
103
the regional difference in susceptibility to damage between the cochlea and the vestibula-semicircular canals (KuMAGAMI, UMEKI, and NISHIDA, 1980). In this experiment, 10 ears of 5 guinea pigs were examined. It may not be possible to draw an adequate conclusion because of the small number of experimental animals. However, the occurrence of severe endolymphatic hydrops after the lapse of 1 year is considered to be a significant result. Further studies are required using animals with the lapse of a long term after the onset of cochlear deafness. In conclusion, the damage to cochlear hair cells in an initial step seems to result in fibrous degeneration of the epithelial cells in the ES, then in endolymphatic resorptive dysfunction in the rugose portion, and finally in development of endolymphatic hydrops after the lapse of a long period. These results are of interest from the viewpoint of development of delayed endolymphatic hydrops. Animal experiments were carried out in the Animal Center of Nagasaki University. I express thanks to Mr. Suematsu, Central Laboratory for Electron Microscopy, for his technical advice. REFERENCES CLARK, S. K., and REES, T. S.: Posttraumatic endolymphatic hydrops. Arch. Otolaryngol. 103: 725726, 1977. EvERBERG, G.: Unilateral total deafness in children: Clinical problems with a special view to vestibular function. Acta Otolaryngol. 52: 253-269, 1960. KAMEl, T., NORO, H., YABE, S., and MAKINO, S.: Statistical observation of unilateral total deafness and characteristic unilateral total deafness among young children with tendency towards occurrence of dizziness. Jibi Inkoka (Tokyo) 42: 349-358, 1971. KIMURA, R. S., and ScHUKNECHT, H. F.: Membranous hydrops in the inner ear of the guinea pig after obliteration of the endolymphatic sac. ORL 27: 343-354, 1965. KUMAGAMI, H., and SASANO, T.: A case of delayed endolymphatic hydrops. Auris·Nasus·Larynx (Tokyo) 19: 51-54, 1992. KuMAGAMI, H., UMEKI, S., and NISHIDA, H.: Regional differences in susceptibility to damages of vestibulo-semicircular canals in experimental labyrinthine lesion. A uris· Nasus· Larynx (Tokyo) 7: 99-109, 1980. KUMAGAMI, H., NISHIDA, H., and MORIUCHI, H.: Changes of the action potential, the summating potential and cochlear microphonics in experimental endolymphatic hydrops. ORL 42: 312-327, 1981. OLIVEIRA, C. A., and ScHUKNECHT, H. F.: Pathology of profound sensorineural hearing loss in infancy and early childhood. Laryngoscope 109: 902-909, 1990. PAPARELLA, M. M., and MANCINI, F.: Trauma and Meniere's syndrome. Laryngoscope 93: 1004-1012, 1983. ROITMAN, R., TALMI, Y. P., FINKELSTEIN, Y.,SILVER, S., SADOV,R., andZOHAR, Y.: Acoustic traumainduced Meniere's syndrome. ORL 51: 246-250, 1989. ScHUKNECHT, H. F., and GULYA, A. J.: Endolymphatic hydrops an overview and classification. Ann. Otol. Rhino/. Laryngol. 92, Suppl. 106: 1-20, 1983. SCHUKNECHT, H. F., NORTHROP, B. A., and IGARASHI, M.: Cochlear pathology after destruction of the endolymphatic sac in the cat. Acta Otolaryngol. 65: 479-487, 1968. ScHUKNECHT, H. F., SuzuKA, Y., and ZIMMERMANN, C.: Delayed endolymphatic hydrops and its
H. KUMAGAMI
104
relationship to Meniere's disease. Ann. Otol. Rhino/. Laryngol. 99: 843-853, 1990. SUTHERLAND, S.D., and FESTING, M. F. W.: The UFAW Handbook on the Care and Management of Laboratory Animals, 6th ed. (Poole, T., ed.), Longman Scientific and Technical, London, 1987. WoLFSON, R. J., and LEIBERMAN, A.: Unilateral deafness with subsequent vertigo. Laryngoscope 85: 1762-1766, 1975.
Request reprints to:
Dr. H. Kumagami, Department of Otolaryngology, School of Medicine, Nagasaki University, 7-1 Sakamoto-machi, Nagasaki 852, Japan
ENDOLYMPHATIC HYDROPS INDUCED BY NOISE EXPOSURE Hidetaka KUMAGAMI, M.D. Department of Otolaryngology, Nagasaki University, Nagasaki, Japan
In animal with cochlear deafness induced by firecracker explosion, fibrous degeneration of the endolymphatic sac was observed 4 months after the disappearance of Preyer's reflex. Endolymphatic hydrops induced by noise exposure may develop as the results of degeneration of the endolymphatic sac due to cochlear deafness by acoustic trauma after the lapse of a long period of time. It is well known that endolymphatic hydrops develops after obliteration of the endolymphatic sac (ES) (KIMURA and ScHUKNECHT, 1965). In clinic, a syndrome that occurs in patients who have sustained a profound hearing loss in one ear, usually from middle ear infection or head trauma, and then develops after a prolonged period of time into either episodic vertigo in the same ear or fluctuating hearing loss in the opposite ear is called delayed endolymphatic hydrops (ScHuKNECHT and GUL YA, 1983). Histopathologically, severe endolymphatic hydrops has also been shown in the temporal bone of delayed endolymphatic hydrops by ScHUKNECHT, SuzuKA, and ZIMMERMANN (1990). Histopathological findings of the ES which were caused by experimental cochlear deafness in animal were studied in order to elucidate why endolymphatic hydrops is caused by cochlear deafness.
SUBJECTS AND METHODS Albino guinea pigs weighing approximately 250 g were used for this experimental study. Each of the guinea pigs having lost the Preyer's reflex by the explosion of a firecracker (made in China) was examined after the lapse of 4, 5, and 6 months, respectively. Two such animals were examined after the lapse of 1 year. Guinea pigs were placed in a cage which was covered by an 80 X 80 em wooden box Received for publication September 9, 1991 This paper was presented at the 38th Annual Meeting of the Ear Research Japan, held in Sendai on February 15, 1991. 95
96
H.
KUMAGAMI
and then a firecracker was fired. The noise level of one firecracker explosion was 130dB or more at the distance of 50cm as measured by a sound level meter (NA61, Lion). Frequency analysis of explosion sound showed a flat energy below 3 kHz. Auditory nerve action potential ( AP) was recorded using a click of one cycle and cochlear microphonics (CM) at 0.5 and 4kHz were recorded using pure tone. AP and CM were recorded from the round window. In normal guinea pigs, the detection threshold of AP is 30 dB SPL and the output potential at 120dB SPL is 503± 110 ,uV. The detection threshold of CM at 0.5 and 4kHz is 50 dB SPL. The output potential at 120dB SPL of 4kHz is 343± 151 ,uV and that at 120dB SPL of 0.5 kHz is 820±220 ,uV. The method used for measurement was reported previously (KUMAGAMI, NISHIDA, and MoRIUCHI, 1981 ). Animals showed no abnormal posture and walking for 1 year. Animals were sacrificed by intraperitoneal injection of pentobarbital sodium after the AP and CM recording. The otic bulla was fixed in 10% neutral buffered formaldehyde, and decalcified for 4 days in 10% EDT A solution, and then part of the cochlea and part of semicircular canals (posterior part) were transsectioned. The medial bony wall of the ES was removed as a SEM specimen. The specimen was washed in phosphate buffer solution (PBS) and fixed in 2% tannic acid containing 1% glutaraldehyde for 2 hr, then immersed in 2% osmium oxide for 3 hr, washed thoroughly in PBS and dehydrated in serial ethanol, replaced by isoamyl, critical point dried, and coated by AU. A JSM-35 scanning electron microscope was used for observation. The cochlear part was further decalcified in 10% trichloroacetic acid, embedded in celloidin, sectioned in 20 ,urn at modiolar horizontal plane, and stained with hematoxylin-eosin. As a control, a 1-year-old guinea pig (n = 1) without any treatment was used. RESULTS As a preliminary examination, one guinea pig having lost the Preyer's reflex was examined under SEM after the lapse of 1 month in order to know how cochlear hair cells are damaged by a firecracker explosion. The outer hair cells were severely damaged from the basal turn to the upper middle turn (Fig. 1).
Cochlear pathology In the month 4 animal, no endolymphatic hydrops was seen. In the rrionth 5 animal, a slight degree of endolymphatic hydrops at the apical turn was seen. In the month 6 animal, slight endolymphatic hydrops was seen in all turns, and no atrophy of the stria vascularis was found. In the year 1 animals, endolymphatic hydrops increased in intensive degree varying from moderate to extensive extending to all turns (Fig. 2). No atrophy of the stria vascularis nor abnormal findings of the spiral ganglion cells were found except in the left year of the year 1 animal No.5, showing
ENDOLYMPHATIC HYDROPS
Fig. I. SEM showing severe damage of the hair cells in the middle tum. AP output potential as 120dB SPL showed 108 t.tV (X 1,000).
Fig. 2. Animal No. 5, year I, the left ear. Photomicrograph showing extensive endolymphatic hydrops.
97
98
H. KUMAGAMI
Fig. 3. Animal No. 5, year 1, the right ear. Photomicrograph showing a few floating cells and precipitates stained with eosin in the ES.
the disappearance of spiral ganglion cells in the basal turn. In the vestibule and semicircular canals from month 6 to year 1 animals, slight to moderate endolymphatic hydrops of the saccule was found, but not so intensive as to extend to the footplate. No abnormal findings were found in the sensory epithelia of the otolith maculae and semicircular canal. In the month 4 animal (No. 1), the ES of the left ear showed many floating cells and precipitates stained with eosin in the lumen of the vestibular aqueduct and rugose portion. In the month 5 animal (No. 2), the ES of the right ear also showed the same findings as in animal No. 1. In the month 12 animals (Nos. 4 and 5), the left ear and the right ear, respectively, still disclosed a few floating cells and precipitates stained with eosin covering the epithelial layer in the vestibular aqueduct and rugose portion (Fig. 3). SEM findings of the ES In the month 4 animal, the ES of the right ear already revealed degeneration of epithelial cells with remarkable proliferation of collagen fibers on the cell surface. Floating cells were found scatteringly among the epithelial cells (Fig. 4). In the month 5 animal, epithelial cells disappeared in some portion of the ES of the left ear, particles measuring 1 f.Lm in size were adhered to the surface of the preserved epithelial cells, and the proliferation of fibrils was observed on the surface of some of the cells (Fig. 5). In the month 6 animal, the ES of the left ear showed no great difference from that in the month 5 animal. However, the proliferation of fibrils covering the epithelial cells was more intensive. In the year 1 animal (No. 5), epithelial cells of the ES of the left ear showed deposit substances covering the surface of sac cells as in animal No.4 (Fig. 6).
ENDOLYMPHATIC HYDROPS
Fig. 4. A: Normal control. Note well arranged epithelial cells in the rugose portion (X 1,300). B: Animal No. 1, month 4, the right ear. Note fibrous change of the epithelial cells (X 1,500).
99
100
H. KUMAGAMI
Fig. 5. Animal No. 2, month 5, the left ear. SEM showing a remarkable change of the sac cells in the rugose portion (X 2,000). AP and CM responses in the month 4 animal showed a low output potential, but the responses in the year I animals were absent or extremely low (Table 1). In Table 1, blank space without D (degeneration) for SEM, sac means that SEM examination was not done because the whole inner ear was observed using the celloidin specimen. A control guinea pig showed normal findings in both cochlea andES. DISCUSSION Endolymphatic hydrops divided by SCHUKNECHT and GULYA (1983) into symptomatic and asymptomatic, each being subdivided into embryopathic, acquired, and idiopathic endolymphatic. The acquired group was further divided into postinftammatory and posttraumatic. Delayed endolymphatic hydrops belongs to the symptomatic acquired group. Acquired endolymphatic hydrops is caused by syphilitic labyrinthitis, virus infection, and bacterial infection. Cases of posttraumatic endolymphatic hydrops accompanied with Meniere's disease-like attack have been reported (CLARK and REES, 1977; PAPARELLA and MANCINI, 1983) and acoustic trauma-induced Meniere's syndrome also has been reported (RoiTMAN, TALMI, FINKELSTEIN, SILVER, SADOV, and ZOHAR, 1989).
ENDOL YMPHATIC HYDROPS
101
Fig. 6. Animal No. 5, year I, the left ear. SEM showing the deposit substances covering the surface of sac cells (A, X 1,000; B, X 6,600).
H. KUMAGAMI
102
Table I. Endolymphatic hydrops induced by noise exposure. Animal Lapsed No. month 4
Hydrops
SEM, Sac
AP (J.tV)
R
R
R
L
R
L
R
L
125
120
10
15
10
50
L
D
L
4kHz CM (J.tV) 0.5 kHz CM (J.tV)
110 120 20 20 20 50 D + + D 85 50 10 5 8 0 6 3 + + 0 0 D 0 0 0 0 4 12 ++ ++ 10 D 50 0 10 0 0 5 12 ++ +++ +, slight; + +, moderate; + + +, extensive; D, degeneration; AP, CM, output potential at 120
2
5
dB SPL.
It is also known that vertiginous attack is caused by unilateral total deafness of unknown etiology (EVERBERG, 1960; KAMEl, NORO, YABE, and MAKINO, 1971; WOLFSON and LEIBERMAN, 1975; OLIVEIRA and SCHUKNECHT, 1990). There is a long time lag from inner ear damage to the development of endolymphatic hydrops or to the appearance of vestibular and cochlear symptoms. For this reason, SCHUKNECHT, NORTHROP, and IGARASHI (1965, 1968) stated that there is a great difference among animal species in time requirement before the completion of endolymphatic hydrops after the disturbance of endolymphatic resorptive function. The time required is a few weeks in guinea pigs, 3 years in cats, and a longer period in human. It is said that 1 year of guinea pig corresponds to approximately 10 years of human life considering from a viewpoint of the average life span (SUTHERLAND and FESTING, 1987). In animal experiments, review was made on endolymphatic hydrops upon inducing cochlear deafness by acute noise exposure. It was considered that endolymphatic hydrops begins to develop 5 months after the disappearance of the Preyer's reflex and gradually increases thereafter. Degeneration and fibrous changes in both intradural portion of the ES and rugose portion were already observed in the month 5 animal in which the development of endolymphatic hydrops was minimal. It is considered that fibrous changes may advance with time and endolymphatic hydrops may increase as endolymphatic resorptive function in the rugose portion is disturbed. The severity of degeneration of the epithelial cells in the rugose portion and the degree of endolymphatic hydrops seem to be proportional to the severity of cochlear damage. Previously, we reported a case of a 30-year-old male with delayed endolymphatic hydrops (KUMAGAMI and SASANO, 1992). In this case, the ES showed fibrous degeneration and disappearance of the epithelial cells. In our experiments of inner ear damage due to firecracker explosion, AP and CM showed a remarkable low output potential compared with normal guinea pigs, suggesting that a severe damage was caused to the cochlea. In the same firecracker explosion induced cochlear damage, AP and CM responses seemed to decrease with time. On the other hand, the shape of the vestibule and semicircular canals was well preserved light microscopically. This may be due to
ENDOLYMPHATIC HYDROPS
103
the regional difference in susceptibility to damage between the cochlea and the vestibula-semicircular canals (KuMAGAMI, UMEKI, and NISHIDA, 1980). In this experiment, 10 ears of 5 guinea pigs were examined. It may not be possible to draw an adequate conclusion because of the small number of experimental animals. However, the occurrence of severe endolymphatic hydrops after the lapse of 1 year is considered to be a significant result. Further studies are required using animals with the lapse of a long term after the onset of cochlear deafness. In conclusion, the damage to cochlear hair cells in an initial step seems to result in fibrous degeneration of the epithelial cells in the ES, then in endolymphatic resorptive dysfunction in the rugose portion, and finally in development of endolymphatic hydrops after the lapse of a long period. These results are of interest from the viewpoint of development of delayed endolymphatic hydrops. Animal experiments were carried out in the Animal Center of Nagasaki University. I express thanks to Mr. Suematsu, Central Laboratory for Electron Microscopy, for his technical advice. REFERENCES CLARK, S. K., and REES, T. S.: Posttraumatic endolymphatic hydrops. Arch. Otolaryngol. 103: 725726, 1977. EvERBERG, G.: Unilateral total deafness in children: Clinical problems with a special view to vestibular function. Acta Otolaryngol. 52: 253-269, 1960. KAMEl, T., NORO, H., YABE, S., and MAKINO, S.: Statistical observation of unilateral total deafness and characteristic unilateral total deafness among young children with tendency towards occurrence of dizziness. Jibi Inkoka (Tokyo) 42: 349-358, 1971. KIMURA, R. S., and ScHUKNECHT, H. F.: Membranous hydrops in the inner ear of the guinea pig after obliteration of the endolymphatic sac. ORL 27: 343-354, 1965. KUMAGAMI, H., and SASANO, T.: A case of delayed endolymphatic hydrops. Auris·Nasus·Larynx (Tokyo) 19: 51-54, 1992. KuMAGAMI, H., UMEKI, S., and NISHIDA, H.: Regional differences in susceptibility to damages of vestibulo-semicircular canals in experimental labyrinthine lesion. A uris· Nasus· Larynx (Tokyo) 7: 99-109, 1980. KUMAGAMI, H., NISHIDA, H., and MORIUCHI, H.: Changes of the action potential, the summating potential and cochlear microphonics in experimental endolymphatic hydrops. ORL 42: 312-327, 1981. OLIVEIRA, C. A., and ScHUKNECHT, H. F.: Pathology of profound sensorineural hearing loss in infancy and early childhood. Laryngoscope 109: 902-909, 1990. PAPARELLA, M. M., and MANCINI, F.: Trauma and Meniere's syndrome. Laryngoscope 93: 1004-1012, 1983. ROITMAN, R., TALMI, Y. P., FINKELSTEIN, Y.,SILVER, S., SADOV,R., andZOHAR, Y.: Acoustic traumainduced Meniere's syndrome. ORL 51: 246-250, 1989. ScHUKNECHT, H. F., and GULYA, A. J.: Endolymphatic hydrops an overview and classification. Ann. Otol. Rhino/. Laryngol. 92, Suppl. 106: 1-20, 1983. SCHUKNECHT, H. F., NORTHROP, B. A., and IGARASHI, M.: Cochlear pathology after destruction of the endolymphatic sac in the cat. Acta Otolaryngol. 65: 479-487, 1968. ScHUKNECHT, H. F., SuzuKA, Y., and ZIMMERMANN, C.: Delayed endolymphatic hydrops and its
H. KUMAGAMI
104
relationship to Meniere's disease. Ann. Otol. Rhino/. Laryngol. 99: 843-853, 1990. SUTHERLAND, S.D., and FESTING, M. F. W.: The UFAW Handbook on the Care and Management of Laboratory Animals, 6th ed. (Poole, T., ed.), Longman Scientific and Technical, London, 1987. WoLFSON, R. J., and LEIBERMAN, A.: Unilateral deafness with subsequent vertigo. Laryngoscope 85: 1762-1766, 1975.
Request reprints to:
Dr. H. Kumagami, Department of Otolaryngology, School of Medicine, Nagasaki University, 7-1 Sakamoto-machi, Nagasaki 852, Japan
