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Saccular damage in patients with idiopathic sudden sensorineural hearing loss without vertigo
Otolaryngology–Head and Neck Surgery (2008) 139, 541-545
ORIGINAL RESEARCH—OTOLOGY AND NEUROTOLOGY
Saccular damage in patients with idiopathic sudden sensorineural hearing loss without vertigo Seok Min Hong, MD, Jae Yong Byun, MD, PhD, Chan Hum Park, MD, PhD, Jun Ho Lee, MD, Moon Suh Park, MD, PhD, and Chang Il Cha, MD, PhD, Chuncheon and Seoul, Korea OBJECTIVE: Saccule could be damaged in patients with idiopathic sudden sensorineural hearing loss (ISSHL) with vertigo and with high-frequency sensorineural hearing loss. Thus, the saccule might be deteriorated subclinically in ISSHL cases without vertigo. Therefore, we investigated saccular damage in ISSHL patients without vertigo through vestibular evoked myogenic potentials (VEMP). STUDY DESIGN: A prospective study. SUBJECTS AND METHODS: Fifty-two patients with ISSHL without vertigo were enrolled in the study. We identified VEMP in patients with ISSHL and analyzed the association of VEMP with initial hearing threshold, each threshold according to frequency, the type of audiogram, and hearing recovery. RESULTS: For cases with absent VEMP, we found significant differences between patients with 90 dB or more hearing loss and those with a hearing loss less than 55 dB with frequencies over 1000 Hz. Patients with profound hearing loss presented significantly high abnormal and absent VEMP than patients with audiograms of other types. CONCLUSION: These findings suggest that the subclinical deterioration of the saccular neuroepithelium is associated with patients with ISSHL having profound hearing loss at the high frequency. © 2008 American Academy of Otolaryngology–Head and Neck Surgery Foundation. All rights reserved.
S
udden sensorineural hearing loss has been defined as a sensorineural hearing loss of 30 dB or more and covering at least three contiguous audiometric frequencies, which occurs within 3 days or less.1 Most of these cases are idiopathic. Idiopathic sudden sensorineural hearing loss (ISSHL) remains controversial and equivocal with regard to diagnosis, treatment, and prognosis. Several prognostic indicators have been ascertained including age, the severity of the initial hearing loss, the presence of vertigo, and the audiometry pattern.2 About 30 percent to 40 percent of patients with ISSHL have accompanying vertigo.3 Studies have found that vertigo appears more frequently in association with profound hearing loss and that hearing recovery is worse in patients
with vertigo than in patients who do not experience vertigo.3-5 A recent study showed that the lesion site of vestibular disorders in patients with idiopathic sudden hearing loss with vertigo appeared to be within the labyrinth and that in these cases the saccule could be involved more frequently than the semicircular canals.6 Another report suggested that patients with high-frequency sensorineural hearing loss had subclinical disturbances of the vestibular system, especially in the saccule.7 Thus, we thought that ISSHL without vertigo might be associated with subclinical involvement of the saccule. However, no studies have reported on saccular damage in patients with ISSHL who do not have vertigo. Saccular damage can be identified by vestibular-evoked myogenic potential (VEMP), which is recorded on tonically contracted neck muscles by stimulating the ear with a loud sound. VEMP testing has been validated to reflect inner ear function, in particular the saccule, but not the cochlea and the semicircular canals.8 Therefore, we used VEMP to investigate saccular damage in patients with ISSNH without vertigo and also to evaluate the differences in saccular damage according to the initial hearing threshold, the frequency of hearing loss, and the hearing recovery rate.
METHODS The study was approved by the institutional review board, and, from May 2006 to December 2007, a prospective study was designed for 52 patients with ISSHL. Patients were included in the study if they had a sensorineural hearing loss of 30 dB or more with over three contiguous audiometric frequencies that occurred in less than 3 days. The authors obtained informed consent from patients, and we excluded the patients with ISSHL that had vertigo, Meniere’s disease, tumors, and a treatment onset of over 15 days. For all patients, we performed initial standard treatments by administering oral steroid for 8 days in tapering doses while also
Received March 18, 2008; revised May 18, 2008; accepted July 1, 2008.
0194-5998/$34.00 © 2008 American Academy of Otolaryngology–Head and Neck Surgery Foundation. All rights reserved. doi:10.1016/j.otohns.2008.07.003 Downloaded from oto.sagepub.com at Flinders University on December 5, 2016
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Otolaryngology–Head and Neck Surgery, Vol 139, No 4, October 2008
treating with other medications, such as a peripheral vasodilator and Ginko biloba extracts. Pretreatment and posttreatment audiograms were obtained for all patients. Puretone averages were calculated by averaging the pure-tone hearing levels at 500 Hz, 1000 Hz, 2000 Hz, and 3000 Hz. Audiograms were categorized as high- or low-tone hearing loss, flat type, and profound hearing loss. The group with high-tone hearing loss was defined as those patients with an average loss of 4 to 8 kHz who surpassed the average of the 0.25- to 0.5-kHz hearing loss by 30 dB or more. The low-tone hearing loss group showed an average loss of 0.25 to 0.5 kHz and surpassed the average of the 4- to 8-kHz hearing loss by 30 dB or more. The flat-type group consisted of patients with a 20 dB or less difference between the worst and best hearing levels among six frequencies (0.25, 0.5, 1, 2, 4, and 8 kHz). In the group with profound hearing loss, at least two frequencies produced results that were off the scale. Furthermore, in this group, the difference between the hearing level and the maximum sound level generated by the audiometer was within 10 dB at all six frequencies.6 Hearing recovery was expressed as complete recovery, partial recovery, slight improvement, and no improvement using the hearing threshold at 1 month posttreatment according to Siegel’s criteria.9 The VEMP testing was performed by using the initial hearing threshold test when possible and was recorded with patients in a sitting position with the head rotated away from the stimulated side during recording. The surface electrodes were placed as follows: on the middle third of the sternocleidomastoid muscle as the active electrode, the upper sternum as the reference electrode, and on the forehead as the ground electrode. Clicks of 0.1-ms duration were presented at a rate of 5 per second through a headphone. The click intensities were 95 dB, and an electromyographic signal was amplified and bandpass filtered (20 Hz-2 kHz) using a Nicolet Viking IV (Madison, WI). The analysis window was 100 msec wide. Responses to 256 stimuli were averaged. When we read the VEMP findings, we used our own VEMP response data as the reference value that was already reported at our department10 and two objective parameters, the abnormal VEMP rate and the absent VEMP rate. The abnormal VEMP category included cases with prolonged p13 and n23 latency, increased VEMP asymmetry, and an absent VEMP. An absent VEMP indicated no p13 or n23 wave formation in response to a loud sound. We investigated VEMP results in patients with ISSHL and analyzed the association of the VEMP findings with the initial average hearing threshold, several frequency thresholds, audiogram type, and hearing recovery.
Statistical analysis Statistical tests were performed by using the 2 test and Fisher exact test with Bonferroni correction (SPSS ver.11.5; SPSS, Chicago, IL) to analyze the abnormal and absent VEMP rates from several groups.
Table 1 Demographics and characteristics of the patients (n ⴝ 52) Parameter Age (y) Mean Range Affected ear Right Left Sex Male Female Days to treatment Mean Range Severity of hearing loss Mild Moderate Moderate to severe Severe Profound
N*
55.1 13-79 21 31 22 30 4.8 1-14 13 7 8 7 17
*Unless otherwise indicated.
RESULTS The average age of the patients was 55.1 years. The right to left ear and male to female ratios were 21:31 and 22:30, respectively. The time period between disease onset and the commencement of therapy averaged 4.8 days. The distribution in the severity of the hearing loss is listed in Table 1. Fourteen of the total 52 patients (26.9%) showed an abnormal VEMP response. This included eight patients with an absent VEMP. Moreover, abnormal VEMP responses were observed in 8 of 17 patients (47.1%) with a hearing loss of more than 90 dB, in 4 of 15 patients (26.7%) with a hearing loss between 55 and 90 dB, and in 2 of 20 patients (10%) with a hearing loss less than 55 dB. We found a significant difference between the patient group with a hearing loss more than 90 dB and those with a hearing loss less than 55 dB (P ⬍ 0.05). Furthermore, seven of eight patients with an absent VEMP had a hearing loss that was more than 90 dB (Table 2). When the data were analyzed according to the type of audiogram, the abnormal VEMP rates and absent VEMP rates were as follows: 8.3 percent and 0 percent in patients with high-tone hearing loss, 14.3 percent and 0 percent in patients with low-tone hearing loss, 18.8 percent and 6.3 percent in patients with flat-type hearing loss, and 47.1 percent and 41.2 percent in patients with profound hearing loss, respectively. Patients with profound hearing loss showed not only significantly higher abnormal VEMP rates than patients with high-tone hearing loss (P ⬍ 0.05), but they also presented significantly higher absent VEMP rates than patients with either high-tone hearing loss or flat-type hearing loss (Table 3).
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Table 2 The rate of abnormal VEMP formation and findings related to the extent of hearing loss expressed as pure-tone average Extent of hearing loss
% (n)
90 dB or more 55 dB-90 dB
47.1 (8/17)* 26.7 (4/15)
55 dB or less Total
10 (2/20) 26.9 (14/52)
VEMP findings: n Absent: Absent: A:1 A:2 Absent: P and
7, P and A : 1 1, P and N : 2,
8, P and N : 2, A : 1, A : 3
Absent, absent VEMP; P, prolonged p13 latency; N, prolonged n23 latency; A, increased vestibular asymmetry. *P ⬍ 0.05, significantly different from 55 dB or less group.
When hearing thresholds of each frequency were measured by using the initial pure-tone average and were divided into groups that had hearing losses of 90 dB or more, between 55 dB and 90 dB, and 55 dB or less, we found no significant differences among the groups with regard to abnormal VEMP rates (Fig 1). However, with regard to absent VEMP rates, we found significant differences in patients with hearing losses of over 90 dB at 1000-Hz, 2000-Hz, 4000-Hz, and 8000-Hz frequencies when compared with patients in the other two groups (P ⬍ 0.05, Fig 2). All of the hearing recovery rates showed no significant differences between patients with normal and abnormal VEMP findings that were composed of only complete recovery, incomplete recovery ⫹ partial recovery, and complete recovery ⫹ partial recovery ⫹ slight improvement (P ⬎ 0.05, Fig 3), although patients with abnormal VEMP showed relatively low recovery rate rather than those with normal VEMP.
Figure 1 Abnormal VEMP rates reported according to the extent of hearing threshold in each frequency (P ⬎ 0.05).
DISCUSSION VEMPs have been used as a clinical test of the vestibular system, particularly for the saccule and inferior vestibular nerve region.11,12 Clinical studies have suggested that this response is of vestibular origin, especially in the saccule and inferior vestibular nerve region.11,12 Neurophysiological experiments in guinea pigs and cats have shown that primary vestibular afferents, especially saccular afferents, respond to relatively loud clicks.13 In our study, we found that abnormal VEMP responses might be observed in ISSHL patients who do not have vertigo. These findings suggest that the vestibular system, in particular the saccule, has a subclinical involvement in ISSHL patients. A previous study reported that 77% of the ISSHL patients with vertigo exhibited an absence of click VEMPs on the affected side.6 In our study, only patients without vertigo were included. Therefore, when compared with previous report, lower abnormal VEMP rates was found in our study. But in patients group that had the hearing loss of 90 dB or more, abnormal VEMP rate was 47.1 percent. In addition, seven of eight patients with absent VEMPs were distributed in the patient group with a hearing loss of 90 dB
Table 3 Abnormal VEMP rates and absent VEMP rates related to the type of audiogram
Type of audiogram High-tone hearing loss Low-tone hearing loss Flat-type hearing loss Profound hearing loss
Abnormal VEMP rate % (n) 8.3 14.3 18.8 47.1
(1/12) (1/7) (3/16) (8/17)*
Absent VEMP rate % (n) 0 0 6.3 41.2
(0/12) (0/7) (1/16) (7/17)*†
*P ⬍ 0.05, significantly different from the high-tone hearing loss group. †P ⬍ 0.05, significantly different from the flat-type hearing loss group.
Figure 2 Absent VEMP rates reported according to the extent of hearing threshold in each frequency (*P ⬍ 0.05, significantly different from the absent VEMP rates of 55 to 90 dB and the ⬍55 dB group).
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Otolaryngology–Head and Neck Surgery, Vol 139, No 4, October 2008 estingly, in our study, we found that saccular damages that were identified by the VEMP findings did not affect hearing recovery (ie, we found that the subclinical involvement of the saccular neuroepithelium was not associated with ISSHL patient prognosis).
CONCLUSION
Figure 3 Hearing recovery rates of subjects who showed normal and abnormal VEMP findings. (I: complete recovery, II: partial recovery, III: slight improvement, P ⬎ 0.05).
or more. This finding suggests that the more severe the hearing loss, the more frequently the saccule was involved. When the VEMP findings were analyzed according to the type of audiogram, the patients with profound hearing loss showed relatively high abnormal and absent VEMP rates compared with other types. In particular, for absent VEMP rates, the profound hearing loss group was significantly different between the high-tone and flat-type hearing loss groups, although the number of patients with low-tone hearing loss was much smaller and did not show any significant difference. Because an absent VEMP indicated no wave formation and did not have any normal range or deviation, like latency or amplitude, the absent VEMP type might be thought of as a more reliable parameter compared with the abnormal VEMP rate (which includes prolonged p13 and n23 latency as well as increased VEMP asymmetry). In addition, the absent VEMP rates also were significant in patients with hearing losses of 90 dB or more and with high-frequencies over 1000 Hz, compared to the patients with hearing losses of 55-90 dB and 55 dB or less. These findings suggested that patients with severe cochlear damage of over 90 dB in a high 1000-Hz or more frequency could have a subclinical involvement of the saccule. The saccule has not only anatomic proximity to the acousticenergy delivery system, but the great similarity between the cochlear and vestibular hair-cell ultrastructures and the common arterial blood supply of the cochlea and vestibular end organs via the same end artery supports the possibility of vestibular involvement, in particular saccular deterioration that is associated with cochlear damage.14,15 One report has found that hearing recovery in ISSHL cases is worse in patients with vertigo than in those cases without vertigo.16 A previous report investigated the histopathological characteristics of the temporal bone in ISSHL cases with and without vertigo and found no direct relationship between the presence of vertigo and damage to the vestibular apparatus. The authors of this previous study hypothesized that vertigo in ISSHL cases was caused by the transmission of biochemical changes in the inner ear fluid between the cochlea and the vestibular apparatus.17 Inter-
Cases of ISSHL without vertigo could lead to abnormal VEMP responses, and, in particular, cases with a 90-dB hearing loss with a frequency over 1000 Hz or more could have a high rate of absent VEMP. These findings suggest that the subclinical deterioration of the saccular neuroepithelium were associated with severe hearing loss in cases of high-frequency ISSHL.
AUTHOR INFORMATION From the Department of Otorhinolaryngology–Head and Neck Surgery, Chuncheon Sacred Heart Hospital, Hallym University College of Medicine, Chuncheon, Korea (Drs Hong, Park, and Lee); and Department of Otorhinolaryngology–Head and Neck surgery, College of Medicine, KyungHee University, Seoul, Korea (Drs Byun, Park, and Cha). Corresponding author: Seok Min Hong, MD, Department of Otorhinolaryngology-Head and Neck Surgery, Chuncheon Sacred Heart Hospital, Hallym University College of Medicine, #153 kyo-dong, Chuncheon, Kangwon-do, 200-704, Korea. E-mail address: [email protected].
AUTHOR CONTRIBUTIONS Seok Min Hong, study design, writer; Jae Yong Byun, study design, data collection; Chan Hum Park, study design, data collection; Jun Ho Lee, data collection; Moon Suh Park, data collection; Chang Il Cha, study design, data collection.
FINANCIAL DISCLOSURE None.
REFERENCES 1. Whitaker S. Idiopathic sudden hearing loss. Am J Otol 1980;15: 244 – 6. 2. Laird N, Wilson WR. Predicting recovery from idiopathic sudden hearing loss. Am J Otolaryngol 1983;4:161– 4. 3. Shaia FT, Sheehy JL. Sudden sensorineural hearing impairment: a report of 1220 cases. Laryngoscope 1976;86:389 –98. 4. Mattox DE, Simmons FB. Natural history of sudden sensorineural hearing loss. Ann Otol Rhinol Laryngol 1977;86:463– 80. 5. Wilson WR, Laird N, Kavesh DA. Electronystagmographic findings in idiopathic sudden hearing loss. Am J Otolaryngol 1982;3: 279 – 85.
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Saccular damage in patients with idiopathic sudden . . .
6. Iwasaki S, Takai Y, Ozeki H, et al. Extent of lesions in idiopathic sudden hearing loss with vertigo: study using click and galvanic vestibular evoked myogenic potentials. Arch Otolaryngol Head Neck Surg 2005;131:857– 62. 7. Sazgar AA, Dortaj V, Akrami K, et al. Saccular damage in patients with high-frequency sensorineural hearing loss. Eur Arch Otorhinolaryngol 2006;263:608 –13. 8. Colebatch JG, Halmagyi GM, Skuse NF. Myogenic potentials generated by a click evoked vestibulocollic reflex. J Neurol Neurosurg Psychiatry 1994;57:190 –7. 9. Siegel LG. The treatment of idiopathic sudden sensorineural hearing loss. Otolaryngol Clin North Am 1975;8:467–73. 10. Lee SK, Park DC, Yeo SG, et al. Age-related difference of parameters of vestibular evoked myogenic potentials. Acta Otolaryngol 2007;22: 1–7. 11. Murofushi T, Halmagyi GM, Yavor RA, et al. Absent vestibular evoked myogenic potentials in vestibular neurolabyrinthitis: an
12.
13. 14. 15.
16. 17.
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indication of inferior vestibular nerve involvement? Arch Otolaryngol Head Neck Surg 1996;122:845– 8. Murofushi T, Matsuzaki M, Mizuno M. Vestibular evoked myogenic potentials in patients with acoustic neuroma. Arch Otolaryngol Head Neck Surg 1998;124:509 –12. Murofushi T, Curthoys IS, Topple AN, et al. Responses of guinea pig primary vestibular neurons to clicks. Exp Brain Res 1995;103:174 – 8. Golz A, Westerman ST, Westerman LM, et al. The effects of noise on the vestibular system. Am J Otolaryngol 2001;22:190 – 6. Perez R, Freeman S, Sohmer H, et al. Vestibular and cochlear ototoxicity of topical antiseptics assessed by evoked potentials. Laryngoscope 2000;110:1522–7. Nakashima T, Yanagita N. Outcome of sudden deafness with and without vertigo. Laryngoscope 1993;103:1145–9. Khetarpal U. Investigation into the causes of vertigo in sudden sensorineural hearing loss. Otolaryngol Head Neck Surg 1991;105: 360 –71.
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ORIGINAL RESEARCH—OTOLOGY AND NEUROTOLOGY
Saccular damage in patients with idiopathic sudden sensorineural hearing loss without vertigo Seok Min Hong, MD, Jae Yong Byun, MD, PhD, Chan Hum Park, MD, PhD, Jun Ho Lee, MD, Moon Suh Park, MD, PhD, and Chang Il Cha, MD, PhD, Chuncheon and Seoul, Korea OBJECTIVE: Saccule could be damaged in patients with idiopathic sudden sensorineural hearing loss (ISSHL) with vertigo and with high-frequency sensorineural hearing loss. Thus, the saccule might be deteriorated subclinically in ISSHL cases without vertigo. Therefore, we investigated saccular damage in ISSHL patients without vertigo through vestibular evoked myogenic potentials (VEMP). STUDY DESIGN: A prospective study. SUBJECTS AND METHODS: Fifty-two patients with ISSHL without vertigo were enrolled in the study. We identified VEMP in patients with ISSHL and analyzed the association of VEMP with initial hearing threshold, each threshold according to frequency, the type of audiogram, and hearing recovery. RESULTS: For cases with absent VEMP, we found significant differences between patients with 90 dB or more hearing loss and those with a hearing loss less than 55 dB with frequencies over 1000 Hz. Patients with profound hearing loss presented significantly high abnormal and absent VEMP than patients with audiograms of other types. CONCLUSION: These findings suggest that the subclinical deterioration of the saccular neuroepithelium is associated with patients with ISSHL having profound hearing loss at the high frequency. © 2008 American Academy of Otolaryngology–Head and Neck Surgery Foundation. All rights reserved.
S
udden sensorineural hearing loss has been defined as a sensorineural hearing loss of 30 dB or more and covering at least three contiguous audiometric frequencies, which occurs within 3 days or less.1 Most of these cases are idiopathic. Idiopathic sudden sensorineural hearing loss (ISSHL) remains controversial and equivocal with regard to diagnosis, treatment, and prognosis. Several prognostic indicators have been ascertained including age, the severity of the initial hearing loss, the presence of vertigo, and the audiometry pattern.2 About 30 percent to 40 percent of patients with ISSHL have accompanying vertigo.3 Studies have found that vertigo appears more frequently in association with profound hearing loss and that hearing recovery is worse in patients
with vertigo than in patients who do not experience vertigo.3-5 A recent study showed that the lesion site of vestibular disorders in patients with idiopathic sudden hearing loss with vertigo appeared to be within the labyrinth and that in these cases the saccule could be involved more frequently than the semicircular canals.6 Another report suggested that patients with high-frequency sensorineural hearing loss had subclinical disturbances of the vestibular system, especially in the saccule.7 Thus, we thought that ISSHL without vertigo might be associated with subclinical involvement of the saccule. However, no studies have reported on saccular damage in patients with ISSHL who do not have vertigo. Saccular damage can be identified by vestibular-evoked myogenic potential (VEMP), which is recorded on tonically contracted neck muscles by stimulating the ear with a loud sound. VEMP testing has been validated to reflect inner ear function, in particular the saccule, but not the cochlea and the semicircular canals.8 Therefore, we used VEMP to investigate saccular damage in patients with ISSNH without vertigo and also to evaluate the differences in saccular damage according to the initial hearing threshold, the frequency of hearing loss, and the hearing recovery rate.
METHODS The study was approved by the institutional review board, and, from May 2006 to December 2007, a prospective study was designed for 52 patients with ISSHL. Patients were included in the study if they had a sensorineural hearing loss of 30 dB or more with over three contiguous audiometric frequencies that occurred in less than 3 days. The authors obtained informed consent from patients, and we excluded the patients with ISSHL that had vertigo, Meniere’s disease, tumors, and a treatment onset of over 15 days. For all patients, we performed initial standard treatments by administering oral steroid for 8 days in tapering doses while also
Received March 18, 2008; revised May 18, 2008; accepted July 1, 2008.
0194-5998/$34.00 © 2008 American Academy of Otolaryngology–Head and Neck Surgery Foundation. All rights reserved. doi:10.1016/j.otohns.2008.07.003 Downloaded from oto.sagepub.com at Flinders University on December 5, 2016
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Otolaryngology–Head and Neck Surgery, Vol 139, No 4, October 2008
treating with other medications, such as a peripheral vasodilator and Ginko biloba extracts. Pretreatment and posttreatment audiograms were obtained for all patients. Puretone averages were calculated by averaging the pure-tone hearing levels at 500 Hz, 1000 Hz, 2000 Hz, and 3000 Hz. Audiograms were categorized as high- or low-tone hearing loss, flat type, and profound hearing loss. The group with high-tone hearing loss was defined as those patients with an average loss of 4 to 8 kHz who surpassed the average of the 0.25- to 0.5-kHz hearing loss by 30 dB or more. The low-tone hearing loss group showed an average loss of 0.25 to 0.5 kHz and surpassed the average of the 4- to 8-kHz hearing loss by 30 dB or more. The flat-type group consisted of patients with a 20 dB or less difference between the worst and best hearing levels among six frequencies (0.25, 0.5, 1, 2, 4, and 8 kHz). In the group with profound hearing loss, at least two frequencies produced results that were off the scale. Furthermore, in this group, the difference between the hearing level and the maximum sound level generated by the audiometer was within 10 dB at all six frequencies.6 Hearing recovery was expressed as complete recovery, partial recovery, slight improvement, and no improvement using the hearing threshold at 1 month posttreatment according to Siegel’s criteria.9 The VEMP testing was performed by using the initial hearing threshold test when possible and was recorded with patients in a sitting position with the head rotated away from the stimulated side during recording. The surface electrodes were placed as follows: on the middle third of the sternocleidomastoid muscle as the active electrode, the upper sternum as the reference electrode, and on the forehead as the ground electrode. Clicks of 0.1-ms duration were presented at a rate of 5 per second through a headphone. The click intensities were 95 dB, and an electromyographic signal was amplified and bandpass filtered (20 Hz-2 kHz) using a Nicolet Viking IV (Madison, WI). The analysis window was 100 msec wide. Responses to 256 stimuli were averaged. When we read the VEMP findings, we used our own VEMP response data as the reference value that was already reported at our department10 and two objective parameters, the abnormal VEMP rate and the absent VEMP rate. The abnormal VEMP category included cases with prolonged p13 and n23 latency, increased VEMP asymmetry, and an absent VEMP. An absent VEMP indicated no p13 or n23 wave formation in response to a loud sound. We investigated VEMP results in patients with ISSHL and analyzed the association of the VEMP findings with the initial average hearing threshold, several frequency thresholds, audiogram type, and hearing recovery.
Statistical analysis Statistical tests were performed by using the 2 test and Fisher exact test with Bonferroni correction (SPSS ver.11.5; SPSS, Chicago, IL) to analyze the abnormal and absent VEMP rates from several groups.
Table 1 Demographics and characteristics of the patients (n ⴝ 52) Parameter Age (y) Mean Range Affected ear Right Left Sex Male Female Days to treatment Mean Range Severity of hearing loss Mild Moderate Moderate to severe Severe Profound
N*
55.1 13-79 21 31 22 30 4.8 1-14 13 7 8 7 17
*Unless otherwise indicated.
RESULTS The average age of the patients was 55.1 years. The right to left ear and male to female ratios were 21:31 and 22:30, respectively. The time period between disease onset and the commencement of therapy averaged 4.8 days. The distribution in the severity of the hearing loss is listed in Table 1. Fourteen of the total 52 patients (26.9%) showed an abnormal VEMP response. This included eight patients with an absent VEMP. Moreover, abnormal VEMP responses were observed in 8 of 17 patients (47.1%) with a hearing loss of more than 90 dB, in 4 of 15 patients (26.7%) with a hearing loss between 55 and 90 dB, and in 2 of 20 patients (10%) with a hearing loss less than 55 dB. We found a significant difference between the patient group with a hearing loss more than 90 dB and those with a hearing loss less than 55 dB (P ⬍ 0.05). Furthermore, seven of eight patients with an absent VEMP had a hearing loss that was more than 90 dB (Table 2). When the data were analyzed according to the type of audiogram, the abnormal VEMP rates and absent VEMP rates were as follows: 8.3 percent and 0 percent in patients with high-tone hearing loss, 14.3 percent and 0 percent in patients with low-tone hearing loss, 18.8 percent and 6.3 percent in patients with flat-type hearing loss, and 47.1 percent and 41.2 percent in patients with profound hearing loss, respectively. Patients with profound hearing loss showed not only significantly higher abnormal VEMP rates than patients with high-tone hearing loss (P ⬍ 0.05), but they also presented significantly higher absent VEMP rates than patients with either high-tone hearing loss or flat-type hearing loss (Table 3).
Downloaded from oto.sagepub.com at Flinders University on December 5, 2016
Hong et al
Saccular damage in patients with idiopathic sudden . . .
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Table 2 The rate of abnormal VEMP formation and findings related to the extent of hearing loss expressed as pure-tone average Extent of hearing loss
% (n)
90 dB or more 55 dB-90 dB
47.1 (8/17)* 26.7 (4/15)
55 dB or less Total
10 (2/20) 26.9 (14/52)
VEMP findings: n Absent: Absent: A:1 A:2 Absent: P and
7, P and A : 1 1, P and N : 2,
8, P and N : 2, A : 1, A : 3
Absent, absent VEMP; P, prolonged p13 latency; N, prolonged n23 latency; A, increased vestibular asymmetry. *P ⬍ 0.05, significantly different from 55 dB or less group.
When hearing thresholds of each frequency were measured by using the initial pure-tone average and were divided into groups that had hearing losses of 90 dB or more, between 55 dB and 90 dB, and 55 dB or less, we found no significant differences among the groups with regard to abnormal VEMP rates (Fig 1). However, with regard to absent VEMP rates, we found significant differences in patients with hearing losses of over 90 dB at 1000-Hz, 2000-Hz, 4000-Hz, and 8000-Hz frequencies when compared with patients in the other two groups (P ⬍ 0.05, Fig 2). All of the hearing recovery rates showed no significant differences between patients with normal and abnormal VEMP findings that were composed of only complete recovery, incomplete recovery ⫹ partial recovery, and complete recovery ⫹ partial recovery ⫹ slight improvement (P ⬎ 0.05, Fig 3), although patients with abnormal VEMP showed relatively low recovery rate rather than those with normal VEMP.
Figure 1 Abnormal VEMP rates reported according to the extent of hearing threshold in each frequency (P ⬎ 0.05).
DISCUSSION VEMPs have been used as a clinical test of the vestibular system, particularly for the saccule and inferior vestibular nerve region.11,12 Clinical studies have suggested that this response is of vestibular origin, especially in the saccule and inferior vestibular nerve region.11,12 Neurophysiological experiments in guinea pigs and cats have shown that primary vestibular afferents, especially saccular afferents, respond to relatively loud clicks.13 In our study, we found that abnormal VEMP responses might be observed in ISSHL patients who do not have vertigo. These findings suggest that the vestibular system, in particular the saccule, has a subclinical involvement in ISSHL patients. A previous study reported that 77% of the ISSHL patients with vertigo exhibited an absence of click VEMPs on the affected side.6 In our study, only patients without vertigo were included. Therefore, when compared with previous report, lower abnormal VEMP rates was found in our study. But in patients group that had the hearing loss of 90 dB or more, abnormal VEMP rate was 47.1 percent. In addition, seven of eight patients with absent VEMPs were distributed in the patient group with a hearing loss of 90 dB
Table 3 Abnormal VEMP rates and absent VEMP rates related to the type of audiogram
Type of audiogram High-tone hearing loss Low-tone hearing loss Flat-type hearing loss Profound hearing loss
Abnormal VEMP rate % (n) 8.3 14.3 18.8 47.1
(1/12) (1/7) (3/16) (8/17)*
Absent VEMP rate % (n) 0 0 6.3 41.2
(0/12) (0/7) (1/16) (7/17)*†
*P ⬍ 0.05, significantly different from the high-tone hearing loss group. †P ⬍ 0.05, significantly different from the flat-type hearing loss group.
Figure 2 Absent VEMP rates reported according to the extent of hearing threshold in each frequency (*P ⬍ 0.05, significantly different from the absent VEMP rates of 55 to 90 dB and the ⬍55 dB group).
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Otolaryngology–Head and Neck Surgery, Vol 139, No 4, October 2008 estingly, in our study, we found that saccular damages that were identified by the VEMP findings did not affect hearing recovery (ie, we found that the subclinical involvement of the saccular neuroepithelium was not associated with ISSHL patient prognosis).
CONCLUSION
Figure 3 Hearing recovery rates of subjects who showed normal and abnormal VEMP findings. (I: complete recovery, II: partial recovery, III: slight improvement, P ⬎ 0.05).
or more. This finding suggests that the more severe the hearing loss, the more frequently the saccule was involved. When the VEMP findings were analyzed according to the type of audiogram, the patients with profound hearing loss showed relatively high abnormal and absent VEMP rates compared with other types. In particular, for absent VEMP rates, the profound hearing loss group was significantly different between the high-tone and flat-type hearing loss groups, although the number of patients with low-tone hearing loss was much smaller and did not show any significant difference. Because an absent VEMP indicated no wave formation and did not have any normal range or deviation, like latency or amplitude, the absent VEMP type might be thought of as a more reliable parameter compared with the abnormal VEMP rate (which includes prolonged p13 and n23 latency as well as increased VEMP asymmetry). In addition, the absent VEMP rates also were significant in patients with hearing losses of 90 dB or more and with high-frequencies over 1000 Hz, compared to the patients with hearing losses of 55-90 dB and 55 dB or less. These findings suggested that patients with severe cochlear damage of over 90 dB in a high 1000-Hz or more frequency could have a subclinical involvement of the saccule. The saccule has not only anatomic proximity to the acousticenergy delivery system, but the great similarity between the cochlear and vestibular hair-cell ultrastructures and the common arterial blood supply of the cochlea and vestibular end organs via the same end artery supports the possibility of vestibular involvement, in particular saccular deterioration that is associated with cochlear damage.14,15 One report has found that hearing recovery in ISSHL cases is worse in patients with vertigo than in those cases without vertigo.16 A previous report investigated the histopathological characteristics of the temporal bone in ISSHL cases with and without vertigo and found no direct relationship between the presence of vertigo and damage to the vestibular apparatus. The authors of this previous study hypothesized that vertigo in ISSHL cases was caused by the transmission of biochemical changes in the inner ear fluid between the cochlea and the vestibular apparatus.17 Inter-
Cases of ISSHL without vertigo could lead to abnormal VEMP responses, and, in particular, cases with a 90-dB hearing loss with a frequency over 1000 Hz or more could have a high rate of absent VEMP. These findings suggest that the subclinical deterioration of the saccular neuroepithelium were associated with severe hearing loss in cases of high-frequency ISSHL.
AUTHOR INFORMATION From the Department of Otorhinolaryngology–Head and Neck Surgery, Chuncheon Sacred Heart Hospital, Hallym University College of Medicine, Chuncheon, Korea (Drs Hong, Park, and Lee); and Department of Otorhinolaryngology–Head and Neck surgery, College of Medicine, KyungHee University, Seoul, Korea (Drs Byun, Park, and Cha). Corresponding author: Seok Min Hong, MD, Department of Otorhinolaryngology-Head and Neck Surgery, Chuncheon Sacred Heart Hospital, Hallym University College of Medicine, #153 kyo-dong, Chuncheon, Kangwon-do, 200-704, Korea. E-mail address: [email protected].
AUTHOR CONTRIBUTIONS Seok Min Hong, study design, writer; Jae Yong Byun, study design, data collection; Chan Hum Park, study design, data collection; Jun Ho Lee, data collection; Moon Suh Park, data collection; Chang Il Cha, study design, data collection.
FINANCIAL DISCLOSURE None.
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