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ORIGINAL ARTICLE  
Year : 2021  |  Volume : 23  |  Issue : 110  |  Page : 81-86
Acute onset of tinnitus in patients with sudden deafness

1 Faculty of Medicine, University of Belgrade; Clinic for Otorhinolaryngology and Maxillofacial Surgery, Clinical Center of, Serbia
2 Clinic for Otorhinolaryngology and Maxillofacial Surgery, Clinical Center of, Serbia
3 Institute for Biomedical Statistics, Faculty of Medicine, University of Belgrade, Serbia
4 Department of Otorhinolaryngology and Head & Neck Surgery, University Hospital Zurich, University of Zurich, Zurich Center for Integrative Human Physiology, Switzerland

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Date of Submission22-Jun-2020
Date of Decision22-Mar-2021
Date of Acceptance25-Jun-2021
Date of Web Publication27-Sep-2021
 
  Abstract 


Objective: We made hypotheses that tinnitus will appear more likely in patients with sudden deafness with superior hearing in unaffected ear or with more severe acute hearing loss. Methods: A retrospective cohort study was performed. Five hundred forty-one patients were identified with idiopathic sudden sensorineural hearing loss (ISSHL) from January 1995 to August 2006. The exclusion criteria for this study were as follows: bilateral sudden hearing loss and Meniere disease, previous tinnitus or bilateral tinnitus at initial evaluation, and onset of hearing loss less than 7 days. The cohort enrolled 454 patients. The enrolled patients were classified into two groups: patient with acute onset tinnitus in the affected ear and patients without tinnitus at initial visit. Main outcome measures were patient age, the presence or absence of vertigo and tinnitus, audiometric patterns, the severity of hearing loss, and hearing in the unaffected ear. Results: Better contralateral hearing (n = 220 versus n = 72, P < 0.001) and younger age (48 versus 55 years, P < 0.001) were independently associated with the acute onset of tinnitus in patients with ISSHL. The degree of asymmetry between the ears did not differ significantly between patients with and without tinnitus. The sex, presence of vertigo, shape of audiogram, and severity of hearing loss were not correlated with tinnitus occurrence. Conclusions: Tinnitus triggered by ISSHL was more frequent in patients with better contralateral hearing and of a younger age, irrespective of the severity of hearing loss on the affected side or the asymmetry between the ears.

Keywords: Acute hearing loss, acute tinnitus, audiogram, cohort, idiopathic sudden sensorineural hearing loss, sudden deafness, tinnitus

How to cite this article:
Cvorovic L, Arsovic N, Radivojevic N, Soldatovic I, Hegemann SC. Acute onset of tinnitus in patients with sudden deafness. Noise Health 2021;23:81-6

How to cite this URL:
Cvorovic L, Arsovic N, Radivojevic N, Soldatovic I, Hegemann SC. Acute onset of tinnitus in patients with sudden deafness. Noise Health [serial online] 2021 [cited 2021 Dec 7];23:81-6. Available from: https://www.noiseandhealth.org/text.asp?2021/23/110/81/326856



  Introduction Top


Tinnitus, the phantom perception of sound, affects approximately 70% of patients with idiopathic sudden sensorineural hearing loss (ISSHL).[11] Tinnitus is often associated with hearing loss and is thought to result from abnormal neural activity at some point or points in the auditory pathways, which is incorrectly interpreted by the brain as an actual sound.[7] Physiologically, tinnitus can be generated by abnormal, spontaneous neuronal activity in the central auditory system,[14],[26] by a malfunction of a mechanism that normally prevents such activity to be audible, or by both factors.[20] The hearing loss triggers plastic neural changes that result in increased spontaneous activity, bursting, and synchronous activity in the cortical and subcortical auditory regions and also in the nonauditory brain regions involved in attention, emotion, and memory.[23] It is still unclear how such a decrease in afferent drive can result in increased central activity. Hearing loss causes a reduction of the afferent drive of auditory impulses, alters the balance between inhibition and excitation, and thus raises spontaneous neural activity in the central auditory system through the activation of neural plasticity.[23] Neural plasticity requires central activation and attempts to minimize bias between inhibition and excitation.[21] Tinnitus is almost always triggered by hearing loss, but a large proportion of patients with hearing loss do not present symptoms of tinnitus.[25] Authors have shown that tinnitus patients had specific inner ear damage that triggers tinnitus.

Gollnast et al.[6] found, in young patients, lower hearing thresholds in tinnitus patients than in patients without tinnitus, but in the older group hearing thresholds in tinnitus patients were lower at low frequencies, while they were higher at high frequencies. The degree of hearing loss is related to tinnitus, not age,[4],[8] but others have shown that older cohorts have lower tinnitus prevalence that is independent of the level of hearing impairment.[24] Some studies have suggested that only specific audiometric configurations might lead to tinnitus,[10] but others have shown opposite results.[11] Tinnitus has been associated with the degree of hearing loss and the tinnitus pitch dominantly falls within a region of hearing loss.[17],[22]

Sudden sensorineural hearing loss has a variable aetiology and is, in most cases, idiopathic. Any pathologic lesion in the auditory pathway or any reduction in auditory nerve function has the potential to produce tinnitus.[15] The tinnitus pitch is in the same frequency region as the hearing loss in patients triggered by ISSHL, which subsequently alters the activity in the lemniscal pathway and induces an increased neural synchronisation in the auditory cortex.[16]

A recent study showed that tinnitus did not develop in congenital single-sided deafness, whereas most patients with acquired single-sided deafness experienced tinnitus, indicating that the presence of tinnitus was determined by auditory experiences.[12] In this study we analyzed the potential factors implicated in the onset of acute tinnitus in patients with ISSHL.


  Materials and methods Top


A retrospective cohort study was performed in University Hospital Zurich from January 1995 to August 2006. Five hundred forty-one patients were identified with ISSHL. The degree of hearing loss was more than 30 dB over three continuous frequencies occurring in less than 3 days with no identified causes of deafness. The cohort enrolled 454 patients, and the exclusion criteria for this study were as follows: bilateral sudden hearing loss and Meniere disease, previous tinnitus or bilateral tinnitus at initial evaluation, onset of hearing loss less than 7 days, and uncompleted data of patients.

The factors analyzed were patient age, the presence or absence of vertigo and tinnitus, audiometric patterns, the severity of hearing loss, and hearing in the unaffected ear. The standard treatment for sudden deafness in University Hospital Zurich during the analyzed period was carbogen inhalation (95% O2 and 5% CO2 eight times per day for 30 minutes each) and prednisone orally (100 mg in one morning dose) for 7 days. Pure tone averages (PTA) were calculated in decibels of hearing level for four frequencies (0.5, 1, 2 and 4 kHz) and were calculated for both ears. The severity of hearing loss was classified into four groups using the PTA of the affected ear: mild (PTA of 15–39 dB), moderate (PTA of 40–59 dB), severe (PTA of 60–79 dB) and profound or deaf (PTA more than 80 dB). The audiometric configuration was classified into four types using Mazzoli classification.[13] Low frequencies were 0.25 and 0.5 kHz, middle frequencies were 1 and 2 kHz, and high frequencies were 4 and 8 kHz. Audiogram patterns were defined as follows: flat type loss (less than 15 dB hearing loss difference between the means of low-, middle-, and high-frequency thresholds), low type (ascending, greater than 15 dB from poorer low-frequency thresholds to higher frequencies), midfrequency type (U shaped, greater than 15 dB hearing loss difference between the poorest thresholds in the middle frequencies and those at higher and lower frequencies), and high type (descending, greater than 15 dB hearing loss difference between the mean of low frequencies and the mean of high frequencies). In this study, the enrolled patients with ISSHL were classified into two groups: (1) patients with acute onset tinnitus in the affected ear and (2) patients without tinnitus at the initial visit.

Data are presented as count (%) or mean ± standard deviation, depending on the data type. Pearson chi-square test, the chi-square test for trend, and the Mann–Whitney U test were used to assess significant differences between groups. Multivariate logistic regression analysis was used to model the association between tinnitus and significant predictors in univariate analysis. All data were analyzed using SPSS 20.0 (Released 2017. IBM SPSS Statistics for Windows, Version 25.0. Armonk, NY: IBM Corp.) statistical software. All P values less than 0.05 were considered significant.


  Results Top


Participants

The study sample included 288 men and 166 women, with a mean age of 50 years. A total of 313 (68.9%) patients with ISSHL had acute-onset tinnitus. All patient characteristics are presented in [Table 1].
Table 1 Characteristics of patients with idiopathic sudden sensorineural hearing loss

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Variables associated with acute onset of tinnitus

There was a significant age difference between patients with and without tinnitus (47.6 ± 15.7 versus 54.8 ± 17.3, t test, P < 0.001). There was a significant difference in contralateral hearing between patients with and without tinnitus. Patients with good contralateral hearing had more frequent onset of tinnitus. Factors associated with the presence of tinnitus are shown in [Table 2]. The presence of vertigo, the shape of the audiogram, and the severity of hearing loss were not associated with the development of acute-onset tinnitus.
Table 2 Factors associated with the presence of tinnitus

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Pure tone averages of ears and the presence of tinnitus

The mean PTAs of the affected and contralateral ears correlated with the acute onset of tinnitus. Patients with better PTA in the affected and contralateral ears had acute onset of tinnitus significantly more often. We also found that the difference between PTAs of the two ears was not associated with the onset of tinnitus [Figure 1]. The relationships between PTAs and ages for patients with ISSHL are presented in [Figure 2]. The study showed more frequent onset of tinnitus in patients with a better PTA of the affected ear and the contralateral ear. The difference in hearing thresholds between the ears was not related to tinnitus development. The PTAs of affected and unaffected ear and their differences in tinnitus and no tinnitus group are shown in [Figure 3].
Figure 1 Pure tone average (mean ± standard deviation) of affected and unaffected ears and onset of tinnitus (affected − pure tone average of affected ear, unaffected − pure tone average of unaffected ear, delta (aff-unaff) − difference between pure tone average of affected ear and pure tone average of unaffected ear, P value)

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Figure 2 Relationship between PTA of affected ear in dB, PTA of unaffected ear in dB, differences between PTAs of affected and unaffected ears in dB, and age. Scatter plots show individual PTAs and age of patients with ISSHL. dB, decibel; ISSHL, idiopathic sudden sensorineural hearing loss; PTA aff, pure tone average of affected ear; PTA unaff, pure tone average of unaffected ear; PTA aff-unaff, differences between PTAs of affected and unaffected ear

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Figure 3 Relationship between onset of tinnitus and PTA of affected ear in dB, PTA of unaffected ear in dB, and differences between PTAs of affected and unaffected ears in dB. Box plots show individual PTAs in tinnitus and no tinnitus group. dB, decibel; PTA aff, pure tone average of affected ear; PTA unaff, pure tone average of unaffected ear; PTA aff-unaff, differences between PTAs of affected and unaffected ear

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Logistic regression analysis was performed to assess a possible trend for acute onset of tinnitus, PTA of the two ears, and age. Each 10 dB increase in PTA of the unaffected ear reduced the probability of onset of tinnitus by 15%. Logistic regression analysis of factors that influenced the onset of tinnitus is shown in [Figure 4]. In the logistic regression model, Nagelkerke R square is 0.094, which means that the 9.4% variability of the dependent variable is explained by independent variables. The classification power of the model is 72.7%.
Figure 4 Logistic regression model with age and PTA as independent variables and tinnitus as dependent variable, increase by 10 units. CI, confidence interval; OR, odds ratio; PTA, pure tone average

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  Discusion Top


In this retrospective study, we found that two independent factors − better contralateral hearing and younger age were associated with acute onset of tinnitus in patients with ISSHL. The sex of the patient, presence of vertigo, shape of the audiogram, and severity of hearing loss were not correlated with the occurrence of tinnitus.

We supposed that auditory bias would be greater in patients with better contralateral hearing and more severe hearing loss in the affected ear. Nevertheless, the study showed more frequent onset of tinnitus in patients with a better PTA of the affected ear as well as of the contralateral ear. There were a few cases with preexisting unilateral hearing loss in unaffected ear in the tinnitus and no tinnitus group without influence on results. The difference in hearing thresholds between the ears was not related to tinnitus development. Also, the severity of hearing loss had no influence on the onset of tinnitus.

In an earlier report on the tinnitus pitch in patients with acute tinnitus accompanied by ISSHL, the mean difference in hearing thresholds between tinnitus affected and unaffected ears was largest near the tinnitus pitch.[16] These findings suggest that the tinnitus pitch is related to audiometric parameters in patients with sudden deafness. Also, the authors concluded that tinnitus might be related to hearing impairment in the same frequency region in patients with ISSHL or in patients with chronic tinnitus, whereas the development of chronic tinnitus relates to reorganization in the cortical cells. Tan et al.[25] showed that tinnitus may not be strongly associated with outer hair cell impairment and showed a different average pattern of hearing loss among tinnitus patients. They further suggested that inner hair cell dysfunction with subsequent reduced auditory innervation is a possible trigger of tinnitus.

Some studies reported that hearing in the unaffected ear was correlated with acute onset of tinnitus, whereas numerous other factors (age, sex, hearing level in the affected ear, severity of hearing loss) were not.[3],[11] In patients with noise-induced hearing loss, the group with tinnitus had better overall hearing than those without tinnitus.[10] The level of auditory deprivation seems to be subjectively greater in patients with better contralateral hearing, irrespective of the severity of hearing loss on the affected side. Authors suggested that patients might be sensitive to good contralateral hearing in a quiet environment, and those who had good contralateral hearing were more likely to focus on their auditory perceptions, which might be worsened by subjective auditory deprivation.[11]

A few studies showed no significant relationship between hearing loss and the severity of tinnitus.[2],[19] Our study demonstrated that the level of contralateral hearing is more important in tinnitus development than the difference in hearing between the two ears or the level of hearing loss and may be limited only to the development of acute tinnitus. Many patients with ISSHL perceived both hearing recovery and tinnitus remission. Hearing normalization was crucial for the disappearance of tinnitus at the 1 month follow-up.[9] The functional change in the brain may be transient during the early phase of ISSHL, whereas the cochlear component of neural plasticity is the dominant mechanism of tinnitus development in these patients.

This study shows that younger ages were associated with an acute onset of tinnitus in patients with ISSHL. Tambs et al.[24] have shown that older cohorts have a lower tinnitus prevalence, independent of the level of hearing impairment. Others[4],[8] have emphasized that the degree of hearing loss is related to tinnitus, not age. The studies included different groups − noise exposed patients and an unscreened sample group. Al-Swiahb and Park[1] found that tinnitus in older adults is subjectively louder, more annoying, and more distressing than that found in younger patients. Studies in animal models have shown that tinnitus is pathology of neural plasticity. Neural plasticity has two main parts: a molecular, peripheral part related to the initiation of tinnitus and a system-central part related to the long-term duration of tinnitus.[7] Younger patients possess a greater efficiency of neuronal plasticity,[18] which may explain why patients with ISSHL developed acute-onset tinnitus more frequently. It is possible that in younger patients with sudden deafness the mechanism of brain plasticity is triggered to a greater degree to counteract an acute onset of hearing loss. Although cochlear hearing loss can initially trigger tinnitus, the subsequent cascade of neural changes within and beyond the central auditory system is also related to the tinnitus.

The shape of the audiogram was not associated with the presence of tinnitus; however, a large number of patients with tinnitus had a flat audiometric configuration. One explanation for these data is that the more damaged areas of the cochlea produce a greater imbalance (this leads to less stimulation in the production of action potentials through an auditory nerve), which exceeds the capacity of intrinsic plastic processes. In fact, further research is needed to support this interesting theory. In many studies, there was no connection between the tinnitus pitch and shape of the audiogram.[11],[17],[22] A recent study showed that patients with chronic tinnitus tended to experience high-frequency hearing loss. The difference between acute and chronic tinnitus may explain the different audiometric patterns.[25]

In our previous study,[5] using the same database, we showed that the presence of tinnitus had no influence on hearing outcome in patients with sudden deafness, but patients with better hearing levels in the contralateral ear had a better prognosis for hearing improvement.

One of the advantages of the study was that the type of hearing loss, that is, ISSHL, was the same in all patients. The deficiency of the presented study is its retrospective approach. There was no staging of tinnitus by the Tinnitus Handicap Inventory or any other questionnaire and there were no data about the presence of tinnitus following treatment of sudden deafness.

Logistic regression analysis was performed with all variables, and those most predictive of tinnitus were PTA of the contralateral ear and patient age. Each 10 dB increase in PTA of the unaffected ear reduced the probability of onset of tinnitus by 15%. Timely identification of the risk group for acute tinnitus in patients with ISSHL is of great importance in order to ensure they get prompt counselling.. The patient population in general feels frustrated and this modality is aimed at reducing tinnitus-associated distress.


  Conclusion Top


According to our study, the risk of developing tinnitus is significantly higher in younger patients with ISSHL and in patients with better hearing in the unaffected ear. The degree of asymmetry between the ears did not differ significantly between patients with and without tinnitus. The level of auditory deprivation seems to be subjectively greater in patients with better contralateral hearing (irrespective of the severity of hearing loss on the affected side) and that causes an acute onset of tinnitus..

Ethical consideration: This study was approved by the Ethic Board of the Faculty of Medicine, University of Belgrade.



 
  References Top

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Correspondence Address:
Ljiljana Cvorovic
Faculty of Medicine, University of Belgrade, Clinic for Otorhinolaryngology and Maxillofacial Surgery, Clinical Center of Serbia, Pasterova 2, 11000 Belgrade
Serbia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/nah.NAH_42_20

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