Open access peer-reviewed chapter

Ménière’s Disease and Tinnitus

Written By

Ricardo Rodrigues Figueiredo, Andréia Aparecida de Azevedo and Norma de Oliveira Penido

Submitted: April 14th, 2016 Reviewed: October 18th, 2016 Published: October 4th, 2017

DOI: 10.5772/66390

Chapter metrics overview

1,563 Chapter Downloads

View Full Metrics


Tinnitus is one of the Ménière’s disease clue symptoms, but by far less studied than vertigo or other types of dizziness. The typical Ménière’s tinnitus is a low pitched fluctuating one. Although controversial, cochlear Ménière’s disease may account for a tinnitus subtype, a fact that may impact on tinnitus diagnosis and treatment. Further studies focused on tinnitus are necessary to clarify at which extent Ménière’s disease may have a role in some types of chronic tinnitus.


  • tinnitus
  • Ménière’s disease
  • hearing loss
  • vertigo
  • dizziness

1. Introduction

Ménière disease (MD) is a chronic inner ear condition that was first described by Prosper Ménière in the nineteenth century [1]. His initial description of the disease including hearing loss, vertigo and tinnitus was accurate, but the pathophysiology of the condition was only described 75 years later. The endolymphatic hydrops is the main finding, initially ascertained only in post‐mortem exams and nowadays detectable in high resolution magnetic resonance imaging (MRI) [2].

The reported prevalence of MD is 190–513/100,000 cases [3]. Classical symptoms include fluctuating hearing loss, aural fullness and periodic vertigo and tinnitus [2]. The diagnosis criteria from the American Academy of Otolaryngology and Head and Neck Surgery (AAO‐HNS) and the Bárány Society do not recognize an eventual ‘cochlear’ Ménière disease [4], but recent imaging studies (gadolinium contrasted 3T MRI) are more sympathetic with this possibility [5].

Although virtually all patients that fulfilled the AAO‐HNF clinical criteria for MD whose inner ears were evaluated post‐mortem exhibited endolymphatic hydrops (EH), not all the patients with Proven EH developed MD [2]. Many theories concerning the pathophysiology of MD have been proposed, including changes in endolymph reabsorption due to anatomical variations, perfusion/reperfusion vascular changes, autoimmune mechanisms and changes in water homeostasis [6]. Aquaporins (AQP) are involved in fluid regulation in the inner ear, specifically the subtypes AQP 1, 4 and 6 [6, 7]. It has been demonstrated that vasopressin and oxytocin have a direct effect on aquaporin‐mediated regulation of inner ear fluids [7]. Moreover, cytochemical changes in AQP 4 and 6 expressions in the cochlear supporting cells were demonstrated in MD inner ears [6].


2. Current trends of thoughts concerning tinnitus pathophysiology

Tinnitus is the perception of noise which is not generated by external stimulus [8]. It affects approximately 25% of the general population; one third on a frequent basis [9]. Tinnitus may be classified as auditory and para‐auditory tinnitus, with the former representing the majority of cases and the latter being subdivided into muscular and vascular tinnitus, sometimes referred as somatosounds [10].

According to the most recent trends of thought, tinnitus is not considered a disease, but a symptom, which may have multiple causes, sometimes even in a single patient [11, 12]. Noise exposure, metabolic and cardiovascular disease, presbycusis, ototoxicity and cranial and cervical trauma are the most frequently considered causes of tinnitus [12, 13]. Caffeine abuse, dietary factors, temporomandibular joint and cervical diseases have also been described as contributing factors [1416].

Tinnitus is believed to be a central phenomenon that follows an initial peripheral damage [1719]. The cochlear and/or auditory nerve damage may be permanent, temporary or even subclinical and central neuroplasticity, including decrease of efferent inhibition, tonotopical reorganization and activation of, or modulation by, non‐auditory areas have been demonstrated to account for many tinnitus features [17, 18]. Despite the general consensus regarding the role of peripheral damage on the onset of tinnitus, many other factors contribute to tinnitus distress [20]. The correlation of tinnitus improvement and hearing loss recovery in sudden sensorineural hearing loss exists, but is not robust [20]. Nevertheless, peripheral aspects of tinnitus may not be ruled out even in chronic tinnitus, considering that around 45% of the patients submitted to VIII pair neurectomy experimented tinnitus improvement [21]. Ménière disease, particularly, may be an important example of ‘peripheral’ tinnitus, considering that in the initial stages tinnitus (as well as the other symptoms) is intermittent and acute, with no sufficient time for the arousal of a fully manifested neuroplasticity.


3. Tinnitus characteristics in Ménière disease

According to the criteria of AAO‐HNS, MD clue symptoms are recurrent vertigo, fluctuating hearing loss and tinnitus or aural fullness sensation [4, 22]. Tinnitus is probably the less studied of these symptoms, although specific characteristics of MD tinnitus have been observed [23].

First of all, tinnitus is rarely one of the first symptoms noticed (vertigo is the usual one) [23]. Tinnitus is reported by 94% of the patients and considered important by 37% of them [24]. As the years pass and MD disease attacks become more frequent, tinnitus may become permanent and more severe [23, 24].

As tinnitus is usually related to hearing loss, it is not a surprise that MD tinnitus is often low frequencies tinnitus (125/250 Hz) [23]. Nevertheless, according to some studies, this low pitched tinnitus is better tolerated than the high pitched ones [23].

Tinnitus was found to be a less disabling symptom than vertigo by most of the patients [23]. Nevertheless, some patients consider tinnitus an important symptom, and for 19% of MD patients, tinnitus is the most severe complaint, although not associated with a relevant impact in general health and quality of life [24, 25]. According to some studies, the severity of tinnitus does not seem to correlate with the severity of vertigo attacks [23], suggesting that vestibular and cochlear aspects of MD may be independent at some level. On the other hand, some studies demonstrated a strong association between tinnitus and other Ménière symptoms [26].

Diuretics have been proposed as a valuable treatment for Ménière’s disease, although the level of evidence concerning their efficacy is low [27]. The eventual side effects of diuretic therapy must not be ruled out as a co‐factor for tinnitus development, if we consider it direct ototoxicity and the possibility of excessive decrease of the blood pressure, which, according to some authors, may account for direct perfusion/reperfusion changes in the inner ear [27].

The controversial issue concerning the hypothetical ‘cochlear Ménière’ is still a challenge. Current AAO‐HNS definitions do not allow this possibility [22], but there is some evidence that it might exists [2830], so it opens a window for the establishment of a tinnitus subtype. According to some authors, MD may begin with cochlear symptoms only, which may be attributed to other diseases related to hearing loss [30]. According to one study, tinnitus is the first symptom in 6.6% of the cases and the median time frame to develop the symptomatic triad in such cases is 3 years [30]. Having said so, it may be possible that cochlear symptoms occur without vertigo, at least for an initial time frame. The Ménière’s Disease Index (MDI) was developed as an objective correlation of MD, based on audiometric (pure‐tone audiometry air threshold at 125 Hz and pure‐tone audiometry air threshold at 8000 Hz) and transtympanic electrocochleography (summation potential amplitude at 4000 Hz) data [28]. A recent study evaluated the MDI scores in patients with audiological symptoms and without vertigo, concluding that the ‘cochlear MD’ patients may represent a separate clinical entity, with MD’s resembling pathophysiology and/or endolymphatic hydrops (‘Ménière‐like’) [29]. A typical case is represented below. Figure 1 shows the audiometric findings of a possible cochlear Ménière disease with tinnitus. This is a 32‐year‐old woman with complaints of tinnitus and aural fullness at the right ear. She had no vertigo or other forms of dizziness or imbalance. Physical otolaryngological exam was normal. Pure tone audiometry revealed a mild sensorineural hearing loss at the low frequencies on the right ear. Tinnitus pitch matching was centred in 250 Hz. The electrocochleography with ear canal electrode showed a high SP/AP relationship (40%) in the right ear. This may represent a typical case of ‘cochlear Ménière’ in which tinnitus was the major complaint.

Figure 1.

Pure tone audiometry of a 32‐year‐old woman with left year tinnitus pitched at 250 Hz and no vertigo or other forms of dizziness/imbalance. Intracanal ECoG showed a high SP/AP ratio (40%) in the left ear. This may represent a cochlear form of MD with tinnitus as the sole complaint.


4. Possible treatment implications

Tinnitus treatment is still a challenge. There is no FDA‐approved drug for tinnitus treatment and most of the clinical trials with drugs were not replicated, probably due to differences in the samples, tinnitus characteristics, methodology and drug dosage [31]. According to the recent consensus of the AAO‐HNS, treatment should focus on counselling, auditory stimulation and cognitive behavioural therapy [11]. On the other hand, according to many researchers there is no reason that tinnitus could not be pharmacologically targeted, considering the multiple neurotransmitters and receptors involved in tinnitus pathophysiology [32]. The main goal of pharmacological treatment is to deliver the drug, to the right place, in the right amount, in other words, subtyping tinnitus. Understanding the neurochemistry at the peripheral and central areas involved in tinnitus is an important path to follow and may result in the development of successful therapies [31]. Following this line of thinking, if there should be a Ménière’s related tinnitus, this could be a possible pharmacological target.

There is a general lack of studies that analyse the effects of MD treatment on tinnitus distress. In a retrospective study comparing patients with vestibular disorders that were treated or not with betahistine 24 mg bid, tinnitus improvement was significantly better in the group treated with betahistine [33]. There was no mention of the type of vestibular disorders included. These findings, although not specific for MD, may encourage further studies, considering that higher doses of betahistine (even reaching 288–480 mg/day) that have been safely employed to MD treatment could also be tried at patients with tinnitus [34].

Recently, it has been demonstrated that nasal oxytocin could induce an immediate decrease in tinnitus volume [35]. Oxytocin and vasopressin receptors are found at the cochlea and were demonstrated to be related to fluid regulation in the inner ear, via inner ear AQPs [6]. Although central effects of oxytocin may also play a role in tinnitus treatment, this immediate effect may be related to some kind of hydrops reduction.

In the last years, cochlear implants have been indicated for alleviating tinnitus, with encouraging results [11]. One study evaluated the effects of cochlear implants in patients with severe sensorineural hearing loss and Ménière’s disease. Tinnitus distress, evaluated by the Tinnitus Handicap Inventory (THI) questionnaire, was significantly reduced in patients with MD (14 points decrease 6 months after the implantation, p = 0.002) [36].


5. Conclusions

Although, tinnitus is well known as a component of MD spectrum of symptoms, there is some evidence that it may occur alongside with other auditory symptoms in the absence of vertigo or other forms of dizziness. Understanding MD as a possible tinnitus subtype may unveil an important opportunity to study further tinnitus treatment strategies, such as betahistine, oxytocin and cochlear implants.


  1. 1. Atkinson M. Ménière’s original papers reprinted with an English translation with commentaries and biographical sketch. Acta Otolaryngolica. 1961;162:1-78
  2. 2. Gürkov R, Pyyko I, Kentala F. What is Ménière’s disease? A contemporary re‐evaluation of endolymphatic hydrops. Journal of Neurology. 2016;263(1):71-81. DOI: 10.1007/s00415‐015‐7930‐1
  3. 3. Havia M, Kentala E, Pyykö I. Prevalence of MD in general population of Southern Finland. Otolaryngology Head and Neck Surgery. 2005;133(5):762-768
  4. 4. Lopez‐Escamez JA, Carey J, Chung W, Goebel JA, Magnusson M, Mandala M et al. Diagnostic criteria for Menière’s disease. Journal of Vestibular Research. 2015;25:1-7. DOI: 10.3233/VES‐150549
  5. 5. Pyykö I, Nakashima T, Yoshida T, Zou J, Naganawa S. Ménière’s disease: A reappraisal supported by a variable latency of symptoms and the MRI visualization of endolymphatic hydrops. British Medical Journal Open. 2013;3(2). DOI: 10.1136/bmjopen‐2012‐001555
  6. 6. Ishiyama G, Lopez IA, Sepahdari AR, Ishiyama A. Meniere’s disease: Histopatology, cytochemistry and imaging. Annals of the NewYork Academy of Sciences. 2015;22:1-9. DOI: 10.1111/nyas.12699
  7. 7. Eckhard A, Gleiser C, Arnold H, Rask‐Andersen H, Kumagami H, Müller M et al. Water channel proteins in the inner ear and their link to hearing impairment and deafness. Molecular Aspects of Medicine. 2012;33(5-6):612-37. DOI: 10.1016/j.mam.2012.06.004
  8. 8. Heller AJ. Classification and epidemiology of tinnitus. Otolaryngologic Clinics of North America. 2003;36(2):239-248
  9. 9. Shargorodsky J, Curhan GC, Farwell WR. Prevalence and characteristics of tinnitus among US adults. The American Journal of Medicine. 2010;123(8):711-718. DOI: 10.1016/j.amjmed.2010.02.015
  10. 10. Herraiz C, Aparicio JM. Diagnostic clues in pulsatile tinnitus (somatosounds). Acta Otorrinolaringológica Española. 2007;58(9):426-433
  11. 11. Langguth B, Kreuzer PM, Kleinjung T, De Ridder D. Tinnitus: Causes and clinical management. The Lancet Neurology. 2013;12(9):920-930. DOI: 10.1016/S1474‐4422(13)70160‐1
  12. 12. Tunkel DE, Bauer CA, Sun GH, Rosenfeld RM, Chandrasekhar SS, Cunningham ER Jr et al. Clinical practice guideline: Tinnitus. Journal of Otolaryngology Head and Neck Surgery. 2014;151(2):1-40. DOI: 10.1177/0194599814545325
  13. 13. Henry JA, Dennis KC, Schechter MA. General review of tinnitus: prevalence, mechanisms, effects and management. Journal of Speech Language and Hearing Research. 2005;48(5):49-70
  14. 14. Rocha CB, Sanchez TG. Efficacy of myofascial trigger point deactivation for tinnitus control. Brazilian Journal of Otorhinolaryngology. 2012;78(6):21-26
  15. 15. Ferendiuk E, Zajdel K, Pihut M. Incidence of otolaryngological symptoms in patients with temporomandibular joint dysfunctions. BioMed Research International. 2014;2014:824684.DOI:10.1155/2014/824684.Epub 2014 Jun 24.
  16. 16. Figueiredo RR, Rates MJ, Azevedo AA, Moreira RK, Penido NO. Effects of the reduction of caffeine consumption on tinnitus perception. Brazilian Journal of Otorhinolaryngology. 2014;80(5):416-421. DOI: 10.1016/j.bjorl.2014.05.033
  17. 17. Møller A. The role of auditory deprivation. In: Møller A, Langguth B, DeRidder D, Kleinjung T, editors. Textbook of Tinnitus. New York: Springer; 2011. pp 95-98. DOI: 10.1007/978‐1‐60761‐145‐5
  18. 18. Møller A. The role of neural plasticity in tinnitus. In: Møller A, Langguth B, DeRidder D, Kleinjung T, editors. Textbook of Tinnitus. New York: Springer; 2011.pp. 99-102. DOI: 10.1007/978‐1‐60761‐145‐5
  19. 19. Eggermont JJ. The Neural Synchrony Model of Tinnitus. In: Eggermont JJ,editor. The Neuroscience of Tinnitus. Oxford: Oxford University Press; 2012.pp. 154-173
  20. 20. Nogueira‐Neto FB, Gallardo FP, Suzuki FA, Penido NdeO. Prognostic and evolutive factors of tinnitus triggered by sudden sensorineural hearing loss. Otology & Neurotology. 2016;37(6):627-633. DOI: 10.1097/MAO.0000000000001049
  21. 21. House JW, Brackmann DE. Tinnitus: Surgical treatment. Ciba Foundation Symposium. 1981;85:204-216
  22. 22. Committee on Hearing and Equilibrium guidelines for the diagnosis and evaluation of therapy in Ménière’s Disease. American Academy of Otolaryngology – Head and Neck Foundation Inc. Otolaryngology Head Neck Surgery. 1995;113:181-185
  23. 23. Sánchez IR, Garrigues HP, Rivera VR. Clinical characteristics of tinnitus in Ménière’s disease. Acta Otorrinolaringológica Española. 2010;61(5):327-331.DOI: 10.1016/j.otorrino.2010.06.004
  24. 24. Yoshida T, Stephens D, Kentala E, Levo H, Auramo Y, Poe D et al. Tinnitus complaint behaviour in long‐standing Ménière’s disorder:its association with other cardinal symptoms. Clinical Otolaryngology. 2011;36:461-467. DOI: 10.111/j.1749‐4486.2011.02381.x
  25. 25. Stephens D, Pyykkö I, Yoshida T, Kentala E, Levo H, Auramo Y et al. The consequences of tinnitus in long‐standing Ménière’s disease. Auris Nasus Larynx 2012;39:469-474. DOI: 10‐1016/j.anl.2011.10.011
  26. 26. Yardley L, Dibb B, Osborne G. Factors associated with quality of life in Ménière’s disease. Clinical Otolaryngology and Allied Sciences. 2003;28:436-441
  27. 27. Pirodda A, Ferri GG, Raimondi MC, Borghi C. Diuretics in Meniere disease: A therapy or a potential cause of harm? Medical Hypotheses. 2011;77:869-871. DOI: 10.1016/j.medy.2011.07.060
  28. 28. Claes GM, De Valck CFJ, Van de Heyning PH, Wuyts FL. The Ménière’s Disease Index: An objective correlate of Ménière’s disease, based on audiometric and electrocochleographic data. Otology and Neurotology. 2011;32:887-892. DOI: 10.1097/MAO.0b013e318219ff9a
  29. 29. Claes GM, De Valck CFJ, Van de Heyning P, Wuyts FL. Does ‘Cochlear Ménière’s Disease’ exist? An electrocochleographic and audiometric study. Audiology and Neurotology. 2013;18:63-70. DOI: 10.1159/000342686
  30. 30. Belinchon A, Perez‐Garrigues H, Tenias JM. Evolution of symptoms in Ménière’s disease. Audiology Neurotology. 2012;17:126-132. DOI: 10.1159/000331945
  31. 31. Figueiredo RR, Azevedo AA, Penido NO. Pharmacological treatment of tinnitus. In. Watson J,editor. Tinnitus Epidemiology, Causes and Emerging Therapeutic Treatments. New York: Nova Science Publishers; 2016.pp 25-42
  32. 32. Langguth B, Salvi R, Elgoyhen AB. Emerging pharmacotherapy of tinnitus. Expert Opinion and Emerging Drugs. 2009;14(4):687-702. DOI: 10.1517/14728210903206975
  33. 33. Ganança MM, Caovilla HH, Gazzola JM, Ganança CF, Ganança FF. Betahistine in the treatment of tinnitus in patients with vestibular disorders. Brazilian journal of otorhinolaryngology. 2011;77(4):499-503
  34. 34. Lezius F, Adrion C, Mansmann U, Jahn K, Strupp M. High dosage betahistine dihydrochloride between 288 and 480 mg/day in patients with severe Ménière’s disease: A case series. European Archives of Otorhinolaryngology. 2011;268(8):1237-1240.DOI: 10.1007/s00405‐011‐1647‐2
  35. 35. Azevedo, A, Figueiredo RR, Schlee W. Immediate effects of nasal oxytocin in tinnitus patients. In: Annals of the 10th International Tinnitus Research Initiative Conference; 16-18 March 2016; Nottingham, England. Nottingham: Tinnitus Research Initiative; 2016.pp 61-62
  36. 36. Mick P, Amoodi H, Arnoldner C, Shipp D, Friesen L, Lin V et al. Cochlear implantation in patients with advanced Ménière’s disease. Otology Neurotology. 2014;35(7):1172-1178. DOI: 10.1097/MAO0000000000000202

Written By

Ricardo Rodrigues Figueiredo, Andréia Aparecida de Azevedo and Norma de Oliveira Penido

Submitted: April 14th, 2016 Reviewed: October 18th, 2016 Published: October 4th, 2017