Hanyang Med Rev.  2016 May;36(2):81-85. 10.7599/hmr.2016.36.2.81.

The Pathophysiologic Mechanism of Tinnitus

• Chung JH
• Lee SH

• KMID: 2164664
• DOI: http://doi.org/10.7599/hmr.2016.36.2.81

Abstract

Tinnitus represents a phantom auditory sensation without an external sound source. The reported prevalence of tinnitus estimates 15-20% in world population. Although severe tinnitus might be associated with deterioration of quality of life, depression and anxiety, treatment modalities of tinnitus have not been established yet. Considering the heterogeneity of tinnitus, a single theory or a hypothesis cannot sufficiently explain the mechanism of tinnitus. Thus, diverse theories and studies had been conducted to elucidate the secret of tinnitus. Degeneration of outer hair cell in the peripheral auditory system is known to be associated with tinnitus, while auditory plasticity theory, upregulation of excitation of central auditory structures explains the role of the central auditory pathway in the generation of tinnitus. In addition, somatosensory and limbic autonomic nervous systems are also deeply involved with the pathogenesis of tinnitus. Herein, recent pathophysiologic theories and remarkable studies of tinnitus were reviewed. Understanding of the mechanism of the tinnitus generation might be the cornerstone in the development of tinnitus treatment.

Keyword

Tinnitus; Pathophysiology; Mechanism

MeSH Terms

Anxiety
Auditory Pathways
Autonomic Nervous System
Depression
Hair
Plastics
Population Characteristics
Prevalence
Quality of Life
Sensation
Tinnitus*
Up-Regulation
Plastics

Reference

1. Jastreboff PJ. Phantom auditory perception (tinnitus): mechanisms of generation and perception. Neurosci Res. 1990; 8:221–254.

2. Park KH, Lee SH, Koo JW, Park HY, Lee KY, Choi YS, et al. Prevalence and associated factors of tinnitus: data from the Korean National Health and Nutrition Examination Survey 2009-2011. J Epidemiol. 2014; 24:417–426.

3. Coles RR. Epidemiology of tinnitus: (1) prevalence. J Laryngol Otol Suppl. 1984; 9:7–15.

4. Axelsson A, Ringdahl A. Tinnitus--a study of its prevalence and characteristics. Br J Audiol. 1989; 23:53–62.

5. Seo JH, Kang JM, Hwang SH, Han KD, Joo YH. Relationship between Tinnitus and Suicidal Behavior in Korean Men and Women: a Cross-sectional Study. Clin Otolaryngol. 2016; 41:222–227.

6. Han BI, Lee HW, Kim TY, Lim JS, Shin KS. Tinnitus: characteristics, causes, mechanisms, and treatments. J Clin Neurol. 2009; 5:11–19.

7. Van de Heyning P, Gilles A, Rabau S, Van Rompaey V. Subjective tinnitus assessment and treatment in clinical practice: the necessity of personalized medicine. Curr Opin Otolaryngol Head Neck Surg. 2015; 23:369–375.

8. Vielsmeier V, Lehner A, Strutz J, Steffens T, Kreuzer PM, Schecklmann M, et al. The Relevance of the High Frequency Audiometry in Tinnitus Patients with Normal Hearing in Conventional Pure-Tone Audiometry. Biomed Res Int. 2015; 2015:302515.

9. Kaltenbach JA. Tinnitus: models and mechanisms. Hear Res. 2011; 276:52–60.

10. Brozoski TJ, Bauer CA. Animal models of tinnitus. Hear Res. 2015.

11. Lobarinas E, Sun W, Stolzberg D, Lu J, Salvi R. Human Brain Imaging of Tinnitus and Animal Models. Semin Hear. 2008; 29:333–349.

12. Cazals Y, Horner KC, Huang ZW. Alterations in average spectrum of cochleoneural activity by long-term salicylate treatment in the guinea pig: a plausible index of tinnitus. J Neurophysiol. 1998; 80:2113–2120.

13. Kaltenbach JA, Zhang J, Finlayson P. Tinnitus as a plastic phenomenon and its possible neural underpinnings in the dorsal cochlear nucleus. Hear Res. 2005; 206:200–226.

14. Kemp DT. Physiologically active cochlear micromechanics--one source of tinnitus. Ciba Found Symp. 1981; 85:54–81.

15. Probst R, Lonsbury-Martin BL, Martin GK, Coats AC. Otoacoustic emissions in ears with hearing loss. Am J Otolaryngol. 1987; 8:73–81.

16. Baguley DM. Mechanisms of tinnitus. Br Med Bull. 2002; 63:195–212.

17. Stypulkowski PH. Mechanisms of salicylate ototoxicity. Hear Res. 1990; 46:113–145.

18. LePage EL. A model for cochlear origin of subjective tinnitus: excitatory drift in the operating point of inner hair cells. In : Vernon JA, Møller AR, editors. Mechanisms of Tinnitus. London: Allyn and Bacon;1995. p. 115–148.

19. Chery-Croze S, Truy E, Morgon A. Contralateral suppression of transiently evoked otoacoustic emissions and tinnitus. Br J Audiol. 1994; 28:255–266.

20. Sahley TL, Nodar RH. A biochemical model of peripheral tinnitus. Hear Res. 2001; 152:43–54.

21. Jannetta PJ. Neurovascular compression in cranial nerve and systemic disease. Ann Surg. 1980; 192:518–525.

22. Moller MB, Moller AR, Jannetta PJ, Jho HD. Vascular decompression surgery for severe tinnitus: selection criteria and results. Laryngoscope. 1993; 103:421–427.

23. Sasaki CT, Babitz L, Kauer JS. Tinnitus: development of a neurophysiologic correlate. Laryngoscope. 1981; 91:2018–2024.

24. Wu C, Martel DT. Increased Synchrony and Bursting of Dorsal Cochlear Nucleus Fusiform Cells Correlate with Tinnitus. J Neurosci. 2016; 36:2068–2073.

25. Brozoski TJ, Bauer CA, Caspary DM. Elevated fusiform cell activity in the dorsal cochlear nucleus of chinchillas with psychophysical evidence of tinnitus. J Neurosci. 2002; 22:2383–2390.

26. Henry JA, Roberts LE, Caspary DM, Theodoroff SM, Salvi RJ. Underlying mechanisms of tinnitus: review and clinical implications. J Am Acad Audiol. 2014; 25:5–22. quiz 126.

27. Shore SE, Roberts LE, Langguth B. Maladaptive plasticity in tinnitus - triggers, mechanisms and treatment. Nat Rev Neurol. 2016; 12:150–160.

28. Wu C, Stefanescu RA, Martel DT, Shore SE. Listening to another sense: somatosensory integration in the auditory system. Cell Tissue Res. 2015; 361:233–250.

29. Tzounopoulos T, Kim Y, Oertel D, Trussell LO. Cell-specific, spike timing-dependent plasticities in the dorsal cochlear nucleus. Nat Neurosci. 2004; 7:719–725.

30. Adjamian P, Hall DA, Palmer AR, Allan TW, Langers DR. Neuroanatomical abnormalities in chronic tinnitus in the human brain. Neurosci Biobehav Rev. 2014; 45:119–133.

31. Vanneste S, De Ridder D. The auditory and non-auditory brain areas involved in tinnitus. An emergent property of multiple parallel overlapping subnetworks. Front Syst Neurosci. 2012; 6:31.

32. Maudoux A, Lefebvre P, Cabay JE, Demertzi A, Vanhaudenhuyse A, Laureys S, et al. Auditory resting-state network connectivity in tinnitus: a functional MRI study. PLoS One. 2012; 7:e36222.

33. Carpenter-Thompson JR, Akrofi K, Schmidt SA, Dolcos F, Husain FT. Alterations of the emotional processing system may underlie preserved rapid reaction time in tinnitus. Brain Res. 2014; 1567:28–41.

34. Golm D, Schmidt-Samoa C, Dechent P, Kroner-Herwig B. Neural correlates of tinnitus related distress: an fMRI-study. Hear Res. 2013; 295:87–99.

35. Menon V, Uddin LQ. Saliency, switching, attention and control: a network model of insula function. Brain Struct Funct. 2010; 214:655–667.

36. Levine RA, Oron Y. Tinnitus. Handb Clin Neurol. 2015; 129:409–431.

37. Levine RA. Somatic (craniocervical) tinnitus and the dorsal cochlear nucleus hypothesis. Am J Otolaryngol. 1999; 20:351–362.

38. Jastreboff PJ, Gray WC, Gold SL. Neurophysiological approach to tinnitus patients. Am J Otol. 1996; 17:236–240.

39. Jastreboff PJ. 25 years of tinnitus retraining therapy. Hno. 2015; 63:307–311.