The results show a different average pattern of hearing impairment amongst the tinnitus patients, consistent with the suggestion that inner hair cell dysfunction with subsequent reduced auditory innervation is a possible trigger of tinnitus.

References: Tan CM, Lecluyse W, McFerran D, Meddis R. Tinnitus and patterns of hearing loss. J Assoc Res Otolaryngol. 2013 Apr;14(2):275-82. doi: 10.1007/s10162-013-0371-6. Epub 2013 Jan 18. PMID: 23328862; PMCID: PMC3660910.

Tinnitus does not represent a disease itself, but instead is a symptom of a variety of underlying diseases. Otologic causes include noise-induced hearing loss, presbycusis, otosclerosis, otitis, impacted cerumen, sudden deafness, Meniere’s disease, and other causes of hearing loss. Neurologic causes include head injury, whiplash, multiple sclerosis, vestibular schwannoma (commonly called an acoustic neuroma), and other cerebellopontine-angle tumors. Infectious causes include otitis media and sequelae of Lyme disease, meningitis, syphilis, and other infectious or inflammatory processes that affect hearing. Tinnitus is also a side effect of some oral medications, such as salicylates, nonsteroidal anti-inflammatory drugs, aminoglycoside antibiotics, loop diuretics, and chemotherapy agents (e.g., platins and vincristine). Temporomandibular-joint dysfunction and other dental disorders can also cause tinnitus. However, in many cases no underlying physical cause is identifiable. For many years, hearing loss has been understood to be the most common cause of tinnitus,29 and population-based data indicate that excessive noise exposure represents the second most common cause of tinnitus. However, about 40% of patients cannot identify any cause associated with tinnitus onset.

Any pathologic lesion in the auditory pathway or any reduction in auditory nerve function has the potential to produce tinnitus. The location of the hearing problem (i.e., in the middle ear or in the inner ear) and the otologic disorder causing the hearing loss do not appear to influence the etiologic potential. Interestingly, most patients with tinnitus complain about a sensation of fullness or blockage in the middle ear, suggesting a problem with middle ear pressure or increased impedance of the ossicular chain.

Unilateral high-frequency hearing loss combined with poor speech discrimination suggests the presence of a tumor, usually a vestibular schwannoma/acoustic neuroma or a meningioma. Bilateral subjective tinnitus requires assessment of hearing and can be associated with presbycusis, noise-induced hearing loss, endolymphatic hydrops, and a vascular labyrinthine lesion. However, most cases of unilateral tinnitus are not associated with life-threatening otologic disease.

References: Han BI, Lee HW, Kim TY, Lim JS, Shin KS. Tinnitus: characteristics, causes, mechanisms, and treatments. J Clin Neurol. 2009 Mar;5(1):11-9. doi: 10.3988/jcn.2009.5.1.11. Epub 2009 Mar 31. PMID: 19513328; PMCID: PMC2686891.

Tinnitus is the perception of sound in the absence of a corresponding external acoustic stimulus. With prevalence ranging from 10% to 15%, tinnitus is a common disorder. Many people habituate to the phantom sound, but tinnitus severely impairs quality of life of about 1-2% of all people. Tinnitus has traditionally been regarded as an otological disorder, but advances in neuroimaging methods and development of animal models have increasingly shifted the perspective towards its neuronal correlates. Increased neuronal firing rate, enhanced neuronal synchrony, and changes in the tonotopic organization are recorded in central auditory pathways in reaction to deprived auditory input and represent–together with changes in non-auditory brain areas–the neuronal correlate of tinnitus.

References: Langguth B, Kreuzer PM, Kleinjung T, De Ridder D. Tinnitus: causes and clinical management. Lancet Neurol. 2013 Sep;12(9):920-930. doi: 10.1016/S1474-4422(13)70160-1. PMID: 23948178.