By Marcello Cherchi, MD PhD
For patients
Tinnitus (pronounced “TIN‑ih‑tuss”) is the false perception of sound even in the absence of any such sound in the external environment. Tinnitus can take a variety of forms. While there are multiple potential causes of tinnitus, in the majority of cases no underlying cause is found. Tinnitus can be frustrating because in most cases there is no direct treatment. Medications generally are not helpful for tinnitus, despite advertisements to the contrary. Tinnitus masking under the supervision of a tinnitus audiologist can be helpful.
For clinicians
Overview
Idiopathic tinnitus is technically an auditory hallucination — the false perception of sound in the absence of any incoming auditory stimulus. Most people have experienced some degree of idiopathic tinnitus, but a percentage of the population experiences distressing tinnitus. The mechanism of idiopathic tinnitus is poorly understood, though it occurs commonly in association with hearing loss. Tinnitus is difficult to measure since it is a purely subjective phenomenon. Treatment of idiopathic tinnitus is difficult.
Demographics
In 2022 Jarach and colleagues (Jarach, Lugo et al. 2022) published a systematic review and meta-analysis about the global disease burden of tinnitus, which, “estimated that the annual incidence of tinnitus is approximately 1%, with 14% of adults experiencing any tinnitus and 2% experiencing a severe form of it. The prevalence of tinnitus did not differ by sex, but increased prevalence was associated with increasing age, with any tinnitus being present in 10% of young adults, 14% of middle-aged adults, and 24% of older adults.”
Definitions
For purposes of this discussion we focus on idiopathic tinnitus, defined as the false perception of sound in the absence of any acoustic stimulus. Tinnitus by this definition is an auditory hallucination (perception in the absence of stimulus).
There are other phenomena that are sometimes classified as tinnitus.
The first is somatic tinnitus, which refers to auditory perception of a vibration that is being generated somewhere in the body. For example, some people can “hear” themselves swallow; there are actual vibrations being generated by the musculature in the larynx, and the ear can “hear” these vibrations. Another example of somatic tinnitus is pulsatile tinnitus, which is generated by rhythmic turbulent blood flow through vessels. Although somatic tinnitus (such as pulsatile tinnitus) is sometimes classified as “tinnitus,” we prefer to regard it as a form of hyperacusis, in the sense that the ear is unusually sensitive to vibrations that would not otherwise be noticeable. Somatic tinnitus is discussed elsewhere.
The second is tinnitus from middle ear myoclonus, whose subtypes are tensor tympani myoclonus and stapedial myoclonus. In stapedial myoclonus the muscle attached to the stapes (innervated by a branch of the facial nerve) rhythmically contracts. In tensor tympani myoclonus the tensor tympani muscle (innervated by a branch of the trigeminal nerve) rhythmically contracts. In normal circumstances these muscles mediate a protective auditory reflex against loud sounds, but if the muscles pathologically contract in a rhythmic fashion, then the ossicular chain will move (as if sounds were entering the ear from the external environment) and be perceived as sound. Middle ear myoclonus is discussed elsewhere.
Pathophysiology of idiopathic tinnitus
Idiopathic tinnitus, which we will hereafter refer to simply as “tinnitus,” is poorly understood. What is known about the neuroanatomy of the ear is that signals generated by the cochlea travel through the cochlear division of the 8th cranial nerve to the brainstem where they synapse in the cochlear nuclei, then ascend through a number of structures (trapezoid bodies, superior olives, lateral lemnisci, inferior colliculi, medial geniculate nuclei, sublenticular limb of the internal capsules) to the auditory cortices in the transverse temporal gyri. Logically, one would think that tinnitus could arise from a lesion anywhere along these pathways.
Many cases of tinnitus likely arise from damage to the cochlea. Suggestive of this mechanism are instances of tinnitus beginning after noise exposure.
However, it is well reported in the literature (House and Brackmann 1981) that some patients continue to experience tinnitus even after labyrinthectomy and/or vestibulocochlear neurectomy. In cases of labyrinthectomy there is no longer any cochlea to generate auditory signals; in cases of vestibulocochlear neurectomy there are no longer any afferent fibers to carry auditory signals from the cochlea; so in patients who continue to experience tinnitus despite having undergone these procedures, it is clear that the tinnitus must be generated somewhere between the cochlear nuclei and the auditory cortex, even if the tinnitus perhaps originally “began” as a problem in the cochlea.
Studies have shown that tinnitus frequently accompanies hearing loss of any cause (Lockwood, Salvi et al. 2002). One interpretation of this finding is that the brain does not like a “vacuum,” and if the brain is no longer receiving auditory signals it had been accustomed to receive, then it will start “guessing” or “interpolating” what signals “should have” been there. This is somewhat analogous to a phantom limb syndrome, in which a patient may still perceive an amputated limb despite the obvious absence of that limb. On this interpretation, tinnitus following hearing loss is a type of “phantom” perception (Muhlnickel, Elbert et al. 1998).
Studies have also demonstrated clearly that individuals with normal hearing at least intermittently experience tinnitus (Heller and Bergman 1953) — in other words, some degree of tinnitus appears to be physiologic. Taking this observation together with the earlier cited observation that tinnitus often accompanies hearing loss, one possible conclusion is that some degree of tinnitus is “always there” below one’s threshold of awareness, but it becomes more noticeable when hearing loss eliminates the distraction that perception of normal environmental sounds would otherwise have provided.
Diagnosis
Simply diagnosing whether or not tinnitus is present is straightforward because it relies entirely on a patient’s report of a subjective experience. As such, it is also unverifiable.
A basic rationale for “measuring” tinnitus is that a metric is needed to identify/characterize disease and to evaluate the effect of any interventions (Henry 2016), and some data suggest that tinnitus management with a masking strategy that is “customized” to a patient’s individual tinnitus profile may be more effective than a general (non-customized) strategy (Wang, Ding et al. 2022).
Despite the subjective nature of tinnitus, there is substantial literature regarding methods for characterizing it. There are several features of tinnitus that researchers have attempted to measure.
The first feature is tinnitus pitch (McMillan, Thielman et al. 2014). Different pitch matching methods sometimes give different results (Neff, Langguth et al. 2019). Tinnitus pitch matching can be more complex when an individual’s tinnitus is present at multiple frequencies (Tao, Chang et al. 2017).
The second feature is tinnitus loudness (Manning, Grush et al. 2019).
The reliability of measures tinnitus pitch and loudness is suboptimal (Hoare, Edmondson-Jones et al. 2014), which could be due either to variability in the measurement method, or variability in the tinnitus itself, or both.
Proposals for objective “biomarkers” of tinnitus (Kang, Kim et al. 2021) have not gained acceptance.
A third set of features comprise the degree to which tinnitus evokes an emotional response or interferes with an individual’s functioning. This aspect of tinnitus is usually assessed through questionnaire-based investigations, with instruments such as the Tinnitus Handicap Inventory (McCombe, Baguley et al. 2001), Tinnitus Functional Index (Meikle, Henry et al. 2012, Henry, Griest et al. 2016), and Tinnitus Reaction Questionnaire (Meikle, Henry et al. 2012, Henry, Griest et al. 2016), though the reliability of such instruments has been questioned (Newman, Wharton et al. 1995).
Management
Management of tinnitus is difficult, and we discuss this topic elsewhere.
References
Heller MF, Bergman M (1953) VII Tinnitus Aurium in Normally Hearing Persons. Annals of Otology, Rhinology & Laryngology 62: 73-83. doi: 10.1177/000348945306200107
Henry JA (2016) “Measurement” of Tinnitus. Otol Neurotol 37: e276-85. doi: 10.1097/MAO.0000000000001070
Henry JA, Griest S, Thielman E, McMillan G, Kaelin C, Carlson KF (2016) Tinnitus Functional Index: Development, validation, outcomes research, and clinical application. Hear Res 334: 58-64. doi: 10.1016/j.heares.2015.06.004
Hoare DJ, Edmondson-Jones M, Gander PE, Hall DA (2014) Agreement and reliability of tinnitus loudness matching and pitch likeness rating. PLoS One 9: e114553. doi: 10.1371/journal.pone.0114553
House JW, Brackmann DE (1981) Tinnitus: surgical treatment. Ciba Found Symp 85: 204-16. doi: 10.1002/9780470720677.ch12
Jarach CM, Lugo A, Scala M, van den Brandt PA, Cederroth CR, Odone A, Garavello W, Schlee W, Langguth B, Gallus S (2022) Global Prevalence and Incidence of Tinnitus: A Systematic Review and Meta-analysis. JAMA Neurol 79: 888-900. doi: 10.1001/jamaneurol.2022.2189
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McCombe A, Baguley D, Coles R, McKenna L, McKinney C, Windle-Taylor P, British Association of Otolaryngologists H, Neck S (2001) Guidelines for the grading of tinnitus severity: the results of a working group commissioned by the British Association of Otolaryngologists, Head and Neck Surgeons, 1999. Clin Otolaryngol Allied Sci 26: 388-93.
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Wang J, Ding J, Song J, Hu L, Cong N, Han Z (2022) A Prospective Study of the Effect of Tinnitus Sound Matching Degree on the Efficacy of Customized Sound Therapy in Patients with Chronic Tinnitus. ORL J Otorhinolaryngol Relat Spec 84: 229-237. doi: 10.1159/000517631
