tinnitus

Tinnitus

May be either subjective (heard only by patient) or objective (e.g. cranial bruit, can be heard by the examiner as well, usually with a stethoscope placed over the cranium, orbit, or carotid arteries in the neck). Objective tinnitus is almost always due to vascular turbulence (from increased flow or partial obstruction).


Tinnitus is the conscious, usually unwanted perception of sound that arises or seems to arise involuntarily in the ear of the affected individual. In most cases there is no genuine physical source of sound. This nonpulsatile tinnitus is caused by a hearing malfunction.

see Pulsatile tinnitus.

see Non-pulsatile tinnitus.

Tinnitus is not a disease, but a condition that can result from a wide range of underlying causes. The most common cause is noise-induced hearing loss. Other causes include: neurological damage (multiple sclerosis), ear infections, oxidative stress, emotional stress, foreign objects in the ear, nasal allergies that prevent (or induce) fluid drain, wax build-up, and exposure to loud sounds. Withdrawal from benzodiazepines may cause tinnitus as well.

Patients with idiopathic intracranial hypertension can have pulsatile tinnitus, a whooshing sensation in one or both ears (64–87%); this sound is synchronous with the pulse.

Tinnitus distress has been linked to increased beta oscillatory activity in the dorsal anterior cingulate cortex (dACC). The amount of distress is linked to alpha activity in the medial temporal lobe (amygdala and parahippocampal area), as well as the subgenual (sg)ACC and insula, and the functional connectivity between the parahippocampal area and the sgACC at 10 and 11.5 Hz.

Aortocranial fibromuscular dysplasia.

Chiari 1 malformation.

Intracranial hypotension.

Primary otalgia

Geniculate neuralgia.

Meniere’s disease.

Endolymphatic-subarachnoid shunts.

Glomus tumor

Vestibular schwannoma: see Vestibular schwannoma tinnitus.

Aminoglycoside toxicity: streptomycin, tobramycin (tinnitus precedes hearing loss)


Recent studies have adopted the Bayesian brain model to explain the generation of tinnitus in subjects with auditory deafferentation. That is, as the human brain works in a Bayesian manner to reduce environmental uncertainty, missing auditory information due to hearing loss may cause auditory phantom percepts, i.e., tinnitus. This type of deafferentation-induced auditory phantom percept should be preceded by auditory experience because the fill-in phenomenon, namely tinnitus, is based upon auditory prediction and the resultant prediction error. For example, a recent animal study observed the absence of tinnitus in cats with congenital single-sided deafness (SSD; Eggermont and Kral, Hear Res 2016). However, no human studies have investigated the presence and characteristics of tinnitus in subjects with congenital SSD. Thus, the present study sought to reveal differences in the generation of tinnitus between subjects with congenital SSD and those with acquired SSD to evaluate the replicability of previous animal studies. This study enrolled 20 subjects with congenital SSD and 44 subjects with acquired SSD and examined the presence and characteristics of tinnitus in the groups. None of the 20 subjects with congenital SSD perceived tinnitus on the affected side, whereas 30 of 44 subjects with acquired SSD experienced tinnitus on the affected side. Additionally, there were significant positive correlations between tinnitus characteristics and the audiometric characteristics of the SSD. In accordance with the findings of the recent animal study, tinnitus was absent in subjects with congenital SSD, but relatively frequent in subjects with acquired SSD, which suggests that the development of tinnitus should be preceded by auditory experience. In other words, subjects with profound congenital peripheral deafferentation do not develop auditory phantom percepts because no auditory predictions are available from the Bayesian brain 1).

Tinnitus may be an accompaniment of sensorineural hearing loss or congenital hearing loss, or it may be observed as a side effect of certain medications (ototoxic tinnitus).

Tinnitus is usually a subjective phenomenon, such that it cannot be objectively measured. The condition is often rated clinically on a simple scale from “slight” to “catastrophic” according to the difficulties it imposes, such as interference with sleep, quiet activities, and normal daily activities.

Tinnitus and hearing loss in the adult can have profound effects on the quality of life. The imaging workup for tinnitus and hearing loss in adults follows otoscopic exam and audiometry testing. CT and MR imaging have different and often complementary roles in the evaluation of tinnitus and hearing loss depending on the clinical scenario and the suspected underlying cause. Imaging can often identify the cause and evaluate the extent of disease for surgical planning 2).

see Tinnitus treatment.

Bayesian models of brain function such as active inference and predictive coding offer a general theoretical framework with which to explain several aspects of normal and disordered brain function. Of particular interest to a study is the potential for such models to explain the pathology of auditory phantom perception, i.e. tinnitus. To test this framework empirically, Hullfish et al., performed an fMRI experiment on a large clinical sample (n = 75) of the human chronic tinnitus population. The experiment features a within-subject design based on two experimental conditions: subjects were presented with sound stimuli matched to their tinnitus frequency (TF) as well as similar stimuli presented at a control frequency (CF). The responses elicited by these stimuli, as measured using both activity and functional connectivity, were then analyzed both within and between conditions. Given the Bayesian-brain framework, they hypothesized that TF stimuli will elicit greater activity and/or functional connectivity in areas related to the cognitive and emotional aspects of tinnitus, i.e. tinnitus-related distress. They conversely hypothesize that CF stimuli will elicit greater activity/connectivity in areas related to auditory perception and attention. They discuss this results in the context of this framework and suggest future directions for empirical testing 3).


1)
Lee SY, Nam DW, Koo JW, De Ridder D, Vanneste S, Song JJ. No auditory experience, no tinnitus: Lessons from subjects with congenital- and acquired single-sided deafness. Hear Res. 2017 Aug 15;354:9-15. doi: 10.1016/j.heares.2017.08.002. [Epub ahead of print] PubMed PMID: 28826043.
2)
Hoang JK, Loevner LA. Evaluation of Tinnitus and Hearing Loss in the Adult. 2020 Feb 15. In: Hodler J, Kubik-Huch RA, von Schulthess GK, editors. Diseases of the Brain, Head and Neck, Spine 2020–2023: Diagnostic Imaging [Internet]. Cham (CH): Springer; 2020. Chapter 15. Available from http://www.ncbi.nlm.nih.gov/books/NBK554328/ PubMed PMID: 32119238.
3)
Hullfish J, Abenes I, Kovacs S, Sunaert S, De Ridder D, Vanneste S. Functional brain changes in auditory phantom perception evoked by different stimulus frequencies. Neurosci Lett. 2018 Jul 31. pii: S0304-3940(18)30522-6. doi: 10.1016/j.neulet.2018.07.043. [Epub ahead of print] PubMed PMID: 30075284.
  • tinnitus.txt
  • Last modified: 2021/04/17 19:21
  • by administrador