Prevalence

Tinnitus is a common condition and up to 18% of the population in industrialised countries are affected mildly by tinnitus (Coles 1984; Coles 1995). Up to 2% of the population are thought to suffer to a debilitating degree (Coles 1984) with anxiety, depression or altered sleep patterns reported (Andersson 2004; Coles 1984; Coles 1995; Luxon 1993). A minority of sufferers will have an identifiable structural abnormality such as acoustic neuroma, Ménière's disease or otosclerosis which may be amenable to current surgical treatment. Epidemiological data reports are few. The data described by the Institute of Hearing Research (UK) in 1981 refer to a prevalence of tinnitus in 15.5% to 18.6% of 6804 participants who completed a questionnaire in four cities (MRC 1981). This is consistent with the data collected by the American Tinnitus Association (ATA) which points to a prevalence of tinnitus in 50 million, or about 19%, of Americans (ATA 2001). Data exist for Japan, Europe and Australia, and estimates suggest that tinnitus affects a similar percentage of those populations. One to two per cent of the population experience debilitating tinnitus, severely limiting the quality of life of affected individuals (Seidman 1998). In a survey in Germany 1.5 million adults experience tinnitus as being 'considerably annoying' (Pilgramm 1999).

Aetiology

Almost any form of disorder involving the inner ear or the auditory nervous system may produce tinnitus (Brummett 1980; Shea 1981). Around 90% of people with hearing loss experience some degree of tinnitus (Parnes 1997). Tinnitus can occur as an isolated symptom without a recognisable cause. It can also occur in association with a middle or inner ear disorder, such as sensorineural hearing loss (Vesterager 1997), otosclerosis (Shea 1981), intoxication with certain drugs (Brummett 1980), sudden deafness or Ménière's disease (Spoendlin 1987). Environmental factors can also cause tinnitus. The most relevant and frequently reported are: explosions or gunfire (Christiansson 1993; Chung 1980; Melinek 1976; Mrena 2002; Temmel 1999), exposure to occupational noise (Alberti 1987; Axelsson 1985; Chouard 2001; Daniell 1998; Griest 1998; Kowalska 2001; McShane 1988; Neuberger 1992; Phoon 1993), exposure to recreational and amplified music (Becher 1996; Chouard 2001; Lee 1999; Metternich 1999) and more recently as a result of airbag inflation (Saunders 1998). Iatrogenic factors causing tinnitus include drug‐induced ototoxicity caused by, for example, the use of some antimicrobial and chemotherapeutic agents, quinine, aspirin overdose and platinum cytotoxics (Begg 2001; Cunha 2001; Palomar 2001; Sullivan 1988). Tinnitus is also associated with depression, although it is unclear whether tinnitus is a manifestation of depression or a factor contributing to it (Sullivan 1989).

Pathophysiology

The pathophysiology of tinnitus is not yet fully understood. One theory suggests that tinnitus is caused by excessive or abnormal spontaneous activity in the auditory system and in related cerebral areas (Lockwood 1999; Jastreboff 1994; Kaltenbach 2000; Moller 1997). A separate, but not incompatible, hypothesis suggests a genetic origin (Gingrass 1993; Laubert 1986; Snow 1993). This has been recently reviewed (Willems 2000).

Lockwood proposed that the perception of tinnitus arises not in the ears but in the brain (Lockwood 1999). The flow of blood through the brain can be detected and imaged using Positron Emission Tomography (PET). This is a method of computed tomography that detects energy emitted by radionucleotides. Changes in cerebral blood flow have been found in patients with tinnitus. In these studies, pure tones presented to subjects with tinnitus activate more portions of the brain than in control (non‐tinnitus) patients. This suggests that 'abnormal connections' in the central auditory system may play a role in tinnitus perception.

The neurophysiological model of tinnitus (Jastreboff 1990) suggests that tinnitus is primarily a subcortical perception resulting from the processing of weakened neural activity from the ear. During silence there is random neural activity in the auditory nerve (Moller 1984) and in fact over 90% of normal hearing individuals experienced brief tinnitus when placed in a sound‐proofed room (Heller 1986). It is thought that anything that alters this level of spontaneous activity (e.g. cochlear hair cell dysfunction or degeneration) could produce neural impulses that are interpreted by the auditory cortex as tinnitus (Nelson 2001). These patterns of impulses are usually very faint compared to those generated by external sounds (Hazell 1998). In this model, tinnitus could therefore result from continuous firing of cochlear fibres (nerve cells connected to the inner ear) to the brain, from hyperactivity of cochlear hair cells or from permanent damage to these cells being translated neuronally into a 'phantom' sound‐like signal that the brain 'believes' it is hearing. For this reason tinnitus may be compared to chronic pain of central origin ‐ a sort of 'auditory pain' (Briner 1995; Sullivan 1994).

Diagnosis

Initial management of a patient with tinnitus will involve a basic clinical assessment of history taking and examination. The relevant otological, general and family history will be sought. Examination will focus on the ears, teeth and neck and scalp musculature. Referral to a specialist is likely to involve a variety of other investigations including audiological tests and radiological imaging. Persistent, unilateral (one‐sided) tinnitus may be due to a specific lesion within the auditory pathway. Imaging studies of the cerebellopontine angle are important to exclude for example, a vestibular schwannoma (acoustic neuroma) ‐ a benign tumour of the cochleo‐vestibular nerve. This is the most common tumour of the cerebellopontine angle, with an incidence of 1.4 per 100,000 of the population (Dawes 2000; Anderson 2000) and is readily visualised by magnetic resonance imaging (MRI) (Ho 2002). Other lesions, such as glomus tumours, meningiomas, adenomas, vascular lesions or neuro‐vascular conflicts may also be detected by imaging (Weissman 2000; Marx 1999). If an organic, pathological or degenerative cause for the tinnitus is not found, it can be considered to be idiopathic.

Treatment

At present no specific therapy for tinnitus is acknowledged to be satisfactory in all patients. However, the prognosis if untreated is not always severe. In a recent trial (Hiller 2005), the Tinnitus Quotient severity at 18 months in the minimal intervention group (those receiving education alone) fell from 50 to 14 points.

Many patients who complain of tinnitus and who also have a significant hearing impairment will benefit from a hearing aid. Not only will this help their hearing disability, but also the severity of their tinnitus may be reduced.

A recent review (Waddell 2003) showed that the use of tricyclic antidepressants improved tinnitus related disability in people with or without depression and chronic tinnitus (Bayar 2001; Dobie 1993) and this medication has been evaluated in a Cochrane review (Baldo 2006). Other pharmacological agents used in the treatment of tinnitus with less beneficial results include antiepileptics (Simpson 1999), baclofen (skeletal muscle relaxant and central nervous system depressant) (Westerberg 1996), benzodiazepines (sedative) (Johnson 1993), cinnarizine (a cerebral vasodilator and vestibular sedative) (Podoshin 1991), nicotinamide (vitamin B group) (Hulshof 1987) and zinc (Paaske 1991).

Ginkgo biloba for tinnitus has been the subject of a number of studies (Drew 2001; Ernst 1999; Holger 1994; Rejali 2004) and a recent Cochrane review (Hilton 2004) although this did not find any conclusive evidence to support its use. Intravenous lidocaine has been shown to give short term relief of tinnitus in patients with no cochlear or vestibular nerve (following translabarynthine acoustic neuroma removal). This suggests a poorly understood mechanism of action on the central auditory pathway (Baguley 2005), or a peripheral action involving stabilisation of hair cells and cochlear nerve fibres (Hulshof 1985; Lenarz 1986).

Other interventions include acupuncture (Park 2000), electromagnetic stimulation (Dobie 1986; Fiedler 1998; Roland 1993), hypnosis (Attias 1993; Mason 1996), low power laser (Mirz 1999) and psychotherapy (Andersson 1999). In recent years increasing attention has been given to the method known as tinnitus retraining therapy (TRT). This is a therapeutic process that uses a combination of low level, broad‐band noise and counselling to achieve 'habituation'. The aim of the treatment is to redirect the brain's 'attentional focus' away from the tinnitus signal (Jastreboff 2003; Dobie 1999).Cognitive behavioural therapy has also been used to treat tinnitus and is the subject of another Cochrane review (Martinez‐Devesa 2007)

This review will consider the role of masking devices in tinnitus.