Diagnosis and clinical management of tinnitus

There is no standard procedure for the diagnosis or management of tinnitus. There are, however, recent guidelines for doing so from the UK Department of Health (Department of Health 2009), and the international organisation, the Tinnitus Research Initiative (Biesinger 2011). Both guidelines recommend that tinnitus and its impact on the person are assessed using validated questionnaire measures of severity, quality of life, depression or anxiety. Psychoacoustic measures of tinnitus (pitch, loudness, minimum masking level) are also recommended. Although these do not correlate well with tinnitus severity (Hiller 2006), they can prove useful in patient counselling (Henry 2004), or to demonstrate stability of the tinnitus percept over time (Department of Health 2009). Recommended clinical management strategies include directive counselling, relaxation therapy, tinnitus retraining therapy (TRT), cognitive behavioural therapy (CBT), sound enrichment using ear‐level sound generators or hearing aids, and drug therapies to manage co‐morbid symptoms such as insomnia, anxiety or depression (Department of Health 2009). All show variable efficacy and have little known risk of adverse effects (Hoare 2011; Hobson 2010; Martinez‐Devesa 2010; Phillips 2010). Where there is a hearing loss and tinnitus, the most common recommendation is to fit a hearing aid, although this practice also varies according to clinical experience and anecdotal evidence. For example, there is a clearly divided opinion among clinicians as to whether or not a hearing aid should be recommended to someone with a mild or higher‐frequency hearing loss that ordinarily might go unaided (Hoare 2012).

Pathophysiology

Most people with chronic tinnitus have some degree of hearing loss (Ratnayake 2009), and the prevalence of tinnitus increases with increased hearing loss (Han 2009; Martines 2010). The varying theories of tinnitus generation involve either changes in function or activity of the peripheral (cochlea and auditory nerve) or central auditory nervous systems (Henry 2005). Theories involving the peripheral systems include the discordant damage theory, which predicts that the loss of outer hair cell (OHC) function where inner hair cell (IHC) function is left intact leads to a release from inhibition of IHC and aberrant activity (typically hyperactivity) in the auditory nerve (Jastreboff 1990). Such aberrant auditory nerve activity can also have a biochemical basis, resulting from excitotoxicity or stress‐induced enhancement of IHC glutamate release with upregulation of N‐methyl‐D‐aspartate (NMDA) receptors (Guitton 2003; Sahley 2001). In the central auditory system, structures implicated as possible sites of tinnitus generation include the dorsal cochlear nucleus (Middleton 2011; Pilati 2012), the inferior colliculus (Dong 2010; Mulders 2010), and the auditory and non‐auditory cortex (discussed further below). There is a strong rationale to say that it is a direct consequence of maladaptive neuroplastic responses to hearing loss (Møller 2000; Mühlnickel 1998). This process is triggered by sensory deafferentation and a release from lateral inhibition in the central auditory system allowing irregular spontaneous hyperactivity within the central neuronal networks involved in sound processing (Eggermont 2004; Rauschecker 1999; Seki 2003). As a consequence of this hyperactivity, a further physiological change noted in tinnitus patients is an increased spontaneous synchronous activity occurring at the cortical level, measurable using electroencephalography (EEG) or magnetoencephalography (MEG) (Dietrich 2001; Tass 2012; Weisz 2005).

Another physiological change thought to be involved in tinnitus generation is a process of functional reorganisation, which amounts to a change in the response properties of neurons within the primary auditory cortex to external sounds. This effect is well demonstrated physiologically in animal models of hearing loss (Engineer 2011; Noreña 2005). Evidence in humans, however, is limited to behavioural evidence of cortical reorganisation after hearing loss demonstrating improved frequency discrimination ability at the audiometric edge (Kluk 2006; McDermott 1998; Moore 2009; Thai‐Van 2002; Thai‐Van 2003), although Buss 1998 did not find this effect. For comprehensive reviews of these physiological models, see Adjamian 2009 and Noreña 2011. It is also proposed that spontaneous hyperactivity could cause an increase in sensitivity or 'gain' at the level of the cortex, whereby neural sensitivity adapts to the reduced sensory inputs, in effect stabilising mean firing and neural coding efficiency (Noreña 2011; Schaette 2006; Schaette 2011). However, such adaptive changes would be achieved at the cost of amplifying 'neural noise' due to the overall increase in sensitivity, ultimately resulting in the generation of tinnitus.

Increasingly, non‐auditory areas of the brain, particularly areas associated with emotional processing, are also implicated in the maintenance of bothersome tinnitus (Rauschecker 2010; Vanneste 2012). Vanneste 2012 recently described tinnitus as "an emergent property of multiple parallel dynamically changing and partially overlapping sub‐networks", implicating the involvement of many structures of the brain more associated with memory and emotional processing in tinnitus generation. Identification of the structural components of individual neural networks responsible for either tinnitus generation or tinnitus intrusiveness, which are independent of those for hearing loss, remains open to future research, however (Melcher 2013). One further complication in understanding the pathophysiology of tinnitus is that not all people with hearing loss have tinnitus, and not all people with tinnitus have a clinically significant hearing loss. There are possible explanations for this, however. For example, König 2006 found that the maximum slope within audiograms was higher in people with tinnitus than in people with hearing loss who do not have tinnitus, despite their 'non‐tinnitus' group having the greater mean hearing loss. This suggests that a contrast in sensory inputs between regions of normal and elevated threshold may be more likely to result in tinnitus.