1 Neurophysiological Models, Psychological Models, and Treatments for Tinnitus
Phillip E. Gander and Richard S. Tyler
Abstract
This chapter provides an overview of different models of tinnitus according to the two major categories of neurophysiological and psychological models. These models lead to different approaches to tinnitus treatment and the implementation of sound therapy and counseling protocols, which are summarized accordingly.
Keywords: neurophysiological, psychological, treatment, sound therapy, counseling
1.1 What Is Tinnitus?
A clear definition of tinnitus is from the study by McFadden.1 Tinnitus:
?Is a perception of sound (it must be heard).
?Is involuntary (not produced intentionally).
?Originates in the head (not hearing or overly sensitive to an external sound).
The patient's reaction should also be considered. It is helpful to distinguish:
?Tinnitus that is problematic from that which is not.2
?How often the tinnitus occurs and how long an episode is (e.?g., whether it occurs once a month for 10 ?s or is present daily).
Tinnitus has been classified in several ways, such as its presumed site of generation and whether it is audible to someone other than the patient (objective tinnitus) or the patient alone (subjective tinnitus). An objective tinnitus, heard by the examiner, may be of middle ear origin or a spontaneous otoacoustic emission arising from the sensorineural system and can occasionally be identified by physical examination to direct treatment options, such as in vascular causes. However, the terms subjective and objective are not particularly helpful in understanding or treating most forms of tinnitus. Instead, it is more useful to classify tinnitus in a manner analogous to hearing loss according to site of injury or generation3; that is, whether it is middle ear, sensorineural, or central tinnitus. A thorough physical examination and treatment of identified ailments, when possible, are important first steps in patients with tinnitus. However, a physical examination will typically not reveal a clear cause, that is, idiopathic tinnitus. Importantly, in all cases a distinction can be made between (1) the tinnitus and (2) the reaction to the tinnitus, which has become known as the psychological model of tinnitus.4 Regardless of the classification, the treatments described in this book are applicable to all types of tinnitus. See Appendix 1.1 for an overview of this chapter.
The overall impact of tinnitus on a patient is influenced by the characteristics of tinnitus and of that particular patient.5 For example, tinnitus is more likely to be annoying if it is louder or has a screeching quality. Some authors have incorrectly suggested that psychoacoustic factors are unimportant or unrelated to tinnitus annoyance. Psychoacoustic factors are indeed relevant,6,? 7 although they are only one thing to consider in understanding the effect tinnitus has on a patient. An absence of high correlation between loudness and annoyance does not mean that loudness is not important. Stouffer and Tyler8 concluded that patients with soft tinnitus are not under as much stress as those who report a loud tinnitus. Also, patients who are under stress or have not had adequate sleep find the tinnitus more annoying.
Tinnitus is not a personality disorder, but psychological factors are involved in the development and maintenance of this problem (see, e.?g., Folmer et al,9 Fowler and Fowler,10 Nondahl et al11). Although patients with severe tinnitus can have clinical depression, in our experience, serious psychological problems are rare among most tinnitus patients. Very few of us, after all, would not be bothered at all if we constantly heard an unwanted sound that we had no control over.
1.2 Neurophysiological Models of Tinnitus
A likely cause for tinnitus is maladaptive plasticity of the central nervous system.12 In essence, in response to some (typically unknown) causes, mechanisms that keep the nervous system in balance (i.?e., homeostasis) lead to changes that result in the perception of tinnitus. In the normal auditory system, increases in neural activity evoked by acoustic stimuli are the basis for sound perception. Under conditions of a hearing loss, there is a decrease in input to the auditory system in the frequency range of the loss. Normal operation of the nervous system is to restore activity levels that have changed due to this decrease in input, to keep homeostasis.13 A mechanism for this restoration is modification of the sensitivity of neurons to their input and their resultant output activity by increasing the neural response gain.14 The increase in gain also leads to an increase in spontaneous activity in the absence of acoustic stimulation. Therefore, neurophysiological models have logically nominated this increase in spontaneous activity as a mechanism of tinnitus. Wherever the site of origin, most probably this activity change is transmitted to and results in an increased spontaneous rate in the auditory cortex. Table 1.1 reviews a few of the neurophysiological models that have been proposed over the years (for reviews, see Cacace,15 Eggermont,16 Eggermont and Roberts,17,? 18 Jastreboff,19 Salvi et al,20 and Vernon and Moeller21). Some of these are specific to precise anatomic or physiological sites; others are more general models referring to processing principles.
Table 1.1 Examples of neurophysiological models of tinnitus
Kiang, Moxon, and Levine25
Edge between normal and absent hair cells and subsequent neural activity
Tonndorf29
Decoupling of stereocilia between the hair cells and tectorial membrane
Eggermont26
Moeller27
Cross-talk (interneural synchrony) between nerve fibers
Hazell30
Tinnitus is a result of automatic gain control system of central nervous system (e.?g., normally increasing the sensitivity in quiet), linked to outer hair cells
Penner and Bilger31
Spontaneous otoacoustic emissions
Jastreboff19
Discordant inner and outer hair cell damage (damaged outer hair cells with reasonably intact inner hair cells)
Salvi et al20,? 28
Increase in central neurons tuned to similar frequencies following reorganization of peripheral hearing loss
Llinás et al32
Abnormal neural oscillatory connection between thalamus and cortex
Noreña and Eggermont33
Eggermont and Roberts17
Cochlear damage leads to reduced inhibition in auditory system resulting in increased neural synchrony, spontaneous firing, and burst firing
Kaltenbach, Zhang, and Zacharek34
Hyperactivity of dorsal cochlear nucleus
Noreña35
Schaette and McAlpine36
Zeng37
Homeostatic plasticity after hearing loss results in neural hyperactivity from increased central gain
Leaver et al38
Rauschecker et al39
Failed "noise cancellation" system in frontostriatal network that gates and interprets neural noise
Roberts, Husain, and Eggermont41
Basal forebrain cholinergic attention system involved in tinnitus prominence and maintenance
De Ridder, Vanneste, and Freeman42
Multiple brain networks that interact with tinnitus "core" subnetwork
De Ridder et al43
Hearing loss reduces input and brain fills in missing information to resolve uncertainty
Sedley et al22
Brain reinterprets increased neural noise as a sound
In general, many of these models are insightful and clever. For models to be useful, they should be testable or should lead to a broader understanding and eventually a testable hypothesis. Unfortunately, many of these models are mutually exclusive22 and so it becomes difficult to separate testable hypotheses that usefully contribute to broader understanding.
Whatever the initial source of tinnitus, it must be perceived in the auditory cortex (see Tyler,23 p. 136; Vanneste and De Ridder24). Broadly, there are three different ways that the mechanism of tinnitus can be coded in the auditory cortex:
?Increased spontaneous activity fed by increase or decrease in activity or edge in activity.25
?Cross-fiber correlation with normal or increased spontaneous activity.26,? 27
?More fibers with similar best frequency following hearing loss-induced auditory plasticity.20,? 28
Fig. 1.1 shows a schematic representation of how we hear, interpret, and react to sounds. Sound is transformed from...
