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Largely unknown causes and innumerable assumed mechanisms conceivably could be involved in the generation of tinnitus. The systematic classification outlined in this article differentiates conductive from sensorineural and central tinnitus. In addition, the very common, subjective tinnitus cannot be assessed objectively; thus, no concrete evidence at all corroborates the large number of individual mechanisms that supposedly lead to tinnitus, as de-scribed in the literature. In the present situation, a systematic classification based on the anatomical and functional aspects involved in the generation of tinnitus should prove useful. The present systematic classification, parts of which actually have been discussed since 1993 [16,l7], is described here in further detail, taking both the methods of functional and anatomical systematics into account. The first stage in the systematic classification of tinnitus (Table 1) is the conventional division into objective and subjective tinnitus.
From this schematic course of events, which presents a simplified form of the entire auditory system according to its functional and anatomical aspects, an uncomplicated classification can be deduced for subjective tinnitus (see Table 1).
According to function and anatomy, the following three divisions can be made: conductive tinnitus, sensorineural tinnitus, and central tinnitus [11,13]. In the case of sensorineural tinnitus, one of the three sensory functional elements of a resulting sensory tinnitus can be distinguished from extrasensory tinnitus [18].
For these purposes, central tinnitus, [1,9,11,13] can be subdivided into primary central and secondary central [9] tinnitus.
Thus, the systematics presented here provide us with the framework for classifying all known causative models of the symptom tinnitus.
Tinnitus occurring with and in the same frequency range as a hearing disorder, whereby the psychoacoustic loudness is some decibels above the hearing threshold and the hearing disorder is accompanied by a partial or complete loss of TEOAE and a positive recruitment phenomenon, results in a high degree of probability from a disturbed motor function of the OHCs. Currently, diagnosing a sensorineural tinnitus type II in exceptional cases only is possible. If an acoustic neurinoma is detected, a sensorineural tinnitus type III is the most likely diagnosis. The combination of different tinnitus types within this systematic classification generally is acceptable. For tinnitus sensations of up to 3-5 kHz, on the basis of the coherence theory, Feldmann [7] gives guidelines to differentiate clinically between central tinnitus and the tinnitus described here as sensorineural tinnitus. Some therapeutic approaches also can be grouped according to the systematic classification presented here. If the classification is used for diagnostic purposes, the tinnitus also can be registered as compensated or decompensated. If a diagnosis is reached by these means, clearly no single method of treatment can be found that would relieve all forms of tinnitus.
For the diagnosis of a motor disorder (OAE, recruitment), an acoustic neurinoma (ABR, NMR), and primary central disorders, specific diagnostic tools are available. At present, single forms of treatment are considered appropriate without specification for nearly all patients with tinnitus. Indeed, tinnitus is so complex and so manifold that a systematic classification could prove helpful. Sensorineural tinnitus is subdivided into motor (type I), transduction (type II), transformation (type III), and extrasensory tinnitus (type IV), central tinnitus being subclassified as primary and secondary (centralized) tinnitus. In the same way that the visual system can react to disturbances only symptomatically by reducing the ability to see or by "seeing stars", all disorders of the auditory system lead to a reduction in hearing ability or to tinnitus (or to both) without exception.
The various models can then be incorporated into the classification, regardless of their scientific evaluation.
It will enable physicians to classify the large number of causative mechanisms for tinnitus by a more simplified means, to reach a basis for general understanding. To comprehend subjective tinnitus, Figure 1 schematically depicts the individual functional and anatomical steps involved in sound processing, with the middle ear, inner ear, and brain roughly outlined. Systematics of possible generation mechanisms of subjective tinnitus, developed from Zenner et al. This allows every conceivable proposition for a pathophysiological, causative mechanism of tinnitus to be classified in the same way that the physiological courses of events divide the entire auditory system.
In principle, sensory and extrasensory tinnitus include all possible cochlear and neural (auditory nerve) tinnitus models. The pathogenesis of primary central tinnitus is to be found exclusively in the brain; it develops independently of the inner or middle ear. Noises perceived in the outer auditory canal with a microphone or a stethoscope are an indication of objective tinnitus. If, as did Feldmann [7], one assumes a uniform disruptive mechanism to be responsible for both the hearing disorder and tinnitus-in cases of noise induction of aminoglycosides, this is virtually certain; in other cases, it suggests a high probability-a sensorineural tinnitus type I can be diagnosed. A circulatory disturbance of the inner ear (proving difficult for detection) indicates sensorineural tinnitus type IV (reduced blood circulation in the stria vascularis); in cases involving dramatic hypoxia, this leads to a tinnitus type III (swelling of the nerve fiber endings).
The fact that a secondary central tinnitus can be diagnosed is exemplified by phantom tinnitus, which still continues even after neurectomy.
This is especially true of secondary central tinnitus, which always is triggered by a different form of tinnitus.
Tinnitus that can be heard in one or both ears is generated in the ear; a tinnitus perceived in the head may be regarded as central.
The exact description, depending on the course of the disorder, is acute, subacute, or chronic. A secondary central tinnitus can be diagnosed, partially at least, with psychological methods. Here represented is a systematic classification that is suitable for scientific communication, for explaining tinnitus models to affected patients in the course of tinnitus counseling, and as a basis for rational diagnosis of and therapy for tinnitus. For this reason, a broad number of mechanisms can be responsible for the onset of tinnitus, as has been discussed in the literature.
Even some apodictic statements have claimed that one model is responsible for (nearly) all forms of tinnitus: Circulatory disturbances represent one example of this form of misuse.
The signal can be made out, which begins at the point when sound enters the ear and leads to vibrations of the ossicles in the middle ear, which then are transferred to the inner ear. To classify the tinnitus models with respect to the three sensory functional elements, an easy approach is to number them consecutively [16,17].
Secondary central tinnitus is based on the fact that conductive and sensorineural tinnitus can be perceived only as such when the signal is processed in the brain. Systematics can be used clinically in cases in which case history, etiology (if known), and the accompanying audiological examinations allow conclusions of clinical relevance to be made. During one of the initial steps, noise leads to physiological damage of the molecular structure of the stereocilia of the OHCs, thus disrupting their motor function. Apart from these rare events, an additional centralized component of a sensorineural tinnitus canbe considered, especially in cases of extreme emotional overlap with secondary symptoms.
Indeed, some therapies available are designed for specific disorders: drugs for improving blood circulation (sensorineural type IV), caroverine [20] in the case of excitotoxic tinnitus (sensorineural type III), and lidocaine and calcium antagonists in the case of ion channel disorders (sensorineural types I, II, IV). Disorders associated with sensorineural tinnitus types II and III (apart from acoustic neurinoma) still are lacking reliable diagnostic procedures. The therapeutic problem of tinnitus can be resolved only if more sophisticated diagnostic instruments become available, enabling the classified diagnosis of tinnitus.
Focal metabolic activation in the predominant left auditory cortex in patients suffering from tinnitus. Concomitant salicylate-induced alterations of outer hair cell subsurface cisternae and electromotility.
Receptor pharmacological models for inner ear therapies with emphasis on glutamate receptors.
Neural mechanism of tinnitus: The Pathological Ensemble Spontaneous Activity of the Auditory System. Tinnitusmodelle zur Verwendung bei der Tinnituscounsellingtherapie des chronischen Tinnitus. Tinnitus-associated spontaneous otoacoustic emissions: active outer hair cell movements as a common origin? Nevertheless, just as one cannot deduce the pathophysiology from the symptom of hearing loss alone, without case history or further medical evidence, the symptom of tinnitus alone does not allow one to deduce the mechanism involved in its generation. The sensorineural component of the hearing process follows, comprising three functional, anatomical steps. Thus, tinnitus associated with the first functional element, the cochlear amplification mechanism, is termed motor tinnitus [8,10,14,16,19] or sensorineural tinnitus type I.
Mechanisms leading to a response in which the perception of tinnitus first triggered peripherally but then manifesting itself in the brain independently of the original source in the ear can be subsumed within the group termed secondary central tinnitus (centralized tinnitus, or the less scientific but comprehensible term phantom tinnitus, being synonyms).
This then would form a rational basis to indicate a specific therapy for all diagnosed cases. Furthermore, results obtained from therapies that apply specific forms of treatments, such as certain drug therapies or retraining therapy, do not necessarily allow a firm conclusion to be drawn from the host of pathological mechanisms that might be responsible. First, the sound signal is amplified by the motor (i) of the cochlear amplifier of the outer hair cells (OHCs); then the amplified signal is transformed into an electrical signal by the final mechanoelectrical (ii) transduction of the inner hair cells (IHCs).
Accordingly, tinnitus associated with the electromechanical transduction of the IHCs is designated transduction tinnitus [9,15], or sensorineural tinnitus type II.
The subdivision into primary and secondary central tinnitus, therefore, concludes every conceivable, central tinnitus model.
The probability that defective hearing and tinnitus are the result of the same causative mechanism is rated much higher than the probability that they have different origins [7]. If the noise has led simultaneously to a change in the otoacoustic emissions or even to a complete loss of hearing with positive recruitment, the probability of a sensorineural type I tinnitus being diagnosed is much higher.
The signal then is transferred synaptically from the IHCs to the afferent nerve fibers as a so-called (iii) transformation before being transferred by means of the auditory nerve. Following from this, the term transformation tinnitus [4,5,14-16], or sensorineural tinnitus type III, is used to describe disorders arising during the signal transfer from the IHCs and along the afferent nerve fibers (synonyms are cochleosynaptic tinnitus; signal transfer tinnitus). The sensory functional elements, including amplification motor, transduction, and transformation, are supported by such (iv) extrasensory elements as the stria vascularis, which is amply supplied with blood and provides a source of energy. According to this classification, the remaining extrasensory, sensorineural tinnitus mechanisms are called extrasensory tinnitus [18] or sensorineural tinnitus type IV. By way of the auditory nerve, the sound signal reaches the central nervous system, where perception and cognition take place.

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