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Introduction : Tinnitus, the most common auditory disorder, affects about 40 million people in the United States alone, and its incidence is rising due to an aging population and increasing noise exposure. Although several approaches for the alleviation of tinnitus exist, there is as of yet no cure. The present article proposes a testable model for tinnitus that is grounded in recent findings from human imaging and focuses on brain areas in cortex, thalamus, and ventral striatum. Limbic and auditory brain areas are thought to interact at the thalamic level. While a tinnitus signal originates from lesion-induced plasticity of the auditory pathways, it can be tuned out by feedback connections from limbic regions, which block the tinnitus signal from reaching auditory cortex. If the limbic regions are compromised, this “noise-cancellation” mechanism breaks down, and chronic tinnitus results. Hopefully, this model will ultimately enable the development of effective treatment.
Body : The subcallosal area in its posterior portion overlaps with the nucleus accumbens (NAc), which is a major component of the ventral striatum , How do the limbic regions of the subcallosal area interact with the thalamo-cortical sensory/perceptual systems? In addition to corticofugal and transcortical glutamatergic projections from vmPFC, anatomical data indicate that serotonergic axons (from the dorsal raphe nucleus).
“Functional and structural abnormalities in limbic and auditory areas contributing to tinnitus,” Organization of Human Brain Mapping, areas contributing to tinnitus,” Organization of Human Brain Mapping, Barcelona, Spain). Why neurons in some individuals (i.e., those with SNHL but no tinnitus) are better protected from damage than in others (i.e., individuals with tinnitus) remains unclear. However, the use of neuroprotective drugs, such as NMDA antagonists, might aid with the prevention (or even reversal) of chronic tinnitus.
What Breaks the Noise-Cancellation System?
First, it could be a consequence of overload (and resulting excitotoxicity) from chronic firing of NAc neurons trying to compensate for the tinnitus signal.
Second, it is possible that tinnitus patients have an independent, systemic vulnerability in one or more limbic-relevant transmitter systems, such as serotonin (5-HT) (see below), making these individuals more susceptible to tinnitus as well as other disorders, like chronic pain or depression. In affected individuals, underlying transmitter levels may decline faster over time or with age than in unaffected individuals. Although mechanisms driving such “system dysfunctions” (e.g., dopaminergic cells in the basal ganglia are known to fail over time in Parkinsonism) are not yet characterized, they are likely to be multifactorial, with genetic vulnerability, developmental insults, and environmental stressors all considered important and synergistic contributors.

Previous theories of tinnitus have assumed a largely “reactive” role for limbic structures that reflects a mostly learned distress response (Jastreboff, 1990, Jastreboff, 2000). Tinnitus was thought to cause insomnia, depression, or anxiety; limbic activation found in prior PET imaging studies was seen largely as a reflection of these emotional effects of tinnitus and the suffering associated with this condition. The present model assigns a more central role to limbic and paralimbic structures in and around the subcallosal area, in that they participate in a self-regulating gating process that can actually prevent the tinnitus signal from being perceived. More generally, therefore, limbic activity does not only color our perception, it is even in a position to completely suppress or tune out the signal if it is deemed unpleasant and/or redundant. Such limbic influences on thalamo-cortical transmission may prove to be more fundamental in health and disease than hitherto thought and may be realized by a relatively simple feedback circuit.
the long-term reorganization of central auditory pathways following sensorineural hearing loss appears to consist of changes at the cortical as well as thalamic level. It is entirely possible that tinnitus, like many apparently heterogeneous neurological syndromes, may be the end result of various different causes. Different subtypes of tinnitus have indeed been described in cluster analyses, for instance cases in which tinnitus gets better with (i.e., is masked by) noise (a fundamental tenet for many treatment attempts; Okamoto et al., 2010, Roberts, 2007), but also cases in which tinnitus gets worse in noise (Tyler et al., 2008). Notably, tinnitus has been reported to occur in individuals with normal hearing (Heller and Bergman, 1953). In cases of tinnitus with intact hearing, a model of lesion-induced plasticity would not apply, as a lesion in the auditory periphery may not exist. On the other hand, “normal hearing” is often determined on the basis of standard audiological examination, which is performed in octave steps and only at frequencies below 8 kHz. Cases of mild notch-like hearing loss or hearing loss above 8 kHz could easily escape such testing. When audiological testing is performed at finer intervals and at frequencies above 8 kHz, cases of tinnitus with absolutely no hearing loss become more rare in our hands and in those of other investigators (Salvi et al., 2009). It is safe to say, therefore, that the great majority of tinnitus cases do involve SNHL, i.e., damage to the sensory periphery (Hoffman and Reed, 2004). Importantly, the reverse is not true, i.e., not everyone with SNHL develops tinnitus (see below). Thus, although universal models or treatments for tinnitus may not exist, we argue that central auditory system reorganization is a necessary prerequisite for chronic tinnitus.
In this context, analogies between tinnitus and chronic pain may be informative (Flor et al., 2006, King et al., 2009, Møller, 2007). Many forms of chronic pain are modulated by stress, emotions, and fatigue and are comorbid with anxiety and depression (Folmer et al., 2001). Chronic pain often results from previous bodily injury, which could lead to long-term central reorganization.
tinnitus most likely results from the following factors:
(1)
In most, if not all, cases, the process leading to tinnitus is triggered by a lesion to the auditory periphery, e.g., a loss of hair cells in the inner ear resulting from acoustic trauma or aging.

(2)
Loss of input in the lesioned frequency range leads to an overrepresentation of lesion-edge frequencies, which causes hyperactivity and possible burst-firing in central auditory pathways, constituting the initial tinnitus signal.

(3)
Under normal circumstances, the tinnitus signal is cancelled out at the level of the thalamus by an inhibitory feedback loop originating in paralimbic structures: activity from these structures reaches the TRN, which in turn inhibits the MGN. If, however, paralimbic regions are compromised, inhibition of the tinnitus signal at the thalamic gate is lost, and the signal is relayed all the way to the auditory cortex, where it leads to permanent reorganizati.

Conclusions : Tinnitus should not be neglected and should be treated because it is very important and may lead to a complex psychological condition.
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