Tuning Out the Noise: Limbic-Auditory Interactions in Tinnitus

Abstract

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.

Differential tinnitus-related neuroplastic alterations of cortical thickness and surface area

“…It is plausible to reason that a steadily progressive long-term thinning of the subcallosal area fosters the establishment of this vicious cycle. Remarkably, our finding of an anticorrelation between duration and CT in the subcallosal area (even though it is based on uncorrected results) fully concurs with the concept that ongoing tinnitus may be related to progressive reorganistion of the subcallosal anterior cingulate, which is in line with the 'gating' model [12], but would require a modification of the 'phantom pain' model. A similar finding has been reported by Leaver et al [34] who also applied the SBM approach to identify neuroanatomical markers of tinnitus.…”

“…Finally, we used the volumetric estimates of subcortical structures independent of the cortical surface reconstruction stream within the FreeSurfer pipeline in an additional exploratory ROI analysis. ROIs related to the auditory system or tinnitus (models) were chosen out of the available subcortical structures, which resulted in a set including bilateral amygdala [12], hippocampus [29], nucleus accumbens [12], and thalamus [32]. The uncorrected results and Bonferroniadjusted p-values are indicated in Table 7.…”

“…However, our analysis provided no evidence for a link between the subcallosal area and tinnitus-related distress. It is our view that the 'gating' model by Rauschecker and colleagues [12] provides an alternate and more plausible explanation. According to this model, tinnitus is the result of a dysfunction in a cortical-subcallosal-thalamic loop.…”

“…The TRN is meant to inhibit the auditory thalamus and, in so doing, to block the aversive sound from encountering the auditory cortex. In the terminology of Rauschecker and colleagues [12] the mechanism can be termed a 'tuning out' device that filters out the tinnitus signal. The model further proposes that in TI the integrity of the subcallosal circuit is disrupted, in which case the inhibiting projections of the TRN to the auditory thalamus are attenuated, and hence the tinnitus percept is relayed to the auditory cortex without hindrance.…”

“…Although previous research and treatment focused on the inner ear, it has since been widely accepted that tinnitus should not 10 be considered as a sole dysfunction of the ear, even though tinnitus is usually preceded by and associated with substantial to minor or even hidden peripheral hearing loss [6,7]. Instead, it has widely been agreed that tinnitus emanates from a perplexing network that includes the inner ear, the auditory pathway, and non-auditory brain areas [8,9,10,11,12]. 15 In particular, as there is presently no effective medical or psychological therapy available to cure tinnitus, it is of the utmost importance to better understand the sensory and cognitive mechanisms that directly or indirectly may result in alterations of cortical architecture.…”