Role of attention in the generation and modulation of tinnitus

Abstract

Neural mechanisms that detect changes in the auditory environment appear to rely on processes that predict sensory state. Here we propose that in tinnitus there is a disparity between what the brain predicts it should be hearing (this prediction based on aberrant neural activity occurring in cortical frequency regions affected by hearing loss and underlying the tinnitus percept) and the acoustic information that is delivered to the brain by the damaged cochlea. The disparity between the predicted and delivered inputs activates a system for auditory attention that facilitates through subcortical neuromodulatory systems neuroplastic changes that contribute to the generation of tinnitus. We review behavioral and functional brain imaging evidence for persisting auditory attention in tinnitus and present a qualitative model for how attention operates in normal hearing and may be triggered in tinnitus accompanied by hearing loss. The viewpoint has implications for the role of cochlear pathology in tinnitus, for neural plasticity and the contribution of forebrain neuromodulatory systems in tinnitus, and for tinnitus management and treatment.

Increased contralateral suppression of otoacoustic emissions indicates a hyperresponsive medial olivocochlear system in humans with tinnitus and hyperacusis

“…However, in our view, the plausibility of this scenario, in which hyperactivity/hyperresponsiveness develops separately in different neuronal pathways, is diminished by the present data, which add another (PVCN mediated) neural system with distinct innervation and neurochemistry to the list of those manifesting overactivation in tinnitus and low sound tolerance. In light of the existing data, it is worth considering a more parsimonious hypothesis, that overactivation of the auditory brain stem arises from forebrain-mediated neuromodulation broadly distributed throughout the brain stem, and for which there is evidence ; see also Geven et al 2014;Roberts et al 2013). We propose that the patterns of activity in ascending auditory brain stem pathways (e.g., spontaneous activity distribution across characteristic frequency) determine what tinnitus will sound like once heard, but for the tinnitus to be heard, those ascending activity patterns must have an attentional spotlight shone on them via top-down neuromodulation.…”

Tinnitus Suppression by Intracochlear Electrical Stimulation in Single-Sided Deafness: A Prospective Clinical Trial - Part I

“…The optimal stimuli for tinnitus suppression appear to be subject specific. However, medium-to-loud stimuli suppress tinnitus significantly better than soft stimuli, which partly can be ex-and a shift in the balance of excitatory and inhibitory neurotransmitters [Eggermont and Roberts, 2012;Roberts et al, 2013]. The current consensus is that tinnitus is the result of maladaptive plasticity in the central auditory pathway as a result of auditory deprivation [Engineer et al, 2011].…”

Alterations to the attention system in adults with tinnitus are modality specific

“…Recently, the attention network has become a focus of study in tinnitus research (Roberts et al, 2013). Attention is ubiquitous, yet elusive, in that it is difficult to measure or quantify (Fritz et al, 2007).…”

“…Tinnitus, then, may be caused by aberrant engagement of top-down attention, or abnormal bottom-up attention, wherein internal noise gains salience when the external environment is quiet. It may also be an interaction of the two processes, as argued in (Roberts et al, 2013), and further may implicate both an initial capture of attention and a later lack of dis-engagement in a timely fashion (Heeren et al, 2014). Based on the 'effortfulness' hypothesis of (Rabbitt, 1968), both hearing impairment and tinnitus may deplete attention resources thus leaving fewer attention resources for completing cognitive tasks.…”