Neural plasticity due to hearing loss results in tonotopic map changes. Several studies have suggested a relation between hearing loss-induced tonotopic reorganization and tinnitus. This large fMRI study on humans was intended to clarify the relations between hearing loss, tinnitus, and tonotopic reorganization. To determine the differential effect of hearing loss and tinnitus, both male and female participants with bilateral high-frequency hearing loss, with and without tinnitus, and a control group were included. In a total of 90 participants, bilateral cortical responses to sound stimulation were measured with loudness-matched pure-tone stimuli (0.25-8 kHz). In the bilateral auditory cortices, the high-frequency sound-evoked activation level was higher in both hearing-impaired participant groups, compared with the control group. This was most prominent in the hearing loss group without tinnitus. Similarly, the tonotopic maps for the hearing loss without tinnitus group were significantly different from the controls, whereas the maps of those with tinnitus were not. These results show that higher response amplitudes and map reorganization are a characteristic of hearing loss, not of tinnitus. Both tonotopic maps and response amplitudes of tinnitus participants appear intermediate to the controls and hearing loss without tinnitus group. This observation suggests a connection between tinnitus and an incomplete form of central compensation to hearing loss, rather than excessive adaptation. One implication of this may be that treatments for tinnitus shift their focus toward enhancing the cortical plasticity, instead of reversing it.SIGNIFICANCE STATEMENTTinnitus, a common and potentially devastating condition, is the presence of a “phantom” sound that often accompanies hearing loss. Hearing loss is known to induce plastic changes in cortical and subcortical areas. Although plasticity is a valuable trait that allows the human brain to rewire and recover from injury and sensory deprivation, it can lead to tinnitus as an unwanted side effect. In this large fMRI study, we provide evidence that tinnitus is related to a more conservative form of reorganization than in hearing loss without tinnitus. This result contrasts with the previous notion that tinnitus is related to excessive reorganization. As a consequence, treatments for tinnitus may need to enhance the cortical plasticity, rather than reverse it.

Hyperacusis, a hypersensitivity to sounds of mild to moderate intensity, has been related to increased neural gain along the auditory pathway. To date, there is still uncertainty on the neural correlates of hyperacusis. Since hyperacusis often co-occurs with hearing loss and tinnitus, the effects of the three conditions on cortical and subcortical structures are often hard to separate. In this fMRI study, two groups of hearing loss and tinnitus participants, with and without hyperacusis, were compared to specifically investigate the effect of the latter in a group that often reports hyperacusis. In 35 participants with hearing loss and tinnitus, with and without hyperacusis as indicated by a cut-off score of 22 on the Hyperacusis Questionnaire (HQ), subcortical and cortical responses to sound stimulation were investigated. In addition, the frequency tuning of cortical voxels was investigated in the primary auditory cortex. In cortical and subcortical auditory structures, sound-evoked activity was higher in the group with hyperacusis. This effect was not restricted to frequencies affected by hearing loss but extended to intact frequencies. The higher subcortical and cortical activity in response to sound thus appears to be a marker of hyperacusis. In contrast, the response to the tinnitus frequency was reduced in the group with hyperacusis. This increase in subcortical and cortical activity in hyperacusis can be related to an increase in neural gain along the auditory pathway, and the reduced response to the tinnitus frequency to differences in attentional resources allocated to the tinnitus sound.

The impact of age-related hearing loss extends beyond the auditory pathway and impacts brain areas related to cognitive impairment and even dementia. The presence of tinnitus, a sensation of sound that frequently co-occurs with hearing loss, is additionally linked to cognitive decline. Interestingly, structural neuroimaging studies have reported that hearing loss may precede or modulate the onset of cognitive impairment. In this study, we aimed to disentangle the effects of age, hearing loss, and tinnitus on gray matter structure. In total, 39 participants with hearing loss and tinnitus, 21 with hearing loss but without tinnitus, and 39 controls were included in this voxel- and surface-based morphometry MRI study. Whole brain volume and surface thickness measures were compared between the groups. Age-related gray matter volume decline was observed in all groups. Several brain areas showed smaller gray matter volume and cortical surface thickness in hearing loss without tinnitus, relative to controls. This reduction was observed both within and outside of the auditory pathway. Interestingly, these reductions were not observed in participants with tinnitus, who had similar hearing loss and were of similar age. Since we have tools to improve hearing loss, hearing screening may aid in the battle against cognitive decline.

Age-related hearing loss is the most prevalent sensory impairment in the older adult population and is related to noise-induced damage or age-related deterioration of the peripheral auditory system. Hearing loss may affect the central auditory pathway in the brain, which is a continuation of the peripheral auditory system located in the ear. A debilitating symptom that frequently co-occurs with hearing loss is tinnitus. Strikingly, investigations into the impact of acquired hearing loss, with and without tinnitus, on the human central auditory pathway are sparse. This study used diffusion-weighted imaging (DWI) to investigate changes in the largest central auditory tract, the acoustic radiation, related to hearing loss and tinnitus. Participants with hearing loss, with and without tinnitus, and a control group were included. Both conventional diffusion tensor analysis and higher-order fixel-based analysis were applied. The fixel-based analysis was used as a novel framework providing insight into the axonal density and macrostructural morphologic changes of the acoustic radiation in hearing loss and tinnitus. The results show tinnitus-related atrophy of the left acoustic radiation near the medial geniculate body. This finding may reflect a decrease in myelination of the auditory pathway, instigated by more profound peripheral deafferentation or reflecting a preexisting marker of tinnitus vulnerability. Furthermore, age was negatively correlated with the axonal density in the bilateral acoustic radiation. This loss of fiber density with age may contribute to poorer speech understanding observed in older adults.SIGNIFICANCE STATEMENTAge-related hearing loss is the most prevalent sensory impairment in the older adult population. Older individuals are subject to the cumulative effects of aging and noise exposure on the auditory system. A debilitating symptom that frequently co-occurs with hearing loss is tinnitus: the perception of a phantom sound. In this large DWI-study, we provide evidence that in hearing loss, the additional presence of tinnitus is related to degradation of the acoustic radiation. Additionally, older age was related to axonal loss in the acoustic radiation. It appears that older adults have the aggravating circumstances of age, hearing loss, and tinnitus on central auditory processing, which may partly be because of the observed deterioration of the acoustic radiation with age.

Objective: We conducted a retrospective review of medical records of tinnitus patients at a tertiary ENT clinic in Groningen, Netherlands. Our goal was to identify factors that differentiated the intermittent subgroup from the larger continuous group with chronic tinnitus. Design: Tinnitus-related factors such as hearing loss, emotional aspects, and demographics were used to advance our understanding of the subgroups. We analysed the data using descriptive statistics and binomial logistic regression, supplemented by random forests classification. Study sample: Patients presenting with tinnitus visiting the tinnitus clinic. We examined 1575 medical intake records obtained at a tertiary ENT hospital. Results: Duration, total Tinnitus Handicap Inventory (THI), and THI Functional subscale scores differed significantly between the two groups. Increasing age and higher THI Emotional subscale scores were associated with an increased likelihood of intermittent tinnitus. Increases in duration, depressive scores and THI Functional and Catastrophic subscale scores, decreased the likelihood of intermittent tinnitus. Conclusions: Results from this study dissociate the factors affecting those with intermittent and those with continuous tinnitus and point to potentially different mechanisms underlying the two conditions.

The neuronal mechanisms underlying tinnitus are yet to be revealed. Tinnitus, an auditory phantom sensation, used to be approached as a purely auditory domain symptom. More recently, the modulatory impact of non-auditory brain regions on the percept and burden of tinnitus are explored. The thalamus is uniquely situated to facilitate the communication between auditory and non-auditory subcortical and cortical structures. Traditionally, animal models of tinnitus have focussed on subcortical auditory structures, and research with human participants has been concerned with cortical activity in auditory and non-auditory areas. Recently, both research fields have investigated the connectivity between subcortical and cortical regions and between auditory and non-auditory areas. We show that even though the different fields employ different methods to investigate the activity and connectivity of brain areas, there is consistency in the results on tinnitus between these different approaches. This consistency between human and animals research is observed for tinnitus with peripherally instigated hearing damage, and for results obtained with salicylate and noise-induced tinnitus. The thalamus integrates input from limbic and prefrontal areas and modulates auditory activity via its connections to both subcortical and cortical auditory areas. Reported altered activity and connectivity of the auditory, prefrontal, and limbic regions suggest a more systemic approach is necessary to understand the origins and impact of tinnitus.