In conclusion, all indications are that tinnitus, when not caused directly by a central nervous system issue (e.g., stroke), is always associated with one or more forms of hearing loss. As a result, although a treatment of most forms of tinnitus will likely emerge in the years to come, curing tinnitus will first require curing hearing loss."
Getting back to the discussion at hand: the problem I have with the idea of hearing restoration completely eradicating tinnitus is that there's no evidence that it will disrupt the network effect that a tinnitus brain usually develops. I think it will be better perceived with hearing aids and cochlear implants because you are improving the signal-to-noise ratio. Just the same as if you use earplugs; your tinnitus is going to rocket in volume for the reverse reason.
Most research indicates that tinnitus is generated by the brain when hearing loss occurs. Numerous imaging studies show this network effect, or centralisation, as some call it. Fatima Husain is a well-known researcher, and her work shows that there are key differences in the emotional centres of the brain of those with tinnitus compared with controls. There's also been observed differences in the white matter of the brain of those with chronic tinnitus. These are physical differences. The precuneus may also be involved in how tinnitus is perceived. Again, imaging studies have shown that it acts differently in tinnitus brains compared to non-tinnitus brains.
The precuneus is connected to the dorsal attention network and the default mode network which both do completely opposite jobs. The dorsal attention network is active when we are engaged and concentrating on something whereas the default mode network is active when our mind is at rest. When one network is active the other is switched off. The precuneus may be a possible marker. I believe the idea is that some tinnitus brains may struggle to switch off and are always at attention. This could be correlated to tinnitus patients' lack of concentration and inability to sleep.
In that study, we compared a group of patients with mild tinnitus who had developed tinnitus recently, having had their percept for > 6 months but less than one year, to another group of patients with mild tinnitus that had their tinnitus for > one year. We examined three resting-state networks (the DMN, dorsal attention, and auditory networks) and the only significant result was found in the DMN; patients with long-term tinnitus had decreased connectivity between seed regions and the precuneus when compared to the recent-onset group. This finding echoes the results found by Schmidt et al. (2013), which compared the same long-term group from Carpenter-Thompson et al. (2015) to control groups without tinnitus, and suggests that this disruption to the DMN is not immediate but occurs over time in patients.
In the current study, we examined an additional tinnitus characteristic's effect on resting-state connectivity: tinnitus severity. Tinnitus severity in resting-state studies has been variable, ranging from mild to catastrophic (Husain and Schmidt, 2014); it could therefore help to explain the differing results. The existing literature seems to suggest that tinnitus severity has a significant impact on the resting state.
There's also an impact on the resting state:
Results: Data were included from nine resting-state neuroimaging studies that reported a total of 51 distinct foci. The meta-analysis identified consistent regions of increased resting-state brain activity in tinnitus patients relative to controls that included, bilaterally, the insula, middle temporal gyrus (MTG), inferior frontal gyrus (IFG), parahippocampal gyrus, cerebellum posterior lobe and right superior frontal gyrus. Moreover, decreased brain activity was only observed in the left cuneus and right thalamus.
Resting-State Brain Abnormalities in Chronic Subjective Tinnitus: A Meta-Analysis
There's a stack of research indicating other areas of the brain's involvement, particularly emotional memory. The caudate nucleus, which is involved with learning, memory, reward, motivation, emotion, and romantic interaction, etc, is also linked in many studies. I find this deep brain stimulation study quite interesting:
Results: Acute tinnitus loudness reduction was observed at 5 caudate locations, 4 positioned at the body and 1 at the head of the caudate nucleus in normalized Montreal Neurological Institute space. The remaining 15 electrical stimulation interrogations of the caudate head failed to reduce tinnitus loudness. Compared to the caudate head, the body subdivision had stronger functional connectivity to the auditory cortex on fMRI (p < 0.05).
Conclusions: Acute tinnitus loudness reduction was more readily achieved by electrical stimulation of the caudate nucleus body. Compared to the caudate head, the caudate body has stronger functional connectivity to the auditory cortex. These first-in-human findings provide insight into the functional anatomy of caudate nucleus subdivisions and may inform future target selection in a basal ganglia-centric neuromodulation approach to treat medically refractory tinnitus.
Human caudate nucleus subdivisions in tinnitus modulation
I think once tinnitus is centralised, there are too many neural networks involved for hearing restoration to eliminate it. My opinion is that something else will be needed to disrupt the network. However, as I stated at the beginning, I think restoring one's hearing will always work to improve the signal-to-noise ratio. It should always improve the perception to some degree.
We need to figure out is what is causing the maladaptive plasticity and find ways to reverse it.
EDIT:
I was in a bit of a rush writing the above as I had to get my daughter ready for nursery. I want to add further detail by adding more relevant information. I've highlighted parts in bold, but you should read it all because it would make for an interesting debate.
Tinnitus is a common auditory perceptual disorder whose neural substrates are under intense debate. One physiologically based model posits the dorsal striatum to play a key role in gating auditory phantoms to perceptual awareness. Here, we directly test this model along with the roles of auditory and auditory-limbic networks in tinnitus non-invasively by comparing resting-state fMRI functional connectivity patterns in chronic tinnitus patients against matched control subjects without hearing loss. We assess resting-state functional connectivity of the caudate dorsal striatum (area LC), caudate head (CH), nucleus accumbens (NA), and primary auditory cortex (A1) to determine patterns of abnormal connectivity. In chronic tinnitus, increases in ipsilateral striatal–auditory cortical connectivity are found consistently only in area LC. Other patterns of increased connectivity are as follows: (1) right striatal area LC, A1, CH, and NA with parietal cortex, (2) left and right CHs with dorsal pre-frontal cortex, (3) NA and A1 with cerebellum, hippocampus, visual and ventral pre-frontal cortex. Those findings provide further support for a striatal gating model of tinnitus, where dysfunctionally permissive area LC enables auditory phantoms to reach perceptual awareness.
A recent development is the striatal gating model (Larson and Cheung, 2012), which hypothesizes the caudate nucleus to act as a gating mechanism for tinnitus awareness. The striatal gating model is physiologically based, motivated by electrical stimulation experiments in dorsal striatal area LC, located at the junction of the head and body of the caudate nucleus, on awake and interactive humans. Direct stimulation of area LC during deep brain stimulation (DBS) surgery in movement disorders patients with comorbid chronic tinnitus modulates auditory phantom loudness (Cheung and Larson, 2010) and triggers auditory phantom percepts in HL patients without tinnitus (Larson and Cheung, 2012). Furthermore, vascular infarction of area LC results in enduring tinnitus loudness suppression (Larson and Cheung, 2013). According to this model, dysfunctional corticostriatal connections between the dorsal striatum and auditory cortex act as a pathway for auditory phantom representations to reach perceptual awareness. The normally restrictive dorsal striatum becomes pathologically permissive in chronic tinnitus. Although the physiological mechanisms are not clear, it has been proposed that alteration in the balance of excitation and inhibition either within the caudate or in its connections to auditory cortex modulates this permissiveness (Calabresi et al., 2000; Goubard et al., 2011)
Increased striatal functional connectivity with auditory cortex in tinnitus
This is from an article, with Winfried Schlee, that caught my attention many years ago:
It's not just the auditory cortex that is affected when people get tinnitus. Neuroscientists, using increasingly sophisticated brain scans, are finding that changes ripple out across the entire brain. Winfried Schlee of the University of Konstanz in Germany and his colleagues have been making some of the most detailed studies of tinnitus ever, using a method called magnetoencephalography (MEG, for short). They take advantage of the fact that every time neurons send each other signals, their electric current creates a tiny magnetic field. MEG allows scientists to detect such changing patterns of activity in the brain 100 times per second.
Schlee and his colleagues find widespread differences in the brains of people with tinnitus and those without it. A network of regions in the brains of people with tinnitus tend to fire their neurons in sync. Schlee has determined that his tinnitus-stricken subjects have a more synchronized pattern of signals coming out of regions in the front and the back of the brain. (For brain anatomy junkies, they are the dorsolateral prefrontal cortex, orbitofrontal cortex, and anterior cingulate cortex in the front; in the back, they are the precuneus and posterior cingulate cortex.) Schlee and his colleagues also discovered a more strongly synchronized flow of signals coming into the temporal cortex — a region that includes the auditory cortex — in people with tinnitus.
When Schlee compared people who suffer a lot of distress from tinnitus with those who are not much bothered by it, he found that the more distress people felt, the stronger the flow of signals out of the front and back of the brain and into the temporal cortex. This pattern suggests that the network Schlee discovered is important for the full experience of tinnitus. Tinnitus, in other words, extends beyond the ear, beyond a hearing-specialized part of the brain, beyond even any single piece of neural real estate. It is a disease of networks that span the brain.
Clearly the auditory cortex is just an early stop on the journey that sound takes from the outside world to our awareness. Some neurons in the auditory cortex extend branches down to the brain stem, where they link to a pair of regions called the caudate nucleus and putamen. Those regions may be important for processing the signals in several ways, such as categorizing sounds.
Once signals travel from the ear to the auditory cortex, caudate, and putamen, they eventually make their way to regions of the brain that carry out more sophisticated sound information processing: connecting the sounds with memories, interpreting their meaning, giving them emotional significance. It is precisely these regions that Schlee and his colleagues noted were behaving strangely in people with tinnitus. He argues that it is only when signals reach this large-scale network that we become conscious of sounds, and it is only at this stage that tinnitus starts to cause people real torment. Schlee's results suggest that the higher regions of the brain send their own feedback to the auditory cortex, amplifying its false signals. Schlee's model of tinnitus and consciousness could explain some curious observations. Even in bad cases of tinnitus, people can become unaware of the phantom sound if they are distracted. It may be that distractions deprive the errant signals from the auditory cortex of the attention they need to cause real distress. What's more, some of the most effective treatments for tinnitus appear to work by altering the behavior of the front of the brain.
I found this part very interesting:
As a young man, Lowry spent a summer working on a farm with a noisy tractor. The experience left him with partial hearing loss and a high-pitched ringing in his ears that plagued him for 40 years. Then at age 63, Lowry suffered a mild stroke. A CT scan and an MRI revealed that the stroke had damaged his caudate and putamen. But the stroke also brought a pleasant surprise. Lowry was completely cured of his tinnitus, without any further hearing loss.
The Brain: "Ringing in the Ears" Actually Goes Much Deeper Than That