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It is well known that loud noises can lead to hearing problems such as temporary hearing loss or tinnitus (ringing in the ears) and even permanent hearing loss. But this is the first time scientists have been able to identify damages to nerve cells as a result of noise exposure.

The research allows us to understand the pathway from exposure to loud noises to hearing loss. Dissecting the cellular mechanisms underlying this condition is likely to bring a very significant healthcare benefit to a wider population. The work will help prevention as well as progression into finding appropriate cures for hearing loss", said the lead researcher Dr. Martine Hamann, from the University of Leicester in the UK. (Hear-it.org, 2014)

Listening to tailor-made notched sound or notched music reduces tinnitus loudness and tinnitus-related auditory cortex activity (Okamoto, et al., 2010)

Abstract
Maladaptive auditory cortex reorganization may contribute to the generation and maintenance of tinnitus. Because cortical organization can be modified by behavioral training, we attempted to reduce tinnitus loudness by exposing chronic tinnitus patients to self-chosen, enjoyable music, which was modified (“notched”) to contain no energy in the frequency range surrounding the individual tinnitus frequency. After 12 months of regular listening, the target patient group (n = 8) showed significantly reduced subjective tinnitus loudness and concomitantly exhibited reduced evoked activity in auditory cortex areas corresponding to the tinnitus frequency compared to patients who had received an analogous placebo notched music treatment (n = 8). These findings indicate that tinnitus loudness can be significantly diminished by an enjoyable, low-cost, custom-tailored notched music treatment, potentially via reversing maladaptive auditory cortex reorganization.

enter image description here
(Image Source: Notched Music Therapy App for Android)

The hear-it.org website at the paged linked above says:

Loud music played on earphones causes hearing loss by having a similar effect on nerves as multiple sclerosis, research finds. The research shows that noise levels above 110 decibels strip insulation from nerve fibers carrying signals from the ear to the brain. Loss of the protective coating, called myelin, disrupts electrical nerve signals.

Looking for the source, it seems to be coming from John Von Radowitz's article within The Independent newspaper (2012), stating that:

Loud music played on earphones causes deafness by having a similar effect on nerves as multiple sclerosis (MS)

With both articles mentioning Dr. Martine Hamann from the University of Leicester, I found that she was involved with three studies in that year.

The article which seems to be related is Pilati, et al. (2012), which states within the abstract:

Here we investigate mechanisms contributing to excitability changes in the dorsal cochlear nucleus (DCN) shortly after exposure to loud sound that produces hearing loss. We show that acoustic overexposure alters synaptic transmission originating from the auditory and the multisensory pathway within the DCN in different ways. A reduction in the number of myelinated auditory nerve fibers leads to a reduced maximal firing rate of DCN principal cells, which cannot be restored by increasing auditory nerve fiber recruitment. In contrast, a decreased membrane resistance of DCN granule cells (multisensory inputs) leads to a reduced maximal firing rate of DCN principal cells that is overcome when additional multisensory fibers are recruited. Furthermore, gain modulation by inhibitory synaptic transmission is disabled in both auditory and multisensory pathways. These cellular mechanisms that contribute to decreased cellular excitability in the central auditory pathway are likely to represent early neurobiological markers of hearing loss and may suggest interventions to delay or stop the development of hyperactivity that has been associated with tinnitus.

The following is also in the article:

Acoustic overexposure (AOE):

  • induces hearing threshold elevations (shifts of hearing thresholds of 20–30 dB sound pressure level were observed for frequencies above the frequency used during the AOE protocol),
  • decreases fusiform cell excitability,
  • down-regulates auditory nerve (AN) and multi-sensory (MS) synaptic transmission to fusiform cells (FCs)
  • reduces FC maximal firing rate upon AN stimulations
  • decreases the number of myelinated AN fibres in the cochlea
  • reduces FC maximal firing rate upon MS input stimulation and
  • decreases granule cell membrane resistance
  • disables FC gain control by inhibitory synaptic transmission

Auditory Nerve stimulations

article fig.1 B

AN stimulations (25 V, 0.3 Hz) trigger smaller Excitatory post-synaptic potentials after AOE (blue)). Membrane potential was −70 mV. Histogram summarizes excitatory post-synaptic potential amplitudes measured at similar stimulating voltages in unexposed (25 ± 4 V, n = 4) and exposed conditions (28 ± 2 V, n = 6). * P < 0.05,

article fig.1 C

In unexposed condition (black), AN stimulations (40 V, 0.3 Hz) trigger action potentials in a FC (membrane potential of −60 mV). After AOE (blue), AN stimulations (40–45 V, 0.3 Hz) fail to trigger action potentials.

Multisensory stimulations

article fig.1 E

MS stimulations (15 V, 0.3 Hz) trigger smaller excitatory post-synaptic potentials after AOE (blue). Membrane potential was −70 mV. Histogram summarizes excitatory post-synaptic potential amplitudes measured at similar stimulating voltages in unexposed (16 ± 1 V, n = 8) and exposed conditions (19 ± 2 V, n = 6). ** P < 0.01: unpaired t tests.

article fig.1 F

In unexposed condition (black), MS stimulations (20 V, 0.3 Hz) trigger action potentials in a FC (membrane potential of −60 mV). After AOE (blue), higher stimulation voltages (25 V, 0.3 Hz) are required to trigger an action potential.

Not having a background in neurology, I am wondering if altered synaptic transmission originating from the auditory and the multisensory pathway within the DCN equates to brain damage or is the altered synaptic transmission caused by information received from the damaged cochlea?

In other words, has it really been found that the cause of Tinnitus is brain damage which can be repaired through playing sounds or music with a "notch" in specific frequency spectrums?

References

Hear-it.org (2014) Loud music damages the nerves in the brain [Online]
Available from: https://www.hear-it.org/loud-music-damages-nerves-brain

Okamoto, H., Stracke, H., Stoll, W., & Pantev, C. (2010). Listening to tailor-made notched music reduces tinnitus loudness and tinnitus-related auditory cortex activity. Proceedings of the National Academy of Sciences, 107(3), 1207-1210.
DOI: 10.1073/pnas.0911268107

Pilati, N., Ison, M. J., Barker, M., Mulheran, M., Large, C. H., Forsythe, I. D., ... & Hamann, M. (2012). Mechanisms contributing to central excitability changes during hearing loss. Proceedings of the National Academy of Sciences, 109(21), 8292-8297.
DOI: 10.1073/pnas.1116981109

Radowitz J. V. (2012). Loud music played on headphones causes deafness by having a similar effect on nerves as multiple sclerosis (MS) - The Independent
Available at: https://www.independent.co.uk/life-style/health-and-families/health-news/loud-music-on-headphones-causes-deafness-by-having-a-similar-effect-on-nerves-as-ms-8091683.html

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Short answer
Sensory tinnitus is not caused by brain damage, but is due to degeneration of peripheral auditory neurons, and specifically the hair cells in the inner ear.

Background
Tinnitus can be either somatic or sensory in nature. You are enquiring on the latter type here.

Sensory tinnitus is generally associated with sensorineural hearing loss (HL), meaning that the mechanosensory cells, the hair cells (HCs) in the inner ear (cochlea) have been damaged. When this is a permanent ailment, the auditory nerve fibers (ANFs) connected to the HCs may degenerate and the auditory cortex becomes deprived of stimuli. A commonly encountered hypothesis is that the deafferented cortical cells start to actively seek new input (it's also possible that something similar happens in brainstem auditory nuclei; you could perhaps call this "damage" but it would be better described as dysfunction). They might be recruited for visual processing in the process, or they may actually generate endogenous activity on their own. Typically this results in tinnitus corresponding to the frequencies that are lost in the cochlea. This is caused by the tonotopy that is maintained from cochlea up to the primary auditory cortex (for a review see Møller (2016).

To get to your question - the auditory cortex and DCN are not damaged by sensorineural HL. The DCN receives input from the AN. While the HCs and AN are known to degenerate after prolonged HL, more central nuclei and cortical structures do not. They may become remapped but they won't regress.

Therapies for tinnitus often involves the fitting of hearing aids to reestablish input to the auditory system, or masking the sounds that are generated internally by external stimuli, such as pink noise or simply listening to music. Often psychologists get involved in severe cases to deliver coping strategies to the patient. Severe tinnitus cases are associated with considerable suffering, depression and increased chance of suicide.

Early surgical interventions included the severing of the AN, as they thought tinnitus arose peripherally. This made the situation, obviously, often only worse. Currently cochlear implantation is also considered experimentally to reestablish input to the auditory system by means of electrical stimulation (Baguley & Atlas, 2007).

References
- Baguley & Atlas, Progr Brain Res (2007);166: 347-55
- Møller, Int J Otolaryngol (2016): 2830157

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