Recent research has summarized the following the model as one of the leading hypotheses behind the pathological basis of tinnitus:
A compelling hypothesis is that tinnitus results from a maladaptive plastic net down-regulation of inhibitory amino acid neurotransmission in the central auditory pathway. This loss of inhibition may be a compensatory response to loss of afferent input such as that caused by acoustic insult and/or age-related hearing loss, the most common causes of tinnitus in people. Compensatory plastic changes may result in pathologic neural activity that underpins tinnitus.
So basically, one of the current theories is a sequential step wise process:
Loss of auditory input from hearing damage or age related hearing loss
Compensatory loss of inhibitory neurotransmission in the auditory region of the brain
Subsequent further compensatory neuroplastic changes (a "re-wiring" of connections in the brain) cause tinnitus
The evidence for this hypothesis comes from both neurochemical studies and electrophysiological studies. Click here to check out the abstract!
Best,
AudioNotch
Northwell Health researchers randomized 65 tinnitus patients to AudioNotch or standard care and followed them for a year. The results, the caveats, and what they actually mean, with the full citation trail.
An honest, evidence-based ranking of every major sound therapy for tinnitus -- from CBT and hearing aids to notched sound therapy, bimodal neuromodulation, TRT, and more. What works, what might work, and what probably doesn't.
If tinnitus is created by the brain rewiring itself, can we fix it by rewiring the brain back? Two decades of research into neuroplasticity-based sound therapy -- from notched sound to bimodal neuromodulation -- are starting to provide answers.