After irreparable damage to inner hair cells a fraction of auditory signals are not conducted via the auditory pathway and hence do not arrive at the central auditory fields. As a function of this signal loss, neurons in the auditory cortex that are organized tonotopically and that are preferentially driven by specific auditory frequencies encoded by the damaged inner hair cells are rendered idle.
In the absence of incoming auditory signals, these neurons do not fire systematically. Within hours and days after partial hearing loss, however, the subtle balance of lateral inhibition and excitement of adjacent neuronal ensembles changes gradually and slightly.
This loss of balance results in increased firing of the deafferented neurons (Llinas, Urbano, Leznik, Ramirez, & van Marle, 2005) that is caused by a dysrhythmia of exciting and inhibiting thalamo-cortical circuits (Llinas, Ribary, Jeanmonod, Kronberg, & Mitra, 1999).
It is of utmost importance to note that in this understanding chronic tinnitus can be considered a neurogenic phenomenon comparable to chronic pain. The lateral disinhibition is fostered by a thalamo-cortical loop that simply responds to the dormancy of the deafferented neurons and that begins to "nudge" the idle brain cells to "get back to work".
This unsuccessful attempt of the thalamic nuclei to restore the former organization in the auditory cortex serves as an unfortunate example for a maladjusting process based on the neuroplastic nature of the brain.
For this reason tinnitus is often dubbed "the auditory phantom pain" as it results accidentally from the brain's fatal mistake to fix the "hiccup" of the auditory system.
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