14Mechanism: Central Gain and Cortical Plasticity

FCentral gain: the brain’s automatic volume control

Faced with reduced cochlear input, the central auditory system does what any feedback system does when a signal weakens: it amplifies. This homeostatic up-regulation of neural responsiveness is called central gain [2014]. The intended benefit is to restore the loudness of real sounds; the unintended cost is that residual spontaneous activity and neural noise are amplified too, surfacing as tinnitus and often hyperacusis.

The analogy clinicians find most useful is phantom-limb pain: an amputated limb still “hurts” because the deprived cortex remains active. A deafferented auditory system likewise hears a sound that has no external source [2016].

TTonotopic reorganisation and the edge effect

The auditory cortex is mapped tonotopically. When a band of frequencies is deafferented, the cortical territory that used to represent those frequencies does not fall silent — it is invaded by, and begins responding to, the neighbouring intact frequencies [2004]. This over-representation of the lesion-edge frequencies concentrates excitation there.

The result is a hyperexcitable cortical zone tuned near the audiometric edge — consistent with tinnitus pitch typically matching that edge region. Map plasticity thus converts a peripheral hole into a central hotspot [2016].

CThalamocortical dysrhythmia

At the network level, deafferentation shifts thalamic relay neurons from their normal tonic firing into low-frequency burst mode. Llinás and colleagues described how this produces a pathological resting rhythm: excess slow (theta) and high (gamma) oscillation with a loss of normal alpha — thalamocortical dysrhythmia [2005].

In tinnitus, EEG and MEG studies find this signature over auditory cortex, with the persistent gamma activity proposed as the oscillatory correlate of the conscious percept [2016]. The same framework explains other deafferentation phantoms, including neuropathic pain.

CThe limbic system: loudness versus distress

Why are some patients with faint tinnitus devastated while others with loud tinnitus barely notice it? Because loudness and distress are processed by different circuits. Imaging shows that bothersome tinnitus recruits the amygdala, anterior cingulate cortex and other limbic and autonomic structures, with strengthened connectivity to auditory cortex [2010].

The auditory percept may be generated centrally, but it is the emotional appraisal that determines suffering and, through reinforcement, chronicity [2016].

TThe neurophysiological model: tying it together

Jastreboff’s neurophysiological model unifies these strands. Cochlear deafferentation generates a weak neural signal; subcortical detection and pattern-matching amplify it; and the limbic and autonomic systems attach negative emotional value, creating a self-reinforcing loop that drives attention back to the sound and prevents habituation [1990].

This model is more than theory: it is the explicit rationale for tinnitus retraining therapy, whose goal is to break the auditory–limbic conditioning so the brain can habituate to the phantom signal [2016].