Switching Tinnitus On or Off: The Role of the Anterior Cingulate Cortex

Background

Tinnitus is the perception of a sound without an external source — a “phantom sound” — that affects more than 10% of the population worldwide. While hearing loss is a major risk factor, not everyone with hearing loss develops tinnitus. This points to an additional, central factor in the brain that determines when tinnitus is “on” or “off.”
Previous studies suggest that the anterior cingulate cortex (ACC) — a region of the brain involved in emotion, attention, and control of sensory information — plays a key role in this. This research, conducted at BRAI3N in collaboration with Trinity College Dublin and Seoul National University, investigated how activity in specific parts of the ACC influences the onset or disappearance of tinnitus.

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Aim of the research

The aim of this study was to understand:

how brain activity changes when tinnitus is present or absent in the same person;

which areas of the brain function as an “on/off switch” for tinnitus;

how emotional stress or “distress” affects these mechanisms.

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Research design

Participants: 9 patients with intermittent tinnitus (periods with and without tinnitus) and 9 healthy control subjects with similar hearing loss but without tinnitus.

Measurement method: quantitative EEG (19-channel), recorded during a “tinnitus-on” and “tinnitus-off” state.

Major brain regions:

Pregenual anterior cingulate cortex (pGAcc)

Dorsal Anterior Cingulate Cortex (dACC)

Auditory cortex (Heschl's gyrus)

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Results

During the tinnitus-on condition:
Increased theta activity in the pregenual ACC

Impaired functional connectivity (theta) between pregenual ACC and auditory cortex

Increased gamma activity in the auditory cortex associated with perceived loudness

Increased alpha activity in the dorsal ACC associated with emotional distress

During the tinnitus-off condition:

Increase in alpha activity in the pregenual ACC

Enhanced alpha connectivity between pregenual ACC and auditory cortex

This condition is accompanied by temporary suppression of the phantom sound

“On/Off” mechanism:

The “activation” of tinnitus appears to be caused by a shift from alpha to theta in the PGAcc, which weakens the inhibitory control of the auditory cortex.

Tinnitus “shutting down” occurs when alpha activity increases in the pGAcc, inhibiting the auditory cortex.

Stress or emotional strain (regulated by the dACC) can upset this balance and trigger tinnitus.

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Conclusion

The results show that the anterior cingulate cortex acts as a central switch that determines whether tinnitus is detected or not.

The research suggests that:

• increased theta in the PGAcc triggers tinnitus (“on”),
• increased alpha in the PGAcc suppresses tinnitus (“off”),
• alpha in the dACC is associated with stress and distress.

This insight opens new perspectives for treatment via targeted neuromodulation or pharmacological stimulation that promotes alpha activity in the pGAcc and reduces alpha in the dACC.

The research also confirms that tinnitus and chronic pain share similar brain mechanisms, offering opportunities for broader therapeutic applications.