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A Protocol for the Administration of Real-Time fMRI Neurofeedback Training

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Day-night hyperarousal in tinnitus patients.

Xiaoyu Bao¹, Xueji Feng¹, Haiyun Huang²

¹School of Automation Science and Engineering, South China University of Technology, Guangzhou, 510641, China; Research Center for Brain Machine Intelligence, Pazhou Lab, Guangzhou, 510005, China.

|April 22, 2025

Summary

Tinnitus patients exhibit persistent hyperarousal, affecting brain activity during wakefulness and sleep. This hyperarousal impairs sleep regulation and neuroplasticity, suggesting sleep as a key therapeutic target.

Keywords:

Gamma Hyperarousal Sleep Tinnitus

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Area of Science:

Neuroscience
Sleep Medicine
Audiology

Background:

Tinnitus affects 12-30% of the population, often causing sleep disturbances and daytime dysfunction.
The neural mechanisms linking wakefulness and sleep in tinnitus remain unclear.
Understanding these mechanisms is crucial for developing effective treatments.

Purpose of the Study:

To investigate electroencephalographic (EEG) characteristics in tinnitus patients and controls across wakefulness and sleep stages.
To clarify the day-night pathological mechanisms underlying tinnitus.
To explore the relationship between hyperarousal, sleep structure, and state regulation in tinnitus.

Main Methods:

Electroencephalography (EEG) recordings were performed on 51 tinnitus patients and 51 controls.
EEG data were analyzed across different wake states (eyes-open, eyes-closed, mental arithmetic) and sleep stages (N1, N2, N3, REM).
Analysis included power spectrum analysis (gamma, beta, delta, theta) and sleep structure assessment.

Main Results:

Tinnitus patients showed persistent hyperarousal, with enhanced gamma power during wakefulness and elevated gamma/beta power during sleep.
Reduced delta/theta power in deep sleep (N2/N3) and impaired N2 stage stability were observed in tinnitus patients.
Group-by-state interactions indicated deficient state regulation capacity, with wake-related gamma/beta activity aberrantly integrated into non-rapid eye movement sleep.

Conclusions:

Tinnitus is associated with a loss-of-inhibition mechanism extending into sleep, impairing sleep-dependent neuroplasticity.
Deficient low-frequency oscillations fail to suppress hyperarousal, perpetuating daytime tinnitus symptoms.
Targeting sleep may be critical for interrupting the 24-hour cycle of tinnitus dysfunction.