A3 Tinnitus: Abnormal Spontaneous Neural Activity

Topic

When peripheral hearing loss reduces the signal strength transmitted by auditory nerve fibers to the brain, the central auditory pathway—the series of neural relays carrying the signal from the inner ear to the auditory cortex—receives fewer impulses than it did prior to the loss. The central auditory pathway does not merely transmit incoming information passively; each of its neurons constantly integrates excitatory influences (which promote firing) and inhibitory influences (which suppress it). Consequently, the pathway's baseline activity level—its rate of firing in the absence of actual external sound—depends on the balance between these two opposing forces.

When peripheral loss causes a sustained reduction in impulses reaching the central auditory pathway, the pathway attempts to restore its baseline activity level by reducing inhibition and increasing excitation acting upon its neurons—an adjustment that partially compensates for the signal no longer received from the periphery. This shift in balance—less inhibition, more excitation—constitutes "central gain." The longer the peripheral loss persists, the further the balance tips toward excitation, as the central auditory pathway continually strives to regain its pre-loss baseline activity level without ever fully succeeding (since the diminished peripheral signal does not spontaneously recover). Thus, the cycle initiated by the peripheral loss is perpetuated by the pathway's repeated attempts to restore its baseline activity.

This excess of excitation over inhibition does not remain confined within the central auditory pathway awaiting an actual sound; instead, it triggers spontaneous firing—independent of external acoustic stimulation—thereby generating abnormal spontaneous neural activity that either did not exist or went unnoticed prior to the peripheral loss. The greater the accumulated central gain, the higher the rate of this abnormal spontaneous neural activity; as this activity travels along the central auditory pathway to the auditory cortex, it undergoes processing through the exact same stages that would process a real external sound.

Upon reaching the auditory cortex via the same pathway used by a real external sound, this abnormal spontaneous neural activity is interpreted as an internal signal equivalent to a sound: tinnitus. Since the auditory cortex does not distinguish the origin of the signal it receives, it assigns this equivalent internal signal the same perceptual attributes it would assign to an external sound; consequently, the tinnitus possesses a perceptible frequency and level, even though no physical external sound exists to produce them. The frequency and level of this equivalent internal signal are quantified by asking the individual to match it—through repeated adjustments—to a real external sound with a fixed, measurable frequency and level, until both signals are perceived as identical.

Because the origin of this equivalent internal signal lies in an imbalance between inhibition and excitation within the central auditory pathway—rather than in an external sound—none of the available corrections directly reverses the peripheral loss that triggered it. Masking introduces a real external sound that competes with the equivalent internal signal at the same stages of the central auditory pathway, causing the latter to blend into the background activity rather than standing out. Tinnitus Retraining Therapy combines this masking principle with long-term work on the central auditory pathway and the brain areas that assign emotional significance to perceptions; the goal is for the equivalent internal signal to cease capturing the individual's attention, even while the abnormal spontaneous neural activity generating it persists. Cognitive therapy, meanwhile, does not target the central auditory pathway itself but rather the individual's reaction to the equivalent internal signal, thereby reducing the resulting distress without altering the underlying neuronal activity.

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