Tinnitus is the perception of sound, like ringing or buzzing, when no external source is present. While many people experience this phantom noise constantly, others deal with a fluctuating form that appears and disappears without clear warning. This intermittent experience is distinct from chronic ringing because its underlying triggers are temporary. The variability points to transient physical issues, systemic body changes, and the brain’s own neurological mechanisms that govern perception.
Mechanical Factors Near the Ear
The temporomandibular joint (TMJ), which connects the jaw to the skull, is located near the ear canal. Dysfunction here is a common source of fluctuating tinnitus due to shared nerve pathways and muscular connections with the middle ear. A ligament links the jawbone to the malleus, a tiny bone in the middle ear, meaning jaw movement or muscle tension can mechanically influence the auditory system. Activities like clenching or grinding temporarily alter the tension on these shared structures, causing the phantom sound to appear or intensify until the muscle relaxes.
Other local physical factors involve changes within the ear canal, such as cerumen (earwax) buildup. A partial or shifting earwax blockage can dampen the transmission of external sounds to the eardrum. This reduction in environmental noise allows the brain to focus more acutely on the internally generated tinnitus signal, making it more noticeable. The sound quickly disappears when the wax shifts away from the eardrum or is manually cleared.
Changes in middle ear pressure, known as Eustachian tube dysfunction (ETD), also create temporary tinnitus. The Eustachian tube equalizes pressure between the middle ear and the outside air. When this tube becomes blocked by inflammation from allergies, a cold, or rapid altitude changes, pressure builds behind the eardrum. This pressure alteration changes the eardrum’s ability to vibrate normally, which can induce or silence the tinnitus perception until the tube reopens and the pressure is normalized.
Physiological and Systemic Triggers
Body-wide physiological states are powerful triggers for fluctuating tinnitus, particularly stress and anxiety. These states initiate the release of stress hormones, such as cortisol and adrenaline, which put the nervous system into a state of hyper-alertness. This heightened nervous activity increases overall sensory perception and auditory sensitivity, causing the existing neural noise perceived as tinnitus to be amplified. The ringing or buzzing often spikes acutely during stressful periods and then recedes when the emotional and chemical state normalizes.
Changes in the circulatory system can cause pulsatile tinnitus, which sounds like a whooshing or a heartbeat. Temporary increases in blood pressure or blood flow velocity, often following intense exercise or high sodium intake, can make the sound of blood moving through vessels near the ear audible. This increased flow velocity creates turbulence that is picked up by the cochlear structures. This turbulent flow resolves as the body’s circulatory system stabilizes, causing the pulsatile sound to disappear.
Certain substances and prescription drugs can create transient spikes in the phantom sound. Some medications are considered ototoxic, meaning they can disrupt the function of the cochlear nerve or inner ear blood supply. Examples include high-dose aspirin, certain antibiotics, and some classes of blood pressure medications like diuretics and ACE inhibitors. Tinnitus fluctuation correlates directly with the drug’s peak concentration in the bloodstream before it is metabolized.
Beyond prescription drugs, common dietary stimulants play a role in temporal fluctuation. Excessive caffeine and alcohol are known to affect blood flow to the inner ear or increase general nervous system excitability. These substances can reduce the auditory system’s ability to dampen internal noise, leading to a temporary increase in tinnitus intensity. This effect is dose-dependent, meaning a small change in consumption can lead to a quick fluctuation in the perceived noise.
The Brain’s Role in Turning the Sound Off
The cessation of intermittent tinnitus is rooted in how the brain handles internal noise. The auditory system constantly generates background neural signals, and the brain is equipped with a powerful ability for neural filtering. When the temporary tinnitus signal is weak, the brain eventually learns to categorize it as unimportant background noise, a process called habituation. This allows the brain to suppress the perception, making the sound disappear even if the underlying neural activity remains.
The perception of tinnitus is highly dependent on cognitive load and attention, which explains the variability in quiet versus busy environments. The brain actively assigns significance to input through complex neural networks. When a person is deeply engaged in a task or actively distracted, the brain’s dorsal attention network becomes highly active. This heightened engagement effectively suppresses the less-important auditory signal, causing the sound to temporarily fade.
This suppression is partly explained by the inverse relationship between the dorsal attention network and the default mode network (DMN). The DMN is active when the mind is at rest, such as when lying down in a quiet room. Research suggests that in individuals with tinnitus, certain brain regions show altered connectivity, causing the brain to stay more “at attention” and less in the relaxed DMN state.
When a temporary cause, like a stressor or an excessive substance, is removed, the brain returns to its baseline filtering state. The cessation of the sound is thus a neurological act of de-prioritization. The brain stops assigning importance to the signal, allowing the filtering mechanisms to ignore the input, which causes the perceived ringing to vanish. The sound re-emerges when focus is returned to the auditory system, highlighting the brain’s control over perception.