Tinnitus is the perception of sound when no external source is present, often described as ringing, buzzing, hissing, or roaring. This phantom sound can range from a mild annoyance to a condition that significantly interferes with daily life, affecting approximately 10 to 15 percent of adults. While tinnitus is frequently associated with some degree of hearing impairment, the symptom itself is not a disease but rather a signal of an underlying change in the auditory system. Its relationship with measurable hearing loss is not always straightforward.
Tinnitus Exists Without Detectable Hearing Loss
The majority of tinnitus cases are linked to peripheral damage in the inner ear, but many individuals experience the symptom despite having normal results on a standard hearing test, or audiogram. The conventional audiogram primarily tests hearing thresholds up to 8,000 Hertz. A passing result often leads to the conclusion that the ear is functioning normally, but this standard test is not sensitive enough to detect all forms of auditory damage.
Tinnitus with a normal audiogram is often explained by “hidden hearing loss,” which involves damage to the synapses connecting the inner ear’s hair cells to the auditory nerve. This subtle neural damage, known as cochlear synaptopathy, reduces the input the brain receives, particularly at high frequencies. In response to this reduced input, the brain’s central auditory system may attempt to compensate by increasing its internal gain or sensitivity. This neural reorganization and hyperactivity is theorized to generate the perceived phantom sound of subjective tinnitus.
Non-Auditory System Drivers of Tinnitus
Tinnitus can also arise from sources entirely separate from traditional cochlear damage. One common non-auditory type is somatic tinnitus, where the sound can be modulated or triggered by movements of the head, neck, or jaw. This connection occurs because neural pathways from the somatosensory system—which relates to body sensation—project directly to the central auditory structures in the brainstem.
Problems like temporomandibular joint (TMJ) disorders, cervical spine issues, or severe muscle tension in the head and neck can activate these interconnected neural pathways. When the trigeminal nerve, which transmits sensory information from the face and jaw, experiences dysfunction, it can lead to aberrant firing patterns. These patterns are then misinterpreted as sound by the auditory system, explaining why clenching the jaw or turning the head might temporarily change the pitch or loudness of the ringing.
Another distinct type is pulsatile tinnitus, an objective form where the sound source is physically audible. This is often a rhythmic whooshing or thumping sound synchronized with the heartbeat. It is not caused by hearing loss but rather by turbulent blood flow in arteries or veins located near the ear. Causes include high blood pressure, atherosclerosis, or vascular malformations that alter the speed or volume of blood flow, making it audible to the person.
Furthermore, certain medications can induce tinnitus through ototoxicity, meaning they are toxic to the ear. Common examples include high-dose aspirin, certain non-steroidal anti-inflammatory drugs (NSAIDs), and some chemotherapy agents. These drugs can cause temporary or permanent damage to the sensory cells in the inner ear, leading to tinnitus without causing measurable hearing loss. In many cases, the tinnitus resolves once the medication is stopped or the dosage is adjusted.
Clinical Assessment and Next Steps
When a patient presents with tinnitus and a normal standard audiogram, a comprehensive clinical assessment is necessary to identify subtle or non-auditory causes.
Detailed Patient History
The initial steps involve a detailed patient history, including a review of all medications, dietary habits, noise exposure history, and any symptoms related to the jaw or neck. This helps screen for ototoxic drug exposure or signs of somatic involvement.
Specialized Audiometric Testing
Specialized audiometric testing is often employed to look for evidence of hidden hearing loss that conventional screening missed. This may include extended high-frequency audiometry, which tests hearing up to 16,000 Hertz, where subtle damage often appears first. Advanced tests, such as electrocochleography, may also be used to assess the function of the auditory nerve and help diagnose cochlear synaptopathy.
Imaging Studies
If a vascular or structural cause like pulsatile tinnitus is suspected, imaging studies become necessary. Magnetic resonance imaging (MRI) or computed tomography (CT) scans can visualize the blood vessels and surrounding anatomical structures. These scans detect issues like vascular malformations, tumors, or abnormalities in the inner ear bone, helping to pinpoint the precise origin of the tinnitus signal for management planning.