Hair cells can be damaged by exposure to loud noise, which could lead to tinnitus. This can occur gradually as a result of exposure to noises over prolonged periods or may be caused by exposure to louder noises over a shorter period of time. If you are exposed to loud noises, you should always wear ear protection. Find out more about the subject on our How Loud Is Loud article and see if your job or lifestyle could be putting your ears at risk,
Most people who seek medical help for tinnitus experience it as subjective, constant sound like constant ringing in the ears or a buzzing sound in the ear, and most have some degree of hearing loss. Things that cause hearing loss (and tinnitus) include loud noise, medications that damage the nerves in the ear (ototoxic drugs), impacted earwax, middle ear problems (such as infections and vascular tumors), and aging. Tinnitus can also be a symptom of Meniere's disease, a disorder of the balance mechanism in the inner ear.
Age-Related Hearing Loss: Also known as presbycusis, age-related hearing loss results from the cumulative effect of aging on hearing. This permanent, progressive, and sensorineural condition is most pronounced at higher frequencies. It commonly impacts people over the age of 50, as all people begin to lose approximately 0.5% of the inner ear’s hair cells annually starting at age 40.
Take medication for a thyroid disorder, if necessary. Tinnitus can be related to both hyperthyroidism, or an overactive thyroid, and hypothyroidism, or an underactive thyroid. Your doctor can check for swelling or lumps in your thyroid gland, which is in your throat, and order blood screens to test its function. If they find an issue, they’ll prescribe medication to regulate your thyroid hormone levels.[17]
Most people should have a formal hearing test done by either the doctor or a hearing specialist (audiologist). People with tinnitus in only one ear and hearing loss should have gadolinium-enhanced magnetic resonance imaging (MRI). People with tinnitus in only one ear and normal hearing should have an MRI if tinnitus lasts more than 6 months. People with pulsatile tinnitus often require magnetic resonance angiography (MRA) and sometimes angiography.
Paquette et al (2017) reported a prospective study of 166 patients who had brain surgery involving removal of the medial temporal lobe. The prevalence of tinnitus increased from approximately from 10 to 20% post surgery. This study did not include a control -- a natural question would be -- suppose a different part of the brain were removed. One would also think that drilling of the skull from any source might increase tinnitus. We are presently dubious that the medial temporal lobe suppresses tinnitus.

The majority of cases of tinnitus are subjective. Objective tinnitus is far less common. However, a diagnosis of objective tinnitus is tied to how hard and well the objective (outside) listener tries to hear the sound in question. Because of this problem, some clinicians now simply refer to tinnitus as either rhythmic or non-rhythmic. Generally, rhythmic tinnitus correlates with objective tinnitus and non-rhythmic tinnitus correlates with subjective tinnitus. Specific forms of tinnitus such as pulsatile tinnitus and muscular tinnitus, which are forms of rhythmic tinnitus, are relatively rare. Pulsatile tinnitus may also be known as pulse-synchronous tinnitus. Properly identifying and distinguishing these less common forms of tinnitus is important because the underlying cause of pulsatile or muscular tinnitus can often be identified and treated.


Traumatic brain injury, caused by concussive shock, can damage the brain’s auditory processing areas and generate tinnitus symptoms. TBI is one of the major catalysts for tinnitus in military and veteran populations. Nearly 60% of all tinnitus cases diagnosed by the U.S. Veterans Administration are attributable to mild-to-severe traumatic brain injuries.


Supporting the idea that central reorganization is overestimated as "the" cause of tinnitus, a recent study by Wineland et al showed no changes in central connectivity of auditory cortex or other key cortical regions (Wineland et al, 2012). Considering other parts of the brain, Ueyama et al (2013) reported that there was increased fMRI activity in the bilateral rectus gyri, as well as cingulate gyri correlating with distress. Loudness was correlated with values in the thalamus, bilateral hippocampus and left caudate. In other words, the changes in the brain associated with tinnitus seem to be associated with emotional reaction (e.g. cingulate), and input systems (e.g. thalamus). There are a few areas whose role is not so obvious (e.g. caudate). This makes a more sense than the Wineland result, but of course, they were measuring different things. MRI studies related to audition or dizziness must be interpreted with great caution as the magnetic field of the MRI stimulates the inner ear, and because MRI scanners are noisy.
Spontaneous otoacoustic emissions (SOAEs), which are faint high-frequency tones that are produced in the inner ear and can be measured in the ear canal with a sensitive microphone, may also cause tinnitus.[6] About 8% of those with SOAEs and tinnitus have SOAE-linked tinnitus,[need quotation to verify] while the percentage of all cases of tinnitus caused by SOAEs is estimated at about 4%.[6]
Meniere’s disease isn’t directly connected to tinnitus, but people with Meniere’s often experience it, at least temporarily. Meniere's disease is an inner ear disease that typically only affects one ear. This disease can cause pressure or pain in the ear, severe cases of dizziness or vertigo and a ringing or roaring tinnitus. While Meniere’s isn’t fully understood, it appears that several relief options for tinnitus can also help with this disease. Patients are often advised to reduce stress and lower their consumption of caffeine and sodium.
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