Tinnitus, often described as a ringing or buzzing in the ears, is a common condition that affects around 15% to 20% of people. There has long been debate around whether tinnitus originates in the ears or the brain. Research over the past few decades has helped shed light on this question.
What is tinnitus?
Tinnitus involves the perception of noise when no external sound is present. The noises most commonly described are ringing, buzzing, clicking, hissing or humming, although people can hear a variety of sounds. The volume, pitch and pattern can vary. In some cases, the sound may be constant while for others it is intermittent.
Tinnitus can develop suddenly or come on gradually over time. It can affect one or both ears. For some, tinnitus may last just a few minutes while for others it is a chronic, lifelong condition. The severity and impact also varies between individuals. Some may be able to tune out the noises and continue life as normal. For others, tinnitus can significantly impair their quality of life and lead to sleep problems, anxiety, depression and difficulty concentrating.
What causes tinnitus?
There are two broad categories of tinnitus:
- Objective tinnitus – This is caused by sounds produced in the body reaching the ear through conduction in body tissue. Causes can include muscle contractions or blood flow turbulence.
- Subjective tinnitus – This describes tinnitus sounds that only the affected person can hear and that do not have an identifiable source. Most cases of chronic tinnitus fall into this category.
Subjective tinnitus often develops in association with hearing loss caused by aging, excessive noise exposure or other ear conditions. Contributing factors can include:
- Damage to the inner ear – This includes damage to the microscopic endings of the hearing nerve in the cochlea of the inner ear. Tiny, delicate hairs in the inner ear move in relation to the pressure of sound waves, triggering electrical signals that travel along the auditory nerve to the brain. Damage to these hairs can lead to tinnitus.
- Changes in the auditory nerve pathway – This connects the inner ear to the brain. Disorders that affect the nerves can lead to tinnitus.
- Age-related hearing loss (presbycusis) – This gradually occurs over time as part of the natural aging process. The fine hairs in the cochlea may deteriorate and hearing nerves lose some fibers.
- Exposure to loud noise – This can damage the hairs in the cochlea. Examples include loud music concerts, machinery at work, power tools or listening to music through headphones at high volumes.
- Buildup of earwax – Earwax protects the ear canal by trapping dirt and slowing the growth of bacteria. Too much earwax can harden and block the ear canal, causing hearing changes that result in tinnitus.
- Ear and sinus infections – Any infection or condition that blocks or clogs the ears can cause tinnitus. This includes otitis media and otitis externa.
- Abnormal growths – These include noncancerous growths such as osteomas or glomus tumors that press on blood vessels, leading to pulsatile tinnitus.
- Eustachian tube dysfunction – The eustachian tube connects the throat to the middle ear and helps regulate ear pressure. If blocked due to allergies or other causes, changes in ear pressure can lead to tinnitus.
In many cases of tinnitus, an exact cause is never identified. There are also risk factors that increase susceptibility including smoking, hypertension, anxiety, depression and age. The onset of tinnitus can sometimes be linked to a specific incident like an ear infection, exposure to a sudden loud noise or trauma to the head or neck. But identifying one definitive triggering event is often impossible.
Is tinnitus in the ears or brain?
For a long time, it was assumed tinnitus came from damage to the inner ear, particularly the cochlea which transmits sound to the auditory nerve. However, research over the past few decades has shown that tinnitus actually arises in the brain rather than beginning in the ear.
Investigations into the neuroscience behind tinnitus have revealed that it is rooted in the central auditory processing system in the brain, parts of which are activated to compensate for lost input from the ear. Let’s look at some of the key evidence:
1. Tinnitus can occur without measurable hearing loss
If tinnitus originated in the ear due to damage to hair cells in the cochlea, elevated hearing thresholds and reduced otoacoustic emissions would always accompany tinnitus. However, studies show this isn’t the case. People with normal hearing can still develop tinnitus.
2. Cochlear implants don’t eliminate existing tinnitus
Cochlear implants act directly on the cochlea in the inner ear by converting sounds into electrical signals that stimulate the auditory nerve. If tinnitus arose from damaged cochlear hair cells, implanting an electronic device that bypasses the cochlea should get rid of existing tinnitus. However, research shows that the majority of cochlear implant recipients still experience tinnitus.
3. Severing the auditory nerve doesn’t eliminate tinnitus
Surgically cutting the auditory nerve leading from the ear to the brain should eliminate tinnitus if it began as a peripheral ear phenomenon. However, studies of patients who have had the nerve severed due to life-threatening tumors found this did not reduce their tinnitus. This indicates tinnitus maintenance is independent of intact auditory nerve input.
4. Tinnitus can be induced in those with normal hearing
Exposing people with audiometrically normal hearing to loud noises followed by silence has been found to trigger temporary tinnitus and shift hearing thresholds. This demonstrates tinnitus can appear with normal cochlear responses.
5. Brain imaging shows central changes
Advanced imaging techniques have enabled visualization of neural activity in the brain related to tinnitus. These studies have revealed differences in the central auditory processing system between those with and without tinnitus. For instance, hyperactivity and reorganization of neural networks have been found in the auditory cortex.
Brain changes can also occur in auditory pathways involving the thalamus, amygdala and frontal cortex. This indicates tinnitus is associated with altered functioning and connections among brain regions responsible for processing sound, emotions, memory and attention.
How does tinnitus originate in the brain?
Based on neuroscience research, the prevailing theory is that tinnitus arises from changes in central auditory processing in the brain triggered by alterations in auditory nerve input. When signals from the ear are reduced or lost, cells in the brain try to compensate to fill in the missing sound.
This leads regions of the brain associated with hearing to become hyperactive to boost sensitivity to weak signals. It also causes rewiring of neural connections as the system tries to adjust to less auditory nerve input. This generates abnormal neural activity interpreted as phantom sound.
Rather than passively receiving input, the auditory system is dynamically reactive. So when signals from the ear change due to trauma or disease, the central auditory system reorganizes and adapts through neural plasticity. Tinnitus seems to represent overcompensation that leads to the perception of meaningless noise.
Brain mechanisms underlying tinnitus
Research into the neurobiology of tinnitus has uncovered various processes in the central auditory system that are involved:
- Hyperactivity – Loss of input leads to reduced stimulation of neural pathways, causing central auditory structures to increase their sensitivity and firing rate as they try to compensate. Spontaneous hyperactivity is a marker of tinnitus.
- Burst firing – Neurons start firing in abnormal, randomly timed bursts rather than steady, even signals.
- Timing disruption – Central auditory processing relies on finely tuned neural timing. A breakdown in this temporal coding of signals from the cochlea contributes to tinnitus.
- Reduced inhibition – Inhibitory signaling pathways normally suppress spontaneous neural activity in the auditory system. Disruption of these inhibitory mechanisms leads to unrestrained firing patterns.
- Reorganization of neural networks – New connections are formed between neurons in central auditory structures as they reorganize in response to diminished input. This contributes to abnormal neural activity.
- Neural synchrony – Networks of neurons start firing in an overly synchronized and rhythmic manner, producing oscillating patterns of activity associated with tinnitus.
These kinds of maladaptive changes lead to the perception of meaningless phantom sounds that characterize subjective tinnitus.
Treatment implications
Understanding that subjective tinnitus originates in the central auditory pathway helps guide management. Treatment approaches include:
- Using soothing background sounds to mask and provide relief from tinnitus
- Employing hearing aids to amplify external sound and reactivate central auditory networks
- Reducing stress and anxiety which can exacerbate tinnitus through triggering limbic system activity
- Using cognitive behavioral therapy to promote habituation to tinnitus
- Trying techniques like neurofeedback, yoga and mindfulness meditation to address neural hyperactivity
- Applying transcranial magnetic stimulation to reduce hyperactivity and promote inhibition
The central basis of tinnitus also prompts interest in pharmacological options. Research is ongoing into drugs that could target neural plasticity and excitability, GABA inhibition, and neural synchrony in hopes of providing a pharmacological treatment.
Conclusion
In summary, it is now well-established that subjective tinnitus arises from changes in the central auditory processing pathways within the brain, even when no abnormalities exist in the ear itself. Brain imaging confirms that tinnitus is associated with alterations to neural activity, connections, timing and synchrony. While input loss from the ear may be the initial trigger, maintenance of tinnitus involves a complex interplay between different centers of the central auditory system.
Moving forward, this understanding of the neurological basis of tinnitus will be critical for developing treatments that target specific mechanisms in the central auditory system and brain networks. The ultimate goal is to find ways to minimize the brain changes that underlie the phantom sounds of subjective tinnitus.