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Tinnitus Library

How Noise Causes Hearing Loss and Tinnitus

by Barry Keate

How is it that loud noise creates hearing loss and tinnitus? What is the exact mechanism by which this damage occurs? In order to better understand this, it is necessary to first understand the basics of how hearing operates and then review how noise damages hearing and its effects on the ears and brain.

Noise-Induced Hearing Loss

Noise-Induced Hearing Loss (NIHL) occurs when loud noise damages the working of the inner ear and causes hearing loss. It can be the result of a one-time exposure to an intense impulse sound, such as an explosion, or by continuous exposure to loud sounds over an extended period of time.

Roughly 20% of adults in the US, about 48 million people, report some degree of hearing loss. At age 65, 1 out of 3 people have hearing loss. (1)

According to the American Tinnitus Association, Noise-Induced Hearing Loss (NIHL) and tinnitus is currently the number one service connected disability of veterans returning from Iraq and Afghanistan. The total number of vets awarded disability compensation at the end of 2009 surpassed 760,000. (2)

Recreational activities that can put someone at risk for NIHL include target shooting and hunting, snowmobile riding, listening to MP3 players at high volume through earbuds or headphones, playing in a band and attending loud concerts. Harmful noises at home may come from lawnmowers, leaf blowers and shop or woodworking tools.

Noise levels illustrated

Mechanism of Hearing

Hearing depends on a series of events that change sound waves in the air into electrical signals. The auditory nerve then carries the signals to the brain for processing and interpretation.

The Middle Ear

1. Sound waves enter the outer ear and travel through the ear canal to the eardrum.

2. Sound waves cause the eardrum to vibrate and transmit the vibrations to three tiny bones in the middle ear. These are the smallest bones in the body and are called malleus, incus and stapes.

3. The bones in the middle ear amplify and transmit the vibrations from the air to fluid vibrations in the cochlea of the inner ear, which is shaped like a snail and filled with fluid.

Diagram of the inner ear

The Inner Ear

Here is where the magic of hearing really takes place. The cochlea transforms the vibrational sound into electrical signals it sends to the brain.

The cochlea is a small, snail-shaped organ inside the inner ear. Inside the cochlea are row upon row of about 20,000 hair cells. There are two types of hair cells, Outer Hair Cells (OHC), which amplify the vibrations, and Inner Hair Cells (IHC), which transform the vibrations into electrical nerve impulses.

Groups of hair cells respond to specific frequencies of sound. As sound vibrations reach the hair cells, only those that respond to the specific frequency of the sound are activated.

4. As fluid is churned in the cochlea from vibration coming from the middle ear bones, the fluid rushes past these hairs and causes them to bend. The bending of these hairs opens a sort of trap door underneath them, allowing the potassium-rich fluid they live in to reach a sodium-filled fluid underneath, and potassium mixed with sodium makes electricity. Calcium ions then enter the cell and trigger the release of the neurotransmitter glutamate. This is the neurotransmitter used by the cochlea to transmit electrical signals from the hair cells across the synapse to the neurons in the auditory nerve.(3)

5. Glutamate then binds to receptors on the neuron and initiates an electrical potential. From there the information goes to the auditory cortex to be interpreted as sound.

Hearing Loss

As we learned above, hair cells respond to specific frequencies. When the cells are presented with an overstimulation of their frequency their supportive structure becomes swollen and can rupture, destroying the hair cell. As these hair cells become damaged, they lay flat. If enough hair cells in this region of the cochlea die, the frequencies represented by the cells may not be relayed to the brain.

Most NIHL is caused by the damage and eventual death of these hair cells. Unlike bird and amphibian hair cells, human hair cells don’t grow back. Once dead they are gone for good.

image of normal and damaged hair cells of the inner ear.

When hair cells are damaged they produce excess glutamate, which floods the neurons in the auditory nerve. This is sometimes referred to as a “glutamate storm”. This excess glutamate overexcites the neurons and causes them to fire continuously until they become chemically depleted and eventually die. This process is known as glutamate excitotoxicity. The auditory nerve then does not carry signals for the damaged frequencies to the auditory cortex in the brain.(4)

Tinnitus

Our brain likes input and neurons need to be stimulated. This includes the neurons in the auditory cortex of the brain. Just like the hair cells in the cochlea, the auditory cortex is organized according to sound frequency, meaning every neuron is responsible for a different pitch. When hearing loss occurs, certain brain neurons lack input in the regions where the hearing loss is most severe.

If a neuron in the auditory cortex is not getting input from the hearing nerve, it might well pick up electrical activity in an adjacent region and respond to that. Since the neuron is responsible for a specific sound, even though it is responding to a different input, its output sounds like a ringing sound at the pitch that neuron represents. So, even though there is no real sound being generated at that frequency, it sounds as if there is and that, by definition, is tinnitus.

 References:

1 – Hearing Loss Association of America. http://www.hearingloss.org/content/basic-facts-about-hearing-loss.

2 – American Tinnitus Association; How Tinnitus Affects our Military Personnel. www.ata.org/for-patients/at-risk.

3 – National Institutes of Health. www.nidcd.nih.gov/health/hearing/pages/noise.aspx.

4 – Hakuba N, Koga K, Gyo K, Usami SI, Tanaka K. Exacerbation of noise-induced hearing loss in mice lacking the glutamate transporter GLAST. J Neurosci. 2000 Dec 1;20(23):8750-3.