What is Sensorineural Hearing Loss (SNHL)?

Sensorineural hearing loss (SNHL) is a type of hearing loss that occurs due to damage to the inner ear (cochlea) or the auditory nerve pathways in the brain. This type of hearing loss can result from various factors, including age-related changes, exposure to loud noises, genetics, certain medical conditions, and ototoxic medications.


Here’s how SNHL typically occurs:


  • Cochlear Damage: The cochlea is a spiral-shaped structure in the inner ear responsible for converting sound vibrations into electrical signals that are transmitted to the brain. Damage to the hair cells within the cochlea, which are responsible for detecting sound and transmitting auditory signals to the brain, can lead to SNHL. This damage may result from factors such as aging, exposure to loud noises (noise-induced hearing loss), infections, or ototoxic medications (medications that can damage the inner ear).


  • Auditory Nerve Damage: The auditory nerve, also known as the cochlear nerve, carries electrical signals from the cochlea to the brain, where they are processed and interpreted as sound. Damage to the auditory nerve pathways, either within the cochlea or along the auditory nerve itself, can disrupt the transmission of auditory signals to the brain, resulting in SNHL. This type of nerve damage may occur due to conditions such as acoustic neuroma (a noncancerous tumor of the auditory nerve), multiple sclerosis, or head trauma.


What is the relationship between SNHL and oxidative stress?

The relationship between sensorineural hearing loss (SNHL) and oxidative stress is an area of ongoing research, and while the exact mechanisms are not fully understood, oxidative stress is believed to play a significant role in the pathogenesis and progression of SNHL. Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the body’s antioxidant defenses, leading to cellular damage. Several factors related to SNHL can contribute to oxidative stress in the inner ear:


  • Noise-Induced Hearing Loss: Exposure to loud noises, a common cause of SNHL, can lead to the generation of ROS in the cochlea. Noise exposure can disrupt cellular metabolism and mitochondrial function in the hair cells of the cochlea, leading to increased production of ROS and oxidative stress. ROS can damage cellular structures, including lipids, proteins, and DNA, leading to cell death and permanent hearing loss.


  • Age-Related Hearing Loss: Age-related changes in the inner ear, known as presbycusis, are characterized by gradual degeneration of hair cells, loss of cochlear function, and decreased auditory nerve function. These age-related changes can lead to increased oxidative stress in the inner ear, as aging is associated with decreased antioxidant defenses and increased susceptibility to oxidative damage. Oxidative stress may exacerbate age-related degenerative changes in the cochlea and contribute to the development of SNHL.


  • Ototoxic Medications: Certain medications, known as ototoxic medications, can damage the hair cells in the cochlea and contribute to SNHL. Ototoxic medications may induce oxidative stress in the inner ear through various mechanisms, including disruption of mitochondrial function, activation of inflammatory pathways, and generation of ROS. Oxidative stress induced by ototoxic medications can lead to cellular damage and apoptosis (programmed cell death) in the cochlea, resulting in hearing loss.


  • Ischemia and Hypoxia: Reduced blood flow to the inner ear, as occurs in ischemia or hypoxia, can lead to mitochondrial dysfunction and impaired cellular metabolism. Ischemia and hypoxia can disrupt cellular energy production and increase ROS production in the cochlea, leading to oxidative stress and damage to hair cells and auditory nerve fibers. Ischemia-reperfusion injury, which occurs when blood flow is restored to ischemic tissue, can further exacerbate oxidative stress and tissue damage in the inner ear.


  • Inflammatory Processes: Inflammation in the inner ear, triggered by factors such as infections, autoimmune diseases, or exposure to ototoxic agents, can lead to the release of pro-inflammatory cytokines and activation of immune cells. Inflammatory processes can generate ROS and exacerbate oxidative stress in the cochlea, contributing to cellular damage and SNHL.