Understanding The Physiology of Tinnitus
Unraveling the Intricate Symphony
Tinnitus is not just a burden or scar that results from excessive noise or old age.
Tinnitus in the vast majority (>90%) of people is the result of progressive degenerative damage to the ear-to-brain neural connections. I know that may sound scary and overwhelming, but if the truth scares you into reading this and seeking treatment – then so be it!
First, let’s dive into the cochlea (inner ear) and learn about where it all begins in most patients. Then, we will review how the damage in the ear leads to damage in the brain. This means we must provide some detail on how the ear and the brain work together. So yes, let’s dive into the physiology of hearing (how we hear), how it interacts with the brain, and what the pathophysiology (cause) of tinnitus is.
Hearing starts when sound waves enter the ear canal; sound then travels down the ‘S-shaped’ curvy ear canal and activates movement of the eardrum. The sound then travels across the ossicles (aka, the three tiniest bones in the body affectionately known as the hammer, anvil, and stirrup). These vibrating bones then send a literal tidal wave of fluid that travels down the spiraling cochlea (the snail-shaped organ that houses the receptor cells of hearing). Once inside this conch-shell-shaped organ, there are microscopic hair cells that process the incoming wave of sound.
The tiny yet powerful receptor hair cells are the point of origin where the ear and brain establish their network of millions of neural connections that extend from the ear throughout the brain. These expanding neural fibers from the ear extend to nearly every nook and cranny of the brain and interact with the brain centers responsible for emotion, memory, decision-making, processing, and, of course, hearing!
Along this neural superhighway, sound information is analyzed, fragmented, and transformed into a discrete neural activity that tells our brain about the frequency (pitch), intensity (volume) and duration (length of time) of the sound. The higher up and deeper into the brain these neural signals travel, the more neural coding and perception of sound takes place to uncover information like what or who made the sound, where the sound is coming from and what the sound means to you.
The harsh genetic truth is that our mammalian DNA pre-determines the damage to this ear-to-brain neural network as we age. This is why tinnitus is considered a progressive (gets worse over time) degenerative (the nerves become damaged and die) disorder (not normal).
Researchers from across the globe have come to understand over the past 20 years that external factors (not related to our DNA), such as living in a loud world with access to pharmaceuticals that impact the nervous system, can ramp up the speed of the neural degeneration by several decades. Hence, tinnitus starts for many people in their 40s and 50s and only gets worse over time without treatment.
What ELSE can break down the ear-to-brain connections?
While age, noise, and ototoxic (poisonous to the ear) medications can directly result in tinnitus, several other medical conditions can lead to tinnitus.
One of the most common non-auditory medical conditions that affects nearly half of all adults in the U.S. is cardiovascular disease. While people with heart disease obviously worry about their heart, what many don’t realize is that compromised blood flow to the brain can damage the ear-to-brain connections, lead to tinnitus, and diminish cognitive function.
Another medical condition that can negatively alter ear-to-brain neural structures and speed up degeneration is diabetes. Over 130 million Americans are either pre-diabetic or diabetic. There is a significantly increased risk of experiencing tinnitus, living with hearing loss, and marked reductions in memory, learning, and cognitive performance.
The list of ‘other’ medical conditions that impact the ear-to-brain nervous system and result in millions of older adults living and suffering from tinnitus include:
- Cardiovascular Disease (hypertension, arrhythmia and/or Hx of stroke, heart valve complications or heart attack)
- Diabetes or Pre-Diabetes
- Head Trauma (Hx of concussions or unconsciousness)
- Kidney Disease (chronic kidney disease, kidney infections, kidney stones, cysts, or cancer)
- Autoimmune Disease (rheumatoid arthritis, lupus, etc.)
- Thyroid Disease (hyper- or hypothyroidism, cancer, etc.)
- History of Smoking