Your Brain on Vestibular Neuritis
There was a commercial many years ago where you see an egg and a voice-over says, “Here is your brain.” The egg is cracked and dropped in a hot frying pan and the voice-over continues, “This is your brain on drugs.” This week, we want to explore the brain’s response to an acute inner ear disease, specifically Vestibular Neuritis (VN).
In the condition of VN, it is believed that a viral inflammation causes swelling and disruption of function of the vestibular nerve connecting the labyrinth to the brain on one side. Functionally, the opposite healthy ear is sending out a steady signal indicating no head movement, when suddenly the affected side suffers a sudden decrease in output because the nerve has stopped transmitting any signal. The brain registers this (a higher spike level from the healthy ear and a drastically reduced spike level from the affected ear) as movement away from the affected side, causing the eyes to be deflected toward the affected side. Since this asymmetrical spike in activity is prolonged and not associated with head movement, the eyes don’t stay deflected away from the healthy side, but repetitively snap back in place, causing the classic finding of nystagmus with a fast phase beating away from the affected side. It is this rapid eye movement that creates the sensation of vertigo, predictably leading to nausea and vomiting.
The patient is acutely symptomatic, disabled and, frankly, miserable during this time. The brain is trying to resolve this asymmetry between the two inner ears. Since it doesn’t have the ability to restore function on the affected side, the brain starts to shut down its connection with the healthy side. This is a process known as “cerebellar clamp,” which takes 24 to 72 hours to complete. So, after a few days, the brain has a severely reduced connection to both labyrinths, minimizing the asymmetrical firing and reducing the symptoms of vertigo and nausea. This process is not affected by exercise, but can be accelerated by sedating medications. Remember, nothing has changed in the ears. One is healthy and one is damaged, but the brain has resolved the acute conflict.
Now, 72 hours later, the patient feels fine while sitting or lying in bed because the nystagmus has mostly ceased. As long as the person doesn’t move, all is well; the head is still and the eyes are still. But if the person decides to get up and walk around, it will be obvious that something “just ain’t right.”
What patients are experiencing is a condition known as “oscillopsia,” which is used to describe the sensation of visual blurring with head movement. In order to shut down the acute vertigo symptoms, the brain had to disable the Vestibular Ocular Reflex (VOR) to a large degree. So when the patient starts to move their head around, there is not the reflexive corrective eye movement they have depended on all their lives to give them visual clarity when moving. This leads to inability to focus visually while ambulating, imbalance, disorientation, and, eventually, nausea if they push too hard. At this point in the process, the “shut down” which was a blessing in the first 72 hours, has now become a curse because the patient wants to get back to their life.
Next week, we will continue this series with a discussion of the compensation, or “wake up” phase of recovering from vestibular injuries, specifically VN.
Photo courtesy of https://theconcussionblog.com/tag/recovery/
Egg photo courtesy of https://pixshark.com/this-is-your-brain-on-drugs.htm
