Last week, I mentioned that in a healthy system, when the head is still, the eyes are still. When the healthy inner ear is at rest, the signal discharged from each ear is equal. We will refer to this signal as “spikes per second.” So when the head is still, the “spikes” are the same on both sides. In the example last week, when the head is rotated to the right, the “spikes” increase on the right and decrease on the left, causing the eye to move away from the right, toward the left.
There are several situations in which a change in the spikes can occur when the head is not moving. For example, in Benign Paroxysmal Positional Vertigo (BPPV) there is a brief (less than one minute) increase in spikes on the affected side after the head is moved into the offending position (but not still moving). The healthy ear on the opposite side goes back to a resting spike level as soon as the head stops moving, but the affected ear begins and continues to discharge at a higher rate while the otoconia debris is moving. This difference in signal between the healthy and affected ear causes the transient nystagmus and vertigo. The brain doesn’t need to adjust because the abnormal discharge stops pretty quickly.
During an attack of Meniere’s disease, there is an increase in spikes from the affected ear that can last from 30 minutes to several hours. The spike is believed to be the result of increased inner ear fluid (endolymph) pressure on the affected side. At the same time, the unaffected, opposite ear is sitting there at a resting discharge rate. This difference between discharge rates causes the eyes to move involuntarily (nystagmus) with resulting vertigo.
As in BPPV, the duration of this conflicting signal between the two inner ears is temporary so the brain does not need to adapt to the signal. Unlike BPPV, repeated episodes of Meniere’s disease can leave the affected ear permanently weakened, and the brain must adjust to and compensate for that residual weakness.
The inner ear conditions that allow the clearest explanation of the process of central compensation are vestibular neuritis and labyrinthitis. In these two conditions, there is a sudden and frequently permanent decrease of signal or “spikes” from one inner ear, while the other ear remains healthy. In this situation, there is a predictable set of clinical signs and symptoms, and the recovery process is also fairly predictable.
Next week we will address the process by which the brain suppresses the acute symptoms of vertigo and nausea, and the residual symptoms of imbalance and motion intolerance that often follow an acute episode of vestibular neuritis or labyrinthitis.