Function and Dysfunction of the Vestibular System

The starting point to understanding pathology is to have a firm grasp on normal physiology. As a practitioner, you need to fully understand, and be able to simply explain to patients, how and why the VOR works.  The main thing to remember is that most abnormal eye movements can be explained if you understand vestibular physiology. In addition to understanding how and why the VOR works normally, you should be able to explain to patients (and to me) how nystagmus is generated from labyrinthine asymmetry.

The primary role of the VOR is to keep the eye stable in relation to the environment as we move around. A basic (but not always true) rule of vestibular function is this: In a healthy system, when the head is moving, the eyes are still. When something goes wrong, the eyes continue to move even though the head is still. The MOTT list is a good “cheat sheet” but you need to realize that there are exceptions to just about all these “rules.” I put the MOTT list together to hand out at lectures. It is helpful for beginners, but should probably be thrown away after you develop some expertise.

This week, we will be introduced to various vestibular pathologies. By far, the most common pathology is benign paroxysmal positional vertigo (BPPV) Historically, many people have been incorrectly diagnosed with Meniere’s disease (MD). I would guess that about half the people that come to our office believing (because they have been told by a physician) that they have MD, do not have it. This is unfortunate because they have been placed on a bland, restrictive diet for absolutely no reason, and have not received help for the true cause of their dizziness.

The third vestibular pathology that you will see fairly often is vestibular neuritis (same thing as neuronitis). These people typically have a very predictable set of symptoms and recovery. There are more uncommon and controversial pathologies. Perilymph Fistula (PF) is very controversial. Personally, I don’t think it is very common, and when present, I suspect frequently resolves with bedrest. On the other hand, a regional university medical center diagnoses and performs surgery for PF quite often.

Vestibular Equivalent Migraine is more common than most people suspect. We used to think that patients with recurrent vertigo, but no auditory symptoms had a variation of MD that we called vestibular hydrops. Now, we suspect most of those people had Migrainous vertigo. The information on Migraine related vertigo and dysequilibrium is developing, and we learn new things every year. Because of this, many PCP’s, ENTs, Neurologists and Audiologists will look at you funny when you tell them you suspect a patient’s dizziness is from Migraine.

Acoustic Neuroma (AN) is pretty rare, but we find a couple a year. I routinely do an ABR as part of a vestibular evaluation, and have found AN on patients with perfectly normal hearing. Back before MRI existed (not so very long ago), the caloric exam was used to help the surgeon predict the location of the tumor. By looking at the relative difference between hearing loss and caloric responsiveness, the surgeon could determine if the tumor lay closer to the auditory or the vestibular portion of the nerve. Now, the MRI gives a clear picture of the location.

Ototoxicity is more common than you would think. We see a few a year. I remember one particular case, the wife of a retired local physician. She was a diabetic with peripheral neuropathy (numbness in the extremities secondary to poor circulation). She had diabetic retinopathy that severely affected her vision. She developed peritonitis and was treated with aminoglycoside antibiotics. Of course this wiped out her vestibular hair cells. She was left with no feeling in her lower legs, very poor vision, and now, complete loss of vestibular function. Basically, all three inputs were damaged. She was in a wheelchair when we first saw her. With a lot of work, she uses a walker now. She is sure no one ever told her the antibiotics could be ototoxic. On the other hand, she might have died without them.

I have never seen (I should say never found) a patient with superior canal dehiscense syndrome (SC DS). The key here is to know who needs the high resolution CT, as this test is not routinely done. If a patient complains that loud sounds or blowing their nose makes them dizzy, SCDS should be investigated. The symptoms are similar to a PF because the underlying pathology is similar. It represents an abnormal opening of the labyrinth.

That last paragraph reminds me of the dumbest thing I ever heard an audiologist say. Several years ago, I hosted a Mayo Clinic Teleconference at my office. We invited all the audiologists in the area to attend. They could earn continuing education credits, free of charge. I was even going to buy lunch. Well, this one audiologist’s response to the invitation was this: He:” What’s the conference about?” Me: “Early Recogniton of Acoustic Neuroma and New Tests of Vestibular Function.” He: “We really don’t see those kind of patients. Thanks anyway” Me: “That’s the dumbest thing I ever heard an Audiologist say.” Why am I telling you this story? Because you never know what is going to walk into your office. You can’t be expected to be an expert in all areas, but if you don’t consider all possibilities, you are going to miss some important things.

You owe it to your patients to achieve a certain level of expertise before beginning practice. You also owe them the opportunity to see someone more trained if you don’t have the confidence to offer an expert opinion.