vertigo balance testing audiology

Perspectives on Vestibular Testing and More Common Errors

I have done a couple of blogs over the years under the heading “Vestibular Brain Droppings.” Credit goes to George Carlin for the title. Basically, “Brain Droppings” consist of unrelated factoids or opinions that don’t fit neatly anywhere else. I am day five into home quarantine, so my brain is eager to be productive. I will ask it to be organized another day.

Here we go.  Vestibular dysfunction falls under two main headings:  acute or episodic conditions that cause the eyes to move when they are not supposed to (Nystagmus), and chronic dysfunction where the eyes don’t move when they are supposed to move (VOR deficit).

 

Nystagmus

 

Nystagmus can be broken down into spontaneous and provoked nystagmus. Examples of spontaneous nystagmus would include vestibular neuritis/labyrinthitis and Meniere’s episodes. 

Provoked nystagmus would include BPPV triggered by position change, transient nystagmus induced by sound or pressure changes in Superior Canal Dehiscence (SCDS), or vibration induced nystagmus. Provoked nystagmus would also include caloric stimulation, but in that case a nystagmus response is normal. In the other described provoked nystagmus conditions, a nystagmus response is abnormal.

Some nystagmus is the result of a transient unilateral increase in firing rate (Meniere’s, BPPV, SCDS), while others result from a decrease in firing rate (Neuritis/labyrinthitis).

 

Vestibular Ocular Reflex (VOR) Deficit

 

Chronic vestibular dysfunction results from reduced sensitivity, therefore reduced firing rate with head movement, from the damaged labyrinth/vestibular nerve. Classically, this most commonly occurs following a Neuritis/Labyrinthitis event, but can occur from less common conditions such as Vestibular Schwannoma or advanced Meniere’s disease.

Since organization and flow are not top concerns today, I will mention that even in advanced Meniere’s with significant hypofunction measured by caloric testing, VOR function at real life head speeds is often preserved.

VOR deficit results in eye movement that does not offset head movement (eyes don’t move when they are supposed to). From a symptomatic standpoint, this can be expressed through complaints of visual blurring or “after-motion” with rapid head movement (Oscillopsia), and/or increased dependence on visual or tactile feedback for balance and orientation.

From an objective evaluation standpoint, VOR deficit can be detected by informal examination (head thrust), or by advanced testing such as rotational chair or Video Head Impulse Test (vHIT).

 

Errors in Diagnosis 

 

In 2018, I did a post on “Common Errors in Vestibular Management.” We continue to see horizontal canal BPPV frequently misdiagnosed and mistreated as bilateral posterior canal BPPV.  Horizontal canal BPPV is far more common than bilateral posterior canal BPPV, so closely view the direction of nystagmus when a patient is symptomatic on both sides.

We also see a trend where patients with vestibular neuritis are misdiagnosed as BPPV because they have “a positive Dix-Hallpike” as the patient had nystagmus and vertigo when supine.

Keep in mind, the Dix-Hallpike is only positive if the patient DID NOT have vertigo and nystagmus before you performed the Dix-Hallpike test. Unfortunately, viewing for spontaneous nystagmus is still not routinely done in many emergency or primary care settings.

Since we are all stuck at home for the next several days, send us your questions in the comments section below. Be safe and stay home.

 

*Image courtesy USAF

About Alan Desmond

Dr. Alan Desmond is the director of the Balance Disorders Program at Wake Forest Baptist Health Center, and holds an adjunct assistant professor faculty position at the Wake Forest School of Medicine. In 2015, he received the Presidents Award from the American Academy of Audiology.

4 Comments

  1. Dr. Desmond, I always appreciate your insight. I work in a multi-specialty private clinic here in the Caribbean. As our budget is somewhat limited, what diagnostic equipment is recommended or considered essential for establishing an appropriate vestibular clinic. We have family medicine and physiotherapy present, but no ENT physicians onsite.

  2. I’d like for you to blab a bit about the relative importance of taking the time to obtain an accurate and thorough history. If you have 1hr.&15 min. for a VNG (including head-thrust &/or V-hit (&c.) if needed ), how much time do you devote to the Hx? Sometimes I find it difficult to find a happy medium between 1. demanding an answer to my direct questions, and 2. allowing the patient to meander- which sometimes reveals crucial information. Do you always winnow the time a bit by requiring a prior questionnaire to be filled out?
    50 to 60% of my VNG referrals these days have already been seen and questioned (and often Dix-Hallpiked) by an MD, so I often find key information from a very close and detailed history…which can be time consuming.
    ALSO! The referring MD and the patient often appreciate my input re: a potential dx of Personal postural perceptual dizziness, vs. Mal de Debarquement, vs. SEE sick syndrome, vs. blah blah, etc., etc… and in order to tease out the differences of each of these, I find that a really good history is paramount!

    1. Dr. Piner:
      Thanks for the comment and question. I will discuss the importance and streamlining of the case history in my next blog.

  3. Why is it that Ramsay Hunt syndrome is not included automatically when discussing diseases/illnesses that cause CN VIII damage? Our hearing loss does tend to be sensorineural but it appears that many diagnosed with RHs become deaf in that ear, with no hope of bringing back the hearing. Also, because of the CN VIII damage, vestibular issues can be horrendous. Some of us, it seems, have a brain that does not want/is not capable of compensating. Even after BT/VT, we have many of the RHs varieties of damaged cranial nerve issues: difficulty reading (double vision, following a line, blurry, letters jumping, difficulty concentrating, brain fog), difficulty walking in dim light or on uneven surfaces (and with depth perception), inability to complete FSTs, unable to drive (blurring when rapidly turning head, difficulty in judging occupied lanes when at a cross road), hyperacusis, autophjony, dysphonia, dyphagia, tinnitus, lagophthalmos, CFS/ME,
    as well as our CN VII damage – unilateral facial paralysis which leaves us with so many residuals. RHs is so often misdiagnosed as Bell(s) palsy. As such those patients are often given only steroids, which is the typical BP treatment, but that feeds the virus in RHs. Or given the BP strength of antivirals which are about one quarter of the strength needed for RHs. Left untreated (or undertreated), the zoster virus continues to feed off of the cranial nerves and does phenomenal damage. NORD calls RHs a rare disease. It is also classified as an orphan disease. It’s really not that uncommon, just misdiagnosed. Please include us and our issues in your articles. Please, stop ignoring us.

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