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
