Monthly Archives: January 2015

Hyperventilation induced nystagmus

Hyperventilation nystagmus can be induced at about 50% vestibular neuritis patients, but 7 weeks later at about 20%.

The direction of the nystagmus in the acute phase can be to the lesional side or to healthy side, but after the acute phase it’s to healthy side. Hyperventilation nystagmus to the lesional side is usualy very strong, SPV > 25deg/sec.

Here’s what colleagues from Korea got at patients with vestibular neuritis:
Hyperventilation-induced nystagmus in patients with vestibular neuritis in the acute and follow-up stages

HIN (hyperventilation induced nystagmus) to lesional side in the acute phase of vestibular neuritis or persistent HIN are acompained with persistend dizziness.
Hyperventilation-induced nystagmus in vestibular neuritis: pattern and clinical implication

Vestibular function as prognostic factor in SSNHL

Korean authors measured vestibular function in 22 patients with unilateral sudden hearing loss; they did caloric test and cVEMP.

Caloric test was pathologic at 50% while cVEMP in 31.6%. This study showed that caloric test is reliable prognostic factor in patients with sudden sensorineural hearing loss (SSNHL).

Full version of this article is available:
Association between Vestibular Function and Hearing Outcome in Idiopathic Sudden Sensorineural Hearing Loss

and another work showing vestibular function in patients sudden hearing loss:
Involvement of vestibular organs in idiopathic sudden hearing loss with vertigo: An analysis using oVEMP and cVEMP testing

Nystagmus changes direction in acute peripheral vestibular lesion?!?

When you see nystagmus to changes direction, you know that’s a central vestibular lesion. However, can peripheral vestibular lesions have a clinical presentation with alternating nystagmus? It seems to be. This is a more recent work, which describes alternating nystagmus in several patients with peripheral vestibular lesion (Mb Meniere, neuritis, vestibular schwannoma); however in all described cases alternating nystagmus was present for short period, nystagmus was suppressed by fixation (which is not characteristic of central Ny) and all tests for central vestibular pathways were fine.

Periodic alternating nystagmus of peripheral vestibular origin

Atypical BPPV – unidirectional Ny of horizontal canal BPPV

I would like to present you a patient with a classical clinical picture of BPPV. Positioning tests show horizontal nystagmus to the left.
Canalolithiasis and cupulolithiasis of the horizontal canal is not so rare. Canalolithiasis, which is a more common form of lateral BPPV presents with geotropic nystagmus, while cupulolithiasis with ageotropic nystagmus. But in our patient, we see strong ageotropic nystagmus on the right side, on the back also to the left and on the left side we see weak and short geotropic nystagmus. In literature, this rare BPPV type is called Direction-fixed paroxysmal nystagmus lateral canal benign paroxysmal positioning vertigo.

Vannucchi 2011. describes a patient with ageotropic form of lateral canal BPPV, in whom during the treatment, nystagmus changed to geotropic at healthy side, but continuing with treatment in becomes completely geotropic form which is easier to treat.

Califano 2013. describes five patients with an unusual form of lateral canal BPPV. Within these patients, the ageotropic nystagmus was on the affected side, while on the healthy side it was geotropic. The authors have named this rare form of BPPV – Direction-fixed paroxysmal nystagmus lateral canal benign paroxysmal positioning vertigo.

Both works offer the following explanation: it’s canalolithiasis of the horizontal canal, where the deposit of otoconia simultaneously in ampular and the distal part of the horizontal semicircular canal, and in the supine position with the affected side ampullofugal flow endolymph consequence of gravity to deposit otoconia in ampullar part of the semicircular canals, while the smaller otoconia deposit in the distal part is not moving; and when turning on the healthy side ampullofugal flow of endolympha is explained by the action of gravity on the distal, non-ampular deposit otoconia. Switching of one sided nystagmus to a both sided geotropic happens by otoconias from ampullar part of the canal cross to the last non-ampular part of the canal.

In the above-described patient with direction fixed lateral canal BPPV, I did a BBQ maneuver to the right with shaking and Ny transferred to a geotropic at both sides, actualy it was strong geotropic on the right side, and very weak, barely noticeable geotropic on the left side. After that, Gufoni maneuver toward a healthy side was done three times. Over the next two days, the patient had less severe dizziness when turning in bed, and then is completely without any dizziness for the next five days, but than after one bending over she felt very strong vertigo and came to me. This time she had geotropic nystagmus on the right side and a barely noticeable geotropic on the left. Positioning the patient from sitting to lying produced Ny to the right. Gufoni to the left was performed three times. Thereafter, the patient is completely without any vertigo and dizziness.

Downbeat Ny at posterior canal BPPV

Here we present a patient with a classic clinical picture of BPPV. She experienced the same type of positional vertigo a year ago, which spontaneously passed after a couple of weeks.

Dix-Hallpike test to the left: a strong sense of vertigo, and after a long latency, a barely noticeable Ny which suits the left posterior canal (cw). I immediately perform Epley maneuver for the left ear, but in the second position, appears strong Ny, characteristic for canalolithiasis of the right posterior. Maneuver completed and control Dix-Hallpike test was completely bilateraly negative.

The next day the patient returns with worsening of symptoms and even stronger positional vertigo. DH to the right causes a very intense downbeat Ny, while on the left it has also a torsional component in ccw direction. Everything suggests canalolithiasis of the right anterior canal (Ny down and with torsional component to the rightside). However, it sounds unlikely for someone who had a canalolithiasis of the left posterior a day before to return the next day with canalolithiasis counterpart on the opposite side. So since we know that the canalolithiasis of the left posterior is in question, we ask ourselves how is it possible to manifest with downebeathing nystagmus?! However, I am not the first one to encounter this phenomenon:

Posterior Semicircular Canal Benign Paroxysmal Positional Vertigo Presenting with Torsional Downbeating Nystagmus: An Apogeotropic Variant

Anterior canal BPPV and apogeotropic posterior canal BPPV: two rare forms of vertical canalolithiasis

The authors of these two works explain this phenomenon by stating that the otoliths got stuck in the ampular arm of the canal.

I treated this patient with an Epley maneuver for the left ear, and repeated it several times. The patient was much better, but strange feeling in the head didn’t resolved; somthing like “dizziness”, but without any positional vertigo. The patient performed exercises by Brandt-Daroff every day and she complained on discomfort when repeating the exercise on the right side. After two weeks, the patient comes in with a worsening of symptoms; a strong vertigo while going to bed the nightbefore, but sincethan constant dizziness disapeared. Now the DH test revealed characteristic nystagmus for the posterior left semicircular canal. Only one Epley maneuver was enough to completely resolve symptoms of vertigo and dizziness and since than she is cimpletely fine.

After this, how do we know whether the patient has the canalolithiasis of the anterior canal, or an apogeotropic form of the canalolithiasis of the posterior canal? In the aforementioned papers one difference was suggested: canalolithiasis of the anterior canal is downbeat component of the nystagmus is dominant where torsional component is absent or weak, since at the ageotropic form of posterior canal BPPV the torsional component of the nystagmus is more pronounced. In our case this remark wasn’t obvious. Anyhow, it’s important when you see positional downbeat nystagmus to distinguish benign lesion such BPPV from much more serious central lesion, since we know that such lesions could present with positional downbeating nystagmus!
After discard the possibility of central vestibular lesion, you can switch to repositioning maneuvers. I recommend to try with “deep head hanging” repositioning maneuver suggested for both anterior canals; if not successfull than proceed with Epley. The aim is to reposition dislodged otoconia back to utriculus and to resolve patient from vertigo.