Timothy C. Hain, MD •Page last modified: April 13, 2020 •
Just like anything, despite the best intentions of mice and men, things can go wrong. Fortunately, serious complications of BPPV treatments are very rare. We will briefly discuss these possibilities.
This means that debris is moved from one canal into another. It "converts" (e.g. Foster, 2012). At the bedside, this is most frequently seen when posterior canal BPPV, converts into lateral canal BPPV. The previous upbeating/torsional nystagmus converts into a direction-changing horizontal nystagmus. This is generally easily handled by switching over to a lateral canal maneuver.
Babic et al (2014) recently reviewed canal conversion, but unfortunately coined another term for the phenomenon -- "transitional BPPV". We hope that this new term is forgotten quickly.
Much less commonly (2.3% as reported by Park), PC BPPV converts into AC BPPV . (Park et al, 2013) Then the vector changes from upbeating to downbeating. We are puzzled why Park et al (2013) reported conversions as often as 2.3%, as our experience has been much lower. Perhaps technique is the reason.
Babic et al (2014), used a different term - -"common crux reentry", apparently for AC BPPV, suggesting that the DBN often seen after an Epley was not actually due to AC BPPV conversion but rather due to debris hung up in the canal. Here we wish that Babic et al had used the spelling checker in their writing ("crus", not "crux"). We also would wonder how Babic et al determined where debris was located. It would seem safer, in our opinion anyway, to just describe the nystagmus that can be verified by direct inspection rather than the location, which is intrinsically conjectural.
Of course, persons who "self treat" at home, perhaps using "youtube" videos as their physician, may not realize that they have had a canal conversion, and continue to attempt to treat their new lateral canal BPPV, with the home-Epley or Brand-Daroff exercise. This is a risk that one takes when one self-treats.
Epley himself first described canalilth jam (Epley, 1995). The situation here is that the episodic/positional triggered dizziness of ordinary BPPV converts into a constant spontaneous nystagmus. This is attributed to debris "jamming" the canal (Epley 1995; Von Brevern, 2001). So far, there has been no proof that this mechanism is correct. Still, there are few reasonable alternatives to this picture.
It was recently pointed out by Castellucci et al (2019), illustrated in a case report, that a single canal canalith jam can be detected using the VHIT device, looking for a pattern where only the lateral canal is affected. This is reasonable and suggests that this would be a good step to take if canalith jam is suspected..
In our practice (where we treat several BPPV patients on a daily basis, for 20 years), we have only seen this a few times -- perhaps 3 in 20 years. On the other hand, we may be just missing it, as it is fairly common to attribute downbeating nystagmus after the Epley to mysterious and unknown events. Perhaps this is canal jam of the posterior canal.
This condition is very rare and little is known about treatment.
Several authors have pointed out that the plumbing in the inner ear is precarious at best, and that having loose crystals embedded in a gelatinous matrix could plug things up even more. Yamane et al (2014) suggested that Meniere's disease is sometimes due to blockage of the duct reuniens by saccular debris. Hornibrook (2018), provided more support for this theory.
Again, little is known about this. It seems plausible that one could develop hydrops after BPPV. We have encountered patients who complain of aural fullness together with BPPV, or after BPPV is treated. We have also encountered patients with hydrops on ECOG, after canalith repositioning. Overall, we think that this hydrops is an occasional complication of BPPV treatment.
Some of the maneuvers for BPPV (e.g. the Semont maneuver, some of the newer maneuvers for lateral canal BPPV) incorporate high accelerations, similar to some of the chiropractic maneuvers. It is generally accepted that high acceleraiton maneuvers of the head increase the risk for vertebral artery dissection (and stroke).
We have never encountered stroke after BPPV treatment in 30 years. Still, seems possible.
Regarding retinal detachment, again high acceleration would seem to be risker than no head movement, and one would think that it could happen. Again, we have never encountered it. Still, we are cautious in persons who report previous retinal disease.