A few years ago, I did a post here discussing patients that continued to complain of imbalance and “fleeting disorientation” after successful treatment using the Epley maneuver or some other form of canalith repositioning. So let’s revisit that and explore some related newer reports, as well as talk about people that do not improve after repositioning for BPPV.
Some patients continue to complain of positional vertigo after undergoing treatment with the Epley maneuver. First, no treatment works on everybody, but repositioning for BPPV has a very high success rate. In fact, success rate is so high that if the treatment fails, it is more likely that the diagnosis is wrong than it is that the repositioning procedure failed to move otoconia out of the posterior canal. Numerous studies put the success rate for BPPV of the posterior canal in the high 90% range. There are other forms of BPPV where the otoconia enter the horizontal canal, and very rarely the anterior canal. The Epley maneuver is specifically for posterior canal BPPV and would not help BPPV of the horizontal canal. There are procedures for horizontal canal BPPV, but with lower success rates. One particular form of horizontal canal BPPV, where the otoconia is believed to be in the long arm of the canal, close to the ampulla, is particularly resistant to repositioning. This form of BPPV is characterized by ageotropic horizontal nystagmus where the nystagmus beat to the left after rolling onto the right side, and then change to right beating horizontal nystagmus after rolling onto the left side. There is a recommended treatment for this, known as the Gufoni maneuver, but it does not enjoy nearly the same success rate as the Epley maneuver for posterior canal BPPV.
Residual Non-Vertigo Dizziness Following the Epley Manuever
A high percentage of patients will report resolution of positional vertigo after undergoing a repositioning treatment, but more than one in three will continue to describe more vague symptoms of imbalance and movement related visual disorientation and instability in the days to weeks following treatment.
There are two schools of thought regarding these residual symptoms. One theory involves utricular dysfunction. A damaged utricle is the source of BPPV (that is where the otoconia debris comes from). I can’t add much to that discussion, but a review of available literature can be found here.
A second theory is that there is a neural dampening or “cerebellar clamp” process. We know that the brain has the ability to reduce the gain of the vestibular ocular reflex (VOR) in the healthy ear following an acute unilateral vestibular loss. It is also possible, but currently unproven, that the brain’s response to intermittent bursts of increased unilateral discharge (which occurs with BPPV) is to dampen it’s connection to the affected ear, or maybe just the affected canal.
With canalith repositioning, there is not a gradual recovery, but rather an immediate repair. It is plausible that it takes some time for the brain to readjust to a newly healthy labyrinth. This theory has been explored by Faralli et al:
“According to Faralli et al. point of view, the genesis of residual dizziness (RD) could reside in the inability of the vestibular system to readapt quickly to a new functional state: in detail the persistence of debris in the semicircular canal could alter the tonic discharge from the affected labyrinth and could induce a new central adaptation rebalancing the vestibular nuclei activity, in order to minimize the peripheral asymmetry. This new equilibrium tends to stabilize the perturbation produced by the otoconia that is free to float in the semicircular canals. After successful maneuvers, the brain adapted to the new condition is unable to quickly readjust to the old pattern and this could be the cause of RD”
The Bottom Line
Residual non-vertigo dizziness is a common complaint after successful canalith repositioning for BPPV. It generally goes away in a week or two with normal activity, but recovery may be accelerated by performing VOR exercises.