Timothy C. Hain,
Page last modified: January 2, 2022
There are several variants of BPPV (Benign Paroxysmal Positional Vertigo) which may occur spontaneously as well as after the Brandt-Daroff maneuvers or Epley/Semont maneuvers. They are thought to be caused by migration of otoconial debris into canals other than the posterior canal, such as the anterior or lateral canals. It is also theoretically possible for many aberrant patterns of BPPV to occur from an interaction of debris in several canals, location of debris within the canal, and central adaptation patterns to lesions. For this reason, in clinical practice, atypical BPPV is first treated with maneuvers as is typical BPPV, and the logic outlined below is entered into only after treatment failure.
Lateral canal BPPV is the most common atypical BPPV variant, accounting for about 3-12 percent of cases (Cakir et al, 2006; Korres et al, 2002; Hornibrook, 2004). It seem likely that the percentage of lateral canal BPPV depends greatly on the criteria one uses -- allowing diagnosis from smaller amounts of nystagmus is associated with larger prevalence. In the author's experience, most lateral canal cases are seen as a consequence of an Epley maneuver, but others find that spontaneous occurence is more common (Hornibrook, 2004). Diagnosis requires seeing a horizontal nystagmus that changes direction depending on the down ear. In the post-Epley situation, it is generally very strong.
Looking at the diagram above, it is hard to see how anyone could have persistent lateral canal BPPV, because the lateral canal is tilted so that debris should roll down the canal into the vestibule. Just walking around should treat it. By the same token, it is difficult to see how lateral canal BPPV could persist overnight, given that most people roll from one side to the other in bed. It would seem likely from this logic that the simple anatomy of the lateral canal geometry depicted above is not entirely accurate. See this page for more about inaccurate anatomy.
Canalithiasis of lateral canal: (most common)
Displaced otoconia can migrate into the lateral canal as well as the superior canal. For the superior canal, debris would tend to fall out spontaneously unless it was at the ampulated end. For the lateral canal, debris also would tend to fall out spontaneously. This may be the reason that non-posterior canal BPPV is unusual.
Cupulolithiasis, and light cochlea:
Debris can not only migrate into the long arms of the canals, but might also become adherent to the cupulae. This is called "cupulolithiasis". Injuries to the cupula such as due to infection or poor circulation can also, in theory, cause cupulolithiasis. These are examples of "heavy cupula", and cause an ageotrophic nystagmus.
Other substances in the inner ear might also cause a nystagmus resembling lateral canal BPPV. Positional alcohol nystagmus is well known. In theory, protein in the inner ear such as from an intracochlear schwannoma might result in a "light cupula" situation, and a geotrophic nystagmus.
Nystagmus of other disorders such as central positional nystagmus due to cerebellar damage can closely resemble lateral canal BPPV (Lee et al, 2014), but fortunately are much less common. With very sensitive devices to look for nystagmus, it is far more common to see horizontal direction changing nystagmus, that might be mild lateral canal BPPV.
Patients with lateral canal BPPV are usually very dizzy with their head turned to either side in bed. This is very different than the situation with posterior canal BPPVwhere one is dizzy only to the "bad side". In anterior canal BPPV, symptoms are often worse straight back.
Practically, lateral canal BPPV can almost always be seen on the Dix Hallpike test, especially if the examiner does not attain a substantial head-hanging posture but instead tests the patient supine. Nevertheless, the best position to see the direction changing horizontal nystagmus of lateral canal BPPV is not the Dix-Hallpike maneuver. Rather one starts with the body supine, head inclined forward 30 degrees, and then turns the head 90 deg to either side. This is called the "supine roll test". The logic of the supine roll test for lateral canal BPPV is that the 30 degree inclined forward position puts the planes of the lateral canals approximately in the horizontal plane, and thus turning the 90 degrees head to either side causes a larger change in the force on the otoconia. The optimal amount to turn the head for lateral canal is 90 degrees, rather than the 45 degrees which is optimal for PC BPPV.
- Movie of geotrophic lateral canal BPPV • Movie #2 of geotrophic lateral canal BPPV (courtesy of Dr. Dario Yacovino)
- Movie of ageotrophic lateral canal BPPV
The nystagmus of lateral canal BPPV can be either always towards the ground ("geotropic") or always towards the sky ("ageotropic", or "apogeotropic" -- we will use the shorter construction)(Bertholon et al, 2002). Nystagmus that is "ageotropic" (about 25%) is thought to be caused by debris that is further around the canal and closer to the ampulla, than "geotropic" nystagmus (about 75%). It is unlikely that debris is actually adherent to the cupula as this should not cause much vertigo (Hain et al, 2005).
Lateral canal BPPV can cause a very strong and prolonged vertigo. People with lateral canal BPPV are also generally more disturbed by ordinary sideways rotational head-movements than people with posterior canal BPPV. Lateral canal BPPV may occur commonly but may also be self treated as people roll back and forth at night naturally during sleep (Korres et al, 2002).
In some cases, usually ones where the condition occurs spontaneously rather than as a consequence of treatment for regular BPPV, debris is adherent to the cupula. This causes a very prolonged and refractory nystagmus, but it is rarely very strong.
Misdiagnosis is possible : One should be more concerned in lateral canal BPPV, than in PC BPPV, that there is a cause other than BPPV. Disorders that resemble BPPV, including (rarely) brain tumors, are discussed here. Vestibular migraine is certainly possible (Beh, 2018).
When lateral canal BPPV follows a treatment maneuver for posterior canal BPPV, the "bad" ear is considered to be the same one with the posterior canal BPPV.
In idiopathic cases with geotropic nystagmus the "bad" ear is assigned to the side with the stronger nystagmus. With ageotropic nystagmus, the bad ear is assigned to the side with the weaker nystagmus. The rationale for this pattern is that excitation is stronger than inhibition (i.e. Ewald's second law). This mechanism was not supported by a recent study of positional alcohol nystagmus on persons who had only one remaining labyrinth (Tomanovic and Bergenius, 2013).
As the lateral canal, when upright, is mainly horizontal, debris might in theory be distributed nearly anywhere in the lateral canal. Then when one lies down, the nystagmus that appears might be dependent on the initial distribution.
Han et al (2006) suggested that the nystagmus seen on lying supine is can be used to determine which ear is affected. The methodology here is that the patient is initially sitting with head bent down for 3 minutes, and then rapidly brought into the supine position, with the head on a pillow. For geotropic nystagmus, nystagmus is away from the affected ear, and for ageotropic, towards the affected ear. In other words, for geotrophic nystagmus, the nystagmus follows the general rules for paretic ears, and vice-versi for ageotrophic nystagmus.
Some authors feel that a "null point" can be found, and the bad ear is on the side of the null point (Bisdorff and Debatisse, 2001). We find this generally implausible as if debris is movable within the canal, it should always die away, and thus there is no null point. If useful, it should only apply to cupulolithiasis, which is very rare.
Usually there will need to be judgment call on the part of the examiner, integrating together information about nystagmus and other data about which ear is diseased (such as hearing, fullness and the like). When horizontal nystagmus follows an Epley maneuver for posterior canal BPPV, in nearly all instances the most likely "bad" ear is the one in which posterior canal type BPPV was seen previously. In situations where the side is unclear, it is our practice to first treat the more likely side with home exercises, and then switch to the other side after a week.
Treatment of lateral canal BPPV has not been as well established as in typical PC BPPV, but it is based on the same biomechanics and logic.
All maneuvers for lateral canal BPPV take the general approach of turning the body or head around the long axis, from the "affected" side, towards the good side. Variant maneuvers can all be viewed as "pieces" of the log-roll. Thus, if you understand the log-roll, unless you are very interested in saving time by using a variant maneuver, you don't have to read beyond the log roll section. Of the variant maneuvers, the "Zuma" is the closest to the log roll. Is it better ? We don't know.
Oron et al (2015) reviewed numerous maneuvers for lateral canal BPPV. While this certainly was not an exhaustive review, and it was unaccompanied by any biophysical simulations, they stated " No treatment was found to be superior over the others regarding the success rate." Our thought is that in as much as one often doesn't know the bad side, the log roll is a simple and effective treatment.
|Log roll exercises for Lateral Canal BPPV (c) Timothy C. Hain, M.D. 2013|
The "log roll" exercises, are a procedure where an individual is rolled in steps of 90 deg, starting supine/affected ear down, to supine, to affected ear up, to nose-down, and then to sitting at intervals of 30 seconds or one minute. This procedure seems very reasonable and it is the one that we often use in our own clinical practice. There is a report of 75% efficacy (15/20) of a variant procedure (e.g. Fife, 1998) called the "iterative full-contralateral roll", going from supine nose up, a full 360 degrees in 90 degree increments, rotating towards the good ear. This procedure is performed once or twice in the clinic and repeated at home for 7 days. It seems to us that the difficulty of establishing which is the "bad" ear is an obvious drawback of almost any lateral canal treatment and in some situations, we do the log roll to one side for a week, and follow with the log roll to the other side for another week. We also feel that it is preferable to begin with the bad-ear down rather than supine, for situations where there is debris close to the ampula (i.e ageotrophic). Vibration of the mastoid might theoretically add to efficacy of this procedure but no studies are available at the present writing.
Right now, although position 4 says "hands/Knees", actually we just have people roll over to nose down and cradle their head in their hands. This attains the same position without as much moving around.
A newer variant of the log roll, called the "Zuma maneuver", is probably as good as the Log roll. It is similar in positions to the log roll, but done with brisker head movements.
Supplemental material Movie of the log roll exercise
There are many other variant lateral canal BPPV maneuvers -- people think of a another way to position the head, write a paper, and name the new maneuver it after themselves-- this page provides some information about them.
Heavy cupula: (i.e. ageotrophic, non-fatiguing)
Currently it is generally felt that this is a poor prognosis variant of lateral canal BPPV (although not all agree -- e.g. Bisdorff and Debatisse, 2001), and that it is characterized by ageotrophic nystagmus. As ageotrophic nystagmus could theoretically be cause by debris that is either stuck or attached, this means that there could be two explanations for ageotrophic BPPV, as well as of diverse alternatives (e.g. central nystagmus, ? utricular disturbance, neck nystagmus)..
Biomechanical reasoning (no plunger effect of debris) would suggest that strong ageotrophic nystagmus would necessarily be due to loose debris, and thus that lateral canal cupulolithiasis should not be a big problem because either it is treatable or it is weak (Hain et al, 2005).
For the situation where debris is stuck to the cupula, it may not be easily treated by physical maneuvers aimed at dislodging it (called "liberation of debris by some). Debris could be stuck to either side of the cupula, leading to some uncertainty about which is the best way to treat it. Also, this pattern of nystagmus may derive from central disturbances.
Our approach is to initially try the usual treatments for lateral canal BPPV, possibly with the addition of mastoid vibration. If this fails, we will recommend a variant Brandt-Daroff exercise as tried above. Generally anti-emetic and anti-nausea treatment is necessary when treating lateral canal cupulolithiasis.
Light cupula: (geotrophic, non-fatiguing)
This one is a little hard to discuss as there is actually no method of telling a "light cupula" geotrophic DCPN, from some other non-BPPV positional mechanism such as migraine or a cerebellar disturbance. So all literature about the "light cupula", is usually literature about a conjectured entity. Perhaps it doesn't exist. There are notable exceptions involving temporary changes to blood chemistry -- notably drinking lots of alcohol, and drinking D20, which is heavy water (Money et al, 1965).. Both of these are temporary and just don't apply to chronic clinical situations.
It has been proposed that nonfatiguing geotrophic DCPN might be due to a "light cupula". In other words, a cupula lighter than endolymph which is essentially that of just water (e.g. Imai et al, 2015). This is a bit hard to comprehend as there is just not much material in the body other than fat and air that is lighter than water, and neither one of these is likely to be found in the inner ear. However, as noted above, if protein were high in the endolymph, this might increase its density, and make the cupula relatively lighter than endolymph. Protein does vary considerably among different types of fluids in the inner ear with blood having the most (4238 mg/dl), vs perilymph (178-242), and endolymph (38) (Nyberg et al, 2019).
Kim and Hong (2018) reported that the canalith repositioning maneuver (modified) does not work for this clinical picture, and in fact, " had no therapeutic benefit for a persistent geotropic DCPN and suggest that the pathophysiology of persistent geotropic DCPN is less likely to be a light debris attached to the cupula."
It would seem possible that there might be a very few moving particles in the lateral canal that just move so slowly that it is mistaken for cupulolithiasis. One would think that this would respond to the log roll.
If indeed nothing works, this would suggest that this clinical phenomenon may not be due to otoconia at all. It would not be hard to come up with an alternative explanation involving the otoliths or central processing of utricular signals. When we see this picture in our practice, we will make an attempt to treat with the log roll, and after that we often consider more workup and perhaps treatment for migraine.
The Vestibular Disorders Association (VEDA) maintains a large and comprehensive list of providers who have indicated a proficiency in treating BPPV. Please contact them to find a local treating provider.
Our own practice is located in Chicago Illinois. We usually combine a visit to a CDH physician with testing for alternatives and then a visit to the physical therapist or a treatment by the physician.
https://dizzy-doc.com/: Chicago Dizziness and Balance, 645 N. Michigan, Suite 410, Chicago 60611