Timothy C. Hain, MD Page last modified: November 9, 2018
The main BPPV page is here. This page is pretty technical (warning !)
Abbreviations used here:
Anterior canal or AC-BPPV may account for about 2% of cases of BPPV (Korres et al, 2002).
Displaced otoconia can migrate to any of the three semicircular canals. When it goes to the top canal, it is called "anterior canal BPPV". This type of BPPV is thought to be characterized by down-beating nystagmus (DBN) on lying flat, and upbeating nystagmus (UBN) on reassuming upright position.
It is best here to just say that the prevalence of AC-BPPV is low, and uncertain. It is uncertain because the diagnostic criteria are nonspecific, and there is simply a lack of solid evidence that the common DBN seen supine is due to AC-BPPV or something else (see following for a list of the "somethings").
Anterior canal BPPV is probably very rare because the anterior canal is the highest part of the ear. Anagnostou et al (2015), reviewed 31 papers, and suggested that AC BPPV comprises 3% of all BPPV. AC BPPV is probably rare because debris would naturally tend to fall out of the posterior half of the anterior canal, and getting debris into the anterior canal would not be easy. From the geometry of the ear, it would seem likely that anterior canal BPPV might occasionally result as a complication of the Epley maneuver. In persons who don't spend a lot of time upside down, other than perhaps Yoga enthusiasts, it is difficult to imagine a plausible mechanism otherwise.
The Dix-Hallpike maneuver diagnoses both posterior canal BPPV as well as contralateral anterior canal BPPV. Variants of the Dix-Hallpike maneuver may also treat anterior canal BPPV (see below).
The conventional (loose) criteria for AC-BPPV are a supine-position triggered DBN, with or without torsion.
AC BPPV is almost certainly grossly over diagnosed, as the patterns of nystagmus attributed to AC BPPV by most clinicians make no sense.
What logic would say:
From basic vestibular physiology (i.e. Flourens, Ewald), nystagmus from the inner ear is mainly oriented in the plane of the stimulated canal. Because in AC BPPV, the stimulated canal is "up", on lying flat, one would expect that the torsion also would beat towards the "up" side (i.e. opposite side).
Anterior canal BPPV should also be mainly provoked (i.e. strongest) from the opposite ear to the side of the Dix-Hallpike maneuver -- in other words, if you get dizzy with DBN to the right side, the problem ear should be the left. Some authors have suggested that because the anterior limb of the anterior canal is oriented so that parts are near the sagittal plane, anterior canal BPPV can be provoked with a Dix-Hallpike maneuver to either side as well as in the "head hanging" position (Bertholon et al, 2002). We generally agree with this idea and we have also encountered a few patients who ONLY have nystagmus in the head-hanging position (but this doesn't prove that it is due to AC BPPV). On the other hand, the anterior canal as a whole is not at all aligned with the sagittal plane -- it is about 40 degrees away (Della Santina et al, 2005). Just because part of the canal is sagittal, does not mean that stimulation of the canal should cause purely vertical nystagmus in one segment, and mixed in another. It should be mixed all through.
In our experience, supine position triggered DBN more often beats (i.e. torsion) towards the "down" ear or just doesn't have any torsion at all. Both possibilities should be impossible for AC BPPV.
Furthermore, in AC BPPV, considering the physiology, there also should be an upbeating nystagmus on reassuming upright as well as a low level UBN all the time. In our very large experience with BPPV, while DBN supine is very common, especially with ipsi-torsion, UBN upright is rare.
So to summarize -- There are two sets of criteria for AC-BPPV. While people that fit the loose (illogical) criteria are common, almost nobody fits the strict (logical) criteria, and it may be that the whole syndrome is a misnomer.
- Loose criteria -- supine DBN, with or without torsion, in any direction, but usually ipsitorsional referred to the down side
- Strict criteria -- supine DBN, with contra-torsion referred to the down side, and UBN on upright
AC BPPV is supposedly diagnosed by a positional nystagmus with components of downbeating and (sometimes) torsional movement on taking up the Dix-Hallpike position (shown above).
Considering causes within the ear, a mixed-DBN/contratorsional nystagmus might also be caused by debris close to the common crus of the PC. In other words, following along the same logic as geotrophic-ageotrophic LC BPPV, especially after an Epley or Dix Hallpike maneuver, debris in the PC might move towards the ampulla/cupula rather than away. Here, the nystagmus should be strongest with the bad ear down, and the torsion should be oppositely directed. This nystagmus pattern is very uncommon (i.e. contra torsion). Although to our knowledge, this idea was first posted on this web page, this mechanism was also discussed at a 2013 conference in Siena Italy by two different research groups. Califano et al (2014) discussed this mechanism in detail in a recent paper and used the name "apogeotropic posterior canal BPPV". Califano used the term "apogeotropic" rather than "contra" for the torsional component, but they are the same entity. The term apogeotropic posterior canal was first used by Vannuchi and colleagues (2011, 2012).
Yacovino et al (2014), suggested that AC-BPPV occurs "de novo" in about 38%, as a canal conversion in about 35%, and in individuals with previous BPPV but without a recent treatment, in 27%. Califano et al (2014) suggested that roughly 2.5% of all BPPV was the common crus mechanism, and 1.5% of all BPPV was the true AC mechanism. It seems to us that these statistics might depend on how the clinics treat their posterior canal BPPV, as some treatment protocols might tend to be incomplete and result in more of the common-crus type BPPV than others.
To figure this out one has to apply Ewald's laws, actually first described by Flourens. These laws express the general idea that the eyes move in the plane of the canals being stimulated. This means that given that a single canal is being stimulated (i.e. in most types of BPPV), the eyes can only move in certain "vectors" -- mixtures of horizontal/vertical/torsion. This is nicely described in Leigh/Zee's book (figure 2-2, 2006). The anterior canals, when excited, drive the eyes with a mixture of down-beating/ipsi-torsion beating. The posterior canals, a mixture of up-beating and ipsi-torsion. The lateral canals, drive the eyes largely in the horizontal plane beating towards the excited ear.
DBN implies excitation of either AC, or inhibition of either PC. UBN, inhibition of either AC or excitation of either PC. Ipsitorsion implies excitation of the down ear, or inhibition of the up ear. Thus conventional PC-BPPV with UB/ipsitorsion makes sense as there is excitation of the ipsi PC. Logically, one could also get the same pattern from inhibition of the contralateral AC.
Ipsitorsion purely due to excitation of the down ear is not anatomically possible as all methods of producing DBN on the down side (excitation of AC, inhibition of PC) produce torsion in the other direction.
Ipsitorsion purely due to inhibition of the up ear is improbable. To be paired with DBN, this vector would have to be due to inhibition of the contralateral PC. As the contralateral PC is horizontal during the Dix-Hallpike to the ipsilateral side, this would seem improbable, but nevertheless still within the realm of possibility, especially if one allows for the possibility of canals that are not entirely in one plane. Another possibility might be stimulation or inhibition of the posterior canals through the "top" (i.e. debris in the vestibule). This is very conjectural.
A more plausible way to organize this would be to postulate two separate mechanisms for DBN and torsion -- for example, it might reasonably be due to a mixture of a pure DBN, perhaps due to saccular damage or cerebellar damage, and an ordinary PC BPPV. See the next section for possible mechanisms of pure DBN. One would expect for this situation that the timing of the two components would differ - -i.e. the DBN should last longer than the torsion. We do not know if this is the case.
Nystagmus of Anterior canal BPPV.
When there is DBN on supine without torsion -- pure DBN -- (e.g. Cambi et al, 2013), the origin is probably not BPPV of any type, as there is an intrinsic pairing between stimulation of the canals and a mixed torsion-vertical nystagmus. This is very common -- and increases with age. The usual situation is an older person -- 70+, who has a very strong DBN, supine, and feels fine. They do not have any DBN on sitting, but often have DBN prone. Generally speaking, nobody has looked very hard at whether there is nystagmus with the head rolled. With nystagmus present both supine and prone, we have ruled out mechanisms related to just the gravity vector, as they don't reverse.
Here some possible mechanisms for supine and prone DBN.
As noted above, nystagmus that appears supine and prone, without any symptoms is common and scales hugely with age. This suggests that it is a wear/tear phenomenon. What could be wearing out ? Perhaps the utricle or saccule, which are thought to shed otoconia through life. How would this work ? One would think there would have to be some signal indicating a supine position. Both the saccule and utricle have sensors for the sagittal plane, but only the saccule detects the upright position as well. So supine and prone presumably have more otolith activation than upright. Perhaps this leads to DBN. More data would be certainly helpful here.
More commonly, people consider DBN must be coming from the usual source -- the cerebellum. The problem with this idea is that usually these people don't have DBN upright, but just supine and prone. There are numerous causes of downbeating nystagmus. One should certainly consider other possible explanations - -especially cerebellar lesions, in persons with nystagmus attributed to AC-BPPV for the reasons developed above. See this link for a case of a person who was thought to have AC-BPPV, but actually had a brain tumor. It is very rare than anyone with dizziness has a brain tumor. So for this situation - -be wary, but don't expect to find much central disease.
Another speculative cause of pure supine DBN, is central adaptation. This idea allows for the appearance of DBN after treatment for PC BPPV, without attributing it to AC BPPV. Should debris on either the short arm of the PC (this location seems reasonable) or long arm of the AC (this location seems unlikely), it could load down the cupula and cause a tonic UBN. After a maneuver that moved debris out of either place, such as an Epley maneuver, there could be a DBN that had built up to counteract the peripheral UBN, via central adaptation. The rules for central nystagmus are not the same as peripheral nystagmus, they don't have to be in canal planes, and a purely DBN is conceivable. This logic suggests that a supine DBN that follows a successful Epley maneuver might not be AC BPPV, but rather might be central DBN. If there is both ipsitorsion and DBN, perhaps a mixture of residual PC BPPV and central DBN. This should be self-limiting.
A very unlikely possibility is canalith jam. The idea here is that debris from the PC "jams" some canal (presumably the PC), causing a constant nystagmus. It might jam causing negative pressure leading to upbeating/ipsitorsion, or positive pressure leading to downbeating/contratorsion. For this situation you would expect "canal plane" nystagmus, and no response for the canal plugged (should it possible to measure these things -- perhaps with the new "vHIT" device").
Treatment of anterior canal BPPV has not been as well established as in typical BPPV and at least as of 2015, there were no controlled studies. Anagnostou et al (2015) stated that all studies had success rates of approximately 75%, with the sample weighted mean being 856%. This seems pretty high to us, especially given the diagnostic difficulties. One would not think that pseudo-AC BPPV due to, lets say, a cerebellar disturbance (Bertholon et al, 2002), would respond to any maneuver. But still, one has to start somewhere, and thus we will talk here about what has already been tried and what we consider a reasonable approach. You can skip down to "our recommendation" if you just want to get to the take home message.
As a general rule, there is "only one" geometry to a maneuver to treat any particular canal type of BPPV, because however one maneuvers the person, in the end, you always have to bring the debris around the same circle of the canal. Thus, even though things might appear complex below, in essence, all of these maneuvers are just trying to get the person upside down, let the debris fall to the top of the canal, and then put them into a position where it will continue around the circle and go backwards into the vestibule.
Naples and Eisen (2015) reported canal plugging for AC BPPV. This is almost never done, and we think this is generally not going to be a good idea.
Our "in the trenches" experience with these maneuvers is that they don't work nearly as well as the Epley maneuver does for PC BPPV. In other words, our thought is that the response rate of maneuvers for supine DBN is low -- perhaps < 50%, and that this is basically due to the lack of a clear cut method of diagnosing AC-BPPV. In other words, we are treating conditions due to lots of other things than BPPV, with maneuvers. Song et al (2015) reported that treatment responses is less than for PC BPPV. We think it is interesting that there is no controlled study of AC treatment (at least as of 2015). The studies published to date, not only are uncontrolled, but also use loose diagnostic criteria. This is probably because almost nobody fits the strict criteria.
Honrubia et al (1999) mentioned a "reverse Epley" maneuver, and results in 4 cases. Similarly, a "reverse Semont" maneuver has been suggested. These maneuvers, if started with nose down to the side that makes the AC vertical, are logical, and are similar to many other successful maneuvers, but their biomechanics are not as good as ones where the head is literally upside-down, as for the Kim or Yacovino maneuvers discussed below. In other words, less likely to work. They are pretty close to the Rahko maneuver.
In the Korres et al (2010) discussion of the reverse Epley, it is defined instead as a conventional Epley maneuver with "slight-head-hanging". In other words, it is not even a "reverse time order" Epley. It is a different way of reversing the Epley. We think that this maneuver is dubious efficacy for the supposed mechanism of AC BPPV, but perhaps it might be useful for situations where AC BPPV is misdiagnosed as it is actually a variant of PC BPPV as discussed above.
Illustration of Rahko's maneuver, from Korres (2010).
Rahko (2002) suggested a maneuver as illustrated above. Start with the head 45 deg down, then move to 45 up (supine) accomplishing a 180 degree "flip". This geometry resembles the Semont maneuver where again, a 180 degree flip is used (i.e. B to C). Rahko reported success in 53/57 patients, although without any controls. We would call position B the "head looking under the table" position. Because the head is flexed rather than extended, it is perhaps more easily possible to attain a head position closer to pointing 90 degrees down (i.e. head flexed 90 degrees from prone, looking under table), than with maneuvers that depend on head-extension (such as the Kim and Yacovino maneuvers discussed in the following).
Crevits (2004), reported a total of 2 cases in which BPPV was successfully treated with a "prolonged forced position" procedure. In this procedure, there is an attempt to bring the head backwards as far as possible -- 60 degrees beyond supine, (in theory, upside down would be best), followed by return to upright and immobilization of the head in this position for 24 hours. In our opinion, the positions of this maneuver are reasonable, but the rationale for 24 hours of immobilization of the head is difficult to comprehend. It is clear both from biomechanical considerations (e.g. Squires et al, 2004) as well as from experience with other types of BPPV that, at most, debris moves in minutes. Also, the results of Kim (2005) and Yacovino (2009) see below, in a much shorter time, suggest that prolonged positions are not needed.
|Treatment for AC BPPV as proposed by Kim and associates (2005). In position 'b', the head is turned 45 degrees towards the symptomatic side. Note that the illustrations of the canals from the Kim article (shown above) are anatomically impossible artists renditions.||Deep head hanging treatment for AC BPPV as proposed by Yacovino, Hain and Gualtieri. (2009). This treatment differs from that of Kim (above) in that the head is not turned to either side, and it is positioned so that it is further back with respect to horizontal in position 2.|
Just a year later, Kim and associates (2005) described a more logical treatment maneuver for the anterior canal. Their modified maneuver is essentially just a deep Dix-Hallpike. They reported a cure rate of 96.7% in an uncontrolled study of 30 subjects. We find this very difficult to believe, as nothing is ever this good, and there are some other issues (see end of paragraph below), but still the authors seem to be enthused about the maneuver, and maybe it works.
The Kim maneuver is fairly logical, but it could be more logical- -in particular, position 'c' debris close to the cupula might not move around the turn. Also, if one accepts the idea that the most anterior part of the AC is nearly saggital, one should logically start this maneuver with deeper head-hanging to get that segment upside down, then go to the head 40 degrees to the symptomatic side. Note that the illustrations of the canal anatomy taken from the Kim paper (see above) are not anatomically correct -- you should use an actual physical model of the semicircular canals to work this out for yourself. As is the case for uncontrolled studies in general that seem to violate common sense and conventional experience -- like this one -- perhaps this study is simply overly enthusiastic.
Yacovino, Hain and Gualtieri (2009) reported results of using a maneuver similar to that of Kim in 13 patients. This again was an uncontrolled study, and the diagnostic criteria for AC BPPV were not as tight as suggested above (criteria were supine DBN with or without torsion). In 5 of these patients, the nystagmus arose after an Epley maneuver for PC BPPV. From the discussion above, other potential mechanisms than AC BPPV include long-arm PC BPPV, and central adaptation nystagmus. The maneuver in this study, like that of Kim, while designed for AC-BPPV, might also be effective for PC BPPV of any variety as prolonged inversion might move debris from close to the cupula to a position near the common crus for the PC. They reported "symptom free" status in 85%. Similar results were reported in a larger study (Yacovino et al, 2014).
For all of the supine AC BPPV maneuvers, there is a problem in that they may be physically impossible due to neck flexibility. One way to get around this is to use devices that flip the person upside down -- e.g. the Epley omniax, and similar devices. These are generally inaccessible, and thus it seems prudent to think about how to attain an upside down position, without a specialized machine.
Along this line, there is also a "forward" AC BPPV maneuver. The closest one to this is the Rahko maneuver from 2002 (see above). In this maneuver, the patient is prone on a table, with the head over the end and bent forward off the end of the table, as if one was looking for a piece of gum under the mat table. Thus again the head is upside down. After a reasonable length of time (perhaps based on how long the downbeating nystagmus persists), one is flipped onto the back (i.e. goes from prone to supine), so that the debris falls towards the vestibule. One would think that ideally, the head would be rotated so that the AC in question is vertical for both positions. This maneuver (so far unaccompanied by any clinical trial) may be the most reasonable for older patients where the head may be anteriorly positioned due to kyphosis. No study is yet available - -but as the geometry is identical as all of the other maneuvers, it seems likely to have similar results.
In our clinic setting in Chicago, we have had reasonable success in treating anterior canal BPPV -- roughly a 50% response rate -- (defined using loose criteria) with the "Deep head hanging maneuver" as illustrated above (Yacovino et al, 2009; 2014). This can be performed on a mat table, or if necessary, using a tilt table or similar gadget that can turn the patient upside down (e.g. Epley Omniax). It does not seem to us that the added effort of getting the patient upside down, is rewarded by a higher cure rate. Nevertheless, one would think that it should help.
This procedure is essentially the positioning of Crevit's maneuver, without the 24 hours of immobilization. It could also be considered as a simplified and deeper Kim maneuver. All of these maneuvers are really the same thing -- with minor variations. The idea is to invert the anterior canal, to allow debris to fall to the "top" of the canal, and then, on sitting, to allow it to further migrate into the common crus and then vestibule. This maneuver has an advantage over the "Kim" maneuver in that one does not need to know the affected side.
When the Yacovino maneuver fails, we then will go to a variant of the Rahko maneuver, but starting with the body prone to take advantage of the usual greater head flexion than extension, in an attempt to get the head close to upside down.
At this writing (2017), home treatment of AC BPPV has not been studied (unlike the case for PC BPPV).
Suppose the patient really has something else ? Long arm PC BPPV should be treated with the Epley (see below). Central adaptation nystagmus needs no treatment. Other central nystagmus -- an MRI seems reasonable.
A controlled randomized study of a rational AC maneuver is needed.
We, like Hetzler (2007) are unenthused about using the conventional Epley or Semont maneuvers to treat clear cut AC-BPPV (e.g. Herdman et al, 1996; Jackson et al, 2007). Oddly enough, Herdman states in her illustration that for the L AC, "note that the position changes are the same as in the treatment of the left posterior canal". The geometry of the AC is such that one would expect these maneuvers could even make it worse, because they involve nose-down positioning.
Still, these maneuvers would make some sense for debris in the "long arm" -- i.e. top of the PC, and falling the opposite way as usual BPPV. A clue may be that the torsional component for this mechanism should be "contra" -- i.e. directed towards the up ear. Here one is not treating AC-BPPV at all, but variant PC BPPV.
Overall, the diagnosis of AC-BPPV is often not "clear-cut", so it could be reasonable to be liberal with maneuvers.
The Vestibular Disorders Association (VEDA) maintains a large and comprehensive list of doctors who have indicated a proficiency in treating BPPV. Please contact them to find a local treating doctor.
Because anterior canal BPPV is more complex than posterior canal BPPV, and includes far more central nervous system conditions (i.e. brain tumors, strokes, Chiari Malformation) as alternative possibilities, we think that seeing a neurologist experienced with dizziness is usually best option.
Our dizzy specialty practice is located in Chicago Illinois. Chicago Dizziness and Hearing, 645 N Michigan, Suite 410, Chicago 60611