Anterior canal or AC-BPPV may account for about 2% of cases of BPPV (Korres et al, 2002).
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").
AC BPPV is almost certainly grossly over diagnosed, as the patterns of nystagmus attributed to AC BPPV by most clinicians make no sense.
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
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.