Timothy C. Hain,
Page last modified: April 20, 2013
The main BPPV page is here. Spanish Version of Lateral Canal Page
Displaced otoconia can migrate to the posterior canal, which is the lowest part of the ear when one's head is upright. Debris can also 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.
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.
Other substances in the inner ear might also cause a nystagmus resembling lateral canal BPPV. Positional alcohol nystagmus is well known. Nystagmus of other disorders such as central positional nystagmus due to cerebellar damage can closely resemble lateral canal BPPV, but fortunately are much less common.
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 variant, accounting for about 3-12 percent of cases (Cakir et al, 2006; Korres et al, 2002; Hornibrook, 2004). In the author's experience, most cases are seen as a consequence of an Epley maneuver, but others find that spontaneous occurence is more common (Hornibrook, 2004). It is diagnosed by seeing a horizontal nystagmus that changes direction depending on the down ear.
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.
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 to either side. This is called the "supine roll test".
.Supplemental material on the site DVD:
The nystagmus 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.
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).
Han et al (2006) recently 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 BPPV, but it is based on the same biomechanics and logic.
Almost 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. The main exception is the
Gufoni maneuver, in which for the geotrophic variant, the maneuver
starts on the unaffected side, but nevertheless continues to turn
towards in that direction (i.e to nose down).
|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 use in our own 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 this procedure 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. Vibration of the mastoid might theoretically add to efficacy of this procedure but no studies are available at the present writing.
Supplemental material on the site DVD: Movie of the log roll exercise
We offer a home treatment DVD that illustrates the Log-roll exercises.
Simply sleeping with the "affected" ear up has been reported to cure about 75% of patients (see Vannucchi et al, 1997). This positioning is similar to recommended for posterior canal BPPV after the Epley or Semont maneuver, except for the 45 degree angle of the head with respect to the horizontal is not used here. Considering the mechanics of the situation, one would expect that bad-ear up would work only for case where the debris is not close to the ampula. In other words, it would not be expected to work for the ageotropic variant of lateral canal BPPV.
|Gufoni Maneuver for ageotrophic nystagmus, from Appiani et al, 2005.|
Appiani and associates (2001; 2005) reviewed several quicker repositioning maneuvers for lateral canal BPPV. Many of them are named after their inventor -- for example, the "Gufoni" maneuver. They generally involve side-lying for 2 minutes, a turn of the head 45 degrees either up or down, remaining in this position for 2 minutes, and then a return to the upright position. Abrupt movements of the head are suggested in these maneuvers - - but in our opinion, there is unlikely to be a benefit (Hain et al, 2005). The process is as follows:
- For the geotrophic variant of lateral canal BPPV, one starts on the unaffected side (side of weaker nystagmus), and then proceeds to 45 deg nose down
- For the ageotrophic variant, one starts on the affected side (side of weaker nystagmus), and proceeds to 45 deg nose up (see above).
In our opinion the logic of the Gufoni maneuver is questionable -- The procedure -- lying down one one side, and then turning the head 45 degrees up -- seems to us to be unlikely to accomplish much useful as lying down on one side is presumably done by patients every night, and a head turn of 45 degrees seems to us far less than the 360 degree turn accomplished by the log-roll maneuver.
Kim et al (2012) recently published a randomized trial of the Gufoni for the less common, ageotrophic varient of lateral canal BPPV (Kim et al, 2012), and reported a 73% response rate. While we are pleased that an attempt was made to perform a controlled study, this study contained many serious flaws.
This study, like others of lateral canal BPPV, has the intrinsic problem of determining the side to treat. In the Kim study, there were judgments made based on intensity of nystagmus in several positions, that went without documentation. The sham maneuver in the Kim study resembled the active maneuver, but was done on the opposite side. If the side was incorrect, the maneuver might treat. Figure 2 in the paper, which is used to explain the mechanism, does not appear to reflect either known ear anatomy or even a reasonable depiction of rotation of a cartoon of ear anatomy.
For these maneuvers, one must both know if the nystagmus is geotrophic/ageotrophic as well as know the side of debris (which is not always the clearest). Because the usual assumption is that the "affected" side is the one with stronger nystagmus in geotrophic, and the affected side is the side with weaker nystagmus in ageotrophic, in either case, one starts on the side with weaker nystagmus. If the nystagmus is geotrophic, one after 2 minutes, then one proceeds towards nose down. If it is ageotrophic, then nose up. Nausea or vomiting are obvious potential issues with these maneuvers that require one to spend 4 minutes in positions that induce severe vertigo.
Of course if you are just not sure which side is affected, you could end up mistaken as to the maneuver and end up doing nothing at all.
The main advantage of these procedures are that they may be quicker as they cut out some of the useless steps of the Log-roll. We agree with the logic that the full log-roll is not always necessary. Nevertheless, for most situations, and especially when not done with apparatus to examine eye movements, the log-roll is the safer option.
Another variant is to move the head briskly towards the good ear during each step, which might add an inertial component to the repositioning process (Lempert and Tiel-Wielck, 1994). However, theory suggests that inertia contributes very little (Hain et al, 2005). Brisk turns does add risk to the maneuver as it could hurt the treated person's neck as well as, in theory at least, dissect a vertebral or carotid in the same way that forceful chiropractic manipulations can sometimes induce stroke. Brisk head movements may also increase risk of retinal detachment.
Several authors have suggested that rapid horizontal headshaking can resolve lateral canal BPPV (Oh et al, 2009; Vanucchi et al, 1997). This is somewhat plausible considering that the lateral canal is normally tilted so that debris would tend to roll out of it, and by shaking things up, this might be encouraged.
In the author's experience, lateral canal BPPV after an Epley maneuver nearly always resolves without any treatment after a week. Accordingly, the lack of a control population in most of the studies is a serious flaw.
See also the comments above about the dangers of brisk head shaking.
Neuroradiological investigation may be warranted in persons who fail to improve these maneuvers as nystagmus similar to lateral canal BPPV can occur in persons with cerebellar lesions. We have encountered similar nystagmus in persons with cerebellar lesions.
Little is known about recurrence of lateral canal BPPV. Sakaida and others (2003) reported that lateral canal BPPV recurs more frequently than posterior canal BPPV (by about a factor of two). Their report was based on a total of only 19 patients with lateral canal BPPV. We find this dubious.
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 -- stuck debris and loose debris. Biomechanical reasoning (no plunger effect of debris) would suggest that strong ageotrophic would necessarily be due to loose debris, and thus that lateral canal cupulolithiasis should not be a big problem(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. 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.
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.
Our own practice is located in Chicago Illinois. For uncomplicated BPPV treatment, we generally schedule new patients to see one of our physical therapists.
http://dizzy-doctor.com/: Chicago Dizziness and Balance, 645 N. Michigan, Suite 410, Chicago 60611
Published literature referred to above:
|© Copyright April 20, 2013 , Timothy C. Hain, M.D. All rights reserved. Last saved on April 20, 2013|