Lateral canal bppv which is the affected side

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No use, distribution or reproduction is permitted which does not comply with these terms. Introduction Benign paroxysmal positional vertigo BPPV is the most common cause of peripheral vestibular vertigo. Figure 2. References S. Lee and J. Parnes and J. View at: Google Scholar F. Mosca and M. View at: Google Scholar E. Prokopakis, I. Vlastos, M. Tsagournisakis, P. Christodoulou, H. Kawauchi, and G. Lopez-Escamez, M. Molina, M.

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Interestingly, there was a substantial response to the Sham. Figure 2 in the paper, which is used to explain the mechanism, does depict either known ear anatomy or even a reasonable depiction of rotation of a cartoon of ear anatomy.

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. We suuggest for the ageotrophic, continuing on with either the "geotrophic" Gufoni or just the rest of the logroll. 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 abbreviated procedures is 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 for geotrophic BPPV.

We do not agree with the logic that the "ageotrophic Gufoni" is a complete treatment. We think a log-roll is the logical treatment for ageotrophic. The Zuma maneuver is basically a log-roll with different timing and an emphasis on rapid head movement.

In this maneuver there is a combination of gravity and inertial forces. The logic is to begin with the "bad ear down", done "briskly" presumably to attempt to detach otoconia and then let them sediment to the bottom of the lateral canal e. Yacovino et al, Then another 90 degree turn of the head is made, again rapidly. Following 3 minutes, a third turn is made we are now degrees from the start. Instead of going nose-down as in the log roll , the individual is sat up. We find it difficult to follow the anatomy in this figure from the author's paper on the topic, but still we think that the general idea of doing a log-roll with rapid head movements, and long waits between each position is reasonable enough.

The geometry of this maneuver can be appreciated, and it all makes reasonable sense till position 4 which seems less optimal than nose down i. Another variant is to move the head briskly towards the good ear during each step, which might add an inertial acceleration component to the repositioning process Lempert and Tiel-Wielck, However, theory suggests that inertia contributes little to the movement of otoconia Hain et al, Still this is part of some maneuvers e.

Brisk turns adds 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. Actually, we encountered one patient who dissected their vertebral from swimming, and another who dissected their carotid artery from VEMP testing with head turning not the method we favor.

Brisk head movements may also increase risk of retinal detachment. Vibration might be a little safer -- but no studies so far. In spite of all of these thoughts about risk, practically we have never encountered anyone with a dissection or a retinal detachment related to a physical therapy maneuver of this nature.

Several authors have suggested that rapid horizontal head-shaking can resolve lateral canal BPPV Oh et al, ; Vanucchi et al, ; Kim et al, 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.

Kim et al described the maneuver as follows: " For head-shaking maneuver,15 patients were brought into a sitting position. They do not mention the head excursion presumably small -- for convenience lets choose The problem is the small radius, r. There are some interesting issues brought up here -- in our clinic, we routinely use head-shaking as a diagnostic maneuver, prior to positional testing, and prior to any physical treatments. We also use the HIT test, which incoporates a high acceleration head movement.

Could we be treating patients by accident? Neuroradiological investigation may be warranted in persons who fail to improve after 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. Generally speaking however, when a cerebellar lesion creates positional nystagmus, neurological examination also reveals cerebellar signs other than nystagmus.

Little is known about recurrence of lateral canal BPPV. Their report was based on a total of only 19 patients with lateral canal BPPV. We find this dubious, as the geometry of the lateral canal makes it unlikely to develop lateral canal BPPV in the first place LC bppv is much less common than PC BPPV , as well as unlikely for a patient to repeat the same process. Currently it is generally felt that this is a poor prognosis variant of lateral canal BPPV although not all agree -- e.

Bisdorff and Debatisse, , 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. 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, 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. 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, 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.

Imai et al, 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. Kim and Hong 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.