Background: At the end of the 1970s, a combination of circumstances resulted in a manoeuvre being carried out on a subject complaining of positional vertigo. The outcome was “miraculous” – the patient was asymptomatic and the vertigo was impossible to reproduce. Repeating the same manoeuvre on other subjects also suffering from the same complaint gave the same results. These findings gave rise to a technique, which after fine-tuning and additional research became known as the liberatory manoeuvre and then later, the Semont manoeuvre. This manoeuvre is widely used by vestibular therapists as well as by the ENT community all over the world. What is the situation in 2005?

 

Physiopathology: BPPV is a transient rotary vertigo (lasting about 25 seconds) that occurs when the head is placed in a particular position. The vertigo disappears if head position is maintained and it can be reproduced at will. It manifests itself as a torsional nystagmus beating toward the lower ear. The nystagmus peters out after paroxysm, and inverts when the subject is back in an upright position.

 

Functional explorations show no major anomalies except if the BPPV appears on an earlier vestibulopathy or, when post-traumatic, is associated with a vestibular lesion. In most cases, when the BPPV is idiopathic, a slight asymmetry can be observed which disappears following treatment. RCT generally shows a slight irritation that is ipsilateral to the BPPV.

 

When this manoeuvre was discovered, the only hypothesis available at that time was that of SHUKNECHT who called it cupulolithiasis. But this hypothesis was not overly satisfactory. EPLEY employed the term canalolithiasis, while at the end of the 1980s, Th. BRANDT wrote that if the Semont Manoeuvre worked, it was because the debris was located in the canal rather than on the utricular side of the cupula. Presently, thanks to live demonstrations by David POHL in Australia and Lorne PARNES in Canada, we know that it is caused by an egg-shell coloured aggregate moving about the posterior semicircular canal. When the aggregate is gently tapped using a blunt instrument, it disintegrates and turns into a sludge. The aggregate consists of calcium carbonate crystals held together with proteins. This binding agent renders the aggregate somewhat gluey.

 

This information enables us to understand a number of findings discovered during provocation manœuvres or during the therapeutic manoeuvre.

 

The fact that the aggregate disintegrates explains why the Brandt and Daroff dispersion procedures rendered the patient asymptomatic but did not stop it from reoccurring. The same goes for the exercises prescribed by M. NORRE.

 

The fact that the aggregate is somewhat gluey explains the variability of the latent periods as well as, in certain cases, the difficulty in reproducing the vertigo. This also explains why manoeuvres sometimes have to be repeated to induce a therapeutic nystagmus.

 

The quite substantial size of the aggregate also explains why mistakes in manipulation or mistaking the side are responsible for lesions to the cupula. Nowadays, unless there is evidence to the contrary, canalolithiasis appears to be the most logical explanation of benign paroxysmal positional vertigo. This however does not mean that cupulolithiasis should be dismissed.

 

Method: Experience has shown us that the success of therapeutic manoeuvres is closely tied to the quality of therapy preparation.

 

We suggest avoiding, as far as possible, the use of too many diagnostic manoeuvres. Firstly for patient comfort: numerous provocation procedures cause nausea and reduce their tolerance as treatment continues.

 

How to determine which side? Having checked for the absence of spontaneous nystagmus in all gaze positions, all that is required, in the majority of cases, is to lay the subject down on their back, firmly but without excessive force, with the head positioned slightly lower than the body (but not so far as to be in the Rose position). After a variable latent period, a torsional nystagmus is observed, although sometimes a simple drifting of the eyeball as if the torsional nystagmus was about to occur. The direction of the fast phase nystagmus indicates the affected side. After the nystagmus disappears, the subject is returned to a standing position, the head slightly down-turned, to check for nystagmus inversion.

 

If lying the patient down on their back has no effect, turn the head 45° to one side:
- either nystagmus is observed and we find ourselves in the earlier situation
- or nothing happens and the head is turned to the other side:
- nystagmus is observed and we find ourselves back in the starting situation
- nothing happens and the patient is returned to the seated position.

 

If when returning the subject to the standing position nystagmus is observed, do not forget that it is an inversion and that the nystagmus beats to the opposite side to that of the affected ear. If these different manoeuvres have no effect, move on to the DIX & HALLPIKE manoeuvres.

 

It is worth noting that nystagmus inversion is a significant factor. Indeed, it shows, as with the onset of nystagmus, the shifting of the aggregate in the canal in the direction of the endolymphatic current. The absence of nystagmus inversion calls for due caution and it should not be forgotten should the liberatory manoeuvre have no effect. Likewise, our goal is not to aggravate the nystagmus by fatigue with repeated diagnostic manoeuvres. We do not consider this to be a necessary element.

 

The liberatory manœuvre: it is assumed that the side is known and that the nystagmus parameters are present and have been verified.
The following example is for BPPV simulation of the RIGHT side.

 

The subject is seated in the middle of the examination table, their legs dangling, so that the same amount of space is available on either side of the subject. We begin by lying the patient down on their left shoulder, the head at a slight angle, having angled the head 45° upwards for safety (checking for the absence of nystagmus) the head is then turned 45° downwards.

 

Explanation: In this position, the right SCC is on a vertical plain and the debris, while regrouping, migrates towards the ampulla. One would expect there to be no more nystagmus so the subject is then gently returned to the sitting position with their head in the upright position. Then we lie them down again on their right shoulder, the head in any position, as soon as downards “rolling” nystagmus presents itself, the head is turned upwards at a 45° angle. The nystagmus becomes more pronounced, the patient resists. We wait for the nystagmus to disappear.

 

Explanation: The debris that had regrouped in the ampulla gravitates towards the lowest part of the SCC causing an endolymphatic current which in turn causes a movement of the cupula towards the canal. This movement of debris produces the nystagmus. The movement of the head from any position through 45° in an upwards direction is going to increase the speed of the endolymphatic current because of the direction of the canal, "from a slight incline to a vertical position" and facilitate the migration of the debris.
Once the nystagmus has disappeared, the head is brought back to the upright position and then with a firm, brisk movement, but not violently, the subject is brought back to the lying position but this time onto the opposite side, their left shoulder.

 

Explanation: If the head remains turned upwards at a 45% angle (in line with the canal) the inertia of the aggregate when the therapeutic manoeuvre begins will cause it to gravitate in the opposite direction, in other words towards the ampulla instead of towards the canal. Bringing the head upright, the force applied to the aggregate at the point of initial acceleration will adhere it to the wall of the canal where it will remain throughout the whole process until the opposite position is reached.
Once the destination is reached and after a variable latent period, therapeutic nystagmus is observed. As soon as it appears, the subject’s head is turned downwards at a 45° angle.

 

Explanation: In the target position, the part of the SCC that was at the lowest point is now at the highest point. The forces that attached the debris to the wall of the canal disappear. The debris continues to migrate along the slope of the canal towards the crus commune with an endolymphatic movement in the same direction as that of the start. This explains why the therapeutic nystagmus beats in the same direction as the initial nystagmus. As with the starting position, the 45º downward rotation of the head will increase the angle of the slope and facilitate movement of the debris.
The subject is then left for ten minutes in the left-lateral decubitus position with their head turned downwards at a 45° angle.

 

Explanation: Depending on the nature of the protein bonding, the aggregate might disintegrate or fracture during the manoeuvre. Once this is finished, it can be accepted that only sludge will remain. The movement of this sludge towards the exit of the SCC and into the utricle does not happen at the same speed as the movement "en bloc" as at the start of the manoeuvre. For safety reasons, it is best to take every precaution so that the canal empties completely and therefore reduce the relapse rate.
After a period of rest, the subject is gently returned to the seated position with the head fully upright. Sometimes the subject experiences a strong sensation of being thrown forward and reacts by throwing themselves backwards. So the subject must be held firmly when returning to the seated position and be ready for any eventuality should this arise.

 

Explanation: What happens to the debris is unknown. The nystagmus shifts along the SCC. On the hypothesis that the aggregate disintegrates, the subject is left in the lying position, but the opposite might happen; there might be a shift "en bloc " and when the crus commune is almost vertical, when returned to the sitting position, the shift of debris through the latter towards the utricle will cause an endolymphatic current in both posterior and anterior SCC. These two canals work in opposite directions and are responsible for the sensation of vertical movement caused y the stimulation of both canals simultaneously. Moreover, it is not a torsional nystagmus that is observed but rather an inferior vertical nystagmus with, sometimes, a horizontal component beating towards the affected ear.

 

Regardless of whether the event described above occurs or not, the subject is not allowed to leave believing that they are cured. It is best to prevent any ill-advised endeavour on their part upon their return home. The subject is slowly returned to the original starting position facing upwards at a 45° angle to verify that there is nothing left, but if there is a little something left, the manoeuvre is immediately repeated to complete the emptying of the canal. Whatever happens in the starting position, the manoeuvre described above is repeated. Sometimes, when repeating the manoeuvre, therapeutic shaking is sometimes observed indicating that the canal had not been fully emptied.
After the second manoeuvre, the subject is asked to maintain their head rigorously in the vertical position until the following session a week later. They are not asked to do this to ensure the success of the therapeutic manoeuvre but rather to decrease, as far as possible, the relapse rate.

 

Explanation: let us keep in mind that aggregate disintegrates and becomes sludge. It is fair to say therefore that part of the sludge might still find itself in the end portion of the SCC and continues to empty out during an indeterminate period of time. If your subject positions their head so that the sludge moves in the opposite direction towards the SCC, vertigo will reappear as soon as aggregate regroups.
One week later, all provocation manoeuvres are repeated and in more than 92% of cases, the subject is asymptomatic. Nonetheless, they might note a floating sensation or instability. For the majority of cases, this sensation disappears over the course of the following week.

 

Explanation: when the SCC empties into the utricle, the debris falls as rain onto the utricular macula, modifying the symmetry between the two utricular maculae. This effectively gives the impression of instability when walking and sometimes gives the impression, once lying down, of being on a water mattress.

 

Conclusion: When every precaution has been taken, when all the signs point to and enable one to conclude that it is a BPPV, the success rate stands at around 100%. It must not however be forgotten that certain infiltrating tumours can mimic a BPPV. Should this be the case, no therapeutic nystagmus is produced and the manœuvre has no effect. With experience, it can be noted that these subjects have a different nystagmus with a greater vertical component than normal, with projectile vomiting. But it should be acknowledged that it is more a case of phenomenology than anything else, much more a posteriori than an a priori differential diagnostic capacity. All of which is to say that if the manoeuvre is unsuccessful after two or three repetitions, but never more, a more cautious approach would be to start the examinations afresh.