Rehabilitation of a Benign Paroxysmal Positional Vertigo (BPPV) of the Anterior SCC (Example)


Diagnosis through locating the canalolithiasis in the anterior canal is a very delicate thing. The story told by the patient is not the same as one usually hears from a BPPV sufferer. The subject arrives in quite a bad state: nauseas and unsteady on their feet. Conversely, they say that their symptoms improve or even disappear completely when lying down. As long as they do not lean their head back too far.

Observation using videoscope shows a spontaneous torsional nystagmus  with an upper vertical component. This leads us to fear there might be a brain stem disorder. The subject tells us that they feel better lying down, we check for any modification to their spontaneous nystagmus using the videoscope. Sure enough, the nystagmus fades away. When the patient is brought back to an upright position, the nystagmus reappears. The variation of the nystagmus is not sufficiently significant to establish that it is produced by a moving amalgam in the lumina of the canal. It is important to invert it.

Explanation: The vertical anterior canal appears in the head as a ring with its bottom cut off. With the patient in the upright position, the amalgam is therefore in the ampulla on the canal side of the cupula, acting like a cupular lithiasis. While the cupula lens towards the utricle under the weight of the amalgam, a nystagmus is produced. When the subject is lying down, the weight of the amalgam decreases or even disappears as it is supported by the wall of the canal, and the cupula goes back to its normal position.

Vascular disorders in the vertebrobasilar region can provoke this type of nystagmus and its depletion. Taking into account the disposition of the anterior canal in the head, the inversion of the nystagmus requires the canal to be in line with the vertical plain and the head to be in an extension position. Given what we have just learned about the vertebrobasilar region, it would not appear wise to position head in hyper-extension.

In fact, this situation does not allow us to clear up the doubts given that hyperextension could be behind a compression of a vertebral artery and might provoke the same distress and a torsional nystagmus, the origin of which is no longer peripheral.

Once the subject is lying down and the nystagmus fades away, they are asked to change to the prone position and to allow their head to hang off the end of the table. In this bowed position with the head facing down, the upper arch of the anterior canal is lowered, favouring the migration of the amalgam of the ampulla along the branch of the canal. The spontaneous nystagmus that is observed at the start will be inverted and furthermore will indicate the ear responsible for it.

Technique: The manoeuvres and positions used to invert the nystagmus enable us to confirm the mobility of an amalgam in the canal and to determine which side is the affected one. Let us suppose that we have observed a torsional nystagmus rolling towards the right ear when the subject is facing downwards. We then ask them to lie down on their right hand side while keeping their head turned down at a 45° angle.
Explanation: The right anterior canal is on the same plain as the left posterior one. The manoeuvre will take place therefore in the opposite direction to a manoeuvre of the left posterior one. The end position of the left posterior canal is therefore the start position of the right anterior canal, and the end position will be that of the starting position for the left posterior canal. The technique used on one side or the other is the same.

The subject therefore finds themselves lying down on their right hand side with their head turned down at a 45° angle, and one important thing to note: the head should be as flexed as possible. In other words, resting against the highest possible part of the forehead with the chin against their chest. As with the posterior canal, after ensuring that the nystagmus has faded away, the subject’s head put in a neutral position and holding the subject with both hands by the head and the neck, they are rapidly, but without any undue force, repositioned on the other side, in other words to their left. From the end position, the head is turned upwards at a 45° angle and at the same time, the head is put into extension. We then observe the reappearance of the torsional nystagmus beating in the same direction as the earlier provoked nystagmus when we tried to invert it. In other words, the therapeutic nystagmus beats to the opposite side than the one observed when the subject was in the standing position.

Explanation: initially, the nystagmus was produced by a deflection of the cupula towards the utricle. When the subject’s head was turned down, the amalgam migrated towards the upper arch of the canal producing a suction of the cupula and deflecting it towards the branch of the canal. The physiological direction. When we reach the final position of the manoeuvre, the amalgam continues its migration from the arch towards the downwards part, towards the crus commune. The amalgam comes to a halt on the wall on the upper part of the crus commune. Migration continues to take place in the physiological direction, moving away from the cupula.
The subject is then left in this position for several minutes with the idea that the sludge, resulting from the erosion of the amalgam during its migration, continues to flow in the same direction. The subject is then put into the sitting position, maintaining the same 45° angle to the torso with the head in extension. Lastly, we bring the head forwards (in flexion) while maintaining the right ear in a downward position. We then observe an event that almost perfectly mirrors that observed after a manoeuvre of the posterior canal.

The instructions given to the subject are as follows:

The proof of success of the manoeuvre is immediate: the subject comes in with a spontaneous torsional nystagmus, and leaves with no visible nystagmus at all.

Vestibular reeducation: Anterior SCC BPPV