Neurophysiology has taught us that the vestibular system is the primary system.

 

Observations made about patients show that multimodal compensation is only possible when the centres are in good order. A subject with a bilateral deficit disorder is able to move around and walk just as they are able to use their eyes. Saying that they are able to do this does not however mean that they can do it "naturally". It is said that at low frequency, in a static position therefore, proprioception is sufficient. The absence of a response from the otolithic system is responsible for a certain amount of imbalance that the visual input can not manage to fully correct (except after reeducation). The difference between the posture with the eyes open and the eyes closed is significant but is not pathological in the true sense. Dynamically, the subject is able to enjoy almost normal activities; conversely, in complete darkness, they might fall without even perceiving it. It is certain that a vestibular disorder will be all the more obvious to evaluate that there will be no associated neuromotor pathology. This means that: taken in isolation, somato-sensory input functions normally. The same is true for visual input, but should there be a vestibular pathology, oculomotricity, navigated by the vestibular system, will be disrupted. We must therefore deal with the input (the cause) responsible for the disruption (the consequence) of the whole of the balance function: the vestibular system.

We mentioned earlier that the functioning was carried out via a series of reflexes. Furthermore, we know that it is impossible to voluntarily induce a reflex. It is always possible to carry out a task by taking a longer path, slower, using large volumes of energy while fully conscious, something that is known as pre-programming. Using such a path is unsuitable because there are always delicate and conflictive situations that require an immediate response.

 

A subject who has developed a unilateral vestibular disorder tells us that when walking along the street, they can turn their head to look at a window display. Conversely, if, while walking, someone calls to them or something catches their eye and they turn their head without thinking, they will lose their balance. There we have a demonstration of the difference between a pre-programmed action and a reflex action, although the goal is essentially the same: look by turning the head. Only the latency time between the command and the execution is different.

 

What happened in the case of a subject with a fully bilateral vestibular disorder: peripheral and central?

 

Immediately after the lesion, the subject is unable to remain in a seated position, and much less in a standing one. To a discerning eye, the subject presents one major feature: although able to be in a sitting position, they are unable to hold their head up vertically. The head sags and/or leans to the side. Any attempt to correct this is pretty much impossible. If we control the segmental muscular force of the subject lying down, nothing in particular is noted. Having succeeded, through vestibular reeducation, in repositioning the head in the vertical position, one can at last try to get them into a vertical position. They can remain seated or in a standing position as long as there is a voluntary contraction of the extensor muscles. An immobile standing position becomes possible with a voluntary and intentional contracting of the extensors of the lower limbs. The subject is able to move about thanks to these walking aids, but with their legs rigid. Here, one can verify that despite the fact that the muscular force is unaffected and there is an effective proprioception, the subject is unable to use them to their advantage.
But let’s get back to the head: if we ask a subject sitting in a chair with a head-rest to close their eyes, we note that the head moves forward and the subject leans forward too. This compels them to always leave a light on at home.

The subject no longer has the ability to compare and adapt information. This demonstration shows that despite inputs other than the vestibular input being in good order, the subject has a severe handicap.

 

Let us now imagine a section of vestibular nerve following surgery for a debilitating Ménière’s disease or the excision of a vestibular schwannoma. In post-op, the subject presents with photophobia, nausea and vomiting that increase with movement of the head. The destructive nystagmus is present whichever way the patient looks. When an attempt is made to get the subject into a vertical position, a lateral tilting of the head that is ipsilateral to the stricken ear is observed. The standing position can be achieved but only with increased postural deviation. After several days, the head straightens, walking is once again possible, the nystagmus is only present with the gaze in a medial position.

 

Now, let’s take the example of a unilateral peripheral deficit. The subject describes great bouts of dizziness with nausea and vomiting, the inability to move the head without causing vomiting, and of course the inability to stand up. After three days, the dizziness subsides; the subject is finally able to stand up but presents with balance disorders that increase in the darkness. These balance disorders are characterised by an ipsilateral lateral lean towards the damaged ear. At the vestibulo-ocular level, one observes a spontaneous nystagmus beating contralaterally towards the bad ear, indicating a vestibular deficit.

 

What can be learned from these observations?

 

Central multimodal compensation of a peripheral deficit sets in quite quickly.

The speed with which a reeducation programme can be implemented is essential for the quality of the recovery and the speed with which the subject is able to get back to living a normal life.
Without the centres, compensation is impossible.

For what would appear to be an identical disorder, there are as many different behaviours as there are subjects. Reeducation is therefore adapted to each subject. There is no standard.

 

As far as reeducation is concerned, it can be said that:

 

there is no point in carrying out proprioception exercises on mobile platforms until the gaze has become stable.
self reeducation is of no great use although the activity does allow one to maintain the acquired skills.
for vestibular reeducation, one must be able to trigger a reflex using an external stimulus. Specially adapted equipment is required.
conflicts are responsible for slow-downs in the compensation process. Sensory restrain will delay compensation.