Rehabilitation of a Unilateral Vestibular Deficit Syndrome (Example)

To facilitate understanding of how the session develops, we will use a simple example: a right unilateral peripheral deficit disorder.
The pre-therapy evaluation provides the following information:
- the most obvious of these is the presence of a spontaneous left-beating nystagmus of differing degrees according to Nylen’s classification. This provides both temporal and quantitative information. Temporal, with regard to the duration of the disorder, and quantitative with regard to the degree of the disorder
- depending on the severity of the spontaneous nystagmus, there will (or won’t) be impaired eye pursuit in one direction or another. For an intense, spontaneous left-beating nystagmus, for example, stemming from a recent disorder, left eye pursuit will be impaired.
 - videonystagmoscopy protocol: Eye response during counter-rolling testing  tells us if the otolithic has been damaged or not. High, constant-speed rotational impulse testing, depending on the severity of the spontaneous nystagmus, will result in full directional preponderance, or the start of recovery or compensation of the injured side. Rapid rotation of the patient’s head will increase severity of the spontaneous nystagmus.
- vestibule-spinal lateralisations are harmonic in nature and all veer towards the right.
- high-speed rotatory chair testing with a sudden stop indicates asymmetry. Asymmetry is consistent in both eye fixation and vection testing. Vection testing provides information about the degree of central compensation.
If the examination does not give the same results as those described above, everything should be called into question. Referral to a specialist prescribing doctor is essential. They should be provided all information considered to be incompatible with the condition that was originally diagnosed. It is the prescribing doctor who will give the green light to follow up treatment or who will call for additional examinations to be carried out.
It should not be forgotten that we are in a neurosensoral field that is likely to change, fluctuate and evolve. Our observations are those of the moment they were made and only reflect the condition at a specific point in time.
It is acknowledged that vestibular asymmetry will disrupt the direction and the stability of the gaze and distort the straight ahead position. This set of anomalies is going to be responsible for the subject’s complaints. The brain desperately tries to correct the situation, as can be seen by the incidence of the fast phase of a spontaneous nystagmus.
It would appear obvious that the first thing to do is to try to reduce this asymmetry. It should not be forgotten that asymmetry appears in all vestibulo-spinal and vestibulo-ocular lateralisations.
To do this, we will use a rotatory chair to provoke repeated stimulations, which, thanks to neuronal plasticity will re-align to the "straight-ahead" gaze, and as such decrease or even get rid of any vestibulo-ocular deviations. So we see that the work of the rotatory chair does nothing more than what the brain asks of it. The absence of a spontaneous nystagmus and the symmetrical responses do not mean however that the dysfunctional ear is recovered. Remember, this does not deal with the dysfunctional labyrinth, but rather on the consequences of an asymmetry of the tonus between the two systems acting complementarily to each other. The consequences themselves are being controlled by a hierarchal system aimed at adding weight to the system response. A repeated series of rotations on the chair is specifically going to bring about a reduction of the spontaneous nystagmus, followed by its complete disappearance, in other words, its inversion. This modification in the vestibulo-ocular response shall be the proof of the plastic modification of the “straight ahead” position and the return to normality of the ability to stabilize and direct the gaze.
The first manipulation to be carried out is when the subject is seated on the rotatory chair, with video goggles over the eyes and observing the monitor. Observing the signs allows us to know how the patient is behaving at the present moment. It also allows us, in cases of pressure syndromes, to focus on the passage of a critical phase and what comes afterwards. In the aforementioned case, the subject is at their third session. The first two sessions are spent going through the evaluation. What is observed with the video does not risk being any different from what was observed at the first session. Specifically, a left-beating spontaneous nystagmus should be observed.
When the chair is rotated at high speed (> 400°/s), the nystagmus, following a clockwise rotation, is left beating. After an anticlockwise rotation, the nystagmus is right beating. Be careful! It is a provoked nystagmus, and not a spontaneous one. If we continue with rotations towards the right, response from the left labyrinth decreases. This provoked asymmetry appears as a spontaneous right-beating latent nystagmus that is going to counter and diminish the spontaneous left-beating nystagmus. The goal of the exercise is to manage to reduce the left-beating nystagmus. From this point on, the subject is asked to undergo a series of rotations towards the right and to control the response based on the length of the response during eye fixation.
If the results from a session of this type are transferred to a graph, we observe that the curve not only changes with the repetition of the series of rotations, but also with the increase in the number of sessions. Great care must therefore be taken when analysing the shape of this curve.

Here is an example of the responses from an evaluation:

Clockwise rotation12 seconds14 seconds
Anticlockwise rotation3 seconds5 seconds


The right responses are seriously reduced compared to the left responses.
The subject is then rotated in a clockwise direction for a series of three turns (initially). As can be seen by the curve, we will begin by observing an increase in response, followed by a decrease before increasing once again.
One should not expect to witness a major reduction in response from the first session.
And there are many reasons for this: the subject might have some difficulty when it comes to dealing with the number of repeated stimulations. It is difficult to predict 100% the reaction of each subject. The ability of the patient to deal with such stimulations is dependent on them having latent motion sickness. This of course, has nothing to do with the disorder they are being treated for.
Another reason is their general condition: if the deficit disorder is the result of a surgical or accidental trauma, their vulnerability will be different from that of a subject having had a sudden-onset viral disorder.
The final reason does not directly stem from the patient, but rather from the secondary effects of the treatment. In fact, it is essential to respect the rise in responses even of the subject states that they are able to "take a little more". Not respecting this could lead to, with a delay of one or two hours after the session, the emergence of a non-descript, latent, sneaky feeling of unease, aggravated by movement of the head, and associated with heavy-headedness, where the subject finds themselves obliged to undergo some kind of sensory restraint. These secondary effects, depending on their level of intensity, might lead patients to decide to stop the course of treatment.
The vestibular therapist, being knowledgeable on the potential outcome of these incidents, shall advise their patient about the possible appearance of undesirable effects and not to hesitate to phone to provide information about their intensity.
The following session follows the same protocol, and undoubtedly the length of the session will increase. The repetition of the sessions will lead to changes in the response curve until we see the disappearance of the spontaneous nystagmus at the end of the session, in other words, an inversion.
Rotatory chair treatment will be stopped once responses are symmetrical and much less than five seconds for a series of ten rotations. Furthermore, the modification of responses should correlate with asymmetry of responses to vection.
If the responses to vection are not symmetrical, you must persevere, following the same protocol as those of responses to fixation.
If responses are good, the following question is then asked: is treatment over?
Yes, if the subject shows no symptoms. No, if the subject still presents with complaints.
If the subject presents with no symptoms, and they have been attending two sessions per week, they will be asked to come back one week later for a check-up, if the check-up is positive, the next check-up will be scheduled for a month, unless the subject gets in contact of their own volition. If responses to vection and to fixation remain symmetrical and are those that correspond to a normal social and professional life, then at that point, treatment is effectively over.
If the subject is still presenting with symptoms: pre-therapy evaluation should resume looking to focus on the remaining complaints. In most cases (of subjects still presenting with symptoms) optokinetic stimulation sessions should be scheduled.
It should be remembered that the role of the optokinetic stimulation sessions is to reduce the burden of visual input and transfer it to the somatosensory one. The first remark to make, which should be obvious enough, is that optokinetic treatment should not be carried out in the same session as the rotatory chair or if the responses on the chair are not "normalised". In fact the rotatory chair session makes strong use of sight (except for vection) while the optokinetic treatment relies less and less on the use of visual input. These are two types of stimulations that cancel each other out.
We have seen what an optokintic generator is and does and we have calibrated the apparatus to stimulation speeds of 20°/s, 40°/s and 60°/s.
The subject must be standing upright in the room in complete darkness for this apparatus to be used. They are placed at a minimum distance of two meters from the nearest screen. The session begins with a horizontal stimulus at a speed of 40°/s. The patient is asked to focus on the luminous points of light on the wall that are moving past them. The instructions are: "just look without looking to do anything, and without looking not to do anything ". It must be completely passive since it is a question of triggering a reflex where voluntary participation is obviously undesirable.
After a certain time (varies greatly between one subject and the next), we observe a postural deviation on the same side as the direction of the stimulus. This postural deviation is not an imbalance but rather an active correction so as to avoid falling into a universe which, from a visual perspective, is moving in reverse. It should not be forgotten that when the reflex is triggered, the subject senses that the stimulus is motionless but that the room in which they are in is leaning, turning, and shifting in phase opposition to the stimulus. Thus, the source of the active correction. Hence, inversion only in the direction of the stimulus will enable us to bring the subject back to the correct vertical position.
We know that the speed of 40°/s is a starting point, but is not a speed that has to be scrupulously stuck to. Each individual has their own corresponding speed. You just have to play with the dial to discover which speed provokes the most forthright and major postural deviation in the subject.
One must look into the eyes of the subject to check for an optokinetic nystagmus provoked by the stimulus and control the position of the scope of the beating. With a normal subject, this should pre-empt the stimulus.
With the current case, we observe a postural deviation with a preference towards the stimulus. When the stimulus is moved to the same side as the damaged ear, nothing happens. Conversely, when the stimulus is on the opposite side of the injured ear, postural deviation is observed. The session will therefore consist of presenting, by “toggling” between the two directions, the most disruptive stimulus. Repetition will bring about a decrease in the degree of postural deviation. The same protocol will be used for the vertical stimulus. The only difference is that treatment should start at 20°/s and then be adjusted based on the observations of the therapist.
Optokinetic treatment is completed once the subject is completely insensitive to the stimulus, whatever the speed and direction.
In the case of an earlier lesion, it might be that the subject is not completely asymptomatic, which might warrant reeducation sessions for balance through proprioception exercises. These exercises are known by physiotherapists so there is no point dealing with them here.
Nevertheless, certain rules should not be forgotten:
- we have just completed a treatment by decreasing the burden of the visual input. It would be useful to check if the responses on the rotatory chair have changed. One might need to repeat certain rotatory chair sessions.
- to be able to improve input results, it should be worked exclusively without giving the brain any time to use anything else. To do this, the proprioception exercises are carried out with the subject’s eyes closed, randomly, without any potential pre-programming by the subject (so once again, auto-reeducation is not an option).
- place the vestibular system in a situation of conflict.
In conclusion, to increase the results of the somatosensory input, the subject must have their eyes closed, exercises will begin without the subject being told what is going to happen, with the addition of head movements, the frequency and direction of which are randomly changed.

Vestibular reeducation: deficit syndrome