Medical evaluation
What is a vertigo disorder?
- on one hand, the huge difficulty of "getting the message across";
- on the other hand, the fear of not being understood.
These patients explain that: "you have to have experienced these attacks of dizziness for yourself to really understand what we have to live with". Said remark is fully warranted. These patients are not like the “normal patients” that we tend to imagine.
Why?
Because it is not as simple as summing up the symptoms as vertigos and balance disorders. It should be understood that in modern-day language, the term ‘vertigo’ covers a vast number of symptoms and to be able to provide an effective treatment, we must be rigorous when it comes to semantics. Balance disorders are easier to explain, but then again, there is a difference between a sense of dizziness that goes unseen by a third party and a strong lateral lean when walking.
Case History
Far from the ideal scenario presented above, there is an entire group of people who are still suffering from earlier complaints: dating back many months, or even years and who have yet to find a satisfactory treatment. The therapist has the duty to question the patient, to carry out tests that are not necessarily practical for the ENT community, and to ascertain if the subject warrants vestibular reeducation or not. It is essential to find out if the patient has previously been examined by an ENT. Do not forget that with these conditions, extensive procedures of the posterior fossa might not have been detected given that the advice the patient received might have been wrong from the very outset. This does not reflect negligence on the part of the GP or specialist but might simply be a result of poorly asked questions and the confused responses of the patient. This misguidance might result in there being no consultation with a specialist, and veer towards a psychosomatic disorder instead. Given the lack of a well-conducted examination by an ENT specialising in otoneurological function testing, the therapist should not revert to vestibular rehabilitation, except in very specific cases.
We will use this evaluation to tackle these disorders. We will tackle them not through the definitions that doctors describe, but rather through the symptoms that manifest themselves through patients. We are therapists, not doctors. It is up to the reader to do things the other way around, when reading specialised literature, to use to the symptoms to find the diagnostic label.
The evaluation must begin with a comprehensive and rigorous question session, in other words, the task of a policeman, namely trying to “pin” the complaints to a possible vestibular cause.
Vestibular disorders, as we are well aware, are characterised by two symptoms: vertigos and balance disorders. To determine, through our conversations with the patient, if any of these symptoms exist.
Having listened to the medical history of the patient, the aim is to clarify certain aspects.
Vertigo:
How did it all come about?
What was the initial event?
In your own words, how would you describe a vertigo?
When the ailment first appeared, was it sudden or was it a gradual process?
Did your visual scene move and if so, do you remember in what direction?
When the initial episode occurred, were you taking any particular kind of medication?
Did the episode take place while you were being treated for another ailment: an infection, undergoing surgery?
When it happened, were you carrying out any particular activity?
How many identical episodes have there been since this started up until today’s appointment?
How long do symptoms last?
Does vertigo continue regardless of your position? Is there a particular position that makes it worse? Or makes it better?
Can you bring on an episode at will?
If the visual scene does not move, does your head feel like it is spinning? Do you feel like you are drunk? Are symptoms accompanied by any head pain?
Are there any gests, positions, movements that the patient is not longer able to do?
Do they manifest themselves differently depending on whether the patient is standing, sitting or lying down?
Are there any other signs associated with it?
Is your hearing affected?
Is there any tinnitus? Any feeling of fullness in your ear? Any earache?
Are there any balance disorders? At the same time? Afterwards?
Does everything return to normal between episodes?
What are the after effects following the initial episode?
Balance disorders:
Are they at about the same time as the initial vertigo episode?
Which balance disorders?
Did it appear gradually, suddenly or violently?
Do you lean strongly to one side?
Does it cause you to swerve when walking? Do these always occur on the same side?
Is there any sensation of imbalance?
Are there any outward signs of this imbalance?
Do light or dark in some way influence your disorder?
Is there any difference if this occurs at the start or the end of the day?
How do you feel in the morning when you wake up, when you get up, one hour after getting up?
Are you able to move around on your own?
Does it bother you when there is a movement in your visual scene? Tunnels in the underground, department stores, crowds, at intersections etc.?
Do you feel like you are walking on soft ground?
Does your head position change your sense of balance?
Are you able to walk and turn your head to look at a shop window?
Are you able to walk and raise your head to look at an aeroplane in the sky?
When you are walking, does the landscape appear to move at the same pace as your legs?
Do you feel you are walking on a moving train?
Is the distance you can walk limited?
Interpretation:
This is not an exhaustive list of questions. They are based on the essential neurophysiological characteristics which should, when asked by an experienced therapist, point towards signs that one can expect to see during the instrumental testing stage.
We have seen that the vertigo is a visual manifestation that appears as a nystagmus. If the patient says they are having an episode, obviously we should expect to see a nystagmus. If one can not be observed, the series of questions should resume.
Answers to the questions allow us to predict the signs and to determine, a priori, if we should expect balance disorders, if we should expect other dizzy spells, if the subject is normal between episodes, or if it is simply a peripheral vestibular disorder.
Questions regarding the onset of the symptoms may help to guide the therapist. If the onset is sudden and the vertigo can be reproduced at will, preferably in a lying down position, and lasts only a few seconds, there is a strong likelihood that we are witnessing a benign paroxysmal positional vertigo.
If the onset is unexpected within the context of a long-term infection, it could be a bilateral deficit disorder of iatrogenic origin. But it could also be viral damage stemming from a bout of flu.
If it is rotatory vertigo with nausea and vomiting and with a history of ear problems such as fluctuating hearing and tinnitus, we are most likely witnessing a pressure syndrome.
The above questions show the importance of associating the answers provided by patients to give a clue as to the pathology, the signs that are to be observed and the best approach to use for the vestibular reeducation.
With regard to balance disorders: if these are clearly lateralised, and the subject states: "I veer to the right", it is obvious that we are dealing with a unilateral deficit disorder.
If the balance disorders are always slightly lateralised and appear after an increased incidence of rotatory vertigos, we are witnessing an old, recurring vertigo.
Difficulty arises when the complaints are badly defined, when they are closer to imbalance than dizziness, or constantly occurring etc.
We must therefore pay close attention to the age of the subject. If the subject is elderly, concern should be taken about their activities, their daily life with or without sensory restriction, with or without falls etc...
If the subject is younger, an earlier vestibular disorder should be looked for. The disorder presented would therefore be the consequence of a decompensation. One should pay attention to aggravating factors so as not to be misled to believe it is simply a debilitating case of motion sickness. One needs to verify that it is indeed a case of motion sickness and not a phobia. Consultation with a specialist in psychiatry could prove to be useful. But be careful of the opposite occurring: namely the subject has been labelled phobic when in fact the cause of the disorders is organic. The long term prescription of central inhibitors can potentially block any conflict resolution processing of sensory information.
Among the samples of imbalances, there are subjects who symptoms could be labelled vascular. The Anglo-Saxons have a syndrome called "slow blood flow" which is comparable to what G. RANCUREL calls haemodynamic vertebrobasilar insufficiency. The condition is described according to its degree of severity based on imbalance with a sensation of drunkenness only found in the upright position. These are subjects who wake up in the morning in perfect shape, but as soon as they get up or shortly after getting to the upright position can feel their symptoms gradually appear. These subjects feel bad when in the upright position, a bit better when seated and perfectly fine when lying down. It is obvious that vestibular reeducation can do nothing in this case. Only treatment using medication can alleviate this deficiency in their orthostatic supply. VR, on the other hand, can act directly upon the consequences, in other words, imbalance, the sensation of being drunk while walking, uneasiness when walking etc... Once again, here is a wonderful example of the need to work as a team. Generally, when a slight vertical nystagmus is observed, it is a result of a disorder of the brain stem.
Instrumental Testing
If we take the example of a deficit disorder on the right hand side, based on the description provided by the patient, we would expect to see the following:
- a spontaneous left-beating nystagmus
- a standard slow pursuit
- the impulse rotatory test at a constant speed should give comparable results to those of caloric testing, in other words, a deficit on the right hand side
- lateralisations more or less to the right following vestibulo-spinal testing, depending on the longevity of the disorder.
We ask the subject to make horizontal eye movements followed by some vertical eye movements. Meanwhile, we observe the symmetry of speed and magnitude of the two eyes and ask the patients to talk us through any sensations they are feeling. This is then repeated but this time with vertical movements. The same observations are made. We then ask the subject to carry out the same movements again, but this time with their eyelids shut.
If we look beyond the fact that any asymmetry of eye movement would indicate a ophthalmological or neurological issue, any sensations felt by the patient will provide details about their sensitivity to both movement of the visual scene and the existence of a spontaneous nystagmus. This information is carefully collected because even if it has no bearing at the moment, it might at a later stage.
We then use a perimeter rod and ask the patient to carry out a pursuit. This eye movement is impossible without a target and the rod is ideal for this. The movement of the rod should be approximately 40°/s with an amplitude of 20° from the central position per eye on both sides. The test is carried out with a single eye and with both eyes.
Testing with both eyes is essential. The aim is to see if the pursuit is smooth and without saccadic eye movements. Furthermore, it allows us to observe the effect of a spontaneous nystagmus on pursuit. We see a smooth pursuit in one direction and an impaired movement in the other. In the case of a spontaneous right-beating nystagmus, the slow phase is to the left. So the movement of the eye during slow ipsilateral pursuit during the slow phase of the nystagmus will be facilitated and as such will be perfectly smooth. But in contrast, a slow movement in the opposite direction to the slow movement of the vestibular nystagmus will result in an impaired pursuit and even saccadic movement. Pursuit with a single eye is interesting as it allows us to determine the visual acuteness of each eye. It is even possible to determine if the eye being tested is a prosthetic one, something that subjects sometimes forget to point out, out of pure coquetry!! It is therefore useful to know that one must use the other eye to look for a spontaneous nystagmus. Although this remark might at first seem obvious, who has never had a patient pull the wool over their eyes?
Then we are going to use video goggles. Just as a reminder, these are goggles that are sealed against the light and contain one or two video cameras that film in infrared and are not visible to the human eye. The eye is in complete darkness to eliminate any ability to focus and to suppress any visual feedback that might interfere with the nystagmus response.
The protocol, strictly speaking, consists of the following:
Having placed the equipment on the head and over the eyes of the subject, check for the presence or absence of spontaneous nystagmus. If saccadic eye movement is observed, one must wait at least forty-five seconds to be able to confirm that it is in fact spontaneous. Indeed, the test is so sensitive that physiological nystagmus in response to a movement of the head or the simple act of sitting down on the chair are visible in the dark. A spontaneous nystagmus should not change in frequency or amplitude throughout the whole observation.
- Incline the subject’s head to one side, along the naso-occipital axis, moving the ear towards the shoulder at a speed of under 30°/s on one side while observing the contra-rotation movement that should be present. Then bring the head back to the upright position. It appears (at least for the moment) that the compensatory eye movement when returning to the vertical position is of less interest that that observed when the head is initially inclined. The same is observed when the head is inclined in the opposite direction. The comparison between the two observations might show all the degrees of asymmetry. With practice and by using points of reference on the iris, it is possible to check following the inclination of the head that the eye remains "counter rolling". This allows us to observe and to quantify the static component of counter rolling eye movement. This static component is purely otolithic in content. The dynamic component in this test (during inclination) is 75% otolithic and 25% ductal.
- Impulse testing: the subject is seated in a rotatory chair which will be turned through 180° at a constant speed of about 20°/s all the while observing the nystagmus per rotation. When the chair is briskly brought to a rest, nothing happens to healthy patients. But on the contrary, with subjects suffering from a vestibular disorder, when the chair is stopped, one can see the onset of a nystagmus, which we will carefully observe. We will count the number of tremors. Before rotating through 180° in the opposite direction, we have to wait for the nystagmus to abate. A 180° rotation in the opposite direction, observation and counting the nystagmus per rotation and observation and counting the nystagmus with the chair at rest until it fades away. If desired, the vertical canals can be examined in the same way, remembering that: for the horizontal canals, the nystagmus per rotation corresponds to the ipsilateral canal in the direction of the rotation and that the nystagmus observed at rest corresponds to the contralateral ear in the direction of the rotation. For the vertical canals, it is the contrary. When the head is inclined towards the right ear and the chair is rotated clockwise, the response upon stopping (down beating vertical nystagmus) corresponds to the upper-right vertical canal. With the head in the same position and chair turning anticlockwise, after rotation, an up beating vertical nystagmus is observed which responds to the back-left vertical canal. Conversely, with the head inclined towards the left shoulder, following rotation, corresponds to the back-right vertical canal, and upon stopping after an anti-clockwise rotation, to the upper-left vertical canal.
- should patients be non-responsive to the preceding tests (no eye counter-rolling, no canal nystagmus) hold the top of the patients head still using your hand, and rotate the torso. During rotation, we check for a nystagmus that perfectly mimics vestibular stimulation. It is called a somato-axial reflex, whose gain is inversely proportional to the speed of rotation.
- lastly, we ask the subject to close their eyes, shaking the head from one side to the other as quickly as possible, upon stopping, the patient is asked to open their eyes and we observe in cases of vestibular asymmetry, a nystagmus that beats to the side of the ear with the greatest response. Generally, if there is a deficit, the nystagmus will beat towards the healthy ear. In the case of central disorders, one can sometimes see an increase in “downbeat” spontaneous nystagmus.
Carefully observing these different nystagmus has allowed us to arrive at the following conclusions:
- all forms of response disruption are possible and we can now attribute counter-rolling eye movement to the otolithic uricular system because in effect, many elderly subjects have shown very weak counter rolling and today we know that the ageing of the otolithic system results in a decrease in the otolithic mass. Furthermore, following a vestibular nerve section, there is no counter-rolling eye movement on the side of the section.
- in many disorders, rotatory nystagmus are symmetrical and are much less intense than the nystagmus observed once the chair stops, which are closely linked to the degree of vestibular dysfunction.
- the quick rotation manoeuvre of the head is a trustworthy technique of providing supplementary information when there is asymmetry.
- the somato-axial nystagmus is only observed when bilateral vestibular damage has occurred. (by the speed at which the test is carried out.)
One can write down the answers or transfer them onto the COURTAT chart, and these are available from the equipment supplier.
The following is called vestibulo-spinal reflex testing. It is in effect now time to measure and observe the dynamic and static lateral deviations.
The first test, the most well known, is the Romberg test. Remember that this test was originally used for proprioceptive ailments, notably emaciation. The Romberg test is carried out by asking the subject, standing up, feet together, to close their eyes. In cases of emaciation, after palpebral occlusion, we observe a fall backwards. The subject’s body remains straight, and like a caricature, of a plank falling over. If the subject has a vestibular disorder, it should not be forgotten that balance starts from the head and moves down towards the feet. We therefore see the head move first and, in certain cases, the subject can be seen fighting to maintain their balance. It is like watching a tennis ball oscillating at the end of a flexible rod.
We make a note of the direction of the imbalance of the subject. In general, and in the case of a unilateral disorder, the deviation is oblique: backwards towards the right for example.
The subject, with a huge effort, might be able to control their Romberg. We can then render it more sensitive by asking the subject to move their head laterally to one side as quickly as possible, and then to the other side when asked to do so. We then alternate the lateral movements with the vertical movements at random. After a certain time, lateralisation and imbalance occurs.
The subject is then asked to carry out a blindfolded walk test. This test is known by the name of its creators: the Babinski - Weil test.
Having closed their eyes, the subject is asked to walk forwards in a straight line, and then walk backwards and then forwards again when asked to do so. It is essential that this test is carried out in silence, and with no points of light to guide the subject. We observe deviation both when walking forward and when walking backwards in the opposite direction. The completion of all the movements should have formed a star shape on the floor. The lateralisation observed in the direction of the structure of the star should be coherent with the response to the Romberg or the Sensitised Romberg tests.
Lastly, the vestibulospinal test: the walking on the spot test or the UNTERBERGER test. This test was taken up by FUKUDA who quantified it.
The subject, placed in the middle of the room, is asked to walk on the spot, without any visual or sound clues and with their eyes closed for 45 steps. With peripheral disorders, taking into account the start of spontaneous compensation, any deviation will not be immediate, but rather after a certain number of steps.
Interpretation is based in the angle of rotation of the subject from their starting position, as well as the direction.
After the vestibulospinal tests, the evaluation comes to an end with a rotatory test which is similar to Barany’s cupulometric test. It comprises rotating the subject in the chair at a speed of 400°/s. There are three rotations. Acceleration and stopping of the chair must be perfectly identical in both directions. The speed should also be exactly the same in both directions. It should be pointed out that there is no such thing as normality in a test such as this. The differences between one individual and the next are considerable by virtue of the explanations provided in the Neurophysiology section. But it should also be remembered that we are dealing with pathological subjects who, when it is brought to their attention, have a very standard behaviour. The comparison between one subject against themselves therefore becomes reliable and replicable.
Rotation takes place with the eyes closed. The recommendations for the first set of rotations are as follows:
- the chair rotates with the subjects eyes closed and upon stopping, the subject is asked to open their eyes and to focus on a target that is right in front of them. The target will appear to move. "Once the target you are focusing on stops moving, you say "stop".
The therapist takes note of the length of time when the visual scene of the patient appears to move. This value is added to the following table.
Deficit on the Right side | Fixation | Circular Vection |
Clockwise rotation | 14 seconds | |
Anticlockwise rotation | 6 seconds |
Having taken measurements for both directions, the subject is then told:
- "we are going to rotate with the eyes closed and you are going to keep them closed once the chair comes to a stop. The moment you are told that the chair has come to a stop, you will have the sensation that the chair is now moving in the opposite direction. When this sensation dissipates, you say "stop".
As with the test with the eyes open, we time the length of time that the subject has the sensation of movement. The values are them added to the same table.
The values observed in this case are the values that you would expect to find in a subject with a right-hand-side vestibular deficit.
Deficit on the Right side | Fixation | Circular Vection |
Clockwise rotation | 14 seconds | 15 seconds |
Anticlockwise rotation | 6 seconds | 9 seconds |
It should not be forgotten that the per-rotatory nystagmus corresponds to the ear on the same side as the direction of rotation whereas the nystagmus that manifests itself once the chair comes to a stop beats towards the ear opposite to the direction of the rotation. This explains why in a right deficit disorder, the lowest values are obtained following a counter-clockwise rotation.
Interpretation is based on an understanding of how the vestibular system works. A response in a fixed position is quite a reliable response pointing to a peripheral deficit. The moment the subject announces the end of any movement of the visual scene marks the end of any nystagmic directional preponderance.
The response to vection is a cortical response as it is the perception of rotation. This response indicates the condition of central compensation. There could therefore be a lack of ay correlation with response at fixation. Indeed, good central compensation through substitution does not necessarily change tonus asymmetry between the two peripheral sensors. The spontaneous nystagmus could still be present. One must therefore try to determine if there is any correlation between responses to vection and the complaints of the subject. Indeed, a subject who continues to have strong asymmetry at fixation and symmetrical responses at vection might complain about discomfort following quick head movements in addition to movement in only one direction: towards the affected ear. A subject with correlation between fixation and vection will have complaints that are habitually found in subjects with a vestibular illness. There are therefore different degrees of asymmetry, as well as degrees of correlation with vection depending on:
- the longevity of the illness
- the degree of debilitation
- the degree of compensation
- the type of affection
It should not be forgotten that:
- disorders are not necessarily unilateral,
- unilateral illnesses can be both recurring and fluctuating,
- there are centrally caused illnesses.
It is a good idea to have a rough idea as to where to position the results.
The values for a healthy system are 10>X Hypovalency is < 10 seconds.
Hypervalency is >30 seconds.
Here are some typical examples:
Bilateral destruction | Fixation | Circular Vection |
Clockwise rotation | 0 second | 0 second |
Anticlockwise rotation | 0 second | 0 second |
Central | Fixation | Circular Vection |
Clockwise rotation | 35 seconds | 50 seconds |
Anticlockwise rotation | 40 seconds | 50 seconds |
Cerebellar | Fixation | Circular Vection |
Clockwise rotation | 45 seconds | 15 seconds |
Anticlockwise rotation | 50 seconds | 16 seconds |
Peripheral and Central Mix | Fixation | Circular Vection |
Clockwise rotation | 50 seconds | 20 seconds |
Anticlockwise rotation | 45 seconds | 8 seconds |
We can see from these examples that there is a great diversity in the responses. In other words, this test is essential as it serves as the basis for reeducation. These responses form the very foundation of any proposed treatment.