Oculomotor Testing: Theoretical Introduction

In this video, Darren Whelan describes the anatomy and reflexes in eye movements. He then goes on to explain how to perform and measure the oculomotor examination. Lastly, he describes normal and abnormal ocular movements and their clinical importance.

You can read the full transcript below.

Introduction

The purpose of this presentation is really to come back and look at the relevance of oculomotor testing in the modern balance clinic. As we are presently, most modern balance clinics or dizziness clinics are in the combination of hospital-type environments. These can often be either in neurology, ENT, or audiology clinics.

What we find is within these clinics, we have a range of different tests available to us to assess the dizzy patient. The aims of this particular webinar are to describe the anatomy and reflexes in our eye movements, as these do form the basis of the VNG, or videonystagmography, assessments that we undertake in clinic.

I'd also like to discuss how to perform and measure these oculomotor examinations to successfully understand and quantify eye movements, in particular with the oculomotor exam. And also spend some time describing both the normal and abnormal ocular movements and those clinical importance for the assessment and understanding of dizziness in our patients.

Oculomotor anatomy and reflexes

So if we start with the oculomotor anatomy and reflexes, these are a combination of pathways that incorporate the brainstem and central nervous system to both initiate carrying out and facilitate appropriate eye movements, depending on the task that we're trying to undertake.

As part of this presentation, we'll look at various elements of this pathway in relation to some of the oculomotor examinations that we undertake. Whilst it's not key to have a very definitive understanding of where these lesions may be present, the understanding of where some of the changes in the eye movements that we see initiate from certainly allows us to have a better understanding of some of the symptoms that our patients may report.

And also clinical importance when we then go on and look at eye movements further into the VNG test battery.

Oculomotor pathways and reflexes

So if we start with the pathway. So what we have is a motor and pre-motor system that are generating and initiating smooth pursuit or tracking movements. This is predominantly about keeping a small moving target very closely on the fovea of the retina to keep visual acuity at its best and to detect very small amounts of retinal slip to allow the eye to be repositioned to keep this moving target in focus.

These movements are slow and they're voluntary. The optokinetic system acts in a different manner, but it has a very close relationship with the smooth pursuit tracking system. It enables us to keep an image on the retina through a sustained head movement. These are movements that are again slow but reactive in orientation.

The saccade system is different. This allows us to keep an image of a new object again on the fovea. However, it initiates much faster reactions and faster eye movements to initiate this. Again, we can have a look and recap on the purpose of the patient's ability to look at fast eye movements. And this looks at these back-and-forth movements in the vertical and horizontal planes.

Why perform an oculomotor examination?

So why should we perform an oculomotor examination? Often the question is raised. Why are we interested in eye movements when looking at dizzy patients? Well, in my experience in the NHS and in the United Kingdom, over a very large cohort of dizzy patients that have been referred from a primary care setting over a ten-year period, we see the list that I've presented here for you of common diagnoses and conditions that were present in our patients.

Very much at the top we have these vestibular conditions that we're familiar with: BPPV, vestibular neuritis, migraine, and migraine-associated vertigo. But if we go a little bit further down that list, what we can see is dizziness that is present in a central or vestibular vertigo. So these are patients that are presenting to us with dizziness that are not peripheral in orientation but have elements that could be associated with a central lesion.

So that brings us to the question of doing these assessments. Really, what we're trying to do is differentiate between these central causes of dizziness and moving away from what is relatively common in our clinic, peripheral and maybe even a fixed lesion, to more dangerous central conditions that require a different approach to identify and manage for the patient.

Central nervous system etiologies

So looking at some of the etiologies of the central nervous system. And this list is not fully encompassing, but it gives us an idea of some of the diversity that we can see when we see patients who have dizziness that may be central in orientation.

Primarily, the first things we need to think about are ophthalmological conditions. So issues in relation to eye movement and the eyes being able to carry out some of these motor tasks and oculomotor activities.

We also have more degenerative conditions that present to us such as progressive supranuclear palsy. Cerebellar ataxias also can have disruptions within the oculomotor examination. Brainstem infarction. Again, depending on the site of lesion and extent of the infarction, we can start to see more growth changes within the oculomotor.

Alzheimer's disease and the progressive nature of that condition does often change some of the central nervous system function over time. And dizziness, imbalance, falls, and coordination can often be presented into our clinic. And looking at the eye movements gives us some insight of where the changes in the central nervous system may be taking place.

Along with other degenerative conditions such as Parkinson's disease. Neurological changes such as transient ischemia attacks and stroke. Demyelinating conditions such as multiple sclerosis can often indicate some nerve conduction changes that may be a palsy in eye movements.

Again, may start to present in a very subtle fashion in the oculomotor exam. And also space-occupying lesions where we have compression and disruption to some of the central nervous system firing and coordination resulting in dizziness, imbalance in coordination, and often subtle changes in eye movement.

Oculomotor test battery

So coming back to the oculomotor test battery. Initially, one would always look at gaze stability. And we can take these piece by piece as we move forward through this presentation. Followed by saccade testing, pursuit and tracking testing. And also, we can look at optokinetic testing with full-field visual stimuli.

Oculomotor function

Again, the oculomotor function very much sits within the videonystagmography assessment, as this can give us some very non-invasive, well-defined, and easily-quantifiable eye measurements to allow us to further identify any changes that we may see present.

With videonystagmography, it's worth noting that using the video goggle to track and monitor eye movement in high resolution does allow us to quantify those measurements. And often, then allows us to further look in detail to consider attention, head movement, and medication to exclude those so that what we are left with in our measurements are these changes that may be part of a central nervous system condition.

Gaze stability testing

So if we can start with gaze stability testing. With gaze stability, what we're trying to achieve is looking at both primary left and right gaze. Here what we want to see is whether or not we have any changes in the patient's ability to maintain gaze without the generation of other eye movements.

We can check this both with fixation and without fixation. And this becomes important if we then do see some instability within the gaze assessment, the most common instability one would see is something being driven through nystagmus.

So nystagmus being present in any of the three conditions will have an effect on other eye recordings further in our VNG assessment. If that nystagmus is present with fixation, this is going to affect our saccade testing, smooth pursuit testing, and optokinetic testing.

If that nystagmus is present with fixation removed, then this could be present both in positioning testing with a VNG goggle and also more importantly, within a caloric assessment with fixation removed. So quantifying gaze stability as a primary examination before conducting other oculomotor examinations does have some very sound clinical utility.

What we can see here is the eye movement relative to the target. In this case, the eyes moved to the right and we've tracked that with the eye moving to the same position and holding that position. Here, we can see an ideal example where we don't have any eye movement whatsoever and we don't have any ocular movement or flutter.

During this assessment, we often can take the time to check that the patient is just eliciting an eye movement and not a head movement, as it's very tempting for a patient to, when looking right or left, slightly move their head.

Now, that will have an effect in terms of where the eye position is and also, they may make corrective eye movements to reposition their eye. This can again be seen in the trace and reinstruction can be offered. And some mental alerting tasking if needed to keep them in the correct position for the eye examination.

So here we can see some examples of nystagmus that has been elicited in different eye positions. And again, as we move forward through our oculomotor examination and also then further into the VNG, we can take these into consideration when looking at any other nystagmus or eye movements that are present.

So, gaze stability. So, this is the examination of the patient's ability to maintain steady gaze with and without fixation. And as we have said, the most common manifestation of gaze instability is nystagmus. If we just take a quick look at a video here, we can just see some very quick eye movements that allow us to see some videonystagmography being undertaken.

Saccade testing

Our next test moving into the oculomotor examination is saccade testing. And what we can see here with saccade testing is we have random eye movements being generated that are quick and can move both horizontally and vertically. We can track the eyes moving for each of these random steps.

To quantify saccade testing, we need to carry out approximately 20 saccades in each direction to fully utilize the pattern or changes that may be present. These measurements can be indicated as follows.

What we can see here is a step change where the eyes have moved from a left position across primary into the right position. And they track the target and follow the target back once again.

Within this test, we've got some different parameters that we can look at that allow us to quantify some of the abnormalities. So I'd like you to have a little look at our first abnormality here.

What we have is an eye movement and what we're measuring is a latency of eye movement. So the time that it takes for that eye to move after the target has initiated the eye movement. Typically, what we would see are eye movements around about 100-120 milliseconds following the target movement.

Any delay in this movement of greater than 200 milliseconds... If it is a consistent pattern and follows through the saccades, we can look at whether that eye movement is delayed unilaterally, either to the right or left, or up or down for vertical saccades. Or whether it's bi-directional and that it's present in either the horizontal or the vertical plane.

Abnormalities within the latency of eye movement are often described within the central nervous system structures as being frontal or frontoparietal cortex or even within the basal ganglia. We can come back to some of these abnormalities further into the presentation.

The next parameter to look at within the saccade test is velocity. So how fast does the eye move after being initiated, following the target? Again, we can look at normal data, both for age and gender. And we can have a look at whether a delay in this eye movement is present either in a unilateral or bilateral directions. Again, horizontal or vertical.

And delays within velocity give us some indication within the central nervous system of looking at structures such as the supranuclear complex, the brainstem, and basal ganglia, and are often associated with more neurodegenerative diseases such as Parkinson's, Huntington's, progressive supranuclear palsy, or even spinal cerebellar degeneration.

Our other parameter to look at within a saccade test is accuracy. Now, this is calculated as the percentage of distance that the eyes moved following the first target movement. If the eye moves to the same distance as the target has moved, then this is 100% of movement.

But we can then start to quantify that movement both as a percentage and by its nature. So we may have a movement that doesn't fully reach the same point as the target that we would describe as hypometria. And again, these could be lesions that are affecting the cerebellar flocculus or the dorsal vermis.

Or we may have a movement that's actually exceeded the target movement and then a correction has been placed back on the target. And again, these would be more consistent with lesions within the cerebellum.

As an example of an impairment to the saccade test, we can look at internuclear ophthalmoplegia. And that can have palsies both in a unilateral or bilateral direction, where the eye ducts inappropriately, creating either doubling of vision in the horizontal plane and dizziness and unsteadiness if the patient is stood.

Smooth pursuit testing

Smooth pursuit is more of a voluntary and slow reactive test. And what we're doing here is we're looking at the patient's ability to keep a small, slow-moving object in the fovea, identifying the retinal slip and making a correction appropriately.

Now, this can be tested at different speeds either with fixed velocity or increasing velocity to identify any impairment that may be present. So what we can see here is we have our target that is moved in a very sinusoidal fashion and the eye movement is tracking and moving both at the same speed and distance as the target.

We can look at different parameters within the smooth pursuit. So we can look at gain as being a measure of the eye movement versus the target movement. We can look at when the movement is within phase of the target movement. And we can also look at any asymmetry as with our example with internuclear ophthalmoplegia.

We could have an asymmetric palsy. Therefore, the direction to the left or to the right may elicit an abnormal eye movement that would be identifiable through our smooth pursuit examination.

Here is an example of a bilateral symmetric abnormality. So what we can see is we've got correction being applied both to the right and to the left directions to keep the eye tracking with the trace.

Lesions that are bilateral identify within the central nervous system. Often, diffuse cortical changes. Again, basal ganglia changes and cerebellar disease. We do have to be mindful of medication and I'll talk about that a little bit further into our presentation. And also age. Pursuit is very sensitive to age-related changes and therefore we need to consider this as we look at all the populations.

A unilateral change either in the right or left identifies slightly different areas within the central nervous systems being involved in that pathway. So we may be there thinking more of a focal lesion or ipsilateral cerebellar hemisphere, such as an ischemic event. Or within the brainstem or the parieto-occipital lobes.

Optokinetic nystagmus testing

What we have here is an example of an optokinetic stimulation. So what we could see in that example is a full field with the patient sat in front of it. A full field stimulation that initiates a checkerboard or striped pattern to induce a corrective eye movement that very much looks like nystagmus.

So we're generating a nystagmic eye movement that we can measure both going to the right and to the left to assess whether or not the patient is able to initiate those eye movements appropriately and symmetrically.

Here an example of some of those recordings that we can see within our software. And this allows us to quantify the surface velocity of those eye movements and establish whether we have equal gain. Does the eye move to the correct degree of movement both right and left?

And we can look at this at different velocities. So we could look at 20 degrees movement or 40 degrees per second of movement both in the right and left directions. We can also look at the slow-phase velocity of that nystagmus and calculate a symmetry value to see whether we have any lesions or changes that are predominantly moving either to the left direction or to the right direction.

So if we look at the purpose of optokinetic testing. The purpose of the pursuit mechanism is to stabilize small targets within a thinner visual field, whereas the optokinetic is to stabilize the entire visual field onto the retina. So whilst one is voluntary, the other is a reflexive response.

It's worth mentioning that the optokinetic, out of the oculomotor examinations, has the least specificity in relation to identifying a central nervous system pathology. However, as an additional supportive test within the oculomotor examination, you can see where it would show changes potentially both between the pursuit and the optokinetic to see whether we've got consistent findings within our oculomotor examination.

Summary of the oculomotor test battery

So what I'd like to do now is look at the oculomotor test battery as an overview. We've spoken about gaze stability testing and the importance of gaze stability testing in relation to looking at any nystagmus or instability within gaze testing that may influence our oculomotor exam or even more importantly, further into the VNG examination when we look at eye movements with fixation being removed.

So to recap, this is to examine the patient's ability to maintain steady gaze in different conditions with and without fixation.

We considered saccade testing. The purpose of saccade testing is to examine the ability to make fast eye movements in that horizontal and vertical plane.

We've considered smooth pursuit testing. And again, we've addressed that in terms of looking at these slow foveal tracking eye movements to identify that very slight retinal slip of one to two degrees per second and repositioning the eye into the correct area of the retina to keep visual acuity present.

We've looked at the optokinetic and we've identified that that requires a full field stimulation to initiate this reflexive response in relation to these changes.

Abnormal oculomotor test results

Now, we've discussed some of the abnormalities within the oculomotor examination. But now, let's just take a moment to recap some of these abnormalities.

So with saccade testing, what we said we would look at is the latency, accuracy, and velocity of these eye movements. And we would look at these individual components, examine the abnormalities that may be generated, and look for repeatable patterns that may then identify central nervous system changes or conditions.

We've considered smooth pursuit and within that, we've looked at elements of gain, the eye movement relative to the target movement, the phase of that movement of the eye tracking the target, and also any asymmetry that may be present within that eye movement, and whether these changes are bilateral in nature or unilateral, as each change can indicate a slightly separate location within the central nervous system of where the abnormality may be being generated.

And we've looked at optokinetic. And again, whilst normal values for optokinetic testing are not well defined, what we are able to do is look at the gain and the slow phase velocity of the nystagmus that we generate and we can use a qualitative assessment of these findings to see whether the examination of that nystagmus intensity is either reduced unilaterally or bilaterally, or whether there is a velocity change.

We've also said that we can measure the optokinetic at twenty degrees per second and also forty degrees per second. Because sometimes, abnormalities may vary with velocity, with some of the higher velocities eliciting an abnormality that does not present at a slower speed.

And once again, we've said this is not a diagnostic test in terms of location within the central nervous system. It's a complementary test in terms of supporting changes that we may then see in smooth pursuit testing or saccade testing.

Site of lesion

So to summarize within our site of lesion. In saccade testing, we said the abnormalities are consistent with lesions in the medial longitudinal fasciculus, lateral medulla, frontal or frontoparietal cortex, or within the basal ganglia or cerebellum.

Smooth pursuit abnormalities have been identified within the diffusive cortical lesions, basal ganglia, or cerebellar disease. We also can have focal lesions, brainstem, and again, parieto-occipital regional changes.

Conclusion

So in conclusion, oculomotor testing is a valuable examination to identify any subtle central changes for how some of these conditions have progressed. This allows us to identify more dangerous causes of dizziness and imbalance within our clinic that are not peripheral in nature and require different management and investigative modalities to address the patient's concerns.

We've also looked at the identification of these oculomotor abnormalities as allowing us to do more accurate interpretation of other eye movement recordings in the VNG test battery. The VNG test battery we know very much relies on us establishing peripheral function and positioning changing symptoms in relation to eye movements.

So an impairment within the oculomotor or gaze stability can have influences in terms of the VNG recordings that we may then use further in the test battery. This is very important when we're trying to localize the site of lesion and also in terms of then initiating management and treatment options for these patients.

In summary, the oculomotor examination has good clinical utility and the validity of its use within the test battery is very much consistent as a diagnostic tool to separate central causes of dizziness being present from those that are peripheral in our test examinations.