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ICSC01_1.TRANSCRIPT-Sports_Concussion

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ICSC01 Head Injuries
Section 1 – Sports Concussion

Instructor Brett Jarosz
Video Lesson: 02:15:42

Welcome everyone to the FICS sports related concussion management online module. My name’s Brett Jarosz. I’m a fellow sports and exercise chiropractor, based in Melbourne, Australia.

The purpose for this particular online module is for the sports chiropractic world to be able to further enhance our skills, our ability, in the management of concussion. So far, we have gone through the online modules, going through the new update from the consensus statement with the SCAT6 and the SCOAT6 and understanding our way to navigate through those assessments.  What we would use in that acute concussion assessment, on the sidelines, on the field in your office in that acute setting, mainly in that first 72 hours, maybe up to a week we were using the SCAT6. And then when we are dealing with people coming into the office, 72 hours or weeks later, then utilising the new tool from the consensus group. The SCOAT6.

The focus for this module, is to try and further enhance our understanding and knowledge of those assessments, understanding the physiology, the pathophysiology, neural substrates, mechanisms, first principles, whichever way you that sort of makes sense to you. All those words say very similar things there. But when we do our assessments, what do those assessments mean from that first principal mechanisms, physiology, neural substrates perspective? What we want to try and do is go through these key points from the consensus. We will go through the reevaluation or the evaluation process, which is part of SCAT6 and SCOAT6.

Discuss this rest and exercise and understanding why we are describing it, understanding the different mechanisms of exercise, how they impact our physiology but then understanding how concussion impacts our physiology. Therefore, understanding why we want to use certain types of exercise at certain times and why we don’t use other types of exercise.

And then understanding our rehabilitation.

I would like to start with my disclosures and biases so we can set the scene of the importance. You will hear a couple of quotes today about understanding the pathophysiology of concussion and how important that is for the 20 to 30 percent of people who sustain concussion injuries, but don’t get better in that expected thirty-day time frame. So those people that then develop those persisting post-concussion symptoms, understanding the pathophysiology there, proves very important, and my bias of this is very much framed in that space because this is what I see in my private practice.

I don’t get to see too much of the acute concussion injuries. I see the people who have not recovered, so my bias in this presentation is the bias that I see from my clinic.

We need to understand this better to help serve our patients, our athletes, and our community. Then, of course, we will finish off with that return to learning, return to sport. But I will be jumping around through these parts, through the presentation, trying to constantly tie these together for our understanding.

The reevaluation process or more aptly, the evaluation process. The reason they put the “re” in front of it is for this. The thirteen “Rs” of the sport related concussion management model from the consensus group.

The concussion in sports group provide these thirteen “Rs” so that way we can flow through that concussion management, logical protocol, logical clinical flow, whatever words make sense. Recognize, reduce, remove, reevaluate, rest and exercise, refer, rehabilitation, recovery, return to sport or return to learn, reconsider, retire, refine. A lot of those things we have already gone through with the previous online update, and then today, we are going to focus our attention on those four key points.

Let us start with reevaluation. The purpose of the SCOAT6 and the child’s SCOAT6 was to give healthcare professionals a standardised, expansive, and age-appropriate clinical guide to a multi domain evaluation in the subacute phase. 72 hours to a week post a concussion injury with a view to guide individualised management. While that statement there is obviously quite profound from the consensus statement, is because concussion is very much multi domain. We have cognitive components, emotional components, visual processing components of what we are seeing, but then we have the ocular motor components, the parts that move our eyes. We have the inner ear vestibular components that connect our inner ears to our eyes, but our inner ear is also to our spine. For postural stability and balance we have our motor coordination, so our cerebellar coordination patterns, our neck could be involved, and then some of the newer stuff, which we will really emphasise today is some of these autonomic aspects as well. So multi systems, multi domains.

And we must be able to assess all these components in a concussion injury so that we can best create this individualised management.

But we need to understand that physiology, pathophysiology mechanisms, neural substrates, we need to understand those things to truly provide an individualised management strategy. Otherwise, it becomes, I see this, I do this, and it becomes technical cookie cutter approach. I see people who have gone through that approach from doctors, and it fails. The emphasis here is really focusing on that third of patients that don’t get better. If we can do a better job earlier to prevent that 30 percent, then we are helping serve our athletes and communities to hopefully prevent those persisting symptoms, or indeed if they are in seeing you with persisting symptoms, ask yourself, how do we do a better job of providing that individualised management?

The SCOAT6 is broken down there on the left-hand side. All the different steps that are involved in creating that logical clinical workflow so that you can work your way through a concussion assessment, and what we want to focus on today is those areas in bold, and I want to try and integrate this together. We know that the major concern with concussion is it is still based on symptoms. The idea that athletes’ or members of the community, whoever it is that you have in front of you, when we are assessing a concussion, the primary assessment tool to determine concussion injury as well as clinical recovery is their symptoms.

But what we want to try and get a better understanding of is which of the domains, which of the physiological systems may be hypo functioning or dysfunctional or hyper functioning that is in turn driving those symptoms. Trying to look at the world through an objective lens, the testing, objective testing, and understanding that testing versus the symptoms, which is the subjective. And of course, remember patients can lie about their symptoms. They could be telling you, no, I feel fine, especially athletes who want to get back to the game or return to sport.

Try and look at the athletes from the perspective of, we understand symptoms very important, but we want to understand objectively what is going on in our assessment, what those things mean. We want to really get into the detail of these objective vital signs, the cervical spine assessment, our balance or postural stability, our VOMS assessment vestibular ocular motor assessment, graded aerobic exercise testing, and then our return to learn and return to sport.

The orthostatic vital signs there is emerging evidence that has associated concussion with changes in the autonomic nervous system. The postulated mechanisms include trauma to the hypothalamus limbic system, midbrain nuclei, and the regions of the brain responsible for autonomic function. Where we want to go back to is understanding our concussion mechanisms. Remember, it’s an acceleration, deceleration injury to your nervous system. And of course, we hear those words acceleration, deceleration injury to your neck, we call that whiplash.

Well, a concussion is that, but it’s just occurring to your nervous system. So same mechanism of injury. One’s just being impacted to the orthopedic structures of the neck. The other one’s being impacted to the nervous system.

When we create that acceleration, deceleration, we get that stretching, the areas that get stretched are primarily the areas through the midline of your nervous system. If we understand our anatomy, our first principles, physiology, mechanisms. If we understand what lives in the middle of the nervous system, it is all those hypothalamic, the midline limbic areas.

When we go through the middle of that cerebrum, limbic system, hypothalamus, get down to the brain stem, what lives in the middle. Well, that is all our eye movement nuclei. It is all our balance pathways and nuclei, our postural muscle tone, our pain systems, our pain inhibition systems. It’s our ascending reticular activating system, the thing that gets us alert and awake, the autonomic nervous system. If we understand the anatomy that lives in there, which you would have gone through in previous online modules, then we understand that this makes sense as to why the research is showing that the autonomic nervous system is involved in concussion injuries.

The big part now is this orthostatic tachycardia has been described as being associated with a substantial subset of concussion clinic patients. So orthostatic referring to getting upright, Tachycardia, obviously, racing heart. Now the numbers with this, and it’s important here to understand that there are different forms of dysautonomia or dysfunction of the autonomic nervous system.

It just happens to be that orthostatic tachycardia tends to be one of the most common dysautonomias that occurs in concussion. The disorder, the orthostatic tachycardia here, is what they see with a lot of concussion patients that have got persisting symptoms and have got this issue with their autonomic nervous system. When they lay down, and then they stand up. We see that they have a heart rate increase from supine to standing of greater than thirty beats per minute, and it causes symptoms.

That is key to having the diagnostic criteria here will break down this even further in a second. In this example, from laying to standing, their heart rate is 50 beats per minute laying on their back, then when they stand up, their heart rate increases above eighty. If you are an adolescent, so less than eighteen years of age, that has to jump up by forty beats per minute, or it reaches an absolute value of a 120. They might be sixty laying down. All of a sudden, you see it jump up to a 124, and then drop down a little bit. They are upright, it hits 124, and then it comes back down to ninety. But because it reached an absolute value of a hundred and 20, that also counts.

But the importance with this diagnosis for orthostatic tachycardia, and the true name here is postural orthostatic tachycardia syndrome (POTS), they stand up their heart rate increases and is sustained by more than thirty beats per minute, but they don’t get a drop in their blood pressure. It’s the absence of postural hypotension. Heart rate goes up when they stand up by more than thirty and it’s sustained. But there’s no drop in blood pressure. What does a drop in blood pressure mean? It means systolic does not drop by more than 20. Or diastolic does not drop by more than 10. We are saying blood pressure stays level, stays normal, heart rate increases by more than thirty, plus they have symptoms. And what those symptoms are is they feel lightheaded. They feel dizzy. They feel faint. They feel presyncable. In the bad cases, patients even faint. When they are bad, they stand up, their heart rate spikes up, and these people faint.

Understanding that this light headedness, dizziness, pre syncope feeling is the common symptom, but they also develop headache or nauseousness or sweating, or you will see their hands, feet start to go purple from that Venus pooling. We start to see these different other signs and symptoms go along with it, spotty, black vision, feeling of heaviness in their legs. This condition is really, really common in people who have persisting symptoms. So please assess for these symptoms.

Now in the consensus statement, it was put forth this way to assess orthostatic vital signs in the SCAT6, which was to lay someone on their back for two minutes and then take their blood pressure once they have rested for two minutes laying on their back. We are there, two minutes pass, take your blood pressure, take your heart rate. You then get them to stand up, and then upon standing, after one minute, ask them if there’s any symptoms while they are standing, and of course we take their blood pressure and heart rate. Now the problem with this is It’s only for one minute. You will see the bad cases often show up here, but the more subtle cases you will miss, and you can see at the bottom of that table there, it gives you the clinical significance of what you’re expecting to see and symptoms. The drop in systolic by 20 or a drop in diastolic by 10, that would be orthostatic hypotension. Which is still dysautonomia, but that’s a different type. So, the blood pressure dropping in those examples one and two at the bottom of that table. Or the heart rate increases by more than thirty, and the blood pressure stays normal. That’s pots. Or you might see that their heart rate drops. Blood pressure drops. And of course, we see these different variations of dysautonomia.

When we look at it from a pots point of view, blood pressure’s normal, heart rate goes up by more than thirty. That’s going to be one of the most common dysautonomias that we see. But we may miss it if we use this particular protocol.

What I am going to encourage everyone to do is to use the NASA lean test version instead of what’s put in the consensus. The exact same thing. You lay them on their back and let them rest for a couple of minutes. Take their blood pressure and heart rate after two minutes of laying on their back, and then you have them stand up as you can see in the picture, have them with their back against the wall, have their feet one foot length away from the wall, both feet are there. They are leaning on the wall, and then you have them stand there for 10 minutes. Every minute that they are standing, take their blood pressure, take their heart rate, and ask them about symptoms. This is where we can start to see more of the subtle versions of these pots where it starts to gradually kick in after three, four, five minutes. If someone is bad, it will show up in that first minute. But often you must keep them there for a bit to see that autonomic failure or dysfunction.

On the left there, we can see some other prep instructions, because some people come into you and have already been diagnosed with pots, maybe prior to a head injury, or they have seen someone, and they have been diagnosed with pots. To make sure that we do the test appropriately, we want to limit their fluid intake to one liter for the day prior to doing the testing, limit their salt intake for forty-eight hours. No compression garments for the day of the testing, wear clothes, but no compression clothing. Then where it is appropriate and safe obviously, look at limiting or get them to stop the medications and supplements before the testing, as they could affect their blood pressure or heart rate. So that is how we want to do that NASA lean test. Let’s go beyond what’s in the SCAT and SCOAT6.

Let’s do the NASA lean test.

Then when we move into the balance error scoring system, both within the SCAT and within the SCOAT6, we will understand how to do that from our previous online modules as well as your face-to-face training. As you can see in the video presentation “A, B, C”, and “figure C” in the picture on the right, these are our modified balanced error scoring system tests. Feet together on firm flat surface. All of them with eyes closed hands on the hips. We have feet together, single leg on their non dominant leg. Ask the person which foot you would kick a ball with. They kick a ball with their right foot, they are going to stand on their left leg and then in figure “C” the non-dominant leg is the leg that’s behind in our tandem stance. We have our error scoring system there. We know our rules of if they open their eyes, that’s an error. If their hands come off their hips, that’s an error. If they step out of position, that’s an error. If they’re leaning from the hips by more than thirty degrees, that’s an error. If any of these types of things are happening together at the same time, it’s just one error. It’s not three.

We do the test for 20 seconds. Count how many errors are occurring in that 20 second. If they reach 10 errors, just stop the test, and just move on to the next one.  Where it is appropriate, we want to get people doing the testing on foam.

That is no longer the modified “M” bess, the “M” bess, when you do the foam testing, now that is the full bess testing. We got firm and foam. Why do we want to bring this up and go beyond the modified “M” bess and do the foam, then do the full bess. Because of the different systems that this test is testing.

When we look at postural stability here, understanding that when you are upright, we are relying on vision, the vestibular system / inner ears, and our proprioceptive / somatosensory system. We have our muscles and our mechanoreceptors in our joints, and they are all giving us input up into our brain stem and to our cerebellum in order to tell us where we are in space. Why this becomes important is these things.

A real simple rule here is when you are assessing balance on that balance error scoring system, yes, you are counting the errors, I want you to watch for which way the person swaying in the subtle cases or which way they keep falling.

What happens with our balance? If we have a cerebellum, or vestibular or brain stem problems, remember your vestibular system, your balance nuclei, your vestibular nuclei, your eye movement nuclei, those pathways, they are in the brain stem. If we have dysfunction of one cerebellum, in this case, let us say it is the right or my inner ear, my vestibular system on the right or those pathways that go from those parts of the anatomy into our brainstem to then go to the brain or to the eyes or the spinal cord, wherever it is going to go. For those pathways from vestibular, cerebellum, into brain stem, what happens if one side’s down, like doing weights and you watch someone doing bicep curl, and then we watch, this arm coming up, and everyone’s watching the left, but its right arm taking a bit longer.

Everyone at the gym might say “you need to go and work on that right bicep, it’s not as good as your left”. We will see that people with vestibular hypo function or cerebellar hypo function or brain stem hypo function will sway or lean to the side of hypo function.

When we do this test, not only counting the errors, but your count is also observing which direction are they swaying? Which direction are they falling? Do you consistently see they are going to the right, and then immediately in your mind, you say alright, I am making the error count, but I now also know that this person’s either got something going on with their right cerebellum, their right vestibular system, or that right brain stem. Where those vestibular and cerebellar projections go, so primarily into the pons and the medulla there on that right side.

Those things there are important for us to remember because we want to then put that together with other tests.  The balance error scoring system that we brought up before, why do we maybe want to put someone on foam as well? When you stand on a hard flat surface, what is normal in a normal/normal person? Was supposed to rely on vision 10 percent.

Our vestibular system, 20 percent, and our proprioceptive/somatosensory system 70 percent. 10, 20, 70. Neck, ankles and feet, hips in that order of where the most weighting goes for the proprioceptive input, so hard, flat surface.

Norm is referenced as most normal environments, when you are walking around your house, standing in the shops, whatever it is, 10, 20, 70. But as soon as you put someone onto an unstable surface, when you put someone on foam, your nervous system reweights. And that’s what this picture here is showing you. It shows you how your center of mass changes and the weighting of your nervous system shifts. When you are on an unstable surface, you now shift and rely 20 percent on vision, 70 percent on your vestibular system 10 percent on your body. So again, why do we as clinicians in our office want to start going, I want to go beyond the MBess, the modified, balance error scoring system.

Why I want to do the full BESS is because now when I put them onto that foam and unstable surface, it’s now going to give me a different clue of different systems. If I am on the firm surface, I am primarily weighted to my body. Proprioception, but if I am on an unstable surface, I am now weighted to my vestibular system.

It is going to give us clues as to what systems we want to look at. So now you have done your balance testing, and you have seen that they are swaying to the right. We have now thought to ourselves, that could be that right cerebellum. That could be that right vestibular system. That could be that right brain stem.

Now you put them onto the foam and do it, and you see that they fall to the right and now you are starting to think, maybe this is looking more like that vestibular system is the key here. Well, I am going to have to do more vestibular tests to confirm my hypothesis because that is going to start to dictate where I create my individualised management. So far, are orthostatic vital signs for dysautonomia.

Our understanding now of that balance system and what we are seeing when we do balance testing, what it means. We are now going to do more than the modified VOMS that’s in the SCOAT6, and hopefully you will understand why when we get to the neural substrates. Based on concussion, concussion is still remembering symptom provocation testing. It Is about the symptoms, and symptom recovery for determination of clinical recovery. As we can see here, their justification in the consensus statement is that symptom provocation with the VOR and the visual motion sensitivity tests appear to be associated with concussion. The modified VOMS have the same diagnostic accuracy and the applicability as the original VOMS, based on symptoms.

What you are going to see, within these changes to the concussion recommendations, is they have taken out some of the vertical testing, and the near point convergence.  But from an objective point of view, that’s almost like saying that concussion doesn’t affect those areas, which is nonsense because 50 percent of concussions have a problem within the near point convergence. They have convergence insufficiency. We want to do all the testing, even though the modified forms are being used for assessment of symptoms only, and if you are just doing it for symptom assessment, the modified VOMS will be fine. But if we want to be truly objective and start to try and figure out where this concussion has affected that person that is sitting in front of you, we want to do it all. Remember the last point here, it is important to recognise that if symptoms are reproduced during the VOMS, that does not rule in the presence of a vestibular or ocular motor problem.

Really important, you need to practice these tests. Understand that when you do these tests, you may not have had a concussion. You may not have a vestibular ocular motor problem, but you do these tests, and you can feel symptoms from some of these tests, which is why we have got to do more tests and put the whole story together for that individual in front of us.

As we can see here, the table from the SCOAT6 on the left shows you have the various tests, and then we are asking about the four symptoms listed across the top there, headache dizziness, nauseousness, and fogginess. We ask the person to rate those symptoms out of 10 before you do the testing. This is the person’s baseline. Then we go through each of the tests. On the left, you can see, we do smooth pursuits, we do horizontal and vertical. Now when you get to the Saccades, you can see that they have just got horizontal, but I want you to all do vertical as well.

Then you can see with the VOR, the VOR’s got horizontally. They took the vertical out. But again, we want to do the vertical. They have removed near point convergence, as I mentioned previously, that we also want to have in, and then we have our visual motion sensitivity test. The general rule is we do the test, we observe while we are doing the test, to see for objective issues that may be going on and then post the test we are asking about the symptoms as well for the symptom provocation.

Video presentation placement: 29:50
Our smooth pursuits can be seen in the instructions in this slide, we are just moving the pursuits side to side at the rate of two seconds. Basically, from the side to the middle takes a second, and across the other side, we obviously make it flow two seconds from side to side. We do two repetitions.

One, and then two, we ask about symptoms, but I want you to repeat that in a vertical direction as well. We have got our testing there; you record those symptoms after the testing. The point on the bottom there, observe for saccadic eye movements or jerky eye movements. What should happen is your eyes should be able to stay on that moving target. If we see their eyes, doing something like displayed in the video, jumping off the target and back to the thumb, they are losing the smooth pursuit movement. We are looking for the blatant pathology things too, where the eyes show, one eye’s moving, and the other one’s not. Look for our pathology, but we are looking for dysfunction. Why does this matter?

Video presentation placement 31:03
The confusing chart in the video slide on the right, I want us to understand what’s involved in a pursuit of eye movement. The pursuits classically come from this parietal temporal cortex on either side. You can see in the example, if the target’s moving to the right, my eyes are following it to the right. I want to keep this simple. The diagram in the chart is everything, let’s keep it simple. When I follow my thumb to the right, pursuit is pulled by the parietal. Easy way to remember it, pursuit is pulled by the parietal. So, if the pursuit goes to the right, it is the right parietal, that is making it move that way. If the pursuit goes to the left, the pursuit is pulled by the parietal. So, it’s the ipsilateral parietal lobe. Why is it important that we understand more of this? Hopefully, you are going to see the emphasis here, you do the pursuit and maybe you see jerky movements. They have got jerky movements going to the right. So, you are thinking “right parietal lobe”. Maybe?

Maybe, because if we follow the rest of it, when I go to the right, the pursuit pulls it, but that pursuit parietal lobe goes down into your brain stem, and then it decussates across to the opposite cerebellum, and then from that cerebellum, it then goes into your vestibular system. When you look at that chart in blue, that is your VOR. That is your vestibular ocular reflex. Our pursuits use VOR.

If I follow to the right, that is the same as my head turning to the left. Left VOR, the eyes go right, a right pursuit, the eyes go right. This is why the anatomy matters because the pursuit to the right could be a right parietal problem. Could also be a left vestibular problem. This is why these little nuances are going to matter. It also could be obviously that brainstem. It could be anywhere in there, but I want to paint the picture there right now. Pursuits, parietal P and P, but the pursuits also use VOR.

In red there, area in blue, the common pathway shared by the horizontal VOR in the smooth pursuit.  Really important, because if you rehab a pursuit, you see a pursuit, and the rules basically say this, if you see saccadic intrusions in the pursuit, you get told to give pursuit exercises.  What if the problem is in their VOR? You need to give them VOR exercises to fix a pursuit. I hope that makes sense. We have to understand our mechanisms and principles here, so we can give the people the right exercises.

If we do vertical pursuits, it’s no different except its primarily temporal lobe, and it uses your vertical VOR pathways. So same principles, pursuit to the right, right parietal. It’s got the double decussating pathway. Parietal, ipsi brainstem, contra cerebellum into the VOR. That’s my horizontal, obviously, reverses for the left pursuit. Vertical, both temporals down into that ipsilateral brainstem on each side into your vertical VOR pathway, which is what those things are showing you there, to your eyes. The takeaway, your pursuits are using the cortex, parietal temporal lobe, and then they are using the VOR. Key takeaway, parietal temporal cortex, and the VOR. Highlighted in red on the slide.

Now looking at our Saccades, (you will do this in the hands-on module) we have the right left, right left, right left, as shown in the blue italics on the slide, do it for vertical as well because the anatomy is different.

Video Presentation placement 36:31

As we do our testing, ask about the symptoms, and then we observe the objective things we see. When they are doing this, do you see them when they are supposed to look at the thumb here? I am just looking for visual purposes, they are supposed to look at the thumb, that thumb, that thumb. But watching the video you may see them lose focus.  They decide they are pretty good, but when they go back to this side again they lose focus. Do you see that they overshoot the target? Can you see that in order to get to this thumb, they might be going from here and they might go here, here, here, here, and they have these saccadic corrections.

The more you practice this, the better you get at picking this up.  We want to look for those objective issues with the eyes. The other little takeaway here that I want to give you, is the eyes from one thumb to the other thumb, you should basically just see them, be on one thumb and the other thumb, one thumb, other thumb, one thumb, other thumb. If you can see the eyes moving, a bit like a pursuit, if you can see that eyeball moving, their movement’s too slow. 

What does it all mean though when you are looking at those errors? Here we go. If I want to look to the right, a saccade is a voluntary eye movement, basically, the rest of your eye movements are reflexes. Your Saccades are the only voluntary movement you have, which is a bit like moving your hand, it’s voluntary. We know that if I move my right hand, it’s controlled by my left frontal, my right leg left frontal. If I want to look therefore to the right, it’s left frontal. And if you want to remember it frontal, fast eye movements, “F” and “F” so parietal pulls the pursuit, and then we have got our fast frontal, to the opposite side. Activation of your frontal eye field and your superior colliculus generates contralateral horizontal saccadic. 

Keeping it simple again. Frontal lobe. To your brain stem generators, then those brainstem generators, you can see in that fancy picture there. You got all those different paramedian pontine reticular formation, your nucleus prepositus, hypoglossi, medial vestibular nuclear. They are all the words, understanding our anatomy, frontal lobe, to that pontine medulla area in that brainstem, then move the eyes. That’s our fast eye movement mechanism. 

We want to look to the right, left frontal, to the right brainstem, pontine brainstem, primarily. I want to look to the left, right frontal, left pontine area. And again, why does it all matter? Let’s look at this as the example. Let’s say you saw someone falling to the right on your balance testing. You might be thinking, right cerebellum, right vestibular, or right brain stem. Now, suddenly, you maybe have done your pursuits, and as you did the pursuits to the right, you think that looks pretty good, and then you did the Saccades to the right. And now, all of a sudden, you saw that when they are going to the right, their eyes are slow or they are jerky, they are not fast, they are overshooting. Now all of a sudden, you are thinking, I saw them falling to the right. That could be that right cerebellum, right vestibular system right brain stem, and now I have seen that those Saccades to the right, that might be that right brain stem playing up, because when I go and saccades the right, left frontal, right brain stem, and they were falling to the right. I got two tests that are maybe suggesting that. Flip side of it, maybe the saccades are okay they are falling to the right, right cerebellum, right vestibular system, right brain stem, but when I did the pursuits to the right, that looked good. But when I did the pursuits to the left, remember which is left parietal, left-brain stem to the right cerebellum and right vestibular system. Now, this is something which has us thinking, this could be the vestibular system or cerebellum. 

If it’s starting to get overwhelming, it’s okay. We are going to keep going through it over and over and over again, Just understanding the anatomy going through these slides. Fast, eye movements frontal, and then brain stem. But the importance of this is if we truly want to serve our patients and our communities better, understanding this to apply the most appropriate individualised management.

 This matters. It really matters that we own this and that you own this understanding so that we can serve our patients the best way possible. And when it comes to vertical, the difference now, horizontal was contralateral sort of frontal lobe to that opposite Pons. When I do vertical saccades, it’s bilateral frontal, to the midbrain. Different areas of the nervous system now. So frontal lobe to midbrain, always remember this. All your vertical eye movements end up coming from your midbrain. All your horizontal eye movements are generated from your Pons. So, these are going to be our two takeaways now. 

So all of my horizontal has their component come out of the Pons? It just depends on what talks to it. Is it a parietal lobe that talks to it? Is it frontal lobe that talks to it, is it a vestibular system that talks to it? If it’s vertical, it’s the midbrain. If it’s fast eye movements, the saccades, that’s frontal, fast and frontal, vertical eye movements to the midbrain. If it’s a pursuit, it’s going to be that temporal lobe into your vestibular system into the midbrain. So vertical eye movements, for saccadic, frontal, midbrain. 

For pursuits, it’s that temporal area to the vestibular system to midbrain. So again, understanding these parts of our anatomy. We do these tests, observe for the deficits, and then from there, we put our story together of what things has this person got showing up as dysfunction. Now near point convergence, this was taken out of the modified VOMs. So, as you can see here, I have put it there as VOMs. 

Because in the normal VOMS, it’s included. Modified VOMS are taken out. I want us to be doing the near point convergence. Again, 50 percent of concussion injuries have convergence insufficiency. They have an issue bringing the eyes together. Again, we do three tests. As we have learned before, we get our distances of how close these people can get to their nose. We want to see that their eyes can get within six centimeters. 

If they are not converging more than six centimeters, they have an issue. With all the VOMS testing, you ask about the symptoms, headache, nauseousness, dizziness, fogginess, rated out of 10, following your testing.  But remember, we are trying to look at the eyes as they are bringing the thumb in, do you see that suddenly one eye stops converging on the thumb, and then we would stop moving the thumb and measure that distance. 

Why does that matter? Well, your near point convergence is using your midbrain, your mesencephalon. Just some semantics here, there is three, four, not known thought processes of some of the pathways for, seeing it, which is occipital lobe, and then from that occipital lobe, other mechanisms using some cerebellar areas, some vestibular areas. There are question marks in the studies here? A lot of primate studies and monkey studies are used to understand where a lot of these pathways come from. The near point convergence is all of the in between like you have seen with the saccades and pursuits. Not truly known, but what could be agreed upon is those reflexes come from the midbrain. So that end point is from that midbrain. As you can see here, the mesencephalic reticular formation, and the reason I highlighted that, putting all this together now. The midbrain when we talked about saccadic, vertical eye movements all come from the midbrain.  Convergence comes from the midbrain. The midbrain reticular formation also is in control or of the pathway of stimulating your sympathetic nervous system. And I will say that again, the mesencephalic, the midbrain, reticular formation is part of that system that sends a signal down to your IML to stimulate your sympathetic nervous system. What we often see is people who are a little bit anxious, maybe their heart rate’s spiking, POTS or orthostatic tachycardia, you might start to see that there are issues going on with that person’s midbrain. Now you might see that, don’t know, but assess it. 

Start to put that together and you will have done your orthostatic vital sign assessment, and you see that they have orthostatic tachycardia. Their heart rate’s going up by a hundred and thirty. The person’s reporting that they are feeling a bit anxious, sweaty fight or flight, a little bit wound up, whatever it is they are reporting these things to you. 

You have seen they got tachycardia. You do your vertical eye movements, and you see that there are issues with all their vertical eye movements. You then do your near point convergence, and you see there’s an issue with that. And now suddenly, you might think, maybe this person’s got a problem with their midbrain. 

How do we put all these things together? We keep doing our tests. We do more and more and more tests so that we can keep triangulating where the issues look like they are in this person’s nervous system. Because if you just do one test, if you look at pursuits as the example, that could have been that parietal area. It could have been the pathway to the brain stem, it could have been the decussation from that brain stem to that cerebellum. Could be from that cerebellum to that VOR. It could be from the VOR, vestibular nuclei to the eye. Nuclear, oculomotor, the MLF, you can see the difficulty with that. If you do one test, it could have been any of those things show up. We have got to do every test that’s possible that’s in your tool kit, and then try and figure out all the tests and what test are showing dysfunction and where are the common places that have a relationship between each of those tests. We use that example. Vertical eye movements, near point convergence, heart rate, maybe we are looking at something midbrain. Someone falling to the right, maybe that could be a cerebellar vestibular problem. Maybe it could be your brain stem problem. Or which of my other test is showing that pontine area, it could be a saccadic movement, or it could be a pursuit movement. 

Our VOR, at the understanding of the vestibula ocular reflex, now the modified VOMs took out the vertical VOR. Why that again is problematic is why do we want to take out a movement? We don’t know if the person’s got a problem with that vertical mechanism, remember that the modified VOMS are about symptom provocation. We want to go a step above that, and then look at the idea of the neural substrates. We do have VOR. We put a target up in front of the person, metronome at hundred and eighty beats per minute, the person’s moving their head 20 degrees side to side, keeping their eyes fixed on that target. 

After 10 seconds of completing the test, wait for 10, ask them about symptoms. But while they are doing the test, you are looking to see, do the eyes stay on the target. If I just did that, you might ask them to, just turn your head to the right. The eyes jumped off, then they look back, he goes to the left, that looks pretty good. Goes to the right, the eyes jump off, then he looks back. 

If you see someone, jump off, so they eyes move with their head and they come back, we call that a catch up saccade, and that lets you know whichever side they turn to, that example, they have me turning to the right, and then I jump back, that’s letting you know that this right vestibular system is hypo functioning. It’s decreasing function. Obviously, if I went to the left, that will be the same thing, on the left. I should be able to maintain my gaze the whole time and the eyes don’t jump off.

 This is the time to really emphasis why this is important. This reflex from your ears to your eyes is the first and only system that is fully developed when you are born. When that baby comes into the world, the vestibular system is the only system that is fully formed. It is the fastest reflex of humankind. That reflex from your ears to your eyes takes seven milliseconds, seven and a half milliseconds. The idea of you looking at the screen right now for the information on the screen, me moving my hand, for that to go through your eyes to your occipital lobe to see takes a hundred milliseconds.  Slow. This is why when you put something up in front of you, and if you are looking at the screen, you can turn your head side to side if everything’s working in your VOR, and you can keep reading the words that are on the screen.

But if you grab this screen in front of you right now and you moved at 20 degrees to second, you kept trying to read it with your vision. You can’t do it. Your vision’s too slow. We have to have an intact working VOR to be able to be upright and walking. We must have this reflex. You are going to hear me always say our priority in rehab is you must be able to keep someone’s eyes still. They must be able to maintain gaze stability.

This test is really important. So let us go back. I turned my head to the right. The example I said before was my eyes then jump back up, a catch up saccade, when I went to the right, right vestibular hypo function. In rare circumstances, very rare, you may see the opposite where they turn their head to the right and their eyes then come back. They turn their head to the right, they overshoot and they come back. What we call a backup saccade.

In that particular instance, we are looking at a vestibular system that has increased function. Very rare that you see this. Now in certain circumstances, when we see it, we must understand that lets us know that that vestibular system’s up, on that side, it’s got too much juice. If I have this way and I have to catch up, I have dysfunction. Now the general rule with nervous system problems is that with the exception of, seizure disorders, epilepsy, seizure disorders, most vestibular problems are most vestibular. Most nervous system problems are decreased function problems. Epilepsy and seizures are, of course, increased nervous system problems. As a general, everything else seems to be decreased function problems.

Understanding most of the time, you are seeing a catch-up saccade, which lets you know that we have hypo function of the appropriate vestibular system. In this example, if we did a VOR, you saw that catch ups a saccade, like that, you think, that right vestibular system is not working too well. What other tests have you done that might also give you a clue. Well, you might have done the balance, especially on foam. Remember that is going to rely on the vestibular system more, and if that vestibular system’s down, you might see that they also fall sway to the right. Now I have two tests that have seen it. I also now know that my pursuits also use that right vestibular system. So in order to make my eyes go to the left, with that VOR, you may have also seen that when they were trying to do pursuits, that their eyes were jerky to the left because that left pursuit uses the right VOR.

Hopefully, we are starting to see how important understanding of physiology mechanisms/neural substrates are. Of course, for our vertical VOR, it’s the same thing. If I take my head forward, of course the eyes should stay on the target, but if my eyes went down and then look back up, it’s a catch-up saccade. Obviously, if I am doing it that way, it should be able to stay on the target with my head going backwards, if my eyes went with my head and then I jumped back down, catch up saccade. What you just know is that that’s just using the vertical pathways of that VOR to that midbrain. So exact same principles, and we put our picture together with the rest of our tests.

Video presentation placement: 54:30

There is our anatomy, which is somewhat already covered, when we did the pursuit. Head rotation to the right stimulates the right horizontal canal, which leads activation of the left lateral rectus, right medial rectus, so both eyes rotate to the left. I turn my head to the right, both eyes should go to the left. A lesion to the left horizontal canal leads to unopposed action of the right horizontal canal, which causes your eyes to be turned to the left.

The example here, that wording there of the second dot point. If this left horizontal canal, which should drive my eyes this way, another way to view it is that your vestibular system is like two magnets. And you know, when you bring two magnets together, and you can feel them pushing against each other, If I had a magnet here that’s weaker than this one, so we will call this, big magnet, weaker magnet, because there is a lesion here. Well, this magnet is going to push, so therefore, this pushing from my ears should keep my eyes there.

But therefore, if I have got a magnet here normal, and this magnet here less. Now this one is dominant, what’s that going to do? Well, that will push my eyes that way, because this one cannot push the eyes that way. So as a result, if my eyes are being pushed this way, your brain is picking up a signal now, but my eyes are being pushed that way, so your brain asks the question, am I moving? Because the only way to make your eyes go that way in a slow movement is to have a pursuit. I need to be able to follow something. So, your brain’s asking, am I following anything? The brain says no. Then the brain is asking vestibular system, are you turning, are we sitting in a swivel chair, are we in a car doing burnouts and spinning to the right, have I got something going on turning my head to the right? And then suddenly, these systems go, NO. So, your brain goes, well eyes, what are you doing over there, get back there. Then suddenly this pushes your eyes again this way and the brain goes, are we doing any movement, are we following anything? NO. Get back there. That’s nystagmus. The slow phase that comes from that vestibular system, brain going, gets back there because that is where I am supposed to be looking. That’s your basic mechanism of a nystagmus, whether it’s right, left, up, or down.

Obviously, the vertical VOR, so a downward head acceleration chin down, makes our anterior canals make the eyes move up, and then of course if our head goes backwards, chin goes up, posterior canals drive both eyes downwards. Why all these matters are the most common cause of dizziness in the world is BPPV, benign positional paroxysmal vertigo. The crystals in the ear, and the most common one because of the anatomy is in your posterior canals. That is where 80 plus percent of all your BPPVs are going to be. Very rare to see them in the horizontal or the anterior. Gravity is going to cause them to go into the posterior most of the time.

If we understand the anatomy of the posterior canal, if I have crystals going into that canal, posterior canal is the same as doing that. Which means those crystals are going to cause my eyes to get pushed down. The brain doesn’t want that, so the brain goes get back, so you see the eyes flick up.

Now, of course, crystals tend to be in one canal most of the time, so if the crystal is in the right posterior canal only that right posterior canal is going to cause your eyes to go down to the left. So, what are you going to see in BPPV, your eyes go down, like that with torsion, slow, bang, flick back up. And that is what you’re seeing in your classic posterior canal, BPPV, a torsional upbeat nystagmus.

That is our mechanisms of how our anatomy works, but we want to look for it. We want to see it because then we understand what part of the anatomy is involved, and we triangulate that. Take away message, if someone’s got BPPV, you fix that first. You fix all those crystals, otherwise, we have constantly got faulty vestibular reflexes being stimulated. And the number one clue that you are going to get about BPPV from a patient history is when they roll over in bed. That’s the number one clue that you will get for BPPV. When I roll to the right in bed, I get dizzy. As soon as you hear that, it’s not the neck. You need to look and assess for BPPV.

If you are going to do testing properly, you need to remove fixation. Spend the money and get video oculography goggles or goggles where you can put the person in the dark. You could use VR goggles for this, you could go to your optometrist or a cheap shop where you can buy thick round lenses/glasses “coke bottle glasses” to use on your patients because then they can’t fixate. This allows you to see those little eye movements that occur when people have got BPPV. If they have got it bad, you will see it without the goggles, but in the subtle cases, we need to be performing our Dix Hallpike maneuvers, our supine roll maneuvers, etc we need to be performing them without the patient’s ability to fixate. We must remove fixation, in the dark or frenzel lenses so they can’t keep their eyes focused on something.

Really important. So your patient tells you, “I roll over to the right in bed or anytime I roll over to the right, I get dizzy”, you assess for BPPV. Even if it’s not a concussion, that is the first thing you put into your armamentarium, and then, if you find it, you treat it with your appropriate Epley’s maneuver, for the posterior canals, or we go through our barbecue roll for the rare horizontal canals, I personally use the modified gufoni maneuver for horizontal canals. That is some of our options for BPPV.

https://www.interacoustics.com/balance-testing-equipment/visualeyes/support/gufoni-maneuver

Video Presentation placement: 01:01:10

Our final test here in this VOMS assessment and the modified VOMS is visual motion sensitivity. The other way to look at this, is this is a VOR cancellation.

You are using your fixation to cancel the VOR.  So, remember, when I turn my head to the right, my eyes go to the left. If I turn my head to the left, my eyes go to the right, but if I give myself a target, my thumb in this test, and I turn to the right. My VOR wants to push my eyes to the left. But I have kept my fixation on my thumb, so what – that in turn – does, is it cancels the VOR. So even though they talk about this test being a visual motion sensitivity test, it’s a cancellation test.

We use the VOMS principles, you do the test, 50 beats to the metronome, and we do those five repetitions. Five each side. One, two, three, four, five counts, 10. Wait 10 seconds, and ask about symptoms. While they are doing the test, you as a practitioner watch their eyes. Can they keep their eyes on their thumb, or do you see their eyes jump off their thumb?

Why does that matter? Because your cancellation is a reference back to the pursuit mechanism. When I turn my head to the left my VOR should push my eyes to the right. That’s my normal VOR. When I do a VOR cancellation or visual motion sensitivity, if I turn to the left my VOR wants to make my eyes go to the right, but I can cancel it because if I have a left pursuit, that left pursuit is what pulls my eyes that way. So now VOR wants to make my eyes go to the right, and if I have an intact pursuit, I can now use that pursuit to cancel the VOR.

The importance of our physiology, neural substrates, in this example we can see, deficient VOR cancellation, ongoing to the left corresponds to low pursuit gain to the left. If you do your VOR testing, and they are doing those 180 beats per minute, they’ve got no symptoms, and you look at the eyes and the eyes are staying on, but then you did your pursuit testing before and you saw their eyes were jerky to the left, and you are thinking, “is that the parietal area or is that that right VOR?” What’s going on there? But you do your VOR and find, It’s not that. But then when you did your VOR cancellation, you realise that their eyes jump off.  Now you have another clue, that the pursuit mechanism on that left may be the problem. So that pursuit parietal area down into the brainstem pathway, maybe the area that we need to rehab.

That section is full on, and there are hours and hours of modules and books that go into more details about this, but I want to give you a few takeaway key points.

• Pursuit
  • Parietal pulls the pursuit.
  • Ipsilateral side, to the opposite cerebellum and vestibular system.
  • Vertical pursuits, that temporal lobe into the vertical VOR
    • or anterior posterior canals, to the midbrain or vertical eye movements to the midbrain.
  • Our saccades
    • if I look to the left, fast frontal. So fast eye movement is a saccade frontal, so contralateral frontal lobe pushes the eyes and uses the contra from the frontal lobe, Ipsi to the eyes, pons for horizontal movements, swap it around if I go to the right.
    • If it’s vertical, both frontal eye fields, into my midbrain, all verticals midbrain.
  • My near point convergence, midbrain.
  • My VOR
    • right vestibular, left vestibular, into the eye movements
    • if it’s vertical, anterior and posterior canals. So that way, anterior canals. That way, posterior canals to the midbrain.
  • VOR cancellation
    • if I go to the right, it should be the right VOR pushing the eyes, but my right parietal pursuit should cancel it.

There is my anatomy neural substrates physiology for our eye testing. It’s important to emphasize that the VOMS was not designed as a comprehensive tool for vestibular ocular motor function and may not encompass all the screening strategies necessary to examine all aspects of vestibular and oculomotor dysfunction.

It is useful as a screen tool, but that may not be appropriate as a replacement for comprehensive vestibular and ocular motor assessment. We should still be using, all our other testing tools, gaze holding, our video-type goggles, optokinetic nystagmus, subjective visual vertical, dynamic visual acuity, velocity storage testing. You have your advanced testing with video, V-HITs, you have your other types of, C-VEMPs, O-VEMPs, otolithic dysfunction, so you can see there’s a lot of other vestibular ocular motor testing to be performed, saccades, anti-saccades, gap and express saccades, different types of testing. VOMS is good for the screening, so what they provide us in the SCOATS6, what we talked about today goes beyond the SCOAT6, and understand that there’s still more that we can do to go beyond that even more to help our patients.

Video Presentation Placement: 01:07:32

When we look at the neck, the cervical spine assessment there, that is what is provided in the SCOAT6. Muscle spasm, tenderness, paravertebral tenderness, our range of motion. But what are we looking for primarily this? We are primarily looking for bad injuries, such as fractures and dislocations.  From a concussion and Chiropractic point of view we want to go beyond these assessments that are within the SCAT and the SCOAT6. If we look at this clinical practice guidelines, it was published three years ago, (Quatman-Yates et al, 2020) it is a really, wonderful paper. It is a 90-page article that summaries all of the best practice evidence. This paper was written pre the 2022 concussion consensus, but the consensus doesn’t outline all the evidence for every single test and every single rehab strategy. That is what this paper was focused on and shows that there’s clear evidence to suggest that the cervical spine should be examined, but there is limited evidence on which procedures should be used in relationship to concussion. This is the dilemma. We know it should be examined, but what test should we use in relationship to concussion.

There are several different groups out there. Katherine Schneider, who is part of the consensus or the concussion in sport group, did several different studies. These are a couple of things from Katherine.

1. Schneider KJ. Concussion – Part I_ The need for a multifaceted assessment. Musculoskeletal Science and Practice. Elsevier; 2019 Jul 1;42:140–50.
2. Schneider KJ, Meeuwisse WH, Palacios-Derflingher L, Emery CA. Changes in Measures of Cervical Spine Function, Vestibulo-ocular Reflex, Dynamic Balance, and Divided Attention Following Sport-Related Concussion in Elite Youth Ice Hockey Players. J Orthop Sports Phys Ther. 2018 Dec;48(12):974–81.

https://www.chrisworsfold.com/3-neck-pain-diagnostic-tests/

When it comes to neck assessments, our extension rotation test asked the person to extend ask them to rotate as far as they can side to side. Your manual spine exam is basically like what was in the SCOAT6 just then. You know, it’s just your PA like motion palpation. From that PA motion palpation, just feel what you feel is the limitation of motion in one segment on the right or left. They just ask you to rate it as normal, slight, moderate, or mark, but use your feels there for that. Obviously, then palpate, is it sore? Is it tender? Over those same areas, and you can see the criteria that Katherine put there when the person’s pain is reproduced, so familiar pain. It’s greater than three out of 10.

If you are palpating a joint and you feel that motion palp is rated as moderate or marked, if you have those, it is highly predictive that it is facet joint mediated. Whether it’s concussion or not, these tests are a nice group that you can put together to be able to decide whether it is facet joint related. Our extension rotation test, our manual spine exam, and then your palpation for tenderness.

Now the cervical flexion rotation test is when the persons on their back, you passively bring them up into full flexion, and then you rotate them to the right or to the left and as you can see in this slide, you are trying to see if the range of motion is reduced 10 degrees or more. With that blocked end field, standard techniques we have done in our Chiropractic training feel that motion palpation.

If you feel that real blocked end feel and that significant loss of range of motion, we know that it has good diagnostic accuracy for that upper cervical cervicogenic headache relationship components there with that test. We have our extension-based ones, motion palp, tenderness, manual spine exam from the last slide, which is good for C2/3 below, and then you have this test, which is good for C1-2 area.

This is a great deep flexor and neck endurance test which is super important. There are relationships with our deep neck flexors for potentially concussion risk, especially in, our high school age athletes and we also know it is a good predicting value in return to sport. Our testing, these two fingers hold them under the person’s head, they perform a chin tuck, they lift the head up so that they are just above those two fingers, and they hold that for as long as possible. If that occiput ends up coming down and touching your fingers for over a second, or you start to see that they lose the double chins there, the skin folds, they start to lose that, you stop the test from a fatigue point of view. Head touching, the skin folds lost or if the person starts to get a pain reproduction. Otherwise, it is a test until failure, and we are trying to record the time that this person can hold those tests for.

Our head laser, classic whiplash type test. You will see this test and the next one becomes important as differentiating tests for vestibular problems or vestibular from neck problems. As chiropractors, naturally people think, chiropractors are only good for neck problems. But as chiropractors, we need to take that responsibility and go, is it a neck problem or an inner ear problem? So, vestibular problem or a cervical proprioception problem. We need to do a better job of differentiating that for the patient. To give them the appropriate care. So, joint position error testing, we got the head laser on, they have the target about ninety centimeters away from them. They close their eyes, turn their head to the right, come back, they don’t open their eyes and you mark off where they got on the target. You passively reposition their head back to neutral, and you get them to do three tests on each side. Six, alternating or three on each side whichever way you want to do this test, and you get the average for the three trials on the left and the right.

Video presentation placement: 01:13:01

That chart you can see in the picture, the green and the yellow, anything that is outside the yellow, when you are performed at ninety centimeters from the wall, is considered dysfunctional, four and a half degrees. Obviously consider angles and our mathematics there, ninety centimeters away from the wall. Four and a half degrees, if you are sitting ninety centimeters from the target is dysfunctional. So that’s our test for the cervical proprioception, knowing where my neck is, right or left.

The one you couple with that is the smooth pursuit neck torsion test. You do your smooth pursuits like you did before looking for your jerky eye movements. After you have done them normal in neutral, you then have the person hold their head still, and you have them turn their body under their head to ideally 45 degrees. If they have a neck problem, maybe only thirty, and you redo your pursuit testing again. You are looking for those jerky eye movements again, those catch-up saccades. The eye should be able to stay on the thumb smoothly. If you see those jerky eye movements, in particular when the eyes cross midline, that is what we are primarily looking for, and then of course can they reproduce their symptoms when their bodies turn under their head. Why do we do it with the body turned under the head? Because we are trying to stop a vestibular reflex, because as soon as you turn your head, you have created a vestibular response as well.  Keep the head still, and we turn the body under the head to make more of the cervical afferents.

The cervical sensory motor, proprioceptive, checking the neck compared to that vestibular system. CSPR cervical spine, proprioceptive rehabilitation, for dizziness post-concussion.

• Hammerle M, Swan AA, Nelson JT, Treleaven JM. Retrospective Review: Effectiveness of Cervical Proprioception Retraining for Dizziness After Mild Traumatic Brain Injury in a Military Population with Abnormal Cervical Proprioception. J Manipulative Physiol Ther. 2019 Jul;42(6):399–406.

The results have suggested the patients with dizziness after a concussion who had abnormal cervical spine proprioception. The laser, joint position error, If that is abnormal, and or they have abnormalities with that smooth pursuit, neck torsion test, these people respond better to neck treatment and rehab rather than vestibular rehab.

You need to do your vestibular testing too because if someone’s got BPPV, you don’t do neck rehab, you do vestibular BPPV rehab. If you do smooth pursuits, when they are neutral, and you see that they have got jerkiness consistently in one or two directions. It’s not a neck problem, it’s a vestibular or central vestibular problem. If someone’s has a nystagmus, so if you see that they are at the end and they have a nystagmus, it’s a central vestibular problem.

You need to do the vestibular tests, and if you see that there are vestibular problems, whether it’s BPPV or any of the central problems, as we can see here, exclusion criteria for any patients who had clear peripheral vestibular, BPPV or consistent central signs, so jerky smooth pursuits when they are neutral, not in torsion, or you see that there’s like a nystagmus. If you see that, with or without visual suppression, you look at the ear. This is the importance of separating these tests, and as you can see here, properly determining whether concussion or cervical injury is the source of symptoms is vital because the management of each condition differs considerably. I want to emphasis a point here. Your nervous system is a learning machine, which is consistently learning and is built to survive.

The only thing your brain cares about is survival. It does not care about the fact that we can create this technology, I can record this and write these things, we can read it and learn and understand. Your brain just cares about, is this a threat? Is this computer threatening me? Are Brett’s words threatening me? Everything is about survival.

If our brain is a learning machine for survival, it learns all the things that are negative to keep you safe. This is why you don’t run across the road, or you don’t put your hand on the hot plate anymore while it’s on, why you don’t jump in the lion enclosure at the zoo. This survival aspect is learned over and over and repeatedly. So nervous systems are great learning machines. The problem is that you can also learn bad habits.

Why does this matter for us from a treatment point of view? If someone’s got a vestibular problem, and you don’t assess their vestibular system, and you think, I am a chiropractor and I just treat the neck. You keep treating their neck, good adjustments, good soft tissue, good exercises, good rehab, and you keep treating this neck, and it is a vestibular problem. By ignoring the vestibular problem, you are training their nervous system to compensate from their neck.

So, you haven’t really helped them, and you don’t know this because you haven’t assessed the vestibular system. Let’s look at this example, we are going to say it’s a vestibular problem, and all you do is treat the neck. You have a chance that you can train their brain to rely on their neck to override their ear. Where’s the problem? Let’s say they then go and have a car accident, or they develop DJD in their neck. Suddenly, that neck that you used to compensate for is now gone, and now these people go downhill.

So that is one of the risks. The other common type of thing that happens is we get all this great treatment going on the neck, really good treatment going on the neck, but they got a vestibular problem, and then as you are treating the neck, if they have a vestibular problem, the problem keeps coming back. They come in the next week and say, “It was great for a day or two, but then it just come back.” or this treatment aggravates them more, because that’s not the problem. The vestibular system’s the problem, and the neck is the thing that’s trying to compensate. All you are doing is treating or aggravating the compensation. So, we have got to make sure that we differentiate where the problem is.

Video PowerPoint placement: 01:20:07

Where in the nervous system is this problem? Is it a vestibular problem, an ocular motor problem, a dysautonomia problem, a balance / cerebellar problem, a neck problem. Now the big one that has the most research is our graded aerobic exercise testing. This should only be performed when the athlete reports the general resting concussion symptom scale is not greater than the 7 out of 10. When the person you are assessing had a concussion and they are at rest, if they are reporting that their symptoms are 7 out of 10, you can do this graded aerobic exercise test, but if they are reporting that they are 8 out of 10 when they are at rest, wait to do this test until there are 7 or less. Once you do the test, which we will go through, then you can prescribe targeted heart rate treatment based upon 90 percent of the person’s heart rate threshold.

Then if you would like, you can keep repeating this test every few days to a week to determine the appropriate heart rate the person needs to be working at. Where the literature is, the most evidence for any concussion treatment now is aerobic exercise. We want to understand aerobic exercise again for our group. So, the subsymptom threshold we are going to use is 2 out of 10. If someone hits a 3 out of 10, when they are doing aerobic exercise after a concussion, we stop the training. 2 out of 10 is fine, 1 out of 10 is fine, but if they hit a 3 out of 10. Stop the session and try again tomorrow.

Just repeating that, if we use subsymptom sub 3 out of 10, threshold aerobic exercise within 2 to 10 days after a sports related concussion, we know that it is effective for reducing the incidence of the persisting symptoms. If you get people exercising soon, you have got a chance of stopping them from getting persisting symptoms, but it is also effective for the people who have got persisting symptoms, to recover.

This is what is listed in your SCOAT6, and it a matter of ticking the box that you have either done it or not done it, and then just list which protocol you used. Now the Buffalo concussion treadmill test listed here is the one that has the most sort of research behind it. There are little variations of it that are now released, a Buffalo bike concussion test as well, but the buffalo concussion treadmill test is the one that’s got the most evidence. And that is how we perform it, and this is covered in some of the other online modules.  We perform that test to determine the person’s symptom threshold and what their heart rate is when they get those symptoms or when they fail on that test. What is their heart rate when that test ends?

• Clausen M, Pendergast DR, Willer B, Leddy J. Cerebral Blood Flow During Treadmill Exercise Is a Marker of Physiological Postconcussion Syndrome in Female Athletes. J Head Trauma Rehabil. 2016 May;31(3):215–24.
• Kozlowski KF, Graham J, Leddy JJ, Devinney-Boymel L, Willer BS. Exercise Intolerance in Individuals with Postconcussion Syndrome. J Athl Train. 2013 Oct;48(5):627–35.
• Leddy JJ, Willer B. Use of graded exercise testing in concussion and return-to-activity management. Curr Sports Med Rep. 2013 Nov;12(6):370–6.
• Borg GA. Psychophysical bases of perceived exertion. Med Sci Sports Exerc. 1982; 14(5): 377–81.

So, understanding the physiology and the pathophysiology of concussion is especially critical for our 20 to 30 percent of concussion patients who get persisting symptoms.

Video Presentation placement: 01:23:23

Part 2 – Rest and exercise after that big reevaluation of the importance of it.

Let’s understand aerobic exercise. Individuals with acute concussion have impaired cerebral blood flow, that’s our whole stretching, sodium calcium coming into the cell, that creates that energy demand where the sodium potassium pumps are trying to get sodium out potassium back in. The calcium that’s going into the cells creating vasoconstriction, and an energy mismatch.

I have an energy increase in demand to try and help those sodium potassium pumps, but that calcium going into the cell is causing decreased cerebral blood flow. What we can see here with concussions, we have impaired cerebral blood flow, cerebral oxygenation is impaired, abnormal blood pressure responses, dysautonomia. We know that what’s going on with the concussion, so, the question we should be asking is “we need to be doing things to enhance cerebral blood flow, enhance cerebral oxygenation, help the autonomic nervous system”. The second dot point in this slide suggested the cerebral hypoperfusion might be responsible for the provocation or worsening of concussion symptoms. Decrease perfusion into the brain may be responsible for this provocation worsening of some symptoms. Increases in cerebral blood flow, cerebral glucose, brain derived neurotrophic factor, and heart rate variability are considered favorable biomarkers If we see increases in those things, remember, HRV heart rate variability is a simple rule, and people always ask you about it. What do you want to see? The bigger the number, the better. As we get older, that number gets smaller, but the bigger the number in HRV, the better. The better tolerance you have in your autonomic nervous system. We want it to be bigger.

Increases in systolic blood pressure, mean arterial pressure, cortisol oxidative stress and reductions in diastolic blood pressure are considered detrimental. For example, an increase in systolic blood pressure during exercise may elicit a myogenic response in the cerebral arteries, thus stimulating reflexive cerebral vasoconstriction resulting in reduced cerebral blood flow in an already impaired state. The simple takeaway with that example is don’t get people doing weights after a concussion. Because of the increase in blood pressure, then can cause a reflexive constriction, decreases the blood flow even more, enhancing symptom problems, enhancing that system dysfunction.

Understanding aerobic exercise now. Low intensity aerobic exercise, so that is 63 percent maximum heart rate or less, has been shown to increase cerebral blood flow and oxygenation and no adverse effects on exercising BPm cerebral blood flow cortisol, BDNF  levels.

Moderate intensity aerobic exercise is less than 76 percent maximum heart rate, has shown generally positive effects on these symptoms. The top two points, they are low intensity exercise, maybe moderate intensity exercise, in terms of aerobic exercise, keeping someone like in that 65 percent less range has been shown to have those benefits, whereas you can see here high intensity has been shown to increase blood pressure, variable findings on cerebral blood flow, increase free radical production, cortisol synthesis, dangerous increases in mean arterial pressure, and reductions in cerebral glucose. So high intensity aerobic exercise would likely be detrimental for physiologically compromised concussed patients.

When we have a concussion patient, think about the American barbecue, low and slow, low level, low intensity aerobic exercise.  When we look at the consensus statement, they have now come out and said strict rest until the complete resolution of concussion symptoms is not beneficial. This “cocoon therapy”, go into a dark room and wait till all your symptoms are gone, we don’t do that anymore. Relative rest is monitoring your activities of daily living, resting where appropriate when your symptoms get up more than 2 out of 10, go back, rest and reduce screen time. Just get rid of screens for the first 24 hours. No TV, no phones, no computers in the first 24 hours. But after those first 2 days, so day 2, you want to start introducing activity of daily living within the symptom threshold. We recommend early physical activity that is tolerated. Individuals can systematically advance their exercise intensity based on the degree of symptom exacerbation experienced during the prior bout of aerobic exercise.

We can prescribe subsymptom threshold aerobic exercise treatment within 2 to 10 days after a concussion based on the person’s threshold. Now this is where that buffalo concussion treadmill test is important. We do the test, find out what that heart rate is and where they get symptoms, where it goes to 3 out of 10 symptoms. As soon as that 3 out of 10 increases in symptoms occurs, the example being if they are 5 out of 10 when they are doing the exercise, that’s okay, they are allowed to go to 7. So let it go up by 2, but if it hits an 8 on that test, we stop the test, we take their heart rate, and we see what that heart rate is when they develop those symptoms. 

We then give them exercise at the 90 percent threshold. Let’s just say they got symptoms at a 130 beats per minute.  We are going to take 13 off that. They will be able to exercise at 117 beats per minute. We go through the prescription of that in a minute, but that’s our subsymptom threshold exercise, which can be progressed systematically by repeating that test every few days to a week. Or they can just keep doing the exercise for 10 to 20 minutes every day. If that symptom doesn’t increase by more than 3 out of 10, if it only goes up by 1 or 2 out of 10, or it doesn’t increase at all, the next day, they can try and get a little bit more. And we want to start building people’s aerobic exercise up. 

That is how we prescribe the subsymptom subthreshold maximal exercises following your treadmill test. 90 percent of the threshold heart rate achieved on the treadmill test. They do 20 minutes a day for 5 to 6 days a week using a heart rate monitor.

 Terminate the exercise at the first sign of symptom exacerbation, which is greater than 2 out of 10. If they hit a 3 out of 10 increases, they stop, or after 20 minutes, whichever comes first, you can keep doing the tests, as previously said, every few days to a week or every two to three weeks to establish a new heart rate model. The model I personally use in clinic quite a bit is to get the person to increase their heart rate target by 5 to 10 beats per minute every two weeks. And then get the person building that in the background, and then I will assess the vestibular, oculomotor, dysautonomia, and neck. 

In clinic, we are figuring out how we build those things up while they can just build this up on their own in the background.  So, both alone and coupled with other impairment specific active rehab interventions, aerobic exercise training has been linked to faster symptom resolution and rate of return to sport and enhanced neurological recovery. So why is that the case? Because this low level to moderate level aerobic exercise enhances that cerebral blood flow. It enhances cerebral oxygenation, brings in all the good, favorable biomarkers that the brain needs when it’s recovering in a concussion. Remember, we are in an energy crisis in concussion. We are using too much energy, but we don’t have the blood flow coming in, that energy mismatch, that metabolic mismatch, the energy crisis. 

Aerobic exercise at low level, at subsymptom subthreshold level, that is the thing that enhances cerebral blood flow, cerebral perfusion. These are the words I use with patients a lot. It is not about exercising to try and get fit, we are using heart rate-controlled exercise to enhance the blood flow into the brain, cerebral perfusion, to bring oxygen into the brain to help that energy crisis, that mismatch. Educating the patients of what’s going on, so they don’t go and do their exercise and tell you “I find it really hard to exercise at that heart rate” and you tell them you know. We need to let them know that it’s to try and get your autonomic nervous system and perfusion to work effectively, and that’s obviously what is not happening well in a concussion. 

Video Placement: 01:33:13  When you look at the rehabilitation section of the consensus statement, you think about aerobic exercise as the first part of rehabilitation. Get people doing aerobic exercise straight away, then when you look at the consensus on concussion, this energy mismatches this metabolic mismatch, the energy crisis that’s going on inside the brain is when we have that head injury, the stretching sodium calcium coming in potassium out. 

That process is supposed to take about thirty days for it to resolve, maybe up to forty-five. This suggests that a lot of people may recover in 7 to 10 days from that process. But current advanced imaging is suggesting maybe 30 to 45 days. If we start doing this relative rest on the first day, and on day two, you start to get them to do some physical activity, aerobic exercise at a low level. And they are doing all that and trying to make their return to learn or return to sport, whatever the individual is. If we are dealing with athletes as part of being a FICS sports chiropractor, we are dealing with the athletes who we are trying to get ready to return to sport. If they are a student athlete, high school collegiate, whatever it might be, we are asking them to return to learn first. Learning takes priority for the student athlete. If they are professional athletes, of course, it is the return to sport. 

Relative rest for 24 hours, maybe 48. Starting them exercising day two, day three. Aerobic exercise, low level, and if you are doing that, with that return to learn, return to sport program, but they are not getting better, or progressing, that is when the consensus statement outlines.

• If the person’s got dizziness neck pain or headaches for more than 10 days, we want to start doing some cervical vestibular rehabilitation.
• If you have got dizzy balance problems, vestibular rehabilitation or cervical vestibular rehabilitation may be a benefit.

 Our job as chiropractors is to be able to assess properly so we know which thing we should be doing. Should it be neck, vestibular or should it be both? 

We know that the inclusion of the sub symptom threshold aerobic exercise in combination with these other things should be considered. The first thing you are taking away; I get them doing aerobic exercise at an appropriate sub symptom sub threshold level as soon as appropriate. So, two or three days after a concussion.

 In the case of recurrence of symptoms, when progressing through the return to learner return sport, reevaluating and referral for rehabilitation may be a benefit to facilitate recovery. All the things we just talked about before. Reevaluating for the dysautonomia for the oculomotor, for the balance, for the neck symptoms, evaluating all of that to determine what’s the appropriate treatment for this person to help rehabilitate them from their concussion injury. 

Dysautonomia, I want to just give them a few little things for these POTS, and I just want to give you things straight out of the literature that we know that we can sort of do safely, whether it’s in hospital or in home, and then we will obviously build into understanding our other rehabilitation strategies that we have built up today. So, concussed athletes often have altered autonomic nervous system balance, which is reflected by higher heart rate during steady state exercise, versus controls. The primary autonomic nervous system control center is in the brainstem.

I talked about it before, the mesencephalic reticular formation is involved in this. Your other pontomedullary reticular formation is involved in these areas. We have our cardiovascular centers, our breathing centers located within those reticular formation structures in that brain stem. These areas may be damaged in a concussion, particularly if there is a rotational force applied to the upper cervical spine. The upper cervical spine, think of fighters, they will try and rotate the head on the skull to knock someone out. If there’s rotation involved there, if we get this shearing which primarily affects this brain stem structures and with a concussive force, which is significant enough, we could get stretching through that area, and in turn could lead to those autonomic nervous system areas being stretch therefore being affected. The altered autonomic regulation after concussion is believed to be due to changes in the autonomic centers in the brain. So that hypothalamic limbic area and or uncoupling of those areas with the brain stem and then our peripheral receptors. Our arterial baroreceptors and the heart.

 It is proportional to TBI severity and improves during TBI recovery. The worse the head injury is the worse the dysautonomia is. Super important, there is a large subset of concussion patients who have persisting symptoms that tend to get orthostatic tachycardia. We are testing that, with our NASA lean test, we go beyond what the SCOAT6 says. Stand them against the wall, keep them there for 10 minutes, take their blood pressure and heart rate every minute and monitor for symptoms.

If you see an orthostatic tachycardia presenting to you or POTS, postural orthostatic tachycardia syndrome, the evidence suggests that the autonomic nervous system dysfunction because of diffuse axonal injury, including brain stem structures and pathways mediating normal cerebral vascular auto regulation could account for many of the symptoms commonly seen post-concussion. We bring in this idea of tilt table training, so we have aerobic exercise. Now is the time we need to think about this clinically. Aerobic exercise, we said we want to start introducing day two or day three after a concussion. What if the person has also got orthostatic problems? What if they have a problem just standing upright and their heart rate spiking? You are going to try and give them upright aerobic exercises? This is where you have your patient who tells you “I tried to do all of my buffalo concussion treadmill test, and I tried to do all that aerobic training and it wasn’t working”. Were they assessed for orthostatic problems? And often times you find that they are not. As we said, there are a large subset that have these symptoms missed.  These types of people, if you want to do aerobic training with them, you need to make them do it recumbent. They can’t be upright because they will be struggling to get blood perfusion to their brain, because they are upright. This is why you need to do all the tests, otherwise, you don’t know. These people must be in a recumbent bike. In some circumstances, I have had people lying flat on their back, and in those upper body ergometers that you can buy, I have them put one of those up on a chair, so they are laying on their back on their ground, feet up on a chair, and we get them to do their aerobic exercises like that.

That might be how we need to institute aerobic exercise, and while we are also trying to get this orthostatic tolerance up, this is how they can do it in a hospital setting. They just put them on an inversion type table, a high low type of table, and then we can do tilt table training. You can see the model they do in hospital; they lay them on their back for five minutes, monitor their heart rate blood pressure, tilt them up to 70 degrees, and they are trying to keep them there for 30 minutes. They will be measuring their blood pressure and heart rate every 5 minutes. If they start developing fainty feeling presyncope, take them back down onto their back, monitor their heart rate and blood pressure, and they basically just get them doing this repeatedly and training their autonomic nervous system to try and deal with being upright. This is what they are doing in the hospital. So, if the patient can complete, the in-hospital tilt training, once a day without fainting for three straight days, they then refer them home to do home tilt table training, which looks like this.

You look at the picture on the right, it looks like the NASA lean test. Basically, one foot length out from the wall, upper back against the wall, and they try and stay there for 15-30 minutes. Now you may be asking, maybe, what’s the reason for having your feet away from the wall? Because they are leaning on the wall, they are not getting muscle contraction, they normally get from their legs which pushes blood back up. We are trying to get those autonomic reflexes to keep the blood back up, not rely on the muscles from the legs, to shunt it. The idea of having your feet away from the wall and leaning on the wall is designed to take some of those reflexes away. So, we are not using those muscle responses, those muscles squeezing the blood. We are just using autonomic reflexes. And as you can see there, fifteen to thirty minutes twice a day, safe place without risk of injury, stop the session of the occurrence of the first symptom

An alternative to it is just using an inversion table, and then you can see the general process there of having them on a tilt table, they lay on their back, bring them up to 45 degrees for five minutes, see if they can tolerate it. If they can handle 45 degrees, you are progressing to 60 degrees. They can handle that for five minutes, progress to 70, then to 80, then to 90. As you can see, for a max of 20 minutes at or above 60 degrees if they have got tolerance. Any of these things, if you get symptoms of intolerance at any level, you just try and bring them back down to horizontal to allow them to recover. But we have got to build up that person’s ability to be upright and that autonomic nervous system to perfuse the blood into the brain and keep good cerebral oxygenation, energy delivery. That’s what this is all about. Remember, POTS and that heart rate spiking, the heart rate spiking is not the problem. The heart rate spiking is your nervous system trying to help you keep blood into your brain.

For those that are prescribed medications or practitioners who are trying to treat and slow the heart rate down, if that is what you are focusing on, you are treating the person’s compensation, and that can make them worse. We need to do the training to train their autonomic nervous system to be able to effectively keep that perfusion in the brain. Don’t go after trying to decrease someone’s heart rate. That’s the person’s compensation to try and help them. Don’t take away what they are trying to do to help them. You got to try and help their system work properly so that their heart rate can start to naturally drop down on its own.

Now the vestibuloocular rehabilitation we know is associated with reduced dizziness, improved balance, and faster return to sport when it is used in conjunction with your aerobic exercise, or if it’s used on its own. It’s expected that when you do this type of rehabilitation, you may get transient increase in person’s symptoms. I like using that 3 out of 10 rules when I am doing my VOR and oculomotor and other vestibular exercises, but the key point there that I have bolded there, third point down. Patients with posterior and lateral canal BPPV should be treated with canal repositioning maneuvers.

Treat that, clear those otoconia out of the semicircular canals if they are present, and then you are assessing to see whether your patient needs to be doing other vestibuloocular motor rehabilitation.  If you identify something on your tests. We talked about the VOMS, the balance testing and we talked about differentiating the neck with your joint position error – with the laser on your head – and the smooth pursuit neck torsion test. If we identify that there is a vestibuloocular motor problem, we want to provide that targeted rehabilitation strategy, and you then give that that matches what the person needs from your assessment, and this is the key, you can do any rehabilitation exercise as you like, as long as they are appropriate for the person’s assessment. Where we fail is when we just give people exercises because you think, they have got a VOR problem, so you give them a VOR exercise, thinking it may work. But It may not. I have got a greater probability of being able to help someone. If I do my tests, I understand that a right VOR is that right the vestibular system. I understand that if my eyes jump off and they go to the right, that’s a catch up saccade, and that is a right vestibular problem. I am probably going to want to bias that right vestibular system and I am not going to be wanting to bias the left side because otherwise I keep the imbalance there. The same as if I have got a weak bicep and I am doing bicep curls, and this right bicep keeps failing, but if I keep doing barbell curls, the imbalance remains. I am going to go and start doing some dumbbell work and bias that side a little bit more. It’s no different with your nervous system than it is when we’re doing that muscular type rehab.

Keeping your eyes still is the primary focus when it comes to this. If you see that someone’s eyes are jumping off when they are doing a VOR, that is where you go. We must get gaze stability first. Your eyes must be able to stay fixated. If your eyes move off a target, if your eyes are just constantly moving with a little nystagmus or you can’t keep your eyes still, if your eyes are moving less than two degrees, you will feel like you have blurred vision. If your eyes are moving by more than two degrees, you can start to feel like you are getting double vision, and every time your eyes move, at the time they move, which is why they must move so quick, at the time they move, your brain doesn’t know where you are. That is why they must move quickly. So, if my eyes are constantly moving, though, constantly moving, because I have got a problem with my vestibular reflexes, If I have got a problem with that then my brain is constantly going where am I? And that is a threat.

Because if you don’t know where you are, that means you can fall. And if you fall, that means you can hurt yourself, and your brain, because it’s built to survive, falling is equal to the risk of death. So, everything comes back to survival. If my eyes are constantly moving, I don’t know where I am, if I don’t know where I am, that means I could fall. If I could fall, that means I could die. Very simple survival talks there from a brain perspective.

If you don’t know where you are, and there the risks, how do you think these people feel? They feel anxious, and so what you will see in clinic is you will see a number of people turning up to you with high levels of anxiety, and when you do your screening forms and you do your SCOAT6 and you do those anxiety questionnaires like a GAD7 or a depression anxiety stress scale (DASS), if you do those, or even just chatting to the people, people tell you, I’m anxious. And yet, what they will tell you, I have gone and spoken to these different people about my anxiety, trying these medications, and they don’t work.

But then you go and do a whole bunch of vestibular testing, and you finally get vestibular problems. And that vestibular VOR type testing, if that has got a deficit, then you can start to see that these people are anxious. All because of that threat system being wound up. And this is why it is so important that we assess and understand that vestibular mechanism, understanding the different tests, but the important fact is they can keep their eyes still. All we need to do as you can see here, gaze stability training requires a patient to maintain their visual focus while moving their head to facilitate the recovery from the VOR impairment.

We have several different options. Gaze stabilization of VOR x 1. It is designed to increase the gain. If I went like that and my eyes jumped off as I turn my head and I jump back, catch up saccade example or day to day has been this right vestibular hypo function. The other word in neurophysiology, is that would say, the right side got a decrease in gain because every one degree that my head moves, my eyes should move equal opposite one degree. If it’s two degrees per second, my eyes should move two degrees per second. That’s a gain of one. That is the neurophysiology terms.

When you see the design to increase the gain of the vestibular system, it’s designed to make that hypo function, that decrease gain, come back up to level. If I want to do these gaze stabilization exercises, which is just this. If it was to the right, if that was the dysfunction, I am probably going to want to bias doing a VOR like that. Maybe even turning my head to the right, closing my eyes coming back to the middle, so that way I am biasing that right side. Rather than just doing this. Because then I am doing right, left, right, left. How could I bias that person’s dysfunction? If you understand the principles, it doesn’t have to be a standard approach.  I could put someone in a swivel chair, and I just turn them to the right.

The only problem that I have with that is that I don’t have my eyes staying still. And so, we can see we have to make the clinical call of what does this person need I need that person’s eyes to stay still versus if I spin them to the right in the chair, the eyes are flicking because they are not keeping their eyes fixated. How else could I do it?

Video Presentation placement: 01:52:44

I can do a times two. Times two meaning just two things are moving. Again, design increased the gain, so that on the right side, if we use that as example, I could make my eyes look at my thumb. I could make the thumb go to the left. While my head goes to the right, then close my eyes, and bring it back.

And so now I have the vestibular system I have my eyes. If I am just doing my head here, I have my eyes fixated on a target. So, I have my eyes staying still. If my thumb moves, my eyes are still staying still on the thumb, they are just following it, and then I get that double input. So, we know other ways to look at it. Is a VOR x1, one thing’s moving, the head, but you could also view it that that’s going to increase the gain by one.

A VOR x2, I have the thumb and head moving, two things moving. You could view that, which is going to increase the gain by two. It’s going to help it even more. This is where we can start to play with, what is it that I want to try and emphasize a little bit more?

Do I need to emphasize this right side that little bit more because that one version is just not getting enough change, so maybe I will need to get it a little bit more energetic movement.  Flip side of this, is I may need to get the other side down a bit.  When you were doing this testing, you may have seen on your left that they went that way and came back, and there was a backup saccade. There was too much function, too much gain on this side. Or maybe you were trying to do all the increased game things on the right, without any result, and you thought how do I decrease this left side? In this example, I might make them do turns to the left while they keep their eyes on their thumb designed to decrease that gain. This is about understanding different exercises, but the most important thing is understanding our tests.

How do I hit those areas? You might give someone a right VOR because that you saw that when you were doing your balance testing, they were swaying to the right. So, I might do a right side to try and drive up that right balance posture reflex. Starting to understand, I might use an eye exercise for something that doesn’t even look like it’s got anything to do with the eyes, but it had everything to do with balance.

So how do we do this? Other options, you got your VOR x1, x2, x0. But from a home point of view or in clinic, moving people’s heads passively. Because it’s a reflex. If I actively, do it, that actively doing it is also recruiting my neck. So maybe a swivel chair keeping my body still or standing and using my legs and turning the whole body to the right, because now the neck’s not being involved, and the ear is being involved more.

This is where the problem with the rehabilitation is. I can’t give you standard approaches for everyone because we must do our test and then logically think our way through the symptoms. Do I need that neck involved? Is it okay to have the neck involved? Do I need it to be more, pure inner ear? How do I make it more, pure inner ear? Well, I need to do it more passively so it’s more of a reflex, maybe in a swivel chair. Maybe we can do it standing, but we want to progress those exercises as you can see. Progressed from passive to active.

Progress from non-weight bearing. Where’s that relevant? Or what if someone’s got orthostatic tachycardia?

I might need to have them laying on their back, and I do those VOR movements on their back because they can’t tolerate being upright yet. Think about the individuals in front of you and remember there is no standard here. Please understand what the right thing is to give for this person at this point in time.

Our pursuits, you might have found that there was a deficit in the pursuits to the right, but we talked about it earlier. The pursuits to the right, right parietal temporal, ipsilateral brain stem to the opposite cerebellum into that vestibular system.  I might need to be doing left VORs to help a pursuit to the right first.

And once that VOR is working well, then I can start to bring in the pursuits if that’s appropriate. As you can see, practice following the thumb with the eyes, the head stays still in the previously determined abnormal directions, make sure the VOR’s appropriate first, then you can progress to these, like, the head eye coordination where we can follow them in the same directions, VOR x2. Non weight bearing, seated, to standing, depending upon, orthostatic tolerance, balance, abilities.

As saccadic eye movements, Same thing, have we got frontal things here? Now here is where this becomes interesting. Someone has a cognitive problem after a concussion. I can’t think, I’m really struggling to concentrate. Well, that’s frontal, classically. You might start giving them small little saccadic eye movements like in the picture because you now know those saccadic eye movements come from the frontal lobe. Now I am not saying that’s going to fix someone’s cognitive aspects, but this might be a way that we can start stimulating that frontal area and in turn, help these persons cognitive areas start coming back online in a very lower level. Find the directions those saccadic weren’t working too well, and then we prescribe the exercises according to what that person needs. Is it a frontal thing? Is it a brain stem thing? Is it vertical? Is it horizontal?

Our near point convergence the best test is the Brock String. Get that string. Get three beads on it, and you can see different instructions laid out on the PowerPoint slide. Get a string, they try and bring that bead as close as they can to their nose where it’s in focus. Have the third bead arms distance away from you, and then put the middle bead in between those two beads, close one, far one, one in between. Then all the person’s doing is as they look at the string, they look at the bead get the bead in focus, and as they are looking at the bead, they try and make an “X”. So, an example, the lady you can see there, she has a green, a yellow, and a red. If she is looking at the yellow, and then if we look at the bottom picture, let’s substitute the green there for a yellow. That’s what she should see. She should see the yellow bead. She should see it’s in focus. She should see the string makes an “X” and she should see two red beads behind it. As you get that bead in closer and closer, you won’t get an “X” here closer. You’ll just see a “V”. Hitting that bead, and you will see the beads behind it. So that is an important thing for fusion.

Why is this important? Because this is reading. So people who have often had head injuries, concussions, even the people who come into clinic say, “I am getting a headache when I am reading. I don’t know what is going on. I went to the eye doctor, and they said glasses are fine, I don’t need any of that and my visual acuity is fine”. It’s 20/20, we do this near point convergence and suddenly you find that their eyes can only converge at 18 centimeters, and they are supposed to be within six.

As soon as you start working on this convergence, now suddenly, they can see a string, they can see an x, and they are working with that. They come back to you and tell you, “I can read, and I don’t get a headache, or I don’t get tired when I’m reading anymore”.

This movement is so important for our ability to read. For 3D depth perception, it is important. This is why we want to keep that in the actual testing of the VOMS. Here’s the bit that added another layer. Too in-depth to go into for this, but I want to flag it with you. We said that convergence comes from the midbrain. I said that the midbrain is also involved in that sympathetic nervous system.

If you have got a patient who’s maybe got that orthostatic intolerance and that racing heart, maybe making them do vergence exercises or vertical eye movements because they come from that midbrain. If you make them do that, that could make them spike their heart rate more. That may not, you need to test it, but it’s something to put in the back of your mind and think if someone’s got dysautonomia, we have given you a priority that the eyes must be able to stay still when we come to rehabilitation, that is always number one.

Now let’s go back a step. We said that we want to implement aerobic exercise, as soon as possible, like day two, day three after a concussion. Because cerebral blood flow, oxygenation, glucose, all those things, that’s what’s going on in concussion, the energy mismatch, the metabolic mismatch, the energy crisis. That is the priority. If someone’s got dysautonomia, that is our priority in concussion rehabilitation.

We must get that aerobic exercise to enhance cerebral blood flow, and we must get people to be able to get upright. Some of these rehabilitation exercises may not be appropriate to be done with the eyes. Until we have that dysautonomia remedied and working properly first because that is the cerebral blood flow hypoperfusion issue, and maybe if I make people do vergence or vertical eye movements, and that starts driving someone’s sympathetics more, I could get increased blood pressure, increased heart rate, and now I am making the problem worse. So, the importance of us understanding our anatomy and substrates and what it is we are trying to do.

Video Placement 02:03:43

1. Quatman-Yates CC, Hunter-Giordano A, Shimamura KK, Landel R, Alsalaheen BA, Hanke TA, et al. Physical Therapy Evaluation and Treatment After Concussion/Mild Traumatic Brain Injury. J Orthop Sports Phys Ther. 2020 Apr;50(4):CPG1–CPG73.

Now for our neck rehabilitation, we all have a lot of different skills in this space. We know from this study by Quatman and Yates these might be the exercises that may be good to be done after a concussion. Neck strength and muscle strength imbalances have been shown to be associated with concussion risk. We talked about that deep neck flexor aspect, especially in those adolescent high school age groups involved in sports, especially females too.

May be valuable for practitioners to provide cervical musculoskeletal interventions with the goal of decreasing risk for subsequent concussion injuries. We know that deep neck flexor endurance testing is a good test for us to be using as a marker for return to sport. We want them to be able to hold that position for at least a minute. And if they wear a helmet for their sport, they should be able to do at least a minute with their helmet on. We might start a bit low giving them biofeedback so they can learn how to use it. Use a sphig(momanometer) under the back of that neck there below the occiput.

Gentle chin tuck without the SCMs activating, started at 22mm of mercury, 10 x 10 second holds, and they slowly progress, but it’s not shoving the head Into the ground. It’s performing that chin tuck. It is the skull flexing on the neck, not the retraction of the head. Working on that biofeedback.

As they get better at that, we can start to load it with bands to provide more resistance, build up the endurance of how long they can hold those things for biofeedback, 10 x 10 second holds. As they start to know how to do it, start to load it up with bands and start increasing the time ,or the resistance that’s on the bands. But the endurance is the key. These things (deep neck flexors) are going to need to last all day. We would rather have them being able to hold it for two minutes rather than being not able to hold a black band for 10 seconds. We want to go with the endurance first, then we can start building the load. Build them appropriate to what they need. Do they need to be on their back first? Do they need to be seated? Do they need to be standing? Make the clinical determination based on who’s in front of you and what their tests show.

This one’s an important one. We will see a lot of people when we are doing this joint position sense testing. What we want to do is we want to make sure that when we start this rehabilitation, we want to take people’s vision away. We want them, when they are doing joint position training, eyes are closed. You have them turn their head, they come back to the middle, and then let’s just say they did this, then they open their eyes and they will say, “I overshot”.

But this is where it is, remember where this is, they come this way and they come back and undershot that time. We want them to learn how to reposition themselves via that neck. Obviously, their ears are involved with that one as well. Because, here is another little clinical pearl for you, the human brain compensates with vision a lot. So, when you have a neck problem or a vestibular problem or a balance problem, what you will see is that a lot. And you do need some more of the advanced imaging, advanced sort of testing modality. So, force plates to enhance your BESS testing, some of the goggle-type testing to remove vision, so to measure some of these things. It just gives you more of an objective number. But what you can almost know for certain, is that people with neck issues or vestibular issues, they will start relying on their vision. They will compensate from their vision. They will upregulate their visual system. You will hear the stories in the history taking, when the patient tells you “I need to turn on the light when I get out of bed at night, because I bump into things”. Because this person relies on their vision, these are the types of people that don’t want to drive when it’s dark because they are relying on their vision so much.

These are the people who may be walking down the aisles in the shopping center, and they go to the shops, and just everything sets them off, because everything’s moving in their visual world, and their vision’s too slow to process it, because their ears and their bodies should be doing it reflexively.

It is important when we are doing this neck training you start with eyes closed, and they learn how to know where they are without their vision. If you find that when you were doing that joint position error testing before, you know, listen they come back here and they showed that they were outside of the yellow on the target. So outside it is four and a half degrees.

On the right, when they turn to the right and come back, but on their left, they were fine. If we just said it was just neck and you cleared out all the vestibular testing, you might be doing some manipulation, whatever your chosen technique is. You may be doing soft tissue, needling, taping, whatever it may be. Maybe doing that through their neck, and then you are getting them to do, proprioceptive retraining on the right with eyes closed first.

Once they have built up their accuracy, then we can build them to working with eyes open, tracing different patterns. So, then their eyes stay on the target, and the target is the laser, and they are following the laser with the eyes. What do you need to be able to do that though? You need gaze stability. To progress through some of these exercises, there might be another step that’s needed elsewhere, but you might be able to do this neck rehabilitation, because you don’t need your vision right now; they could be doing that while they are also doing some right gaze stability work to focus on being able to keep their eyes stable.

And then as we build along, we build each of the systems up, we can start to couple them. But your assessments are going to determine what it is that person needs. The return to learning and the return to sport, the way to look at this is going ahead of everything we have talked about. You do your evaluation. You are figuring out what is happening with that person, and you make your diagnosis, thinking this is a concussion.

And you have identified that there is something wrong with their balance system, with their vestibular system, with their neck, with their autonomic nervous system. You figured that out, and then you are giving them the advice of one day rest. And then on day two we will start to move them into activities of daily living, and we want to start getting exercise. Now don’t view the exercises of return to sport. View the exercises that we are trying to enhance cerebral blood flow, and that cerebral perfusion. That’s the purpose of the exercise.

While that is going on, for our student athletes, remember the athletes. But in your offices, you are most likely dealing with the general population as well, so you may have some children, adolescents coming into your clinic, that were not part of the event you were working on the sideline for. These people have come in after already having sustained a concussion. As you are assessing them you are working through this return to learn strategy.

As you can see, it’s all based upon 2 out of 10 symptoms. If it hits a 3 out of 10, that session’s over. You rest, and you can go back and try it throughout the rest of that day or the following day, but the progression through the return to learn strategy, as we said, is symptom limited, but they have got to be able to get through returning to school full time before they are allowed to get back to sport. That is why I put this first, because they are getting back to school full time, all classes, all their homework without issue, is the priority over back playing sport.

Return to sport strategy. The quickest you can get through that entire phase is a week. So, the quickest that we can get an athlete returning to sport is one week but be aware that this whole process may take a month. With your testing, if you don’t base everything just upon symptoms, because someone might say to you, I have no symptoms, but you watched the person get knocked out which is one of the key observable signs to remove someone from the field of play. They have been knocked out because of a head collision.

You remove them from the field to play. Hypothetically, lets use this example that the person has been knocked out and has no symptoms. And you go through this return to sports strategy, the catch is they have no symptoms. So, each day, they are going step one, passing that, step two, they are passing that, step three, they are passing that. They have no symptoms, so they have no symptoms at rest. This example they have no symptoms doing step three, so they get clearance to go back to sport. We can go to step four, step five, step six. But what if you did your exam and you found that they had a balanced problem where they are falling to the right, where they have got a vestibular problem, or they have got orthostatic intolerance. Now, we are saying, taking this hypothetical case as our example, the person has no symptoms, however most of the time, these people are going to have symptoms when you do the testing. But maybe they were lying because they want to get back to sports. So, they are trying to tell you they don’t have symptoms, however this is where your objective testing becomes important.

Because we know that if someone’s got a concussion, research has shown that there is an increased risk of a lower extremity injury or a subsequent concussion just because they had a concussion. We want to make sure that we have our objective tests and that we address those objective tests and get the person performing the tests as well as we can. So, we have a nice return to sports strategy here, which is based upon symptoms. But please remember we have our objective testing that we want to be doing as well to match up as we are working through that return to sport strategy.

FICS requires any of the doctors working at international events to update their knowledge of head injury and concussion every two years to remain current. 2023 we have upgraded everything into the SCAT6 and the SCOAT6. And this is our online module to start to introduce some of these rehabilitation strategies and understanding what these assessments mean, as we start to put some of this understanding together. Review these slides, open some of your neuroanatomy textbooks, go and do a couple of additional courses that you can do, to better understand other tests to upskill yourself to become further leaders in this space in a very topical area, obviously, concussion assessment and management.

Happy to answer any questions. I hope that you have been able to take some things out of this presentation and be able to implement them with your patients when you see them next.

To reach me you can email admin@ficsport.org

Take care, Brett Jarosz.

Download English Transcript: ICSC01_2.TRANSCRIPT-CTE_Head-Injury_RobReid

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ICSC01 Head Injuries
Section 2 – CTE
Instructor Rob Reid
Video Lesson: 18:05

I am going to be talking today about Chronic Traumatic Encephalopathy.  We are using the term CTE because that is too long. The question we have is what if we were wrong about CTE and concussion? We’ll talk about that a bit later and you will see where I am going with that. We need to talk about the definition mechanism of injury, and the histological process as much as we could, we know about, but also, we also need to make sure that we look at a potential problem. I have been around for a long time; 40 years and I am a Sports and Exercise Physician in Australia. I have been Chief Medical Officer for a lot of different sports and I have always used a team approach when I look at these.  Whether I am working with an athletic trainer or a sports trainer or another doctor or a chiropractor, or an osteopath, it really doesn’t matter to me. I think the athlete’s well-being is the most important part of the thing, and I am just part of the team. There is no “I” in team.

Let us recap on concussion itself. Sports-related concussion is traumatic brain injury induced by mechanical forces. Now, those forces may be direct to the brain, or they may be to the face neck or somewhere else in the body that transmitted to the brain. As I see it means if there is a rapid short-term impairment of neurological function that results spontaneously. This is important because it means that it is a functional problem, not a structural problem. It does mean that it doesn’t last for a long time or do we don’t have consequences? It just means the definition is that, so, they cannot be explained by things like drugs alcohol, medication use, the interesting, they probably maybe in some cases, be able to be described by cervical injuries, but that may be the cranio-cervical junction but that is not very well recognized in the medical profession, but you guys know much more about this than we do.

There are other co-morbidities that are as well, and we need to keep that in mind. The concussions resulting in neuropathological changes, but the signs and symptoms should reflect its functional disturbance, rather than a structural injury, there is a range of clinical signs and symptoms that may or may not involve consort loss of consciousness, and what we need to remember is that only 10% of concussions are associated with the loss of consciousness. That doesn’t mean that they are not all severe, but it just means that the concussive episode that produces a lot of consciousness is not present in all of them. What about the definition? Well, The Concussion in Sports Group, we met in Zurich in 2016, sorry in 2012, but also in Berlin in 2016 and so it is defined as not having any structural abnormalities. It is a historical term that representing low-velocity injuries of corner because our brain shaking, as you can see there.  It is a subset of traumatic brain injuries and that’s what I am going to talk about. In Europe, they sometimes talk about commotio cerebri as the definition, but we’ll talk about concussion.

mTBI which is Minimally Traumatic Brain Injury is not a concussion. It means by definition, it means that there is some structural damage and this is out of the context of concussion itself. It is used interchangeably in some of the U.S. literature and offering that confusing and they should not be used interchangeably. It is a clinical diagnosis made or presumed at the time of the injury. You cannot go back later and say he did not have a concussion, it is very, very difficult. You cannot go back on a Monday or Tuesday after an injury on the weekend and say, well, he didn’t have a concussion because it is made at the time of the injury, not when you see them later on, that is whether you are a medical doctor or chiropractor, or anybody else. It can be over diagnosed, but mild concussions are more commonly under-diagnosed, it is symptoms of mild can be delayed, they can be delayed for 24 hours. So, you need to be aware of all of these sorts of things. Tim Stark made an interesting comment,  We need a higher level of competency in the outcome clinicians to investigate these things deeper because some of the things that we see in the Medical Profession and not explained by concussion itself but maybe by other problems that Sports Chiropractic can diagnose better and so Sports Chiropractor is should be one of the opinions especially when we’ve got these difficult ones that don’t follow the protocol that they are supposed to. So, Sports Chiropractic should be one of the opinions and I agree with them.

Whiplash, these are interesting. Whiplash has been defined as an acceleration-deceleration force transferring energy to the cervical spine. We have got a head sitting on top of that and the problem is that whether it is the cervical spine, or the head, sometimes it is both and some of the problems associated with concussion, some of the symptoms and signs can be problems with the upper cervical spine, and the cranio-cervical junction. There is some very interesting work in this area done by Dr. Scott Rosa in the United States, looking at changes at the cranio-cervical junction, which I find very fascinating. I cannot do it. Well, I can diagnose it, but I think it is fantastic.

The mechanism of injury for concussion. A blow to the brain sets off a flood of all sorts of things that occur, there is an injury to the brain, it is that the whole of the brain that’s affected and because of that there are all sorts of problems associated. Changes with an influx of calcium into the neurons and then because of this an extra energy that is required by the neurons to try to get better, but the changes also limit the supply of the brain fuel, which is glucose. So, the higher energy demand restricted flow and oxygen debt, and glucose debt create an energy crisis. This leads to the mental confusion failed memory and may take days to restore the balance. We need a full recovery before athletes return to play, but we need a full recovery which might take longer than we think.

CTE is defined as a progressive degenerative, disease of the brain. When people with a history of repetitive brain trauma often athletes, but not always. It is symptomatic concussions but also, we think that asymptomatic is sub-concussive hits, play a part as well. It has been known to affect boxers, it was called the punch-drunk syndrome would dementia pugilistica, but we think it is because of these concussive episodes and Boston University CTE Center is doing a lot of work on this. Obviously, this is a big, big thing in the states. So, the NIH had a CTE Conference in March 2015 and the neuropathology which is pathognomonic of CTE is an accumulation of tau which is a protein in the neurons and the glia at the depth of the cortical sulci.  The problem with that is that it can only be diagnosed after death because post-mortem, you’re a pathological analysis is required to find this tau protein. We cannot use any of the normal methods likes MRI, CT or anything like that to diagnose CTE during life. The concerns that we have is this, we cannot diagnose it during life, but we don’t really want to get to death before we diagnose it. People are not going to donate their brains to science when they are still using them. It is a difficult conundrum that we face, but Boston University CTE Center and a lot of others are doing a lot of work in this area. Tau protein aggregation has been implicated as a result of amyloid protein aggregation, but it is interesting that we actually, we are going to come onto the difference between this and parkinsonism or Parkinson’s disease later on.

A cause-and-effect has not been confirmed we would like to, but we think that repeated brain trauma triggers this Progressive degeneration including the build-up of tau but it takes too long for this to occur to make it easy for us to make the connection. It could be decades after the last brain trauma or the end of the act that led to even caught involvement before somebody really shows the problems with CTE. We do not know the number of head injuries or the type or the amount of head injuries that are required to produce CTE and we also have found that not everyone with a history of repeated brain trauma has it makes it difficult.

When we look at this picture of Parkinson’s disease, we can see that the substantia nigra is a lot smaller in somebody with Parkinson’s. We see something similar in somebody with CTE. So, obviously, it is different to normal, but again, we need to pull the brain apart before we could find it. So, the degeneration in the brain is associated with the common symptoms and these can be all of those that are also post-concussive syndrome or symptoms that we can see.  Parkinsonism is not one, but confusion, headache, depression, impulse control problems and things like that are all seen through all of these. Eventually, we get a progressive dementia and that is probably something that finally has these patients die, but again, we cannot describe it during life, unfortunately. The post-mortem analysis indicated that the symptoms are associated with the neuropathological changes, but their changes because there is atrophy of certain structures as well as degeneration of myelinated neurons. We have a difficulty in trying to describe this or define this during life, other changes with the degeneration of the neurons, etc. We have enlargement of the lateral at the ventricles and septi fenestrations and things that we again cannot define during life. We must have a brain on a table to be able to have a look at these.

Microscopically. There is accumulation in the neurons of tau protein, as I said before these aggregations and filaments called neurofibrillary tangles, but you don’t need to know all of that. But there are other small vessels in the frontal and temporal lobes but also they are prominent in the basal ganglia. When we talk about parkinsonism, we talk about the basal ganglia as well, but this is a bit more diffuse and so, when we look at this and even if we look at Alzheimer’s there is a very different look to these.  Alzheimer’s. Well, again is similar because the tau protein is increased, but they are different, they are amyloid plaques. What we see in CT is a very diffuse amyloid and tau protein aggregation. So, there are similar other brain problems, it is difficult to define whether they are on your genetic factors or whether it is just because of brain injury.

When we assess these, it is difficult there is a lot of different things that we look at difficulty thinking it involves behavior, depression, memory loss, difficulty planning, the executive functions of one of the things that that are important, but again, it makes it difficult for the person who has it because they don’t have the executive function to follow it up, emotional stability. The problem is this can occur in other neuropathological problems or other diagnoses, which don’t include CTE. We cannot make a definitive diagnosis on these because these are the functions but not CTE’s defined as a structural problem. It is almost the opposite of a concussion.

What about prevention? Yes, it is important really important. Can we prevent it? We don’t have a treatment for CTE. We cannot make these brains better when we can prevent them and we think that the way to do that is, because it is associated with a recurrent concussion, we need to do something about that. If somebody’s had one concussion, we know that they are more likely to have another head injury. We don’t know how long they will likely have another head injury, but we do know that there is some association, we don’t know whether it is because they have not really fully recovered from the first one, or whether they have set themselves up, if you like for a second heading toward the recurrent, current recommendation is to prevent the mild traumatic brain injuries, but don’t play sport that that project can produce these things, but we also need to prevent additional injury after a concussion. If somebody is completely back to normal before a return to sport, they are more likely to have any other injury that includes another concussion. We need to make sure that the concussion’s treated properly.

Can we treat it any other ways? There are some interesting things happening at the cervical cranial junction or creating a cervical Junction I should say, some interesting studies done by Dr. Scott Rose in the States which a lot of you may be familiar with. He is talking about the change in some in this Junction, which may make a difference to some of the things that we see in CTE because of a change in CSF flow. The medical symptom system doesn’t really understand what the CSF flow is or why we can sort of semi-define it, but there is some interesting studies done by Scott Rosa and by a number of other people too, who may be able to change some of the early symptoms and signs of CTE, but this is still in the early stages and we not sure that we have definitive changes that we can do with that yet.   There are a few references there one is the Rosa Clinic by Scott Rosa also the two BJSM references are for the Berlin CIS, The Concussion in Sport Group meeting in 2016, and 2012 and Bruckner and Khan’s book, which has some good information in it as well.

[END]

Download English Transcript: ICSC01_3.TRANSCRIPT_Facial Injuries_Dr Warren McDonald

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ICSC01 Head Injuries in Sport
Section 3 – Facial Injuries
Instructor Warren McDonald
Video Lesson: 53:18

Injuries to the ear, mouth, and eye. We are going to talk about some of the common things that we see when dealing with injuries in that area. My name is Dr. Warren McDonald. I am a sports and exercise physician from Australia. I have worked in both Olympic sports with water polo in particular and was lucky enough to go to Olympic Games with the Australian Olympic team. I have also worked extensively in rugby, and I am currently the chief medical officer of Rugby Australia. Just for clarity, I have no competing interests or conflicts that I am aware of in undertaking this presentation.

During this presentation, we will cover some of the common injuries we see in the ear, the mouth, and teeth, as well as the eye and surrounding tissues. Let us start with the ear. In simple terms, just recalling our ear anatomy, the ear is divided into the outer ear, the middle ear, in which we will talk about the tympanic membrane a little bit later on, and then the inner ear, which is responsible for the fine-tuning of hearing and for balance as well. We are going to discuss how we assess an ear and obviously, the first thing to do when you have got an injury to the ear is to look at the outer ear and see if there is any obvious trauma, which we will talk about in a few minutes.

Do not forget to look at the surrounding tissues. There may well be some bruising or other injuries in the area. Then potentially, if it is appropriate, feel the earlobe. I have to say if there are any areas of significant pain and again the surrounding tissues, looking for both pain swelling but also sometimes you can feel crepitus which is a crackling sensation if there is a significant injury to the region. Special tests of the ear are really best left to doctors, particularly looking inside the ear with the use of an otoscope, and obviously, more sophisticated tests of hearing and balance require much more significant investigation. But I think if you have got a significant injury to an ear, do not forget that they could well be associated injuries, and in particular, thinking about concussion. Any trauma that is severe enough to damage the ear could also cause injury further inside the skull.

In the outer ear, we will often see things like hematomas and lacerations. In the middle ear, we will commonly see, there is rupture of the tympanic membrane or the eardrum. Inner ear injuries are much less common but it should not be missed. Let us start with the outer ear and think about hematomas of the outer ear or auricular hematomas. A hematoma is simply a collection of blood, and given the anatomy of the ear, the pathology associated with this is an accumulation of blood very close to the cartilage of the ear.

There is not a lot of space within the ear obviously, so the significant bleeding can both be a sign of damage to the cartilage or potentially cause damage to the cartilage. The mechanism of injury is either a direct blow or recurrent rubbing of the ear which can happen in quite a few different sports. Things like wrestling, the martial arts, boxing, rugby, and particularly those players that play in the front row or second row of the rugby scrum can get significant rubbing of these, and then other sports like water. polo.

Usually, if a player has injured their ear, they may present acutely after a direct trauma or they might present sometime later after an accumulation of rubbing or blows. Signs and symptoms of an irregular hematoma and, well, it is quite a painful swollen mess, and it can be quite tense when you touch it. It is quite done stretching the tissues above it. There is often a very small soft spot or at least an area of softness that indicates that there is fluid within the ear. You obviously need to make sure that the middle ear and inner ear have not been damaged if there is trauma, and likewise, make sure that you have not missed trauma or there has no associated trauma to the face or to the skull or elsewhere.

Sometimes, and in fact, quite commonly in sports people who have been around for some period of time, there will be a combination of new injury and old injury and the recurrent bleeding of a hematoma may compromise the cartilage over time leading to permanent damage, and that is known as a cauliflower ear. The diagram at the top here shows an acute hematoma, but the diagram at the bottom shows damage to the tissue and the cartilage that is quite permanent and that is known as a cauliflower ear. How do we treat a hematoma? Well, it usually requires aspiration if you can get it early. Aspiration using sterile technique. If you can pick the softest spot, you can often drain the blood from the region quite straightforwardly. Often there is not a large volume of blood that comes out, but removing that blood makes a significant difference to the appearance of the ear almost immediately. The biggest or the hardest part is actually maintaining pressure once you have aspirated the bleeding because they are notorious for regathering. You can see the bottom diagram here shows a person who has had their ear drained with a compression bandage over the top and this needs to be left in place for well, preferably a few days to prevent re-accumulation of the hematoma which is very common and come, unfortunately.

The other one, returning to sports, obviously, the ear needs to be protected and this is best done either with a bandage but to protect it from either rubbing again or often get further blows, then an appropriate helmet should be worn. In a sport like water polo shown at the top here, those headgears are mandatory and must be worn and they have protection for the ears. In other sports like rugby or rugby league, as shown in these players here, there are a variety of headgear that can be worn in those sports and others that will protect the ears from further damage. I would recommend that players that have trauma to the year wear them for some period of time.

Of course, the ear can also be lacerated with a trauma and it is not that common an injury, but the skin of the ear is very thin and especially at the front of the ear. Direct blow or contact with a sharp object will lead to a laceration which can be full thickness and involve the cartilage of the ear or just involve the skin of the ear as we can see in the lower picture there, and that usually presents quite acutely with a painful bleeding earlobe.

As the skin is very thin in some parts, you need to ensure that the underlying cartilage is intact and it has not been damaged but the ear can be sutured quite straightforwardly. But the complication is that you need to be aware of the infection and then slow or poor healing can also eventuate, so they need to be managed and monitored quite closely as they recover. Obviously, any significant laceration should be assessed by a doctor to ensure that the wound is healing and whether it needs to be sutured or when fact, in some situations when there is a very significant injury, surgery may be required. It is best not to return to sport until after the laceration is well and truly healed.

Moving from the outer ear to the middle ear, one of the classic injury in this region is a rupture of the tympanic membrane or a rupture of the eardrum. Just recalling our anatomy, the tympanic membrane is a thin layer of tissue stretched across the ear canal. You can see where it is located on the diagram here at the end of the ear canal. Then when we look inside, it is a very thin layer of tissue that is a crucial component of the process of hearing and also provides a barrier for water or fluid to enter into the inner ear from the outside. How does that get injured? Well, the tympanic membrane is usually damaged following a blow to the side of the head and especially if the ear is hit with a cupped hand. What that does is force a rush of air into the middle ear region and that will rupture the tympanic membrane.

I mentioned water polo earlier on, and it is an injury that we not uncommonly see in water polo but can happen in plenty of sports as well where a cupped hand over the ear will cause problems. The diagram on the right here is showing where the membrane has ruptured. That can be quite painful and cause a loss of hearing and sometimes a sensation that air is moving through the ear as well. The mechanism blow to the head and then immediate symptoms come on with pain and potentially a loss of hearing, not necessarily complete loss, but some loss of hearing potentially ringing in the ears which is known as tinnitus and sometimes bleeding from the ear as well. The player should be assessed by a doctor in this situation to view the tympanic membrane which they can do with an otoscope. You can see here that this diagram on the right shows the rupture or the tear in the tympanic membrane and you can usually see that relatively straightforwardly.

Usually, it heals fairly well, if allowed to. It usually heals over a period of a few days to weeks and antibiotics may be required because obviously, you do not want this potentially a risk of infection getting beyond the tympanic membrane in particularly into the middle ear. But yeah, you do need to make sure that it does heal and is given the appropriate chance to do so.

What do we do if we are faced with one of what we suspect is a ruptured eardrum and they should be assessed by a doctor in the first 24 hours after injury? Just get the assessment right and confirm the diagnosis and then commence treatment. Then once the ruptures heal, they can return to sport, and again, the use of headgear is very helpful and I know I have mentioned water polo a couple of times, but the design of the water polo cap is designed as such to protect from this injury so that the player because of the nature of the sport and the fact that the blows to the head and the ear are not uncommon, then the water polo caps are designed to actually prevent that this injury from happening.

The damage to the inner nearly not right along is much less common in sport but may result if you are unlucky enough to damage the components of the inner ear. It can result in either permanent hearing or balance disturbance. The very structure can be damaged by trauma including the semicircular canals and the small bones of the inner ear and that can happen with a direct blow, usually a very, very significant blow. People will present with hearing loss or balance disturb in following such trauma. They may also have tinnitus. They may have problems with vertigo with the world spinning around them. So, this needs to be assessed by a doctor and they possibly need to undertake significant scanning and potentially hearing tests as well.

The other thing to remember is that if a trauma has been significant enough to damage the inner ear, then again, other injuries may be associated with it such as concussions so the player certainly needs a thorough assessment to make sure that you have covered all the possible diagnosis. These players or these participants should be referred to a doctor immediately, and return to sport should not occur until all symptoms of settled. Unfortunately, with a damage to the inner ear, that will take some time for both the assessment and then treatment to occur. It is not uncommon for these people to be out of sport for months at a time.

Moving on from the ear to the mouth. The significant features we are going to talk about here, we are going to talk about some simple lacerations but also injuries to dentition as well. So, when you are assessing the mouth or the mouth region, then you should look obviously at the mouth both inside and out. I am not a fan of anyone putting their hands inside someone’s mouth without a pair of gloves on but you should assess and look to see where the injury has occurred in the mouth, whether it be the tongue, the cheek, or the other parts of the mouth, whether it is the lips or the teeth that are injured. You can then sort of gently just feel the area to see if there is significant pain. Usually, I do not recommend touching the teeth unless you really know what is going on.

If a player or an injured athlete is complaining that they feel like their teeth are loose for example, then do not go touching them to see that. Let that be in the hands of a professional. Then the special tests of looking at someone with a mouth injury, see if they can move their jaw, both open and close their mouth. Can they move it from side to side? Does it feel normal?  Does their bite feel normal? Are there any unusual clicks or any other sensations that they are feeling? Of course, the mouth is part of the upper airway so do not forget to keep an eye on someone with significant mouth trauma to keep an eye on their airways, their breathing, and their circulation. If they have taken a significant blow to the mouth, do not forget that they can have injuries to the nose or to the eyes, or other parts of the face as well so they do need to be assessed thoroughly.

We are going to have a quick chat about the lacerations within the mouth. We will have a look at teeth injuries and then we will talk about fractures to the face and to the jaw as well in covering this. Then to finish off, we are just going to have a quick chat about temporomandibular joint injuries as well. Lacerations inside the mouth or around the mouth are usually a result of direct trauma or potentially by biting the tongue or soft tissues or from a fall such as from a bike. A child riding a bike or anyone riding a bike, they are going to fall off and unfortunately have direct trauma to the mouth.

Lacerations can occur in both the lips and the soft tissues, such as the inner cheek or the tongue itself and you can see on the diagram on the right shows a quite deep and nasty laceration inside the inner lip. But the good news is, the mouth has a very good blood supply. Lacerations in the mouth will usually, they will bleed profusely but they will also heal very well as well. It is an upside and a downside to that. The initial presentation of someone is obviously that they will, following a fall or trauma of some sort, they are complaining with pain, bleeding, swelling, and a potentially altered speech. They might not be able to talk normally because of either the pain or the swelling in and around their mouth.

See if they can open their mouth, their jaw and move side to side. If a patient happens to be unconscious for whatever reason is part of the trauma, do not put your fingers inside their mouth at any stage. Even if they are semi-conscious, you should avoid that because there is a risk that they can go into trismus and lock their teeth on your fingers and that is not a good outcome for either person.  Assess what you can and obviously be aware of other injuries. You can see that the diagram here shows a significant laceration to the tongue, but that would have been caused by the teeth, for example, jamming down, biting the tongue. It is possible that the teeth are also injured as well. We will talk more about teeth injuries in a minute. If there are certain blows that are that significant that cause injuries in this region, do not forget that they can be associated with things such as concussion as well.

How do we intervene? Do not forget the airways, breathing and circulation need to be assessed in these patients to make sure that the big picture items are intact. Usually, I mentioned before, this is a nice diagram here of someone who has had their inner lip sutured. Because of that good blood supply, you would expect that to heal very nicely for that person. They should not return to sport in general, until it has completely healed. But generally, the healing does occur in a relatively quick time. I am a big believer that people playing sports should wear mouth guards particularly if there is a high risk of contact. These injuries often occur because the tooth goes through the lip or whatever. Certainly, the tongue injury I showed on the last slide could have been prevented in a contact sport situation by wearing mouthguard.

Moving up to just the other injuries around the mouth and the face. The zygomaticomaxillary complex or the area of the cheek can certainly be damaged in with trauma. Fractures of the cheekbone occur from a direct blow, which can be a fall, but it could also be a fist such as a punch, it can be a hockey stick injury or a cricket ball hitting them on the appropriate region. Do not forget that a fracture is a crack through the bone and that it can be either displaced or non-displaced, they can be separated or not and it can extend into the orbit of the eye from its location.

Generally, fractures to the cheek occur from a direct blow to that region. They present with a very painful tender area. Perhaps there is going to be some swelling, some bruising as we can see in the picture here on the right. It may be looking a bit flat compared to the other side, so they may be asymmetry between the two sides. There may be some crepitus or crackling of the skin when touched, and there may be, again, unusual, again, extension of symptoms to involve the eye. There may be double vision, there might be numbness of the cheek because of the involvement of the nerves underneath that have some swelling and therefore some pressure on them. Movements of the eyes may be limited and asymmetry as I mentioned. The player needs a thorough assessment in that situation for the generalized facial illness and injuries, I should say, and do not forget the ABC, the airways, the breathing, and the circulation.

Anyone with a significant injury needs to be referred to a doctor for review and then X-rays and scans. Often, I will need more than just plain X-rays because the intricacies of the bones in that region sometimes make it hard to determine whether there is a fracture. So, things like CT scans may be more appropriate. At the top there, I have got other injuries such as eye injuries and other fractures and concussions as we have mentioned. Depending on how bad those injuries are, the treatment ranges from rest at the time or on some occasions, surgeries are required if there is a displaced fracture to relocate the fracture and then allow it to heal over time. When returning to sports, that should only happen when all injuries are healed.

Other fractures around the maxillary and the facial bones, well, yeah, they usually occur from a direct blow, and again, the things I mentioned before. A fall, a fist, a hockey stick, or a cricket ball or baseball. Again, remembering that there might be greater fractures extending to the whole face and affecting the palate or the orbit as well. True facial fractures as shown in the diagram down below, usually require a large amount of force. Things like falling from a height, falling from a bike onto your face can cause these sorts of injuries. They are significant injuries and usually need to be, well, in the vast majority of cases, will need surgical treatment.  Someone who has really damaged the maxillary or the facial bones will have a lot of pain and a very tender touch. There may be swelling, there may be flatness in the cheek, there may be crepitus, there may be double vision, numbness again, and movements of the eyes might be limited, there might be asymmetry in movements in the eyes, and the patient’s face might look asymmetrical or unusual, and there may be a malocclusion. When they bite down, it just does not feel like their teeth a lining up the way it should be. These people need to be thoroughly assessed for facial injuries and again, with significant trauma to the face. Remember that their airways and their breathing, in particular, may be compromised. So, they often want to sit up these people and are probably better managed sitting up because lying down will potentially compromise their airways. But that is obviously only if they are alert enough and awake to be able to assist you in that situation.

Significant fractures and other injuries like to the eye, to other fractures in the face or elsewhere, concussion in the airways and breathing, they need to be referred to a hospital for doctor’s review and X-rays and scans and further management. In many cases, they need ambulance transfer for significant injury. They cannot return to sport and would not be returning to sport until after all their injuries are healed, which may be many months down the track. Mandibular fractures are more common and we see the fractures of the mandible of the lower jaw. In many sports, and again, on the other pictures here we see sports like boxing, the rugby sports, any other contact sports.

Mandibular fractures are not that uncommon but it can also occur from a blow from a ball as well, whether it be a baseball, cricket ball, or any other way, other hard ball that strikes the right place. Most commonly, the jaw will fracture at what we call the angle of the jaw or up at the condyle at the temporomandibular joint. The mandible fractures it often fractures in more than one place. You need to thoroughly assess the mandible if you suspect there is a fracture. The mechanism of injury usually results from a direct blow or from a fall. A painful, tender swelling and malocclusion are common. When assessing these, there may be bruising on the floor of the mouth. You will see malalignment of the teeth and that is what the diagram on the right is showing. The teeth do not line up completely as they should. There is a significant malalignment there on the mandible. There might be tingling or numbness of the lower lip and of the chin as well. Do not forget your first aid approach, the ABC. The airways may be compromised and again, what we spoke about with the other facial fractures, they might feel more comfortable sitting forward which helps maintain their airway if they are conscious.

The complications or potential problems, airway complications can be considered. Concussion needs to be considered and other head and neck injuries. They need urgent referral to a hospital. An ambulance might be required to do that quickly. They need X-rays and scans and they may need surgery. Obviously, the X-ray on the right-hand side, the white arrow shows the line of the fracture. That is relatively easy to see. Often, they are not quite so easy so sometimes you need further scanning such as a CT to ensure that there are no fractures there. They should not return to sports until all the injuries are healed, and that they may be for some months before everything is settled.

Temporomandibular joint injuries are not uncommon in sports. There is a range of injuries from the very mild to the very severe. Generally, any blow to the mandible can injure the temporomandibular joint but the range of injuries can vary from a dislocation of the joint, bleeding into the joint, which is a hemarthrosis to a meniscal displacement to an intracapsular fracture out of the head of the condyle. The diagram on the right there shows a small fracture through the condyle and within the joint.

The mechanism of injury is usually a blow to the jaw. The person will present with pain, tenderness, limited opening of the jaw, they potentially cannot open it properly, they might have malocclusion, their bite does not feel right, they might be unable to close their bite. If they cannot properly close their mouth, that might indicate dislocation and there might be asymmetry as well. When you are assessing them, you need to assess the tender areas and movement of the jaw and the occlusion of the teeth, and you can remember that there may be other injuries associated with it as well. These people should be referred to us for assessment which may include X-rays or scans.

Dislocations or fractures occasionally may need surgery, many times, they do not. But remember that these people again should not return until it is completely healed, which may take some weeks. I know I have spoken a few times around fractures around the mouth area. You can see that the majority of the cases involve the condylar process. That is the most common reason for fractures. Then around the angle of the jaw is the second most common. These are the areas where it will commonly fracture, and as I said, always consider that there might be more than one place where this happens.

Dental injuries are very common in sporting instances and they can range from anything from a small chip of a tooth to loosening of teeth or complete avulsion of a tooth. An avulsion is where the tooth is completely removed from its socket and that is what you can see clearly here on this upper diagram. The lower diagram shows a picture from an Australian rules football where you can see quite clearly the tooth sort of sitting and have been accidentally blown. It received a blow to the face that it actually popped right out of the mouth and will need to be found.

Usually, teeth injuries occur with a collision with an [inaudible] or trauma from an equipment of some sort such as a hockey stick or a fall onto the face from a bike. They will present with pain, bleeding, swelling, and an uneven bite. The signs and symptoms are usually pretty obvious, and especially if you have lost a tooth as that last diagram showed, then the first thing is to find the tooth. Even if that takes some time, it is worth doing. If a tooth can be found and replaced into its socket, then that will potentially have the best outcome. So, if someone loses a tooth, it is worth spending the time to try and find it.  When touching the tooth, you should have some gloves on. It is best to just handle the tooth by the tooth proper, not by the root of the tooth, which is the area that goes into the jawline. Basically, the tooth should be, if it is intact and if it is possible, then as this diagram at the top is showing, it is ideal if it can be replaced quickly, then do so. Wash the tooth down and then replace it before getting to emergency care. If it cannot be easily replaced, then a couple of options. One is to pop it into milk or there are some special solutions that are produced. The worst thing you can stick it in is water. Saliva is better. You can sit in the, I would say, at the cheek of the person whilst they are transferred to emergency dental care. Now, obviously, you do not want the person to swallow the tooth, and that is the point that is made here in the script here. If a tooth or fragment of a tooth cannot be found, then do not forget that it not only might be swallowed but it could be aspirated as well. Obviously, if a tooth gets into the lungs, then that can be a real problem. So, if you cannot find a fragment of tooth or a full tooth that is gone missing, then the person should have a chest X-ray and especially in children to make sure that the tooth is not somehow made its way into the lungs.

To all significant teeth injuries like the ones that I have shown here, they require immediate specialist treatment. You need to get them to a dentist as quickly as you possibly can. But it is worth the effort because you cannot quite often save the tooth and, basically, that will then require weeks and sometimes months of treatment, to get things back to normal. But basically, once the teeth have been healed, then they can return to sport.

Moving right along the eyes. The eye anatomy is very complex. I am not going to go into much detail, but it obviously sits in the bony orbit, which is shown at the bottom here. But the eye itself is a very delicate and complex organ whose purpose is to provide vision. That is a key feature obviously. One of the keys of assessment is making sure that the person has the ability to see out of the eye. If you have got someone with an eye injury, then obviously you need to look at the eye and at the surrounding tissues to ensure to discover what you can. You can feel around the eye to see if there is significant tenderness or numbness and then you can move the eye to see that its movements are full and equal.  The eyes move together usually, but if there is asymmetry in movement, then that is important and we will discuss that in a couple of minutes. Is there any pain with the movement of the eye, and importantly, does light bother the eye as well? The other important thing you might just see here on the diagram on this page is the person here has one red injured eye. The other eye, again, we cannot see clearly, but it looks relatively normal in what we can see. There is an old saying in medicine, “Beware of the one red eye.”

If someone presents with one red or potentially injured eye, they really need to be thoroughly assessed so that we understand the pathology that is going on. There are a range of pathologies, and as a result, we need to fully assess them. There is the specialist test around, can the person see out of both eyes, can they see in all directions, and can they see all of the visual fields at a full? Each eye needs to be examined individually. Is their vision blurred at all? Are there unusual spots? Obviously, looking inside the eye requires specialist equipment such as an ophthalmoscope and also some specialist drops some time to help you such as anesthetic drops, but also down here I am showing fluorescein drops or fluorescein strips, which are very important in helping assess the other services of the eye which again, we will talk about it in a second. Do not forget the associated injuries such as fractures of the nose or the face and concussions, which can also occur as well. There will be a consideration of a few different injuries here, things like corneal abrasion, subconjunctival hemorrhage, hyphema, retinal detachment, and orbital fractures as well. So, let us have a look at these. Corneal abrasions are very common. The cornea is the outer layer of the eye. Basically, it is a common injury in which that outer layer of the cornea is scratched and that can occur with a multitude of things. It could be a foreign body, it can be a fingernail accidentally in a sporting context. It can be things such as metal fragments in people who are working with metal or whatever it might be.

Usually, the person presents with pain, irritation in the eye, a sensation that there is something in the eye, and they might have blurred vision. For anyone who has had something in their eyes, it can be quite an annoying sort of sensation, and you can see on the diagram, the fluorescein drops which are typically orange, sort of show a scratch running across the eye. They should be referred to a doctor for assessment because this is potentially a serious injury and you do not strongly recommend against messing around with eyes. They have one job and if people are not able to see properly then, they need to be assessed as soon as possible.  Basically, the complications of corneal abrasion, usually they will heal, they will often need antibiotics drops to prevent infection and maybe those drops to actually see the inflammation. If it does not heal, just occasionally, you will get scarring if not treated appropriately, but the vast majority will heal quite comfortably with the right treatment. They should be referred to a doctor on the same day to be seen as soon as possible and then usually they can return to their sport after a few days after all symptoms have settled.

Subconjunctival hemorrhages are also very common. The conjunctiva is in the outer layer of the eye away from the cornea. A trauma can lead to bleeding under the conjunctiva and that can happen from either a direct blow, a scratch, a finger in the eye, or a range of things can cause that to occur. Often, it will present as a bright red area, much like what I am showing here in this diagram, a small area of bleeding. Sometimes they just happen spontaneously as well, which often scares people, but is usually, thankfully, not too much to be concerned. But they are not always quite simple as this nice little simple red area. They can be quite extensive as the diagrams here show and so much larger. If they are small, it is usually of no concern. But if they are large, they can cause visual symptoms and photophobia, which is irritation from light, and they should be assessed in that situation. The other important issue is if you cannot see behind a hemorrhage, then it may indicate that there is further injury to the bony structures, particularly the zygomatic bone or the zygomatic arch, but also the orbit as well. What do I mean you cannot see behind it? Well, on the diagram on this page shows the subconjunctival hemorrhage and you can see as we move away from the iris, we cannot ever see this clearer at the back of this eye in this region here. We can just see blood all the way around. So, that is always a concern. There is also obviously a fair bit of bruising around this person’s orbit. The concern is that there is something else going on or significant with this person.

You have got to be aware of fractures and significant injury in the eye. A doctor’s referral for anyone with some subconjunctival hemorrhage if their vision is impaired, you cannot completely see behind the hemorrhage. The good news, unless there is some other significant injury, if it is just a simple subconjunctival hemorrhage, then they can usually return to the sport very, very quickly. In fact, almost immediately. So, that is the good news. A hyphema is an unusual injury but it does occur occasionally where you get bleeding into what we call the anterior chamber of the eye. It is right at the front of the eye, and you can see the picture here shows a fluid level. It shows just fluid sitting in that anterior chamber starting to really block out the iris of the eye. That potentially comes from a blow. It is usually a blow to the orbit or blunt trauma. Sometimes they can be a lot smaller, and I will show you a smaller one on the next page. But these need to be referred immediately to an eye specialist for review. You certainly do not mess around with these. If you see this injury, this person needs to be treated appropriately because if you do not get it right and treated appropriately, then you can have permanent visual problems in this person.

You can see in this case, there is a much smaller fluid level than on the last diagram but again, that person still needs to be referred. It is bleeding, as I said that has gone in there, and if it is not treated appropriately, then they can end up with significant scarring in that anterior chamber and can further damage the cornea. You do not give them aspirin, you do not give them anti-inflammatories because they can both increase the risk of bleeding. They need bed rest. It is what they need but they also need referral to an ophthalmologist to be seen urgently, and then further treatment will be guided by the ophthalmologist depending on their particular preferences. But in most cases, the bed rest will allow the bleeding to settle, and without any scarring, it will allow people to move forward.

Retinal detachments are an uncommon injury, but a very, very significant injury and there are a couple of keys here that sort of make you think, wow, is this person telling me that their retina is detaching? Now, the retina obviously is the sensitive part of the eyeball where the light is directed, and from the retina, the signals are taken to the optic nerve and to the brain for interpretation of our sight. If the retina detaches from the orbital wall, then we break this mechanism, we damage the mechanism and therefore, we can end up with permanent visual impairment. The pathology here is, as I said, the retina is stripped or lifted off the posterior wall of the orbit and it can follow a blunt trauma or a perforating trauma, and sometimes it occurs sometime after a trauma as well. It is almost like the area becomes weakened and then a relatively small event can accelerate what is happening there to go forward.

There are a couple of key things that the patient will tell you in this situation. They often report that they potentially had a trauma, but then they will report flashing lights in their eye, and which worries them. Sometimes, they will say it feels like there is a curtain coming down across the field of vision and that is a bit of a giveaway. If you look at the diagram on the lower diagram here on the right, you can see that the picture above is relatively normal, what normally the inside of the eye will look like. But on this occasion, it just looks abnormal at least you can imagine. It looks like the tissue back there, the retina, is actually sort of sitting and almost sort of waving in the background.

Do not expect to be able to see those. That takes a specialist to be able to identify these issues. But if you think about the tissue sort of sitting forward and therefore damaging the line of the signal, then that explains why they present either with the flashing lights or with a sense that they vision curtain is coming across it. It needs an immediate referral to an eye specialist. You do not mess around with this one at all. If it is not treated immediately, it may result in permanently lost or impaired vision. Even if it is treated immediately, there can still be some loss of vision. But the sooner it is seen and dealt with, then the better. The emergency care protocol is, get them referred immediately. Unfortunately, for the vast majority of people, this needs for the future, that they need to avoid risky or contact sports. Not uncommonly, these people have to retire from the sports that they have been involved in such as contact sports because there is a risk that it could happen again. Having had one retinal detachment usually means that the person should reduce all risks that have been happening again.

Orbital fractures are not uncommon and obviously, the orbit is the bony structure around the eye. The walls of the orbit are very thin both inferiorly, the floor of the orbit, and medially. They can be quite easily fractured with a direct trauma. It results in what we call a blowout fracture. In this situation, a trauma, a blow to the eye region or the orbit, the contents of the orbit, or the eye structures can be compressed and damage the bony structures around them. Then the contents of the orbit can herniate through the fracture line and possibly be trapped by the fracture, which is quite uncomfortable.

People will usually present with these injuries following a direct blow to the eye such as with a squash ball, which is well known for potentially causing these issues. Anything else that directly blows onto the orbit or creates a blow onto the orbit will potentially cause this injury. The person will complain of pain, blurred, or altered vision, they will often be a lot of swelling around the orbit and quite scarily, these people will sometimes present where they have had a trauma, and they feel as if there is something not right. They feel sometimes like they have got to blow their nose, and then they blow their nose, they get an enormous amount of swelling around the eye and sometimes report that they feel like the eye is going to fall out of the socket.  That Is a key giveaway. If someone presents with that story, then in my mind they have got a fractured orbit until proved otherwise.

The other thing I present with is restricted eye movements and that is because of, the muscles around the eye will get trapped in the fracture. If you would have a look down at the diagram at the bottom right, you can see that person is trying to look up and the one eye is going up and the injured eye is not going up there because the muscles have been trapped. The person above that, there is significant swelling and bruising around the eye here and much more than you might just expect to see with a non-fractured injury. This person has had a CT scan which shows the fracture line where the arrows are pointing to.

You need to be a little careful here as a doctor if you order X-rays of this area because the X-rays are often inadequate to see the fracture and the CT scan as this is showing is much better required. If they have the right story and they have history of a blow to the eye, the sense that the eye is blowing up, that maybe crepitus if it feels like it is jumping out of their eyes or out of their eye socket then they do not need to do that but do if you suspect that they have got a fracture of the orbital floor or the medial wall of the orbit.

Complications that are potentially there, well, they can get infected, they will often have impaired vision if the fracture is not reduced and stabilized. Depending on how big the fracture is, these people sometimes need surgery to put it back together. They should be referred to a doctor as soon as possible for assessment and X-rays and scans as I have described. Then they can return to their sport after appropriate treatment and surgery, but it usually takes, you know, several weeks to months for this to settle down. The good news is that usually they will heal quite successfully, and people can return to their previous sports.

That is just a quick skip through some of the injuries we see around the ear, the eye, and the mouth and face. I guess we need to make sure that we take a team approach to the treatment of any athlete. In the absence of any emergency services in an event, the emergency care goals are to first stabilize the patient and provide basic life support, which is the importance thing here. You will notice that quite a few times through the presentation, I referred to going back to the simple ABC. Do not forget those things because the injuries around the head and the face can certainly cause compromise to the airways, the breathing, and circulation.

If there are other sports medicine members, who are emergency care certified workers who are working at an event, they should be the primary care providers in the event of life-threatening trauma. Then finally, any rapid return to a sport may compromise the long-term health of the athlete. It is always wise in my books to just take a little bit longer, make sure you have got them right, and then you will do the best thing you will and not harm the athletes.

If in doubt, sit them out and then see how things progress from there.

[END]

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ICSC01 Head Injuries in Sport
Section 4 – Intracanial Bleed & Haematomas
Instructor Rob Reid
Video Lesson: 16:49

Intracranial bleeds and hematomas are a consequence of head injuries but not really of concussions, although it can be a consequence of the head injury that we can’t diagnose. We will talk about the definition, mechanism of injury, histological processes, and potential problems as last time.  Firstly, its definition. I found this from Wikipedia, and it was quite a good definition, so I am not going to really change anything. This is nothing abnormal or nothing unusual for a lot of you. ICH is also known as intracranial bleed, because of bleeding in the skull obviously but I am going to talk about it as a bleed rather than a hemorrhage. I just don’t like the term. The subtypes, you can get into intraventricular bleeds and intraparenchymal bleeds, but these tend to be not associated with injury, so I am just going to talk about the ones that are associated with injuries. The bleeding can occur when obviously, a blood vessel leaks or is ruptured, which are two different things from a medical point of view and it can result from physical trauma, but also can occur in hemorrhagic strokes, people with high blood pressure. I am only going to talk about trauma-related ones today.

These bleeds, they are much more likely at high-speed impact. So, a low-speed impact has less of a chance of doing this but it is still a bit unclear because I will talk a bit about some of the ones that we see, which are unfortunate, I will just mention them, but downhill mountain biking, motor vehicle racing is common, and equestrian events. It is quite common because of the link that how far they fall, ice hockey and it can occur in other sports but less common in more common sports, if that makes any sense.

Complications make it a serious medical emergency. This is important for everybody to remember. It is a buildup of blood within a fixed volume of the skull. It occupies space and it makes a difference both to the brain tissue and whether somebody can in fact survive, so increasing intracranial pressure is not a good place to be. The ICP increase can cause the brain to be pushed out of the foramen magnum, which puts more pressure on the mid-brain and brainstem, and an increase in blood pressure is one of the signs that we see but also a decrease in heart rate and these two are important symptoms or signs I should say because they can lead to death.

Early symptoms and signs similar statistics to those of a concussion. You can’t tell the difference. I cannot tell the difference as a medical practitioner, and I dare say that you won’t either. If you can, then you are better than I am. There is nothing to distinguish them, so any head injury, whether it is a concussion, a mild traumatic brain injury, or severe traumatic brain injury has to be treated with respect. It is a medical emergency, and we need to treat these on a presumptive diagnosis. You don’t need to do a CT scan to start appropriate treatment for these people. If you know the force of the injury, then you’ve got a better chance of making this decision early. You should have a high level of suspicion when there is a serious head injury or concussion or would you think is a concussion, so early recognition and prompt management are vital. We need a referral to an appropriate facility. The CT scan is in fact the definitive tool for a diagnosis of an intracranial hemorrhage. Sometimes MRI scan can also be used but a CT scan shows the difference in the bleeding area and the brain tissue better than it sometimes an MRI, so a CT scan is the way to go.

Symptoms. Same as for concussion. Headache, dizziness, amnesia, disorientation, tinnitus or ringing in the ears, lightheadedness, emotional changes, sometimes you might some changes and irritability, I [inaudible]. I had one athlete who is we really had to get him off the field because he was quite irritable and although he was sort of thinking okay, he is very irritable. We must take that into account. Double vision, memory loss. They are all symptoms. Signs include loss of consciousness. These people with a bleed will often have a loss of consciousness because the injury is a high-speed injury. Vomiting is common, and they are always drowsy and want to go to sleep. Fainting, loss of balance, slurred speech, slower reaction [inaudible]. The other stuff is there as well but if you can, you need to look at the blood pressure and the pulse, even adjusting the pulse will give you some idea. What about the classification? Well, when we look at these, it is a focal brain injury. Traumatic ones are what we call a focal brain injury. Something that is a localized spot in the brain that may or may not directly involve the brain. Tissue, it might just push it out of the way. There are three different categories. The Extradural, Subdural, and Subarachnoid Hemorrhages. I will talk it to them one by one.

An extradural is sometimes called an epidural, although that’s normally left to a hemorrhage that would occur in the spinal cord occurs between the dura mater and the skull. It is caused by trauma, but it is an artery. Laceration of an artery means that they bleed quickly, so there is a rapid increase in the size of the bleed which means they rapidly go downhill. It is very uncommon because you almost need to have a skull fracture because of mostly the middle meningeal artery but you still see in 1% to 3% of these significant head injuries. Vomiting, agitation, and loss of consciousness are common. The clinical onset occurs over minutes sometimes hours quite often minutes but they have a history of head trauma but then a lucid period and then the increasing symptoms, these are the ones that go off quickly, so you got to keep an eye on them. You must keep an eye on these guys because if they have got one of these, they can go off very quickly. It doesn’t cross suture lines on a CT scan, and you can see it on the CT scan quite easily, but we need to evacuate that bleeding. It can push the brain out of the foramen magnum and the brain doesn’t like going there. Its potential complication is death but normally It is pretty good, and these are often recognized quite early and treated early. We certainly hope so.

A subdural is almost more difficult because it is a tearing of a bridging vein and because of that, It is a low-pressure system, it doesn’t occur as fast. They may still have a loss of consciousness, but they are usually associated with cerebral cortex injury because it is underneath the dura mater, and so, they can be associated with long-term problems, but the problem is that they don’t hit you in the face like an extradural. Depends on the side of the injury as well but they quite often get knocked out or have a loss of consciousness and they get better for a while but then over hours, they just become worse and worse. This is the reason why we tend to get people to who’ve had a head injury really watch for 4-8 hours. If you go to the hospital, they will nearly always keep somebody in 4 hours, sometimes 8 hours, because we don’t want these subdural to come up later when somebody’s asleep because this is the sort of person who can fall asleep after they have had a head injury and they just never wake up. We would like to prevent that. A crescent-shaped hemorrhage compressing the brain on the CT, shows quite well on a CT scan.

The management, same thing. We need a surgical evaluation. The problem is that these can still produce a significant pressure effect on the brain with all its problems. It just is not as fast as an extradural. Unfortunately, there are people quite often who’ll be left with long-term consequences of this because some of the brain tissue because it is almost within the brain. Some of the brain tissue can be affected by this and so, although, the herniation through the foramen magnum is not as common, we still need to make sure that these people are treated properly so that we minimize the amount of long-term brain damage they have.

Subarachnoid hemorrhage. This is uncommon with a head injury. It is mostly older middle-aged people and It is bleeding into the subarachnoid space obviously, subarachnoid hemorrhage, but they quite often start with a sudden severe headache often at the back of the head and quite often nausea, yes, but vomiting is prominent and neck stiffness is actually very common in these. Confusion, a lowered level of consciousness, and seizures occur but these are normally the severe ones, not the ones you see very often. The rapid headache sometimes called the thunderclap headache is the prime thing with these. It is diagnosed clinically, again, confirmed with a CT, occasionally by lumbar puncture. If somebody’s got a sudden severe headache, we would prefer not to do a lumbar puncture because it changes the pressure inside the CSF area, and therefore, if somebody has a significant brain bleed or a bleed around the brain, then it can cause more problems. The CT scan is fairly typical when you see these, you can diagnose them very and they look very different on the CT scan.

Management. It is actually treated by surgery of neurosurgery or angiography because it is an arterial defect but because of the way the arterial defect is, it is a form of stroke, considered a form of stroke, and so, the spontaneous ones require further investigations as the source of the bleeding by either putting a clip in with neurosurgery or a stent in through angiography, these can be treated very extremely. Well, again, you’ve got to have the correct facility.

Basic Emergency Care. This is the same as everything. Now, in Australia, we use this DRABCD. Danger. You look for any dangers surrounding the player/athlete. This is stuff that you should do. It should be just there all the time. Response. You need to respond early. Now, you need to know your sport, if you are dealing with a sport, because, in some situations, you can come onto the field straight away and in some situations, you must wait until the referee or [inaudible] calls you onto the field. Let’s say you need to know your sport but if you see it happen or see you are potentially worried about these things, the earlier, the better. You need to respond very early. Airways. Always with cervical spine control. We need to maintain an airway because if somebody doesn’t have an airway, they are not going to survive anyway. We need to make sure that if we don’t know if it is a high-speed impact, we don’t know what the problem is, then we maintain cervical spine control. It doesn’t fix and prevent all cervical spine injuries, but we want to try to make sure that we don’t do any further damage. Breathing. Circulation or Compressions. It depends on where you are. Some jurisdictions called circulations; some people called compression. The D is the Defibrillator or Drugs. If somebody has collapsed and you don’t know whether they have had a head injury or if they don’t have a pulse, then a defibrillator is important. It may be some drugs that are important as well and this is where the emergency services or paramedics are excellent at looking after they sort of [inaudible], but you also need to remove and refer them to an appropriate facility. A facility that can look after them because if we suspect that they have got an intracranial hemorrhage, then you really need it somewhere we can get something mechanical done about that because it is a mechanical problem.

Luckily, FICS Doctors are trained and certified as primary contact practitioners which means you have a duty of care. This means that if you are the only person there, you are the one to take control and provide basic life support. If there are other people around, we need to work as a team. We need to make sure that the athlete is looked after appropriately. It might be somebody in the crowd who’s emergency trained, it might be a sports trainer or something like that, or an athletic trainer who’s working with you. It might be a physiotherapist or another chiropractor or a doctor. Doctors don’t necessarily know all of these things, but you need to train in this to keep up to date. If there is any question, whether it is an intracranial hemorrhage, it needs a prompt referral, early diagnosis, and treatment are the key to looking after these people. We really need to make sure that these people get the appropriate help quickly.

This is an interesting one. Return to Sport. The problem with any sort of intracranial hemorrhage is It is likely to cause long-term problems. We need to take a considered approach within an appropriate time frame. Again, this is a team approach to do the best thing for the athlete to make sure that they don’t end up in the same situation again. Sometimes they won’t be able to return to the sport because it is too dangerous and you need to make sure that they don’t return rapidly because that make compromise their long-term health. One of the things that, as I said, with concussions before is that we need to make sure that they are completely back to normal before they return to sport. Now, sometimes, after an intracranial bleed does never occur but we need to make sure that they are ready to return to the sport because we don’t want to put them in danger of other injuries as well. I hope this is helpful and thank you very much for listening to me.

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