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Christine: Welcome to the ICSC manipulation principles with Dr. Tim Ray. The we will bring, Dr. Rick Ames in the second half and he is going to  be talking about some motion palpation type stuff and soft tissue stuff as well. We will begin with Dr. Tim Ray and there is so many things for me to-to highlight for his professional career. I almost do not even know where to start.

Tim Ray: Thanks Christine. I appreciate the introduction. I am not going to spend a lot of time talking about myself. I, I would just wanted to say that I have been involved with FICS for a couple of decades and my chores in the International Federations Committee with the games commission, that deals with logistics and selections for International games for FICS. It is really a pleasure to speak with so many different people from so many different countries, and I find that very exciting. I would like to also acknowledge Dr. Brian Nook because he was the one that was really responsible for the majority of the content of this presentation. I have just added a little Tim Ray twist to it and we do this to ensure each presentation covers the same material no matter who is presenting it or where it is being presented.

My portion of this ICSC educational series deals with Basic Biomechanics and Kinesiology of Manipulative Therapy. I will cover some of the foundational principles of Osteo and Arthrokinematics in manual therapy because this will allow us to pr-provide us a baseline of understanding. We will follow in the hands-on section of the program. Understanding these principles allows us to model our clinical practices and prevents us from becoming technicians. We always want you to strive to be a clinician, not a technician. We wish to provide you a practical evidence-based, outcome-driven education, to be able to understand, defend, and appropriately apply this practice or this important aspect of your practice in your care.

According to Sarah Sharman to facilitate movement the body functions as an interdependent, interrelated scheme where the muscular, skeletal, and nervous systems work separately and collaboratively to produce motion. Our care focuses on analyzing the dysfunctional and functional relationships of this regional interdependence.

My good friend and colleague, Dr. Rick Ames, and I will attempt to cover the biomechanical, physiological, and neuromuscular aspects underlying manual therapy. And then, as you move into the hands-on portion, we will stress these concepts of what w-w-we have reviewed today. assessing joint function requires an understanding of what really happens with manipulation or mobilization. And we have to realize that the old historical description of bones, or moving bones back into places is not really valid any longer. But you will see from today’s discussions, the effect of our manual therapy is improved motion and a beneficial alteration of motor control.

So let us start by looking at the osteological mechanics of movement and that is basically turned- termed Osteokinematics. Which is nothing more than a big word that describes how bones and joints move in relation to each other. These types of motions  there are basically 3.

The first of these is called translation, which is really linear, and as to say, along a line. But this line is not only straight but can be curved, and then you have rotational movement, which is angular around an axis. But in most cases, particularly in human movement, it is a multi-segmental combination of this translation and rotation. Then this is dictated by the architectural anatomy of the joints that we focus on.

So when we start looking at motion, we have to review the standard references of cardinal planes of motion.  I am sure you are all familiar with this, but we just go through it. Examples of frontal plane motion in-in human motion are things like flexion and extension, plantar, and dorsiflexion.  sagittal plane movements are like lateral flexion, abduction, adduction, inversion, and eversion. And then examples of transverse plane motion a-are like supination and pronation.

Then with each of these motions, there is a point where there is an axis of motion that occurs. In some cases like in this middle picture where we illustrate the interphalangeal joint, there is a single axis of motion and the single-axis refers to what is called the instantaneous axis of motion. But in other joints like the knee, it is a little more complex because there is  a combination of motions that include translation and rotation, and these occur in more than one plane. So when there are multiple axises of rotation, the composite of these axises of motions is called the evolute.

The takeaway from this comes from our motion palpation assessment of a joint in differentially diagnosing normal from abnormal joint motion. It is important to understand the joint-by-joint approach made popular by Gray Cook and Michael Boyle. It essentially states that joint architecture from the foot up alternates between stability and mobility in terms of motion. Because of this when joint dysfunction results in symptomatic pain, it can often be traced to the joint above or below the pain. A good example of this is when you sprain an ankle, and it loses its mobility because of this. The pain usually shows up in the knee because the knee loses stability in compensating for the lack of mobility in the ankle. I think it is pretty obvious that you can see manipulating the knee would not be the best location for most effective outcomes.

If we motion palpate joints, we try to evaluate the joint’s ability to displace  or resist displacement. And this is a way of n-not only assessing joint stability but also looking for indication of the joint centration or what is called the close-packed position. We also check to see if there is maximal joint surface contact, balance between the co-contraction of the agonist and antagonist, and even loading of the joint services. But do not confuse this with a closed-packed exercise or the distal aspect of the extremity is anchored to the ground  during the exercise.

We have to look at the open-packed position which really allows us to assess passive range of motion and this allows partial joint contact, and within that, we may be able to feel an imbalance between the agonist and the antagonist and then palpate on even joint motion. But do not confuse this with an open-packed position for an exercise where the distal segment is free like, in a seated leg extension exercises.

Man, if we move to look at Arthrokinematics, another big word, which just describes the way articular surfaces move in relation to each other. We can use this information in helping us differentiate motion between our palpation, whether it be static or dynamic palpation of the joint. But to do that, w-w-we need to look at kinetic chains and realize that when we evaluate somatic dysfunction using Sharman’s approach to regional interdependence. We have to understand that there is more than one kinetic chain. That the nervous, the muscular, and the skeletal systems all have their own kinetic chains, but we are not going to talk about all this today. W-We will stick- stick with the articular chain. And in- within the articular chain, you will notice that there are two sub-chains. The postural and, and the kinetic which are Illustrated in the bottom part of the slide.

The postural chain is more about static posture and it is illustrated by this Brugger illustration that shows changes in pelvic tilt also alter the curves and the  curves of the spine and, and then the way that the  rib cage moves. And then the kinetic chain is more about evaluating dynamic posture. Man, this shows an example of how  excessive pronation  creates kinetic changes within the skeleton,  from a functional perspective.

Joints have various degrees of freedom of movement. Most mobile joints have 1, 2, or 3 axises of motion and other joints have none at all. Like our teeth or the sutures of our skull. Each motion is dictated by the joint’s architecture and then that is enhanced or inhibited by the muscles, the ligaments, the Joint capsule, fascia, and of course, the neurological motor control which then supply varying degrees of motion.

In addition to this gross movement, joints have accessory motion or joint play, and this really refers to  the flexibility of the joint capsule. This helps the joint maintain optimal position and prevent loss of contact between articular surfaces. So, if we are looking at the actual joint movement, there are 3 fundamental movements, and then the first of these is called roll, which is pretty much like a tire rolling or, or on the ground. But, in anatomical terms, we have to realize that if there is too much roll within an articular surface, that can lead to dislocation.

Then there is glide and slide which is similar to a tire skidding on the ground, or on ice and this is sometimes also called translation. Then anatomically or clinically speaking, pure slide can  create impingement and we see that when the humeral head slide superior and creates subacromial impingement, or we can see it in the spine with impingement of the articular facets.

We have spin and swing which is rotation around a stationary axis, and this, we commonly see with hip and shoulder and, and radius motion. But again, in reality, please remember that these occur in a combination in most movements. Roll and glide usually occur in opposite directions to each other. Like we see here with the knee.

Within joint motions, we have to look at the convex-concave rule, which basically states, the fixed end of a convex or a concave joint really determines the direction of accessory motion. Each side has its individual motion. So, when we motion palpated joint, we want to make sure to palpate the motion of the fixed end, as well as the moving end.

As you see in the picture here, if you focus on the green dots, you see each motion has a point where the axis of motion occurs. This is what we term, the instantaneous axis of rotation or motion and in like an interphalangeal joint, this axis of instantaneous or axis of motion never changes. But in reality, in human movement, that rarely ever occurs because movement occurs on different planes. When we have multiple motions in multiple planes, this instantaneous axis of motion is constantly changing. We describe the composite of these constantly changing  movements as the evolute.

Most movement, as you can see, is in a curved linear post??? motion. It is always a combination of translation or rotation and that is what commonly happens in most body motions. This freedom of motion gives each joint the capability of having 3 translational, and 3 rotational movements resulting in 6 degrees of freedom of movement in all the cardinal plane  planes. So what this means is joints should exhibit these characteristic movements, flexion, extension, right and lateral flexion, right and lateral rotation, A to P, P to A, lateral to medial, and medial to lateral glide, internal and external rotation, compression, and then distraction.

I think we all realize that since the body motion is really 3 dimensional. The actual description for 3D motion is called the helical axis of motion. And this describes some curved linear translation without rotation,  and without any, spin associated to it. but again, because motion curve occurs on a regular surfaces, there is no real pure planes of motion.

If we switch our attention to the kinetics of motion, which is the branch of biomechanics dealing with the forces causing motion. We really need to review Newton’s Second Law, which is basically force equals mass times acceleration. This relates to our application of thrust with manipulation. We use this in teaching our Chiropractic students, how to use their mass to deliver efficient directions of force during our manipulation courses.

Later in the program, you will learn how to use kinetics in analyzing  athletic movements. So, when we review, we have to look at the different types of muscle activations and we commonly have, are aware of this, but we need to review, and have you remembered that different types of forces that muscles can produce are divided into these categories where concentric contraction is muscle force while the muscle are shortening. Eccentric contraction is muscle force while the muscle is lengthening. Isometric contraction is where there is no change in the muscle length, and then I would like you to remember that eccentric contraction produces twice as much force than concentric contraction with half the energy.

If we started this slide by looking at the bottom of the slide  under a length-tension relationships. This refers to the amount of force a muscle can produce in relation to its actin and myosin cross-bridge connections. We see, in a resting state, there are a greater number of actin and myosin connections. When one elongates or shortens a muscle the percentage of cross-bridges decreases along with the amount of force a muscle can create. And this is called active and passive insufficiency. We see this very commonly in a condition called pattern overload. And pattern overload is when you do the, the same exercise or the same movement over and over again, repetitively like a racket swing, jogging, a particular weight lifting exercise, or pitching a baseball, or a, a cricket ball. and then what occurs from this is pattern overload creates these imbalances in length-tension relationships.

I think that most of us think about muscle function in what is, is just the concentric phase of the muscle contraction because that is how we were taught in school. We learned that the origin and then the insertion, and then we learn the concentric function of a muscle.  I feel that this is carried over into our soft tissue techniques  because we tend to work on the tight muscles in removing muscle tension, removing trigger points in the hope of balancing the soft tissue to allow appropriate joint centration and appropriate motion of the joint. But what I see many neglecting is the other half of the equation where the antagonist is also involved in co-contraction of the joint a-and creating joint stability. And I feel that this must be considered as part of our manual therapy. If we do not activate the weak antagonist while releasing the type agonist or vice-versa, how can we assume that there is balance and force available for joint stability and centration?

Research has provided many instances where this reciprocal inhibition of an overactive agonist, neurologically shuts down the neural drive to the antagonist. And this is basically what neurogenic inhibition is. This creates another condition called synergistic dominance and that is when the neural drive of a prime mover is shut down. Then the synergistic muscles that  aid in the execution of that movement, now become the prime mover. When that occurs this leads to further decentration of the joint and a higher risk of injury and loss of performance.

The reason why this occurs is not only because of the changes in the  length-tension relationships of those muscles but in their coordination of what is called force couples. When you have a synergistic action of muscle groups and this is illustrated in the illustrations on the, on the far right of this slide. Most cases, force couples are considered  a-an gross movements but not that is not true in every scenario. But when you have this scenario of altered length-tension relationships from pattern overload, creating a reciprocal inhibition, and synergistic dominance then you have this agenesis of impairment of performance. I like these  charts here  because I think they are very informative, but I, I think the arrow should move in, in both directions since each component of these  adaptive responses are the result of the body always sacrificing quality of motion for quantity of motion.

Then our neural plasticity, our nervous system creates engrams that quickly learn this dysfunctional movement pattern and then these circles move on to the next stage. Now, regardless if you would know what movement we are talking about. Whether it be everyday movement or athletic movements, there are various forces that act on the musculoskeletal system, and these are composed of tension, compression, stress, shear, torsion, or more times than not a combination of these things take place.

Now, I would like to switch our attention to the articular neurology of, of synovial joints. There are the primary innervation of synovial joints are 3 types of nerves. The primary and accessory articular nerves and then mechanoreceptors, and I want to concentrate on the mechanoreceptors today. We often think of these in our, our, our Kinesio taping techniques because  these assist afferent communication through using the skin as a handle or in our internment, instrument assisted techniques. but it is interesting that joints also have this similar innervation like the skin. I find that fascinating because they allow the body to perceive where it is in space. This is critically important in athletic movement because controlling your balance is so critical. Controlling your balance outside your center of gravity is what I feel is the ultimate athletic skill. Therefore, our optimizing a mechanoreceptor function is really central to what we do.

As you can see, there are 4 types of mechanoreceptors. Types 1 through 3 are found in joints and periarticular tissues. Where type 4 are just free nerve endings surrounding the joints that mediate pain or nociception. When stimulated these type 4 nociceptors do not adapt. They just keep on fire. They just keep on screaming. And then this trigger, triggers muscle tension which then restricts motion from neurogenic inhibition and they get sensitized, and that increases pain perception. The nice thing about types 1 through 3 is that during motion, that stipulates the type 1 through 3 mechanoreceptors and these guys block type 4 nociception from transmission to higher centers.

The other thing you have to remember is when the joint motion is restricted or immobilized or even when the joint has decreased motion from like pattern overload, this stimulates the type 4 nociceptor firing. And this is where we come in because our osseous manipulation like joint motion and exercise stimulates type 1 through 3 nociceptor activity resulting in presynaptic inhibition of the nociceptor afferent transmission at the spinal cord level so it never really gets to the higher centers. I feel that this is how our manipulation helps relieve joint pain.

So let us take a closer look at these guys. If we look at type 1, Ruffini mechanoreceptors, there are numerous and subcutaneous  and fascial connective tissue  joint capsules, apophyseal joints to the spine and they are in the TMJ.

Unique thing about these guys is that they are more numerous and proximal joints. They have a low threshold. They are slowly adapting and they are always active even when the joints are mobile. They discharged at a rate of 10 to 20 times a second and have a tonic effect on muscles. Alterations the discharge rate increase or decrease with active or passive manipulation, isotonic or isometric exercise, or when the pressure gradient of a joint is altered sufficiently like we see in when we cavitate a joint.

The other cool thing is they supplement our visual components of balance and those cutaneous mechanoreceptors in the skin. But alternative, alternative so if you damage the joints capsule, it also causes degeneration of type 1 mechanoreceptors. Then the reverse occurs, this can lead to impairments of posture and balance.

If we look at type 2 Pacinian corpuscles they are, they are kind of strange nerve endings because they have a multilaminate connective tissue capsule and closing the terminal end of the nerve. They are present in periarticular tissue, fibers capsules of the joint, and the periosteum. These guys are a little different because they are more numerous in distal joints as opposed to proximal ones, like the type 1’s. They are low threshold. They are rapidly adapting. And for this reason, they are really inactive when we immobilize the joint. They only become active at the onset of movement, and then they emit a brief high-frequency burst that occurs 20 to 40 milliseconds prior to the type 1’s firing. So there are main function is to signal joint acceleration and deceleration and they have a phasic effect on the muscles.

Then type 3’s are combined to intrinsic and extrinsic ligaments and they are identical to the Golgi tendon organs that were familiar with. They are found in collateral ligaments of the knee, cruciate of the knee, longitudinal and interspinous ligaments of the spine. Their high threshold slowly adapting but like type 2 they are inactive when we immobilize the joint because they only become active at end ranges of motion. So, their function is to mediate breaking reactions, directions of motion, and warn of harmful movements.

Then back to the type 4 nociceptors, they represent a small plexus of unmyelinated pain receptors. Remember that they are active with mechanical deformation,  tension, and chemical or mechanical irritation. When you have  an injury that causes  an  excess of  inflammatory exudate, when the concentration of histamine or bradykinin gets high. These guys set off and they continue firing as mentioned causing muscle tension, increased pain perception and this leads to inactivity from  neurogenic inhibition, and then if unchecked they continue firing into the  upper centers of the brain, and this causes sensitization that we recognize as chronic pain.

So let us move our attention to how we assess joints and we really ask ourselves a lot of questions. How do we assess joints using these biomechanical principles that I have just discussed? let us look at a few theories of why joints become restricted? Why they lose motion? What exactly causes the joint to lose its freedom of motion? And really the answer we see most often is that it is related to so-some type of trauma.

I have, you know, touched on the concept of pattern overload, creating changes in length-tension relationships which then causes adaptations to motor control. But in reality, there are not really a lot of explanations out there and we have not been able to really pin down the precise reasons. Current research does not really explain everything but here are a few of these that I would like to talk about. Paterson and Steinmetz showed that there is a neurological patterning causing decentration of the joint. This is because the brain will pattern quality or quantity of motion over quality of motion and on our brain neuroplasticity quickly creates the engram for the joint function to adapt to the changes that are imposed upon it.

The next research article is by Gattermann and Koch, who really questions this classic chicken or egg question? Is it the joint centration that causes muscle imbalance or is it the muscle imbalance that causes the loss of joint motion? Well, their research agreed with Janda’s explanation that it is really the muscle tension and imbalance that are the causative factors calling causing alteration of joint mechanics. Then Triano created a research paper that proposed a biomechanical or a biomedical model which looks at the mechanical forces acting on the joint that alter its motion and what effect that this has on periarticular tissues.

Normal motion occurs when appropriate joint stiffness support centration of the joint when in proportion to the loads applied to it. Triano reported various stresses cause buckling to articular tissues and these stresses include prolonged postural positions which sort of explains, why we sit here for a long time and then we get up and we feel a little stiff and achy. Well, over time this creates tissue fatigue below the injury threshold, which results in buckling of articular tissues. And then, in addition to this, chronic postural change. You found out that buckling events come from single events like trauma or rapid loading higher than 500 pounds per second. Static postures that have progressively increasing loads, and then he also showed that chronic vibration also reduces the injury threshold and then creates buckling in the soft tissues. But then he went on to prove that we can resolve these buckling events by the application of external forces and actually restore movement through restoring normal movement patterns,  through corrective exercise, and through our manipulation.

As we palpate, we really analyze joint play and joint play as relieved as small discreet ranger motion of passive movement, palpated in the neutral position. We look for the quality of the joints’ resistance to movement, in this neutral, loose pack position. This should have a really small magnitude springy feel to it and when we do not have this springy kind of reaction to our motion palpation, this is one indication of joint dysfunction.

Now, we have all seen these joint range of motion diagrams, and I will go through these rather, rather quickly cause we have seen them before.  but be aware that, you know, there are neutral, active, passive physiological barriers and re- and play zone, elastic barriers joint play zones  Para physiological spaces, and then  the absolute and is the anatomical barrier.

Our palpation attempts to analyze is these different aspects of these barriers during motion palpation. Our motion palpation also looks to discriminate differences in tissue, tension, texture and to assess the end range or, and feel of the joint. This is evaluated by applying  additional overpressure to the joint at end range where we feel a sense of it increasing restriction to the tissue with firmer resistance until it stops its motion. And we are actually looking to find it as it comes as complete as it can be, but we also have to judge the quality of the end feel. So let us look at the qualities or different qualities of end feel. Some are normal. Some are abnormal. I have listed a few examples as described by Magee. In here you will see that there are normal end feels  bone to bone being like elbow extension. Soft tissue approximation being like elbow flexion or knee flexion and then tissue stretches  similar to when you  bend your finger backwards.

But there are also abnormal end feels, and in order to tell the difference between these 2, these are basically very similar  to what you would feel in normal end feels. But they occur where you would not see them, within the normal range of motion, where it is not expected, and that is what makes them abnormal. If you have a bone to bone end feel, for instance, in the middle of a range of motion that stops with that end feel, that commonly occurs when we have like osteophytosis.  spasm is, is basically self-explanatory. That is when muscle spasm like you would see in a torticollis  prevents normal range of motion. Then springy block is when you have some type of intra-articular palo-pathology that is very commonly seen in the knee or the TMJ. Then empty is when pain blocks the motion or when the joint have so much hypermobility that they are, there is just excessive range of motion. The last of these, we need to look for is, is capsular patterns and we need to watch for these to tell if our patterns of, if these patterns of stiffness are leading to capsular fibrosis. In this feels like a thick tissue stretch but not where you would expected in the range of motion. Capsular patterns, only occur in joints with muscular attachments. So, for instance, in the sacroiliac joint and the distal tibiolo- tibiofibular joint, that is not going to happen there.

It is important to show consistency in evidence for what we find in our motion and palpations. So, so we can provide outcome measures for what we are doing. Currently, w-we have not standardized the process and there are not enough outcome measures to really defend our, our credibility.

Our methods are not as sensitive or reproducible enough to produce reliable outcomes. And so, to better help us show better consistency. One of the tools we would like to introduce you to is algometry. If you are not using it already, this measures pain threshold, and face it, our assessment could be better and this is one tool that can help us. Algometry has excellent reliability and repeatability. Correlates well with other measures and it is a really good tool to, to defend and add credibility to our outcomes in ma- manipulative assessment and  in our treatment.

Another tool we use to direct our decision-making  with what joint to manipulate, is what we find in the clinical presentation. As we palpate joints, we look to identify reliable indicators that tell us which joint to manipulate. There is a lot of data out there of indicators that help us identifying that, and here are some more reliable studies to help us with what that looks like. We are more familiar with Triano’s review of methods used by chiropractors to determine the site of applying manipulation.  and, and he uses and made famous the parts acronym, which is basically pain  asymmetry and bony landmarks,  alterations and range of motion,  and as refers to the postural and kinetic chains that we have talked about. Changes in the tissue whether that be temperature, texture, tone, and then special tests revert back to alterations and motor control with gross movements. And, and the kinematics that  we have already discussed. But he was not the first and was not the only one.

Back in 2009, Chase had  his acronym called TART, which is very similar  tissue, texture and temperature changes, asymmetry  of  bony landmarks,  range of motion, changes, and tenderness. Even before him,  an osteopath by the name of Dowling, had his  STAR acronym which again is very similar. Sensibility changes, tissue texture changes, asymmetry landmarks, and then alterations and ranges of motion.

We recognize motion palpation is larger, largely subjective and that is really a problem for us. It has good inter-rater reliability, but pretty bad inter-rater reliability. This caused us to lose consistency in what we are reporting and how we report it. We need more standardization in our approach along with a mutual understanding of these biomechanical principles in what we are, we are trying to assess. We encourage you to try to become as consistent as you can in your assessment and your reporting.

Another tool we would like you to incorporate is called the Orth tool kit. It is an online app and it has  a lot of additional outcome measures for  extremities like the lower extremity functional scale, the Foot and Ankle Disability Index, the knee injury outcome score, and lots of different outcome measures for the shoulder, elbow, wrist,  cervical spine, lower back. And it is interactive between you and your patients. It will track your progress and it is HIPAA compliant. And I am not sure if you understand what HIPAA compliance is, since that is  kind of a, a thing in the States but that is a, a regulation that controls how  patient health information needs to be protected and who can see it and who cannot. This app that you can see online here is, is fully compliant.

One of our tools. Another one of our tools is in treatment is, is joint mobilization. In, in my time we kind of ignored mobilization because we wanted to be identified for our manipulation, not mobilization. But as time went on, we realized that mobilization does have it placed in our manual therapy. It is basically a form of non-thrust joint manipulation typically applied within the physiological ranges of motion. their passive, rhythmic, graded movements of controlled depth and rate and they can be applied with fast or slow repetitions at various depths. Movement can be applied singularly or repetitively within or at the physiological range of motion. But the thing that separates it from manipulation is that there is no thrust or impulse. This lack of thrust is really what separates it from grade 5 manipulation that we are familiar with. But it also has the goal of restoring joint mobility.

You will see in this slide that grades 1 and 4 are small amplitude movements at the beginning and end range of joint play, respectively. Then grades 2 and 3 are large amplitude movements at the beginning and mid-range of joint play. At the bottom, grade 5, the one that we all know and love the high velocity, low amplitude thrust at a-anatomical endpoints of the joint. Now, I think I am pretty close to the end of my time here. I think I will stop at this point.  Maybe answer some questions if you have any take a little break and then I will let Dr. Ames take over to  tell you a little bit more about manipulation. Thank you for your time and attention.

Christine: Thanks so much, Tim. That was really just absolute terrific and very informative. I really love getting that concept of quality of motion over quantity of motion. I think that is a really important concept particularly with athletes that we need to think about when we are, when we are evaluating the kinematic chain, which is a hot topic now. but  thank you. I do want to you know, really appreciate all that you have contributed to the sport, to the profession and  providing teams for games around the world, for a very long time for FICS., and also your expertise at the University of Western States as associate professor and program director of Sports Medicine, not to mention Colorado Chiro of the year, 2 times. So thank you for all you have done for our profession and for joining us today and helping the students grow and learn more as we kind of dive into sports chiropractic.

Tim: Thank you, Christine, and, and thank all of you out there. It is been a pleasure to have the opportunity to speak with you and I, I hope you learned a lot of things from, from our discussion today.

Rick: I do not have… I needs that [smash noise]… hmm, some reason I am not getting my notes. I am going to stop sharing and, and  change this.

Short break in video:

Christine: welcome back everybody and I would like to introduce Dr. Rick Ames,  who will be presenting the last portion of our module today,  functional peripheral joint  technique. This once again is getting at you ready for your hands-on module. So just as a reminder, when we see you at your hands-on module, please come appropriately clothes so that we can do all the adjusting techniques on you, upper and lower extremity. If you are doing just an upper program, just a short-sleeve shirt. If you are doing a lower, shorts as well. We will really be looking forward to seeing you all at your hands-on modules and get   be working now. At those modules there will be no powerpoints,  it will all be hands-on the entire time. So super exciting content that will be going through with you there.

Dr. Ames is a senior lecturer in the discipline of Chiropractic at RMIT University of Melbourne, Australia. There, he teaches diagnosis technique and management  as well. He has graduated from LACC. He has a fellowship in Orthopedics and Neurology. He has worked with National Olympic Weightlifting and Table Tennis teams based out of Melbourne, as well as focusing on treatment and rehabilitation of amateur and professional athletes in his private practice. He is organized Health teams of chiropractors there in Melbourne for major sporting events.

Dr. Ames is also coordinated the sports chiropractic and postgraduate programs for RMIT University and Federation Internationale de Chiropratique, FICS. He is actively involved in the presentation of postgraduate seminars and chiropractic as well as publishing numerous articles with sports chiropractic focus. His main clinical practice is emphasizes postgraduate study and research continues to be a sports chiropractic focusing on extremity conditions. He is published and lectured extensively on management of extremity conditions particularly on how to treat patients in everyday practice, super applicable to today. So welcome Dr. Ames, very excited for you to come all the way from the other side of the world, at a way different times on.

Rick: Thank you, Christine.  hello everybody. These things have changed quite a bit  in the world over the last year and a half, and the last year,  when we are on lockdown here in Melbourne  we had a 5k rule, you could only visit the areas within 5 kilometres of where you live. Well, 4.8 kilometres from where I lived was this  beautiful State Park known as Westerfolds and in  Westerfolds lives what they call a mob of kangaroos. It is really wonderful to be able to walk to there, drive to there and be able to see this  during lockdown. So that is how we will start today. I want to acknowledge first of all, Dr. Brian Nook  who presented a lot of this material at the Madrid seminar back in December 2020. I also want to acknowledge the excellent presentation that Dr. Ray did today.

I thought it was fantastic. A couple of the our final year students who partisan videos that I am going to show in a minute, and  you guys, you are our inspiration. This is what took me from being what I thought was an ordinary chiropractor and to a  much better chiropractor was a seminar  for FICS that they had in Hamilton Island in 1993. It just changed my whole  focus in my whole ideas of, of doing adjusting. There is a- very much we learned a dysfunction-based  functional technique, so they call a couple technique. I tend to call it functional technique  because it is not just straight adjusting  it is  based around the coupled concepts that I am going to be talking about.

Most of us have learned a more traditional approach  where we  diagnose a dysfunction in a joint, and then and then we adjust it. But we can also take some of these coupled concepts and  incorporate those and  improve our ability to  function, and to adjust. The coupled contexts, number 1, Obviously, you are- you want to make sure that you are around the joint capsule.  you want to get as close and into the joint capsules possible when you are doing your  palpation. You want to spring the joint. This is something that you have always learned in your motion palpation,  and Dr. Ray was talking about  with either your joint play or end feel. and you look to find the most restricted position but the other things that you want to do is you can put them in a coupled position. You might add  2 or 3 different positions to that joint and look for the most restrictive position.

You can add muscle contractions so you might be taking a contact around the hip in a flexion position, and you contract the quadriceps, or you contract the psoas. and then the other things that you can do, you can add weight-bearing and sport-specific, so you can do these things in a standing position, you can do them in a position, say a patient who, who was lifting weights. I just happen to use an old wooden stick and get them to simulate a position for  say at the end of a clean and jerk. In that particular position, that is when I do my motion palpation. Use that sport-specific position particularly if they are complaining of pain in that particular position and of course, you adjust then in the position of greatest restriction.

These are what we traditionally learned  you know, we learn, you know, kind of adjusting for dysfunction. We looked at open and packed positions, that is when we would do our adjusting. But then like I said, we can add in these other coupled  aspects, and particularly what I liked is that you can, you can bring in your assisted techniques, your drop pieces, your instruments if there is a range of different type of adjusting instruments that are  in our profession and developed by our profession that make it to If we use a coupled concepts and coupled the approach to doing this. that we can add, add those to our- the way we do it.  Technique principles you guys gone over this before, you would have done it in your undergraduate and you should be doing it now.

One of things, the principles that I find that when we do a technique is the same as in sports. We do these pre-performance routines. You watch  any of your athletes. They do pre-performance routines. They go through and they start off in that pre-performance, they imagine what they do, we focus the attention, you execute and then evaluate and we do the same thing. When we do an adjustment we ready ourselves, we should be imagining the anatomy underneath our hands, focusing our attention, concentrating on what we are doing and then you know, the Nike just do it, and many times that is what we do with our manipulations with our adjustments.

Tim talked about this. why these benign pain syndromes develop? Now there is a professional jargon  that is out there. I do not shy away from the fact that I utilize the term that chiropractors called subluxation. I tend to use it  from the gathering consensus approach. and I know in  the book by  Bergmann and Peterson.  they talk they would have turned it subluxation joint dysfunction,  whatever you want to call it. it develops because there is changes usually within the kinetic chain, maybe this dyskinesis. What Tim was talking about  changes in motor control, changes in utilizing synergistic muscles rather than the primary contractors, a post-trauma, whether it is micro-macro trauma in overuse type situations or if there is been pathological change. What the patient ends up with is many times just a benign pain syndrome. You cannot link it to one specific aspect.

I have always, in working in sports, think it is important. We have the professional jargon that we use of a subluxation. What we have to remember is that in the medical profession their definition of a subluxation is at this end of the continuum just below a dislocation. Whereas, usually, we had talked about that subluxation at the other end of the continuum which has that fixation hypermobility type of aspect, neuromechanical aspect. Make sure that when you are discussing  with the practitioners in other professions that  you, you understand what your definitions are and make sure that they understand what their definitions are. So that you talk in the same language, obviously, the contraindications to adjusting, you guys have covered all of this in several different places. Both the red flag and cautions and modifications because you are going to come across all of those in our practice and so you can work through those.

I like using these particular definitions Bergmann, Peterson’s  always had this again, you should know this. You would have covered this in your undergraduate using joint manipulation as the overreaching concept.  For us as chiropractors, we use that specific form of joint manipulation, we call it adjustment. chiropractors typically have been looked at, and utilize the short leverage aspect of, of the adjustment, but we also have many long lever adjustments. Obviously, there is a controlled force, lever direction amplitude, and velocity. I think the big word here is controlled and that is where that  pre-performance routine comes into it, it allows us to do the control.

Tim talked about joint m-mobilization using those grades  developed out of the European  manipulation models Maitland, highly influenced by cattle born and  some of the UK and European approaches to manipulation. We do teach a range of mobilizations. and Tim went through those grades 1 to 4 with the manipulation being in grade five. If you wanted to classify it,  we have got joint manipulation procedures, you know, our mobilizations in our adjustments and also adding traction to do that. Then there is soft tissue manipulation procedures,  I will show you a soft tissue manipulation at the end of this  talk.

So really manipulation that some of the early work by Roston and Wheeler Haines, where they looked at cavitation of the joint and producing that cracking noise that when they separated. So they have, using x-rays they filmed and they found the initial separation 1.8, and as they increase the tension, it jumped to 4.7 and there was a cracking noise. Their idea was that  this traction like said, it tends to invaginate the, the, the  synovial fold and capsule. they a forced a part of the, of the intra-articular pressure drops and this gas bubble forms, and they felt that the collapse of the gas bubble was what produces the audible crack or the cavitation.

However, subsequent studies suggest that there is a different mechanism involved. It is about a refractory period of 20 minutes and that is been  confirmed by other studies, one of things is that during mobilization, so your grades 1 to 4, there, there is no cavitation, and there has been research suggesting that a-at least for a flexion of the metacarpal, phalangeal joint mobilization is not as effective as actually the manipulation with the production of the cavitation for increasing flexion. You know studies by Kramer on the zygapophyseal joints in the spine shows that there are differences  in there looking at side posture, upside joints, downside joints,  gender, and of the fact that there was more cavitation on joints that are sore more gapping in the joints that cavitated. This is it back again from Roston and Wheeler Haines, looking at two types of patients, looking at the  typical one but this one showing a wide preliminary separation. So perhaps somebody that is in either, hypermobile, hypermobililty or generalized hypermobility  in the way in which that cavitation or cracker.

Study by Kawchuck  was very important in that they  show that the  mechanism joint cracking or the cavitation is related to the cavity formation rather than the bubble collapse. That cavity formation is known as tribonucleation process where the opposing surfaces resist separation until the critical point where they separate rapidly into vapor cavities and do not collapse instantaneously. This tribal nucleation so it is a different idea than that collapse of the bubble that was originally  suggested. They found that there is a 20-minute refractory period before the next cavitation.

Start looking at about biomechanics of spinal manipulation. As Tim noted, we are utilizing  these  peak force-time profiles and teaching students on how to  manipulate.  We are looking at, you know, the pre-loading force into the into the phase, into the thrusting phase and then resolution phase and looking at this  change in force or the rate of rise, and we also look at the speed.

Another thing that we look at is something, which I think is important is the incisural dip or this notch that sometimes as the pre-loading force, people get a little bit of a notch and when they let the tension go out of the joint when they are taking an adjustment.  sometimes I, I found that, that can be a painful aspect. So, Herzog did a really nice review on this. The peak and preload forces very dramatically, depending on location, cervical thoracic sacroiliac and whether we are using a hands or using a  adjusting instrument. The treatment forces very dramatically between clinician. Plenty of research that is come up out of Canada in regards to that and the fact that both experience has a big aspect of it and gender may play a part in it as well. The detail force mean to might not be the important characteristic of success while the direction of thrust might be. We have got multiple hypotheses, is not in mention, there are quite a number of hypotheses out there. Many things, have not been proven, we have got lots of information out in or out in the literature that we can look at his background for our manipulation.

This really nice review article that I came across by some osteopaths out of  the UK  looking at the different theories of  changes with particularly spinal manipulative therapy. Again these biomechanical changes that are produced, which Tim Ray talked about, he talked about the buckled motion segments may be entrapment. This has been around awhile, synovial folds are in these voids adhesions, and  then Tim Ray also talked about changes in the musculature, and so their ideas that these changes in spinal biomechanics trigger a change of neurophysiological responses.

You look at this study, they have this what I think is a quite nice, a representation  within the article which looks at  different aspects of activation of mechanoreceptor of nociception and efferent fibers.  Look at  changes in the  alpha and gamma motor neuron excitability as well as cortical, spinal excitability, we look at  autonomic activation.  All of these having an effect on analgesia, and so changes in pain. We have an effect by activation of the sympathetic nervous system and a activation in what is known as the hypothalamic-pituitary-adrenal axis,  which  changes  tissue healing.

One of things they say in the article that has been well established that both the sympathetic nervous system and the HPA axis plays a significant role in modulation acute and chronic inflammation and are involved in pain relief and teal tissue healing processes. Then one that has been around for a while. Looking at the gate mechanism that Tim Ray talked about where we, you know, alter peripheral sensory input. We get this, hypogeusia from segmental inhibition and then again, there is activation of descending pain pathways.

These are all theoretical aspects of particularly pain control that we come along and that we utilize within our background to manipulation.  A couple of things that  neurological conditions and to mention about this particularly in regards to, to neural plasticity. That is the brain learns to be dysfunctional, and that many times it  goes through a maladaptation process that might be associated with some of the chronic pain. Some of the research has shown that the speed of thrust is very important and  I personally think and look at some of the sports psychology that the visualization of positive outcomes. Going back to that pre-performance flowchart.

This visualization that we have both as a practitioner and that we impart into our  patients is very important. Of course you know we talked about particularly so you go back to what Tim Ray was talking about, about those mechanoreceptors that when they are stimulated you get some  inhibition  for better word of the nociception, the nociceptors. Really nice article, in I like to look at different articles that help with my understanding of what happens in clinical practice so there, there is  this idea that if you try change pain without changing  motor control, it is going to result in the return of pain.

Out of  Haavik and Murphy’s article looking at where you have got this abnormal sensory motor integration with altered motor control that by incorporating, in this case spinal manipulation  into  that flow that you end up with appropriate sense of motor integration and accurate motor control which improves your function. There is also an article just lately  by Malayil  in Texas looking at dual-task performance. Looking at both tasks and posture and looking at manipulation of the extremities they used a pattern of adjustments, and found that  it definitely improved the this dual-task performance.

We know then that our manipulation has activated in pain reduction. We know about it activating  mechanoreceptors particularly but normalizing both mechanoreceptors and nociceptors. We know about inhibiting the central transmission of pain, and I do not have a problem with the idea that there may be some placebo effect associated with all of this.

So our therapeutic approaches that, that, that we  use. we want to see decrease in the patient’s symptoms. We want to change objective findings even though some of them are  more subjective, and less objective. One of the ways that we can objectify is perhaps using some of the things out of the Orthotool kit that Tim Ray discussed. When we are looking at adjusting if you are just doing straight adjusting maybe we need to change what we do to fit better with our patients, who are the athletes. So, again those two concepts, dysfunction-based functional technique that is mainly what we are going to be going about. Like I said, you can take some of these coupled concepts and incorporate them into your normal traditional approach to adjusting.

We are going your, your traditional, I have already gone through that, so we are going to look again about the coupled motion contact around the joint capsule, spring the joint, find the most restrictive position add in muscle contraction, add in different aspects of weight-bearing that are perhaps sport-specific, sport-specific position, but also you can add in equipment. So have the patient grab onto a tennis racket. Have the patient grab onto a cricket ball. Have the patient grab onto  a volleyball or water polo ball, or  hockey stick or baseball bat or whatever and during  our motion palpation  assess with that equipment or in the position that they are utilizing within their sport. While we do with this, we feel for springiness in multiple positions. We feel for springing this in coupled positions. We do not just  do it in a neutral position. We might add in flexion-extension, we might add in supination, pronation, we might add in internal, external rotation, and then we can add in those muscle contractions like said we can add in weight-bearing or sport-specific positions on this. We find them most restricted direction of movement and then we adjust the joint in that position with an impulse-type thrust. We started looking at a quick screens, you saw the, the picture that Tim Ray had of the kinetic chain looking at  the changes in kinetic chain with excessive pronation. I started making up some motion palpation approaches for myself.  Basically, I just call it pelvic hip drop. I get them to bend the knee, I may add in a transitory or a sliding action, and then I will add in rotations. So let me just play you this video. Let us see if it will play.

Video

I just found that there were many times where I would have patients with a low back pain, a sacroiliac pain that was not responding to our normal treatments. I started looking at the hip. One of those  general aspects of motion palpation that allows me to say, “Well, the, the low back seems to be moving fine, the sacroiliac seem to be move fine but the hips are moving awfully and therefore  that maybe is where I should be looking at  reintroducing some motion.

Video

The video cut out at the distal tibiofibular joint and that is the subtalar joint. I use with this general kinetic chain palpation. It lets me focus on which joint I should be paying attention to, again we cannot motion palpate every joint on every patient, particularly, if we are going to be looking at function in combination with perhaps pain, but definitely want to focus on function.

When we are looking at hip, we can do a, a range of, of quick screens. We can just do flexion. We could just do internal and external rotation. We could add in abduction and adduction. Brian’s picture here is probably a nice combination where he is got flexion, internal and external rotation.  You can see this is where these coupled theories or the coupled approach comes into it. It is right down into the joint system. It is doing a coupled motion of both flexion and in this case, internal rotation and then flexion and external rotation.  You could do things like extension and internal and external rotations as well. Looking at it is this, you can either do them singularly or then come on down and start doing them as a couple. You spring in this particular around the joint. In this case, you actually work your way around the entire femoroacetabular joint, feeling for the point of greatest restriction. If we wanted to, we could bring in things like the sartorius. We could get the patient to contract the psoas.  We could get the patient to correct to contract the quadriceps. We could get them to contract the hamstrings. We get them to move the foot.

Now bring in a range of different aspects and of course, some of these you can do in a standing position so you throw them up into a weight-bearing position. But you put them up into a weight-bearing position and obviously it is going to be much more difficult to do flexion and most of the joint. But again, you could get the patient to bend the knee, which creates a flexion inside the joint. You look at their particular sport-specific position to do these  motions. So same thing in the knee you know that we, we look at  we can do singular ones but in this case we are doing a flexion with internal and external rotation. You could do this medial to lateral, lateral to medial. This is done in a neutral or in the extended position which you could do the same thing in a flexion position. Same with the fibula we can put the fibula when we are testing A to P, P to A, we can do this in a flexion position, we could also do it in an extended position. Many times I do both of these in a weight-bearing position particularly if patient is  coming in complaining of knee pain in a weight-bearing position and staying with the patella, I have got them in a neutral lying position. You could do all of these in a standing position or in a closer to a sport-specific position.

With the ankle and foot, one of the things I do find that is really important, just thinking about the superior and inferior aspect of the fibula the fact that during the one of the most common  sports injuries, the ankle sprain, particularly the inversion ankle sprain, what we tend to find a lot is an inferior fibula with a posterior fibula and but we have also got to make sure that the what is called syndesmosis is not  compromised. So, doing our motion palpation of compression  also allows us to assess instability in that area.

We could do things in the mortise joint. In this case  we looking at A to P, P to A, in dorsiflexion and plantarflexion.  We are looking at the subtalar joint, one common  conditions you see  patients who were doing lots of running particularly social running,  but also in the  higher levels  in track and field  is a problem at the subtalar joint. The subtalar joint is the one that tends to lose flexibility  in ankle sprains as well as the  talus in the mortise joint they tend to have problems with dorsiflexion.

You know, we can look at  all of these different areas. We can add in dorsiflexion, and plantarflexion  where we look at them. Perhaps we do A to P, P to A, add in dorsiflexions, look at the cuneiforms in the metatarsal, phalangeal joints maybe add dorsiflexion and internal rotation dorsiflexion or plantarflexion external rotation. So again, you can couple all these different motions. Same thing with the toes, just they always get asked about a patient just before they leave the room. They go, “You know I stub my toe and it is it fractured?” best way to tell about a fracture compress the joint, add a bit of rotation if they are really painful, yes this is a good possibility that the toe is fractured.

I tend to find it was actually Mark Charette, a  lecturer on extremity manipulation adjustments that I saw that he had a certain pattern of  fixations and  so I have not really been thinking about that.  I started looking for myself and this is what I found. I found that there tend to be common fixations. I keep those in the back of my mind so when I am doing the quick, quick screen, that is one of the things that I am looking for. Things like an anterior talus after somebody has an inversion sprain, something like a posterior calcaneus, and patient comes in with plantar fasciitis,  things like a medial navicular, post  fracture of the, of the foot. They might have had a fracture dislocation  up at the  tibia-fibula area. Many times you will find this medially fixated  navicular and cuneiforms are associated with that. A quick screen in the upper extremity you can use long, axis traction, you look and feel for tension in the different joints.

Video

All these motion palpations, when we look at doing these as an adjustment, we are going to do the motion palpation, and then many times, we will have the position that we can actually do the adjustments at that time. We want to look at the AC in the SC joints. Looking at these coupled ideas while I have given you single motions here particularly seated, horizontal, abduction, and adduction many times. You might  substitute your fingers for  your thenar, or for your pisiform but I tend to do use the thenar and do the adjustment at that time. I do find that these lend themselves to also using an instrument.

Looking at the glenohumeral joint and this is a really good joint in bringing in many of these coupled ideas.  For instance, you can bring in abduction and external rotation, and while they are in that abducted, externally rotated position, test internal rotation or the same abduction and internal rotation.  Not only test internal rotation but test external rotation. You can utilize this with bringing in equipment which is important.  Doing the different ranges of motion palpation to kind of screen through but also, you can go ahead and test and adjust with an impulse with these patients. I do think in your quick screen of the, of the shoulder,  there is enough information out there, enough research out there, suggesting that dyskinesis of the scapula  system has a big effect regarding a range of particularly overuse conditions. You should always do scapulohumeral rhythm  do it in abduction, do it in flexion , take a look at the clavicle as well.

Quick screen of the elbow  again, you can do it in flexion-extension. You can do medial-lateral, lateral-medial. You could combine the two of these together for the most part. The pictures showing medial-lateral, lateral to medial in an extended position, but you could do this in a flexion position as well.  Same thing with the radial head, A to P, P to A, now we do it both in supination and pronation,  so you should do both actions, and of course, you can  set yourself up while you are doing it,  to do it as an impulse thrust at that time. Same thing I have used to see  I was taught that when people had problem with extension of the elbow, it was always called a posterior ulna. But instead, I found it was quite commonly a superior ulna and it did not shift the olecranon was not centered  within the joint and it was seemed to be shifted superior.

I definitely use this a lot with any of my elbow conditions. Wrist and hand are very easy to do. A lot of much as the ankle and foot, a lot of the coupled ideas, so, like the idea of the A to P – P to A in supination and pronation of the different carpals.  Same thing you can do radioulnar deviation, or looking at distal radioulnar joint and you know, looking at doing it both in supination and pronation.  I tend to find a lot of risk problems has the scaphoid just does not shift well from its lateral position into its medial position and you will find that many times in either or supination or pronation.

Same thing we should look at the metacarpal phases, particularly any of the  athletes that  have sports where they involve equipment, whether you are looking at tennis or hockey sticks or   doing weightlifting,  and again we look at the thumb and finger joints. I have a, a range of different fixations that I have identified as a pattern. You should be doing this yourself, you can use these ones. Keep them in the back of your mind when you are doing work.  Just to quickly finish up here, we have finished looking at the joint adjusting, at motion and using the coupled motions to test the joint and whether if necessary to then adjust then.

We can do our soft tissue adjustments,  Brian Nook was the one who  I first heard talk about what they called grip and rip, which is basically this post-injury collagen-binding so adhesion scars and adhesions in the soft tissue. You can use it on the different muscle systems and on the myofascial  slings.  Myers,  If you have not looked over anatomy trains admires a myofascial slings, you can use it in relationship with that. There is a dysfunction in the tissue flexibility and what we do, we look for the barrier that is there within the tissue and then we can use manual muscle testing or functional muscle testing  to give us an idea just as a contraindication to your, obviously, inflammation and pain. You do not want to do a high velocity, low amplitude thrust.  When you have inflammation or you have particularly damage to the tissue, we are going to take the tissue to the barrier and we apply a high velocity, low amplitude thrust in the direction. I use the drop piece table a lot with this, as I find it just aids my ability to do it.

That is what I have for today. Thank you very much for listening and I  hope I was able to give you something to start in your practice on the week on Monday.

[End]

FICS ICSC UE Assessment – Shoulder 

Dr. Christine Foss: Hi, and welcome to Assessment of the Shoulder. We are going to spend a good amount of time going through the shoulder today and talking about assessment skills and how we’re going to tease apart different shoulder injuries. I’m Dr. Christine Foss, Education Chair for FICS. I really don’t want to go through all of the things I’ve done would take much too long. So let’s just move forward with the lecture.

Let’s talk about what we’re going to accomplish today in our class. We are going to learn how to tease apart a shoulder injury. So when a patient comes to you in your office, we’re going to be able to kind of better understand which structures were looking at, how to specifically assess each particular structure, and how we can kind of think about moving that into a treatment regime and getting that athlete back to play. Whether we have it, what I call a go or no-go injury, or something like that which kind of needs to take a little time to heal.

So we talked about the shoulder. We need to start with our anatomy. We need to consider what structures are in what layers and that’s how I look at a patient when I evaluate them. I start looking at the layers. I start on the outside and work my way in with my assessment. However, some injuries will require you to start on the deepest level, the bone level, and work your way out. So we’re going to talk a little bit about this. So just a refresher of your structures in the shoulder; your clavicle and your acromion, your acromioclavicular joint up here on the top of your shoulder with the supraspinatus muscle coming out from underneath that acromial beak. Three muscles attaching to the coracoid process, which we’re going to talk about later, very important pec minor bicep short head, and coracobrachialis. Then your long head of your bicep and how that’s different than your short head in what we consider. Then the superior, middle glenoid ligaments that hold the integrity of the shoulder.

So I want you to think about these structures, not only statically but dynamically, and then what does your athlete need to get from you? What do they need that shoulder to do and that’s how you have to think about your evaluation, not only the anatomy but the functional anatomy? What kinematics, what kinetic chain do we need that shoulder to be able to do to get my athlete or patient back in the groove again?

Let’s just start with first looking at our inspection always when we have a shoulder injury or any extremity that you’re looking at, please appropriately disrobe the patients so we can get a good idea for confirmation of the muscle symmetry of how the muscles are getting used and we can go forward and really get a good idea of what we’re looking at. Let’s look at this particular patient here. Very interesting to notice the symmetry of the shoulders, the deltoid muscles, and the biceps. We’re going to be noticing particularly how the shoulder transmits to the kinetic chain across to the opposite Iliac crest.

I’m going to look at that pattern as we start moving forward in our rehab section. I want you to notice this particular patient right here. You might notice, pretty welded but muscularly developed; however, let’s look a little closer. I want you to take a moment. I want you to really focus on this particular inspection because you’re missing some stuff right at first glance. I want you to notice the contour of this pec muscle here and the contour of this pec muscle here. And you notice how we have kind of this little bit of a bolt here. This is a partially torn pec major that is scarred over, and if you really take the time to look at your patients and that’s why it’s so important to disrobe them appropriately and really look at what’s going on because he might not have noticed that. And so, that’s going to affect his kinetic chain here. And of course, we’re going to be looking at scaring which we see some scars here from surgical intervention, scar here from surgical intervention, scar here from surgical intervention.

So we’ve got a lot going on. So I just want to kind of stress how important it is to really get a close look. After we do our inspection, we’re going to move on to palpation. And when we start palpation, we’re going to start by looking at that symmetry and palpating both sides. When I evaluate the shoulder, I stand behind the patient, and I have both hands on the shoulders. This way, I can feel the good side, bad side. I can feel hypertrophy, atrophy. I can feel inflammation and tenderness. I can really get a good handle on what’s happening and what’s different from side to side. So, while we’ll right behind, and I’ll start my inspection with my hands on the shoulders and working down towards the biceps and the deltoids and just getting a good idea for that overall symmetry. All right, so that’s really important to start palpating structures looking for tenderness.

We’ve done our inspection, our palpation and now we’re going to go on to range of motion, really important for the shoulder. Again, I stand behind the patient, looking at forward shoulder flexion up and AB duction thumbs over your head.

This is really important because we want to notice how that glenohumeral joint is moving. We need 180 degrees in flexion and AB duction, but we need to also understand is that we need to have the quality of motion. The neuroplasticity with injury tells us one thing. It tells us that the body will cheat for motion and steal it from somewhere else. That doesn’t necessarily mean it’s a good motion. So you can’t just see somebody put their hands over their head and say that’s 180 degrees. Is that 180 degrees of quality motion? Is the glenohumeral joint doing what it’s supposed to do or is it just cheating the system and getting there a different way? So that I want you to make sure that we have the proper order of events happening with a range of motion.

All right, let’s look at the range of motion of the shoulder and forward flexion. We should have a stable scapula. The glenohumeral joint should drop down in the glenoid fossa and roll. So we should have a drop in a role in flexion. Then, if we move on to AB duction, we should notice a couple of things; With AB duction, in the first 30 degrees of AB duction, there should be no scapular motion. In the second 30 degrees of  AB duction, there should be 30 degrees of scapular motion, and that scapular motion this way with an opening up. So, first 30 degrees, nothing. Second 30 degrees, 30 degrees. Then above 90 degrees, we should get 30 more degrees. So I should get a total of 60 degrees of scapular motion, but nothing should happen inside that first

30 degrees. If we get scapula motion inside the first 30 degrees of  AB duction, you have scapular instability, and that scapulothoracic dyskinesis is something that needs to be addressed in order to have a normal glenohumeral motion of the shoulder to have a normal function of the shoulder.

So I take a lot of time obsessing over my motion. So let’s look at her AB duction here. We’re going to notice that she has pretty good scapular dynamics, but I’m going to play it again, and I want you to notice what we can pick up on this: the right shoulder is different from the left shoulder.

Did everybody see that? I want you to watch the right shoulder when she goes into AB duction. This glenohumeral joint doesn’t drop and roll as much as the left side. It kind of stays up there a little bit higher. So let’s watch again. So it’s going to be your first sign that there’s a little problem with that right shoulder. Want you to see. There. Do you see how that right side is not dropping as much as the left? Did everybody notice that? You see on the way down just a little bit higher. She’s working harder to stabilize that joint on that side.

So we’ll work through her case a little bit later, but I want to stress the importance of that scapulothoracic motion. This is a post-surgical patient that came to me. He had actually had a very large bony osteophyte excised from the inferior aspect of the humerus. So he’s had poor motion for the last 12 years, at least. So, this is after his physical therapy was completed. And after the surgery was completed, he was not satisfied with his results, and this is a left shoulder post-surgical.

We’re going to watch his motion, and I want you to see and really notice, see it forward and watch that scapula moving way too soon. Did you see that? Can you see how that just looks very different than that? He’s lost flexion, so scapular instability, watch his AB duction now.

There, you see it rolling in that first 30 degrees? That is aberrant scapulothoracic motion. That is poor scapular stability. So he’s working very hard to try to stabilize that scapula.

So that’s something that’s really huge to notice. When you’re evaluating your patients, get them in the appropriate position, let’s get a look at what’s happening? So we talked about what we do about scapulothoracic and let’s just jump right into talking about thinking outside the box sometimes. You get somebody that’s had 12 years plus of aberrant motion has completed a long-term of physical therapy with finishing looking like that, which is inadequate, I feel, and he was not satisfied. So he knew that something was wrong.

You now need to think outside the box; what’s actually happening, is that not that physical therapy did anything wrong except they didn’t teach his brain to find the muscle. That’s an important concept to think about when you’re rehabilitating somebody after an injury. Sometimes your brain just can’t tune into it. It’s lost that muscle or that control for so long, we’ve got to reintegrate that motion. So what we did first is I put him in front of a mirror so he could see what normal motion was supposed to look like. We put Russian stim on the scapular border, and as the Russian stim would come on, I would have him go through his range of motion. So now I have the kinesthetic sensation of muscle contracting and I have the visual of him looking in the mirror. So I’m working on all the senses to get that motion going. This is just sometimes you got to be a little creative to try to get things to happen.

Here it is. There’s the Russian stim kicking in, holding that scapula and place. It’s up kind of high and not super comfortable for him. But we got to get the job done, and he’s looking at that mirror and he understands what’s supposed to happen to that glenohumeral joint. How it’s supposed to drop and roll with forward flexion and drop and abduct and that scapula is supposed to stay in place with AB duction. So once he progresses and I feel as though he’s got that visual kinesthetic going, I move him to a wall slide. Again, same thing Russian stim on the scapular border. And when that stim comes on, he is supposed to raise and push against the towel activating serratus anterior, but also activating scapular stabilizers and get that range of motion. So, I’m trying to get more flexion out of him and get that scapular stability going at the same time. Just kind of some creative rehab here.

So we talked about the progression of strength. Now, this is looking better. He’s starting to motion better here. Here’s our forward flexion. Here, he’s starting to get a little bit of better scapular stabilization. It’s starting to get a little less motion in those first 30 degrees. And here’s his AB duction.

Better. Better. Okay, so he’s learning. So it took us about four months to get him retrained in scapulothoracic motion, and it’s so critical. It’s so very critical. Here’s his before and here’s his after. So we actually did really well with him. He’s super happy, full range of motion, full control. So we’ve gained that scapulothoracic repositioning and understanding that that is so important. I can’t stress that enough with shoulder rehabilitation and shoulder assessment because without that, I think that’s what was missed in his PT.

So we do something for the shoulder range of motion called Apley’s test. An Apley’s test is an easy way for us to get a concept of is somebody’s missing flexion, internal rotation of the shoulder, or flexion and external rotation of the shoulder. So we have them do this exact protocol reach across and touch the opposite shoulder. Take their hand up over their head and touch the superior angle of the scapula, take their hand behind their back, and touch the inferior angle of the scapula.

Boop, she can’t do it on that side. Remember we saw that shoulder with a little funky motion before? She did not realize she couldn’t do it. So here’s the good side. That’s the comparison. So we’re going to move on further as we assess her as we go on. But the first clue for us was that range of motion showed that aberrant humerus not dropping in that glenoid fossa.

So that’s Apley’s test.

When we do a shoulder assessment, we’re going to make sure we took off all the boxes in hitting all these muscles. These are the muscles that you need to make sure you’re assessing in every shoulder assessment. What’s very important is as you start developing your shoulder assessment, you do the same order of events for every patient and in doing that we don’t miss anything. I still do everything on every patient because sometimes I’m surprised. I might find something that I wasn’t expecting to find.

So here are the muscles that we’re going to go through today. We’re going to look at their assessment and how we find some tricks in uncovering some of these muscles. So we’re going to look at this patient here is she’s kind of a workout fanatic. Notice she has the KT tape on her left shoulder, but we found a problem with her right shoulder. We assess her, right? So what type of compensatory mechanisms is she using there?

So let’s move on and talk about special tests of the shoulder. Before we kind of jump into that and really dive deep into these special tests, let’s talk about some of the most common things that happen in the shoulder. All of us see biceps tendon apathy in our patients, right? Why is there such a huge prevalence of biceps tendinopathy? I’m going to put that little teaser out there and we’re going to come back to that later. And I want that to kind of sit and stew with you for several slides. So we get a little further along. I want you to think about the anatomy and I want you to think about that bicep here. This, right here. Here’s this biceps sheath. Here’s this transverse humeral ligament that holds that bicep tendon in the intertubercular groove. Understand that the pec major comes over and wraps over on top of this bicep tendon too. So we have layers and investments of tissue in that area and we have the bony conformation of that intertubercular groove as well.

So that’s kind of you know, thinking about that whole biceps tendon apathy, which we’re going to come back to. I just wanted to set a little teaser up there. We talked about tendinopathy in the shoulder and we understand what causes somebody to be prone to different tendinopathies. These remember to check your patient’s medications. That’s an important caveat when we see certain types of injuries, particularly ruptures of tendons, chronic tendinopathies. Checking some of the medications that you have or make somebody more prone to certain tendinopathies. We know tendon ruptures with certain antibiotics. There’s a Levaquin class action suit for spontaneous Achilles tendon ruptures. So also high levels of testosterone, you’ll get spontaneous ruptures of tendons such as bicep and pec. So we’ll see that a lot in our bodybuilders.

Understanding that we’ve got to uncover not only the what when we’re evaluating somebody but the “why”, right? Because we’re not doing somebody justice if we’re just myopically looking at the injury. We need to be able to step back and say, “Why did that injury happen?” That’s the true fix, right? That’s the true fix because you’re going to have to fix the myopic problem, but you’re going to have to fix the why also before that patient can safely return to sport.

So I want you to look at this and I want you to tell me which one you think is the injured side. So let’s see just post right in the chat who you think is our left or our right? What do we think is the injured side of this patient?

Right or left? Right is correct.

This is a ruptured bicep tendon. This is called a Popeye sign, right? That Popeye sign is when the proximal head of the long head of the bicep ruptures and rolls up, causing an increased peak. And we see that increased peak, that’s called Popeye sign. So the rupture’s up here of the long head, and it curls the muscle-up. This is his normal side. So also noticing we have a surgical intervention here too on that side, but this is the normal side. So what happens is if it’s a long head that’s ruptured, that’s non-surgical.

The surgical bicep fix at the proximal head is the short head. So they all function very nicely with the long and actually not so bad, they feel like they have a bigger bicep, right?

So me being the everlasting anatomist and staring at everybody’s body, this was one of my husband’s friends that was over at our pool a couple of weeks ago and he’s sitting there and I come home from work and he’s sitting there in the shirt talking to my husband without a shirt on. I said, “Oh, do you mind if I take a picture of you?” and he’s like, “Sure.” So he was all excited thinking that he look good and everybody always wants to be in one of my lectures that seems to be the talk and I asked him to make a muscle on both sides. Here, can everybody see what we see here?

So look at his left arm. On his left arm, we have a reverse Popeye sign. He has ruptured his distal bicep here. So we get the peak in the opposite direction. So that’s different, it’s opposite to the other one that we saw. We saw the proximal bicep was Popeye sign, this is reverse Popeyes. So he ruptured here. Alrighty? So here he was thinking is looking good and I took all the pictures and I said, “Well, you have a ruptured bicep tendon.” and he’s like, “What? What are you talking about?” So I said, If you don’t mind, I’d like to use your pictures for my lecture.” He’s like, “Sure. You could use them for your lecture at my expense.” So all for the sake of education, right?

Nobody’s safe when they’re at my house at all, especially for a pool party.

Okay, so let’s move on to the rotator cuff muscles. Four rotator cuff muscles. Supraspinatus, infraspinatus, subscapularis, and teres minor. One internal rotator, which is your subscapularis that rotates your shoulder medially. We have your supraspinatus, which is the first 15 to 30 degrees of AB duction. We have infraspinatus and teres minor, which is external rotators, but the difference with the teres minor is the job of the teres minor is external rotation but proximation of the humerus to the thoracic wall.

Okay, so understand that the teres is going to help not only with this action here, external rotation, but it’s going to hold your elbow to your side with external rotation. That’s the difference with teres minor and infraspinatus. That’s how you can tease them apart. We’re going to show you that later.

Let’s start with the most commonly torn rotator cuff muscle, that’s your supraspinatus. We’re going to see that most commonly in middle-aged females. We will see that quite frequently and athletes. Most times we get a tear out in this muscular tendonous junction, right here, or you can get a complete avulsion right here on the humeral head. The interesting thing about this here is it creates a lot of inflammation in this subacromial region. That inflammation, the subacromial region reaches a little bit of havoc which were going to talk about later. You’re presenting factors for a supraspinatus tear is that they’re going to say they can’t lift their arm away from their side or they can’t lift their arm forward. It’s too painful.

I actually just had a patient last week who came in and said she was putting on her pajama pants in bed instead of standing up and pulling up her pajama pants and she couldn’t lift her arm up. She actually tore her supraspinatus. So these type of things, it doesn’t have to be huge and traumatic. I had another very, very active athlete, multi-sport athlete, pick up a bag of Chinese food and he called me up. He says, “I can’t lift my arm anymore.” It’s not that the trauma was so big that it caused the rupture. It was the last fiber that gave way. So this was waiting to happen. So don’t always look for the big thing. Don’t always look for like the giant colossal trauma.

So here’s how we test that supraspinatus. We do it in first 15 degrees of AB duction with your arm 45 degrees forward. And 45° elevated, not at 90. You want to keep that arm down and forward. So in this range of motion here. So we’re checking that supraspinatus just right there. Only two fingers. You do not have to force that sucker down and tear. If there are any fibers left, you don’t have to tear them and you don’t need to prove how strong you are. Two fingers pressure, they just have to meet your resistance. That’s actually just plenty to check that supraspinatus. We do what we call a full can and an empty can for checking the supraspinatus and the difference is pretty important. The full can we just saw. Just two fingers right here. That’s your full can. That’s if you’re holding a can up. The empty can here is when we take that arm and we internally rotate it.

Why is that different? Because now I’m not only checking the supraspinatus. I’m rotating the humerus and I’m assessing if there’s a little bit of impingement going on as well. By impingement, I mean inflammation in the subacromial region. That’s how we’re going to tease apart an older tear versus a newer tear. If we have a newer tear, we have more inflammation. So when I roll that hand in there going to be like, “Ah, nope, that hurts.”  Even if you just roll in and they’re strong, that’s telling me there’s some impingement. That means there’s some inflammation in there. That internal rotation is a little bit of a key for you.

Let’s move on and look at the infraspinatus muscle. Very thin flat muscle, its job is external rotation of the shoulder. So kind of that winding back to throw a ball motion here. The thing about this one, if we get trigger points in this area, it refers down to the last two digits. So it’ll cause numbness, and you’ll think it’s like C7 radiculopathy, right? You’ll think we have some discogenic problem but check for trigger points down in this infraspinatus. When it gets angry, it refers down to the arm. It’s kind of a little clinical pearl there. But our presenting factors are going to be a weakness with external rotation. But what’s interesting about this muscle, the same thing as the supraspinatus is they’re not going to tell you they have pain back here up here. They’re going to tell you they have pain down their arm. Just around that deltoid tubercle area. It’s kind of interesting and we’re going to get into why that is later on. So when a patient is pointing down their arm, don’t forget to go back and look at that whole rotator cuff. Really important.

So, how are we checking that infraspinatus were assessing muscle testing external rotation. So we’re going to do that in two planes. We’re always going to start your first muscle test in a closed-packed neutral position.

That’s this with the arm down at 90/90 and then your second check will be in an open pack external rotation with the arm, less stable. So down here is going to pick a bigger tear up. Up here, a more discreet tear will get picked up. So let’s just demonstrate that neutral position. If they’re strong and okay there, then I’m going to challenge her a little bit more, and I’m going to bring her up here. Remember we’re diving into this shoulder because she showed me that poor glenohumeral motion before. So we’re going to dive into the shoulder just a little bit more and try to figure out what’s wrong with it.

We talked about the subscapularis next. So we did supraspinatus, which is the first 15 degrees of AB duction. We did infraspinatus, which is external rotation. Now we’re moving on to subscapular, your big internal rotator. It’s a big muscle. It lines the interior portion of the scapula and attaches to the anterior aspect of the humerus. So rolls that shoulder-in. They’re going to have pain and weakness with internal rotation. So the thing about the rotator cuff and the thing about rotator cuff injuries that you need to think about is it’s not always the throwing motion that causes the rotator cuff injury. It’s the eccentric load of slowing the arm down after it’s thrown or after a golf swing. The brakes that hold that humerus into the glenoid fossa. So it’s the eccentric loading of the muscles, and that’s usually causing the problem, not the release. So it’s not that concentric throw. So if we think about a throw here, that’s your subscapularis usually isn’t the problem. Usually, we have the external rotator tears with a throw because that’s your brakes. So let’s kind of really think about that function, not so much the concentric action, but the biggest load goes on the eccentric portion of the motion.

So we’re going to check the subscap. I’m going to show you some tricks for checking the subscap. We’re going to check-start with internal rotation. So for unsure in the beginning, again, starting with that closed pack position, looking at internal rotation, and then moving on to that open pack position or that unstable humerus position of internal rotation there. Making sure you’re really holding at that 90/90 angle good. So here we’re doing a little external rotation as well.

Okay, a trick. It’s called your scapular liftoff test, really great to find a subscapularis tear. It’s a little trick. So watch this on her bad side. Now, when I evaluated her she had no idea what was wrong with her shoulder. See how little she can lift that away from her back. Look at the other side. That is a positive scapular liftoff test. This is an old subscapularis tear that was not treated appropriately that healed poorly. So she has a compensatory mechanism to try to get that 180 degrees with compensation. So remember earlier, I told you that your body will cheat itself to try to get normal motion. So if we were to say she has 180 degrees fine but she has 180 degrees of faulty motion, let’s see why. So she has a subscapularis tear that’s kind of healed poorly.

So now we’re going to jump on. We didn’t talk about the teres minor. A trick to evaluate the teres minor and tease it apart from your infraspinatus is your teres minor test. It’s a little trick. You’re going to check to see that she can hold her elbow to her side as she externally rotates her arm. Remember we said the teres job was to kind of approximate that humerus to the body with external rotation. So here is your teres minor check right here. Negative. She can hold her elbow to her side nicely. Somebody that has a teres minor tear will not be able to do that. They’re going to kind of do this thing. They’re going to bring their arm out away from their body as opposed to this. Check that in particularly your middle-aged females. You’re going to see that more commonly than we want to.

Okay, I will get to questions last if that’s okay because we have a good amount of slides and I want to kind of get the role of our content.

Let’s talk next about the glenoid labrum.

The glenoid labrum is the cartilage around and inside of that glenoid fossa. So here’s what it looks like right here, kind of looks like this little ridge right here. It deepens that glenoid fossa a little more so that humerus has a little more area to kind of sink in without dislocation. So kind of deepens the cup a little bit. It actually creates a very nice continuity of the joint so the joint can glide. But what happens very frequently is we get tears of the labrum, particularly with pitchers or somebody with a throwing sport.

What happens with the labrum in this superior aspect of the labrum up here is where the long head of the bicep attaches. So that long head of the bicep comes up through the intertubercular groove and attaches right here to the superior portion of the labrum. So when you get a labral tear, what we call a SLAP tear right here. A SLAP tear is a tear that’s between 10 o’clock and 2 o’clock if we were to look at the labrum as a clock or look at this glenoid fossa as a clock. If I get a tear between ten and two, that’s called a SLAP tear. The problem with the SLAP tear is your bicep tendon attaches up there. So every time you use your bicep, it pulls on that tear and makes it worse.

The very interesting kind of caveat with that is when we have baseball players. We almost want them to have a SLAP tear, particularly high-level baseball players. Because with a SLAP tear without pain, they have increased range of motion and external rotation. With increased range of motion and external rotation, what does that tell you that we have? So if I have normally this much external rotation, but if I have a SLAP tear, I can go here, I have a bigger range of motion to increase my overall velocity for throwing. So what actually happens with somebody that is a SLAP tear that doesn’t have pain, I am going to make sure I’m clear on that, they have increased range of motion therefore greater velocity of their throw.

So when we’re evaluating athletes for high-level sport and for consideration for pro teams, they almost want to see that SLAP tear without pain. Kind of an interesting note, a Bankart tear is a tear that’s between two o’clock and six o’clock as we look at that clock. I’ll show you a picture of this. So that’s a little bit different, that’s not going to affect the bicep. So here’s the difference between your SLAP tear right between ten and two at the top. Where your bicep tendon coming in and attaching right up here. And here’s your Bankart tear down here and that’s going to cause some pain with rotational motion.

Here’s how we test the labrum. We do something called the Grind test. Pretty much you’re just pushing it as you bring that elbow out to that 90-degree mark. You’re pushing that humerus into the glenoid fossa, your circumducting to try to agitate the labrum. You’re looking for a noxious stimulus. So you’re looking for the patient to say., “Yeah, that hurts.” Just like most of the Orthopedic tests. So there’s the Grind test using compression and circumduction.

So we talked about this subacromial impingement and I want to just kind of take a breath here for a moment. And I want to emphasize impingement or inflammation in the subacromial region because it is the number one complaint for shoulders. Just like patella-femoral maltracking is the number one complaint for knees. If you want to really own something in the upper extremity, it’s this condition in particular. You really want to be super familiar with it because it is very common. A lot of patients will present with it. Now that you’re kind of aware of it, you know how to assess it after today. You’re going to say, “Oh, boy, a ton of people have this.”

I want to talk about it. Impingement means that under the subacromial roof, here’s your acromion, under the roof of the acromion, there is not enough room for the infraspinatus, the supraspinatus, and the structures. This is your coracoacromial ligament here, causing the anterior portion of the roof. There’s not enough room for them to cohabitate. When we have weakness of certain muscles, particularly the serratus anterior, which is super common after a certain age is one of those muscles that just degenerates. We get a rise of the humerus in the glenoid fossa. Weakness of the serratus anterior,  I’m going to say it again. Weakness of the serratus anterior takes your humerus and rides it superiorly. So now we have less room in that subacromial region with a weakness of that serratus anterior.

So if my humeral head is riding superiorly, I have less room for my supraspinatus to exit, less room for my infraspinatus to come around, and less room for my bicep. Since this is such a very large area for inflammation to begin with. Now, we move on to aging degeneration, compensatory mechanisms, and we have a whole host of problems. So impingement could mean a myriad of things gone wrong. It doesn’t have to be one thing, it’s not just meaning in supraspinatus too. It could mean that you have spurs on the inferior aspect of the acromion which is uncommon. It could mean that you have what we call a Type 3 acromion, which these acromion shapes are different. A type one is a flat shape like this. A type 2 is a little bit beaked and type 3 is curved down so that we have less room in that subacromial space.

So with that weakness of the serratus anterior and a Type 3 acromion impingement syndrome is inevitable with age unless you really are diligent in your exercise routine, corrective exercises. So the trick with this is with impingement syndrome, what happens is you get inflammation in the subacromial region and where does it go? Imagine that this intertubercular groove and this bicep tendon in the sheath around the bicep is the gutter system for that inflammation to drop down into.

That’s most frequently why we’ve seen so much bicep tendonitis. That is precisely why when you see bicep tendonitis, you need to go back and look at the whole rotator cuff because there’s something else going on. It’s a sign of something bigger because most times, that’s an accumulation of inflammatory modulators that have dropped down that gutter system of that intertubercular groove in the biceps tendon and sheath and kind of sat in there because it got stuck. We have that transverse humeral ligament as we talked about, we have the pec major investing over that and holding that inflammation in that area, bathing that tendon in those inflammatory modulators would actually degenerate the tendon.

So kind of thinking about that bicep tendon and think about how you might treat that myopically. But again, the why and what else you need to treat to truly get the bicep tendon better.

So testing for impingement syndrome, we want to tease apart. Are we talking about subacromial impingement or coracoacromial impingement? To different areas, we can have impingement. So subacromial, we talked about here, but coracoacromial is very common as well. So we’re going to tease those apart by doing this rotational test here. We’re going to take the arm and internally rotate it that bring it across the body and one more time.

They’re going to say, “Yes, that hurts.” here in this position for subacromial impingement. When you bring it a little bit further, now we’re doing subacromial and coracoacromial. All the way over is coracoacromial impingement. This way we are going to treat those very differently. So we’re not going to treat the subacromial region if it’s a coracoacromial impingement.

So we need to really understand what we’re treating so we can apply effective treatment to an area. So, that’s your impingement tests. Per site is pretty straightforward. We have many bursa that can appear in the shoulder. And understand that a bursa is an inflammation. Bursitis is inflammation of the bursa in an aberrant way due to aberrant friction most times between a bone and a tendon. So the bursa will enlarge when we have too much friction, and it does that as a protective mechanism. But when that Bursa gets too large it actually causes more friction in the area. So kind of a catch 22 where it kind of defeats itself.

So most times we’ll see what the patient is this subacromial bursitis, it’ll be right here in the anterior shoulder and we call that Dawbarn’s push-button test, and that’s what I start with again when I talked about at the beginning of the lecture. I put my hands on the patient’s shoulders right from the back and I’m feeling if they’ve got a bursa inflamed right out of the bat. Then I’m going down and seeing if they have biceps tendonitis. That’s my first two things because then I know I’ve got to look at other stuff because if I’m seeing bursitis, there’s friction there, again, why is there friction, right? We’ve got to go to that, why. I can’t stress that. You can’t hammer that home enough.

We talked about that coracoacromial impingement. I just wanted to show you the mechanism here. So we can have impingement because the pec minor is inflamed or the short head of the biceps tendon or the coracobrachialis.

Or we could have this coracoacromial ligament causing inflammation here. If we have inflammation of bursitis in this area and this coracoacromial ligament is here, that would cause a coracoacromial impingement.

So going back and thinking of anatomy and then applying the anatomy functionally and then applying the anatomy into how that person is using it or needs to use it. So step three, step process to that.

Here’s that Dawbarn’s push-button test which I told you about. Just getting behind the patient and feeling. And here’s an example of what that Bursa looks like when it’s inflamed, and it actually causes more impingement, right? Because now we have zero room for that subacromial region in that anterior aspect of the shoulder.

Let’s move on. Let’s talk about an AC joint sprain or acromioclavicular joint sprain. We call that a shoulder separation. A shoulder separation is a sprain of this joint up here, which is your acromioclavicular. A shoulder dislocation is a dislocation of the glenohumeral joint. They’re two different things, separation is the AC joint and dislocation is the glenohumeral joint. Very important we understand this difference. We have a severity of 1, 2, 3 for AC joint sprains. Understand that there are three ligaments that comprise holding this integrity or this alignment of this acromioclavicular joint. What actually happens is when they sprain, we get separation of that joint a little bit and it looks like this.

So when we have a type one, we have the acromioclavicular ligament that gets disrupted and we get just a little bump and a little swelling. When we have type two, we have a greater tear of that acromioclavicular ligament and then disruption of your coracoclavicular ligaments. We have two branches of the coracoclavicular ligament; your conoid and your trapezoid. This is your acromioclavicular ligament and this is your coracoacromial ligament. I should really get some type of award for being able to say all that without getting tongue twisted. Okay. And a Type 3 is greater. So how you’re going to differentiate this when you’re looking at a patient the shoulder separation is you’re going to see how springy that is. You’re going to actually palpate the distal end of the clavicle. You’re going to push down, and it’s going to spring, but you’re going to see the deformity. You’re going to see that deformity there. We need to understand that that’s a little bit different than a shoulder dislocation.

When we get into the live class, we’re going to talk about how to tape for an AC joint and how to treat it as well too. So a dislocation we talked about is a separation of the glenohumeral joint. Most commonly with a dislocation, that humerus is going to pop anteriorly. All right? They’re just not the same protective mechanisms and structures and anatomically in the anterior capsule so that joint can more easily pop forward. Testing for dislocation, it’s caused an apprehension sign and you’re going to take the arm of the patient. You’re going to bring it up and out here and they’re going to say, “Nope. I’m not going to do that.” That’s apprehension because they’re going to feel it’s going to pop out again. They’re not going to let you get back here. If they’re feeling like they don’t want you to get back there. Don’t push it because you don’t want to pop the shoulder out, right? Either. So that’s called an apprehension test.

We can also get dislocations inferiorly and posteriorly as well. Just not as common as an anterior dislocation. A shoulder dislocation here’s your biggest clue right here. Nice rounded deltoid on the good side. Do you see the sharp step off? Here’s your acromion. That humerus is drop-down below the glenoid fossa. That’s why we get this drop-off. That’s how you’re going to be able to tell your patient has a dislocation. It’s going to be that shelf. And that’s pretty obvious for any dislocation on x-ray, it looks like this. This is an anterior dislocation. So we’re not really truly appreciating it as much as we could if we had a lateral view.

Let’s talk a little bit about rehabilitation considerations. We want to talk about what’s your plan? We talked about a lot of conditions. We went through the rotator cuff. We went through AC joint separation, dislocation, tendinopathies, what’s your treatment plan? We have to think first in the same order for almost every condition that we treat extremity-wise.

Your first order of business is to decrease local inflammation. We can’t get anything done without getting rid of inflammation. Give it a couple of days to get rid of that inflammation, and get your patient on board with you. Make a team effort out of getting better. This, I notice actually catapults their recovery much quicker because now they’re part of your team as opposed to going out and throwing a hundred balls a day and they’re not on your team.

So, I’ll have this talk with the patient that does that I say, “Listen, we’re in a fight right now because I’m trying to get you better and you’re inflaming, and every time we put inflammation back into the area, takes 72 hours for that inflammation to peak and two weeks to evacuate the area. So every time you re-inflame something, you’re putting yourself two weeks and three days behind.” So give that little bit of education to your patient so they’re like, “Oh, crap. I don’t want to do that. I want to keep moving forward.” So better to move forward in small increments than to do a giant leap forward and go way backward.

So keeping that inflammation out of the area. Passive range of motion is always where you’re going to go next. So, you’re going to put the patient through a passive range of motion trying to work on quality synchronization of the motion. We talked about that in this particular athlete here who is doing the aberrant AB duction. That’s how we detected the subscapularis tear with her. We need to start getting quality motion. Making sure we’re looking at the motion of the glenohumeral joint. Is the joint itself or chiropractors, right? Let’s not forget about is the joint itself sitting superiorly? Do we have good motion? Do we have motion in superior, and inferior? Do we have medial-lateral glide?

We’ve got to check these things on a humerus because maybe it’s just an old injury that now we have a tight capsule so that we can mobilize, we can adjust the shoulder, some great results with adjusting the shoulder on this. So, making sure you’re challenging the joints, and then getting that passive motion going, then we move into active motion. We saw me doing this with the scapular dyskinesis, right? We have him actively raising his arm and lowering his arm against the wall. Even if we need assistance, we need quality active motion next then we’re ready for strength. If we do strength too soon, you’re cementing in the problem and you will never get rid of it. They need to have quality motion first before you can add the strength.

Otherwise, you will never unpeel the injury. You’re just kind of loading it back in there. And as you’re adding strength, you’re gradually and systematically increasing load and repetitions. That’s our newest research out of Jill Cook’s research on tendinopathy, and tendon healing is you want to gradually increase that load. We know a lot of tendinopathies are actually a degenerative process of the tendon and the tendon undergoes a necrotic state, where it actually is losing blood flow to the area. So we need to think about increasing blood flow to the area. So that motion is actually good but we need to slowly load the tendon again. So the tendon itself can hypertrophy with injury and disuse just as muscle a tendon atrophies as well.

We need to grab that concept and think about re-educating strength and ability to function with that tendon. So we need to load it very incrementally. So we can gain the hypertrophy of the tendon as well as the muscle. Okay, so that’s a really important concept to grab.

So if we want to talk about our athletes how we’re going to get them to perform better. That’s always my thing is I want them to go back to sport better than they were before they got injured. Those are the things we need to look at. We need to look at the ‘why’, not just myopically slap some stim pads on them, do some scraping, adjust them, and send them back. We’ve got to look at the bigger picture here. That separates the average doctor from the elite doctor. So just take a little extra time, a couple of extra tests that we went through today. And now your level is much higher. You’re performing better so that that athlete can perform better.

Again, what we’re going to do is we’re going to think about getting that stability in the shoulder. We’re going to think about getting flexibility, normal motion, and then gradually increasing that load. Very important to think that we’re adding in sports-specific drills as early as possible into the rehab process. So here’s where the creativity of rehab comes into play. What type of athlete do I have? What do I need to bring to the table for my athlete? What motions are going to help that athlete achieve their overall goal? What type of sport is it? Is it a javelin player? Is it a baseball player? Is it somebody that’s an American football player? What did they need to do?

So thinking about that and introducing them, I typically will have my tennis players bring their tennis racket into the office and show me their swing. So I can look at their technique and I add rehab on with their tennis racket in their hand, because if that’s what they need to do, I need to get them to do that early on in their rehab. We’re looking at this graded return right here. This is Jill Cook’s research, talking about tendon injury. You’ll want to start with isometrics, then increase strength and then functional strength and then moving on to speed and then, of course, like plyometrics too. Increase in tendon load, intensity volume, and frequency. All right, really important in that order. I love this picture right here. If we look at these athletes that are in this training drill right here, we can kind of see so many things. I’m huge on game analysis and I’m huge on kind of videotaping my athletes and getting a look at their motion and their aberrant motion and their faulty motion. And we really can kind of pick up this quality of motion, increased flexion of the hip open up of what we call ‘Triple extension’ here. Good angle up here with the shoulder good formation.

Can you see how this athlete here is just kind of lost her overall conformation? See how this athlete has it together. She’s got good trunk control. She’s got good pelvic controls. She got good arm control. Can you see she’s kind of just all over the place here? She doesn’t have that opening up of her leg as much. Her arms are uneven, her shoulders are twisted. We don’t have good core strength.

There’s no surprise to me that she’s last in this race right here. So kind of really get in the habit of staring at people and getting an idea of movement and quality motion and why things are happening. It’s if you’re working with active people, we need to be tuned into noticing motion and movement in the body. Understanding that past injuries change function. So is that acceptable or unacceptable? We might have an injury where it is changed, let’s say we’ve had a fracture and the angle of the bone is different. I can’t change that. So I might have to cheat the system in rehabilitation.

What strength changes have happened from past injuries? How has the body compensated? Do I need to unpeel that or do I need to work with it? Do I have an aberrant range of motion? Can I not get a range of motion back now post-surgically, possibly? So if somebody had a surgical intervention like a rotator cuff repair, they’ve lost external rotation. So what do I need to do differently to have them recover? So taking the past injury and how that changes function is also super important as we consider accessing injuries and rehabilitating.

And lastly, as we start winding down this lecture. Make the functional change. Understand that just doing some scraping is really great and some taping is really great but we need to functionally improve that person. Get them the right muscles facilitated and inhibited. And understand that an inhibited muscle doesn’t mean it’s weak. It just means the brains not finding it. We’ll talk a lot about we go through this in your hands-on module.

We’re going to talk about kinetic chain and how we can facilitate inhibited muscles, but if you notice somebody has a really weak muscle, I want you to look at the antagonistic group because most times that’s over-facilitated. So we almost need to shut down the antagonist to turn on the agonist. So just think about looking at things that way.

QUESTIONS
Questions from the live recording.

1. Why do we not do the supraspinatus press test at 90°? Supraspinatus press test?
   Supraspinatus is tested the first 15 to 30 degrees of AB duction. You don’t check it up here if you’re going to be using the deltoid too much. Is that what you’re asking?
2. Why does that supraspinatus happen more in older women?
   Oh, that’s a great question. I love that question. I’m going to tell you why. Women have 50% less muscle mass in their upper body than men. That’s number one. So what we noticed for women when we look at the supraspinatus, it’s really atrophied and think about the fraying of the muscle that happens over time and it deteriorates. So they don’t have a good fabric of that muscle, to begin with. So we see that fail more frequently in women. The interesting thing is we see that muscle re-rupture post-surgically most commonly in middle-aged women.
3. Can you repeat the pain referral to the digits of the infraspinatus?
   Oh, that’s a good one. Infraspinatus will refer down the medial aspect of the arm to the pinky and sometimes the fourth, the ring finger when it’s really bad. But when they tell you they have numbness down to their pinky, and you’re going to look at the neck. We’re going to rule out discogenic but don’t forget to look at that Infraspinous because we have that suprascapular nerve in there that can get impinged.
4. Trigger point referral down the lower pane in the deltoid tubercle, up not back at the shoulder.
   Okay, so pain down in the deltoid tubercle tells us a little to go back and look at that rotator cuff because most times when someone has a supraspinatus tear, they have this weird referral pattern down to the distal arm. So everybody’s treating this distal arm, and they’re not paying attention to where it’s coming from. Again, I think it comes into play with that inflammation coming down that intertubercular groove or down the shoulder, just like we get dependent edema.
5. Not sure how the serratus anterior helps keep the humeral head down. Oh, great.
   The function of the supraspinatus is kind of like inferior scapular stabilisation. So when we have inferior scapular stabilisation that pulls those scapulas down and out which pulls the humerus down as well. So it’s inferior scapular stabilisers. All right? That’s serratus anterior is so critical for shoulder motion and postural awareness too. I pretty much put almost all my patients on a serratus anterior recovery.

[END]

 

FICS ICSC Upper Extremity Assessment: Wrist, Hand and Finger

 Hello and welcome to this next part of your ICSC seminar on the elbow, wrist, and hand. my name is Dr. Henry Pollard.

So as a part of my background with FICS, I have been a long time lecturer with FICS for about 20 years now, and I also I am on the education committee, and also, Chair of the Research Committee. So the course objectives are there for you to read about. we have got a lot to get through in a short amount of time, so you can have a read about that at a later time. I will, however, acknowledge that this course is for educational purposes, and I acknowledge that the pictures and the videos used in the presentation are owned by their respective copyright owners, and I strongly encourage you to seek out these vendors because they’ve got some great material that can assist your learning.

So, before we actually get into looking at some of the injuries of the elbow, wrist, and hand, and also some of the key examinations, I think there are some concepts that we probably ought to cover now. A lot of these concepts will be covered by other lectures, as well. So, I am going to go over a couple of them very quickly knowing that lower body assessments are going to go be covered in great detail, and a lot of the shoulder assessments which are very relevant for elbow, wrist, and hand are also going to be covered by Dr. Foss.

When considering all this, just general rules of operation I like to move from a central. So, from a spine to the extremity peripheral in the direction of my examination, golden rule of extremities is always examined bilaterally. As a general rule, patients like it if you check out the area that they’re complaining about first, and then, roll through your entire routine. Now, that routine should look at functional assessments, whole body screens, the FMS, and other assessments, a spinal assessment, as well as then the extremity itself.

With regard to that, you inspect, look, feel, and move. This will include palpation and MOPAL which we covered by other lecturers during this course including range of motion and muscle testing. Then, we follow through various stress testing and orthopedic tests which will cover a little bit more today as well as, some neuro, and with the upper and lower limb, particularly upper limb, there are a lot of neuro-type conditions.  I have had the truncate how much we go through because we haven’t got that much time. I have just talked about the really common ones, but you really need to know your neuro for upper limb peripheral neuropathies. And then, after that, there are some special tests and then referral and performance testing which comes into play as well.

So, moving right along, one of the key concepts, I think that you will hear time and time again from the sports chiropractors is that you’ve got to look at the whole body. Now, elbow injuries are incredibly common in pictures for a few reasons that we will talk about shortly but have a look at how dynamic that movement is. There is movement coming from all over the body, particularly hips, and spine, and shoulder. And these things must be looked at when you are looking at, particularly, overuse injuries, of the elbow, for example and to a lesser extent, the wrist. So that should be a part of your assessment. Once upon a time, a lot of these assessments were really in the realm of the coach where they assess motor function, and strength, and things of this nature, but increasingly good practitioners look at these things as well, and not just the straight orthopedic and neuro testing.

Another concept which is Michael Boyle’s concept of the joint by joint approach. This is a concept where alternating areas of the body have a tendency towards getting stiff or loose and that alternates all the way from the ground up to the cervical spine and that is located there. The idea being here is that, sometimes, pain may be located at a particular location, but the loads that are acting on those tissues to cause the pain in the first place, maybe coming from elsewhere, and so, it is a good idea to have a concept that, you know, for example, the thoracic spine has a tendency to become very stiff and mobility is an issue that you need to chase there because if you don’t have the mobility there, that mobility will be thrown off into other areas such as the shoulder or the elbow. These are important overall concepts that you might want to consider as a part of your assessment.

Another one here is again from another coach strength specialist Mike Reinhold, has suggested that when we are looking at this whole chain of events, the kinetic chain that probably the biggest impact is going to be on the joints, either side of the main area. So, for example, thoracic spine is directly relevant for the shoulder, shoulders directly relevant for the way the elbow works, et cetera, et cetera. So, as a concept, that is another one to bring into play.

Now, Tom Myers with his fantastic work on anatomy trains, I think this is something if you have not encountered this sort of work, you really need to get a copy of this textbook, which, I think, is now gone into a third edition, which- that is the second up there. it is really important. Now, this is essentially, together with the posterior line and the functional lines, really do connect the lower body to the upper body. And as you can see there through the spiral line, you’ve got the contralateral hip connecting the shoulder function through the scapula on the homolateral side. And so, straight away, the transfer of power, and in rotation, again, think the pitch and how much the hips contribute to the power that gets translated up into the shoulder, and then the extremity. This is how it happens, and so, it is an important concept to know that, and then, to have a look at, well, we may need to look at the hip flexors. We may need to look at the external you know, obliques and the serratus anterior, because they might have a lot to do with the way the shoulder is functioning either more or less than it should, and then how that may then be translated further down the outline. So, they have an effect on how the scapula works. And then, the scapular is also governed by the superficial and deep arm lines. And so, this is an idea where, again a series of muscles, transmit forces from the spine, posteriorly down to the hand, and also, occurs anteriorly as depicted in those pictures.

When we are using techniques such as IRT or instrument-assisted work factor, things of that nature, you know, we will look at all of this and we will take the arm into functional positions to apply techniques. We can also do that as an assessment point to reproduce pain as well. So, conceptually, these are important things, I think, that give you a reason why, pain and inflammation tends to happen in the locations that it does. And so, it is something that we should consider as a part of our management.

Here’s an example of a nicely dissected superficial posterior arm line and how the trapezius connects to the deltoid and the deltoid through the intramuscular septum and that vents into the extensors of the forearm, which then, ultimately, got it down into the fingers. So, this is a continuous structure. I know that as I learned anatomy, these are all described as discrete structures that there was no continuous connection, but it stands to reason, and you can determine this as soon as you try to do a stretch that the overall function is limited by tight muscles within it.

When we look at this diagram, just to the right here, we will see the traditional model where you have an origin and an insertion into the bone. But where it differs and where, I think, Tom Myers has brought this idea of fascial planes is that some of this content does not attach into the bone and just is continuous with the next set of muscles. So, what we end up having is an anchoring point forces, but we also have an ability to then distribute forces as well through an entire plane of movement. It makes sense that this is a protective mechanism, so we can help the distribute forces rather than have them overload a particular spot. I really like this simple little diagram here, because it describes a lot and it really does describe a lot of advances that have occurred in the last 30 years in terms of the concepts of why we get some of the injuries we get.

So, these kinetic chain concepts, once again, I have listed here from the big toe, all the way up through to the neck, a whole series of areas that are worth looking at. the various lectures will spend more time going through that. I will not go over that today other than to note them there for you to have a look at.

Here’s an example of a test which begins to look at all of this. As a couple of sports chiros Dr. Nelson and Dr. Henry, are from Melbourne, and what you will see here is this, particularly on this right side here, this flexion or inability to extend this arm up through here, slightly increase thoracic curvature through here, but also notice that there are a difference in the leg length here, that this is elongated on that side which tends to load, and, again, think the transmission of all the forces here. So, there is some, certainly, some problems here, and within the thoracic spine.

So, these are just areas you might like to look at, but clearly, if this person needs to get up to this higher level this immobility here is one way to show in a functional way the limitations that are involved because you might be able to do this in a sitting position and you have full range of motion, but when the entire system is engaged, then you may see some shortcomings in the overall movement. So, it is probably a good idea, if that occurs, that you then, treat it in those functional positions, which is an important concept, I think that sports chiropractors need to embrace.

Here is an example, here again, of a more functional thing. What you will see here is an increase thoracic curve, very much reduced external rotation. Have a look at how much wrist extension is occurring here because of a lack of range of motion here at the shoulder. As opposed to our picture over here, he has got an extensive amount of external rotation at the shoulder and a much more relaxed wrist posturing. The loading that would go on in these muscles would, obviously be a lot more advantageous because this is mid-range loading. Where over here, we now have a lot in range loading, so there’d be a lot more of a pool going on the medial aspect of the elbow here, simply because there are a loss of external rotation in the shoulder. So, these are the sorts of analyses that you should familiarize yourself with and practice whenever you can.

So, there are various functional movement screens that are available now. And once again, these describe all the basic functions of life essentially. The trick here with these things is to look for symmetry left to right. So, if we draw a line up the middle here, there are left equal, right? Or if that leg rotates a little further one side, do we get a change in the opposite lane, which we often do to balance. There is this proprioceptive feedback here. There is vestibular feedback that comes into play here, and so we need to analyse all of this. We often look at injuries from largely, a sort of a hardware perspective, if you know what I mean, where there are just broken tissues, or there are inflamed tissues, but sometimes it is the software. So, it is the integration of the movements and things of that nature and I think that is where more the functional neurology side of things tends to come on and something I think we are going to be hearing a lot more about in years to come.

So, here is another example. I am sure Pete Garbutt, and a few others will talk about this a lot in their assessments, but, you know, something like an overhead squat. If someone has an inability to come down into a full squat, their ability to get their arm vertical then becomes a real problem, so they can overload a shoulder simply because areas lower down is not doing what they are doing. If we draw a line straight up and down the frontal plane here, we can see that this ankle here is pronating and somewhat externally rotating. We got a lot more valgus going on here compared to here, but that marries to a lot less abduction over on the opposite limb. So, this is out this way, so this has to go out this way to balance and so that can then create changes in the opposite shoulder. It is for these reasons that we need to look at the whole person and not just the painful spot.

As I mentioned earlier, we can look at the range of motion issues, we could look at tightness issues, we can look at strengthening issue and then more functional issue. All of these really a good sports chiropractor should be looking at those and there are some issues there for you to review. Now, we will talk about the idea of weakness and relative weakness. Now, weakness is not something you are going to often see in athletes just frank weakness. You will see that more in your non-athletic population. But you will see relative weakness where one particular movement or function is not as good as opposing functions. Now, this really shows up, because if a muscle is less strong than it needs to be, it tends to go into spasm to create enough force to do what it needs to do about a joint.

In addition to that, there are the whole concept of eccentric loading. So, if we go back to that lack of shoulder external rotation, and then you get an eccentric increased eccentric loading with a lag on the elbow flexors and it is well known that the eccentric loading is associated with injuries. I have a few references there for you to have a look at in that regard. Now, not only is it more likely that you are going to get an injury with an eccentric loading. So, for example, hamstrings eccentric loading, low back pain eccentric loading inflection, whiplash injuries eccentric loading infraction and extension. Rotator cuff injuries eccentric loading at the point of the catch or in the follow-through. There is a real thing there, and there are reasons for that, you know, you tend to recruit fewer muscle fibers with eccentric loading and as a result of that we end up having increased injury potential. It is worth noting well of these things have some relative weaknesses or not, because they do contribute to injuries.

The management is also about exercise therapy as well and particularly eccentric loading and eccentric loading exercises have been known to be useful, for common extensor tendonopathies of the flexors and the extensors at the elbow and I have thrown a few references there for you to show that the concept of doing manipulative work plus exercise is better than exercise alone, and that is you know particularly adding C and thoracic spine therapies onto concentric and eccentric scheduling, which is probably what most practitioners do in the chiropractic world, but not necessarily outside of it as much. It is something that I think that we need a lot more research on because I believe it will show some good things in the future. But that is hopefully a few of you might move into research in time.

Let us now come into the actual injuries a little bit. So, starting with the elbow as with all things, one thing I will say before we get into this is that elbow, the further you go out in the extremities, I think you got an increased likelihood of fractures and dislocations that occur. Whilst that is not really the scope of practice for a lot of practitioners, it is certainly is for those that are involving combat sports and those that are involving collision sports. All your football codes, MMA, UFC, your Jiu-Jitsu, all of these things target elbows, your wrist locks, elbow locks armbars, all this sort of stuff, and then there are the ball injuries as well, which can cause a lot of wrist and finger injuries as well.

The types of injuries you get a little bit different than what you would expect that as a shoulder where you get a lot more, avulsions, you get primarily things like impingements and tendon issues, so slightly different set of conditions but it is worth noting. As with all areas you observe, if you are in one of these combat sports or high-velocity sports, collision sports, you have the potential for fractions and so you have to look at that. Look for traces. Look at the deformity. Are they moving? Are they not? Always check the whole body and always check bilaterally.

One thing as a concept that I will say about the elbow, is that on the medial side, injury tends to be traction-based, so they are stretch injuries. Now, there is also the ulnar nerve there as well, so that can also come into play and be irritated. You can get on your neuropathies quite readily from injuries of that area. Now, on the lateral side, things tend to be more a compression-based mechanism, so for that, in the younger folk, you get OCD which can spawn loose bodies, which can lock up joints, and road joint surfaces, but you can also get radial neck and head fractures as well. Then when we look at the posterior aspect, and so, we are talking about the electron on foster and the articulation there, we can get stretch factors. We can also get shear-based injuries which can lead to tricep tendonitis and things of that nature in a chronic sense.

One thing we do get a little bit of particularly in the weightlifting crowd bicep ruptures. The most common bicep fracture is the proximal end which gives you the Popeye deformity, but you will also get some distal bicep ruptures. And the best way to test for that is to look for the hook test. I have got one here, where it is not a rupture, but I will show you the process, so here we go.

Watch Video: I want you to look at his hand then what you do is you take this index finger, you bring it right in here and you can see where I am hooking that right around the distal biceps tendon. If he had a distal bicep rupture, it is very difficult to find that tendon in to get to be able to hook your finger behind it. As you can see, I have got a really nice hold on Brian’s here.

Dr. Pollard: It is quite easy to find that tendon if you ask them to load it you will just pick it. There is a nice thick tendon there, which is about the size of your thumb. In a lot of people, maybe a little smaller. But if it is not easy to find and they have talked about a mechanism, you know, the last one I saw was a fellow who did not quite park his car in the garage far enough and brand-new Lexus and the garage door came down and he tried to stop it by holding it up, and he blew his bicep doing that. Not a common injury, but one you might want to consider.

As I mentioned, three nerves pass through the upper limb and I am not going to go into a lot of detail about this, because this is a lecture all by itself. but we have got the ulnar nerve which is associated with the stress-based injuries, and the common flexor group, of the elbow. Then you’ve got the median nerve, which is can also be associated with the pronator, but obviously, then carpal tunnel. And then you have got the radial nerve, which can be compression injury higher up around, the arcade of froze in between muscles and coming over the radial head and then over a Wartenberg syndrome down into the thumb, and in the first couple of fingers. There are multiple compression points in the arm, and, with the overuse injuries that tend to occur in the forearm and hand it is something that I think that you probably want to school up on a little bit moving forward.

One of the ways to do that, which we will not go through today, but I will just bring it to your attention, is the upper limb tension tests that describe how they’re all done, or I suggest that you go and have a look at the physio tutors. They have got some great videos on how to do all of that. So, make your way to their website and have a look at that.

When it comes to the ulnar nerve, as with all nerve injuries you probably want to start out by mapping the exact location of the sensations, and so they could be pain, pins, and needles, numbness, or if it is associated with motor weakness. These things are all present. Generally speaking, you are more likely to incur just pain and pins and needles, before they start becoming more serious. It is something you want to jump on quite quickly you know, tapping on the area of the nerve. You need to have an idea of where the nerve runs. The cubital tunnel is a classic one for the ulnar nerve as well as the down a guidance tunnel down in the wrist, the two compression points. Pitchers get a lot of ulnar nerve type issues at the elbow, cyclists get a lot of issues, maybe golfers get a lot of issues at the wrist, so there are various tests that you can do for all of that which are located there, but I will point one out for you, which is here, which is the ulnar nerve scratch collapse test. let us have a listen.

Watch Video: So, the way you test this is you assess external rotation strength. I want you to hold right here. Give me everything you have got. Do not let me push it in. Hold, hold, hold, hold, hold. Good.

Then you scratch the area of suspicion. Hold again. Hold, hold, hold, hold, hold.

 

Notice he has weakness there. So, that would be considered a positive scratch collapse test. You can see that happened with the carpal tunnel and other areas where you suspect nerve compression and they will develop some weakness on the second go around. It is not just weakness because he is tired from the first one, but it really kind of gave out, did not like you have you think about it, but it is just not there. That is called a scratch collapse test.

Dr. Pollard: So, this is an inhibition-based test. It is got some good statistics to support it, so I encourage you to practice that test. That common elbow injuries are the epicondylopathies or epicondylalgia which is the old tennis and golfers elbows. On the lateral side, we have got the so-called tennis elbow or lateral epicondylopathy if it is a chronic thing. Most of this test is quite a few variants, but essentially they palpate the origin of extensor carpi radialis longus and brevis on the supracondylar ridge and over radial head. You palpate that painful and then you muscle test those muscles with wrist extension or long finger extension and third finger. Either way, you get a reproduction of symptoms, and you have a positive test. Now, moving and the same thing applies to flexion as well, so, you are doing the same type of testing there as well.

We will move on now to injuries which are a little bit more serious and, on the medial side at least common and this is collateral so ulnar collateral ligaments at the elbow and then the radial on the on the lateral side. This is where the concept for stretch based injuries comes into play, and so it is quite common for those that have got restricted shoulder function, that are doing a lot of pitching, tennis serves, even swimming, you know, archery. There is a whole bunch of things where you need a good external rotation of the shoulder. If you do not have it or you have developed good, which is going to humeral internal rotation deficiencies. You can end up with these problems where forces are increased at the elbow and then the elbow begins to break down under the load.

One thing with testing collateral ligaments is a golden rule regardless of whether they are in the elbow, in the hand, in the knee, wherever. You test in two positions, you test in at zero degrees, or in full extension and then somewhere between 20 and 30 degrees, so always test both positions. So, that is an important point moving forward. Now, this one has a slightly different story. This one now we are talking about elbow instability and this can occur very much so in traumas, but on the medial side, it can also happen as a part of repetitive injury to the elbow and it is the sort of thing that Tommy John operation is used for in pitchers, and it is the one of the reasons why particularly in the younger pitchers, they limit the amount of pitching that they are able to do. That being the case it can be quite difficult to do this with the pain remaining because the patient tends not to relax. Just focus here for me, around this area here and have a look at the movement albeit subtle.

So, this movement is analogous to the pivot shift maneuver at the knee. It is a subtle movement, but you will see that that large movement that occurs. Now, in the instability phase, there is a continuum between this and then in the acute scenario, say for someone like a, you know, an armbar with the UFC maneuver where actual frank posterolateral dislocations can occur. That is just gone significantly further past instability to just frank, you know, instability. One is an elongated ligament whereas the other one is a torn ligament. So, not that these things are going to probably walk into your office too often, certainly not the UFC based injury, you would have to be on the spot, usually, they go to the hospital, but some of these overuse ones here whether there is some instability through ligament lengthening and chronic injury. Those you will see particularly if you have got anything to do with baseball pitchers and the like.

Fractures do occur and so as a general rule, obviously, a traumatic background is usually there. It tends to happen more in people older than 55 although it does happen in sport as well. You generally ask people to walk four steps, that will show if there is anything in the lower limb. But also, what happens is that people have an upper limb, they will carry and protect the limb that is involved. You will see changes in posture around the deficit. Look at the area for the darkness, bruising etc. As a general rule, ask them if they can move first, if they cannot, light palpation and then percuss, not at the suspected site, but away from the site and you also apply a squeeze test away from the site and then you look for the reproduction of pain at the site. Once all that is done, and you have an idea of what is going on, you can add resisted isometric contractions as well and you will find that they will be voluntarily limited and range of motion obviously, limited. So, there are a couple of meetings there for you to see and examine of an actual fracture so you can have a look at that at your leisure. What we will do is there is a test here, called elbow extension test. It is a fairly basic test, but it does outline something to do if you suspect an elbow fracture.

Watch Video: To perform the test, have the patient seated with exposed and supinated arms, then ask him to flex his shoulders to 90 degrees and then fully extend and lock both elbows. Injured and uninjured sites are compared visually and those would equal extension recorded as four extension. Patients who cannot fully extend the elbow after injury should be referred for radiography as they have a nearly 50% chance of fraction.

Dr. Pollard: You probably get an idea before that, but that is a test that you can do to confirm. So let us move now into the wrist and the hand to discuss some of those issues. So first of all, let us look at the inspection of the wrist and look for the posturing of the hand with if it is held? Is it not? Look at any gross deformities, there are a couple there, which are fairly obvious, but also, look at the palmar creases if they are still present, have they’ve been filled in? Are they cuts locations of, for example, blistering can be associated with fractures callus formation can be sign of loading and obviously, swelling? Always compare bilaterally.

One area that we probably need to mention does not happen all too often, but it does occasionally. This is vascular injuries. We can get vascular injuries as well, and these are much more serious concern when they do come and they occur in the hand. You can get compartments and rooms and other things that happen in the forearm, but we really have not got time to go into all of those. We will talk about some of these ones that can have that you can get simply by catching a baseball or a cricket ball or something a hard, object that it is travelling at a great pace. You can get basically an injury to the vascular structure itself, and so it swells, and they can present particularly like this one down here and this one down here. Now these two here are acute injuries. These are not things that we are going to be applying soft tissue work to. This we need to have this settle down. You might want to ice this down lightly and allow this just to settle, but we certainly not going to do it.

This one up here is a different one again. This is a ganglion in the wrist and, I certainly was taught that if you get a ganglion, you find the largest book on your shelf and you belt the thing. Now whilst that might be okay on the dorsal side, I still would not go that way, but some would suggest you do. on this side here, a ganglion here is adjacent to the radial artery and they are often, they tether against it. So, if you break this structure, you possibly can break the radial artery. So, it is another reason why we do not use violent techniques in around these types of structures, and these particular group of injuries. So just a couple of quick test for vascularization.

Watch Video: This is going to be a quick test to determine distal blood flow in the finger. To perform the test, compress your patient’s nail bed and note the time that it takes for the colour to return. Normally, the colour should return within three seconds.

Dr. Pollard: It is a fairly simple test, but obviously, colour changes, temperature changes end stage type of thing, you can get trophic changes as well in the nail bed and other things always compared to the other fingers and to the opposite side. This one here is a little more involved, so let us have a look at this one. Allen’s test.

Watch Video: Ask your patient to open and close the hand several times as quickly as possible, and then squeeze the hand tightly. Then compress the radial and the ulnar arteries with your thumbs. Hold it quickly and then ask your patient to open the hand and release the radial artery and you can see how the blood is streaming back into the hand quickly. We will now repeat the same process and release the ulnar artery.

Dr. Pollard: So delayed refilling of the blood into the hand implies that there may be a vascular structure involved and that is something which should gain a quick referral to a medical practitioner. Let us go into some of the more overuse-based syndromes that you are likely to encounter. An intersection syndrome occurs at the intersection of these two groups of muscles here as indicated here, and so this is a relatively common structure. Remember that this is an overuse friction-based syndrome, and so managing this is not about applying a lot more friction to this, but it is having a look at what is going on around it and that is where we might consider again the role of the superficial and deep arm lines that I spoke about earlier in the anatomy trains. That is something that you are looking at any entire limb, rather than just focusing at one point. For very recalcitrant cases we can also use cortisone as a part of the management strategy in the short term to quickly put down the inflammation, but for the most part, you don’t need to do that, and you can manage these with manual therapy approaches.

The next one on the list is the De Quervain’s situation. Now, the difference between the two, is that with the De Quervain’s think of it as occurring adjacent to the radial styloid at about that level whereas the intersection syndrome tends to happen a little higher. That is the way you differentiate the two of them. Both of them will be determined by the Finkelstein’s test, which is like so and then just radially deviates in a reproduction of pain happens. Management is essentially the same. Then we come into wrist instability. This is an area I think that does not get done particularly well, by a lot of folks and it is something that we really need to focus on. What I will say with a lot of these tests it is very much like, motion palpation of the wrist and the hand. In terms of, you need to be extremely specific between two adjacent carpal bones and that you need to block one whilst you create movement over the other. You can then also put combined movements in, so you can add that you can put it in radial or on the deviation or you can even look to rotate as well and do these types of movements and do the combined movement.

So, here is an example of the Watson’s test around the scaphoid. Say you are feeling for clicking and thudding around these movements and it is not a particularly difficult test, but you just need to be on the right spot. So, visualizing your mind when you are testing these the carpal rows and where exactly you are looking for that. So, the best thing to do in this situation, come to the proximal end of the thumb and work your way up into the scaphoid around that.

The other side of the wrist now the TFCC, which of triangular fibrocartilage complex, there is a little disc in there and there are a series of ligaments as well. Now, these ones are acutely often managed with a brace for four to six weeks followed by, often associated with management away from the healing site, but they do tend to become quite chronic. If they tear the structures enough, they will require a surgical outcome and I have an example of one of those that are following. Let us have a look at this one first.

Watch Video: There is a suspicion that he had a TFCC, a triangular fibrocartilage complex injury to this area, and I will show you how we derive that, okay? So, the first thing I did with him was a supination test. So, I am going to have you hold your hands like this. He has a hard time supinating, because he also has a small impaction fracture at the radial neck. Okay, so I want you to lift up on my fingers as hard as you can, and that hurts, doesn’t it? Okay, right around this area. Now, we are going to take you here, so that is a supination test. Then we are going to do the TFCC load test, where we take the wrist, and we bring it into ulnar deviation. And he doesn’t like that, okay? I am not even 50% of the motion getting into that area. If I palpate, we are tender right there also. Okay. Now, the next one we are going to do is going to be the piano key test and I am going to have individual videos and show notes of this video so you can go to those two. So, I am going to do a little piano keys. I am going to stabilize the wrist and radius. I am going to take the ulna, and I am just going to depress it a little bit and obviously, that is painful, so I am not going to push any harder than that. The last thing we are going to do is going to be a press test. So, I am going to have you go ahead and sit in the chair and we are going to keep an eye on his left wrist. I would like you to put your hands on the armrests and I would like you to try to push yourself up and you do not have to if it hurts, tell me. Yeah, it is quite painful right there to try to get it. Okay, great, you should just sit back there.

Dr. Pollard: Okay. So, that is very nicely done. Always, watch your patient all the way through their movements because he was guarding, he was protecting that wrist and the practitioner did a great job of not overloading the risk. Particularly, when we are talking about, more serious injuries that have, you know, longer-term outcomes. We do not want to overload it and add to the problem with our testing. So, be gentle and progress the testing slowly.

So, here is another example now of the distal radioulnar joint, which can be associated with the TFCC tearing as well as other structures as well. Let us have a look at that one now and we will go up to there and way we go.

Watch Video: If you see this, ulnar deviation you will see that there is some movement at the DRUJ (distal radio-ulnar joint) region. This is physiological movement. You can translate the ulnar shaft both dorsal-ly and volar-ly. This is physiological movement. How do you differentiate whether it is physiological movement or pathological movement due to instability? All you need to do is instead of [ulnar deviation] taking the wrist to [radial deviation]. You can try the same thing I can barely move it. So, you will see some movement because it is not [awful?] if the joint has got some mobility for the moment decreases. So, this tells me that the previous movement was physiological and once I have collected from all our deviation to reveal deviation, I can barely see this movement, and this is pretty normal for me. Now, I am going to demonstrate the same thing in the patient, and I will also demonstrate a piano key sign. This is a [gentleman from] a year ago and has been troubled by painful rotation, especially [pronation] and supination. So, if I do the same thing ulnar deviation, you can see it is already [subluxed]. You can see how much it is moving. There is a lot of movement at the ulnar region. It’s a lot deviated even when I do radial elevation still there is lot of translations, this tells me that this is pathological movement like the piano, it will go down and it will pop up. So, you can see here I am pressing it down and it is popping up like a piano keys. This is also is kind of be a redistribution when I press it down, it goes down when I lift it up, it goes up. Looking from this profile, so you see I can press it down and as I leave it pops up. So, this is piano key sign for instability of the region.

 

Dr. Pollard: So, that was very nicely demonstrated there. Hopefully you won’t see too many of those, but when you get your positive findings on those tests, it really is off to the surgeons after that because they have to weave their magic and then you can be involved in the rehabilitation post-surgery.

Another test, which is commonly done, for well, in this case lunotriquetral, but you can apply it across all of the carpal bones, and I will just get that ready and load it.

Watch Video: Place it on the treatment table. The test is a Dorsal Palmar Shear test. So, the fingers of one hand, locate and grab the lunate, and the fingers of the other hand, grab the adjacent triquetrum. Then you fixate the lunate and perform a dorsal palmar glide of the triquetrum.

Dr. Pollard: So, some of the positive test is pain, reproduction of clicking, particularly painful, and an excessive movement compared to the other side and also surrounding articulations. So, as I said to you before, it is quite similar to a lot of the motion palpation work that you will do for the wrist. I think that we have the potential to be quite good at assessing these things, but we just have to be in a have in our mind’s eye. I think, an image of what it is exactly you are fixating and what it is you are exactly moving so that you can then put the movements in the correct locations. And then when you get good at it, you can combine movements as well with radial and/or on the deviation.

Another common one is a fall on the outstretched hand and the so-called FOOSH injury can have problems with fractures in the carpus particularly the scaphoid radial pylon fractures. You can get a radial head, which usually involves a bit of rotation, but then also shoulder injuries with rotator cuff and in particular supraspinatus or then all the way through up to even AC joint grade three-tier. So, a fall on an outstretched hand, FOOSH injury, is an extremely common mechanism and you will see a lot of injuries in your careers with that mechanism. But anyway, this basic one is fairly straightforward. It is about power painting the scaphoid in the anatomical snuff box, which is just located here. So, you will see this happening now.

So, you palpate first and a lot of the time, just the palpation will be painful obviously, compared to the other side, but you can also get painful palpation too if the joint has some significant fixation or if there is some laxity present as well. So, obviously, degree and then when you add the radial deviation or compressing of the scaphoid, that probably gives you a better and if you get a positive and it was not a problem beforehand before a fall and you’ve got an immediate positive afterwards, that is an issue. Just remember that scaphoid fractures have the potential to heal with avascular necrosis, and so it is not something that you want to actively pursuing. They need to spend time in a brace to allow healing and you need to monitor the fact that that is occurring, and they usually follow up with CT scans afterwards to make sure that there is healing going on and you are not having that non-union going on in the scaphoid of the two poles.

We are starting to get close to time. So, we have got carpal tunnel syndrome. It is extremely common. These are the three tests, that you need to have a look at. I think they are fairly straightforward, so I won’t go into those too much. Just remember, it is the first three fingers that are involved with the symptoms, as well as a loss of power as well, so in the theorem and so, check for that and that should be quite clear. Now, the thumb itself basic range of motion, and then we come up to the radial collateral.

Watch Video: Place this finger, you push. Normal finger. Try this to dislocated finger.

Dr. Pollard: Yes, exactly. So that is a relatively uncommon injury, radial collateral injury of the thumb. far more common is the next one, which is the ulnar collateral ligament. Let us have a look at that.

Watch Video: Clinical examination of a patient ulnar collateral ligament injury showing gross instability of the metacarpal phalangeal joint on radioulnar deviation.

Dr. Pollard: So, inabilities, is one way to do all these but quite often what occurs when you get a tear of the- you see a ligament, this upon neurosis here the proximal end of that pops out and so there are no way for that ligament to occur to heal, sorry without having that being reattached. This is called a Stenner lesion, when this occurs and generally with excessive range of motion, you are going to get one of these things, so it needs to be screened for that, with MRI. I will put it down now that we are seeing more and more masters levels at level athletes, immobility with the various arthritis is common. Just know the most common arthritis is probably AC joint for in the upper limb closely followed by the CMC joint. So, mobilizations of these structures and assessing of the basic range of motion and you can get deformity with these things as well. These are all injuries that we should follow up.

Now, as a part of that, always when looking at the dysfunctional side of things rather than just, she broke in things, you know, the scaphoid there is a, you know, a keystone of the arch this way, but equally, there are a keystone of the arch that way, and the scaphoid sits at the intersection of the two of them. It is one of the reasons why I think we get as many problems as we do in this area. Add to that then the fascial attachments, of adductor pollicis, then you have got the extensor carpi radialis and on the flexor side as well, on the heads of the metacarpals, this whole area here, tends to lock up a lot responds really well to soft tissue procedures, as well as mobilizations, that target, the heads of the second and the third metacarpals, whereas you often get a lot of high permeability at the CMC joint over here. So, just consider this because this is very common in tradespeople, who are using their hands heavily for a living as well as sports folk that are doing the same type of thing.

We are going to finish up with just having a look at the fingers now. So, the first thing that I will say is your basic range of motion. The key thing here with the fingers is because they are little joints, it is easy to sort of make a movement and have movements flow off into other joints around the target joint. So, the key here is to be as specific as you can be with your assessments. Here is an example, looking at the palmar side on the flexors where they have stabilized the proximal end of the finger and they hare just muscle testing in this particular case, the dip joint. Then they have moved up by stabilizing the other one and the placement of the finger is in between are on the phalanx here, middle. So that only the joint movement is occurring here. So, this specificity is really, really important.

Now, on the extensor side, one of the ways that we do that is to use the edge of your treatment table where the hand will come over and that you can specifically focus, a movement using the table here, so that we can get a specific movement like so, and then you move down like that so you get like so. We are not getting these combined movements and particularly in assessments. Now, the same thing also applies, with assessing of the collateral ligaments, you stabilize the proximal segment and then you move with finger either side of the shaft of the finger here and then you move into varus and valgus. This is important to be specific when it comes this because they are little joints.

Common injuries, particularly with all the ball sports is catching a ball on the end of the finger, and then, tearing the tendon or avulsing the tendon out of the proximal end of the distal phalanx, so we can get injuries here. Have a look here at the way one of these presents. Here you go.

Watch Video: Not too severe and there are not very much in the way of swelling. The most obvious finding is these flexed fingertips. When you feel, you are looking to see if there are any tenderness, there are not much tenderness and the normal bony alignment is within normal. There is no dislocation of the joint, and there is no obvious swelling, or synovitis. There are no temperature changes and that is really it for palpation. Then when it comes to movement, you want to ask the patient to make a full fist. Make a full fist for me. You can fully flex and open up straight and when you also do extend, you see that you cannot fully extend. you cannot fully extend. So, now when a patient can’t fully extend, the question you have to ask is that, is there a fixed deformity called a fixed flexion deformity? Or is it an inability to extend called an extensor lag? So here, you can see this patient. She has full passive extension. I can easily extend there, but when I let go, it droops down and that is an extensor lag as opposed to a fixed flexion deformity. FFD, fixed flexion deformity. The same goes for the ring finger.

Dr. Pollard: You will see that with the cricketers and anyone who has got to catch a hardball that type of the not so much in the baseball because you wearing mitts, but certainly cricket, you will get a lot of that type of thing. Basketball, you get a lot of that type of thing. Note it, I can recall a patient I had who was a rugby player. He got the next injury that we are going to talk about the Jersey’s finger, as well as he had a few of these. Because he had done nothing about them, he essentially had a fairly unusable hand because they all eventually from being just an extensor lag, they moved to a fixed flexion deformity and he ultimately could not move the joints, and they were the source of a lot of pain. At the time he was 28, so he had a lot of problems in his future. Obviously, if you get that with the avulsions you should get an X-ray for these things, because if the avulsions are passed, 20 or 30% of the joint size, are they really ought to be pinned, and so that will be an orthopedic consult required.

let us have a look at the other common injury now, and this one’s based about grabbing jerseys and things of that nature. So, really all of the footy sports and all that type of thing. Let us have a look flag football, I think you guys call it, as another example.

Watch Video: Caught somebody’s jersey and had an aggressive flexion pull on his flexor tendons and had immediate pain. Went to the emergency room, had X-rays and as you can see, we have some bruising along the finger. 2 to 3 days ago, was significantly worse than that, had a lot more swelling. This is now starting to settle down a little bit. And in looking at him, notice that he was having some difficulty flexing. Extending, he is doing really well with that. But if we take your hand and hold it like this, do not let me push the tip down, hold it. So, he has a very good resistance into extension, has a little bit of bruising over the back of the finger also, but on the volar side, you can see here, we will have him bend the finger. Okay. Good. Good motion there. We will do our PIP joint and bend there. And we have some motion there. And now we are going to isolate the DIP joint and flex, and really does not have anything there. You are just getting full-finger motion.

Dr. Pollard: Nicely performed, gentle in the application, and very specific once again on the assessment, so, good practitioner. So, I am just going to finish up with a couple of slides on fractures, because finger fractures and dislocations are quite common, again with all the ball sports. So, again, it is all about the inspection. A lot of these things you know, they will play through them in a lot of cases if they are not too bad and so you will use your buddy taping as demonstrated there. But, have a look at the fingers, you know, bruising under the nail for a distal phalanx fracture. You run the risk of not only with the fractures, but you know you have got a dislocation possible. You have got a motions of the tendons, the central lift slip on the flexor side and on the extensor side you got the extensor hood are all structures that can be damaged as a part of, excessive finger motion.

Now, one thing I will put up, you will notice that these photos here, on this picture, all done with the fingers in extension. Now, a lot of the time there is some rotation component or a side bend component to a broken bone, which may not be obvious when you just simply look at the hand when it is in a sort of natural extended posture, but it will become evident when you ask them to flex the fingers and when you do so, you begin to see rotations of the fingers occur, right? Whereas normally we would just come up and you will see no differences whatsoever, but when we start seeing fingers cross over like so that is a sign that you are looking at a fracture or dislocation. So, it is a simple little test, but one to just kind of take note of.

So, that is brought me to the end of our talk. So, thank you very much for your attention. I believe that you are going to go away and practice some of these things if you have not already. Thank you for your attention and good luck with the rest of the course.

[END]

FICS ICSC Taping

Dr Isaksson: My name is Martin Isaksson. It is a pleasure for me to have this presentation for you. So, what we will go through today is quite a lot of slides. We have about an hour and twenty, depending on how quickly we can go through this material. It will be a lot of talk about taping. However, I will also talk a lot about fascia and the skin and how we can work with them to literally help us tune the brain a little bit better the way we want to. Okay. So let us get on to it.

Firstly, I would like to let you know that I work for RockTape Scandinavia. I am a master instructor, so I do a lot of taping and a lot of other things like instrument recesses of tissue, capping, and a lot of other things as well. But you are not required to buy any of their different types of tape or anything else. It is important for me to let you know that I do work for them.

This is from one of our hands on seminars that I and team started doing in Norway 2020. I like the simple thing that Mark Twain put up “Education is the path from cocky ignorance to miserable uncertainty”. I will take you through maybe a lot of uncertainty at times but hopefully, you will see that there is a red line following the whole presentation. Just read the words.

WATCH VIDEO:

I absolutely love these videos. They really talk a language and talk a story about how well the nervous system communicates. If we can harmonize or balance that nervous system even more, to help our athletes perform better, I am all for it. What we will go through today is kinesiology taping. Some ins and outs about that and research and so forth. Go through some biomechanical taping in terms of dynamic. I will quickly talk about the rigid taping at the end. This will give you a smaller overview of what we’re going to talk about. There will be a lot of other things as well. But we will get to that.

I like to talk about kinesiology taping in terms of Kenzo Kase as well. He was the founder of kinesiology taping method in 1980 which is a long time ago. He did really amazingly considering that was early 80s. I think what we’ve done today, we have taken that concept and just expanded it. I do not think the Kenzo Kase himself really thought that was his grand idea was that so I think he would be pretty happy when he would have seen what’s happened in these days as well. I do like to put up literally one of these slides to show some appreciation of what he did.

When did it start? It started in 2008 Olympics. Kerri Walsh obviously had it on her shoulder and from that point It is just been growing. We see today on our regular patients. We see it on the early population on our kids. We see it on a range of different people and I think that is why we start to see pretty cool research coming out from it as well. Now, “Does kinesiology tape really work or do we just ‘throw it out with the sweats’?” This was a systematic review that came out in 2015 and we will come back to this specific research article. I do like It is headline on, “Do we actually use it or do throw it out with the sweat?” So, let us come back to that.

Skin has been considered the largest organ of your body for a very long time. I would say, research start to shift maybe the idea here. So, is it really the largest organ of your body these days? I am going to let you be the judge of that, but I am going to leave this as a cliff-hanger a little bit and come back to it. We have a lot of different mechanoreceptors in the skin and that’s why we called it skin intelligence. Our skin is the megaphone to give our brain’s attention. Obviously, it is a two-way street so whatever happens in your skin will be a tentacle or some form of satellite for your brain and vice versa. We can have a lot of everything from chills or whatever in your feelings in your skin. When we think about something, it is the same way. It is going the opposite if I blow on top of my skin, I will feel it. The skin is very tactile stimulus to our brain, and they do come from the same neurological tissue. As you all know from your Embryology classes, you have the endoderm, mesoderm, and ectoderm. We all know that the ectoderm is where we have the skin is being made and the brain tissue.

Skin is having a key to your brain as a largest organ on your body or maybe not. This is how we prime in our system through the skin, and we like to use them. If the skin is a liver, let us try to use it and let us try to prime the brain. We do not touch muscles, specifically we do touch the skin. If we dive a little bit deeper into this, what we will see is a lot of mechanoreceptors as you can see here. We have the epidermis and the dermis layer and the hypodermis layers. Then we have the mechanoreceptors coming in everything from your Ruffini to Merkel discs to also our hair follicles. Now, the sense of touch what we talked about is tactile pain, temperature, pressure, vibration, proprioception, interception.

I think everyone has heard about the first six. The interoception, however, I think is something that might be new to some people. If we talk about hair follicles: Why is that important? The reason why it is important is because it has a low-threshold mechanoreceptor in your arms which is really interesting. When I learned how to use kinesiology taping, it was always to talk about to make sure that the skin is always dry and clean. But we also talked about that you should shave it first. Now, the recent years that has shifted. We talked about today, making sure that you have a couple of millimetres of stab in that case, if you have hair skin. Do not use a razor, instead use a trimmer. So you keep some of those low-threshold mechanoreceptors which is in the hair follicle. That will only add to what you are already doing with the tape. If I can add to whatever I am doing to some form of tissue to be a sensory part to the brain, I am all for it as I said before. Do keep it. Do not shave it, use a trimmer.

So what are we dealing with? Obviously, software. We are not dealing with hardware here. We are dealing with software, we are dealing with the sensation to the brain. Fun fact, there is 72.4 kilometres of peripheral nerve in human body. So that is every cubic centimetre of skin organ has a nerve or portion thereof, supplying it, embedded into it. This came from Diane Jacobs at dermoneuromodulation.com. Really interesting website and quite an interesting way of thinking through how to work with pain. She works a lot with people with chronic pain and so forth. If you have couple of minutes to spare, do check out her webpage.

The satellite systems will help us to visual the vestibular and proprioception. Now, we do want to have something more to that to help our brain even better and that would be the exteroceptive and the interoceptive mechanoreceptors. If we look at proprioception, everyone should know of proprioception. It is the kinesthetics sense that enables us to sense the relative position of the parts of the body, so we have learned about posture balance, and motion and so forth. Exteroception pertains to the stimuli that originates outside the body. That would be, if we have something that is very hot or something that pushes pressure unto us or something similar. However, interoception is more defined as sensitivity to stimuli originating inside of the body.

We talked about free nerve endings. We talked about literally the fascia here that is located in blood vessels, organs, and connective tissue and so forth. Interoception is where we have our most of our fascia layers. Do we have it in the proprioceptive part as well? Yes, we do because it is close and we talked about Epimysium, so there are different layers of fascia but most of our mechanoreceptors in terms of the interoceptors are fascial in derivation[?]. What is mechanoreception? We know the connective tissue and fascia are highly innervated. The fascia network possesses approximately 10 times the sensory receptors as compared to its muscular counterpart. We know that these are Golgi, Ruffini, Pacinian, free nerve ends and so forth.

Fascia is considered more of a perceptual organ than a mechanical organ. Think about that. Think about how smart the body is and what it can do when we think about the word perceptual organ. Let me lieu you with that a little bit so that you can think about that because it is important when we go on a deeper dive into what fascia does. I just put the slide up to inform you about where do we find the different mechanoreceptors in the skin? Meissner [inaudible] Pacinian, Ruffini, Merkel, and free nerve ending are found in different places. However, they are also very different as mechanoreceptor. Some of them are slow adapting. Some of them are fast adapting, some of them refers more of a vibration type of receptor while others are more of a, if you think about grabbing a tool in your hand and you have an even pressure on the tool the whole way, so that’s why you have a different mechanoreceptors will provide different stimuli to the brain which helps the brain to control it better.

I could probably talk a few hours about all these different mechanoreceptors in the skin and how they work. However, I am going to let you guys to do that on your own spare time. I do find it important so do go through it. Take the time to really think about what we do and what do we want to do. The effects and benefits of kinesiology tapes specifically is pain mitigation, decompression, and neurosensory input. We are going to go through all 3 of those. Our relationship with pain is obviously complicated. Pain science has taught us that for a long time now. The old way of thinking from textbooks and some stuff that we have gone through in our school, in our college, the inhibitory interneuron, nociceptor fibers, and by an alpha-motor neuron and that inhibits the nociceptive inputs and that goes up to the brain and we feel less pain.

The Pain Gate Theory is a simplified into slow and fast. Slow fibers, C fibers which is the pain fibers are slow for the reason that they do not have myelin in it. Then we have the fast myelinated fibers and the Aβ neurons which comes from our muscles and tendons and so forth. They are fast acting and are really fast. By then increasing the input of the Aβ motor neuron fibers, we can then decrease the pain to the brain. That is how they thought what the mechanism was. Gray Cook’s “Are you moving poorly because you are in pain, or are you in pain because you are moving poorly?” Pretty good talk, I reckon, I think I could talk about that for a very long time because there are so many things you can think about when you read that quote.

To lead from that, pain is an opinion of the brain. So, what do I mean with that? Depending on if you have an environment or a tissue that hurts, your brain will think about or scrutinize that into “Okay, am I sensing pain or am I sensing something that is completely normal?” Pain only lives in the brain. I think, we can all agree with that. However, how people see pain is very different. Some people feel pain very differently than others and that has something to do with our physiology and that has something to do with our behavior or the things that we have done before. The brain always looks for “Has this happened before? How did I feel? What happened?” and so forth. An easy way to think about this is, say when you were small, and you ran and then you fell or did something and you were crying and your mom came and she was just telling you that “It is alright, let me look at it. Maybe I can blow some or kiss it better.” When she did that, you felt better. So that is such a beautiful way of explaining that pain only lives in the brain. If we can change how we feel about pain, then we can change the pain perception as well.

That’s why I am saying that pain size has really changed the way we think about pain these days. It is a paradigm shift fueled by pain science. And we all know that the insula, which is in the limbic system, far in the brain is the judge of pain. So, it has a lot of other things, but it is connected to everything. So, the insula and the limbic system, where we have a lot of emotions, are literally connected to every part of the brain. That is why it can judge as well. Now, the interoceptive pathway, all the way from the C fibers for those people that are really interested in the physiology of this, you have the free nerve endings, the lamina, the prebrachial nucleus, the thalamus, and the insula. So, all the way up.

Lorimer Moseley, if you have not read any of his studies, or if you have come across him before, really interesting. I highly recommend his stuff and if your get a chance to maybe YouTube him and stuff like that, you will find an incredibly interesting. He said, “To reduce pain, we need to reduce credible evidence of danger and increase credible evidence of safety.” I do not think this can be said enough. If we want to help athletes and we want to help them to get better, we really must increase credible evidence of safety and make sure that they feel comfortable and okay with what we are doing. That would produce so much better results for you in your practice or with athletes on events or whatever you are doing. So, do think about that as often as you can.

Melzack more recently developed a more of a model of inputs and outputs. We can see the input is cognitive, emotion, and sensory. Output is pain, motor, stress, or emotion. In terms of sensory, if I can change any form of sensory, I can also change the output in pain or if emotion is triggered by something, that could also trigger an output as pain or some form of stress or anything else. Input is quite important that we start thinking about “Okay, what we can put in that’s going to help our athletes in terms of sensory? Can I put it something like tape? Can I put tape on someone and decrease their stress or decrease their motor output or do I decrease their pain? Emotionally, do they feel safe in the care we are providing? In cognitive, how are they thinking?” We all know athletes can have a stressful mind and do think a lot about things that have not really happened. So, can we change that? Can we blend that into our work with them and talk about things that help them do better in that section?

Consider the whole human. The biopsychosocial model of pain or biopsychosocial model of care, I think, is a beautiful way of thinking when we are dealing with our patients and/or athletes. Psychology is important. The social aspects are very important. We all know that if we are very open and happy and like working or being there, we’re going to have better results. We have all met those people if their medical doctors or whoever they are, they can have a very crappy attitude and we all know how we feel.  It is very important what we bring into the conversation, what we bring into the treatment room with the athletes or the patients. Their bio will make some sense to us if they have biomechanical issues or anything else that we need to look at.

Evidence informed, I like to think of evidence as a research and patient considerations, healthcare environments, and clinical judgements. In my opinion, that is informed practice. That is way of thinking to be guided by science but not necessarily shackled by it. There are a lot of things that we have evidence for but there are also things that we do not yet. That does not mean that you cannot do it, that just means that we need to research that and eventually someone will put a hand up unto it. It is an important way of thinking at least.

WATCH VIDEO:  Voice over: Pain perception in the human brain. Part of the survival value of pain is its association with learning centers in the brain. The brain circuitry associated with nociceptive and neuropathic pain involves areas consider to be essential in emotional learning, memory, and reward. The insula and anterior cingulate, together with the thalamus and basal ganglia are most consistently activated in acute pain. The brain stem and the descending pain modulatory system also play a role, where activity is observed involved the anticipation and perception of pain. Clinical chronic pain causes increased activation of prefrontal cortical regions which implies that chronic pain disturbs the cognitive and emotional perception and processing of everyday experiences.

Hypervigilance and an impaired ability to extinguish aversive associations of fearful or painful events seems to involve interaction among medial prefrontal cortex, basal ganglia and amygdala which is consistent with clinical data indicating that chronic pain patients usually suffer from elevated anxiety, depression, and decreased quality of life. These observations demonstrate that the brain in healthy subjects is distinct from those with chronic pain indicating that chronic pain is at least partly a neuro degenerative disease.

Martin: Awesome video. How do we think when we come to the part of chronic pain? Most of us and I will put up my hand to this as well, when I started to practice and work a lot with patients with chronic pain, I thought it was to restore normal motion to whatever that was. If I restore the normal motion, that will feel better. Lo and behold, they did not. Many of those patients were not getting better. So, that was something I was quite interested to know why that is,  and that led me to Lorimer Moseley in the first place. But if we want to think about nociception in terms of chronic, we got to stop thinking about just like what this article said. The shift is to stop trying to restore normal motor control in case of chronic nociception in patients with musculoskeletal disorders. The trick here is to start working with their pain and let the pain be your guide. What do I mean with that? That means if I can do the least amount of things to literally get them feel less of pain without trying to restore every single joint in the body to normal function, you’ve done something amazingly good for them.

Just as what this article is stating it. Let us try to work with nociception interactions instead and shift that and work with Okay, I can maybe do some light force technique. Maybe if you can adjust them just one segment. Leave it at that. Do not try to do too much because that is just going to make them a lot worse. Think differently when you work with patients with chronic nociception or just the normal guy that comes in with an acute trauma or disc or whatever that is. Chronic nociception is different so let us start treating it that way.

Here we come back to the article I have in the beginning. Now, this systemic view with meta-analysis focus on pain and also methods of taping applications. The conclusion of this was that KT is superior to minimal intervention for pain relief. KT as an adjunct is beneficial to pain relief. That is interesting. What we could see is that research is telling us that when we use it without other intervention, KT is good. However, KT should be used as an adjunct for treatment. I think most of us would use tape as an adjunct, not necessarily the only thing we do, and we could do even better if we use significant improvement when combining tape with corrective exercises. So that is another great thing you can add on to whatever you are already doing in terms of exercises or rehab programs for your patients.

Subacromial impingement has been on discussion for a long time but what we could see there was that KT as good as steroid injection plus exercise for subacromial impingement at both 1 and 3 month follow up. I think that says it all, really. If we can just use tape and exercises instead of using that nasty steroid injection, I put my hand up, I am all for that every time. It is such an easy way to work with so please keep that in mind. Where we going to see most the benefits of kinesiology tape or most tapes are with the compromised population. If we are just looking at people who are already feeling great and doing great, putting tape on those people, will we see huge improvements and see huge differences? I do not think so.

Do I think that if we take a compromised population and do the same thing? Yes, I do think so. Just as this research report concluded as well where they could see that the application of KT is effective in improving both the isokinetic quadriceps torque and reducing pain in knee osteoarthritis. I think that is pretty cool. We talked about decompression and taping. You have all seen this and some people do look for this convolution in the tape and said that is what you need. Research has shown us that that is actually not what you need. It does not matter if you have convolutions or not. However, what they signify is that when you put the tape on the body, you create something that we call a lift. So, you lift the skin towards the surface.

If we want to learn a little bit more: how does it look like? We have the skin, we have the adipose tissue, the superficial adipose tissue, the superficial fascia, the deep adipose tissue, and then the multilayer structure of the deep fascia and then you have the loose connective tissue in the bottom and then the muscle. Let us go through and look at what are these things a little bit more. This is important. RCS and RCP, Retinaculum Cutaneous Superficialis, you see on the left side, and RCP, Retinaculum Cutaneous Profundus. Why is that important? If you want to understand why the skin is connected to the fascia layers, there you have it. This is what we call skin ligaments. They are extremely important. They will provide a framework for the fascia to connect between the fascia layers all the way up to the skin. If we do something to the skin, then that means we can manipulate the tissues underneath. That is the cool idea about it.

I am sure you have seen an ultrasound before so let us have a small tutorial before we go further. Now, that is the skin. The superficial fascia is that white line you can see all the way through. You have the deep fascia which is that white line and then down there, we have the muscle. Let us look at this, on the left-hand side, we have the VML, that is without tape. You can see, if I put my pointer here, you can see that those two layers, you cannot even see the difference between the superficial fascia and the deep fascia. It is like they are one single layer. So here is the adipose tissue, that is why It is darker. Then you have the skin on the top here. What we see here on the opposite side is that we see the skin and it is a little bit wider, and that is because we have the tape on. You can see the superficial fascia is right there, and the deep fascia is right there, and here is the muscle.

So, look at this again. It moves like a solid block, and you can see quite a lot of movement in the muscle as well. The muscle moves quite a lot, and the skin moves quite a lot as well. Now, if we go over to this side. There we go. Here we can see the differences in the fascia. You see that? We do not have so much movement up here anymore. We can really see the differences. What we’re trying to do here is we’re trying to get the deep fascia which is there, and the superficial to actually move in between. We want to have movement between those fascia layers. That will create a better optimized signal for the brain because we want the brain to feel. We want the brain to know what we are doing. We want the brain to know proprioception and what is going on. So that is pretty cool. We can see it if we put tape on.

So here we have an untreated ITB on the left hand corner or left hand picture. Then in the middle, we see we have done some fascia release, and what we call a fascia release in this case, it is just some instrumented assisted soft tissue therapy. Then you can see on the right-hand corner or right-hand picture, we have a rock tape or a tape on the top. So, the differences here is there is the deep fascia layer, there is the superficial. We can see it starts to come loose a little bit here. But those two are hugely different. Here we can see It is just one single layer. We know through research, and this is why It is so important that if you increase the space between the fascia layers, you actually decrease pain in edema. For instance, of the soft tissue trauma, it was a histologically shown that KT increases epidermal distance and may reduce the sensation of pain in the main inflammation, that I think is pretty cool. That is why we use the tape in terms of pain.

If you increase the subacromial space, the KT obviously increases the AAP in healthy individuals immediately following application compared with Sham tape. So, AHD is acromiohumeral distance, so everyone knows what that means. Here is what they did, so you can see the tape job is very simple. You go from the anterior part of the shoulder model, chest muscle pectorals, and then you just follow the shoulder back and put it or lay down flat over the back of this shoulder blade, and that is literally what they did. Then they took an ultrasound to see if there was a difference. That was pre-tape, and then right picture post-tape. I would say that is pretty significant.

Which leads us into neurosensory. But I would say this is my favorite part with kinesio tape. If I can change something or if I can create something additional for the brain, in terms of movement or in terms of function, I am all for it.  This particular tape job I used on an athlete not too long ago, he plays on the higher soccer league in Norway. He came back to Sweden for a visit. This is obviously before the pandemic anyway. He had issues with chronic instability of his ankle. Now I tried a few things and obviously he had been with a physio and done rehab exercises for years.

It helps a little bit but he never gets the feeling that he can actually trust the ankle. What I did well, I thought to myself, we have got to increase the proprioception and we got to increase the sensory components of the brain here. Whatever we can do with that ankle, the better he will be off. So did I adjust it, yes, sure I did. But did that change anything for him when he started working here? No, it did not. Did he have issues in his ankle? Yes, he did.

However, once I put the tape on, and specifically this tape job, and I tried a few different ones before this one, everything else did not make him feel different. This one however, got him 100% better. He could literally jump up and down in my gym room with no pain. He was thrilled. This is all I did. It kind of blows me away sometimes how much it can do for an athlete. I mean, try different things, if one thing does not work in terms of taping, try a different way of doing it. We are all different. We are all wired a little bit differently. So different things can work for different people.

This also comes from www.dermoneuromodulation.com, we have the hindbrain, we can all see that back there, and we have the higher cortical function. Now we have a body around this and our nervous system. Whatever we do to that nervous system is either going through the hindbrain, before it gets to the higher cortical areas. Now, why is it important? Well, if the patient does not feel safety if the patient does not feel or athlete. It is a nice environment, and you are good enough to let them feel like they can trust you, that stress level they will have will activate that hindbrain and you will never get through to that higher cortical function, which means that whatever changes you see short term will not last.  This is a brilliant way of thinking about what we can do. Everything is important. How we move, what we say, what we do. Keep this in mind, please. Yes, that is what we want to see.

Now, Hilton’s Law 1863. That is a while ago. Does it hold true? Yes, it does. 2009, and you can read about it in PubMed. There was a researcher that took it on to see if it actually is correct. It still holds true. So why is this important? Well, if we think about it through muscle, skin, and joint, the same trunks of nerves whose branches supply the groups of muscles moving and joint also furnish a distribution of nerves to the skin over the insertion of the same muscles.

If we work with the skin, that means that we can literally think about the nervous system as being that trunk or branches and so forth, all the way down to the source. So do think about this Hilton’s Law when you use the tape and that’s kind of a nice little research article for you there. So go ahead and look that up on PubMed. Pleasantly surprised that was. Effects of tape on the brain. Yes, this was a fairly small study, only eight subjects, they looked at with their functional MRI. However, what they saw, I thought it was pretty cool. So just patellar taping on the brain activity during knee joint proprioceptive tests using functional MRI. We can all see on the left picture, that we see those red yellow areas and the right hemisphere we see, the right picture, we see the blue areas. Now the yellow and red areas is the areas that light up and become more activated when we put tape on the patella and on the right-hand side, we see the blue areas which is actually decreased activity. Now why would that be?

Well they postulate in this research article that It is actually due to that if you put taping on the lower extremity, you will see a decrease of sensitivity in your upper extremity. That is the only way they or what they possibly thought was the case here. If that is correct or not, I do not think we know yet. But it is quite an interesting idea for sure. What they did was they used a simple application of taping or covering 50% of the skin over the knee, and that had effects on the brain associated with sensation, coordination, decision making, planning, complex coordination tasks, and coordination to the unconscious aspect of proprioception. I would say that is pretty cool. Now, is this being all end all? Oh, absolutely not. But it definitely makes it interesting for the future to see what can come out in terms of when you use tape and the effects on the brain.

Another research article showed that if you put kinesio tape on a patient’s ankle, now look at this chronic ankle instability, what we could see was improved balance with chronic instability for 72 hours after removal. I find that quite interesting because some sports, it is impossible or not impossible, it is prohibited to put tape on different body parts due to rules in that sport. An easy way to get around that, obviously, is to put tape on and then use before they go out on this event or whatever it is, ring or so forth, you take it off.

We can still see a difference. We can still see something positive even though we have taken the tape off. Chronic pain is a cortical dysfunction. That is, we have seen both in the video before that I showed you. But we also can see it in terms of we talk about nonspecific low back pain. So chronic low back pain patients, we can see tactile thresholds are impaired compared to normal people without back pain. What they did was in this study, looked at both the vertical line and the horizontal line. So tactile acuity, and you probably seen these two-point discrimination tool so you can use and what they saw was that people with chronic pain were harder to feel when you go closer and closer if you have one or two.

You probably seen this, it is almost like two little spikes, and you push them into the lumbar spine, both in vertical and horizontal, and you mark how far or how close you can get between the two spikes before they send one or if they still feel to. We can see that there is a difference between normal population and people with chronic low back pain. If you improve the tactile acuity, you improve the body representation, which means decreased pain and improved control.

Whatever we do in that region, we can use tape, or we can use a lot of other things but taping specific, then we can definitely see also decreasing pain and improved control. Try it on your next patient you have walking in your room with chronic pain, put a piece of tape on, see what they feel, see if it is different. Sometimes you might be surprised of how much it can do.

In summary, we can talk about decompression and lift the skin and superficial fascia and the deep fascia and so forth. What it creates is neurosensory stimulation, it changes the neural input, and that has a positive effect on both reducing pain and increasing or changing movement. How do we move? We thought in the old days was if we contract the bicep, the only thing that moves is the biceps. Like we can go and train biceps in the gym, the only thing you will train when you those curls is your biceps. Well, we do know that is a car analogy of thinking and it does not hold true for anything, even though we talk about different perspectives here.

We do know that more and more in terms of research that we might have to look at the body as a whole and see that there is a lot of things happening without us knowing. Our current thinking in terms of anatomy, I would say is the anatomy trends, where everything is connected to the soul of the feet, connected all the way up through the lower back, the midback, the neck, and all the way across the eyebrow. Anatomy Trains by Tom Myers. Great book, in my opinion. It is a very easy read, and it is a nice read. Can we take a lot of things from them, Myofascial Meridians and so forth in manual therapy? Yes, I think we can. See, if you have not read it, I encourage you to do so. This is the superficial backline that Tom Myers has been able to show us. You can see, follow us all the way up through, from the soles of your feet, big toes, and all the way to the forehead.

Fascia layers, which is obviously what we talked about here. The fascia layers that connect everything and we can see it in almost every single tissue in your body. First cliff-hanger I left you with was the longest organ of your body is the skin. Is it now? Now if you look at this list of things, do we still think that the skin is the largest organ? I have come around and I think that we probably are all looking at the fascia as the absolute largest organ. The fascia has the ability to do so many things. We will get to a video later that will show you even more how intricate and amazing the fascial system is. Fascia has the ability to change its tonus autonomously, independent of outside muscular forces. Dr. Jochen Staubesand found that using electron photomicroscopy, smooth muscle-like cells embedded within the fascia’s collagen fibres aka myofibroblast. Staubesand also found a rich interfascial supply of sympathetic nervous tissue and sensory nerve endings. Now based on these findings, he concluded that it is likely that these fascial smooth muscle cells enable sympathetic nervous system to regulate a fascial pre-tension independent of muscular tonus. That is quite interesting, if we look at this video, let us see how cool fascia is.

WATCH VIDEO: Voice over: In order to make this new film easier to understand, we first need to review what the previous film strolling under the skin showed. It seems that the body consists of an inner architecture, a gathering of calendulas tissue in a novel continuous network, a web in multi micro fibrillar shapes, and in a pseudo fractal irregular organization, enclosing multi microvascular spaces from 10 to 100 microns in size. These structures not only participate in the elaboration of form, but they also represent the framework of this form and play a major role in movement and gliding.

Ultrastructural studies have shown that this tissue is composed of these microfibrils that have a diameter of about 10 to 20 microns, and are made up predominantly of collagens type one and three. By intertwining, they determine the volume of the micro vacuole, which is filled with the glycosaminoglycan gel. By accumulation and superposition, these multi microvascular polyhedral patterns will build an elaborate form fibroblasts, in charge of maintenance fit perfectly into the structure and have similar dimensions ranging from 10 to 60 microns.

The adaptability of the space that is created is insured by the inner properties of the fibrils, the most important of which are attraction and retraction. But other properties also play a role such as the mobility of the fibers along one another, involving a de-polymerization phenomenon, deformation and re-formation, a function not previously reported, as well as division, a phenomenon which enables an immediate dispersion and distribution of the forces on the tissue space.  Thanks to these three movements, but there may be other properties, the micro-vacuole can therefore adapt to all mechanical solicitations in the three dimensions of space while keeping its volume. The movement of one of these structures influences the other, and by connection, maintains form and tissue integrity, dissipating from the slightest to the most violent forces. Leads to this multiple micro-vacuum structure, all the distortions are made possible in three dimensions. Our bodies, our forms can then be described using this mobile in an architecture, which introduces a real structural ontology.

The movement of the tendon which without any influence on nearby tissue, ensures an optimal, almost frictionless sliding movement, as well as simple gestures such as pinching or stretching the skin with the ability to slide back to its original position can be logically explained. But this global observation of living matter, based on a micro fibrillar and multi micro-vacuolar inner architecture has its anatomic limits. This limit is the skin, the border between me and others, between two worlds, the human form and the outside environment. One is susceptible to aging, the other timeless. The skin constitutes the boundary between these two worlds. So now let us go and discover the skin in order to learn what has become of all these fibrils that we’ve seen going towards the surface of the skin.

 

Martin:. Those videos, I do have permission to use them in my presentation, but they are all over YouTube. So good, my two beautiful videos about fascia, I absolutely love them. I think it is so cool how fascia can literally work around and taking all those muscular forces or any type of force and just redistributed that through the fascia to be able to create those pretty damn cool things. As you can hear, I love fascia, I could just go on forever to talk about it. We have different types of fascia. You will see that the fascia in the lumbar spine or in the truck along the fascia is different to the skeletal muscles, the [inaudible] that surrounds every single muscle. We also know that the internal structure of fascia looks different depending on where it is in the body. Tension and integrity and so we have tense integrity, it is the structures to maintain the integrity due to the balance or continuous tensile forces through this structure. Now this is a perfect explanation of what actually fascia is. When you watched the video, and then you think about tense integrity, you can really see how AB is connected and how it works.

We talk about fascia as a sensory organ. Stecco, these slides are more densely populated mechanoreceptor stem tissues situated more internally. If you have not read any fascial stuff, please have a look at Stecco. The Stecco family has put out tons and tons of research articles in terms of fascia and there is even a pretty good fascial international group these days. If you Google that, you will come up with that as well. It is great to be a member of that as well if you want to read a lot of the research coming out. I think this next one is pretty interesting for us. Scar practice is now believed that joints only provide joint feedback when at end range on motor movements and not during physical motions. Isn’t that interesting? They provide feedback at the end range. Now where we go to middle of that then the parent physiological space. Who is giving the brain information here? It could be interesting. But I will look that up.

Proposed timeline and mechanisms for fascial, adipose and muscle changes in the multifidus muscle after intervertebral disc lesion. I put this up because I want you to see how a lot of this is bound together in terms of fascial and how everything works. I am not going to go through this 100% now but I do want you to look at this picture and think about everything you see here and then take that in the back of your mind when you have a de-escalation patient or so forth.

It is quite cool how everything is bound together and how much of that is due to the fascial and adipose and muscle changes we see. We know the fascia, It is alive, it senses, it transmits force globally. What is also quite interesting I would say is that we have different fascial membranes. The depression membranes can be divided into the aponeurotic fascia, and the epimysial fascia.

So epimysial fascia surrounds the muscles itself. What I find interesting with the epimysial fascia is that it actually handles 30 to 40% of the muscular force. Very interesting, in my opinion. So previously, we thought of everything is by muscle, it is the muscle that takes everything with the tendon. Well, we got to look what sits outside the tendon here. What is the epimysial layer is made up of, and how do they work? I think that is quite important to consider, when you look at how the body works in terms of changing the way or working with the body to create changes in those muscle layers. Aponeurotic fascia is where we find a little bit more superficial to that. They can have two or three parallel layers. They are a little bit thicker than epimysial layers, well, what is important with them is that they have very well vascularized and have well developed lymphatic channels. So here is where we can see a lot of that, if they have inflammation or some acute injury, that is where we will find a lot of that swelling.

High lauric acid matrix, or Howard acid rich matrix is also what we find in those layers now. High lauric acid is almost a lecture on its own and I do encourage you, if you do not know how it works in the fascial layers, I do encourage you to look that up and be well familiarized of what happens and how it works. Because that could actually change the way you think in terms of using different modalities for treatment of certain athletes.  I give you all these golden little nuggets for you to look up on your own time, because if I go through them now, I am not going to have time. So it is that simple. Now, I think you want to listen to me for the next three hours. So that is why. Schleip is very interesting. Robert, he has done a lot of work with fascia, and he is just putting out research article after research article. If you really want to learn a lot more about fascia, please look at his work.

Tissue manipulation. If we look at this turning wheel here, we can see that if we do any form of intervention, whether it is big fat on the left-hand side, and then we can see that the tissue manipulation, soft touch and sheer tape. Tape is what I am thinking about here. The arrow, here they go. Stimulation of mechanoreceptors is that when we get to the end, then we obviously have the interstitial receptors and Ruffini’s endings, the autonomic nervous system changes, the brain changes. The inter-fascial smooth muscles, so here is where we get that myofibroblasts change, and we get that palpable tissue response.

We have all gone through this with people when we work on them. We can see or we can feel in those tissues what happens. It is just to create an understanding of what actually happens when you do any form of intervention and what happens on the global and also their local blank. Reflective activation. What we talked about is if you touch or you tape or you do something that stimulates receptors, which stimulates brain, which in turn stimulates those myofibroblasts and what we see is that palpable tissue response. Now, does direction of tape matter? No, it does not. We can tape it from organ to insertion or the opposite or whatever you want to do, is it going to change anything? No. So to make it clear, stop talking about it because it has been so well researched now. We do not see there is a difference. Do we see any if we apply direction in terms of muscle strength or flexibility? No.

 

According to this study, and multiple others, there is no evidence to support directional taping at all. Facilitatory or inhibitory effects of kinesiology tape, do that exist? Have not been able to provide any evidence so far that we can say that, and nor do I think we do. Because the body will do what the body will do. If we will facilitate on inhibit, I do not think we can say either, because we can only stimulate the brain. Whatever happens in the brain, happens in the brain. That is going to be different from person to person. Effects of kinesio tape application direction on quadriceps strength. Now, regardless of application direction, there was a significant difference in quadriceps peak torque before and after kinesiology tape application. Do we have any effect on that? No, we do not. Does the amount of stretch of the tape matter? No. So I will say the only thing you ever going to create if you stretch the tape is blisters and problems with skin irritation. If you instead work with the tissues and stretch the tissues instead, instead of the tape and just lay down tape, you will get a lot of better results. First, you will not get any issues with their skin unless they have an allergy. That is what actually has some research behind it. Does stretch have any research behind it? No, we have not seen any.

So MED, Minimally Effective Dose. The smallest dose that will produce a desired outcome. It is important to think of less is more. That goes for everything in my opinion but taping as well. Start taping small amounts and see if you can change anything. Do not take their whole body. Do not cover everything. Start with some stuff and see what happens. So kinesthetic guidance translates to behavior 30 times faster and then visual guidance and many thousands of times faster than auditory guidance. This was published back in 1971. If I can put a slice of tape on someone and I actually get kinesthetic guidance better, then I am on, sign me up. Let us look at this video.

WATCH VIDEO: Voice over: Not so long ago, many scientists believe that the brain did not change after childhood, that it was hard-wired and fixed by the time we became adults. But recent advances in only the last decade now tell us that this is simply not true. The brain can and thus change throughout our lives. It is adaptable like plastic, hence neuroscientists call this neuroplasticity. How does neuroplasticity work? If you think of your brain as a dynamic, connected power grid, there are billions of pathways or roads lighting up every time you think, feel, or do something. Some of these roads are well-traveled. These are our habits, our established ways of thinking, feeling, and doing. Every time we think in a certain way, practice a particular task, or feel a specific emotion, we strengthen this road. It becomes easier for our brains to travel this pathway.

Say, we think about something differently, learn a new task, or choose a different emotion, we start carving out a new road. If we keep traveling that road, our brains begin to use this pathway more and this new way of thinking, feeling, or doing becomes second nature. The old pathway gets used less and less and weakens. This process of rewiring your brain by forming new connections and weakening old ones is neuroplasticity in action. The good news is that we all have the ability to learn and change by rewiring our brains. If you had ever changed a bad habit or thought about something differently, you have carved a new pathway in your brain and experienced neuroplasticity first-hand. With repeated and directed attention towards your desired change, you can rewire your brain.

Martin: Principles on neuroplasticity. Repetition helps drive home the information in the long-term memory. Now, we love repetition as humans. Adaptation occurs according to the stress that is applied repeatedly. Now, if we want to change something and we want the change to be measured and we also want to have change that will last, well, why do not use tape? If we can get that message to the brain constantly because that is what It is trying to do, by working on all those mechanoreceptors on the fascia and so forth. If we can drive home that message to the brain, so the brain can help change itself, that makes a huge difference for that athlete or that person.

I do not think that holds true for only kinesiology taping, I think that holds true for most tape. Regardless of if you use biomechanical tape like Dynamic or use kinesiology tape or even rigid tape to some degree. But what we’re trying to do with kinesiology tape is trying to get that hand to become clearer. Putting a piece of tape on will help the brain to function better in terms of knowing where that hand is in space, by working on those mechanoreceptors.

Gray Cook and Mike Boyle came up with Joint-by-Joint Approach. If you have not looked that up before, I think It is quite interesting to look at, where it goes through different parts of the body as mobility and stability. Between two mobility joints, we obviously need some form of stability. If you are looking at, for instance, in this case, take the ankle as a mobile joint, if it is hypermobile, could that be due to something as simple as lacking in the stability of the knee? Yes, it can. Do I always look at the knee when I have ankle instability? Of course, I do. Do I say that it always is the knee? No, I do not. But those instability portions, I can say, for instance, that I have seen very positive surprises by using the tape on those specific spots. That could be one way of thinking about it.

There are contraindications which you can read on your own. I do not have to go through it. The biggest thing is adhesive allergies. That is the biggest thing I talked about most of the time. Caution, if there is a history of past skin irritation, and you can do a test patch if that is the case. Some tape manufacturers can do really well in terms of having an adhesive that doesn’t seem to irritate the skin and some do not. Sometimes, you just have to play around a little bit and see what works.  Kinesiology tape or I would say every form of tape we have used is not protocol-based. Not the way we teach and fix, and not the way I have ever taught in RockTape. It is more the fact that it is a framework, and you rule the tool. Whatever you want to do, you have a couple of things you can train yourself to, but how you want to play it is completely up to you. So let us go into Dynamic Tape. Let us see what Ryan has to say about it.

 

WATCH VIDEO – Ryan Kendrick: Hi. My name is Ryan Kendrick. I am the developer of Dynamic Tape. At Dynamic Tape, we never really set out to start a tape company. We were just looking for solutions for our athletes and our patients, clinically. We recognized that load was a key driver in a lot of our patient’s problems. Be it tendinopathies, muscle tears, and those sorts of things. Also, loading was really critical in their recovery. But we also, at the same time, recognize that a lot of normal activity was too much load for them. Unloading completely also results in fairly lengthy recoveries and was certainly not the popular option with our athletes to cease their activities. At the same time, we had our neurological patients, where their function was really heavily impacted by the load. It might have just been the load of gravity acting on their foot, that they had a foot-drop and weakness and they were catching their toe and had an increased risk of falling and those sorts of things. We were looking for something that we could put on the body externally to do some of the work to either take the load off or to overcome gravity or to increase stability by creating some compression, and we really could not find anything out there to do the job. We did not want to lock up the movement like a lot of existing tapes do. Movement is our friend, particularly when it comes to dissipating load. We dissipate load primarily through movement, but also very important for our balance, strategies, and those sorts of things that we’re taping the lower limb, foot, ankle, and so on. We needed to preserve that as well.

What we came up with was a very strong elastic type that stretches very well in all directions so we do not lock anything up. But it has this very strong resistance and strong recoil that it acts likes a spring or bungee cord or if you like an external muscle to do some of the work. It is very much like what we use in our hand therapy without dynamic splints, where we have a big rubber band that we can resist against it with our intact muscle, and then it springs back to protect our operated muscle or tendon, for example. That is where the name came from, dynamic splint, this was a dynamic tape. Similar to a splint, but we could apply it anywhere on the body. That is how it developed, and it is been quickly adopted into all areas of manual therapy, physiotherapy, chiropractic, osteopathy, podiatry, etc. Because of that ability to manage load while maintaining function.

Martin: Ryan says tissues do not fail because of pain, they fail because of load, and I could not agree more. Load is obviously the driver of pathology such as tendinopathy. Load is obviously also necessary for recovery. It is an interesting play between those two. Dynamic Tape is used to reduce the load and to allow some of that functional stress to be applied without overloading an already sensitized tendon. That is why I tend to use Dynamic Tape a lot when it comes to tendon problems or issues with loading that the patients or athletes have issues with. Jill Cook and Purdam 2009 came out with a critical research article that I encourage everyone to read if you have not. When they look just on load and force transfer, and you can see the normal tendon in the middle there. You have the stress, something happens, increase or excessive load and it has become reactive and then reactive tendinopathy. If you appropriately modify that load, what will happen is that you will obviously optimize the load better, and the tissue will adapt in terms of the tendon will adapt, and then it will strengthen and that becomes a normal tendon.

It all works really well. However, if you do not do what you need to do in terms of appropriately modifying that load, well, what might actually happen is that then you will see a next level instead, and that is tendon dysrepair. Now, when it comes down to that, it becomes a little bit more tricky to work with. Tricky to treat and tricky to get better quicker, and now we are talking about a long-term problem. Once it gets down to degenerative, there is nothing to do. Research has shown this a few times, or all times, I have not read of any that has come back from degenerative tendinopathy. It is very important to take it seriously and to look at it. If you did hear Jill Cook talk in the symposium, the fix had a few months ago, an excellent discussion about her thirty years of research of tendinopathy.  As she said herself, that a lot of people think they can feel or they can take an MRI and say, “Well, this is what you have, and this is how it is,” and she literally said that is impossible. You cannot feel which part or where they are in the cycle and you clearly can’t take an MRI to even show that there’s a reactive tendon or anything else. It is done by clinical knowledge and making sure that you appropriately modify that load.

Obviously, different sports will have different problems here, and how you need to work with them to modify that load that they are feeling. Modifying it would obviously entail the training and competition schedule, the equipment they are using, the environment they are in, biomechanics, and kinetics. Limitations of the traditional approaches with respect to load and function. If we talk about now, rigid tape, for instance, there is a restriction of range of motion. Reduced capacity to dissipate load through movement, we all know that tape does not last very long, and they can’t take much of that force anyway. Possible adverse effects on balance. Limited or no deceleration through range. That is, in my opinion, a huge issue. Limited capacity to functionally assist, well, there is no functional assist. Tape fatigue, it takes twenty minutes. Twenty minutes is what they can gain some help from in terms of rigid tape. That’s important to consider when you put white support tape on, regardless of if it is Johnson and Johnson or which other brand it is. Twenty minutes.

Fundamentals of taping mechanically. If you use biomechanical tape, there are three critical factors that have to be met in order to affect the mechanisms of motion. First is you need to cross a joint or multiple joints. Secondly, you need to apply it in a shortened position. Remember, when I say shortened, I do not say fully shortened, I do not say loose either, we will get to that point on what that means later on, and we will back it up with some research. Get good purchase on the levers. Now, that doesn’t mean that you should pull the tape with everything you got, but it means that you need to have a small pull on the tape to get the effect you are after. Because the greater the force of the load that goes through that tape, the better it will help you to sustain that load. Modifying load or movement with tape, unaccustomed load; acute overload; permit early functional loading and reduce compensation strategies, very, very important, if you want to get that reactive tendon back to normal; permit optimal tissue healing, obviously also very important; functional impairment or techniques, depending on who you are talking to or how they look like. Like the gentlemen on to your right there, his arm is a bit different from the other arms you might have seen in your practice. Now, how will you tape that? You got to stop thinking about what you are after and what you want to do. The mechanisms, if we look at some research that is done on Dynamic Tape so far, there’s not overly much yet. There are being done a fair bit though, and we can see that if you look at EMG activity, we can see that statistical analysis shows the increase in EMG activity was statistically significant and not coincidental. What happens is we do gain response with the force contribution or in the EMG activity if we use Dynamic Tape.

The effects of Dynamic Tape on DOMS. It is an interesting study, you can all read about as well. But in conclusion, the clinical markers associated with DOMS can be seen to have been reduced through the application of Dynamic Tape. What they did was measured the PPTs, range of motion, and muscle girth. There we see what I just talked about. All right, let us see what we have talked about.

WATCH VIDEO Brian: We often hear that because the tape attaches to the skin that it cannot possibly affect mechanics. Really, what we are talking about here is kinetics quite often. Can we introduce a force that crosses the joint, that changes the joint movement there, and in doing so, reduce the required workload of the structures that would normally create that force? Or maybe by introducing a force, we can actually change things like position, so change our kinematics, our movement, our position, and in doing so, once again, that can also have an effect on our kinetics by changing lever arms, either of things like the ground reaction force, or of the muscles that are acting upon that joint can change things like the axis of motion, for example, your subtalar joint axis and so on. This is just a quick demonstration, we are looking at the Achilles tendon or a calf-type application here, I just want to pay attention to a couple of things. First, have a look at the resting angle here when there is no tape in place. Also, have a look at the way the foot springs back and then the force that is required to take this through full dorsiflexion. You will see here, as we go down, that takes about 3.2 kilograms or 32 Newtons of force, and we see it spring back there.

If we go a little faster, we just reproduce that here, it is about 3 kilograms. Again, a little faster, we are only getting about 1.8 kilograms or 18 Newtons of force if we move at speed in that outer range. Again, there is 2.3. Now, with the tape on, let us have a look at our angle once again. We are now actually resting in full plantar flexion. Again, watch what happens now, as we come down, we already hit 3 kilograms, not even a plantar grade. If we keep going to the end of range, then it is well up, almost 9 kilograms, and you can see it springs straight back, and it springs back into that same resting position, full plantar flexion.  If we go with a little speed, we can see that is about thirteen and a half kilograms. If we just do it in outer range with speed, we are still 7 kilograms, seven and a half kilograms of resistance, and we are not even reaching plantar grades, that is just in that outer range of motion. We will often use this technique for calf tears, for Achilles tendinopathy, particularly those reactive ones where we’re trying to get an initial reduction load to allow them to settle down a little bit as we reintroduce the load in a way that they can handle it. It may be in transitions where we are increasing the amount of activity and there’s potential for them to relax a little bit. Or it may be in those late-stage sorts of degenerative tendinopathy where they have lost their own intrinsic energy storage and release capacity within the tendon. We can tape them to give that to them, sort of externally, and they will say they feel like they have a bit of a spring back in their step once again. We may be able to maintain function, even though we are not directly going to reverse some of those more permanent changes in the tendon itself. But as you can see there, you know, we are getting 5 up to 10 kilograms additional resistance to dorsiflexion. Every time that foot lands on the ground, the tape is absorbing or taking some of that load off the structures that would normally have to control that. If your athlete is a marathon runner or a jumper or volleyballer, then that can add up to a very significant amount of force throughout an event or throughout a training session, or throughout a season.

Martin: Another EMG study, they looked at the activity of the upper trapezius, pre and forty-eight hours after application of cervical offload PowerBand technique in a group of office workers. What they saw was, results showed a significant reduction in the EMG activity with the tape.  Another one came out of Brazil where Dynamic Taping improved both pain and active range of motion in the subject with accessory nerve injury post lymphadenectomy. We do see small amounts of research coming out on biomechanical tape in terms of Dynamic which is nice to see.  A lot of athletes are showing it more and more. A lot of athletes seeing the help it can actually do. Personally, I had a tennis player that came back to Sweden after being in the States for a few years with significant problems with his shoulder. I did such a simple little offload of that shoulder with Dynamic Tape. We taped her up for a couple of weeks and we did, some other soft tissue work and adjusting and so forth, and some corrective exercises. She went back to the States in January this year and she came second in the league. She is outdone herself in every possible way. It can really change a lot for a lot of people when you start using these things for the right reason.  As you can see, there are a lot of different sports that you can start to see Dynamic Tape today. If you want to modify move or position, which is kinematics, you got to understand that kinematics describe the motion of objects, in the case of bones, without consideration of the forces or circumstances leading to that motion. Kinetics examines the forces on an object and potentially, the effect of this motion on the object.  As certain kinematics have been associated with painful conditions and poor performance, we can target our technique to simply improve the movement patterns by pulling the body part on one way or another, by playing external force on modifying kinetics. You are gliding movements like Mulligan techniques and stuff like that into the position of ease correcting a deformity, or anything like that, we can use the Dynamic Tape for that. The aim may be to change the way they are loading on a particular structure, to improve function, permit better healing, to resist deformity. But a change in movement or position can have additional effects. We can use the technique with Dynamic Tape and have multiple layers to it. Emerging research on large hip joints is showing an effective change in magnitude velocity of movements with Dynamic Taping. There are coming out studies both in Australia and so forth are showing just this which I find quite interesting. I am looking forward in the future to see where that can bring us in terms of research in Dynamic Tape.

 

Does Dynamic Tape change the walking biomechanics of women with greater trochanteric pain syndrome? That was a double randomized control trial with a crossover. What we see is obviously, positive results on these people. A couple of interesting movement positions and how much you will literally push the patient on, if you are going to resist or load up these joints and how painful those conditions can be unless they have worked on. Remember what I said before about taping them in a shortened position? Now, if you go too much, you actually force inefficiency and functionally weakens them. But if you stick around in the mid-range, in a resting or neutral position in the mid-range, you have a lot better positive change when you use Dynamic Tape. What we are trying to obviously do with the tape or can do with the tape is something that we call Force Closure. That will help when you use Dynamic Tape circumferentially. That will create the compression force, which may augment that force closure. As I said before, depending on which technique you use, you can do more than one thing at the same time. There is another interesting study that came out of Brazil, which you can read about in your own time. This nice little tape job is something that once you take the courses in the Dynamic Tape with us, when we go through taping in our class, which we will show you, I absolutely love this tape job. It is simple, it is effective, and you got that ankle covered, in my opinion.

Do I ever use rigid Y tape? Yes, I do. Is it rare or very seldom? Yes, it is. Please, think about the possibility to use Dynamic Tape in these situations as well. There are a lot of other things, which we will go through with you once we have the live sessions. We will go through how you work with the soft tissue offload and so forth as well, which is really handy and positive if you have patients with a lot of pain in terms of muscle strain and so forth. The aim is that we want to work with the load. That is our biggest thing here, to provide a strong mechanical compression. We help with or resist the deceleration or acceleration. Permit applications which augment stability or introduce accessory motions and rotation. There are a lot of good things we can use the tape for. Patients may not have pain and function may be limited by load. On the other hand, depending on the pain process involved, the pain may well be load-dependent in a way. Once you clear that load out of the picture, a lot of the pain disappears.

The same thing with the skin reactions to the tape. We need to be vigilant about this and ask about allergic reactions. Skin reactions are obviously the same thing as kinesiology tape. You can have mechanical irritation and that is when we see when you pull the tape a little bit too much. It is good with a pull. But if you do too much, you will see mechanical irritation.  As I say to all my patients, regardless of what type of taping I use, if you experience any itching, burning, stinging, irritation, or similar, take off the tape, just remove it. If you want to reach out to Dynamic Tape out there. Now, rigid tape, I will just simply brush on this, we will go through in the live session how you tape an ankle and how you do things like that.  But the same thing here, it is like what we do in the live sessions is built upon you understanding what and how you do it, obviously. But also, that there are things that you must think about in terms of contraindications in the skin irritation, it is that simple. Make sure you think about skin irritation, circulation, and nerve supply, those are the big things. For crying out loud, use the right scissors, or use the right equipment if you do not want to like the top picture there. Please, be mindful of how you work with the tape, how you take it off, and how you put it on. Obviously, check for a capillary refill and so forth, we will go through that in the live sessions. Would you consider taping these injuries? I hope that with your previous understanding, and what you have done so far, is that you would consider maybe think twice about applying tape to these injuries. First of all, you want to make sure that it is not an injury that would sustain or create huge issues for the patients or athletes, think about that, please.

Obviously, you can see in the very picture that we have a dislocated finger. The second one down there, we might have a fracture because of the swelling and so forth. It is important, can we still tape once they are cleared? Obviously, when they are cleared if there is nothing there, yes, we can. Do I put tape on this before? I have sent them off or if I have made sure that you have checked it properly with the medic or X-ray and so forth, so, just think about that. When you understand the technique, you know a technique. But when you understand a concept, you know a thousand techniques. This guy knows a few things, “Education is not the learning of facts, but the training of the mind to think.”

I hope after this lecture, you have understood there are a lot of extra layers to everything we do and everything we have seen so far. Not to say that what you know already is not useful. What I am saying is take what you want from my lecture or my presentation but try to add on to what you already know and try to add on a little bit more of that fascial understanding and how much understanding of the fascia can change your practice. It changed my practice and my way of thinking. I mean, there is education or learning and knowing, it is not hard to bear or to walk around with. Please, stretch your mind as much as you can.

[END]

V2 2023 SCAT 6

DOWNLOAD ENGLISH – Concussion Scat6 2023 Transcript

Dr Jarosz:

ICSC01 Head Injuries  Section 1 – Sports Concussion Update 2023

Instructor Brett Jarosz
Video Lesson: 02:22:03

Welcome everyone to the Head-Injuries Annual Update. What this update is going to serve, is two purposes. We have got people who are already qualified with their ICSC. There is a requirement that they update their Head-Injuries Module every two years. This module will serve a role for the group that has already gotten their ICSC, this will be their update. Then we have got the group for those practitioners who are seeking to become ICSC qualified and achieve that ICSC certification. As part of the certification process, there is a Concussion Module which is what we are doing here now as the online component. Plus, during the hands-on, there is then a hands-on Clinical Application and Assessment of what it is we are going through today.

For those who already have their ICSC, this will be the update of the latest information. We are very fortunate to have had the Consensus Papers of the 10 systematic reviews, the consensus statement, and the 5 new tools that have come out, SCAT6, SCOAT6, Child SCAT6, Child SCOAT6, and the Concussion Recognition Tool. It is a very current update and looking forward to being able to share this information with everyone.

As we go through it, I will try to the best we can to separate it for the people who had doing the hands-on material. We will emphasise when this material where we are expected to know as the prerequisite before we get into the hands-on. That way we know what we should be studying, revising, and practicing before we go into the hands-on module and do our assessment at the actual Symposiums of the particular courses.

My name is Brett Jarosz, I am a fellow Sports and Exercise Chiropractor and Neurorehabilitation Chiropractor in Melbourne, Australia. My main thing is private practice here in Melbourne, Victoria. I also serve as a role as part of the Allied Health Team for the World Surf League.

The Disclosure from FICS. FICS makes every effort to provide contemporary information. Obviously, this module, is very contemporary, being only based on material released in June 2023. Hopefully, everyone gets a lot out of these next couple of hours plus in the hands-on for the new learners. FICS desires to build the best of the best in International Sports Chiropractic. I am hopefully demanding a little bit more from everyone in the field of Concussion. I will emphasize those sections throughout this presentation of how I would like to see our group become better and be some of the best practitioners in this particular space. FICS and their instructors are vetted by the FICS Education Commission, composed of academic members and leaders from most regions of the planet. The information instructed by me today has been established and approved by the FICS Education Commission, and FICS will not be held liable for any injuries as a result of today’s instructions. The majority of the material, what we will really be covering today is about assessment. That will be the overarching aspects of what we would be doing hands-on when you attend the Upper Extremity Seminar. We will also try and go into some aspects of, we call it Management for now. We will discuss some of these rehabilitation aspects later on, with those differences and nuances coming into play as it relates to Concussion.

The objectives of this presentation are, will go through the definition of concussion, the updated definition, and you will see there are still some issues with the actual definition. We will go through the Pathophysiology of concussion. We will go through of course, these new aspects that are going to be important for our Sports Chiro practice. If we are working sideline at an international event, such as the World Games or other events with FICS Sports Chiro practice, part of that team, or maybe the sole provider there, we must understand these things there that are in blue.

The SCAT, SCOAT, the Return-to-Learn, Return-to-Sport.

In the last bits in the end, there are going to be questions that are potentially that will be coming up from patients down the track. We just want to be across some of those topics, so that we can be better informed in our communities, in this particular Concussion space.

We will start here with the two groups here listed in the yellow list. The Concussion definition and the Pathophysiology. If we just look at some occurrences of concussion, everything, as for everyone recognizes that I will reference every slide where possible. Those references are at the end. If you want to go in and see the details and get further material out of that, all those references will be there for you in the final few pages of this presentation.

A concussion is among the most commonly occurring injury in sports. Globally, there is a one in five-lifetime risk of concussion. When you start to hear that number that’s up there, one in five, an estimated 3 million people, 50% are children and adolescents, sustain a concussion in North America annually. This is the important part, the majority of the concussion research comes from North America, the United States, and Canada. There are some that come from Europe, Scotland, I can think about with professional soccer, football. Limited but growing research coming out of Australia, with also football and rugby but the majority of the literature that we have with concussion, really big databases of this information comes from the US and North America. Of those 3 million people in North America that could get a concussion every year, 30% of them have recurrent concussions. They have had a concussion; they get another one. Then 30% remain symptomatic for more than one month. We will go through these definitions a little bit later on. Basically, that idea is becoming or remaining symptomatic for more than one month is where we are starting to get into realms of trying to separate concussion injuries versus persisting symptoms and how we want to look at these things differently. We will go through that throughout the course of this presentation.

Sport-Related Concussion when you see SRC (Sport-Related Concussion) reportedly accounts for 36% to 60% of concussions in children and adolescents. Children Adolescents, the basic ages for that, children would be said to be 5 to 12 years of age. Adolescents would be said to be 13 to 18 years of age. That pediatric population not including, obviously, the 0 to 4 age group here but 5-12, 13-18, you can see that the majority of Sport-Related Concussion is occurring in this age group. In Canada, one in nine adolescents sustain a concussion annually.

The concurrent concussion definition. The Concussion in Sports Group meets every 4 years to come up with a consensus statement. Now, because of the pandemic, the original consensus statement, although the consensus meeting was supposed to have occurred in 2020 got delayed until 2022. The meeting occurred in Amsterdam in October of last year, October 2022. The Concussion in Sport Group, the Expert Panel, you can attend the conference as an attendee for 2 of the 3 days, on the third day the Expert Panel is basically in a locked door room going through the research, and the evidence. They are debating, arguing, and voting for things. If we look at what is written here, in preparation for the Amsterdam Concussion Conference, the Scientific Committee considered that the Berlin definition, which was the definition from 6 years prior, should have been 4 years but 6 years prior, they considered that the definition that they had from Berlin required modification to align with more recent scientific evidence relating to advances in our understanding of Sport-Related Concussion pathophysiology.

Research evolves, science evolves, and as our understanding evolves so do our definitions, our management strategies, our assessment strategies. All of it has to continue to evolve. We will see that there are similarities, for those people who currently got their ICSC, you will see a number of similarities that have continued from when you have done this material a couple of years ago. For the new learners, this will be new. At the same time, we will see for the people with the ICSC already, you will see what things have been updated into this new consensus, SCAT6.

The conceptual definition and this is where the consensus statement in the Concussion in Sport Group becomes important because for them to achieve consensus they need to get an 80% consensus vote from their Expert Panel, which I believe is 28 people. They need to get an 80% agreement in order for something to be put into the consensus. The conceptual definition was accepted but as a majority decision, because it was 78.6% but not reaching an 80% consensus. The definition that now is currently in play, for the definition of Sport-Related Concussion is that it is a traumatic brain injury caused by a direct blow to the head, neck, or body resulting in an impulsive force being transmitted to the brain that occurs in sports and exercise-related activities.

Symptom 1, where I just want to get a visualization concept for everyone, is I want you to take that first line and realize that I do not need to get hit in the head in order to have a concussion. I could take a blow to my chest or somewhere in my body, for example, and then my head gets thrown. That impulse gets thrown into my brain, through that impact through my body. Let us use an example here to sort of define this. I was driving my chiro and I got hit from behind. I have that acceleration-deceleration injury that we then call, whiplash. Let us break that down, the mechanism was an acceleration-deceleration injury that occurred to my neck, and we call that whiplash. A concussion is an acceleration-deceleration injury to the nervous system. If we can visualize that as a concept and look at that first sentence again it is a traumatic brain injury caused by a direct blow to the head. If I get hit, this gets accelerated-decelerated, or get hit in the neck, accelerated-decelerated, or to the body, accelerated-decelerated, that impulsive force is transmitted to the brain that occurs in sports and exercise-related activities.

Naturally, some, hopefully, a lot of you guys, would be thinking, therefore in a concussion you can have a whiplash but hopefully, when you flipped open a yellow light, if you have a whiplash injury you can also have a concussion. As this presentation evolves on we are going to start to realize that if you are dealing with whiplash and/or dealing with a concussion, you are going to have to start to learn that we have to assess a lot of things. It is not just the neck, and it is not just a couple of little brain tests. We have got to assess a lot of things.

That particular force being transmitted to the brain, sentence 2. This initiates a neurotransmitter and metabolic cascade, with possible axonal injury, blood flow change, and inflammation affecting the brain. Conceptual here, again, for everyone. I want you to view sentence 2, neurotransmitter, metabolic cascade, axonal injury, blood flow change, and inflammation. I want you to view that sentence alone. I want you to think that is a concussion. Think of it just like if I tear a muscle, I get a bruise to a muscle, a hematoma, the inflammation that occurs, all that healing process, will just be the same thing going on with the brain. When that comes in, you have got a concussion, and when that inflammation, metabolic cascade normalizes, the blood flow returns to normal, and the concussion is over. This is an important part. We have a couple of slides on this coming up. I want you to view that that sentence, sentence 2, that is what the concussion is. This inflammation within the brain.

The symptoms and signs may be present immediately, or they may evolve over minutes or hours, commonly resolved within days but may be prolonged. They are generally there immediately, and the tricky part with concussions is someone may get what looks like a concussion injury. The athlete or person that is not playing sports has a fall, for example. We are talking about sports in this presentation. They are playing sports, they have an injury, which looks like a concussion. When they get up, they have no symptoms, you cannot see any signs. If you do your exam there is nothing that you can see, you are right, they are cleared to play. Then in an hour, half an hour, a few hours later the symptoms start kicking in.

This is where concussions can be problematic because we might be returning athletes to the field because we have done all the appropriate assessments and exams. Nothing is present on the exam. We will discuss the little nuances with that. The symptoms, usually, resolve within days, but may be prolonged. You are going to see the slides coming up. Basically, they will say, we expect most people to be able to go through the basic concussion recovery process. The concussion being there, inflammation, and metabolic cascade inside the brain. That process, can recover from that in about a week but they are now starting to show, through advanced studies, coming up in sentence 3 or 4, that this process may actually take up to probably 4 weeks, maybe up to 45 days. That idea of most people recover from that metabolic cascade within about a week, but they are starting to say that may be about a month.

No abnormality is seen on your standard structural neuroimaging, CTs, and standard MRIs, but in the research setting abnormalities may be present on our functional MRIs, Diffusion Tensor Imaging, Diffusion Tensor Tractography, PET scan, SPECT scan, and QAGs. What we are saying here is that they are starting to include some of these advanced imaging studies that use research because these have been starting to show, there are changes in the brain in a concussion, even though our standard imaging, CTs and MRIs, we normally use do not show anything. We are saying that there is no real structural problem but there appear to be functional problems that are occurring when we have a concussive injury.

Sport-Related Concussion result in a range of clinical symptoms and signs that may or may not involve the loss of consciousness. A general rule, there is only about 10% of people that have lost consciousness during a concussion, and 90% of concussion injuries do not lose consciousness. There are clinical symptoms and signs of concussion that cannot be explained solely by drugs, alcohol, medication use, or other injuries such as your neck or vestibular system or anxiety, depression, and other comorbidities. The clinical signs and symptoms cannot be explained solely by those things but you may have concurrencies. Someone may have depression or anxiety or a neck injury and then go and play sports and they go get the head injury and those previous symptoms can concurrently with that concussion injury. There’s our current concurrent definition.

We want to go through and break all these down more in detail. Before we do that, we talked a couple of slides ago about they could not get to a consensus. Sport-Related Concussion has long endured the absence of a universally accepted definition, complicated by different terminology such as concussion, and mild traumatic brain injury.  When you guys look through the literature, what you will see is the research that talks about concussions, and then you might see another research article that talks about Mild Traumatic Brain Injury (mTBI), and that mTBI research article is actually talking about concussions. They use the words interchangeably and this is what starts making confusion.

The actual Concussion in Sport Group in Amsterdam, they were trying to create a more universally accepted definition. As part of that, they recognized that the Concussion in Sport Group (CISG) recognize the American Congress of Rehabilitation Medicine (ACRM) that that group had a Mild Traumatic Brain Injury Task Force, and they were doing a similar thing. The consensus group, the Sports Group, they were trying to come up with an updated definition. The Concussion in Sport Group was trying to take the ACRM diagnostic criteria for an mTBI and they were trying to blend them in, the two groups trying to work together. I will talk about where the numbers went on the next slide. You can see there, this was taken from the Davis article, from one of the systematic reviews from the consensus meeting.

We have got now, the Sport-Related Concussion definition here on the left, which we just talked about in the last slide, they used the words there. Then we can see that the American Congress of Rehabilitation Medicine on the right side, they have their diagnostic criteria there for Mild Traumatic Brain Injury. You are going to see the similarities there, but then there are differences. The point that I really want to emphasize here is in the next slide.

Only 16 out of the 28 of the expert panel, not even 60% voted to incorporate the ACRM diagnostic criteria into the consensus. Remember we said, we have to get 80% to have a  consensus agreement for the Concussion in Sport Group. The point of divergence was the scenario where an athlete with the biomechanically plausible mechanism of injury presents with acute symptoms of Sport-Related Concussion but no signs. The athlete has an injury and maybe they are saying, “I have a headache,” or “I am dizzy,” or whatever it is. They have one or more of the possible 22 symptoms that are considered to be the common symptoms of concussion. They have the symptoms but when you test them there are no signs. Their memory is okay, their neck is okay, their orientation is fine, their balance is fine. We will go all through this in seconds. There are no signs, there are no observable signs. They did not lose consciousness, they are not having seizures, and they do not have the staggers. There are no signs but they have symptoms.

It was recognized by the Concussion in Sport Group Expert panel that this a situation that the ACRM criteria classified the athlete with a suspected Mild Traumatic Brain Injury but the Concussion in Sport Group has consistently maintained that clinical signs of a concussion may frequently be absent and that in such cases the diagnosis of a Sport-Related Concussion can be established by the presence of symptoms alone. That is an important point, because when we look at the research the majority of concussion research, including in this consensus, the assessment and management, and clinical recovery, I used the word “clinical” importantly, which is based around symptoms. For you to have recovered from a concussion, it is about whether or not your symptoms have gone away. We also know that the more symptoms you have, and the more severe those symptoms are when you first had the head injury, the greater probability that you will have a prolonged recovery. The symptoms are still the number one driving thing as it relates to concussion and that is where I am going to ask our group to try to be better. I will explain why throughout this presentation, especially towards the second half of what we are doing here today.

The Concussion Pathophysiology, as we said, is the direct blow to the head, neck, or body that results in an impulsive force being transmitted to the brain. The yellow there is what I would like you to think is a concussion. In the red, think, that is my acceleration-deceleration mechanism. Yellow is what is a concussion, the inflammation in the brain. In the blue there, as we said, nothing is shown up in standard imaging but when we looked at the advanced imaging that is being used in the research setting, that is where we are starting to see the evidence of concussion functionally, and that is an important part. These are functional things where we are seeing different blood flow aspects, and different metabolic aspects in different areas. The advanced imaging which we cannot use as clinicians to refer and go say, “Can we get a DDT for assessment to see if this is a concussion or not.” They are only using that in the research right now.

Here is the Neurometabolic Cascade of Concussion. This is still the model that is considered that is going on within the brain in 2014, this was where it was talked about. When I want to think about the mechanism, I have that acceleration-deceleration injury. As part of that acceleration-deceleration think about what happens to your neck. If that head goes forward, the back of the neck stretches and when I go backward the front of the neck stretches, or if it happens sideway.

I want you to think the same things are happening to your nervous system. Because the head sits on this 3D neck, when that acceleration occurs, because the head is on the neck there is generally an element of rotation that always occurs. As that occurs, we have these nerves that are stretching inside the nervous system. Now, think about wringing out a towel, if I wring out a towel, the water will come out in the middle of the towel. That is probably where we look at these advanced imaging aspects, we do see frontal lobe things, but we will see a lot of these midline pathways through the brain areas that are being affected. We will talk to you about what that essentially means for our assessment and management later.

For this perspective, for this cascade, when I get that stretching of the axons, you have the nodes around the area if you go back to your whole neuron anatomy physiology, you have different sodium, potassium pumps and all these gates that allow these ions to move in and out. These are usually regulated. You have plugs on them, you have gates that allow things to get in, but when you have that stretch, suddenly those gates just open and the ions start flooding in. What happens now is that the sodium starts flowing into the cell, and calcium flows into the cell and that is what creates action potentials. I have all these increased activities going on in the cell, especially once calcium starts getting in there, you are starting to release glutamate which is an axonal neurotransmitter, another side story.

Now we got a situation that your cells are firing like crazy but, in step 2 you can see there is an energy crisis. I will show you in the next slide in a graph what actually happens at the same time all of the ions are going into the cells while potassium is going out. The important one here is sodium and calcium are going in, which is activating the cell. Glutamate is released to the next cell. That cell is firing like crazy. Everything is firing the brain. The blood flow into your brain is decreased. We have decreased cerebral blood flow. What is the blood doing? It is bringing nutrition and it is bringing oxygen. This is your bread and butter for producing ATP. You need your glucose, you need your oxygen to be brought in in order to produce ATP. Why is that important? Because the ATP is the energy that you need, if you look at the picture there, it says the potassium pump. You need ATP to get those sodium, potassium pumps, to pump the sodium out of the cell and get potassium in, to get re-polarization of the nerve cell. But because you are losing that oxygen in the blood flow, you are losing the oxygen and the nutrition in the cell. What starts to happen is now you have an energy crisis. We have all these cells firing but we do not have the ATP to keep the balance, the re-polarization, getting things back in and out. Everything is just flooding in.

Now, because of all that stretching some of the advanced imaging is now showing that stretching might actually cause shearing and sometimes even complete “snapage”. You might get this absolute separation of some of the pathways, or some of the axons can completely be separated. We get this non-continuity of the actual axons that sort out cytoskeletal damage, axonal dysfunction, altered neurotransmission, and inflammation and the cell can die. If you keep a cell going and you do not have that ATP coming into a cell, nerves can blow up from that. That is not good. That is the Neurometabolic cascade. If we look at it in a graft sense you can see the calcium is going in the cell, at the top in green. Potassium is coming in. What we can see at the very bottom in the blue or gray-blue is you can see that cerebral blood flow is down. You can see the percentage of normal there, it is nearly 50% of where it normally is. Look at those amounts, calcium is not good to have a bunch of that going into the cells because it creates toxicity. That is actually the thing you need to create, plasticity in the brain. You can see here how calcium, at that level, can potentially draw faulty plasticity.

We have cerebral blood flow being decreased there. Then when we look at the graph from the bottom and what they suggested is that this process normally takes, they used to say, about 10 to 14 days in adults to recover, you can see in this graph, it shows 10. They used to say it takes 4 weeks in children. They are now saying that this process can take up to 4 weeks. Most people tend to recover from their symptoms in about a week, but they are saying that this process may take up to 4 weeks, and that is because of what we are seeing in advanced imaging.

Go back a step to our definition, which talked about this Neurometabolic Cascade. We said that this here, on this slide, and on that previous slide, that this is what I want you to think a concussion is. When this process starts, that is a concussion. When all these chemicals and the blood flow and everything get back to normal, homeostasis, the concussion is over. The question starts becoming after that, what happens when people still have symptoms after that period? Now we are getting into a realm of different diagnoses, and a different conversation.

If we look at just the concussion, the metabolic cascade, the associated signs,  and symptoms, as we can see there at the right. They are the 22 symptoms that are considered common in a concussion. This scale is the post-concussion symptom scale. This is the second step of our SCAT6 that we will be going through. This is where we write these symptoms. Headaches and dizziness are the most common symptom that tend to happen but you will also have other people who have a concussive injury and they talk to you about they feel like they are in a fog, they do not feel right, maybe a little confused, and maybe some fatigue. We can see here that these symptoms are very nonspecific. There are a lot of other conditions out there that can have symptoms like these. They are sensitive to light, and immediately what people would think of that, is a migraine. This is the way our thought process work.

The importance of the concussion is, I want us to be better than just these symptoms. As important as these symptoms are, I want us to be going better than this.

Clinicians and athletes can expect a minimum of 1 week to complete the full rehabilitation strategy. We will go through that towards the very end of the presentation. Based on what we are talking about, being able, in an ideal scenario, from injury to Return-to-sport, you can say a minimum of 1 week to be able to achieve that. Typical unrestricted Return-to-Sport can take up to a month. This is a big change from what was previously said. It was said that it would take 10 to 14 days normally in adults, and 4 weeks in children but now, they are saying typical Return-to-Sport takes up to a month post-Sport-Related Concussion.

The time frame for Return-to-Sport may vary based on individual characteristics, necessitating an individualized approach to clinical management. This is the part where I really want to emphasize here is, individualized nature. We will see that there is a lot of generalization. This is what we do from an exercise point of view, this is what we do from a generalized rehab point of view. We want to get good enough at our assessments that we can tailor how we are prescribing our exercises or our rehab strategies to that individual to hopefully, enhance better outcomes for that individual rather than trying to cookie-cutter some rehab protocol for every concussion. Then on the bottom there, you can see, 30% of adolescents experience persisting post-concussive symptoms beyond 1 month.

When we look at these persisting symptoms, the Amsterdam consensus recommended to include the use of the term “persisting symptoms”. The words used to be in Berlin it was “persistent symptoms” or “persistent post-concussive symptoms”. Whereas now they just refer to using the words, we now just have “persisting symptoms” and they do not use the idea of concussion in there. Persisting symptoms are to be used for symptoms that persist greater than 4 weeks across all age groups, children, adolescents, and adults. Again, it used to be, until this consensus made in these papers, it was said that adults would have 10 to 14 days. If you have symptoms lasting longer than that, that was considered persisting symptoms. Children and adolescents were considered 4 weeks, and if they had symptoms after it, that was considered persisting symptoms. Now, it is everyone. No matter what your age is persisting symptoms is if you have had a concussion and have not clinically recovered in 4 weeks you are said to have persisting symptoms.

Symptoms attributed to concussion are non-specific, as you have heard me say before, commonly also reported by healthy individuals, think like you had a bad sleep, light night. You wake up the next day you have a number of these symptoms just because of poor sleep. We can also have other conditions, other than concussion that could cause those symptoms, either migraine or depression. The other aspect is those other conditions can be exacerbated by the concussion or they can be exacerbated by biopsychosocial factors aside from the concussion.

All of these things need to be assessed in the context of persisting symptoms. Other problems may exist prior to injury that can be exacerbated by concussion co-occur with persisting symptoms or mimic persisting symptoms but do not arise from concussion.

A mouthful of writing but if we got this, here is a person at baseline, and that baseline, let us say, they have anxiety and they have migraine as well. They have anxiety and they have migraines. They now get hit with a concussion. They also have this stuff beforehand. They have whatever concussive symptoms that are going on, that concussion may exacerbate this, which is their anxiety or their migraines. The injury may exacerbate that or these things here may exacerbate these symptoms, and then, that period, that metabolic cascade, the concussion is now over but the person still saying that I have symptoms after this concussion. The question then becomes did the concussion injury create, when we will talk about these external changes, miscommunications, damage, et cetera to the different areas of the nervous system, it did that. Metabolic cascade, once that was over as part of the external injury, did that create problems that are creating the persisting symptoms or is it that the previous stuff that they have, the migraines and the anxiety, is that causing it? We can see the complexity of this.

I can tell you that when you got concussion patients and I see, unfortunately, I’m a little bit biased when it comes to this that is why I say I want everyone to be better because I see all the concussion cases that failed. All of my concussion cases are people who are months to years after having a head injury and they still have got persisting symptoms and could not get their life back. My bias is because that is what I see, so I want everyone to do a better job because we don’t want to see people like this. But that part is one of the biggest things we spend time in my clinic educating patients about previous stuff, concussion, persisting, and how they interlink with each other, and it is an important education process especially when we are dealing with the biopsychosocial stuff, mental health, depression, anxiety, and have those things can be sensitizing this and vice versa.

A multimodal clinical assessment is indicated to characterize individuals with persisting symptoms, including the types, patterns, and severity of the symptoms. Of course, that is where we can just use that symptoms scale, plus some other scales as well that are out there. We will talk about them and any associated conditions and other factors that may be causing or contributing to the symptoms. Let us talk about it.

Mental health issues. We have to assess and discuss these things. History of these things maybe some patients reported the outcome measures to quantify those things. Learning and attention difficulties with these people like ADHD, dyslexia, et cetera. Visual, oculomotor, cervical, and vestibular problems. Visual processing or movement issues, neck issues, inner ear balance, reflex issues from ears to eyes, ears to spine. Headache disorders or migraine. Sleep disturbances, that is a huge one, we will get to that a bit later on. Dysautonomia, I’m going to get to that one later on because that is a bit exciting for me personally because of what the consensus group has brought in. Postural orthostatic tachycardia syndrome, orthostatic intolerance, as well as pain. When we look at these, that there, and I can suggest to you guys, there is actually a couple of more things in there that we should also be considering but that is your multimodal clinical assessment for someone who is coming in after concussion and they have got the symptoms still going after 4 weeks after the injury. We have to be doing all of that and more. That is a lot of stuff and if people are looking at that going, “Yeah, I want to be able to work in these concussion spaces but I don’t have time in my clinic.” One of my suggestions to you is, you either start creating new appointment types and charge for them accordingly, or you book these types of patients as the last patients of your shift so you can run overtime because you do not want to worry about your clock. You want to make sure that you get all the appropriate assessments done and to give you an idea, for me to do my physical assessment in the clinic, it takes me a bit over two hours or two-and-a-half hours to run through my complete assessment of someone with persisting symptoms after a concussion.

All right, the SCAT6. For the people who have got their ICSC, this would be the update for you guys to know where the differences are in the SCAT6. For the new FICS Sports Chiropractors who want to attain their ICSC, this section now is what we are going to need you to review this, and again, once you have done this section with me, maybe you want to review this. Just grab your SCAT6 hard copy, and download it free from Google, just type in SCAT6 and you will get a free PDF. Download that as a hard copy and start reviewing, working through it, and practicing it because when we get to the hands-on module, so for those that are coming to the Adelaide module here in Australia, that is about 3 to 4 weeks’ time. I will be running through that hands-on module here and this material that we are doing now is assumed knowledge, it is a pre-requisite knowledge so when we get to the symposium, it is right where we are into the hands-on. None of these makes blinding how any of it works because it is assumed knowledge from this and we want you guys to practice this as many times as you can, leading to the hands-on because we will have instructors around the room assessing your ability to perform these tasks on each other. All right, here we go.

SCAT6 is endorsed by the International Concussion Symposium. These points are bolded here. This cannot be performed correctly in less than 10 to 15 minutes. These assessments cannot be done 3 minutes out on a pitch. Part of this is the concussion in Sport Group’s attempt to try and get sporting organizations to change, I’m going to pick on soccer here because soccer has a time limit of how long a doctor has got on the field to assess an athlete and make a decision as whether or not to remove him from the field play. Why that is important in soccer because if you take an athlete off to assess them, that player cannot return to the field. This is the concussion in Sport Group’s attempt to start, say, “Hey, in order to assess a concussion properly, you need at least 10 to 15 minutes. We got to have to make some rule changes within the sport in order to allow us to be able to do a proper assessment.” That being proper I want to use the word maybe “the minimum standard assessment,” this is the minimum standard. We can do more than this, but this is the minimum that we need to do and it is going to take a minimum of 10 to 15 minutes on the field and on the sideline to run through this to try and help you make a decision. The SCAT6 is designed for the acute phase. It is designed realistically to be used in the first 3 days and it can be used up to 7 days. But it starts losing its clinical utility in about 3 days and definitely after 7, but 3 days about that window with the exception of your symptom scale. That post-concussion symptoms scale, we keep using that as we said because the biggest predictor as well as the indicator of recovery, is this clinical recovery which is the symptoms that have resolved. If it is 7 days post-injury, we want to use the new SCOAT6, which is the Sport Concussion Office Assessment Tool and we will be touching base on that. That will be new for our ICSC current holders, and for all of the new attendees, this is going to be a brand new section that would be brought into this presentation and into the hands-on module.

The Child SCAT6 is for children aged 8 to 12. For an adolescent 13 or older, you use the Adult SCAT6 that we have on the previous page but if we are talking about 8 to 12, we are using the Child SCAT6. The same thing, cannot be performed correctly in less than 10 to 15 minutes, still the same thing with 72 hours up to 7 days. The thing that is a little bit different, and we have not gone through the SCAT6 yet but just sort of flagging it, where the child one is different is that symptom scale. You have the option to choose[?] well, that is so the children fill them in but you also have an option for the parent to then also fill in their child’s symptoms, so, there are two symptom scales. One with the actual athlete child fills out himself and then we have the one that the parent fills out. When we get to the orientation questions, which is called the Standardized Assessment of Concussion, the orientation section does not exist in Child SCAT6. I will talk about that a bit more when we do the SCAT6 as well as the Maddocks questions.

The Maddocks questions do not exist in Child SCAT6. There is one part of the sideline test that they now do, which is new to the adult and the child. This was never in the SCAT5 but they are now using tandem gait and the difference with the child one is they put a complex tandem gait into the Child SCAT6. Where are the differences? They have two sets of questionnaires for reporting the symptoms in the child. There is no orientation, no Maddocks questions and they have the complex tandem gait in that SCAT6.

From our perspective, if we look at this from 13 years and up for adults, the diagnosis of concussion is a clinical determination made by a Health Care Professional (HCP), or Health Care Profession. SCAT6 should not be used by itself to make or exclude the diagnosis of concussion. As I said before, this is a minimum standard. The important point that you can see there is to note that an athlete may have a concussion, even if their SCAT6 assessment is within normal limits, and that is the point that we want to be able to do more. We want to be better than the minimum wherever we can.

Part one, again, from the learners attending the hands-on module. This will be part one of what we are going to be expected to work through and understand. This is the immediate assessment. You see an athlete get a suspected concussion injury on the field, so, you see a collision, you see someone down on the field, you are going out onto the field to perform an immediate assessment, neuro screen, and everything about this is basically think first-aid principles. Do we need to get this person transported to a hospital? We want to be thinking about this. When you are going out there, we are doing our whole Dr. ABC stuff. Some simple rules, if you see a collision, and you see someone go down, and they are unconscious, you think neck until proven otherwise. The whole process of if someone is wearing a helmet, we are not removing the helmet unless it is about airways, and then you have got to have the qualifications in order to do that. We are protecting the neck. We are not moving these people unless, again, it is for airway purposes. It is all about spinal and spinal cord injury prevention, so, the process of spinal boards, and we will do these emergency procedures through the FICS courses. But we have got first aid principles. If you see them get hit, and they go down and they are unconscious, you are always thinking about the neck and spinal cord injuries. But if you see someone go down away from play, they just go down and there is no one around them, you think cardiac. Some simple things here, even though this is a concussion course, we are healthcare providers, and you are assessing through and you might be running out on the field to look at an ACL or an inversion sprain or Charley horse. We have got all these different types of injuries, but obviously this one is specifically for concussion. You run out onto the field, you immediately assess and we are looking for our red flags, we’ll go through those in a second.

There are 11 different red flags. If we see the red flags, are there any of those there, you can see they just follow the flowchart, remove from play, have an immediate medical assessment, or transport to Hospital Medical Center because we are worried about things like brain bleed, spinal cord injuries, et cetera. We do the red flags. If there are no red flags, then we move into the positive observable signs. We will go through those. If you see those signs, again, is the whole removed from play? Anytime you see the yes, it’s removed from play, and we will think about medical assessment, transport to the hospital, and it’s all depending upon the scenario that you are in as the health provider. Are you the only one there? Do you have the medical training to be able to be doing all those things? Well, you can say, “No, I’m not a medical provider. We are going to have to probably get an ambulance.” Are you part of a medical team? If I am, let us say, working the surfing at Bells Beach, we have our water safety patrol that is out there on the jet skis in the water, we have a shark drone, we have our TV drone, we have then our emergency doctor down on the beach, we have an emergency nurse down on the beach, and then we have allied health up the top to go down and help if we need.

The medical doctor is at the top and it’s this whole team process of knowing where obviously, we have got the water safety for obviously trying to prevent drownings and things like that, shark attacks if those things happen, and obviously shark spotting and getting athletes out of the water. Then we have got the injuries and then doctors, nurses, and team, and knowing what each of our roles is in each of those scenarios. If there was a head injury at Bells Beach, for example, our medical doctors would be running through this stuff first, and then I am there as part of that team to then to help in basically the next section, knowing where our roles are in each of those scenarios. You just work through this flowchart here and we are going to go through each of these things in a second. But if any of them is yes, it’s the removal from play, thinking medical assessment, hospital transfer as required. If it’s no, it’s like no, no, no, no worked through, and we just continue to work through the SCAT. This is part one of the SCAT. This is you running out onto the field, and trying to assess immediately, and we are thinking all the bad stuff.

Box one, the red flags. Is there neck pain or tenderness upon that initial injury? We are worried about fractures and dislocations, those things, the bad stuff. Are they seizing or convulsing? Is there double-vision? If you see double vision, we are naturally starting to, the bad one that we’re worrying about, is we got a blow and we have damage that is going to occur to obviously some of these cranial nerves that are occurring. We get someone that has an eye looking this way and this way. That is not how it is supposed to be. Our eyes should be yoked together.

Loss of consciousness. If someone has lost consciousness and we will talk about some of the other observable signs coming up. If they are unconscious on the ground, naturally, as we said, we are thinking neck if we see the blow. If it happened away from the field of play, the athlete has just gone out with a cardiac event. Someone has some weakness, tingling, or burning in more than one arm or in the legs, again, red flags.

Deteriorating conscious states. They have not lost consciousness, but you are watching them go in and out and are starting to become dazed, falling asleep, or these types of things. Not good.

Vomiting is the interesting one. If we look at some of the guidelines, you will see that some people say, if you vomit twice, then other people say one projectile vomiting, that is going to be a clinical judgment. But if you have gone out there, someone has had a blow, and they throw up straight away, you are removing them from the field of play for further medical assessment.

Severe increasing headache. Obviously, you are worrying about brain bleeds, intracranial pressures, and things like that. Increasingly restless, agitated, or combative. Glasgow Coma Scale less than 15. Obviously, from a red flags point of view, you can see here that you are performing the Glasgow Coma Scale to a degree because of a part of your observations. For those that are not familiar with it, we are going to be running through that. I have an attached video, that is actually a brilliant video. It does a better job than I’m going to be able to explain it. We will just share that with you. Then a visible deformity of the skull. If we see any of these red flags, removal from the field of play, medical assessment, and is it at a hospital transfer. There are clinical judgments to make.

Then our observable signs. We have done the red flags. If there are any of those, remove them from the field of play, where we go then, our medical process.

Next step, did you see someone lying motionless on the playing surface? Unconscious, falling unprotected to the surface. This is someone who gets hit and when you watch them go to the ground, they do not put their arms out to protect themselves, because falling unprotected means they are ragdoll, which means they got hit and they are unconscious now, and they are unconscious, falling to the ground unconscious. Of course, what happens then, they tend to hit their head again on the ground. The first two there are really about unconsciousness. You see these things; it is removed from the field of play. Balance gait difficulties, motor and coordination, ataxia, stumbling, and slow laboured movements, a simple way to view that point there, just picture someone drunk, staggering around. If you picture that in your mind, it is that type of stuff when somebody stands up and they collapse back down to the ground. They are staggering around, but they get up and you see their legs go on them, see them wobbling everywhere. They are the things that we are thinking about in that observation.

Then you have got your disorientation, confusion, staring, limited responsiveness, and inability to respond appropriately to questions. You will see, this is where we start to get into some of the Glasgow Coma Scale types of questions, our Maddocks type questions. You will see that there is interchangeability with some of these steps. But where did we see any of this blank or vacant look? That sometimes can be tricky. You must know the athlete sometimes to know, is it just how they look? Or, do you make a judgment call to go do that that looks like a vacant look? Facial injury after head trauma. Impacts seizures. That one is an interesting one so, for those that follow American football, or if you do not, Tom Savage’s concussion that he had that was missed several years ago. He had an impact seizure that was missed. Jump up on YouTube, and type in Tom Savage’s concussion. It is so subtle. It looks like a regular hit. He gets tackled and goes to the ground, nothing malicious. But if you carefully watch his right hand when he rolls over is having little seizures like this, and that was missed. That changed the NFL spotting concussion gameday guidelines. Impact seizures are now part of those observable signs and then it is at a higher risk mechanism of injury as someone fallen from jumping in the air and standing up on someone’s shoulders and neck and they had fallen to the ground. This is in chiro racing activities. This is surfing and we are in a pipeline or choke, and we have some big 15-foot wave, and it’s slamming the surface into the reef, underneath it. Did you get the idea? High-risk mechanism of injury. We are observing these things and when you see any of these things, we are moving them from the field of play. Medical assessment, transport to the hospital, making those clinical decisions, and what needs to occur there.

Now the Glasgow Coma Scale. As I said, this video is going to do a better job than me explaining it. I will put this on in a second. But as you can see, that is from the SCAT there on the left, our responses, our verbal responses, and our motor responses to get a Glasgow Coma Scale out of 15. If we see a score less than 15, it is removed from the field of play. Let us run through this Glasgow Coma Scale.

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Sir Graham Teasdale: Current assessment of consciousness is often crucial in the care of a patient with an acute brain injury. This film will provide a practical guide to using the Coma Scale that we developed in Glasgow, to ensure reliable assessment and clear communication about the patient. We will show you how to make a series of standard observations of three aspects of the patient’s responsiveness. Eye-opening, verbal, and motor responses for stimulation. Steps in each component can be rated according to defined criteria to show the degree of impairment present. We will show you how to record and communicate your findings, how these can be used, and provide you with a downloadable sample.

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Narrator: When assessing a patient, there are four steps: Check, observe, stimulate, and rate. The preliminary check is used to identify any factors that might interfere with your assessment. It is important to identify local factors such as a hearing impairment that could cause a lack of capacity to respond. Following these preliminary checks, we observe the patient, noting any spontaneous behaviours in any of the three components of the scale: Eyes, verbal, or motor. The patient is rated in each component by matching findings with a corresponding criterion.

There are 4 criteria for eyes, 5 for verbal, and 6 for motor score. For each component, the top criterion is a normal response. Whilst the lowest criterion is no response. If the patient’s eyes open spontaneously, spontaneous is recorded. Remember, there may be local factors such as swelling that prevent eye-opening. If the spontaneous opening is not demonstrated, a verbal stimulus is used by introducing yourself clearly and requesting eye-opening, if necessary, by shouting. If the patient opens their eyes, the sound is recorded. If the patient does not open their eyes when you speak to them, a physical peripheral stimulus is then applied. Stimulation starts at a low level by pressing on the nail tip and is applied with increasing intensity for up to 10 seconds until the patient demonstrates a response or until maximum stimulus has been applied. If the patient opens their eyes, record the pressure. If they do not open their eyes, record as none. If there are local factors such as swelling interfering with eye-opening, record eye is not testable.

To assess the verbal response, ask the patient to tell you their name, where they are, and what month it is. If answered correctly, record orientated. If during the conversation, the patient can speak in phrases or sentences but is unable to give the correct answers to these questions about orientation, record, confused. If they do not talk sensibly, or talk to single words, record words. If the patient moans and groans with no recognizable words, record sounds. If the patient makes no sense at all, then record none. Remember, speechlessness may result from factors other than depressed consciousness. For example, the presence of an endotracheal tube. In these cases, record, verbal is not testable.

To assess the motor component of the Coma Scale, first, ask the patient to perform a two-step action by asking them to grasp and release your fingers with their hand or opening their mouth and sticking out their tongue. If the patient does this, record, at base commands. If the person cannot move their arms, for example, because of a spinal injury, you should ask them to open their mouth and stick out their tongue. In a patient who does not obey commands, a peripheral stimulus alone is inadequate to assess the motor component to the Coma Scale, and an additional central stimulus is needed. This is first applied by the trapezius pinch. To perform this, place your hand over the patient’s shoulder and press your fingers into the muscle above the shoulder blade. Apply pressure with increasing intensity for up to 10 seconds until you are sure that the response you observe is a patient’s best response.

The second location for central stimulus is a super orbital notch. Apply this stimulus if there has been no localizing response to the trapezius pinch. This stimulus is applied by placing a hand on the forehead with a thumb over the upper rim the orbit feels for the notch in the supraorbital margin. Apply pressure with increasing intensity for up to 10 seconds until you observe the patient’s best response. The patient should not be rated as having an absence of response until the maximum stimulus has been applied. This stimulus should not be used on patients with facial injuries adjacent to the supraorbital notch. If the patient moves their hand above their clavicle, or collarbone, in an attempt to move the stimulus away, record, localizing. If their upper limb does not reach the clavicle but does flex, then they are either normally or abnormally flexing. In clinical practice, the assessment of these non-localizing responses is based on a combination of both peripheral and central stimuli. In normal flexion, the elbow bends and the arm move rapidly away from the body and from the stimulus. In abnormal flexion, the elbow bends slowly and the arm comes across the body. If in doubt, record, normal flexion. If the patient extends their elbows rather than flexing them, record, extension. A patient who makes no responses is recorded as, none. If they are paralysed by other factors such as paralysis by drugs, record, motor not testable. If different responses are exhibited between limbs on the right and left sides, record the better side response as the best index of overall responsiveness. The response of the worst side may reflect focal brain damage or local injury.

To recap, check for factors that might interfere with your assessment. Observe the patient for spontaneous eye-opening, speech, and movement. If necessary, then stimulate the patient, first, verbally, and then physically. Findings should be documented clearly on a Coma Scale chart.

Brett: All right. As we can see this process there, we go through the idea of observing. Observing, obviously, is what we really want to see with our eyes, our verbal responses, and our motor responses. They are the things that we are hoping that we will see straight away. If not, we then have our sort of verbal aspects so that you did respond to the verbal stuff. Then, we have our palpation and pressure, pain generation stuff. The Glasgow Coma Scale, step one, when we go through this and the hands-on, you will have your SCAT with you. I will have this up on the presentation board. We will have all of these things there. You will work this through with a partner, working through and talking through those red flags. What it is that we are looking for, those observable signs talking what you are looking for, then you will go through the Glasgow Coma Scale. You could talk about how we can create a couple of different scenes during the hands-on module and score these things.

Then, step 3 will be a Cervical Spine Assessment. Now remember, this is immediate stuff happening out on the field. This is not like what we are doing in our office as chiropractors. It is just quickly going out there. Remember, as we said, if a patient is unconscious, as they can see here, or is not fully conscious, a cervical spine injury should be assumed, and spinal precautions taken. Does the athlete report neck pain at rest? Is there tenderness to palpation? Obviously, we are palpating spinous processes along those paraspinal muscles. If there is no neck pain and no tenderness, does the athlete have a full range of active pain-free motion? This is basically your myotomes and dermatomes, are they normal? They are going to be our quick on the field, neck assessment and again, if we see anything there, so if they go, “Yes, my neck hurts,” let us remove them from the field of play for further medical assessment.

Step 4, your coordination, and ocular motor screens are basically just finger-to-nose with the eyes open, and then finger-to-nose with the eyes closed, and then we are going through standard cerebellar testing there. Do you see an intentional tremor? Do you see dysmetria, whether it is hypometric or hypermetric? Eyes open, or eyes closed, oculomotor stuff without moving their head looking side to side, up and down. The idea that we are looking to see, do both eyes move together? Are they yoked? Or do we see the situation where someone is moving from one side to the other and they are going like this instead of both eyes moving? Do they have double vision? When they are doing that, which is likely what would happen with that and can you observe whether the eyes are yoked properly, or whether we are seeing one eye not moving properly?

The standard ones are Maddocks questions that most people think about when running out onto the field. I’m going to ask you a few questions. Please listen carefully and give me your best effort. First, tell me what happened. The athlete is down, and then you are asking them the questions. Now, you got to think about the particular environment that you are in. Surfing is a different environment to what it is when we think about things like American football or basketball or Aussie rules football, rugby, or soccer. What venue are we at today? What half is it now? Who scored last in the match? What team did we play last week? Did your team win the last game? For certain sports, you will create sports-specific questions in place of those, but they are the classic five questions.

The 5 steps there, in the hands-on module, we will go through all of those, review those red flags, our observable signs, our Glasgow Coma Scale, the neck assessment, the coordination, oculomotor testing, and then our Maddocks questions. If we see any of those, remove them from the field of play, and throw the medical assessment. When the question comes up, if we are worrying about things, what about imaging? Well, we know with a head injury concussion is not going to show up in any of our structural imaging. In the research setting, if we talk about that, we may get those abnormalities with functional MRIs, DTTs, DTRs, PET, SPECT, et cetera. But our purpose for imaging is to exclude any red flag symptoms. We may refer for a CT straight away because you are concerned that there is a brain bleed, or you are concerned that there is a fracture. That is where the imaging role comes into play, which is that you ruling out a red flag. You are not referring to imaging to diagnose a concussion. Concussion diagnosis is a clinical thing. Imaging, again, is about the red flag aspects.

Some indications there for you, for imaging, we have the Canadian Cervical Spine guidelines, and we have the Canadian CT Head rule. We have our different factors there as to what would be considered indications for going and getting imaging after a potential cervical spine or a head injury. The point there on the right, though, is the advanced imaging is starting to suggest, this is again our functional MRIs or DTTs, PET, SPECS, advanced imaging, those things, is suggesting the brain is physically not recovering for greater than 30 days, and I said one recent paper suggesting 45 days. This is where some of the changes are occurring in the consensus definition. Advanced imaging, again, is used as part of the research to help these definitions and our understandings but for us as clinicians, we may want to be referring them based upon these guidelines in ruling out red flags based on your assessment on the field.

Once you have gone through the on-field assessment of the SCAT6, and those first 5 steps, basically, you are then going, well, I have made the decision that these obviously need further medical assessment or transport to the hospital. But if not, and you have suspected that there is a concussion injury, and there is none of those referrals for a medical assessment hospital, we are taking them off the field and we are then moving into the off-field assessment of the SCAT6. The first part was the immediate assessment, that neuro screen. That is part one of the SCAT6, and then part two is the off-field assessment. The recognition of concussions is the first step to initiating appropriate management. Removal of play from the field of play should be done if there is a suspicion of a potential concussion to avoid further potential injury.

The rules still exist to this day. If in doubt, sit them out. So, if you’re in doubt, sit them out. It’s a concussion.

It is better to be safe and monitoring and observing and continuing to do your serial testing than it is to return a player to the field. This may be based on the play symptoms or signs observed by other players, medical staff, or officials on the field or video and again, depending on the sports that you are involved with, we may have those video spotters that can obviously radio down and say, “We are going to get that athlete off the field.” Obviously, in amateur or local sports, we may not have access to that but we may have a parent who sees something on iPad or phone because everyone’s got a phone out now filming stuff. Signs that warrant immediate removal from the field include actual or suspected loss of consciousness, seizure, and tonic posturing ataxia to those observable signs. If you see those observable signs, it is an immediate removal from the field of play.

Our Maddocks’ questions as we said accepting the children. We do not worry about those. Those five questions, what venue are we at? What half is it? Who scored last? Did you win your last game? Incorrect answers warrant a more comprehensive off-field evaluation as does any clinical suspicion or concussion. Symptoms and signs of a concussion may evolve over minutes, hours, or days. Whether acute concussion is suspected or confirmed, the player should be serially reevaluated in the coming hours and days. Recognizing it removing them from the field of play, and then performing the remaining parts of our SCAT and continuing to follow these athletes up.

The off-field assessment as we can see here, you have got basically the history part of it here. You have got the athlete background and we have got the symptom evaluation. The beautiful thing about the SCAT is you can see the blue italics there; it talks you through how to do each section. That is why I said review this but get out the SCAT and read it and start practicing doing it, and practice doing it, and the more you practice doing this the more efficient you will become at it and you will not necessarily need to be reading off of the SCAT. You just know what the next steps are each time. Filling in the data of the athlete’s background, getting them to record their symptoms or scoring those symptoms like 22 possible symptoms and a total score out of 132.

Then we move into the Cognitive Screening. This is the standardized assessment of concussion, so we do our orientation questions. Again, this part is not in the Children’s SCAT, but it is what month is it, what is the date today, what is the day of the week, what year is it, and what time is it right now so within the nearest hour. We are scoring that. Then we go through this immediate memory, and you can see there are three lists of 10. The old SCAT5 used to only have five-word lists and ten-word list options, but what they have now done is they have made it 10 to remove any ceiling effects, and when we look at the scope a little bit later, they have actually even provided 15-word options as well.

The way it works is that you basically say, “I am going to test your memory. I will read a list of words, and when I am done repeat back as many words as you can remember in any order.” You might choose list A, list B, or list C. You can choose whichever one and you read each of the words at about one word per second. In this case, if I read off list A there, jacket, arrow, pepper, cotton, movie, dot, et cetera. After I’ve said the 10 words, then the patient is to recall as many as they can, and you obviously circle which ones they got correct or missed, and then you do three trials of this. I am going to repeat the same list. Repeat back as many words as you can remember in any order even if you said the word before, and you repeat that same list out again and you circle through the trials. You see, pretty straightforward.

Then we go to the concentration and then we got a similar type of process here with testing digits. You are going to use one of those lists of digits and you are going to give them, say, the first list A there you can see is 4-9-3. The patients got it, they will hear the words 4-9-3, but they have got to say it backward, that will be 3-9-4. Then you work your way through that list. Then you will go through the months in reverse order, but that is timed now. That is where that is a little bit different. You are going to get a stopwatch here. Their job is to do the months of the year backward and do it as quickly as possible. They want to see this basically no errors, so they get the months backward correct, so obviously December, November, and if they were then to go August, that is an error. They do not get a point, or if they can get it correctly all the way through from December to January but they cannot do that within 30 seconds, they do not a point for that either. This is going to become important because there is now a total cognitive screening assessment.

Then we do our Balance and Coordination Exam. M-BESS as you can see in the picture on the right there, the M-BESS is basically the top ABC. D, E, and F is the foam section, and that is optional because you must think about it you are on the sporting field, and having a bit of foam to test someone may not be available nor it may be not applicable in those situations. We do the M-BESS, we will go through this and the hands-on, of course, along with everything here. But the basic principles here you can see, it is hands on the hips, eyes closed, and it is about staying in those balanced positions. You are trying to stay there for 20 seconds, and we are counting the number of errors in each of those positions. What is an error? If you open your eyes, that is one error. If you take your hands off your hips, that is another error. If you stumble or fall out of the testing position, that is another error. If you stay out of the testing position, i.e. if you keep your eyes open for more than five seconds to recalibrate yourself, that is another error. Now, if you open your eyes and your hands come off your hips all at the same time, it is just one error. It is not all the errors together; it is just one. Now, when it comes to the M-BESS, if someone has made 5 errors in any of those positions, that is considered a failure.

With the M-BESS, after you have gone through that if they pass the M-BESS, you can then go to Time Tandem Gait. If they do not pass the M-BESS, then you do not have to worry about doing the Time Tandem Gait. Now, this Time Tandem Gait is new. Basically, you put a three-meter strip of tape on the ground, and the test is to get the person to walk heel to toe along that line, go all the way up to three meters, and then back, and you time that. They get three trials, and you get the average of those three trials. As you can see, the words, they are in blue. Please walk heel to toe quickly to the end of the tape, turn around, and come back as fast as you can without separating your feet or stepping off the line.

Then again, if they can do that, not falling over and not stumbling, et cetera, if they can do the three trials, then you can go to Dual-Task. All of this, it is the exact same test. They are walking heel to toe along that three-meter tape to the end and back. But while they are doing this, one of the common ones here that they were using this test is you are going to start at 100, and you are going to count backward by sevens. Now, what you do is give them a practice go at this first. Start at 100 and count backward by sevens. They are just sitting or standing, they are not moving yet, so 100, 93, 86, 79, 72, and they are doing that, right?

When they are working through that, you can see that there is your practice aspect there where they have got the score, so, you can see those and record them. If you are not good at math, you have got the answers there. Then you get them to do their three trials where you time it and you have also got those numbers there, but you will start them at different numbers so that way they are just not memorizing what the correct numbers are. You can see trial one, start at 88 and count backward by sevens. Now, why do we choose sevens? Because there is no pattern to it, all right? You have got to keep thinking because there is no pattern to the number seven. All the other numbers tend to have a pattern to it. That is the purpose of step 4. We do our M-BESS into our Time Tandem Gait. If you pass the M-BESS, then you go into the Dual-Task Tandem Gait optionally if you pass the Time Tandem Gait.

Then, the tricky part is then you say to the person, do you remember that list of words we gave you earlier? I want you to tell me back as many words as you can remember in any order. You do not give them any clues this time. They had three trials earlier before, but now you are seeing if they have got any of those words there in that delayed recall. You can see there on the bottom of the screen, you have got a total cognitive score there where you get to score all of those out of 50 now, and this is believed to have helped with the ceiling effect that occurs with the SCAT.

Again, when we get to the hands-on module, we are going to run through that first section there, all our immediate assessment neuro-screen, red flags, observable signs, Glasgow Coma Scale, the neck assessment, oculomotor coordination testing, and Maddocks’ questions. Then after that, we will run through, and all of this you are going to have the SCAT in front of you, and you are going to just work through this. We will not worry about the hands-on, we are not going to worry about filling in the symptom score. We know that that is there, and you can have a look at that, but we will start to work through this standardized assessment of concussions. We will have a look at those practicing the orientation questions, going through obviously all of these immediate memory questions, our concentration questions, our balance coordination questions, and then this delayed recall.

Then the next step of the SCAT is then to come to a decision. Are you making a decision that this person has had a concussion? As you can see, you can fill in the SCAT there, and use this as part of your clinical assessment when you are working sideline, whether you are working in an office, and someone attends to you with an acute concussion, and this can help you come up with making that clinical decision.

The off-field assessment, typically the process conducting that screen to evaluate the concussion takes at least 10 to 15 minutes. Sporting organizations are strongly advised to allow for at least that amount of time for an adequate evaluation and to accommodate such an assessment off-field. We talked about that before with soccer. For athletes with a potential sign of concussion, any screening assessment short of a multimodal evaluation of symptoms, signs, balance gait, neuro, and cognitive changes associated with a potential concussion may be inadequate to allow continued sports participation. The idea of you walking out onto the field and doing this and flashing a light in people’s eyes is just not good enough is what they are saying. If you are going to use that to make your call that someone is safe to go back, the consensus group is saying that is inadequate to allow continued sports participation. We have got to be able to do the SCAT6 as a minimum, knowing that is going to take 10 to 15 minutes if you are competent at performing it. Now sports whose rules currently do not facilitate such evaluation should strongly consider enacting rule changes in the interest of player welfare. The one we talked about again, of course, is soccer’s the big one there.

The SCOAT6, again, is new. The SCOAT 6, for those that did their ICSC, is brand new. All right, for those that did this a couple of years ago, the SCOAT 6 is the new office assessment that they have created as part of this new consensus. For all the people trying to achieve their ICSC and this is the first time doing it, we are going to run through certain aspects of the SCOAT6 during the hands-on. Let us get into this. The purpose of the SCOAT6 was to give healthcare providers a standardized, expansive, and age-appropriate clinical guide to a multi-domain evaluation in the sub-acute phase. This is designed for after 72 hours. We do the SCAT first, and then if we are past 3 days to 7 days, we then start to use the SCOAT. Various components may assist the clinical assessment and guide individualized management. This is where we are starting to get into beyond the removal from the field of play and diagnosing a concussion, and now we are starting to look at this as okay, yeah, we have had the concussion and now we want to start to look at the various systems domains that may be involved in your injury and what things we need to do to help manage that. Now, again, it does not replace you as a practitioner, or your clinical acumen, but it provides a standardized framework that can be adapted to help inform your evaluation in your office. Again, the SCOAT6 is for 13 years and older and there is a Child SCOAT6 for children 12 years or younger.

SCOAT6, we have got very similar components to the SCAT. Step 1, you have got on the right side of the page there, we can see it gives you a structured way to help you take a concussion history or a concussion history. Not history for all your different types of injuries, but for specifically for concussion. It gives you that structure, the current injury, any history of head injuries, have you got a history of neurological, or psychological learning disorders. Then on the next page is what you will also see that then there is there any of those types of things within the family. They have got those there as well, which is obviously pretty interesting that we start to then bring in the family history component of some of those things. Then when we get into the symptom evaluation, that is the same as what you saw with the SCAT. We have got our post-concussion symptoms scale, our 22 symptoms. But then on top of it, they are also asking questions about your symptoms that they are bringing in autonomic nervous system questions. They are bringing in, do your symptoms get exacerbated by physical activity? Do those symptoms get exacerbated by cognitive activity?

Our verbal cognitive test is step three. They’re the same as the SCAT6, so that is all of your standardized assessment of concussion, so your orientation, your immediate memory, your concentration aspects. But then this is where we get into some new stuff. The examination, now, the things that we have got here in bold, these are the things that I want to go through, obviously here today. But when we get to the hands-on and we do the actual practical aspects in the hands-on, we are going to be going through orthostatic vital signs, the complex tandem gait, and step 5, the modified VOMS. We are not going to be putting people on treadmills. We do not have enough time at the symposiums to do those and we do not have enough time to obviously go through the return-to-learn a return-to-sport. But I want to cover that here now, obviously, one, for the things that we are going to do with the hands-on and step 9 and 11, obviously, being very, very important components for the education and help management of athletes and people that have had potential concussion injuries.

Then you can see step 6, they have included an anxiety screen, which is the GAD, the Generalized Anxiety Disorder-7 questionnaire. The depression scale is two questions. That is a quick screen, and it suggests that if you get a certain score on that scale, which is a three, if you get a three on that scale, they are then telling you to then probably perform the Patient Health Questionnaire-9, so the PHQ-9, which is a more sensitive and more in-depth depression screening questionnaire. Then there is also a sleep screen. They are patient-reported outcome measures that are built into the scope.

Then you have got your delayed recall, just like the SCAT. Then if people are using impact or cog sport, that is just step 8. You just fill that in if you have been using computerized testing. Then our graded aerobic exercise test will go through that. Then it is like the SCAT6, we have got our overall assessment, management, follow-up plan, and discussing our return-to-learn and return-to-sports strategies.

Orthostatic Vital Signs. This was the new one that has been brought into the SCOAT6. Emerging evidence has associated concussion with changes in the autonomic nervous system. Postulated mechanisms include trauma to the hypothalamus, limbic cortex, midbrain nuclei, and regions of the brain responsible for autonomic function. Orthostatic tachycardia has been described as being associated with a substantial subset of concussion clinic patients.

Now, orthostatic, meaning, people who go from laying to standing, sitting to standing. Basically, when you get upright, we start to see that your heart rate spikes at least 30 beats per minute in adults, and 40 beats per minute in adolescents or younger, but their blood pressure does not change. We do not see the blood pressure drop. We see the blood pressure stay the same, laying down as it is standing, but we see their heart rate from laying to standing go up by 30 and there have to be associated signs with that, being, signs and/or symptoms, I should really say, light-headedness. They feel like they are going to faint, that presyncope feeling. Their vision gets like stars in it. They get spotty vision. You may see their hands and feet going blue or purple with that venous pooling. Temperature aspects, getting a headache, feeling nauseous. Legs feeling numb or weak. They have got to have light-headedness plus something else.

Now, this is a very specific area that I have a lot of interest in so I published an editorial and case series in this particular space. If you guys want to see that, just type in POTS, my name, and then Chiropractic Journal of Australia. It is a free PDF download where I go through the assessments and the relationships of a lot of these tests that we are about to talk about in the SCOAT and creating a multi-system, individualized management program and how, in my opinion, going after the dysautonomia first is very, very important in the management because that dysautonomia is all about cerebral perfusion. If I cannot keep blood into the brain, that was just like the concussion stuff we talked about before. It means I am getting less oxygen, and less nutrition in there, which means that my brain’s not able to get ATP, so I am going to get different failures of different systems. If I am trying to rehab areas in my brain with whatever exercise I am doing if I’ve got dysautonomia, dysfunction of the autonomic nervous system, POTS is a form of dysautonomia, orthostatic intolerance is a form of dysautonomia. If I cannot keep that blood perfusing into the brain, then my rehab is potentially going to fatigue and fail because I do not have the energy systems. In my clinical opinion, this aspect is super important.

You can have a little bit further read into that space, but how do we perform it? Well, it is pretty simple. You have the person laying down on their back, blood pressure cuff on. A lot of the automated blood pressure cuffs now have blood pressure and heart rate so an automated one works really nice. Obviously, if you have got a manual one, you will have to have a manual one, plus you are going to be taking their heart rate as well. You lay them on their back for two minutes and they rest quietly. After two minutes, you take their blood pressure and heart rate and then you stand them up and then you are watching their heart rate, and then you are taking their blood pressure in a minute.

Now, that is how they are telling you to do it in the SCOAT6, in my opinion, that is not good enough. In order to assess this properly, now we are going to do it like the SCOAT6 when we get to the hands-on component. But for me to you clinically, as I said, I want you guys to be better, I want you to use the NASA Lean Test. Now what that is, you lay them down for two minutes still, and you take their blood pressure and heart rate. But when you stand them up, you stand them up and you put their backs against the wall, you have their feet out from the wall a little bit so that they are leaning on the wall, and then every minute for a minimum of five minutes, you are taking their blood pressure and heart rate, asking them about symptoms, just like you are in this one here from the SCOAT. Two minutes of laying, five minutes of standing, and every minute of blood pressure and heart rate. But then at the end of it, you then lay them back down, and after a minute to two minutes, you take their blood pressure and heart rate. Why this is important? Because of the actual diagnostic criteria for POTS, which is what you are assessing for here, in order to diagnose POTS, yes, you need to see that heart rate goes up by more than 30, and the blood pressure stays normal. But you need to lay them back down and you need to see that their heart rate returns back to normal and their symptoms resolve upon getting recumbent again.

We can see this is good that they have introduced it, it is just not good enough. Again, I want us to be better. We have got our criteria here. When we get to the hands-on module, I will have another little bit of a rant about that quickly, but we will just practice this version. Two minutes laying, one-minute standing, that is what is the minimum requirement, as we said, the minimum requirement in the SCOAT6.

Now the Complex Tandem Gait, we talked about tandem gait before, and we showed you how we will do that Time Tandem Gait, three minutes up, and then back time at three trials, get the average of the three trials. We then said we have got our dual-task version, so we do the same thing, start at 100, and count backward by sevens. This show that tandem gaits are validated and practical tests, and the evidence suggests that dual-tasking increases the sensitivity for concussion diagnosis. We went through that idea of the different dual-tasking, but the complex tandem gait, what is different about that, is once you have done the dual-tasking option, you have now got this complex version, which is just simply doing the tandem gait, but you are now going to walk forward, eyes open, and then you will do walking forward, eyes closed, and then you will do the same thing, walking backward, eyes open and eyes closed, but we just do that for five steps. As you can see there, you get scoring one point for each step off the line, one point for truncal sway, or holding onto an object for support.

We have got timed tandem gait, three meters up and back, three trials. We have got our dual-task version, still, the three meters up and back, timed, but that is when you are getting to do something cognitive, the hundreds by sevens, every second letter of the alphabet, months of the year backward, giving them words and getting to spell these words backward. Lots of things you can throw at them and a lot of those things are in the SCOAT there for you to use. Then you have got this complex tandem gait version, five steps forward, eyes open, five steps forward, eyes closed, five steps backward, eyes open, five steps backward, eyes closed.

The VOMS testing. Now personally, I thought and I had suggested for those people that had obviously attended the online module of this from last year and those that attended the hands-on last year. I really thought that this would have been included in the SCAT, what turns out it was, is that they could not come to a consensus, again that this should have been in the SCAT, but it is in the SCOAT6. Now the VOMS, they have modified it. As we can see here, symptom provocation with the VOR and the visual motion sensitivity tests appear to be associated with concussion. The modified VOMS has the same diagnostic accuracy and applicability as the original VOMS. It is important to recognize that if symptoms are reproduced during the VOMS, this does not rule in the presence of a vestibular or oculomotor problem.

The diagnostic accuracy of VOMS for concussion, my point that I have made before is I want us to be better, and the reason I want us to be better is because the things that they have taken out that I am about to show you here is you can see that the modified VOMS is we do smooth pursuits. We are going to go through each of these in a second, saccades, VOR, visual motion sensitivity. You can see the smooth pursuits, we do them horizontal and vertical. The saccades, we just do horizontal, but in the full VOMS, you do saccades back and forth, as well as up and down. But they have taken the up and down out. Now, what happened? You are not assessing for up and down. What happens if the concussions cause an up-and-down problem but you are not assessing for it? Okay, as I said, I want us to be better. In the SCOAT that says to do the modified VOMS, I would encourage everyone to also learn how to do the full VOMS. We will go through the SCOAT because that is the minimum standard that we expect everyone to know and that is what is been included from the research. But see if we can be better and add those other things. It is the same with the VOR. We have got a horizontal VOR, then we are doing this to a metronome at 180 beats per minute, but they have removed the vertical one. Then we got our visual motion sensitivity test, we will go through that, which is the same. But then they have also removed the near point convergence, which is basically bringing a bead of a focal point in towards the nose, and then you are measuring when that becomes a double vision, not blurry, but when it becomes a double vision, we measure the distance from the nose. They have removed that from the VOMS.

Here is the thing, the research suggests that 50% of concussions have a problem with this, with convergence, okay? Some of these things in here, great that they have been added, but again, as a group, I would like all of our sports chiropractors to go that step further and be assessing each of those things. The smooth pursuits, as we can see, we will go through this hands-on, but it is just following a target over two seconds side to side. I prefer around saying the distance, I prefer to move that target to the patient’s shoulder width so that way, you know that you are doing it the same each time. Then when you do the vertical to the top of their head to the bottom of their chin, that way it is staying the same each time. Move it at a rate of two seconds so basically from one second from the middle to the out, which therefore means it is two seconds across, two repetitions in each direction and you are recording whether or not a headache, dizziness, nauseousness, fogginess is aggravated from the test. Again, I want us to be better. I want you to also look at the eye movements and see if the eyes are jerky, or if are they following smoothly. During the hands-on module, we will go through those things and what that look like, and what that means.

Start practicing those things now. But really the VOMS from the SCOAT perspective is all about does it provoke symptoms. Does it provoke headache, dizziness, nauseousness, or fogginess? Now, for horizontal saccades, again, I use the patient’s shoulder width. They will talk about being one and a half feet to the right and one and a half feet to the left, so three feet. I like using that so it is standardized to that patient every time because do you know exactly where three feet are in the air unless you are like holding a string and you have practiced it and you know exactly where it is each time? I standardize it by keeping it to the patient’s shoulder width. Back and forth, back and forth, back, back, back, forth, 10 repetitions in each direction. Does it aggravate symptoms of headache, dizziness, nauseousness, and fogginess? But from our point of view, going that step further, do we see the eyes are accurate? Are they hitting the target the way they need to, or are they overshooting or undershooting? Or are they going to the eye and get hit to that eye? We want to observe all of those things because that means something.

The VOR, getting metronome out, and when we have that metronome going, a bit of a nasty one. We set this metronome to 180 beats per minute. They look at the target and in time to the beat. They are doing that horizontal VOR. After that, wait 10 seconds. Do they have headaches, dizziness, nauseousness, or fogginess after that VOR? But you also want to look, were they able to keep their eyes on that target? Or when they turn their head, did their eyes move with their head and then come back to the target? Because that is going to mean something when it comes to time for our rehab. Yeah, we want to assess this for symptoms, but we want to also do it for our purpose of what might we have to do to help this person recover from their particular head injury.

The Vision Motion Sensitivity test is very similar in that we use a metronome, slower, 50 beats per minute. But what we then have the person do, I like having both hands together, thumb up, they are standing, they look at their thumb in time to the beat, they turn 80 degrees to one side, and they turn 80 degrees to the other side. The beat, hopefully, you can hear that. Looking like this, they would do five repetitions on each side, and wait 10 seconds. Headache, dizziness, nauseousness, and fogginess, we are asking for those particular symptoms again.

It is important to emphasize that the VOMS was not designed as a comprehensive tool for vestibular and ocular motor function and may not encompass all the screening strategies necessary to examine all aspects of vestibular oculomotor dysfunction. Therefore, it may be useful as a screening tool, but it is not appropriate as a replacement for a comprehensive vestibular and oculomotor assessment. The point I am trying to make. That is not me saying that. That comes from a really great physical therapy, the American Physical Therapy Association paper that they did on concussions a couple of years ago. But what they are talking about there is exactly my point. How do we be better, okay? We have got the modified VOMS, great for putting that into the SCOAT and great for us using that to further assess our patients, but going that step further, what do those tests look like and mean? We will go through that more in that hands-on module. What do which of these tests look like? What does it mean? Because then that is important for our rehab. But then adding those old exercises that we talked about, the old tests back in that have been taken out of the modified VOMS, because that can mean something for us too.  All right, going that step further.

The Greater Aerobic Exercise test. Arguably the thing that is got the most research for concussion management. When we look at exercise testing, it should be performed only when the athlete reports the general resting concussion symptom burden is not greater than a 7 out of 10. If they are sitting they are going, “Yeah, all right. Yeah, my headache sucks, but it is like a 6,” or “My dizziness,” whatever, you do not do the exercise testing on the treadmill until it is less than a 7 out of 10. Clinicians can prescribe targeted heart rate aerobic exercise treatment based on 90% of the individual’s heart rate threshold at the more than mild symptom exacerbation point. I will show you how to do this test on the next slide. Basically, you are trying to figure out when the person becomes symptomatic or exhausted and whatever that point is of monitoring their heart rate throughout it. When they have a 3 out of 10 increase in whatever symptom it is, we stop the test and we get the 90% mark of whatever their heart rate was when that symptom went up to 3 out of 10. That is what the more than mild symptom exacerbation point means.

Then the sub-symptom threshold aerobic exercise treatment can be progressed systematically based on the determination of the new heart rate threshold on repeat exercise testing. You can keep going back to that treadmill test, keep repeating it every few days to every week, determine what the threshold is, and then have the person keep progressing with their aerobic exercise.

Prescribed sub-symptom threshold aerobic exercise within 2 to 10 days of having a concussion is effective for reducing the incidence of persisting symptoms. It is also effective for facilitating recovery and athletes suffering from symptoms lasting longer than one month. Why? Aerobic exercise enhances cerebral perfusion. It is helping blood get to the brain is one aspect of importance when it comes to that along with all the other things. But I want to talk really about that part there about making sure that we are getting that blood going to the brain. Using sub-symptom threshold aerobic exercise helps reduce the chance of getting persistent symptoms, but it is also going to help the people that have got persisting symptoms get better. Aerobic exercise is the message right now that we are going to make sure that we are all prescribing to our concussion patients and we want to assess and prescribe. But we can also understand now that if there is an inability to put people on a treadmill, there are also ways that we can start prescribing aerobic exercise in a very safe manner. This of course allows us to be very specific and safe because we can figure out the heart rate very specifically to work people out.

This here is how to do it, people. This is the one slide, so if you want to take a screenshot of this, take a photo of it. When I first started to learn how to do it, I literally had this as a printout page until I learned how to do it off the top of my head. You are basically setting the treadmill at 3.4 miles an hour or 5.5 kilometers an hour, treadmills at zero incline, and basically you are watching the person’s heart rate and you are asking them about symptoms. We will just keep it that simple. They are walking away, walking away, and every minute you are increasing the incline by one degree, asking about symptoms while checking their heart rate, monitoring their heart rate with a pulse oximeter or chest strap or wristwatch, monitoring that heart rate, and each minute the incline gets up and up and up and up. Basically, you are going through the point if they can, where the treadmill maxes out on its incline, and when it maxes out on its incline if the person’s symptoms have not increased by 3 out of 10 if the person’s not complaining of feeling complete exhaustion, so their perceived exertion has not got to like a 9.5 out of 10, then we start increasing the speed. As you can see 0.4 miles an hour to 0.6 kilometres an hour, obviously is for the Australian to American conversion. Each minute, we start increasing the speed because the treadmill is maxed out, but we keep basically going with this test until the person’s reached maximum exertion or they have an onset of new symptoms or exacerbation of symptoms of 3 out of 10 or the person talks about I do not feel safe. They cannot continue to do it safely.

As soon as you terminate the test, whether it is the exertion, whether it is the symptoms, whether it is a safety thing, terminate the test and you record the final measurements of their heart rate. Whatever that heart rate is that you determine from the test, whether it was the 3 out of 10, whether it is the exertion, you take 90% of that heart rate and that is where we start our aerobic exercise treatment from. We will talk about that a little bit later, but that slide there, remember it, practice it, get the hang of that one. Again, in the SCOAT6, that’s literally what’s there. It says, Graded Aerobic Exercise Test and you put the protocol used. And there are a few different options that you got the Buffalo concussion treadmill test. You got the Buffalo concussion bike test. There are a couple of other different versions now where the University of Cincinnati is putting a stethoscope on and they are listening at the carotid artery and they are listening for breweries and they are obviously waiting until I hear the brewery and they are measuring what the heart rate is at that point in time. That is an interesting test that has been published too. There are a few different options that are out there.

This part here is not in the SCOAT6. Before we get into this section, sorry, for the hands-on module, we are going to go through the SCAT6, the immediate assessment neuro screen, and then we will be going to the off-field assessment, which is a lot of that cognitive and balance stuff. Then we are going to go into SCOAT6 hands-on and in the SCOAT6 hands-on component, we will go through orthostatic vital signs, complex tandem gait, and the VOMS. Practice those things and get printouts of SCAT6 and printouts of SCOAT6. Review this presentation, review those things, and then when we get to the hands-on module, we will be performing those things with most of it as assumed knowledge and me adding a couple of little nuances to the actual performance of the tests, okay? Really work with that over the next few weeks.

There is clear evidence to suggest that the cervical spine should be examined after a concussive event, but there is limited evidence on the examination procedures for cervical musculoskeletal dysfunction specific to patients who experienced the concussive event. Low-level evidence suggests that a concussive event can cause cervical injury and cervical musculoskeletal impairments can cause symptoms that are often reported after a concussive event. But when we look at SCAT6 and the SCOAT6, as it relates to the neck, the majority of the assessment base in there is just the on-field screening for the red flag stuff, so like fractures, dislocations, the bad stuff, spinal cord injury.

When we get to SCOAT6, still pretty similar. It is just that palpation really all that they add in is the specific ranges of motion. But from our point of view, again, going that step further, that next bit is better. What are some of the things in the research that we know that we can do? Because as we 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.

If you are going to sit there and go, “I’m a chiropractor, I treat the neck.” But if someone has got a vestibular problem, driving a neck problem, we better understand how to assess that vestibular system. But vice versa if someone has got a selection of symptoms like headaches and things, and we need to differentiate whether that headache is coming from a Dysautonomia problem or whether or not that headache is coming from a Cervicogenic problem, we need to be able to differentiate those things. Then our profession, obviously being one of the better professions as it relates to manual therapy for treating cervical spine components, but we have got to understand the next step of being better at how we differentiate those things before we make those decisions over neck versus vestibular oculomotor, dysautonomia.

Different Forces, Different Systems. Julia Treleaven, obviously a great physio from the University of Queensland here does a lot of studies in that whiplash space. What she showed is when higher forces or a direct blow to the head occur, additional injuries such as concussion or damage to the central nervous system or visual or peripheral vestibular apparatus are more likely. Basically what we are saying here is if we look at the picture, the higher the forces that occur, the higher up we go. It takes less force to injure your neck but if we are getting more force and more speed that we are being hit, then the more likely are we to have the actual damage occurring higher up to the systems from neck to vestibular oculomotor, brain, et cetera because we can see that up to 35% of those with traumatic neck pain associated with high forces may have peripheral vestibular damage.

Someone that has got a chiro accident, 35% of those people may have a vestibular problem. We need to understand because chiropractors see whiplash stuff all the time. We need to understand how to differentiate a vestibular problem from a neck problem or how that happens concurrently and be treating them both. Injuries induced by axial rotation versus linear. Obviously, these types of injury fighters, punching, MMA, boxing, trying to rotate the head on the neck to try and knock someone out. Those axial rotation things may result in different types of neuro otological injury. But as you can see there that force is required. Nice little visualization there from Julia Treleaven, but that relationship between the nervous system and neck and from our perspective, understanding how to separate or concurrent components of having multiple injuries at once or differentiating so that we know which injury we actually need to be treating.

Great little test here, the Deep Neck Flexor Endurance test.  A simple little test. Those two fingers under the head, get someone to perform a chin tuck, lift that head just off those two fingers, and hold that until fatigue or pain, all right? Basically, if the person’s head touches that for more than a second, or you see that they lose the chin tuck, we stop the test. Some numbers that are out there, in general, talk about females should be able to last longer than 29 seconds, and men should be able to last longer than 39 seconds. If we are talking about athletes, we want our athletes to be able to hold this for longer than a minute. If they are an athlete that plays a sport that does wear a helmet, like American football, equestrian stuff, you get the idea, right? Lacrosse, any of these helmet-based sports, we would want them to be able to do that for a minute with their helmet on too.

One first test, then there is some evidence between the deep neck flexor endurance test and being able to go longer than a minute as a predictor of helping return to play. There is research out there suggesting that this one should be part of our return-to-play criteria. It is not part of the SCOAT. These ones I’m adding in now are additional bits of information for us, especially as chiropractors who have an interest in that neck. But I’m trying to just show you guys this next step of how we separate this from vestibular. We get to this one here, cervical joint position testing, put a laser on the head. You can get these targets off of the internet really easily now. There is one that comes as a PDF design so that you set it up 90 centimeters away. You sit on a chair 90 centimeters away from that laser and basically close their eyes with a laser in the middle of the target. They turn their head and I’m going to do this on purpose. They come back here and then it is checking where that laser is in relationship to the target.

Basically with that target, you can see there in the picture when they turn their head with their eyes closed and come back to the middle, they tell you when they think they are back in the middle, you mark that off. Then they keep their eyes closed, you reposition their head to where the middle was. Then they go to the other side and come back to the middle. They tell you when they think they are back in the middle, you mark that off and you position their head to wherever the middle is again. They go there and they are doing three on each side. Basically, if you look at that particular target there, if that red laser is outside of the yellow, they are greater than 4.5 degrees, that is where it said that they have got a cervical proprioception problem.

The idea is that they do not know where their neck is as a way to put it. They do not know where the head on their neck is or where their head is in relation to their body. However, that makes sense to you, but our cervical proprioception test, this one here very, very important as it relates, especially into the whiplash literature, but us integrating this for the next step of now we go. Well, what happens if we load the neck and we do some of those pursuits as we did there in the VOMS? Same thing, we do our pursuit testing and we are looking at the eyes now, are the eyes tracking smoothly? Then what we do is on the chair, as you can see in the picture there on the right-hand side of the screen, we then keep the head still and we get the person’s trunk turned 30 to 45 degrees to one side, and then we do the pursuits again, and we are watching them follow. What we are primarily looking for is do the eyes get jerky, so they are not smooth. They are jumping, especially when they cross the midline. We do it this way and then we do it the other way. We are looking to see if are there differences in the eye movements from just straight ahead to when there is torsion, okay?

What the research has shown is that for patients with dizziness after a concussion, mild traumatic brain injury, who had an abnormal, laser on the head, cervical joint position testing, and Cervical Spine Proprioception is what the CSP stands for, Joint Position Areas, the JPE, and the SPNT is the Smooth Pursuit Neck Torsion test. If we have got someone who has got dizzy after a concussion and they were doing the head laser one, and that was abnormal, outside of 4.5 degrees or we did this one and when there was torsion, there was jerkiness, those people responded better to Cervical Spine Proprioceptive Rehab compared to Vestibular Rehab.

You hear the word dizzy and immediately people go, if you are dizzy, you got to do Vestibular Rehab. But if people had those neck-based proprioceptive problems, they did better by doing neck rehab. However, exclusion criteria included any patients who had clear peripheral vestibules. This idea if I went here and there was jerkiness, if you saw that there was jerkiness consistently with those types of testing, that would suggest more of a central type of problem, a central vestibular type of problem. If you saw nystagmus in someone’s eyes, as a screen, if you did a Dix-Hallpike for BPPV, if we have got clear vestibular signs, we treat from a vestibular perspective. Those types of people got excluded from this study to allow us to narrow down the actual neck component. But if you see nystagmus, if you see consistent psychotic intrusions in this Smooth Pursuit Neck Torsion test, if you do a Dix-Hallpike and they have got obviously BPPV things, you go after the vestibular system. That comes from that particular paper there again, everything referenced there for you guys. Understanding the pathophysiology of concussion proves, especially critical for the 20% to 30% of concussed patients who develop persistent post-concussion symptoms.

I know I have done another presentation online for FICS, where I start talking about these reticular formations and the way that those different pathways integrate. Understanding the pathophysiology is really, really important for these people that don’t recover in that normal four-week period. We want to try and make sure that we are better at our neuroscience, our assessments at our management strategies to try and help these people who are not recovering.

Awesome 2 slides we have here. Referral to clinicians with specialized knowledge and skills in concussion management should be considered for the targeted treatment of persisting symptoms. This is straight out of the consensus paper. Referral to clinicians with specialized knowledge and skills in concussion management. Now, it is super important if you are going to be working with concussion patients, you need to be current with concussion literature assessment management strategies. You cannot know a concussion from 5 years ago. The research is changing too quickly. You have got to be current with it to be able to help assess and manage symptoms. But the exciting bit is what the Sport-Related Concussion clinician network may include, put it in bold, this is for the first time in history that the word chiropractor has been listed in this network, and specifically, it is sports chiropractors. We are considered part of the network if we have got the knowledge and skills. At FICS this is part of developing those skills and I’m asking everyone to try and be better than what it is that we are presenting here for you at FICS. We want to go to that next step, the next level.

From the consensus paper, our role in the management because we are now recognized as part of that clinician network for the first time. Our role is the assessment of the athlete, it is the SCAT6 and the SCOAT6. That is number one, it is the assessment first, recognizing it, removing it from the field of play, and doing all the appropriate tests. Now, depending on the sports chiropractor’s competency and expertise, Cervicovestibular rehab for dizziness, neck pain, or headaches in people that have had symptoms for more than 10 days. This is the words out of the consensus statement. Vestibular rehab or Cervicovestibular rehab for dizziness-balance problems. If you have got the competency and the expertise in those areas, this is obviously the stuff that the consensus group is saying, “Yeah, the sports chiro is good for this.” The prescription of that sub-symptom threshold aerobic exercise and the implementation of our return-to-learn and return-to-sports strategies. It is a very exciting time to have our names in the consensus statement and these are those things according to our competencies and expertise that we can have a role in as part of that clinician network.

The rest of the exercise part. I am going to go through these things at a pretty good clip. You will obviously have the recording of these things. This is the additional information that the take-home messages. I am really going to emphasise the stuff in bold.

Relative rest, 1 to 2 days max of rest after a concussion is all it is now. There is no more cocooning. There is no more rest until your symptoms go away. Relative rest, basically immediately first 2 days after injury, we were allowed to rest. Actually resting from screens at that time too, get off your phones, get off your computers, and TVs, basically. Do cognitive stuff, thinking, reading, like paper-based things, some homework, those types of things, activities of daily living, it is okay to start building and introducing those. We will go through the specifics of that in return-to-learn. But once the 1 to 2 days are over, stop resting. We have got to start doing stuff. It is recommended after 24 to 48 hours to return to physical activity, that is the PA. Physical Activity is tolerated. Prescribing sub-symptom threshold, aerobic exercise treatment within 2 to 10 days after the concussion. The big emphasis here is relative rest for 1 to 2 days. Getting people to do physical activity is tolerated. What does that look like? Well, here is our return-to-learn and return-to-sports stuff.

The Return-to-Learn. This is so important for the children. The emphasis is getting kids back to school, not back to sports. We will use aerobic exercise to help them in their return-to-learn but it is not about getting them to sport until they can do this return-to-learn strategies. You can see here, progression through the return-to-learn strategy is symptom limited. Basically, you just look at step 1, step 2, step 3, step 4. You are just doing those things 2 out of 10 is fine. You hit a 3 out of 10, stop. If this is a person who has got a headache, light sensitivity, whatever it is, start doing some of those gradual activities of daily living. Just the normal reading you might do. Minimizing your screen time at step 1, though. Step 2, maybe start doing some work at home or some of the homework you are supposed to do, not in the classroom, no. Just doing some of that homework, 3 out of 10 seems like if your headache or light sensitivity increases by a 3 out of 10, that is the end of that, got to wait till it is gone, okay?

You just basically going to work through each of these based on your symptom-limited capacity. Again, as we said, student-athletes should complete a full return-to-learn before unrestricted return-to-sport. Now as part of this, the relationship between you as the healthcare provider and the schools becomes very, very important as part of maybe there is going to be some academic requirements that are needed to put in place, i.e. handing assignments in a little bit later, allowing extra time for examinations, testing, et cetera, depending on when a head injury might happen as to what is happening in that curriculum for that student in their particular school at that time.

Now Return-to-Sport Strategy. As we talked about expect a minimum of one week to return to full return-to-sport, but typically unrestricted return-to-sport can take up to one month. Now, when we look at these, it is guided again, step by step. Everything here as we progress through this idea of it is okay to have symptoms, one to two, increase out of 10, increase by 3 out of 10, the session is over. There is that basic rule. You can see step 1, symptom limit activities, just do your daily activities that do not exacerbate your symptoms. Then in step 2, this is done without doing the treadmill test. This is just saying, “Hey, you can start doing up to 55% of your max heart rate as long as the symptoms stay in that mild range, one or two, hit a three, and the session is done.” Then you can progress to the moderate 70% of your max heart rate, 1 or 2 out of 10 is fine, not allowed to get to a three if the session is over, then you can start moving into the sports-specific stuff.

At this point here in the middle of steps 4 to 6, you can start moving into the sports-specific things once there are no symptoms. All right, this person is going to be symptom-free. There is SCAT testing of cognitive function, concentration, delayed recall, all of those numbers’ backward orientation, all of those things, cognitive function, and any other clinical findings they had. The M-BESS, duel-tasking, whatever you found in your SCAT6/SCOAT6, all of those signs that were related to that person’s injury, they need to have been resolved. Their symptoms need to have been resolved and then when they are doing their physical activity you can see in steps 2 and 3, during the physical activity and after the physical activity that they cannot have any of their signs or symptoms at all. Before they can get to step 4, they have basically got to have a clinical resolution, symptom resolution and all of their signs have been resolved and that includes when they are doing physical activity. Basically, each of these steps is considered to be 24 hours, and if you cannot do step 1 or step 2 without the symptoms, you have got to stay at that level until such time that you can move until you can do stage 2 without the symptom exacerbation, then you can move to step 3.

Again, the consensus statement and the SCAT6 have obviously all of this with all of your further details in there, but nice, easy step-wise progression. I’m just saying, here is the concussion, here is the education on getting people back to learning and back to the sport. That process there, a step-wise process from the consensus statement. The newer things that they have started putting in the consensus statement this year is this section called the Reduce. The consensus statement created like the 11 hours where the idea of recognizing the concussion, removing from the field of play, I will use the word re-evaluate just to keep the hours there. They had this whole section there like rehabilitation, return-to-sport, return-to-learn, but what they have added this year is this idea of the Reduce. How do we prevent concussions? Because prevention is better than cure. What some of the research has shown the consensus statement has now included is to say rule changes have helped reduce concussions.

Disallowing body checking in children and adolescents ice hocking has reduced the rate of concussions in games. Policy and rule change is going to be a big thing moving forward for a lot of sports and they showed in American football, the limiting the number and duration of contact practices, the intensity of contracting practices, all of those collision-based things, reducing the amount of that that occurs in practice has had an overall reduction by 64% in practice related concussions and to reduce head impact rates. Policy changes are very, very important.

Now, Mouthguards. This has always been an interesting one because the mouthguard stuff has been, “Does it help, Does not help.” Mouthguards were associated with a 28% reduced concussion rate in ice hockey across all age groups. Mouthguards are being encouraged now as part of that prevention strategy, obviously, as well as the whole teeth strategy.

Neuromuscular Training Warm-up programs are completed at least three times per week. It is been associated with lower rates of concussion in rugby union across all age groups. Just think of our FIFA 11-type programs for these neuromuscular programs. These types of things here as part of a warm-up shown to help reduce concussions. So far we have got policy changes in the sport, wearing a mouthguard, doing a neuromuscular warm-up, and then of course, all of the management strategies, the idea of our role in this is being able to recognize it and remove the player is mandatory from sports. If we see it, the mandatory removed from sport and they then got to get clearance from a healthcare provider in order to return to play. They just cannot say anymore, “Yeah, I’m good to go,” and now they have got to have clearance. Having coaches educated about it, not pushing athletes back out. They are going, “Oh, that is my best athlete and I need them to win the game.” They go, “No, the health and well-being of my athlete is the number one priority, not the game.” Educating parents about concussions, and educating the athletes themselves about the concussion signs and symptoms, but all of that whole management protocol has been associated with a reduction in recurrent concussion rates. Having a concussion and then getting that second concussion or third concussion or whatever it might be. Reducing the recurrence.

The next one that they brought in was the reconsider the long-term potential effects. This is the one that is getting all the media attention. This is the area that got all the negativity that is driving this sort of concussion message and making concussion very, very topical all over the world, but especially around the US and the NFL, ice hockey, it is obviously starting to come into Australia here now with the AFL and rugby. We had our first female ever diagnosed with CT and she is in her 20s that just happened. This stuff is obviously full-on in the media here at the moment in Australia and obviously continues to be a worldwide thing.

There is increasing concern about possible problems with later in-life brain health in former athletes such as mental health problems, cognitive impairment, and neurological diseases. Previously what was known as survey studies. This is important to understand what type of studies we are talking about here. Because of the consensus statement, they used cohort case-controlled studies. That is what they looked at in this systematic review. It is very different from these ones and it is important to understand the different types of studies. As a result, you get different types of results. Survey studies said that some former contact and collision sport athletes report difficulties with cognitive function and mental health.

Cross-sectional studies. Former contact and collision sports athletes have identified changes in brain structure, physiology, and biochem. Some death certificate studies of professional soccer players, particularly Scotland and American-style football players have reported associations between ALS, Lou Gehrig’s disease, and dementia as causes of death that was previously known.

When they did the consensus statement and looked at their systematic review, cohort studies, these case-control studies. Former amateur athletes are not at an increased risk for depression or suicidality in that type of study. Professional soccer players are not at risk for psychiatric hospitalization. Former professional American football and soccer players are not at increased risk for mortality from psychiatric disorders or suicide. Men who participated in amateur sports are not at increased risk for cognitive impairment, neurological disorders, or neurodegenerative diseases compared to men from the general population. Men who participated in professional sports, however, have reported an association with neurological diseases, eg, ALS and dementia. In professional football players, American style, as well as soccer players. But the consensus statement did not identify any published case-controlled or cohort studies. This is what they were looking at in their systematic reviews are very, very specific.

They could not find any case-control or cohort studies that examined the age of the first exposure to a head impact and later-in-life health risks. They did not find any of those studies that use neuroimaging as an outcome. They did not find any studies that examined later-in-life risks for women. They did not identify any of those studies were considered post-mortem cohort studies for CTE. Of course, that is the big topic is the CTE stuff. Everything that we have got right now is all the brain bank stuff. Of course, the challenge with that as an area, is the people who are donating their brains to these brain banks are generally people who have played sports and have got those concerns. We are going to definitely, therefore, see a bias in potentially seeing these CTE types of neural, neuropathological changes. It is tricky.

So what the consensus statement is saying is what we need to help better identify these things are case-control and cohort studies. We need more of these longitudinal studies. That is what we need. Any of the researchers out there that have got an interest in this space, that is what is being sort of put out there that we need this to help answer these questions better to go, are there concerns for us? Long-term effects? Do we really need to know what these numbers and percentages are?

Then, of course, the new one now, of course, is when should we retire after concussions? There is no clear evidence of the factors that, if present, would unequivocally lead to retirement. They have not been able to collect what these factors are to say, “Yes, you need to retire.” Basically, the conversation is a complex one. It is multifaceted. It needs to involve clinicians with expertise in traumatic brain injury, and concussion. They need to have expertise in sports. We need to have neurologists, sports physicians, psychologists, and sports chiros. We need to have that multidisciplinary team and the athlete and their families having this conversation. I personally have been involved in this conversation with three of our high-profile athletes here in Australia about retirement. It is a tough one. It is a tough conversation to have, and it is a collective input from multiple sources so they can make the best-informed decision for themselves cause we do not have any specific evidence that says this is when you have to retire, this is the data we know, we are going to collect more of it.

But here is the important part. Given the positive benefits of exercise on health, all athletes who ultimately retire from contact or collision sports should be encouraged to continue noncontact or low-contact physical activity. The importance of continuing to exercise, even though it may not be contact or collision sports.

Obviously, we are not time for any questions here because it is not interactive, but if you do have any questions, feel free to reach out to FICS, to get any of those afforded over to me. Any of the Australian cohorts will be in Adelaide, feel free to obviously ask me, we will go through all of these things in their hands-on.

To all the people that are attending the Adelaide symposium, print out the SCAT, print out the SCOAT6. Start reviewing this presentation, work your way through the SCAT6, the SCOAT6 hard copy, and practice those tests. Again, we are going to do the entire SCAT6, the immediate assessment neuro scan screen that we are going to be doing hands-on. We are then going to be doing the off-field part of SCAT6. We are doing all of that hands-on and then we will be doing those specific components of SCOAT6: Orthostatic vital signs, the complex tandem gait, and the modified VOMS.

Please, when you are attending these hands-on symposiums, bring a hard copy of the SCAT that you can complete. Bring at least the one-meter tape measure so that we can do our time tandem gaits. We can obviously get three meters out on the floor. Bring a metronome on your smartphone, and bring a blood pressure cuff and heart rate monitor. Obviously, an automated one often comes with both, but if you have got a manual, bring some form of heart rate monitor, a pulse oximeter, something to wear, a chest strap, or a wrist strap. Obviously bringing a timer that you will need on your smartphone as well.

Just making sure that we have got all of those tools that we are able to utilize when we are doing those hands-on and keep in mind, again, all the FICS-ICSC practitioners have to update their head injury module every 2 years. For those that are currently needing to get updated, this will form that new update for you guys this year. Obviously, for the people next year, they will have their new one references. All are available for you here at the end of this presentation. You can go and look up all of those, but the majority of the information that I have presented to you here today is taken from these current 10 systematic reviews and the consensus statement.

I hope that you have been able to take some of these things out here for our ability to assess people on-field to then be able to make decisions about recognizing, removing from the field of play, off-field assessment, in-office assessment, starting to understand what some of these further testing and understanding that pathophysiology relationship between the autonomic nervous system with orthostatic intolerance, exercise testing, using exercise for recovery, vestibular oculomotor testing, neck, how to separate some of these with some of those tests.

If anyone has got any questions, please feel free to reach out to me via FICS. Thank you very much.

 

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