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Upper Extremity - Mopal/CMT - Drs Tim Ray & Rick Ames

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]

Upper Extremity Assessment - Shoulder with Dr Christine Foss

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]

 

Upper Extremity Assessment - Wrist, Hand and Finger

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]

Upper Extremity - Taping Techniques - Dr Martin Isaksson

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]

Upper Extremity - Concussion and Head Injuries - Dr Brett Jarosz

Dr Jarosz: Welcome, everyone. This is the Head Injuries Annual Update for FICS. For myself, obviously, I just had a bit of an introduction on my background.  I am a practitioner here in Melbourne, Victoria, Australia. I do a little bit of work mainly stateside, but with COVID, that’s not happening as much, obviously, the last couple of years.

From a disclosure point of view, so these are disclosures from FICS for today’s presentation. For myself, as an individual, no disclosures from me for today’s presentation. Meaning, I don’t receive any money for anything I’m about to present, by any of the companies that’s working in the concussion field, any of the technologies that are available in the concussion field. No disclosures from my perspective.

The objectives of today, we just look at those points there on the screen. We want to sort of break this down into those overviews, sort of epidemiology and pathophysiology. We’ll look at that as a collective group here, which is a little bit of that didactic information literature research science. Then what we want to also look at here is the actual practical skills that FICS would like everyone who performs the ICSC, we would like everyone to be competent in these particular skills.

The purpose of today is not only to get that latest update, the information, the actual science, the evidence, the physiology, that understanding of what’s happening with head injuries, and concussion. But also, to then be able to build the skill base to be able to perform an on-field exam. So, when we’re actually working on the sidelines at a particular event and we have to move out onto that sporting arena, whatever that arena is. What do we need to do on the field when we’re examining someone for a suspected head injury, concussion and the other sort of injuries that may come along with that. Then making a decision, bringing those people back to the sideline for further evaluation or making a decision whether or not someone needs to be referred off for emergency medical care.

So, we want to be able to identify those things on the field. We want to be able to make a decision as to whether or not we’re referring off for further medical interventions assessments. Whether or not we’re bringing them to the sidelines to perform further sideline evaluations. And then we want to move into the next step of the best practices’ clinical examination.

Now, when we’re talking about assessing concussions specifically in the clinical environment, so in your practices in your offices, the actual clinical examination is quite extensive. We’ll go through some of that literature. But what I wanted to present to you is what are some of the biggest thing for your buck assessments, for you to start to put into your assessment tool bag, knowing that there’s a lot more than what I’m going to present. I’ll expand on those types of assessments a little bit further. But I really want some key aspects of the science and the literature and hand it over to you guys, so that you guys can start to take that information, start to apply it with your patient base.

After we go through that clinical examination, we then just want to have a look at an overview of what, and I always emphasize it as the return to academics. Because when we’re dealing especially with the children and the adolescents, even the adults, it’s about return to work. We want people to be able to return to school, return to academics, return to work before we actually return people back to sports. Hence, the order there, even though you’ll often hear people say return to sport guidelines. We want to be returned to academic, return to school, return to work first, then we move into the return to sport.

We’ll break those things down. We’ll have a bit of an overview of what are some of the injury prevention strategies that are out there that you will get as questions from clients themselves, from parents of particular injured children or adolescents. We just want to try and have some ideas of what the literature and the science is saying as it relates to these injury prevention strategies.

When we start to look here at some of the epidemiology, motor vehicle accidents are the leading cause of concussions. Now, I’m going to set this up and get our minds into this physiology. When we think of concussion injuries, I want us to start to think about forgetting about a label. I want us to start thinking about physiological mechanisms. I personally, my bias, what I would like to see everyone have that attitude with all types of conditions, whether it’s a knee injury from an ACL perspective, whether we’re talking about a shoulder dislocation, a rotator cuff injury, low back pain, etc.

If we look at what concussion is, the literature is starting to suggest to us that it’s an acceleration-deceleration injury of your nervous system. If you hear those words acceleration-deceleration injury, maybe one of the conditions that you’re starting to think about is whiplash. Whiplash being an acceleration-deceleration injury to the neck, so, orthopedic structures of the neck. Whilst the concussion is an acceleration-deceleration injury to your nervous system. That first point there, motor vehicle accidents are the leading causes of concussions. Whiplash mechanism, acceleration-deceleration mechanism of injury. One affecting the neck, one affecting the nervous system.

Let’s plant that seed there. We’re going to come back to that through today’s presentation and be able to expand on that. So, then we look at some of the numbers here and nearly 3.8 million concussions occur in the US alone, per year during competitive sports and recreational activities. You’ll start to see some of the numbers as it relates to children and adolescents on the coming slides. But the important part here is up to fifty percent of concussions occur may go under-reported. If we’ve got someone having particular injuries out on the field, this obviously becomes a big deal when we’re talking about elite and professional level sports, where people are being paid to be on the field for their sport. If they’re not on the field, they may not get a paycheck.

We have some of these issues with concussions not being reported because of financial, other aspects of life that may go along with that. Obviously, an important aspect of concussion injuries with them being quite profound. Obviously, very topical especially with a lot of the media attention that’s going on now in this world of head injuries. Especially now, collision combat sports and of course, a lot of other contact sports that are out there also have high rates of injury, with head injury and concussion.

Then, our final point there at the bottom is concussion rates have doubled in the last decade with an estimated seven hundred and fifty thousand pediatric acute concussion visits to emergency departments, occurring annually in US. That was in 2016, of course, five years has moved on from that. The thing that we’ll see is that the literature for concussion just keeps expanding almost at an exponential rate and we’re starting to see papers on various elements of concussion constantly coming out on a weekly basis. The data that gets collected in hospitals and in sporting context and from events, those injury rates we keep learning more and more and more as that research and evidence continues to be added to our databases.

One thing we’ll talk about primarily as our backbone for FICS, is we are going to use the International Consensus Guidelines. The Concussion in Sport Group meet every four years and they come together with particular goals of how they’re going to sort through the literature, and then they create a consensus statement from the collection of the experts after sorting through, say like, sixty thousand articles. They’ll create systematic reviews and then a consensus based on those reviews, as to what is the best overall summary of what concussion understanding is, what we need to do to best assess it, what we need to do to best manage it, and all the other components that go along with that. They meet every four years. They should have met last year in Paris, in October, but of course, because of the pandemic that has been moved forward to this year. To my knowledge, it’s still going ahead in Paris, in October this year, so we will have the new one.

This particular paper that we’re looking at, the American Sports Medicine Group, is they meet basically, every other two years in between. If we’ve got the consensus group that meets saying 2020, these guys here will meet in 2022. What they do is they try to create a little bit of an in-between update, but more from a clinical applications perspective. Not so much of the research, the evidence sorting through that, but they try and give a little bit more of an update of here’s how we use this information clinically. A great group, both groups that is in terms of the consensus group as well as this American Sports Medicine Group, of providing some of this nice overview of all the data that’s there.

If we look at the consensus group here from American Sports Medicine, the epidemiology from this particular study showed concussion is common in organized sport, but it’s also common in non-traditional recreational activity. The idea of extreme sports or activities such as, like surfing or skateboarding or rock climbing, things like that, and as well as those like individual style of sports and recreational activities that are out there. As well as just routine activities of daily living. We’ve already talked about that, like motor vehicle accidents are the leading cause.

But the numbers here at the bottom, become like really interesting when we start to see the age groups of zero to eighteen with an estimated one to 1.8 million in SRC, sports-related concussions. So, one to 1.8 million sports-related concussions per year in the under eighteen years of age, and then there’s a subset of about four hundred thousand sport-related concussions in high school athletes.

Now, of course, this data is coming from the US. And the US model, of course, is a model of schools playing sports. For those that are in the Australasian area, it’s classically a club sport type of model and different models exist around the world for how the sporting system works. A classical club sport. The US is classically done through that high school sport. The data that we get through concussions is often through that high school and college system.

However, this is where we start to have some of the problems with our numbers. Because the numbers are limited and not available for recreational club sports. When we’re dealing with Australasian types of reporting, we don’t have that same reporting that we get with the data that come out of the US high school and college systems. And then also, to your activities, as you can see here, such as bike riding, skiing, snowboarding. There were different combat sports. Obviously, with the UFC and MMA being a big, a popular sort of combat sport following now. We don’t have as much data on the incidences and the rates of how often these injuries are happening per hour of sport being played.

The final big point is we really lack the research on youth-adolescent athletes, and especially differences between males and female. One of the emphasis that’s going into research is to try and look at the differences in the youth-adolescent athlete, and especially differences between female and male athletes, because we do respond differently in our genders.

It’s estimated that over fifty percent of concussions in high school-aged youth are not related to organized sports. Over half of the injuries are not occurring in the American Football field or on the Australian rules football field or playing rugby or playing ice hockey or playing soccer, world football. These things are happening when we are riding around on our bikes, walking around on the streets, driving our cars, etc. Only twenty percent, as we can see, are related to organized school team sports. But then, between two percent and fifteen of athletes participating in organized sports will suffer a concussion during one season. In this data from two years ago, just starting to show how prevalent this particular injury is within that age group, as well as, within a different sporting context.

We talked about the consensus group, the Concussion in Sports Group, and we’re going to be using their definition and we’re going to be using their paper now. This is a freely accessible paper. Everyone can go to the British Journal of Sports Medicine or just type into Google the concussion consensus statement. This one was from 2017, published in the British Journal of Sports Medicine. We’re going to be using their information as our standard model that we will use.

You’ll realize that there’s a little bit of a different variation from different sporting groups. The American Sports Medicine Group has slightly different variations. But similarly, you’ll realize there’s different things that come out of Canada. In the end, we want to use the international guidelines, as it’s taking the research experts from all over the world and putting them together. That’s the group that we want to use.

Sport-related concussion is a traumatic brain injury induced by biomechanical forces and it may be caused either by a direct blow to the head, face, neck, or elsewhere on the body with an impulsive force transmitted through the head. A few slides ago, we talked about whiplash. From an education point of view, a lot of people think I have to hit my head in order to have a concussion, we don’t. If I get hit in my shoulder and my head gets accelerated and decelerated, the problem we have, of course, is because we’ve got this neck that is really mobile. It’s got all these freedoms of movement.

Depending on the position your head is in while you get hit, whether that’s to your body, to your neck, to your face, to your head. Depending on previous injuries, depending on whether or not you could see a hit coming and could brace and protect yourself for it or you could not. All of these factors mean that each individual concussion will be different. That’s not even us talking about pre-existing psychological problems that people may have. So, with depression, or anxiety, learning disorders that people may have had. Where someone’s inflammatory state is before they have it, where someone’s hormonal levels are, where a female is in the timing of a menstrual cycle. All of these factors make concussion very tough to research because it’s very individualized.

There’s a professor out of one of the universities in Canada. I have forgotten his name and I apologize, but he said this line and it was so profound to me and I’ll always remember it to this day. It was, “Once you have seen one concussion, you have seen one concussion.” Because they are so individualized, so we have to be very thorough in how we assess the person for a suspected concussion. Because we need to investigate a lot of different systems. I will use that word now and plant the seed for different physiological systems.

Take away biomechanical force directed anywhere to the body, neck, face, head with that force thing gets transmitted through the head. Again, for our concept today, think of a whiplash mechanism of injury, the classic acceleration-deceleration injury. We have got the neck and the nervous system both being affected in that particular injurious movement.

Now, the next point here with their definition is very important, and we are going to expand on this in a few slides. The clinical signs and symptoms cannot be explained by drugs, by alcohols, by medication use, or other injuries, such as a neck injury, a peripheral vestibular injury, or other comorbidities, such as, psychological factors, coexisting medical conditions. Again, let’s set the scene.

We are going to look at concussion in a few slides, just straight out of literature and look at it as a neurometabolic cascade. That is one of the best models that we have. But we are going to look at it as this chemical inflammatory response, blood flow changes that are occurring inside your nervous system. Where these factors on this slide, neck, vestibular system, cognitive, where these types of factors come into play is when we’re dealing with the patient who is not recovering the way we expect.

Our concepts so far, think whiplash injury, could affect the neck and or nervous system. Concept two, an injury that can create a concussion doesn’t have to hit your head. You can hit your body and that force is transmitted to the head. Concept three is we’re saying that concussion, we’re going to view as a neurometabolic inflammatory blood flow type of chemical reaction going on inside your nervous system. Then post-concussion syndrome, and we’re going to hear the words persistent symptoms later on. But post-concussion syndrome for now, we’re going to view as that’s where these factors come into play that we’ve got on the screen now. So, setting the scene here with sort of four concepts so far.

An important fact from the consensus group is the idea that when we see the words MTBI, so a Mild Traumatic Brain Injury. Concussion and MTBI get used interchangeably in the research. The problem is it leads to some confusion because you can have an MTBI and it’s not a concussion. That’s the point that they’re just trying to make, is that concussion is a form of mild traumatic brain injury. But you can have a mild traumatic brain injury, such as, let’s just say, archery’s on at the Olympics right now. We could see that maybe someone by accident gets an arrow penetrating into their skull for whatever reason. That penetrating injury is a mild traumatic brain injury, but it may not cause a concussion. The importance of understanding that MTBI and concussion are used interchangeably in the literature, but they are separate entities. Concussion is a form of MTBI, but we could have another form of MTBI that’s not concussive.

Now, when we start to go through this pathophysiology, I’m a little bit biased to this area of wanting people to really understand it. Now, the model that we have by Chris Geezer and his group, they’ve published the paper in 2014. I believe was the first, and then they updated it in 2017. This is the best understanding that we have of how concussion works.

The problem is how do you research this on a human. It is not very ethical to be able to do this type of injury to a human, and then they have to extrapolate from animal models. The animal model studies are pretty relevant to us as humans to understand what’s going on, but at the same time, they are animal studies and animal brains are different to us. But again, we’ve got to take the best models that we can from the science to try and understand what’s actually occurring for us, in humans.

The exact pathophysiology is not fully understood. It’s extrapolated from animal studies but the important part here, it’s generalized as a force. Let’s think acceleration-deceleration and occurring wherever to the body or to the head, and then I can have my nervous system being stretched. If you think if I’m from side on here and I have this acceleration, the classic whiplash mechanism, and my nervous system is now being stretched. Now, let’s think about it. What happen if I got hit on an angle and my head was here and I get this type of motion occurring and now there’s rotation?

The theory is here. Imagine a wet towel. You’re getting that wet towel and you’re wringing the water out from that wet towel. Picture that, and that’s what’s going on through the nervous system. When we look at some of the studies that they have been able to do with some advanced imaging, what tends to happen is it appears to be the midline pathways of the human that get stretched most easily. All right? But again, these are animal models and we’ve only recently started to develop these advanced neuroimaging techniques where we’re starting to collect some data on adults.

We will break it down. This is what I wanted you, guys, to think of as concussion. I want you just for the purpose of getting the concept, points one and two, I want you to think that’s concussion. All right. There’s more to it, but our concepts to take away from this points one and two, that is our concussion.

The pathway stretch, picture your nerve cell, your axon. Think of it as like a big thing that we can see in front of us. I’ve got my cell body and I’ve got my long axon. I create that acceleration-deceleration injury, so I create this stretch. Because I create this stretch, I’ve got those ion channels, if we remember all of our anatomy from our neurons and neuron theory and neuron physiology. I’ve got like nodes of Ranvier. I’ve got my sodium-potassium pumps. I’ve got all these channels that allow ions to come into the cell and get ions out.

When I stretch and, again, I am giving you this for visualization. When I stretch those channels open, so they’ve been stretched open. Now, what happens is because of the whole chemical cascade that you learned over creating an action potential, sodium starts to flood into the cell as does calcium. I get this ionic influx, but at the same time, potassium moves out of the cell. We can see that there in the picture. You’re not seeing the sodium being really shown there. But we can see potassium going out, we’ve got sodium and calcium coming in. We know that when sodium comes in, if you get enough of this, the neuron fires.

We get that action potential. When calcium comes in, that actually makes the cell more efficient at firing, just for the detail. Calcium comes in, sodium comes in, potassium’s going out. But what we needed to do in normal cell function is we had our sodium-potassium pump right. That would pump the sodium back out of the cell and allow potassium to come back into the cell to get that resting membrane potential.

However, what also happens is point two there we can see this energy crisis. I want you to think of this, conceptually, is we get a decrease in cerebral blood flow when we have a concussion injury. I’ve got this flux of ions, but I’ve got a decrease in cerebral blood flow. Blood flow is what brings your energy, your fuel, your oxygen to wherever you need it to go, whether it’s the working muscle, to the skin, to your brain, to your nervous system. If I don’t have that fuel delivery going there, I’ve got less ability to bring in or create ATP. Your sodium-potassium pumps need ATP to pump those things out.

We have got this problem where we have got this ionic flux, but I have got decreased cerebral blood flow. Now, stuff’s going into the cell, but I do not have the energy to pump it back out of the cell. If we take this sort of concept there of understanding, this appears to be the problem with concussion. It’s this flux of ions, this cerebral blood flow energy crisis that’s occurring. We have got all those other things that are listed there. All important, but if we can take that concept of points one and two and if we think of that as concussion, what they have then shown is that when we look at it from a graph, there is your process of when we see the different ions, the blood flow return to normal levels.

When we look, calcium, potassium, glucose, we can see in the very bottom in that light blue. We can see the cerebral blood flow. Look at the time frame that these things are occurring over, and you can see that it says that this process takes about ten days to recover from. This chemical process going on inside your nervous system, and I’ll point up here but that could be brain, that could be cerebellum, it could be brain stem. Think of that as just nervous system. This process is going on through there and it depends on all those mechanisms of injury — how are you hit, the direction you were hit, the speed you were hit, et cetera, et cetera.

That time there that we can see, ten days, you’re going to see it start to pop up in the literature that we hear about. Which is in adults they will suggest in the consensus statement, that it takes adults ten to fourteen days to recover, clinically from a concussion injury. This is where that data comes from is this model. We’ve got this chemical response, blood flow, ionic flux that takes about ten to fourteen days.

I am going to drop a hint here for you, but some of the research now is starting to say that this process may actually take thirty to forty-five days. Leave that one with you for now. But for now, we’re just going to keep going with what the big consensus data says. That process should take about ten to fourteen days in adults to go through the ionic flux, and then the cerebral blood flow changes.

When we have that mechanism of injury, what we’ve got there is a collection of symptoms. Now, those symptoms that we create are going to depend on really where that ionic flux, where that energy crisis, where is that occurring. Where is that neurometabolic cascade occurring? Some on frontal lobe, middle of their brain stem, et cetera. All those are based on the mechanism of injury. The most common symptoms that we see occurring are headache and then dizziness. The reason I’ve got that particular chart there on the right is you can see that there have been identified twenty-two possible symptoms that someone may experience in a concussion injury.  Now, headache and dizziness are the most common, but there are twenty-two other possibilities.

This is one of our important points for concussion, is that the more severe, so you can see on that scale there. That is the post-concussion symptom scale and that is part of the SCAT5. I’ll expand on the SCAT5 in a minute because this is what we’re going to be using as part of FICS. What we want you to be competent in using for our on-field sideline/in-office. Not so much the office, but on the field sideline evaluations.

It’s step two that you can see there, that is also called the post-concussion symptom scale. If someone has a suspected concussion injury, any of those twenty-two symptoms may pop up. The people who have more severe, meaning towards six and the ones that have more symptoms, that is more prognostic that these people are going to have a probability of having delayed recovery. The more symptoms someone has and the more severe they are, that is more prognostic of a potential probability of delayed recovery. The symptoms, to this date, symptoms, are still our best predictor based on the literature of concussion, sort of assessment, and recovery.

When you hear the words clinical recovery of concussion, they’re talking about symptoms. Not objective testing, nothing to do with balance or eye movements or vestibular or neck or cognition. It’s about symptoms. Okay? The research, of course, is trying to investigate this further to go, are there objective markers that we need to be using to assess and use for monitoring progress. But for now, it’s the symptoms.

Approximately eighty to ninety percent of athletes that sustained  concussions report clinical recovery of symptoms. All right. The clinical recovery, we just talked about that. eighty to ninety percent of people will recover. Adults, in ten to fourteen days. In children, four weeks. This becomes the important part. Eighty to ninety percent of that adult athletes… Because when you start to look at children, adolescents it’s more like seventy to eighty percent recover in the time frame.

We’ve really got nearly like twenty percent of people who don’t recover in the expected time frame. That neurometabolic cascade has passed, so it’s gone. We’ll use these ten to fourteen days. That’s how long that neurometabolic cascade. We showed you the graph. That should pass in ten to fourteen days in adults, and it should pass in four weeks in children. But there are some people, who still, unfortunately, have sustained symptoms.

The consensus group, they said that we want to use the word persistent symptoms rather than calling it post-concussion syndrome. The consensus group suggested the use of term persistent symptoms following sports-related concussion should reflect failure of normal clinical recovery. The chemical cascade has gone, but the person is still symptomatic. What we’re talking about is symptoms that are longer than two weeks in adults and longer than four weeks in children. Persistent symptoms does not reflect a single pathophysiological entity.

Let us reflect back. I tried to plant a seed earlier on. I wanted you, guys, to get the concept concussion equals this neurometabolic cascade, this chemical energy crisis in the nervous system. The definition said concussion is not a neck or a vestibular or a cognitive problem. What we’re saying in this particular consensus statement is once this neurometabolic cascade ends… In adults, it should be ending in about two weeks. In children, it should be ending in about four weeks. If you still have symptoms after that, those symptoms are most likely coming from your neck, your vestibular system, your oculomotor eye system, your cognitive-emotional psychological system, or your autonomic nervous system. We’ll leave that for now.

You can see here, the second point there is persistent symptoms describes a constellation of non-specific, post-traumatic symptoms that may be linked to coexisting or confounding factors. The chemical stuff’s done. Now, I’ve got these other factors left over. These other factors are what are contributing to the person’s symptoms. Therefore, a detailed multi-modal clinical assessment, the other way to say that is multi-system. We’ve got to look at the musculoskeletal sensory motor system of the neck. We’ve got to look at this vestibular, vestibulospinal, vestibular ocular system. We’re going to look at these ocular vision processing types of systems, cognitive systems, physiological autonomic nervous systems.

We have got to do a detailed assessment in the clinic to identify are there any primary or secondary pathologies that may be contributing to the person having the persisting symptoms beyond that two weeks in adults, four weeks in children. At a minimum, the assessment needs a comprehensive history and focused physical examination. I want to try and give you, guys, at least five of those things today and that’s part of that special tests we’re indicated. I want us to be able to walk away with knowing what some of these key special tests are that focus in on some of the systems.

What we have going to try to do here is look at this section of sideline examination red flags. We are going to break that into two things, the on-field part, and then when we’ve removed the person to the sidelines with quiet environment, locker room, et cetera. We want to take these sections now. This is what we will be doing during the hands-on modules and you will be getting assessed while you’re at the hands-on module. We are going to go through the theory here now, and then the hands-on module, you will be with a partner. I have created as like each case, there will be something that will be up on the board for the patient to pretty much act out. The doctor will come in and they will run through an on-field assessment and they will be evaluated by one of the speakers, presenters, lecturers and the people who are in the room and they will be ticking off whether or not you have the competency in those particular skills.

We’re going to break down these skills. First tip, everyone’s going to go into Google again or to the British Journal Sports Medicine. We’re going to be downloading, obviously, one, the consensus statement, but we’re also going to start to download the SCAT5. If you guys are sitting there now, I want you to do that as we’re getting ready for this next section because we’re going to be using the SCAT5 and working our way through each of the steps, so we start to understand those steps. That way, you’ve got this presentation. You’ve got the recording of this. You’ve got the SCAT5 with its instructions there. You can review and perform this. The key thing is to actually perform it.

Start to practice this in clinic, on your friends, whatever it may be. Just to start to practice it and rehearse it. Of course, if you get a real-life case, we then start to use those methods that are within the SCAT5. Let us look at that. I want to get into on-field. Once we finish on-field, we will just have a little five-minute break at that point, and I will answer any questions coming out of the break. The Sports Concussion Assessment Tool 5. For those that end up going and looking in detail and the others, no SCAT4. What happened is they realize that they started creating the SCAT during the consensus meeting so there have been five consensus meetings so far. What happened is they created the SCAT, and they created the SCAT2, and then a SCAT3. But what happened is they created the SCAT3 during the fourth consensus.

What they just did is when they went to the fifth consensus, they just made the label the SCAT5 because this came out during the fifth consensus meeting. Okay? SCAT5 was endorsed and created at the fifth international symposium. The SCAT5 contains your neurophysiological tests, some cranial nerve testing, some balance testing and your symptoms scoring, plus a few other things in there. It’s sensitive for sport-related concussion sideline screening, but it loses utility after three to five days for concussions assessment. The symptom tracking, remember we said earlier that symptoms still are our biggest indicator of prognosis but also of recovery. We can keep using the post-concussion symptoms scale, that’s within the SCAT5, to track the person’s symptoms progress.

Now, they also created a Child SCAT5. The SCAT5 adult version is for ages thirteen years and older. Now, it gets interesting because the definition of the age group is children is five to twelve and an adolescent is thirteen to eighteen, then adults are eighteen and above. Adolescents, we use the Adult SCAT5 or just theSCAT5. For five to twelve-year-old age groups, we use the children SCAT5.

What’s the difference? The SCAT5 for children has the symptoms scale. They have the child gets to report their symptoms, but they also have the parent-guardian ability to report the symptoms from the child. There’s two sort of symptoms scales in it. The other part is that they don’t have the Maddocks’ questions. We’ll talk about the Maddocks’ questions in a second, but they’re the classic five questions that you may be familiar with when you’re running out onto the field play of play, whatever that field of play is. We’re going through the five classic questions of like the where are we, who are you playing school. Go through those in detail, but five questions of the Maddocks’ questions, that’s not in the child’s SCAT5. It’s in the adult but not in the child.

The other one is the orientation questionnaires. These are our neurocognitive psychological questions. Orientation, is are you orientated to place and time, (month, year, day of the week, date, time within the nearest hour). Maddocks questions and the orientation questions, not in the child’s SCAT5. In the adult, but not in the child’s SCAT5, and the child’s SCAT5 has the two symptom reporting components. One from the child itself, and then the other from the parent or the guardian.

If you haven’t downloaded it already, make sure you got a note there to download it. Maybe you grab it during the break. Ideally grabbing it now so you’ve also got a copy of it as we go through each of the slides here. It’s a free evidence-based tool. You can freely grab this off of Google, off of the British Journal Sports Medicine. The only equipment that you need is basically a watch, whether it’s a stopwatch on your phone or an actual stopwatch, or just a normal wristwatch. Now, this is a key point. It’s not the gold standard, it’s the minimum standard. Hence, when we’re assessing concussion, we need to know it fixed, that you have the minimum standard competency to be able to perform these assessments. This is the minimum standard.

For those that are in Australia, here’s the little bit of, I guess, nuance. We need to be trained in its use. That is what we’re trying to do now and between now and your hands-on module by repetition. But when we complete this in Australia, we, as chiropractors, cannot sign off on the SCAT5. It has to be signed off by a medical practitioner. You’ll see on the very top there of the SCAT5, it says for use by medical professionals only. Be aware of that. In Australia, you need to do this as the minimum standard assessment, but then this needs to be signed off by a medical practitioner. Okay? Important part. For New Zealand, for the US, for Europe, South America, Africa, et cetera, not exactly sure of what the legal aspects are in each of those regions. But please be aware of what the legalities are as it relates to your role in this particular space.

Remember, it’s not the gold standard. It’s the minimum standard, and it’s not something that needs to be passed or failed. It is helping you do your assessment and put together the entire clinical picture of that particular patient that’s in front of you. We do not use it as the sole basis for making a diagnosis. Again, because it’s the minimum standard. We ideally want to do more than this as a part of our assessment. For us on field and on the sideline, this is the minimum amount of stuff we need to do.

The immediate or the on-field assessment, this is the second page, basically, of the SCAT5. We can see there on the left. What we want to get is the first three hours that are there. We want everyone to recognize the injury. If you are on the sideline, there’s a lot going on in sport, and you may be looking primarily where the actual play is. But there’s things that go behind play, and something may happen there.

Now, if we’re at very elite professional sport, we may have video spotter. We may have cameras and medical practitioners sitting up in booths, who are actually watching plays in the field and can report down to the sideline, can report down to the referees, the umpires that are on the field that to go, “There was an incident. This needs to be having a medical practitioner come out.” But our first job is to try and go from watching the field of play, can I see it, did I see it. I need to be able to recognize the injury. When you recognize the injury, we’re trying to make those assessments on the field and remove the person from the field of play and refer for medical assessment, especially when we’re looking at some of these red flags.

Here’s first of the two rules. Point at the top. The on-field assessment, really thinking first aid. Is this something that needs to be taken to hospital? All right. First aid principles. Running out onto the field, that’s what we’re trying to rule out. If someone is unconscious on the field, if you saw the actual injury and someone is lying unconscious on the ground. You saw the mechanism of injury and they are unconscious; it is a neck injury until proven otherwise. However, this got polarized only a few weeks ago. If someone collapses on the field away from the field of play, there was no mechanism of injury occurring. We think cardiac or cardiovascular. Christian Eriksen, just recently with the soccer, collapsed on the field, was in cardiac arrest.  If you see someone unconscious, if you see an impact, a mechanism of injury, an acceleration-deceleration injury, direct blow with the head, whatever it is and someone’s unconscious, you think that it’s neck until proven otherwise. Spinal cord injury. If they’re unconscious, they can’t talk, they can’t respond, we think neck. If there was no mechanism of injury, it’s away from the play, someone collapses, you think cardiac. That said, our red flags, loss of consciousness is there in the middle right box. If someone’s unconscious, we’re thinking neck. We’re thinking cardiovascular. Red flags. Is this immediately initiating a call for an ambulance to take this person to hospital.

Now, neck pain. Attendants, remember. Neck pain, neck injuries, here’s rule number one. Has this person got potential fracture or damaged that could lead to nerve damage paralysis, et cetera? It’s all about red flags. Now, this is, of course, especially relevant when we’re talking about our collision sports. Rugby, Australian rules football, ice hockey, American football. Contact sports — soccer, the world football, basketball, lots of different sports here that we, obviously, have a higher risk of having a concussion injury. Neck pain or [inaudible] We’ll go through how we’re assessing each of these steps. Severe or increasing headache. What are we worried about here? We are worried about brain bleeds. If I get a direct blow to the head, especially that temporal area…

When we jump on the FICS online portal and you’re looking at the head injury section, you’re going to have the actual online presentations, where they’re going to go through the different types of skull fractures, brain bleeds, facial injuries, et cetera. Temporal bone, being softer, direct blows to this area, you could potentially create a fracture and start developing a brain bleed. Any other head direct blows or any of these accelerations-deceleration injuries could be enough to maybe shear one of the sinuses within the brain and skull area. Brain bleed, increasing severity of headache and then deteriorating conscious state. I might lose consciousness and be unconscious on the ground and then I come to, but then my conscious state starts to deteriorate. We need to know how to assess that, which we will as part of step four of the SCAT5.

Double Vision. If someone is complaining of double vision, we are thinking about brain bleeding into the area. The nerves that actually go to your eyes to control your eye movements, what will happen if they’re not moving together. If one eye moves, you can do this to yourself you just get your finger and push it on the side of your eye just gently so you’re almost forcing that eye in. Welcome to double vision. If you lose one of the nerves to your eyeballs via maybe a bleed into the area creating pressure. Remember, your cochlear nerve has got to go all the way from around the back and wrap around the front runs along path, any nerves that run long path are more susceptible to injury. Double vision, red flag.

Caught someone seizing or convulsing on the ground are red flags. Vomiting… Now, we’re trying to be risk-averse. By some of the definitions that exist, and you’ll see this when it comes to making a decision to image someone. We can say that if someone vomits twice, we think about red flag. If someone has one projectile vomited, we think red flag. If someone vomits once, you might be like, “Oh, they’ve vomited once.” But we could air on the side of caution and just go, “If they vomit, we’re done.” But if you do look at some of the guidelines for what we would initiate an emergency head imaging for or the absence of suspicion guidelines in the state of Ohio in the states, that’s if you vomit a second time or you have one projectile vomiting, that’s red flag. Okay? That’s where sort of the number is. You’re on the side of caution. Someone vomits once, I’m not happy.

Weakness or tingling burning in the arms or limbs, because we are worried about spinal cord injury or neck injury there. That makes sense. Loss of consciousness, we’ve already talked about. The tricky one is this increasingly restlessness, agitated or combative state. Tricky because sometimes you don’t know the athlete. If you don’t know the athlete, well, you don’t know if that’s just them or if that’s actually a sign of this particular injury. It’s an actual red flag, but at the same time can be a little bit tricky when you maybe not know the actual athlete that you are assessing. We’re out onto the field and we’re looking for these red flags. We see these red flags; we’re initiating an emergency process.

The observable signs. Red flags are in mind. The observable signs, you’re going to see there’s a little bit of overlap between each of these steps. Step one will have a bit of step two in it as well as step four and step five. You’ll see that there’s a bit of interchange, but we’ve got the steps here so that you can follow all of these logically. These observable signs have been shown to be reliable things that parents or spectators can see. We need to be able to see them as well. Again, if we’re on the sideline, watching a field of play over here and something happens there, and well, maybe we miss it but we see someone down.

As you are going out there you might be yelling to people what happened to the players on the field. People on the sideline, especially your local community, sports on the weekends, “Has someone seen what actually happened? Was there any observations?” Of course, the elite professional levels might have a video observer reporting down going, “This person just got hit, we need that investigated. “Did you see it? Did someone else see it? Can we get those reports of what actually happened?” If you can see someone loss of consciousness. Very bottom point there you’ll see, loss of consciousness is only there in about ten percent of cases. Sort of two education points for the general community to the consumers. I don’t have to be hit in the head to have a concussion and I don’t have to lose consciousness to have a concussion. Ninety percent of concussions don’t lose consciousness. But if I see loss of consciousness, we’re starting to think red flags. Because that was an injury that was significant enough to create lost of consciousness.

What does it look like? This is the types of person, especially you want to see this if there’s an incident, maybe someone’s jumping in the air for something. And then what you see is that as they’re falling to the ground, they don’t have their arms moving to protect them. It’s a rag doll, so they’re falling to the ground. They’re already out before they get to the ground They’ve lost consciousness. There is no protective action.  You may not have seen any of that, but they just may be unconscious on the ground. Do you see it within the field of play? Do you see the results of it and they’re unconscious on the ground?

Impacts seizure or tonic posturing. The tonic posturing, one, is more of one of our obvious ones. That’s when the people have their arms, legs whatever it may be, one or the other, where they go stiff. Their arms may be up in the air. Their arms may be down by their side and turned in. Their toes may be pointed forward and they are rigid. They may be stuck like this. These are all our tonic posturing types of signs.

The impact seizures are where people get hit and you may see obviously arms, hands. Now, why this one’s profound? If you, guys, want to jump on the internet, not right now, but look up during the break at the end of the day tomorrow. Look up Tom Savage and his concussion injury because he had an impact seizure and this literally started changing some of the NFL rules a few years ago because that impacts seizure was missed. This is where some of these whole video observers and the process that went on, we got to see these impact seizures and you can see his hand, his left hand on the ground. Because he was basically assessed, sent back out onto the field and then deteriorated later in the game. But if they had have seen the impact seizure, he was removed and he was not returning. We will come back to that point. If we remove someone from a concussion, they don’t go back to play.

Motor incoordination. That is where you start seeing people maybe stand up and they are unsteady on their feet. They are staggering around. It look like they are drunk. Their are sort of visualization that you can give to yourself. They are ataxic. Their balance is off set. Motor incoordination and then confusion. Now, confusion is when we start to talk to them and how do they respond to us. What is their understanding of what I’m asking them and how do they respond back. Those types of signs, if we see any of those, we’re removing them from the field of play. Those observable signs are removed from the field of play and, of course, like a loss of consciousness, seizures, tonic posturing, we’re calling in medical examination evaluation with these.

Step three is our Maddocks’ questions. The five classic questions we talked about before.

  1. What venue are we at today?
  2. Which half is it now?
  3. Who scored last in this match?
  4. What team did you play last week?
  5. Did your team win the last game?

We’re running out onto the field. In this particular picture, we can see the player is down, face down on the ground. We don’t know right now if that person is unconscious or not. We don’t know if they’re responding. But we are running out there talking to the person and you will see the next step which is the Glasgow Coma Scale.

  1. First, what happened when you’re trying to ask the person what just happened?
  2. Do they know if they got hit?
  3. Do they know what happened?
  4. Do they just go, “I just collapsed.” or
  5. “I got hit from the side”

You asking the person what happened and then we are going through those five questions to try and identify some of that memory neuropsychological aspect. Now, of course, if as an example, when I work at the surfing, I am not out on the jet skis as water safety patrol. I am up on land in the rooms. But when we are out there and we have got our medical professionals there and we are going to water safety team. One of these athletes maybe has a head injury out in the water, they are getting brought in and then this process is starting to be asked of the actual athlete there. The difference is surfing’s not that. We change the actual questioning based on the environment that we are in for those particular athletes. As long as you are replicating similar questions, you just change it to those specific sports.

The Glasgow Coma Scale. What I want to do here is I want to show you a video because this is obviously, a really nice way to learn the Glasgow Coma Scale. On the left here, we can see the process of how we score it in the consensus statement and we’re looking for eyes, verbal responses, and then motor responses, and we score each of them. Now, the video is a really nice way. It’s here as a reference for you, guys. You can go back and they have also got some nice resources on the website. I will let these guys talk these through so we have an understanding of what that Glasgow Coma Scale looks like in the SCAT5. 

Assessing their consciousness is often crucial in the care of a patient who had an acute brain injury. This film will provide a practical guide to using the commerce skill that would develop 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 person’s responsiveness.

  1. Eye opening,
  2. verbal and
  3. motor responses stimulation.

Steps in this component can be rated according to fine criteria to show the degree of impairment present. We’ll show you how to record and communicate your findings, how these can be used and provide you with a downloadable summary

When assessing a patient, do the four steps:

  1. check,
  2. observe
  3. stimulate and
  4. 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 behaviors in any of the three components of the scale. Eyes, verbal or motor. The patient is rated in each components by matching findings with the corresponding criterion.

There are four criteria for eyes, five for verbal, and six for motor scale. For each component, the top criterion is a normal response, whilst the lowest criterion is there’s no response. If the patient’s eyes opens spontaneously, spontaneous is recorded.

Remember, there may be local factors such as swelling that prevent eye opening. 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, to sound is recorded.

If the patient does not open the 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 ten seconds until the patient demonstrates a response or until maximum stimulus has been applied.

If the patient opens their eyes

  • record to pressure.

If they do not open their eyes

  • record as none.

If there were local factors such as swelling interfering with eye opening

  • record, eyes not testable.

To assess a verbal response, ask the patient to tell you their name, where they are and what month it is. If they answer correctly

  • record orientated.

If during conversation, the patient is able to speak in phrases or sentences, but is unable to give the correct answers to these questions about orientation

  • record confused.

If they did not talk sensibly but at a single word

  • record words.

If the patient moves and groans with no recognizable words

  • record sounds.

If the patient makes no sounds at all then

  • record none.

Remember, speechlessness may result from factors other than depressed consciousness. For example the presence of an tube. In these cases

  • record, verbal not testable.

To assess the motor component to 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 obeys the commands.

If the person can’t 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 components of 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 where the shoulder blade. Apply pressure with increasing intensity for up to ten seconds until you assure that the response you observed is the patient’s best response.

The second location for central stimulus is a supraorbital notch. Apply the stimulus if there has been no localizing response to the trapezius pinch. This stimulus is applied by placing hand on the forehead with a thumb over the upper end of the orbit. Feel for the notch in the supraorbital margin. Apply pressure with increasing intensity for up to ten 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 localizing does not reach for 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 stimulus. In normal flexion, the elbow bends and the arm moves rapidly away from the body and from the stimulus. In abnormal flexion, they overbend slowly and the arm comes across the body. If in doubt

  • record normal flexion.

If the patient extends the elbows rather than flexing them, record extension. A patient who makes no responses

  • record it as none.

If they are paralyzed by other factors such as paralysis by drugs

  • record motor not testable.

If different responses were exhibited between limbs on 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 assessments. Observe the patient’s spontaneous eye opening, speech and movement. If necessary, then stimulate the patient, first verbally and then physically. Finally, it should be documented clearly on the Coma Scale chart.

The observations can then be clearly communicated and the trend rapidly appreciated so that any improvements or deterioration in a patient’s condition can be seen. Patient observations can be documented numerically, as a short-hand aid to quickly record findings.

Brett. We will leave that there. Obviously, we will get into some more detail in a hospital-style setting, but let us just relate that back to the Glasgow Coma Scale within the SCAT5. We can see it is the same thing on the left there about eyes, verbal and motor response. We can see at the top left there, we have got time of assessment, date of assessment so we can keep monitoring this Glasgow Coma Scale to see if people are deteriorating. Are they having decreases in consciousness? Because this is a sign for a medical referral for us in a sporting context. You can see here now, let’s go to that verbal response or the even the vision. You’re running out there, you’re observing observable signs. Are they unconscious on the field? As you run out there and you start to talk and you are yelling, “What happened.” They may not be responding and then you might start to be looking are their eyes blinking or are they having spontaneous movements. But then you can start to ask some of your Maddocks’ questions. You can see where it talks in the verbal response there, which is they’re orientated or confused. We can start to ask, what venue are we at, who scored last. We could start to ask like the orientation questions. What’s the time? What day of the week is it? What’s the month? What’s the year. Are they giving us appropriate responses back or confused responses back. You can see how there’s a little bit of an overlap here with just by going through your Maddocks questions. We’re starting to get some of those responses from the Glasgow Coma Scale.

Now, an MTBI, which concussion falls into, gets a score of thirteen to fifteen. You can have a concussion with the perfect score here on the Glasgow Coma Scale. Four, five, and six and score fifteen there, you can still have a concussion. It just means that there is not a consciousness component to it. There’s not a consciousness problem. But you could have a lost, so someone may not open their eyes spontaneously but they open it to speech. They might score a three there initially when you run out on to the field. They might give you a confused response, where you get a four. That could be where we get our thirteen out of fifteen, so mild traumatic brain injury. Obviously, if we start to get more than that, now we’re starting to get into the moderate traumatic brain injuries and we’re starting to think about, we need to get this person off for further assessment.

Let’s just go to that next slide here. Here we go. Part four after the Glasgow Coma Scale, we have got the cervical spine assessment. Now, remember we’re examining this person out on the field. This is not an in-clinic, in-depth cervical spine. This is first aid principles. Has this person got a spinal injury that needs to be stabilized, braced, boarded. Does the athlete report that their neck is pain-free at rest.

“Do you have any neck pain?” They are say “No. No neck pain.” This is important to step two. They are “No, my neck’s fine.” Then you’re asking can you move your neck fully. Do they have full range of motion and then is limb strength and sensation normal. Asking them, “Can you feel both your hands and feet? Can you move your fingers and hands?” We can see how that could overlap with some of the Glasgow Coma Scale. Can you get your hand, reach it up and grab my hand? We are just ticking those off to make sure that there is nothing there cervical spine-wise.

Remember, if someone’s unconscious, it is a cervical spine injury until proven otherwise. So, we want to make sure we’re using the first aid principles, those emergency techniques appropriately to stabilize someone’s neck before we’re actually attempting to move them off the field. On the imaging part, because if we’re starting to think about these red flags, if we’re looking at imaging for concussion, there’s no imaging out there for concussion. You cannot diagnose concussion on an MRI or a CT. What we’re thinking about for imaging is, “Do I need to get someone in for an acute emergency CT scan or an MRI?” Now, CT’s are more accurate in those first one or two days. MRI’s are better after that. But CT is going to identify any of those emergencies, whether it’s a fracture or a bleed better than an MRI in the acute stage. We don’t have to think about the concussion here. Now, we’re thinking red flags, “Do I need to get this person off to get a CT, because I’m worried about a red flag?” A fracture to the neck, a fracture to the skull, a bleed there.

Now, what are our rules for that? We’ve got the Canadian cervical spine, where we’ve got these risk factors there, that might let you know you need to go and get an X-ray of that person’s neck so we can see in, older age person who’s had this injury, if there’s a dangerous mechanism of injury. So if someone basically falls from their height, so if you were standing on your own head and fell, that’s a high-risk thing. If someone has a direct collision, axial load to their heads, they land directly on their head or head-to-head like that, high-speed motor accident, paresthesia into the hands, these are our high-risk factors. You’re go, “We might need to get these people, imaged of their neck straightaway.” We can see those other ones with the low-risk factors that you’re sort of going, “I probably don’t need to go and get that x-rayed.”

From a CT perspective, we can see that if your Glasgow Coma Scale is less than fifteen, that would be, i.e, the person, their eyes do not open to speak. They don’t spontaneously open. They’re not even opening to speech, may not even have to be that. But if I’ve got a Glasgow Coma Scale of less than fifteen, we might be thinking about “Uh-oh,” and especially two hours after injury. If someone’s lost consciousness on the field, we’re examining them. We’re doing those types of things, but we’re doing a serial exam on the sidelines and monitor them, and if we’re seeing deteriorating consciousness or sustained poor Glasgow Coma Scale, we’re thinking about referring these people off for medical evaluation, and maybe a CT scan. Of course, if you’re suspecting any of that types of fractures, if someone’s got CSF from the nose, CSF from the ears, if they vomit twice or if they have one projectile vomiting, we’re starting to think about, “I need to go and get a CT scan. I’m worried about bleeding. Then we’ve got our other risk factors there, which are pretty similar to the neck ones. Obviously, a dangerous mechanism of injury, falls from greater heights.

The other rule for imaging is if someone’s had a known concussion, been diagnosed with a concussion, they come to see you in your clinic and in your office, and it’s already been longer than a month. You can say greater than thirty days or greater than forty-five days, you haven’t used those words before. Some researchers saying thirty to forty-five days. If we have got someone who’s still got symptoms at that time frame and hasn’t been imaged, this might be the indication that you go and get the imaging at that point in time.

What we’ll do now is we will have a five-minute break. I’m going to look through these questions and as we come back from that five-minute break, I will answer any of the questions that need to be answered now. Then we will come back in and start the sideline evaluation and the clinical evaluation.

Just looking at the questions there. Dr. Foster’s answered a few of them in the chat. Two main ones were about the model of what concussion is, and whether or not that is scientifically proven, so the neurometabolic cascade is the best evidence-based model that we have for what concussion is, and again, based primarily from rodent, animal models. The other question that came up was about the age and asking whether or not it’s about the age from a chronological point of view, as in you’re eighteen years old by the date, or whether it was by brains development, which is brain development is not twenty-five. That one gets interesting, too, because the difference between male and female brain development. Female brains were actually developed earlier. Male brains are later. But when it comes to age, age is actually just chronological. If you’re eighteen years old because of your date of birth, that makes you adult based on these guidelines. Not based on brain development. Any other questions that pop up through the time, feel free to put them in the chat. And then when we get to the end, happy to take, obviously, face to face answers as required.

Going through what we’ve just done on the field assessment; assessing using the SCAT5 to assess them through those four steps; red flags; going through our Maddocks’ questions; going through our Glasgow Coma Scale; going through our cervical spine assessments there, trying to make sure that we’re making a decision to go, “Is this person needing to go off for medical evaluation? Is this stuff that is not sidelined or returned into play? Is this stuff that’s more serious?” You may have some observable signs that you saw. Maybe some loss of consciousness, tonic posturing, impact seizures, staggers, et cetera. Maybe it’s just a collection of symptoms that the person’s reporting, and they’re saying they’ve got a headache or maybe they’re dizzy or they’re light sensitive, whatever it may be. And so, you’ve made that decision on the field now that you want to remove them from the field of play to bring them over to the sideline, because it’s safe. Because they don’t have a neck injury, they don’t have any risks there because they got no neck pain. They weren’t loss of conscious or they didn’t even have any changes in their conscious state. We bring them to the sideline, and then we start our sideline evaluation.

On field, think red flags, safety first, then we move them to the sideline for further evaluation. Any player who manifests signs or symptoms of a sport-related concussion should be removed from play for examination. They’re on the sideline now or they’ve, obviously, been into an ambulance to hospital. The sideline evaluations or rapid screening assessments, again, we’re going to continue to use the SCAt5, intended to screen for a suspected sport-related concussion, but not to produce a definitive diagnosis. We’re trying to make the call on the sideline there. Is it a red flag? Is it concussion? Obviously, one’s heading off to hospital, the second one is, “You’re not playing, we’re done. And we’re going to monitor this person while they’re on the sidelines.” And then of course, we need to then do future in-depth clinical evaluations to further look at the different systems that may be involved in causing the person’s signs and/or symptoms.

The office, let’s just call it the off-field assessment, not the office exam right now. We need to take this person into a distraction free environment. Even though we’re saying on the sideline, we might be back into the change rooms, the locker rooms, maybe there’s a medical examination room. The NFL, we see the classic pull, the actual blue hood over the top of the athletes of being a distraction-free environment. As we can see there, the office or off-field assessment of the SCAT5 is on the left. We fill in those details. You’ve got your athlete background, so you can feel and complete those. Then we’ve got our symptom evaluation.

Now, part one of the symptom evaluation, is you hand the SCAT5 to the patient, and you ask them to read that paragraph aloud. This will form part of the rest of the SCAT5, which comes later. Ask them to read that SCAT5 about the symptom evaluation of the SCAT5. Have them read it aloud and then they complete the symptom questionnaire to rate their symptoms. Remember, the more symptoms someone has, and the highest severity of symptoms that someone has, is sort of our biggest indicator, especially, for prognosis of delayed recovery. But it’s also our biggest indicator of a concussion injury, but you could just have one symptom. That can still be a concussion. It’s just that the more you have, and the more severe, more indicative and also gives us a little bit of prognostic factors.

Then we move into step three, which is your cognitive screening. They talked about this being the standardized assessment of concussion. Now, orientation’s in there, now orientation’s considered to not really be reliable in the context of concussion, but it’s in. It’s not, remember, in the child’s SCAT5. Orientation, as you can see, asking the person what month is it, the date today, the day of the week, what year is it and the time to the nearest hour. We’re getting that idea of orientation and we score that one point for each correct question. Obviously, a zero for an incorrect. We then work through these immediate memory digit backwards, months in reverse order questions. The immediate memory, we either choose the five-word list that you can see there or we choose the ten-word list depending on the patient athlete that you have got with you, and knowing their background if you have got baselines of this and you understand the actual athlete, but the standard one is the five words. You would say to the person, “I’m going to test your memory. I’m going to repeat five words to you. I want you to repeat as many words back to me as you can”. So, it is going to be finger, penny, blanket, lemon, insect. Now, when we do it, we’re going to say one word at like a one-second sort of interval. It’ll be finger, penny, blanket, lemon, insect. And then we get that person to repeat those words. You would repeat it again for two and three trials to see how many words they can get right in those three trials, and we score that out of fifteen, how many words they get right in the fifteen.

What’s going to be important for us is later on, after we’ve completed the rest of the exam, we are going to go back to that person and go, “What were those five words I asked you earlier?” We are going to ask them to see if they’re delayed memory is there. Then the concentrations, we’re going to ask them to go through the digits backwards testing, which is I’m going to put a string of numbers together for you, I want you to repeat them back to me in the reverse order of what I say to you. For example, if I say 7, 1, 9 you would say 9, 1, 7, and then what you do is just start going through the lists. So, you would say 4, 9, 3, and then see whether or not they can repeat 3, 9, 4 back to you. You can see with each particular test, they start to increase the amount of numbers. We go to four digits, then to five digits, then to six digits, and we’ve got six different options tested.  Then we would ask the person, “Can I please get you to repeat the months of the year backwards.” You’ll say December, November, go ahead, and then we see whether or not they can do those.

Then the next step after the cognitive screen is we run through this neurological screen and balanced examination. You can see here, we’ve got a checklist. We asked the person before to read the symptom scale out loud. Could they do that? Because of course, we’re looking at the ability to read. So vision, can they see? Can they comprehend the words that are there? Can they then articulate them out? Again, it’s a neurological screen, even though we might think of taking that for granted, but that does a lot of neurological process. Did they read out aloud properly? Circle “yes” or “no”. Did the person have full-range pain-free passive cervical spine range of motion. We are assessing the neck. Now, the next bit is we do our six positions of gaze. When we do this gazes, you’re taking those targets across for them and they are looking with their eyes only, not with their head. When they are doing that, you’re asking blurred or double vision, blurred or double vision. We are doing our height and space, but also remember to do up and down. So, really, we’ve got sort of nine points — middle, here, here. Asking if someone’s got double vision while you’re doing it. You as a practitioner, watch their eyes. As we’re moving side to side, you might see if I’m looking at the camera, and you, guys, are looking at me in that small window. As they are following that thumb, you might see that they do this and one eye, obviously. Now, they will report double vision in that particular case, most likely, but we are also watching for the gross movements of their eyes to see, can they move both eyes together? Then we are asking the standard cerebellar tests so a finger to nose test to look for those coordination components. And then can they do tandem gait. Can they stand up and walk heel to toe? Remember, this is just being done on the sideline. What we are doing in our clinic goes more detail than this. We have got more tests than this, but we are screening them. Keyword, screening them.

Then our balance examination is a modified version of the balance error scoring system. The full balance error scoring system is there on your right. We can see that there are three stances performed in two different environments. However, in the sport on-field sideline assessment, we’ve removed the foam testing. Because thinking about it, if you’re out there on the soccer pitch or on the basketball court or wherever it may be, we may not have pieces of foam. We just use the modified testing.

How do we do it? We have the person stand in each of the positions. Position A, feet together, hands on the hips. They close their eyes, and they’re trying to stand there in balance for twenty seconds. Now, as they are standing there with their eyes closed, you are watching the person for errors. If you haven’t done this test before, what you’re looking at is do their hands come off their hips. That is an error. If they open their eyes, that’s an error. If they, of course, step out or fall out of the test position, that’s an error. If you see them tilt their hips or they’re leaning their trunk more than thirty degrees to one side, that’s an error. If they stay out of the testing position, i.e. they open their eyes, so they got an error and if they kept their eyes open for five seconds for whatever reason, or their hands off their hips, that’s an error. However, if someone took their hands off their hips and open their eyes at the same time, it’s just one error. You don’t give them two, because they happened at the same time. If someone opened their eyes, hands off the hips and stumbled, one error.

If someone makes ten errors, as soon as they make ten errors, just stop the test. All right? But otherwise, you keep them going for twenty seconds. You do it as you can say feet together, and then position two would be we stand them on their non-dominant leg. If you try to figure out some people go, “Oh, my ambidextrous.” “Which foot would you kick a ball with if you had to?” “I would kick the ball with my right foot.” So, they are going to stand on their left. Okay? If they are going to kick the ball with my left foot, they would stand on their right.

Then when you go to the tandem gait, a set of ten gaits or the Tandem Balanced Assessment, it’s the non-dominant foot is the back foot. In that particular test, generally, what happens is the rear foot will take about seventy to eighty percent of your body weight in general. We’re getting them into those positions. Each test is for twenty seconds, and you are counting the amount of errors they make. You can see that on the chart on the left, that allows you to input how many errors they made in each of those positions, and also to the testing environments that you tested them in.

Then we come back, as we said before, “Do you remember the list of words I read to you before? Tell me as many words from the list as you can remember in any order.” We’re seeing can they get those five words from before. The idea is delayed recall is supposed to be about five minutes after you have done those original cognitive tests. Then in the SCAT5 is once you’ve performed these, you’ll have your little decision sheet. Obviously, their symptoms, symptom score, their orientation score, so you’ve got all of that decision assessment there and you’re trying to make a call of whether or not this person has a concussion, whether you’re not sure, whether you’re definitively sure. But as you can see, the bottom line there, relevant for Australia, has to be signed off by a medical professional. We need to perform the assessment because that’s the minimum assessment that needs to be done, but from a legality point of view, needs to be signed off by a medical practitioner.

What I wanted to share with you is the SCAT5. You’ve got the paper there and you just work your way through the paper and you tick it off. However, a nice way developed by Jim Bovard out of Canada to run through the SCAT5 would be this ABCDEF’s. It just allows you to follow that alphabet so that you’re covering all of the points when you’re out there on the field. You work through it hierarchically, I run out onto the field. We are thinking first aid principles. If you are going out onto the field, the first thing you are looking at is the whole danger of this situation. I will use a personal example. I worked the Nitro Circus event at one of our big stadiums down in Melbourne. We are looking at these motorbike riders and these bicycle skateboard, all this stuff, so the x-game stuff, and we have got these motorbike riders jumping like seventy feet in the air. Our rules on the sideline, though, for that event were if something happened, we which was myself, an emergency room medical doctor, another physiotherapists, physical therapists and then our paramedics, our ambulance guys, we had to stay there. What would happen is the Nitro Circus team, they would run out there and make sure something wasn’t going to explode, like clear the site for danger. One other step back before we started in here this is, even though we’ve been systematically trying to go through it, step beforehand is if you’re there as a lone individual, having a plan, having the numbers that you know that you need to call. But if you’re there as a team, knowing and communicating what each team member, that medical team member, what each person’s role is. That example was the Nitro Circus team, they would make sure that the actual arena and that the environment was safe. Then the emergency room doctor and the paramedics would run out for the life-threatening stuff. Then the role was then I came out and I examined for all the concussions, head injury, musculoskeletal stuff. We made sure that our processes were either they’re off to hospital or was taken in the back room along with the physical therapist, the doctor.

Having that communication is important. This ABCDE is a nice little way to work your way through it. Going out onto the field, did you see the injury? If you saw the mechanism of injury and they are unconscious, it is neck until proven otherwise. If someone collapsed on the field away from the field of play, again, if you are not sure what happened we’re thinking obviously, neck first, but it could also be a cardiac problem. As you your then going out into the field and all the danger of the particular environments are appropriate, because remember, some of the sports continue to play, even though someone may be down on the field. We are going to make sure of safety first, but you get out there to the athlete. The first thing is you’re working through those Maddocks’ questions, the orientation style questions, Glasgow Coma Scale style questions. Are they alert? Are they aware?

If they’re not alert or aware, that’s removed from the field. So, the question becomes is this refer for emergency or to the sideline? Step one, alert awareness, you’re running through those Maddock style questions, Glasgow Coma Scale things. If they are alert and then they’re aware, you’re moving into that behavior, are these people becoming agitated? The tricky bit, of course, with behavior is do you know the athlete beforehand. But also, too, if this person is able to be getting to their feet on their own before you even get out there? Are they able to balance? Are they staggering around? Can they stay steady on their feet. If they’re able to do all that, we’re moving down to the neck.

Having this conversation because this is where the cognitive and then C-spine come in overlap, so painful, midline spinous processes. Remember, just assessing red flags here. Do they have any headaches? Do they have any of those symptoms with their neck pain? Running through your cognitive tests, running through your symptoms with that person. Then we can move down to the dizziness which is  all those finger to nose test, tandem gaits, mBESS can fit in there. Then we have got all of our eye movements tests, flashing lights in the eyes. Then out there on the field, the purpose of Jim Bovard was thinking of, “Well, if you feel this person’s passing everything, they’ve passed the alert, awareness, their behavior, their balance is good, their C spine, their cognition. You’ve pretty much worked your way through the majority of the SCAT5 at that point”.

You then got down to the dizziness where you’ve done all the remaining parts of your neuro screen. As you have gone through that neuro screen and the mBESS, then they are passing all of that, that’s great. “Well, let’s actually get you to maybe sprint ten meters back and forth, three, four or five times.” Does that bring on any of your symptoms? Does that cause any problems. If it doesn’t, with exertion, you go, “All right, I’ve made a clinical decision that I don’t think you’ve had a concussion. Maybe you just had the wind knocked out of you. I’m happy for you to continue to play. You continue to play. If you develop any symptoms, if you feel something’s not right, take a knee on the field, tap to your head, and then that’s the F for follow up, we’ll get you from the field of play.” Regardless if the person plays out the entire match, after the game, you follow them up and we’re running that full assessment sidelines, the serial examination. But those “ABCDEF” is a nice other little mnemonic that you, guys, could potentially follow to implement the SCAT5.

Now, the King-Devick test. This is a common test that gets talked about. I’ve just got it in here for your understanding. Most of the King-Devick test now is, I believe, owned by the Mayo Clinic. It’s created as an app on an iPad. Once upon a time it was charts. It’s a little bit harder to get your hands on the charts now, because it’s been turned into an iPad app. But it’s about moving the eyes rapidly. It’s the cards reading numbers that are on a chart, saying them out loud, and these things are timed and measured for errors. The cards would actually you have to be showing that to the patient and you, as the practitioner, would have the responses and the timeframes on the back. And so, the problem we’ve got with it, it’s been shown to be somewhat of a good test to be using in the assessment of concussion, but you need to have a baseline. This needs to be used on our athletes before we run out there and actually use the test as part of your assessment process. If you don’t really have your baseline, it’s not going to be a good test for you as part of your diagnostic assessment battery. It’s not clinically sufficient for concussion diagnosis. It needs to be used together with other tests and it needs to have a baseline.

Before we get into this best practices clinical exam, let’s just, again, emphasize the points there. That on-field assessment, the sideline assessment, that SCAT5, when we get to our hands on module, we’re going to be running through those real-life scenarios. Each practitioner student that’s an attendee of the hands-on module will be assessing every one on those components using an example mock case for each doctor and patient and reverse the roles each time. Also, as part of that, we’re going to try and give you guys some of these best practices, clinical exams. When we look at it, I said it before, understanding that pathophysiology of concussion proves especially critical for those twenty to thirty percent of concussion patients who develop persistent post-concussion symptoms.

Why do I spend that time trying to emphasize that science and that pathophysiology? Because as we follow the research here, understanding how the neck could be involved, the vestibular system, the eyes, cognition, autonomic nervous system, et cetera. Very important for these people who have the ongoing symptoms, those people that don’t clinically recover in that fourteen days as an adult, four weeks as a child.

The correlated systems evaluation. You’ve heard me use the word systems. Research has demonstrated a complex relationship with the brain, the neck, vestibular ocular system, the jaw, other structures that are related to the signs and symptoms that people can have with concussion. Because the problem is someone can have a headache because it’s a concussion, but someone could have a headache because it is the neck. Someone could have a headache because it is their eyes. Someone could have a headache because it’s their inner ear. These systems need to be evaluated. Now, the Berlin consensus statement, the Concussion in Sport Group, the fifth one, and similar research has demonstrated common signs and symptoms that occur with concussions, with whiplash associated disorders, with vestibular ocular disorders at the time of head injury.

The concussion process is based upon this chemical metabolic process. Once that passes, it is no longer a concussion and its persistent symptoms post-concussion and that is because of either a neck, ears, eyes, cognitive, physiological, autonomic nervous system, combinations there off. Once the time frame ends for that metabolic cascade, it is no longer a concussion. It’s persistent symptoms after a concussion, and it is other systems that are causing those signs and symptoms. Any system involved with the signs and symptoms that are experienced by a patient should be thoroughly investigated in a clinical environment. We’re all chiropractors here and, hopefully, we would be happy to say that we would feel pretty confident and good with our neck assessments and understanding that. What I want to try and do here is to try and allow us to how do we differentiate neck from, say, inner ear, especially as it relates to dizziness.

We know that if someone’s hurt their neck, we could have neck pain. But one thing I’ve also say to you is go back and it’s not in the notes that, but a problem with your vestibular system can cause neck pain. A problem your eyes can cause neck pains. The roles can reverse. A problem with your jaw, as you can see there, could cause neck pain. But a neck problem could also cause jaw pain. We’ve got to be evaluating all of these systems. As you can see with the neck, maybe you’ve got neck pain, headache, dizziness, gait instability, feeling, let’s use the word brain fog, gaze stability issues or problems keeping your eyes still on a target that you’re looking at, difficulty with Sicard, so Sicard are your fast eye movements. Okay? Looking side to side, up, down, diagonals. Sicard are fast eye movements, body coordination problems, balance issues, so your neck can contribute to all of those things.

Your vestibular system, everyone thinks naturally of dizziness and balance. I want to flag this with you as to how we think with our patients. If a patient says to you that they’re dizzy, I immediately want you to say to that patient, “Can you describe your dizziness without using the word dizzy?” They will often look at your like, “Hmm?” If they’re struggling to try and describe it, because I try and keep an open ended, maybe say to him, “Does it feel like you are lightheaded like you are going to faint?” If they go “yes”, you, as a practitioner, start thinking autonomic nervous system, cardiovascular. All right? Now, it could be neck as well, but I want you to think first thing, cardiovascular or autonomic nervous system. If someone says that they or the room feel like this spinning, it is vestibular until proven otherwise. If someone feels that they are rocking or bobbing or swaying, or feel that they are being pulled in a certain direction, they feel like they floating, think otolithic organs, vestibular system. Think that again until proven otherwise. Once you have ruled out all those, then think neck.

We’ll show you how we’ll break this down, but that dizziness question is really important ,and then, we can see obviously oculomotor, we can have vision problems in balance. Convergence, of course, is our eyes coming together. Accommodation is when we converge, pupils constrict, lens bends, the triad. All right? Accommodation is convergence with two other things, smooth pursuit areas, pursuit is following the target, side to side, diagonals, up and down, in whichever direction is. Smooth pursuit is following, and then Sicard, as we talked about before, and then we’ve got our jaw components.

This here is your clinical multisystem exam that we need to be performing in a concussion patient in your clinic. Now, I will let you know, my concussion exam in clinic takes three hours. Of course, we don’t have the time to run through a three-hour exam here via webinar. Obviously, that is a long process, that entire exam. We have to be able to run our neurological examination which we need to assess people’s vision, auditory system, sensory processing, motor control, coordination, I think, cerebellar type testing, their hearing testing, sensory, so your pinwheel, joint position, sense, light touch, vibration, visual processing, obviously, lots of stuff going on. We might think about optometry, ophthalmology, if we don’t have that training in those systems. You have got your mental status cognition. We have got certain tests that we can do for that in clinic, maybe with questionnaires such as many mental status exams, part of the SCAT5. We can be using with that, the MoCA, or the Montreal Cognitive Assessment, and then, of course, neuropsychological referral to a neuro psych.

Then we’ve got these autonomic. I’ve highlighted the three here in bold that I want to try and emphasize for us. These autonomic exertional intolerance impairments, vestibular ocular motor impairments, your postural stability and your balance, and then our cervical spine, sort of musculoskeletal sensory motor impairments. But that there is what we need to cover and, obviously, all the tests that go with that, as part of our examination in clinic for a concussion. I like this chart as a way to start to think about. You look at the top, the person’s had a concussion, they have done the examination. But then it’s greater than three weeks later, and you are doing the follow-up on this person. Just look at the model, don’t ask why it’s three weeks, but let’s just look at it from that point of view. You’re doing your follow-up and it’s been greater than three weeks, and now you’ve got the person sitting in front of you and you’re asking, “Do you still have symptoms?”

Remember, symptoms are our biggest clinical recovery indicator. “Do you have symptoms still?” The person, if you follow the chart, they say, “No, I’ve got no more symptoms. Symptoms have been fine.” We’re going to do a treadmill test, which we’ll talk about in a second. On that treadmill test, does that cause you any symptoms. If they get no symptoms, you can follow the flow chart that says, “All right. You’ve got no symptoms or risk. I physically exert you. You get no symptoms when I physically exert you. That suggested that you’re recovered. We can start the return to play protocol.” If they’re back at work and if they’re back at school, or back at school or both. But if I’ve got no symptoms at rest, and then I put some on the treadmill, we can see over here that we’ve got the no symptom pathway, and then we’ve got, I put them on the treadmill and then their symptoms get exaggerated. This is starting to make us think of a physiological mechanism, an autonomic nervous system type of problem.

Other side of the chart, we can see, I go to examine the person, “Do you have symptoms?”, “Yes, I have still got symptoms.” “I will put you on the treadmill. If I put you on the treadmill and your symptoms worsen, I’m thinking autonomic nervous system.” I have got symptoms at rest, put them on the treadmill, but the symptoms don’t change. They stay the same. Now, we’re thinking that it could be the neck or it could be their vestibular ocular system. A nice flowchart of clinical thought process and we want to be able to start to use these tests to figure out which system or systems are involved with that patient having ongoing symptoms.

Let’s just say this in general. If this is the only thing you take away from today, this test, I want you to know that we need to make our concussion patients perform this test. If you don’t have a treadmill in your clinic, make sure we’ve got someone in your network that we can actually get this test performed. Out of all the evidence that’s building, this is the test that’s getting the majority of the evidence behind it as a test and as a therapeutic intervention. We can get a lot of information from this particular test. As you can see, the instructions are all spelled out. I’m going to hit the high points here for you.

  • We set the treadmill for, obviously, Australia, five and a half kilometers an hour. For the US, 3.4 miles an hour.
  • Treadmills at a zero percent incline. Every minute, you’re going to make the treadmill incline move up one percent, one degree, depending on the measurement of your treadmill.
  • The incline goes up.
  • Every minute, you measure the person’s heart rate. You ask them about their symptoms and you ask them how hard the effort is.
  • An RPE, rating of perceived exertion.
  • Is this a ten out of ten effort or one out of ten? Whatever it is for them.
  • Do they have symptoms? What’s their exertion effort level and what’s their heart rate?
  • Then I increase every minute going through that process. Incline increases, symptoms, effort, heart rate.
  • Next minute, incline up, symptoms, effort, heart rate.
  • We keep going until the treadmill maxes out on incline, the example there’s like twelve degrees, fifteen degrees or percentage, and then if they’re still going because their symptoms are fine, they’re not exhausted, we then start to increase the speed or we slowly start to make them run.
  • The purpose of this test is to push someone until they’re completely exhausted so their RPE is 19.5, or 9.5 out of ten. The 19.5 comes from the old Borg scale. Is the effort at a ten, a nine and a half out of ten?
  • If that effort gets there, we stop the test. We see what that heart rate is for the person.
  • If they’re walking away on the treadmill, and then they report that they’ve got a symptom increase. They’ve developed dizziness or their headache has increased by more than three out of ten, whether that symptom was there at baseline, maybe a three out of ten, I walked them, walk them, walk them and all of a sudden, it is got more than a six, we stopped the test. We see what their heart rate is.
  • If I’ve got no symptoms at all, I’m walking away on the tread. I’m fine. Everything’s going great. As I start walking, all of a sudden I start to feel nauseous and that goes up by more than three out of ten, I stopped the test. I see what the person’s heart rate is.

The purpose of this is to take someone basically to failure, symptom provocation or exertion and see what their heart rate is at that time. Okay?  “There is our rules just there”. We come back to it.

Then we have got our VOR, our vestibular ocular motor screen. Now, when we are looking at this, I have got an expansion of this in the FICS ICSC Learning portal as part of the module (ICSC01) with the rest of the head injury and concussion learning.

We will go through this more when we do the hands on training. I want to hit the high points with this right now. But the screening process is five tests and we’re doing eye movements and head movements to see if we can aggravate the person’s symptoms. Everything is always about symptoms when it comes to concussion. But again, I would like us to be better as a profession. I want us to look for objective things as well. Because those objective things on these tests, give us the clues as to what we might need to be rehabilitating what is not working properly. Watching someone at the gym do this, and then you watch that happen, and everyone goes, you need to go work on that left bicep as an example. Maybe I am doing these eye movements and find out that they can’t do a smooth pursuit to the left. They are jerky and therefore, we know that that pursuit pathway to the left might need to be worked on.

That is freely available for you online. You can jump onto Google and type in VOMS for concussion and you can fill these types of things in. You could create a template chart for yourself in your own records. All we do is we ask the person about headache, dizziness, nauseousness, and fogginess out of ten. “Do you have any of those symptoms out of ten? If so, what do you rate them out of ten?” We then perform each test and we ask the person after each test, “How are your symptoms? Did it aggravate headache, dizziness, nauseousness, fogginess?” We get the person to report that out of ten. Now, if any of the tests aggravate the symptoms, you then wait for those symptoms to go back down to baseline level then do the next test. Okay?

Smooth pursuits, all that information is there for you, but the bit I want to take out of this is when you’re trying to follow the target, you want to see are their eyes following smoothly or do you see their eyes jump? Do you see one eye move and the other ones stay still?  Red flaggy type of stuff versus jerky functional things. Yes, we record the symptoms, whether it provokes it, but we also want to see, do they have observable objective findings? We’re going to do it horizontally and vertically. We’ll go through this in the hands-on in more practical detail. Sicard, we give them two targets. They’re going to look left, right, left, right, left, right as fast as possible. Up, down, up, down, up, down as fast as possible. Does it aggravate your symptoms?

Our perspective we want to see if they look to the right. Do they look straight to the right? Do they have one eye move and the other one not? Does gross motor inappropriateness there? Red flags, of course, if we’re not moving one eye compared to the other one. And then also this accuracy of do they get straight from here to that target or do they one, two, three? Their eyes sort of jump a few times. If we see more than two jumps to get to a target, that’s an objective error, whether that’s up, down, left, right. We want to look for some of these objective findings.

The new point convergence you do, that’s the one test in this that we look for problems. Now, this is bringing the target in your normal accommodation types of tests. But really, with this one, they are just looking to see do the eyes come in. We are asking the person, “Tell me if you see double.” They ignore blurriness, but do they see two images? Usually, as a practitioner, at that point, you will see as their eye comes in, one eye goes out. Instead of both coming in, one will just go boom. That’s when they’ll see double because their eyes aren’t focused on the target. We measure that distance for when the person either reports double, or you see one of their eyes, or both of their eyes stopped moving. Why this becomes important is that fifty percent of concussions are reported to have a problem with convergence. We call it convergence insufficiency.

If people can’t converge, they are going to have a problem reading. This becomes profound for us with learning, with going back to work. This could produce headaches and everything, and it’s based upon an eye movement control. Does it cause symptoms when you’re doing it? Do you see an objective issue where if their eyes can’t come in to six centimetres or closer? If they’re beyond six centimetres, that’s considered an objective error. Then we have got our VOR, which is setting a metronome to a hundred and ninety beats per minute. In time to the metronome doing that, can they keep their eyes on the target? Does it cause aggravation of symptoms? Can they objectively keep their eyes on the target? Because if I do this, and then my eyes jump back, I’m getting a clue that left vestibular system is not working.

Obviously, the opposite. If I’m doing that, then my eyes jump back, I’m getting a clue that that right vestibular system is not working. Not only symptoms, I want us to identify whether or not someone has got and, of course, also do it in the vertical plane. I want to see if the person’s also got objective deficits.

Now, visual motion sensitivity, this as you can see, is they’re moving whole body, keeping their eyes looking on their thumb. Now, this one here you want to do with stuff in the background so you get them facing a busy part of your clinic. Maybe you have got pictures on the wall or bookshelf, something that’s busy in the background. What happens is when they’re doing this, your eyes should be able to stay on the thumb. But because there are things in the background, their eyes exaggerated, their eyes might look over there and then come back to their thumb. Can they keep their eyes on their thumb is another aspect that we can look for with that. But we are again, asking the person about those symptoms.

The points I want to bring up here is that the VOR this one in terminal 180, either of those, the visual motion sensitivity one or the new point convergence, if you put all three of those together, if someone’s got a problem with all three of those, they are suggesting it’s clinically useful in identifying concussions. If you see abnormalities with any of those tests, whether it’s symptom provocation, which is what the main thing is, or objective findings, eye movement dysfunctions, referring to the appropriate healthcare professional for more detailed assessment and management. You can see here this quote and this is a great article. This is the American Physical Therapists Association. They did practice guidelines on concussions like eighty-five pages of all literature of what tests got good evidence behind them, which ones don’t, which are the test we should be doing, not be doing to truly assess a concussion patient. But as they quote here,

“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 of the screening strategies necessary to examine all aspects of vestibular and ocular motor dysfunction. Therefore, it may be useful as a screening tool, but it is not appropriate as a replacement for a comprehensive vestibular and ocular motor assessment”.

There’s more to assessing those systems than just this. But this is a great start to be bringing this into our repertoire to help serve our patients and our communities. The point that I wanted to bring up here, is the next link of that whiplash concussion, and this idea of if you have had a concussion, you have had a neck injury. The question becomes if you have had whiplash to your neck, have you also had a concussion?

There are some basic guidelines that we can use from the literature. It’s that different forces and basically, the more force that you get hit with, whether it’s to your body to your head, et cetera. But if I create a whiplash acceleration-deceleration injury, or mechanism of injury, the more force that I get hit with the more G-forces, the higher the G-force, the more the nervous system gets involved. The lower the G-force, the more it’s the neck.

  • As you can see here, when higher forces are a direct blow to the head occur, additional injuries such as concussion, or damage to the central nervous system, or the vestibular system are more likely. When I get a high force or a direct blow to the head, we think nervous system injuries.
  • Up to a third of those with traumatic neck pain associated with higher forces may have peripheral vestibular problems, e.g. BPPV. Classic one. Remember, BPPV is the most common cause of dizziness. Hence, what we are saying before, if someone says dizzy, get them to describe their dizziness. If they say they are spinning, it is vestibular until proven otherwise. The probability is its BPPV based on probability. It’s the most common cause of dizziness.
  • Injuries induced by axial rotation, as I said before, this acceleration movement that may result in different types of neurological injury. There we go, guys.

To injure someone’s neck, four and a half G’s. But you can see here to start to then increase it. The way to do it, lower G-forces, as I start coming up, more likely to get that brainstem vestibular system. As I keep coming up, more likely to get the brain higher levels of the nervous system. We can see that for a concussion, different researchers out there. So, 60 to 160 G’s, I’ve seen 80 to 160 G-forces is what’s required for a concussion injury, whereas your neck is four and a half G’s.

Therefore, if you have had a concussion injury, there will be a neck injury. The question then starts becoming role reverse. If someone’s had a whiplash injury, a neck injury, have they also had a concussion injury? Because the mechanism is the same. It is just whether or not there was enough force, enough speed to induce further injury to the nervous system.

As it relates to the neck, we want to bring in some tests into our toolbox to help this as it relates to concussions specifically. The deep neck flexes and testing their endurance has been one that has getting a lot of research following, and they’re starting to suggest that it may be one of our good return to sport predictors. To be able to say, if I’ve got enough strength and endurance in this, this has given me a better indicator that you’re ready to return to sport. If you don’t, we can’t return you to sport. All we do is we have the person laying on their back with their hips and knees flexed, we’ll go through this hands-on. We put two fingers underneath their head, we have the person perform a chin tuck while their head’s resting on your fingers. They gently lift the head up. You can see that in picture B down there. They hold that position with the chin tuck for as long as they possibly can. When the head drops and touches your finger, they reproduce some pain and they can’t hold the position any longer. Well, that you see that they lose the skinfolds here, they lose one of those, we stopped the test. Basic rules, if we’re dealing with athletes, these athletes should be able to hold their neck in that position for at least a minute. If they’re a sport that wears helmets, ice hockey, American football, to polarizing ones, they should be able to do that with their helmets on. We want to make sure it’s minimum a minute, and then of course for some people are going to say there is data out there because it’s just normal data for males and females, when we are not talking about sports that says males should be able to hold it for greater than thirty-nine seconds. Females should be able to hold greater than twenty-nine seconds. But we’re talking about sports and athletes here now. Beyond the minute, and some people are pushing the two-minute mark is what we should be looking for.

Now, our joint position testing, some of you have seen this one. Dealing with the head laser. Basic principle. Laser on the top of the head, get them to close their eyes. We have them turn their head, they come back to the middle, they tell us when they think (they’re in the middle) they go, “Yes, I’m in the middle.” You would then mark on that target where that laser is, you don’t give them any feedback, you keep their eyes closed. You move their head back to the middle for them, and you go, “That’s where the middle is. Keep your eyes closed. Turn your head to the other side. Come back to the middle. Tell me when you think you’re there.” (They’re there) you mark it on the bull’s eye again.

Personally, I laminate mine. That way, I just use a whiteboard marker and a market with a whiteboard, and then when I’m done with it, just wipe it off with a wet wipe. So we use that. We do six times alternating each side. Right, left, right, left. You can do up and down as well. But the big ones they talk about is doing right and left. And then we get an average of the right and left trials. Anything that’s greater than four and a half degrees. Now, how this gets measured, is if you download one of these off the internet, you will see that you do the testing ninety centimetres away from the target. So, where that person’s ears are needs to be ninety centimetres away from the target, and then that target is designed so that if that laser is out in the yellow, you already know it’s four and a half degrees.

In a smooth pursuit neck torsion test, we get people to do the pursuit again. Can they follow the target smoothly? Then as they are following the target smoothly, you will have the person keep their head straight, and then they turn their body underneath it. Why are we doing this? Because if I turn my head, I activate my vestibular system as well as my neck. If I keep my head still, and I move my trunk underneath, I’m just activating cervical efference. Now, while doing a pursuit, seeing what their eyes do, are they smooth? And then if I load up the person’s neck, and now do the pursuits, do you see that they become jerky with those pursuits? In particular, as they cross the midline? From there, they’re following, and then their eyes do this. Oh, there it is. Back and then it’s like, ah there it is.  Does that neck by intorsion them right or left, does that cause their eyes to become jerky or does it start to reproduce these symptoms? Try to differentiate between ears versus neck.

Why do I want to bring up these particular important things with this particular paper? Its results suggest that patients with dizziness after a concussion, who had abnormal cervical spine proprioception, which was the head laser and the smooth pursuit neck torsion test. Joint position error, JPE, SPNT, smooth pursuit neck torsion test. Those people who had abnormal head laser, and then this with intorsion, they responded better to a cervical spine proprioceptive rehab program compared to those who received vestibular rehab therapy. Here is the important part, the exclusion criteria is this. If someone has BPPV, you have got to treat that. It’s their vestibular system. It’s not their neck. If someone’s got BPPV, a peripheral vestibular problem, or if you’re doing the smooth pursuit neck torsion test, so if you do this, and their eyes are jerky there, it’s the central nervous system. It’s not their neck.

If we have got holding here, and you’ll do in your six positions of gaze as part of your cranial nerve assessment, and as they’re looking, if their eyes are moving, so if they’ve got intrusions or nystagmus or doing that, it’s the central nervous system. It’s not their neck. This is how we start to differentiate these types of aspects. If I throw someone into a Dix-Hallpike maneuver, or a supine role to look for the canalithiasis or cupulolithiasis, crystals in the ear, BPPV, so I said the same thing three different ways. If I’ve got that going on, that is a peripheral problem. It’s not the neck, it’s this. We’ve got to treat the vestibular system first. If someone’s got intrusions in the smooth pursuits, if they’ve got it when they’re straight, and then they’ve got it when they’re here, if it doesn’t get worse, if it’s just the same or if we’ve got nystagmus or jerky movements when we’re doing any of these gaze holding six positions of gaze, it’s a central nervous system problem. It’s not the neck. We’ve got to investigate those vestibular ocular motor system appropriately.

Our role, in summary and trying to come to the finish of this, we are well suited for evaluating signs and symptoms associated with concussion, especially as it relates to the neck. Because remember, every concussion is going to have a neck component. Question is what’s the neck components? We can, of course, make a decision as to whether or not we need to refer for the appropriate imaging. We worry about neck fractures, dislocations. That’s obviously significant. Skull fractures, facial fractures, bleeds, assessment, diagnosis, refer out, and then of course, we can implement our return to academics, return to sport protocols, and our aerobic strength and conditioning protocols. The buffalo concussion treadmill test.

If you’ve got further training in neuro rehab, in vestibular ocular motor rehab, that is another tool in your tool belt to also help deal with that. We have got referrals to colleagues, other professionals who have strong practice interests and qualifications in those fields.

Return to academics, return to sport injury prevention. We will hit these pretty quick because they’re nice and easy to follow when they are available on your consensus guidelines. These are straight out of those. A return to school guidelines. It’s academic school first. Look at the very bottom points there, guys, that I put there. Children and adolescents should not return to sport until they have successfully returned to school. That is full-time school, full-time workload, full-time homework, no problems. That is return to school. The same thing for work. If you’re more of an adult going to work and not a child, it is are you back at work, full-time work, full-time workload, normal eight days of the week, hours, no symptoms. That’s what you’ve got to be able to achieve before you can go and start playing sport again. However, doing aerobic exercise, the buffalo concussion treadmill test, and prescribing the exercises, that is absolutely appropriate. That is not sport. That is the therapy. We are using aerobic exercise as a therapy.

A graduated return to sport. You can see here. No return to play before clinically recovered, on the bottom. Meaning no symptoms. Then we work through each of those phases. Symptoms at any stage. If you’re doing aerobic activity, let’s just say stage two, and you’re doing your buffalo concussion treadmill test aerobic activity, if that’s aggravating your symptoms, you move back to stage one. You got to do stage one without symptoms before you can move into stage two. You’ll do stage two without symptoms. Now, what I want to flag here, guys, is this is the international consensus.

Just recently, and obviously, Paul McCrory, who’s a neurologist, sports and exercise physician here in Melbourne, Australia, the lead author of that group, Michael Makdissi, who is also one of the key authors and the lead author of the persistent symptoms systematic review, and Gavin Davis, who’s a neurosurgeon here at our children’s hospital. We’ve got three of the guys that write these consensus papers. They’re actually here in Melbourne. Very fortunate to have some of these experts right here in our town.

But when we look at the current return to sport, Australia has actually increased this. You could have returned to the sport following that protocol in about eight days because you would have had a day off. You would have gone through those stages, and then what would have happened is at stage five, before you can go to full-contact practice, you had to have medical clearance. To be able to go back to full contact, you need a medical clearance. Then once you have gone through that, then as long as you can pass through each of these stages without symptoms, we can return to sport.

Australia has just implemented these guidelines, which means the earliest you can be back is thirteen days. The idea of the seven-day, eight-day return to sport in Australia doesn’t happen anymore. It’s now a thirteen-day recovery. As you can see that there whether this gets implemented into the new consensus statement, I would suspect it does because those guys that I just mentioned in the consensus group are also involved in our Australian Football League.

This protocol here, it’s there. Basically, it’s a day of rest, two days of rest max. Then you start to do your normal activities of daily living. Can you do that without provoking symptoms? Yes. You get a rest day then you move into your aerobic exercise program, which is from the buffalo concussion treadmill test.

Injury prevention strategies, guys, let’s hit the high points. Do helmets help? They help with skull fractures and contact injuries, but they don’t stop twisting and moving of the nervous system inside the skull and spinal column. There’s no evidence to show that helmets reduce concussion occurrences, but they do help with the more significant things. Lacerations, fractures, et cetera. Mouth guards, same thing. They help with jaw dental things, but nothing with concussion. However, technology now is starting to put gyroscopes and things into the mouth guards. They are actually doing research right now here in Australia, where they’re trying to measure some of these rotational effects to see if we can get more numbers. We do not only have the G-forces. This 60 to 160 or 80 to 160 G’s for a concussion. We might start to be able to pick up what are the rotational accelerations that are required. But that’s a research thing, not about preventing concussions.

Strength and conditioning. Especially in high school female athletes, there’s research to show that if they’ve got increased neck strength, that that can be helpful. The research right now for return to sport says deep neck flexes strength and endurance is a potential return to sport criteria that you need to be able to be strong and for long to be able to be cleared for return to sport. But when we start to talk about elite level athletes, there’s a mixed sort of result on the idea of neck strength on professional athletes. But the high school athletes suggest that neck strength may reduce the rate of concussions. Hence, this idea of the deep neck flexor endurance test seems to be a big one that’s starting to get, especially Canada, a bit of following and research behind it. Now, University of Cincinnati, very fortunate enough to have been able to do some work and training under professor, Dr. Joe Clark, who’s a neurologist there. University of Cincinnati has been doing these visual training processes with hand-eye coordination, vision processing, eye reaction, vestibular ocular motor, and they’ve got some data that they have published that suggests that by improving vision ocular motor hand eye reaction times reaction times, that they have been showing signs through their university program compared to all other college American football programs. But the University of Cincinnati has one of the lowest concussion incidence rates out of all college football. So much that their concussion rates in their football program are equivalent to what the general public would sustain compared to, obviously, American football, which is obviously significantly higher. They’re doing further research on that. That is an interesting bit of research that’s coming out of the University of Cincinnati.

On that note, are there any questions from today?

Christine: There are a couple of questions in the chat for you, too, Brett. If you want to take that up.

Brett:
The first question here is with neck pain or tenderness being a red flag, is it any presence of pain or is it only when present at rest that it’s a red flag? At this point in time, Michael, it’s like thinking about the hierarchy of red flags and being safe. The presence of that pain or tenderness, not just at rest, but when you’re palpating and when you’re getting them to move, we’re trying to look at have they got their full range of motion. Of course, if they’re unconscious, we’re thinking its neck until proven otherwise. But that idea of the red flag if we’re palpating and all that, we’ve got that decreased range of motion. We’re thinking more about concern about protecting the neck.

The next question was is it significantly more beneficial to have a full team’s baseline preseason scout results for comparison? This one’s up for debate. Now, when I say it’s up for debate, what the research suggests is you do not need baselines to make a concussion, assessment, and diagnosis. However, if you had a baseline of people, you would actually have a better idea objectively of what that athlete needs to get to as a standard for return to play. But right now, that is not suggested as being mandatory or required. If you could get it, it’s going to help you and help that particular patient.

The next question is to get the SCAT5 signed off by a medical professional, do we send it to a GP with a referral letter? Yes, depending on how that network works. I work in a sports medicine clinic. I’m very fortunate I could walk down the hallway and tap on the door and have our sports and exercise physician, obviously, quickly assess that. We have that relationship so we’ve got that ability to do it. The problem that we also have is we need people who were actually trained in concussion to assess concussion. Unfortunately, we’ve got to be able to also find someone in our network, a medical professional, who’s actually got training in concussion. The SCAT5, you need to have medical training in its use. Like we’ve been trying to do here today and in the hands-on and hopefully, you guys will be practicing this between now and then. So we want to be able to have a medical practitioner who’s trained in the SCAT5 as well.

Then we’ve got the graded treadmill test. Only test or can it be done on a cycle EG as an ECG testing? The graded treadmill test has actually been created as a buffalo concussion bike test now. They’ve actually validated. It’s used in being able to do it in adolescence. The protocol is a little bit different because it’s got to do with wattages on the bike. But yes, a graded treadmill test can be done on a bicycle as well.

What equipment are we using to record heart rate? Up to you. You could use a pulse oximeter. The most accurate way we’re going to be able to do it in the clinic is with obviously a chest strap connected to a watch. If you are going to do something off the wrist, Apple Watch is actually the best technology that it comes off the wrist. If you’ve got a Garmin or a Fitbit, the Apple Watch is going to read based off the wrist. But remember, the wrist is not good. But if you’re going to use something off the wrist, use an Apple Watch. Chest strap pulse oximeter. Do not put your hands on the rails on a treadmill. Those hand sensors are not going to detect heart rate accurately. There are options for the equipment that we can use.

Then coming from a third-year student, is it safe to adjust an upper cervical with a patient that has a history of concussion? If yes, any preferred technique? Now, the question becomes with that, it depends. Now, I know you guys are wanting a direct answer, but the answer is it depends. The reason it depends is because is that indicated in the assessment? Is it their neck or is it something else? Is it their eyes? Is it their vestibular system? Is it their neck? Is it their autonomic nervous system? We have to examine the person to determine is that appropriate. And then when it comes to which technique do you use, of course, that’s always going to depend on what was the significance of the injury. It’s got to have to do with the actual patient’s comfort level, with you as the practitioner, with manipulation. So many various factors, but you generally should always would start with most of these circumstances on more lighter, lower force, and then you can move up to more of the HVLAs where you deem appropriate. The answer for sure, is going to be depends. I hate doing that to you, guys, but it is the honest, truthful answer.

At what point do you stop the SCAT5 tests or would you always try to go through the entire test as much as possible? We would work through the entire SCAT5 from basically from cover to cover. After three to five days, it starts to lose its clinical utility. Really, it becomes more about using the symptom scale, post-concussion symptoms scale to monitor their symptoms and their recovery. You would potentially have your other tests, but you know a key for that person. It’s your tag test that you would keep reviewing to see objectively when they’re improving.

Christine: Really lucky for everybody listening. Super informed, very accurate, up-to-date, and really dynamic lecture.

[End]

Upper Extremity - Soft Tissue Inventions - Drs Jon Wilhelm & Mika Janhunen

Dr Janhunen:  Welcome everybody to this lecture on soft tissue interventions here on FICS hands-on modules or hybrid modules, as they may be. My name is Mika Janhunen, and I’m a sports chiropractor here in the UK.

Today, I’m joined with Dr. Jon Wilhelm from the USA. We’re going to be covering this vast topic of soft tissue interventions not necessarily in all the nitty-gritty detail but we’ll give you a broad spectrum overview of our favourite techniques and how these things can be utilized effectively and efficiently in the clinic whether it’s indeed in clinic or pitch side or any other setting where you might be practising. Welcome, Jon. Thank you for joining me for this amazing lecture today.

Dr. Jon Wilhelm:  Glad to be here, especially with someone of your calibre. let’s get going. I am going to go ahead and share my screen here.

Okay, here we are. Soft Tissue Interventions. First, some important housekeeping details. Disclaimers. Of course, this is for educational purposes only. We’re not rendering any specific medical diagnosis or a substitute for your own unique evaluation for your patients’ own unique problems. We hope that the information that you find in this is helpful. Remember your treatment decisions are your own personal choices. Exercising your own professional judgment needs a situation.

Again, we hope this is a helpful primer[?] on soft tissue interventions. We also have no commitments to or relationships with outside sponsors. We’re not going to discuss any unlabelled products or investigational use of products, and all the images and videos to the best of our knowledge are open source or produced by us. Any violation of intellectual property or copyright, of course, is unintentional.

What is soft tissue work? We all do it. We’ve heard of it. What exactly is soft tissue work? Well, found this definition and added to it and refined it. Skilled hand movements that really try to produce a number of different changes. Teaching extensibility, range of motion, mobilization of soft tissues. Sometimes, the soft tissue intervention is simply meant to induce relaxation, to change or modulate pain, or to reduce some sort of movement restriction or tissue swelling or inflammation. Mika, here we go.

Mika: That in my opinion is a great definition of soft tissue interventions. Of course, in its own right, pretty much covers more or less what we’re going to be discussing today. We always have to remember that sports chiropractic is not only about adjusting. Even if adjusting and manipulation, whatever you want to refer to it really, it’s your number 1 go-to technique in most situations, but there are all these other tissues as well. It’s not all about bones and joints. As sports chiropractors, we need to be able to really influence most of the tissues. We can, of course, manipulate fascia. We can manipulate muscles to a degree. Sometimes, mobilization is the appropriate thing. All of this is geared up towards producing the absolute best performance in the athlete.

First, of course, it can seem quite overwhelming if you’re a newcomer to the scene. There are all these acronyms and all these seemingly, very different techniques, but we’ll try and cover and put a little bit of clarity into that, that makes today. At the same time, is it a good idea to be a purist so that you only use 1 particular technique, or is it better to just mix and match and find bits that work for you amongst lots of different things? Even more importantly, when you’re first starting out, what is the correct soft tissue morality and how do you know which one to use?

Jon: I remember being a student sitting in school and lectures would come in and they’d talk about this technique or that technique. I remember one particularly saying, I’ve spent my whole life learning XYZ technique. That seemed overwhelming as I was a student sitting there in my chair, the whole world of diagnosis and treatment and clinical management in front of me. How do you decide that? We’re going to touch on that, aren’t we?

Mika: We’ll try and make sure that you have a bit more of an understanding of which techniques to use for which situations and how to gauge your appropriate response to these situations. Going back to the old uni days, I could definitely remember there was a lot of chatter about which technique is the best. Everybody has their own ideas and this sort of polarized views on these. Some people absolutely swear blind that this technique that I’m using is by far the best thing and everything else is of secondary importance. That’s their opinion. That may not be the best suitable technique for you, your style and indeed your patience for any given day.

What about all these new shiny techniques, Jon? What about all these things you see advertised on Facebook and Instagram and promising you the Earth and only costing you $1,000 for the seminar? What do you think about these?

Jon: Well, I’ve run into those a lot in my sixteen years of practice and obviously, my years of schooling before that and I think it’s a slippery slope. I think it’s hard to vet those out to know exactly what’s there to stay. As you said, what shiny and repackaged, nicely marketed and meant to hurt you with some of your hard-earned money. Another one of our goals in this soft tissue interventions approach is to give you some of our favourites, some that we’ve learned that are tried and tested and true on the battlefield. Like you said, on the sideline, on the pitch and maybe help you wade through these new shiny techniques.

Now, don’t get me wrong. Sometimes, the new technique may have the best new research and maybe the best approach and that may be worth paying for. Again, one of our goals is to help you with that, but buyer beware as well, I’d say, Mika. How about you?

Mika: I agree. Sometimes, I tell patients or athletes when I’m treating them. When there’s a particular situation, you just stick an elbow into a trigger point, which is that sometimes, an old trick is better than a bag full of new ones. Sometimes, the simple approach is the best, and these things have to happen around for thousands of years. They’re definitely worth it. Like you said, sometimes, the new techniques that come about, yeah, they have the latest research behind them and the latest understanding maybe. Maybe it’s just shedding new light on the old theme, but at the same time, it’s whatever makes the most sense in your own head and how they’re able to communicate that to you. That’s the most important thing.

Jon: Yes. Let’s look at a little bit of the history of soft tissue therapies. There’s nothing new from the biblical records of laying on of hands to the father of modern medicine in the 5th Century, combining prone traction with manipulation and on and on from Arabian medicine to medicine from around the world whether it be Eastern or Western approach. There have been combinations of joint manipulation with soft tissue treatments for centuries. Now, the research behind those, the application of those and the sharing of that knowledge, I think, has spread just like technology has spread and through the use of technology has spread, wouldn’t you say, Mika?

Mika: Looking at the European shamanic traditions and things, I suppose that would be also Northern American traditions, the adjustments and those kinds of things, they’ve been around for thousands and thousands of years. Equally in China, equally in Egypt, all these things were taking place, and these were the modalities before the new shiny, shiny surgeries and those kinds of things. Yeah, they’ve always been around. The human body hasn’t really changed in the last 30,000 years. I can only see that this is going to stick around for another few thousand years, I would say.

Jon: I think you’re right. Nothing new under the sun. I put this slide together just to show you what I talked about already is there’s a world of soft tissue techniques out there. Now, this could be ten slides, but each of these is a unique approach, a unique body of knowledge and of background and of application. You see things like an active release, which may be a lot of us are familiar with at least in the United States. That’s quite a pop, a common one. Rolfing, you may hear of a lot and then others, NMT and fascial unwinding that maybe aren’t so widespread but if found their way into the literature and into good hands of good practitioners. Really, I put this just to show you you could dedicate your whole life to even one of these methods and maybe not even master it.

Mika: That’s right. There’s such width and depth in these things that you can argue whether positional release or active release or fascial unwinding is significant and different from one another, is one better than another? In a way, you’re missing the point by that argument when you say.

Jon: I would say so. I would say, instead of trying to pit one against another, be curious. Be curious about why a practitioner would choose that, why it might help that type of patient and why you should consider it for your patients. While you’re in that learning process, which we always are but especially when you’re a student getting into sports chiropractic and you’re probably listening to this lecture, look around as much as you can and when you find one that resonates with you, grab onto it and then utilize that. I would say, exclusively for the first number of months. If not, the first year to gain good clinical acumen with it. That’s the approach I took, personally. Mika, did you take a different approach in your background?

Mika: Well, my background was a little bit different. First, when I qualified in 2007, back in a dark old day, I came out of college, and I was relatively burnt out. I was quite tired and didn’t really have too much money burning a hole in my pocket, so I decided that I would just try and learn to be a good chiropractor before taking too many seminars. I just focused on the basic techniques I had from school and used those. I didn’t want to know too many techniques right away. I just wanted to learn the basics well and teach myself the touch and get my hand sensitive and so that I can actually feel what I’m supposed to feel. Only after that, I felt ready to take on more techniques, more seminars and started attending those then. To begin with, I just wanted to focus on the basics and be a good safe, competent practitioner.

Jon: Fantastic. I think that’s brilliant, Mika. When I train the new doctors that come into my clinics here in Montana in the United States, I always tell them, “Be a chiropractor first. If it’s a pyramid, that’s your base.” Then once you have that solid base, and part of being a good chiropractor, of course, is being able to diagnose. Of course, having that palpatory skill, having that communication skill, developing where you can move your patients from where they are to where they need to be and communicate plans of care, approach, and safety of your treatment. Then start building the blocks. One of the second tier blocks I always say is a good soft-tissue technique. I believe a good taping technique and a good rehabilitative approach make up that second line.

Mika: I completely agree. Oftentimes, when students are getting near to qualifying or just having qualified, there’s almost that fear of missing out, wouldn’t you say, when it comes to all the differences. Everybody’s comparing notes and having a chat about, “Oh, I have attended all these different seminars,” and it’s easy to feel left out and it’s easy to feel almost deficient that you haven’t. I have confidence and have that peace of mind that you’re doing what is right for you. If somebody can handle all that information straight away, that’s great, but personally, I never could. What was your experience with that, Jon?

Jon: Yeah, the exact same thing. I think that last year in University and chiropractic education is so important and I felt that same deficiency, that same motivation maybe to learn everything all at once. Really, what you do is you just barely skim and that results in… What I find, especially in my new docs, I like to call analysis paralysis. They overanalyse everything. They have thirteen techniques they sort of touched on, instead of two that they really learned well. They’re looking at this Achilles tendinosis or this rotator cuff tear or the cervical strain saying, “Oh my goodness, I did this for 1 visit and it didn’t work and I switched and I did this for 2 visits and it didn’t work. Now, what should I do?”

When really, if they stuck with instrument-assisted soft tissue mobilization for 6 treatments, that would have resolved instead of bouncing around and around. I think we’re saying the same thing and that’s, look around at first but then don’t be afraid to find something and stick with it that resonates with you. Here’s what’s resonated with us. We’re going to take you through 6 of our favourite techniques. Those are therapeutic dry needling, PNF/PIR, fascial manipulation, cupping therapy, instrument assisted and trigger point work as well as a global analysis approach that I think that Mika is going to touch on.

Mika: I think first off the blocks is that dry needling, and that’s more your bag, Jon. I don’t use needles myself in clinic purely because I suppose I’m just not that happy with needles.

Jon: Fair enough.

Mika: You’re happy to needle people, so you crack on and tell us about dry needling.

Jon: Well, I’m happy to do that. I’ve been dry needling for the better part of a decade, done several certification courses and utilized dry needling every day in my practice. Not with 100% of my patients because I don’t think any one particular modality is a magic bullet. Therapeutic dry needling is certainly not that, but it’s one that I find very good success with. What is dry needling? Well, it is a manual soft tissue therapy in which fine needles, we call them acupuncture needles because the acupuncturists invented them first, are inserted into muscles, tendons, teno-periosteal junctions or other areas of the body to stimulate a healing response, particularly with neuromusculoskeletal conditions.

Now, don’t be confused. Dry needling is not Eastern acupuncture. It doesn’t have the purpose of trying to change the meridian in the treatment of multiple disease processes. It’s really the Western medicine equivalent to that. What it is it’s a science-based, evidence-informed soft tissue treatment for pain and dysfunction in musculoskeletal conditions. Yeah, let’s interpret that to the real world. Why do I use a needle? Well, if there’s a tissue that’s affected. I always call it an affected tissue. It’s painful. It’s restricted. It’s damaged. It’s inflamed.

The body is not doing a good job handling what’s happening there. Maybe it’s an acute injury. Maybe it’s a chronic injury. Maybe it’s subacute. It matters not. The body’s having a hard time in that area. The needle is a hygienic instrument that we use to put right into that affected, tissue to stimulate the body’s healing response. I often explain it to my patients like this. If you get a sliver in your finger, a wood sliver or maybe a bee sting, your body knows exactly what to do to that poking intervention. It knows to bring blood flow to the area, to clot that up, to bring white blood cells, to stimulate this inflammatory cascade of healing. Dry needling does that with a hygienic instrument. It goes to the affected tissue and really stimulates, sometimes, I say, tricks your body into bringing healing to that area.

Now, there’s a lot of ideas of why this makes a difference. Is it a sympathetic response? Is it a nervous system based? Is it purely chemical? Is there an electrical component? Actually, we’re finding out that if you look on the slide, on the right-hand side, there’s a number of effects that are being well researched in therapeutic dry needling. It has just gained and gained in evidence basis, in evidence information. Let’s look at the video.

Okay, I’m going to quickly demonstrate some dry needling. There’s tons of different approaches to dry needling. We’re just going to show intermuscular dry needling for her cuff. Of course, we always practice clean techniques, so alcohol wipe before we insert the real key like any good soft tissue technique is palpation that we’re going to find a good spot. Over here, you can see that there’s different sizes of needles. Of course, we’re not going to use the hundred for this, but there’s also different gauges, so different diameters and different links that we’re going to use for her. We would use this, which is a 25×40.

You’ll see that the needle is stored hygienically, go back, palpate the trigger point. Okay. We’re contacting little poke, and the needle’s already in the skin. Then we are in. Now that the needle is in, there’s a few things that we can do. We can twist the needle. We can piss[?] in or pulse the needle. We can also put electric stimulation through a pointer or through clips and a different type of machine depending on the need of the patient, the type of tissue that’s injured, the chronicity or acuteness of the injury. There’s a lot of factors that go into that, but this is a simple demonstration of insertion of therapeutic dry needling.

That’s intramuscular dry needling. I found through my experience, you can find someone that’s new at dry needling. Usually, the first approach you learn is in the extremities intramuscular. In the biceps, in the gas tracts, in the very safe areas away from vessels, away from lung fields. Then as you gain experience and go through advanced training, you learn to needle safely into tendons, into teno-periosteal junctions and of course, over and around the more important vessels and the lung field. There is some training that goes with it. Of course, you should not just grab needles and start poking them into yourself or something else without appropriate training.

There are some soft tissue modalities where you can do this. For instance, cupping therapy is quite safe, and you could grab a cupping set and really start cupping yourself or someone else quite safely. Do not do that with dry needling. What are we green light on dry needling? Well, pain and dysfunction of various origins. Myofascial trigger points, centers of coordination, anything that’s restricting range of motion causing multi-layer adhesions or limitations. In my experience, really, Mika, almost all musculoskeletal conditions can benefit from properly and safely applied dry needling.

Mika: I agree with you, Jon. I’ve had dry needling done on me a number of times and I have to say that the results have been near on miraculous. I completely understand the application. Personally, I don’t use it, but my associates use dry needling. If a patient of mine need’s needles, then I’ll send them down their way and they will get their needles done.

Jon: Let’s talk red flags on this. Obviously, we’re not going to needle a pregnant female. We’re going to stay away from systemic infection, uncontrolled hypertension, any peripheral neuropathy. Of course, if they can’t feel what you’re doing, you don’t want to be putting needles in. If they have a hard time controlling bleeding, if they have anti-coagulant dysfunction, you don’t want to be poking into capillaries. By the way, because it’s not uncommon, we don’t have X-ray vision to see all capillaries. We’re educated where the big vessels are. You’re not going to needle the femoral artery or over the carotid or jugular. There are capillaries all through.

I would say, when I needle, there is a very pinpoint or what we call a pinprick of blood. You have to have proper boundary training and proper body substance isolation and to understand how to control a very small amount of bleeding. We’re not going to dry needle over someone that has trouble controlling their bleeding. Of course, acute skin infections, we don’t want to spread that around. What are some of our cautions? These are yellow flags. You can needle somebody with cancer. You just have to be aware of what your needling, what type of cancer they have and coordinate with their oncologist or their primary.

Generalized infection viruses, I needle patients all through the COVID pandemic, but of course, precautions were made and we’re using the clean needle technique. You can see some other yellow flags listed there. I don’t have to read all of them. I needle around post-surgical scars all the time. I don’t like to needle around burns myself. There are times I’ll needle around a hematoma. That’s fresh, but I think there are better techniques for that. For instance, some taping techniques or some cupping techniques can help to decompress that a little bit better.

Why use needles in your treatment? Why do I use them? Well, they preserve my hands. A lot of times, I’d be using a more aggressive manual therapy, soft tissue technique and active myofascial release approach or fascial manipulation approach that are much tougher on me. I find it offers you a very ultra-focused therapy that gets right down to the effect of tissue. It’s a light force alternative approach to some of these more aggressive, soft tissue techniques, and I really like that I can treat multiple areas on a patient and multiple patients at the same time. I go into a room, do an adjustment, put needles in, depart the room while the needles set. I’m in another room with another patient. Go back in, check on them, maybe piss and remove the needles, maybe apply some stem and so I can get a lot of treatment simultaneous. That’s one of the reasons, Mika, that I like it.

Mika: Yeah, I really like your point there about preserving your hands. That’s one of those things that we can’t. We can’t reverse the damage when the damage is done on us or it will be very difficult anyway, so it’s a great idea to get into good habits early on for all the students watching and listening here. These things here, you’re stuck with them for the rest of your career. I always take as much care as I can and try and spread the load as they say. That’s why earlier, I said you stick an elbow into a trigger point rather than trying to thumb it or using, of course, all these different modalities we have available that are less intensive on your fingers and your hands. That is just very, very important to remember.

Jon:  Now, we’re moving on to instrument-assisted.

Mika: Here we have, again, a big broad topic and is something that there’s a lot of contention perhaps in the ranks. What is the best way or what is the best particular brand of technique or whatever you want to call it? I know most of you have heard of Graston and their range of instruments and those kinds of things. Here, you can see a picture. This is my favourite, favourite tool in the clinic. I carry this little thing with me everywhere. It’s a fascial edge tool. I just love it because it does pretty much everything I wanted to do. It has a bit of a point at the end. It’s got a big broad service at the other end. I call it my big spoon just because it looks like a weird spoon. It has a little depression there on one end as well, so it would potentially even work as a spoon.

Of course, you got a nice big edge on the side there that you can utilize again in a number of different ways. When we’re talking about instrument-assisted soft tissue mobilization, you can use whatever instrument you have handy and you could use a specialist tool, you can use a golf ball, you can use a tennis ball if you got one of those handy if you need that extra little bit of help. If you happen to be at the beach, you can use a pebble. I mean, it’s not something that is limited really to specific manufacturers or specific instruments, but you can use your imagination to a massive degree.

Jon: Isn’t some of the backgrounds in Graston, I see you have Gua Sha listed there, in stone or bone or even animal horn.

Mika: Various different materials for these instruments is used across the board. This particular tool that I like, the fascial edge one, that’s a sort of special alloy that is slightly different from stainless steel. It’s meant to give the best vibrational frequency when it comes to the human connective tissue and imparting an effect on that. I’d already know about that, but to me, it gives great results. Hence, I like using it. Some of them, of course, make huge promises about their specific quality of the metal alloy. I really couldn’t say which one is the best.

In the Gua Sha realm, which is more the Chinese techniques, they use the animal horn, shells and those kind of things for the scraping and what else you have there. Mainly, to me, it comes across like the natural substances work the best. Generally, they don’t really use the plastic stuff, potentially, for a reason. Also, I found that wooden instruments don’t work that well as these kinds of instruments. I mean, I like using a rolling pin on myself when I’m doing fascial release and stuff like that after running. I love rolling pinning my calves, quads and hamstrings and things like that rather than using a foam roller myself, but that, again, is just personal preference.

Why would you use instrument assisted is basically when there is a pain when there is tension and tightness, restricted range of motion when the tissue starts getting a bit clumpy, twisty and tight so that you may have that typical feeling of rubber bands in muscles, where the muscle fibres are slightly starting to get twisted around each other. That’s when something like instrument-assisted can be really, really helpful because of course, you understand the flow of the fascia, you understand the flow of the muscles. When you start instrument-assisted releasing, it can help that tissue recoil so much quicker. No, not recoil. I meant to release, of course.

Mika: That recoil is something different. That will also help with the recovery rates. Hence, even post-competition, you can use something like instrument-assisted straight after competition or training. You don’t have to really sit there and wait for too long before you can get stuck in. Why does it actually help? Well, it says here, the 3 things at the bottom, about the increased circular exchange, increased vascular response and breakdown or realignment of collagen fibres. What does that actually mean? Do you know what that means, Jon?

Jon: Well, yeah, I certainly do.

Mika: For those people who may be new to this, it really just means that we give those tissues a good old shake and a shiver and let them get on with it. I like what you said earlier about the needling, how you trick in the system, you’re giving them a stimulus, you poke them with a stick and something happens. It’s kind of the same thing with this. You can study it scientifically until the cows come home, but really, you’re giving it a stimulus, you’re producing a response from the human body. That, of course, is a very important thing. Rest of it, it gets down to the nitty-gritty and it gets down to the real fine detail when you want to study that deeply. These 3 things at the bottom here, which seem to be, what really happens. That, in my opinion, can only be a good thing.

Jon: A hundred percent. One of the things, Mika, that I like best about using an instrument and I’ll echo what you say, I prefer a metal tool over a plastic tool or over a stone piece of jade maybe for Gua Sha. What I like about any instrument is that it’s both diagnostic and therapeutic very quickly and broadly over a trapezius, find the adhesion, find the limitation of motion and then it resonates especially through a metal instrument and then you can go to work, breaking it down, go back to scanning and multiple plains very efficiently, very quickly and then go back and break it down. Then you can add motion to the patient. You can add isometric resistance. You can do all sorts of different things, and there’s some advanced approaches in it. I love that it’s both diagnostic and therapeutic and very efficient and quick.

Mika: Like you said earlier, you can study this one modality your whole life and become a seeming expert in it. I suppose this is another one of those where you can spend your whole life just doing soft tissue releases using instruments. On first glance, you think, “Well, what’s so special?” Like you said, when you start looking into the adding movement, passive-active movement, when you’re looking at potentially combining it with a bit of taping modality, you can really entertain yourself for years and years with this kind of approach. That really comes down to imagination and how far you want to take it.

Jon: The first one I ever learned postgraduate was the Graston technique, just had touched on it in university. I want to go out and certify in it, and they were just starting to learn. This is in 2005. They were just starting to put together what now is FAKTR. FAKTR is applying functional movement and rehabilitation to instrument-assisted mobilization and of rehabilitative approach. Shout out to our friends at FAKTR even though Mika and I are not sponsored by them. I’m a fan, personally. Putting it all together. If you want to start, there’s a lot of different instrument-assisted camps and tools and approaches. Then the next level would be applying a FAKTR with it. That applies to all the wonderful movements. I’ll happily give a shout out to them. They’re doing great work.

Mika There’s a whole bunch of things that you can, of course, use instrument assisted for. This list is pretty straightforward, pretty self-explanatory in that sense. When you have muscles that are in trouble when, you have tendons that are in trouble, when you have a potentially bit of compression or restriction across compartments, you can use it and that’s really it. When you look at the specific like rotator cuff tendinosis or plantar fasciitis, it’s just an application of the same theme. Equally, we could replace those words with any other muscle or any other tendon. That’s where the instrument-assisted really comes to its own, I would say.

Jon: Do you have a condition or top 2 or 3 conditions that you find to respond the best?

Mika: Well, I find the very stubborn stuff that is oftentimes difficult to shift and can be quite irritating and even debilitating for our patient, something like plantar fasciitis or Achilles’ tendonitis, even golfer’s, tennis elbow. They really respond well to instrument-assisted.

Jon: I think you’ve listed my top 3. Plantar fasciitis, certainly a lateral or medial epicondylitis, and I’ve had really, really good results. It’s interesting, we run into the same things across the same things.

Mika: Oftentimes, these are the ones that you can’t really release them just by working on the muscles distally from the side like for your Achilles, you would be releasing the gastroc and soleus. Just by releasing those muscles, you can’t really get that full effect, but getting onto those tendons directly. You can really start poking a hornet’s nest with a stick like we said earlier so you can start getting the body producing a response. Usually, it turns out for the best hands, you get a healing response coming out of this poking of the hornet’s nest with a stick.

That is a good way of doing it. Of course, there are other ways. I’ve heard about… Hold on. I was just going to use an example of a technique that is very specific. I’m drawing a blank here now. What is it called?

Never mind. Shockwave. Oftentimes, you have people start using shockwaves for these kinds of things, but I’ve never actually learned shockwave. I can’t really comment too much about that. Have you got experience of shockwave yourself, Jon?

Jon: I do. I have the storage units in my clinics, and it’s a really solid soft tissue modality. I’ll use it after I’ve tried a few others where maybe we haven’t had the results that we want. Then I’ll plug that in. I don’t specifically address that in this lecture, but it’s worth looking into for sure. Now, there are some things to stay away from with instrument-assisted too, yeah?

Mika: That’s absolutely right. These again are very common-sense. If you have a patient who has an open wound or an unhealed fracture, something, if you have a bone sticking through the skin, you don’t want to be using instrument-assisted on those. Same again with the cancers and high blood pressure, pregnancy and anticoagulant therapy, and blood clotting disorders, you want to be careful in regard to the bruising and those kinds of things. It’s very, very common sense, really.

Here are a few different instruments courtesy by Dr. Christine Foss. I stole this picture from her. There are a few different instruments there, and they can all be very, very useful. For your pleasure, later on, all the students, have a look at some of these papers. They give a bit of evidence to support instrument-assisted interventions.

Jon: Yeah. This is a great picture. Just shows the variety of treatment edges and tools. One of these instruments, I gave to Christine Foss as a present. I won’t tell you which one. All right, let’s move on. Now, we’re going to talk about PNF/PIR. Some more acronyms. PNF stands for Proprioceptive Neuromuscular Facilitation and PIR stands for Post Isometric Relaxation. This is a type of assisted stretching developed to treat some really tough conditions, polio and MS.

There’s a number of different approaches that you can take with PNF and PIR stretching, but what you’re really trying to do at a very basic level is to stimulate a stretch reflex in that to inhibit something else, though when you stretch one area, something else turns off. For instance, when we flex our biceps, our triceps need to turn off and lengthen. When you go the other way with the triceps, the biceps need to lengthen. Our brain is constantly working to let something go at the same time we’re telling something else to contract. This approach harnesses that.

PNF really relies on reflexes to induce a deeper stretch. Really what it does is it tells the brain, “Hey, something’s going to happen here and maybe something’s going to tear, so you got to let it go a little bit for it to move more normally.” I’ve got a video of this as well. Nice way to demonstrate.

Okay, we’re going to demo PNF stretching Proprioceptive Neuromuscular Facilitation or PIR which is Post Isometric Relaxation. Corina’s is here to help us out. If we were doing it for her hamstring, we’d go up until we feel a point of tension. I actually let off of that a bit and pushed it into me about half your strength. You hold that. She’s contracting right now through the glute, through the hamstring and relax. You’ll see now that the point of tension’s changed.

We can go a little further, push against me again, pull. Three, two, one, relax. In each time, we gain a little. Another way that we can do it is we’ll have you contract against me again and hold. When I count down, afterwards, I want you to bring your leg up with me, okay? Three, two, one, relax. Then bring your leg up with and we can run through several of these. Really great for gaining a quick range of motion. We’ll talk about the indications and contraindications in the lecture.

What are those indications? Well, if we want to induce or increase flexibility, I would say rapidly, we want to improve the range of motion. It has been shown to increase strength in the published literature and to help with neuromuscular control. There is some research that it improves running mechanics as well because it does change range of motion so quickly. What’s nice about it is you don’t significantly increase heart rate while you’re doing this, but you can get quite a good stretch. For instance, similar to an active warm-up, but there is some research that shows that it decreases immediate athletic output.

For instance, one study showed that vertical jump actually decreases after PNF/PIR stretching. We have an understanding of when to utilize this type of modality. Personally, I’ll use it as part of a post-treatment cool down or maybe an evening treatment, if I’m travelling with athletes where they’re not competing right away. Maybe it’s right before bed or something like that. There have been a few cases where something and it’s just splinting and spasm. You need the range of motion. You need them to be able to just perform and you’re willing to sacrifice 10% or 20% of their speed or their explosiveness so they can just perform. In that case, PNF is something that I would certainly use.

When do you not want to use this? Well, if you feel a bony block on the end of the range of motion, don’t use this. You should feel a soft tissue block and you should be able to gain as you saw in the video. Of course, if there’s a recent or unstable fracture, you’re putting a lot of range of motion into an area. If there’s a brand new acute soft tissue injury, please, don’t be putting so much motion into that. If there’s an active infection or a lot of bruising. Obviously, if there’s a post-surgical repair, we don’t want to pop any skin grafts or repairs or sutures. If the patient’s hypermobile, you’re probably not really going to be able to find a barrier of range of motion on this.

Some clients or patients don’t like it. They just refuse the approach. I haven’t found that a lot, but I guess that’d be a contraindication to any treatment feedback.

Mika: I was going to ask you actually, in terms of the post-surgical repairs and those kinds of things, how soon after surgery would you be able to use this? Are we looking at a couple of months or are we looking at 6 months? What’s your take on that?

Jon: My personal experience is about 8 weeks post, you’re probably safe. You’re really good if you wait until that 12-week window. A good rule of thumb is when their treating surgeon clears them, then you’re always golden… Having good communication with their physio if you’re managing the rehab with the surgeon themselves, but I’d say, between the 8 and 12-week mark, you’re probably safe to apply this. Anything past 12 weeks, in my experience, you’re not going to tear anything loose. Again, that’s a general broad answer. Each specific surgical procedure is different and so you have to have an awareness of what you’re dealing with. Really, really great question.

Mika: Here are some things about cupping. Now, cupping is actually quite a unique modality in its own right because it doesn’t aim at squashing things or pulling things so much but it’s actually decompressing. There are not that many ways how you can directly decompress tissues. Obviously, you can see my favourite cups there in the pictures. Little silicone cups, very easy to use, very easy to get acquainted with. Like Jon said earlier, you can really just purchase yourself a set of cups and go nuts with them because with these kinds of cups, there’s very little you can do wrong. You’re pretty good to go.

Obviously, there are different types. You have the old-fashioned wet cupping, which would be almost like a bloodletting cupping, which I definitely would never use. You can utilize sliding cupping which actually is very, very helpful. You would have to have a bit of cream on the skin or a bit of oil, you get the cups on and you can utilize that to lift the tissue across a broad area. If you have, say, a big muscle like a quadriceps muscle that is tight and tense and holding on to that tension without being able to release, something like sliding cupping can really lift those tissues and lift that fascia, allow that drainage to happen and also then let that muscle again to release and relax.

Jon: Is there a progression that you take, Mika? You said you can leave them on the skin and you can also slide them. Do you start with one? Is it condition-specific? Is it practitioner dependent? What’s your take on that?

Mika: There’s a lot of intuition in this one. What feels like the right thing to do with a given patient? With the sliding, it can feel a bit more uncomfortable, bit more painful for the patient. Some patients may not be very happy for you to use it. Some people are absolutely fine with it. There is that element of what patients can tolerate also. Now, the easiest application, of course, is to just apply the cup, leave it on a particular spot in the tissue and you can then do stuff around it with your fingers or instrument-assisted or whatever else you choose or even treat a different body part while this cup is taking effect.

With the sliding cup, that’s a bit more of a direct approach where you are really homing in on this issue and you’re focusing a lot of effort into it. I was thinking about it earlier. What is a good way of introducing a similar decompressing effect without using cups? The only thing I could come up with is a very ancient technique that we learnt in uni. I remember our teacher said that this is the only way you can decompress a tissue. It was basically where you grab bits of skin with your fingers, and you just roll your fingers along. Very effective. That’s the only thing I could think of that is somewhat similar. Everything else is more compressing than decompressing. That was a very cool thing.

Jon: I was at a seminar once, Mika, and a massage therapist brought a toilet plunger, fortunately, a brand new one and hadn’t been used for but really just a large decompressive cup and she was showing us how she used it over the lumbosacral region. She said with great effectiveness for relieving pain and mobilizing, but you’re right, there are limits to the modalities that decompress and that’s one of the things I love about cupping. Quite an old technique, yes.

Mika: Again, we go back thousands of years to the bloodletting cupping and using animal horns and those kinds of things. You can probably see it happening now often. You can use the silicone cups or you can use the actual- They use glass cups with a certain pump to produce the degree of decompression and suction in the cup so that you can be very, very specific with those kinds of things as well. That is a bit beyond my scope, using the suction pumps and things like that. I just like this very basic approach myself.

Cupping, why would you use it? Well, there’s a number of reasons. Yeah, thank you, Jon. Like we said before, it helps to reduce painful inflammation, improves blood flow and can be rejuvenating for the body organs, and that’s very good indeed. Hence, we get that deep tissue effect very easily with cupping.

Jon: Really great modalities. Probably my wife’s favourite soft tissue modality to receive. He’s a big fan of cupping.

Mika: Now, talking about those toilet plungers, would that be more instrument-assisted or cupping? I don’t know which one that would qualify as.

Jon: Combo technique, Mika.

Mika: When should you not use cupping? Of course, again, we have a very similar list here of open wounds and ulcers and broken bones and fractures and dislocated joints. It’s very straightforward. We generally don’t recommend cupping in young children and when there is excessive swelling because that can be, of course, meaning something very different. So, you got to exercise a little bit of caution and always, always play it safe.

Now, there is a couple of pictures here of different kinds of cups. In the top picture, you can see one that has a bit of a rubber squeezy thing at the top so you can help use that to produce the suction. At the bottom, there’s the very fancy looking equipment with glass cups and a suction pump. That again is another way of producing the effect. Now, one thing we have to mention is that some patients don’t like the bruising.

Sometimes, using cups can produce discolouration of the skin. Of course, when you’re utilizing these pumps there is a lot stronger effect, a lot stronger suction in the cup, which can then lead to bruising coming out later on. I found that when I’m using little silicone cups, even if I’m being quite vigorous with it, I don’t really tend to bruise patients, which is actually quite nice and they seem to appreciate that as well.

Jon: I’ve only recently started using the silicone cups only because they’re easier to travel with when I’m attending to athletes. In my clinics, I have a set very similar to what you’ll see in the bottom picture. I think you’re right. I never thought of that before me, but the bruising is quite a bit different with those. Yeah, I’m curious as to why, but maybe somebody will research that down the road. If there’s a really smart student sitting around, there’s your project, right?

Mika: That is a great project. Absolutely. I know that sometimes when you put cups on a patient, you can see almost a different colour of the skin as it comes up under the cup. Sometimes, you see this almost like a pinkish colour. Sometimes, it comes across as more purple. A discolouration can change as you leave the cops on. Oftentimes, I find when the colour comes more purple first, it seems to be more acute. Then gradually, oftentimes, it changes to more towards a healthier pink, which to me is a signal that, right, that cup has more or less done its thing so it’s time to remove that and move on. Would you find that, Jon, yourself?

Jon: I’ll usually give feedback to patients that, If there’s darker discolouration, it tells me that there’s more work to do there. That’s my simple explanation to them. Yeah, I like sliding the cups. That’s one of my favourite approaches. I like having the patient move through what they feel is a functional range of motion whether that’s an athletic motion, whether it’s throwing a ball or twisting with their hockey stick or something like this with the cups on. Sometimes, I’ll combine those where I’ll move with them in the range of motion, gliding the cup while they’re moving. Sometimes, I’ll move against their range of motion while they’re moving.

I like to progress, usually starting static than sliding on a passive patient and then to a patient moving and then to sliding on a moving patient. That’s the approach that I’ll take and then it’s also easier to educate them as to why it may take 6 visits for us to get the ultimate effect. We’re doing 4 different approaches and progressing through those as quickly as we see change. That’s the approach I like to take.

Mika: That’s right. As we said before, you can have so much fun with this and learning the specifics of a given athlete and even the specifics of different sports because of course, the demands from ice hockey to soccer or football or volleyball or sprinting, running, swimming. The movements and the biomechanics employed by these athletes are very different. Hence, I don’t know about you, but for me, it’s that immersing myself in the world of this athlete and in their movement. I find that very, very gratifying where you can really picture, what is it doing? How are they producing this movement?

Therefore, it usually makes perfect sense at that point why they’re exhibiting this particular problem or restriction or tension in their system. It’s almost too simple at that point. When you put yourself into their shoes.

Jon: It’s fun. That’s the fun part of it. It’s not a dead modality at that point. It’s not something that’s just you’re blindly putting cups on somebody. You’re applying your knowledge of the human body and biomechanics and then specifics of their sport. That’s when this becomes fun. When it’s not just cupping, but it’s cupping for that athlete for their moment.

Mika: There are some more evidence food[?] research papers, again, support evidence for cupping, but I think that’s enough about cups for now. Let’s move on.

Jon: Fascial manipulation. One of my favourites. This came to the United States about a decade ago, but it has its roots in Italy for the Stecco family. If you’ve been around fascia or studied or read any research or been to any symposiums, you probably heard the name Stecco. If you haven’t, you may want to look it up. They’re really pioneers in fascia and understanding the inter-workings of fascia from the histological perspective all the way to the functional perspective.

The fascial manipulation approach is both an analysis and treatment. In the analysis part, you can see they’ve mapped the fascial lines, the fascial planes and really what they call a centre of coordination. That’s the dots or the triangles you’ll see. You’ll see the arm lines and the deep centre line and the superficial leg line and a number of these different lines. It brings up memories of Tom Myers and myofascial meridians. Fascial manipulation is quite similar to that.

Looks like me because reaching for his texts as it is right there. Absolutely. Yeah, anatomy trains a great and would highly recommend that. If you want to even go to what I would call the Master’s Degree level that fascial manipulation is what I found in that book. How does it work? Well, you find these limitations in the fascia, and the real key is not just in localizing them but in finding a way to unwind them.

They talked about creating manual friction over the specific points, creating 80% of your pressure down into that point and 20% staying on that specific point until you create a thixotropic effect, which is a fancy doctor word for enough heat and pressure to feel and unwinding. If you apply fascial manipulation correctly on the correct facial centres, you can feel these tissues unwind and what’s really neat because you can chat with your patient while you’re doing this. Although sometimes, that treatment is quite intense, they’ll tell you they feel it unwinding. Right before you say anything, I’ll do this all the time with patients, I’ll say, “You feel that unwinding? The intensity got a little less, didn’t it?” They’ll say, “Yeah, I felt that.”

Sometimes, they feel referral from these fascial centres that change, but basically, you’re trying to modify that extracellular matrix. This affected tissue that’s not gliding well that balled up, you’re trying to create enough heat and pressure, unwind that and restore gliding. Really, what we’re trying to do with Graston technique and active release and pin and stretch and a lot of these approaches. I’ve just found fascial manipulation to be deeper, more focused. Honestly, the treatment applied for longer at a specific point to create a more permanent change in unwinding. That’s what I love about fascial manipulation. I put some links on there so you can go back and read more about it. Let’s look at a little demonstration of it.

Now, we’re going to talk about fascial manipulation. This is Stecco’s theory. What we do is we find the area or centre of coordination and we’re going to put pressure into that area until we get a thixotropic effect, which is a loosening of the tissue, glide and slide. The 3 contacts we use are elbow. Fascial manipulation looks like this. We’re going to give you a good ergonomic position right on a good spot with all the retro help we’ve got. Eighty percent of your pressure is down, 20% back and forth. You’re going to maintain this very focused contact on this point of densified tissue for 1 to 3 minutes.

If we were doing it in a more focused spot, I would use a reinforced knuckle, for instance, at her QL. We call this the retro lumpy point, and I’m going to put that pressure in again, the same thing, to get enough heat and pressure for it to unwind. What you’ll feel is the tissue unwind. It’ll actually feel like that very dense specific point kind of let’s go. The third contact or even a more specific point is a reinforced fingertip. We might use this on a hand or on a foot. Reinforced fingertip. The key to this is your palpatory skills, okay? Maintaining that contact, enough heat, enough pressure to unwind the tissue. That’s fascial manipulation.

Now, I’ll tell you right now, disclaimer, Mika. Fascial manipulation can be quite intense for a patient. I’ll use it on complicated cases that are maybe unresponsive if I have a patient that presents. You’ll see these in the clinic. I’m sure, Mika, back home that they say, “I’ve been to 3 other chiropractors. I’ve been to 4 physios. I’ve had a bunch of different soft tissue approaches, and nothing’s worked.” My mind immediately goes to fascial manipulation.

Really, any myofascial pain syndrome, repetitive strain or repetitive stress movement imbalances where you can really see it on their gate or their movement pattern. Maybe you take them through a selective functional movement assessment and see a real limitation or something they’ve compensated for. Maybe they’re post-surgical in an ankle and they’re moving the QL and the hip strange. I’ll really like to get around that with facial manipulation.

It seems to work really good in some cases of visceral dysfunction. There’s a whole approach to visceral fascial manipulation. I’ve had some good success with some organ issues, working on the viscera and the fascia that surrounds them.

Mika: I think there’s a little point to be made here. It’s doesn’t only apply to athletes, this kind of stuff, because when you have people who do the same thing over and over again, so you have your taxi drivers or your lorry drivers or accountants who always are in the same position. They’re using a very small range of muscular activity, even if they’re not very active. They will produce really nasty fascial tightness and things. Therefore, using this kind of approach can be so helpful.

Jon: You’re absolutely right, Mika. How do I want to say it? There’s working on a Ferrari and there’s working on a Chevy Cavalier in the United States. There’s plenty of working persons in multiple fields of work that need this exact thing whether they’re digging ditches or shooting baskets. This is a technique that can work really, really well. That’s very perceptive. When do we want to stay away? Well, we don’t want to be digging deep and creating heat and pressure around a malignancy or an aneurysm.

Some of these common-sense contraindications. If they have advanced diabetes and can’t feel or they have a breakdown in the tissues from a neuropathy, if they have severe osteoporosis, you have to be careful. If you have a seventy-five-year-old female with osteopenia and you’re digging an elbow deep into that hip or over the ribs, of course, common sense contraindications just to stay away from treatment.

Like I mentioned earlier, it may feel intense to the patient. My vast experience with this technique has shown me over and over again that though they may cry and howl a bit during the treatment, they get up and say, “Oh my gosh, I haven’t felt so free in a while.” The usual post-treatment explanation to the patient is, “You’re going to feel lighter and looser. If you press into the area I just worked on, that’s going to feel a little bruised and tender for twenty-four to forty-eight hours. We need to follow up within 3 days to build on our progress.” That’s the take-home message.

Jon: Now, we’re going to move on to trigger points.

Mika: Well, trigger points are something that everybody has heard of. Everybody kind of knows what they are. Here’s a definition for you. It is a hyperirritable spot in a skeletal muscle, painful and causes referred pain or even autonomic phenomena. Now, is it an important definition in the sense of, if you find a tender spot, just poke it or do you have to be very, very fancy about it? I think you don’t need to be that fancy about it. Is there a difference between a trigger point on a myofascial or a facial tender spot? Again, does that even necessarily matter? Not really.

Jon: Depends on who you ask?

Mika: Well, quite. If you want to be a real purist, then I suppose it does matter. For us who are firmly working in the trenches, it doesn’t really make a difference. Trigger points can be quite unpleasant, quite nasty. They can happen across the whole band, so they can be in muscles, fascia, tendons, ligaments and even periosteal trigger points. You have experience with those as well, Jon. Periosteal trigger points can be, well, very, very unpleasant for the patient as well as the practitioner because you have to be extremely pinpoint accurate with your contacts.

I suppose that’s where you come down to using acupuncture needles or dry needling and those kinds of techniques. Can this be very much more helpful for you to release them? We got lots of different types of therapies we can use to release trigger points. There is not just one modality, not just one thing you can do to influence trigger points. I remember our instructor back in my… When I was doing my FICS hands-on modules, we had Dr. Mike Murray from Canada came to do a lecture for us in Lausanne, Switzerland.

They would see what’s going through his thing about trigger point, and somebody said, “What kind of techniques can you use?” I can’t do it with Mike’s accent or any of that. He just said something like, “Well, you can use whatever’s handy, whatever you like.” On the left-hand side of the screen there, you got these manual things you don’t need any equipment with. Whether it’s just a typical ischemic compression, put a thumb into it or an elbow into it, whether indeed you want to use a passive stretching or PIR, whether you want to do some strengthening, you can of course do that. All these different things are absolutely fine.

On the right-hand side with the blue background, you can see the things that you can do use that has some equipment with them. Indeed, you have acupuncture, dry needling and lasers and taping, and foam rolling. All these kinds of things. Whatever you want to do, you can really do a trigger point. Chances are, it will respond, but you got to go and poke it. You can’t just leave it there because that’s not going to do anything.

Jon: The roots of trigger point therapy really are in pharmaceutical management, right? With Janet Travel and actually thinking that it wasn’t the medicine that she put in but so much as the needle into these points that made the difference and started mapping those, right?

Mika: Absolutely. There are people who use various different, find pharmaceutical products to influence trigger points and inject them also into things. Well, we’re not going to go into that too much today at all. Let’s move on to the next bit. Again, same contraindications really when it comes to bleeding disorders, anticoagulants, local infection. The very common-sense way of looking at it again. There’s a couple of articles for you there. By all means, have a look at your leisure later on and see what you think.

This one is a little thing that I use a lot in the clinic, actually. For the lack of a better term, we’ll call it movement flow. It might be a new copyrighted thing just now, but we just call it movement flow. It’s a simple repetitive movement to help the fascial gliding. It doesn’t have to be anything strenuous. It really doesn’t have to make a patient painful, even better if it doesn’t. All you’re trying to do is influence how that fascia moves, how the skin moves. It’s not necessarily resisted. I wouldn’t say resisted at all.

If you’re looking at something like an elbow or a wrist problem, which is probably easiest to demonstrate here, but if you got a bit of a problem coming up through those forearm musculature and the tide is in there, it’s very good to have the patient simply utilize a little bit of a movement like that where you’re getting or even assisted with the other hand, so you’re just getting that tissue gliding. I get patients to do this regularly, and you make it up as you go. You find out what is the good movement for that patient to do during your treatment and you’d ask them to copy that at home.

I can’t remember now who was the inventor of the Kinesio tape who said that they wanted to have his hands on a patient in between treatments. This is another way of doing exactly the same thing. As the patient is working on these little movements that are repetitive and oscillating and not too taxing, it gives them also a sense of continuing that treatment effect in between treatment. Hence, it gives them a little bit of ownership. It gets them activated in a treatment process and can be very rewarding in that respect as well.

It’s a key to keep it simple in my opinion. Don’t get too technical. Don’t start overprescribing because that just gets confusing and then they’ll get overburnt, overwhelmed and they won’t do it. So always keep it real simple.

Jon: Mika, I think this is brilliant. It sounds like what you do is you do your soft tissue intervention in the office. You understand what movement is provocative or what’s giving relief or what gets that tissue moving. You simply send the patient home with instructions to do that and to keep it moving once you’ve made the change in the office, creating a more permanent change, correct?

Mika: That’s right. It’s not a strengthening thing, it’s not rehabilitation, it’s something that you ask the patient to adhere to specific patterns. I say, “Look, if it feels like it eases better with the slide rotation, then do that.” We are here to learn. The patient and I, learn together at the same time. We learn about that patient’s body, what works for them. There is really no right or wrong answer, and it’s not only possible to write a textbook on this one.

Jon: I love it. Mika’s movement flow.

Mika: Again, it comes back to intuition and figuring out what is right for a given patient in a given time. It’s great fun I find.

Jon: Yeah, absolutely. I love it too. Okay. Now, we’re starting to get to where we’re wrapping up. These are some of the nuggets that we’ve tried to share through the presentation. Look, there’s a lot of approaches. We’ve already said that a number of times. The more tools you have in the box, the better and the more capable you’ll be at treating different athletes. Having said that, you need to learn and get to where you’re competent with the technique before you start trying to learn ten techniques. Isn’t that a good take on, Mika?

Mika: My particular favourite thing on this slide is the bit in the middle that says good decisions are made based on experience. Oftentimes, experience is gained from making bad decisions because we got to learn. We will make little mistakes; we will be able to patch them up because we’re not doing anything permanent. Hence, you need to practice, you need to learn, you need to try and you start figuring it out. Most of the time, you probably will make good decisions, but sometimes, you make a decision that you realize, “Oh, oh, yeah, I better not do that again.” That’s equally valid and equally important to know.

Jon: Don’t give up on something just because it doesn’t work one time for a particular condition. They work on the next athlete or the next patient. Be patient with yourself. Apply soft tissue modalities. That’s why I like using the same one as you’ve learned it for 6 months and try it on everything. See if it works great with the Achilles. Maybe it does wonders with the rotator cuff but not with the Achilles on certain types of athletes. This is what clinical acumen is all about. These are some of our nuggets, but I think my favourite is to be patient.

Be kind to yourself and understand you don’t always have to have the right answer right away that your patient doesn’t even expect that. They just expect you to have a plan and to communicate that plan, respect their time and give them choices and feedback.

Mika: As we said before, I suppose many a time, all techniques are great for something. There’s no silver bullet. There’s no one thing that fixes everything. Sometimes, you need to try these things in combination. Sometimes, you need to use that technique that you haven’t used for the last 8 years because all of a sudden, that little bump of intuition, just tells you, “Oh, hello. I better go back to that real basic thing I did then, and it might just be the best thing.” So the more tools you have in a box, like we said, the better because they will come in handy one day.

Jon: Understand that they take some years to gain those tools and that’s okay too.

Mika: Absolutely.

Jon: Do we have a little time left for case studies and stories?

Mika: We got a few minutes. Absolutely, a good one to share?

Jon: I do. I actually was excited about this. I put together a little case study. This is an Olympic gold medal bobsleigh pilot that I worked with a quad complaint. It’s with his permission that I shared this story, and he’s actually holding the tribunal left-hand side. This quad complaint bothered him pre-Olympic. In the 2 years prior to the last Olympic games, for eight months, he had an unknown onset of quad pain. He said, “It might have been when I was sprinting. It might have been when I was lifting, but all I know is it happened and I can’t get rid of it.”

Had multiple multidisciplinary interventions, multiple images, MR, CT, x-ray, musculoskeletal ultrasound. When he presented, we were on a World Cup tour. He talked about how he’s limiting his training volume, his push speed and velocity and his ability to load into the sled, which you can see on the bottom left-hand picture. He has to push in then and then drive off that quad and get in. He said it’d be uncomfortable when he was even in the sled, which was severely limiting just his velocity.

As failed interventions were multiple soft tissue approaches, including massage therapy, active release cupping, EMS, ultrasound, therapeutic exercise like crazy injection therapy, even therapeutic dry needling in the area hadn’t worked. It was through evaluating him over about a two-week rotation. I was on the road, we were in Europe and we found successful interventions with deep fascial manipulation, which we discussed. We’re talking elbow right into the quad to the point he would sweat profusely on the table. It was that intense.

What we actually determined was that it was a vastus intermedius strain and that had been missed thinking it was something more superficial, everything from a VMO issue to a hip flexor issue because the pain would travel. When I was able to get a hundred-millimetre needle directly into a point in the vastus intermedius and twist the needle to gather the fascia, it was at that very moment. This athlete who was very in touch with his body said, “That’s the spot,” right there that nobody else has been able to get.

What we found is that through the deep fascial manipulation and very focused needle with twists… Mika, I would put the needle into his quad, he has big powerful quads, and twist that needle and I was unable to pull it, the needle, out.

How hard I pulled. There was that much adhesion that had built up over those 8 months and that’s why I used both the needling to stimulate blood flow and then my elbow with the fascial manipulation to create unwinding in that area. Notable was that the problem was deeper than we expected. The treatment was very intense, but with immediate notable post-treatment relief, he would get up and say, “Oh my gosh, that was it,” and the training was immediately better the next day.

He would come in basically, “Okay, Jon, do it again,” begging for that same approach. He would say, “Make me sweat, make me cry,” a motivated athlete that wants to hold… By the way, he’s holding the World Cup championship trophy there that same year. That was at the pre-Olympic test event in Korea prior to the games. You’re working through this and other challenges. It was nice to be able to help that.

One take-home I want to say is that therapeutic dry needling had already been applied to this area but not a technique I used and not by me. Not that I’m the end all be all by far of dry needling, but I want students and experienced practitioners to understand, just because somebody comes in and they give you the list of things that haven’t worked, that doesn’t mean that your hands and your palpatory skills and your skills in that treatment whether it’s an instrument or cupping or fascial manipulation or dry needling or adjusting.

What if every patient that came in said, “I was already adjusted,” and we just said, “Okay. I’m not adjusting you then. It didn’t work for you?” Sometimes, we do that with soft tissue approaches, don’t we, Mika?

Mika: It’s easy to get a bit defensive or it’s easy to back off too soon. The important thing here is to remember that not everybody has the same skills even if this soft-tissue stuff, even if your athlete had the soft tissue techniques applied by a person who wasn’t very good. I mean, that’s a possibility. I’m sure they had good people working on them, but what if? Therefore, if they say that, “Oh, yes, I had a masseur massage my quad. It didn’t work so that’s why massage doesn’t work.” Well, that’s just tarring everybody with the same brush, which is quite unfair.

At the end of the day, I personally always want to examine and assess patients from fresh without really taking too much notice of what they tell me that happened before. Like I said, not that I’m the be all end all when it comes to sports chiropractic and treating all athletes. I’m probably far from the best there is in the world, but I’d like to make that call for myself. Therefore, sometimes, we repeat treatment modalities that they’ve had, sometimes, we don’t. It just depends.

Jon: Yeah, that’s a really, really good take-home. Mika, I’ve got one more case study, but I’m sure you came with some.

Mika: Do you know what? I’m thinking I’m quite enjoying listening to yours. If you got one with another slider, crack on.

Jon: Okay. This is one from this year, earlier in 2021. This is an Olympic high jumper. With her permission as well, I share this story. This is just about a month ago, a Lithuanian. She came with a hamstring origin complaint of about 2 and a half weeks duration. Onset was at a training camp in Turkey. When I showed up, she had thirteen days to her national competition. We’re in an Olympic year now. She’s in the lead up to the Olympics. It’s important she jumps to a certain standard.

She’s a former European Champion, is coming back off some injuries as every athlete does, but this particular one was a new injury that everybody was calling a hamstring. What she was feeling was limited acceleration, yet explosive feel and confidence in jumping that a high jumper needs. Her personal best is 2.01 meters. This young lady can jump very high when she feels good. Her failed interventions had been simply resting it, hamstring rehabilitation exercises and a pretty good regiment of hamstring soft tissue from a good physio that travels with her all the time.

What we found was that it wasn’t the hamstring at all. In fact, that was one of the things I said during our initial assessment. Yes, your hamstring origin is which they thought it was, was tender and it was a bit inflamed, but this didn’t seem like a hamstring issue to me. Her coach who’s also a physio in a different country than she’s from and her physio was saying, “No. It’s a hamstring. This is a hamstring.” I said, “No, this isn’t barking like a hamstring.”

In America, we say, “If it quacks like a duck and walks like a duck, it’s a duck. If it doesn’t, it’s something else.” What we found was actually a strain of her deep hip stabilizers and rotators, particularly to the obturator internus and to the adductor longus insertion, in fact, determined without imaging but through orthopaedic modalities and palpation that she had an inflamed point at the attachments or co-attachments or shared attachments of the obturator internus and the adductor longus.

With fascial manipulation to that area, which is obviously a sensitive area and therapeutic dry needling to that area with appropriate, obviously, covering draping and boundaries, we were able to get the same sort of feedback. This is something I’ve learned to really listen to an elite athlete. When they say that’s it, you found it because you can flap[?] around for a while, we say. Maybe that’s not the best word to translate, but you can root around in a dark room and finally find the light and then you need to be confident that you found the light.

The notes on this one. I’ll back up a little. We added a specific activation and a loaded isometric to the obturator, which is something that’s not so easy, I found. I had to do a little bit of research to find out how to really activate that obturator internus. Mika, my notes on this was the problem was initially misdiagnosed by a really good coach and a really good physio. By the way, the physio worked with me on this and was present there through treatments and really was open to feedback.

It was nice- it wasn’t like, “You’re wrong, and I’m right.” It was a lot of dialogue, a lot of respect and communication with the athlete’s outcome being the motivation. The buy-in was not immediate from the patient. She thought she had a hamstring issue, too. Really, Mika, I had about 3 days to be wrong with thirteen days to the competition and knowing how bodies respond and how much intervention. I had to be really confident that I was on the right track and if not within about 3 days.

Mika: There you go. I love the way you put it there. “I had 3 days to be wrong,” because that’s oftentimes how tight the timeline for us is. We are looking at athletes pre-competition or during training camps, you have limited time you can work with them. Then know your obturators from your hamstrings and you have to understand the difference between iliopsoas and the cord. Those are the kind of things that oftentimes do get mixed up though and understanding that.

Jon: Even by good practitioners, I’ve got to say. I miss them myself. Sometimes, I totally miss the boat. Fortunately, we were right in this case. She was able to jump and win her national competition and do a season’s best at the end of the competition. Of course, I’m going to share a good case study where it all turned out right, but they don’t all, Mika, do they?

Mika: No. That’s right.

Jon: On our misses, we learn.  Mika: That’s right. Exactly.

Jon: Or at least we should. If you’re humble and learn from your misses, then when an athlete needs you in their moment, you can be right. This was a fun one. That was more of an acute issue that required a deeper kind of dive. Again, understanding and really listening to what the coach and the physio thought but also remaining independent, thinking from my own 2 feet and applying a theory and then an approach with treatment that the athlete was confident with and communicating that to the team around them. A fun case study I thought I’d share.

Mika: That’s a great case study. I love that one. I think we are more or less getting to the end of our time?

Jon: We are. If there’s time for questions we’ll be happy to follow up or the coordinator a response for you. Please email admin@ficsport.org and we will pass your question onto the instructors.

Mika: It’s been great having to talk with you, Jon, about stuff that we both feel very passionate about. Obviously, you got an absolute world and wealth of knowledge. You’re a great advocate for our profession, and all the students are very fortunate to be learning from the likes of you. We can’t really finish on a better note on that.

Jon: Well, you leave me hanging there with all those great compliments and accolades. Listen, we stand on the shoulders of giants. I appreciate sharing this stage with you and these lectures with so many great competent providers and lecturers that are sharing information. Students, you’re very lucky to have Mika and all the other lectures share with you today. Thank you to FICS. Good luck to all, and thank you for listening.

Mika: Thank you, everybody. Yeah, we’ll look forward to seeing you soon.

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