Concussion series, Part 2: Management and Return to Play

**Disclaimer**: I am not a representative of Complete Concussion Management Institute (CCMI), nor am I endorsed by them. I am a Certified Complete Concussion Management Practitioner (CCCMP) through CCMI, but am not paid to present this material. The following post is of my own, and does not represent opinions of anyone but myself.

Now that we have the basic physiology of concussions out of the way, lets talk management and return to play. This topic will be split into 2 parts; A and B. So an athlete comes off the field and tells you they don’t feel good, with c/o headache, dizziness, blurred vision, and nausea. They say they took a hit a few plays back but didn’t lose consciousness. Now what?

Until about 2012, the NFL had been using guidelines from the American Academy of Neurology’s 1997 Practice Parameters, which allowed an athlete to return to play if their symptoms resolved in 15 min. It also graded concussion severity based on loss of consciousness (or not) which we know, now, is not true. They also used to take the players and put them in a dark room to “help alleviate” symptoms – but we know that that also does not work, nor is it evidence based. There used to be a protocol where following a hit, in order to determine if they can return to play that day following resolution of symptoms, the athlete would be asked to do squats (bodyweight) and pushups and some battery of exertional movements. Increased body temperature has been shown to increase glutamate levels in the body – and from what we know about glutamate in Part 1 of this series, increased glutamate increases Ca+2 into the cells which is the main problem with concussions.

However, thankfully the 2012 Zurich Consensus happened and now there are rules against same day return to play if the athlete has either a clear MOI and/or exhibits signs and symptoms of having sustained a concussion.

So the athlete comes to you with c/o symptoms that appear to be from a concussion with an MOI. If the athlete is conscious (the play did not just happen leaving them on the ground and you do not need to activate EMS, and/or you’ve already ruled out the possibly of a spinal cord injury) you’d take them to the side and ask them some orientation questions and go through a sideline assessment such as the SCAT3. You’d continue to monitor their symptoms over the course of the next few hours – DO NOT let the athlete sleep for at least 3 hours. And when they do sleep have someone (or do it yourself if you’re traveling with the team) wake them up every 2-3 hours. The point is that while rest would be nice, you want to monitor their symptoms and make sure they don’t get worse. Make sure you rule out a hemorrhage – send to the ER for imaging if necessary or suspected.

If the athlete is coming to you a day or so after the hit, and you are performing the initial evaluation – make sure to do a full cranial nerve screen and neuro exam. Again, we want to rule out other serious pathology as well as make sure that their symptoms have not gotten worse. Education and reassurance is key in treating athletes with concussions – especially with the media giving it so much attention. There is a large psychological component of concussions and you need to address that at each and ever visit, starting with the eval.

Screen Shot 2016-09-27 at 2.46.20 PM.png

Many of you are familiar with the above chart for return to play. In order to progress from one stage to the next, the athlete needs to have no symptoms for at least 24 hours. If they get symptoms in the next stage, you regress them back one step until asymptomatic. The first step is brain rest. This gets tricky and needs to be handled with care otherwise you will be feeding into the psychological aspect of concussions. You want rest, but not for more than 3-4 days. Max, 14 days is the point at which you need to start encouraging them to perform light physical activity (stage 2). Many physicians will tell the athlete to rest until they have no symptoms – a month may go by and they are still having symptoms (Now, Post Concussive Syndrome). This can increase their anxiety levels and increase their risk of depression as well as decreased overall physical conditioning.  14 days is our turning point, at which, rest can become detrimental to the athlete. Exercise is the most important rehab intervention and has the following effects: increase brain derived neurotropic factor, increase blood flow, increased sense of control (for the patient), improving neurocognition, decreasing inflammation to name a few. So the idea is that you want them to exercise and progress to stage 2 as soon as possible, after an initial resting phase.

One point I’d like to stress is that most athletes will recover from their physical symptoms around 8 days, however research shows that METABOLIC RECOVERY can take up to 30 days in some cases. Therefore, I find the above RTP guidelines too simplistic in some cases because it does not TEST physical capabilities nor does it apply to work/school scenarios. Rather it is based on a reactionary scheme – if they do not have symptoms, progress, if they do then regress. But there is no mention on how to TEST the athlete to know if they can progress/regress.

Screen Shot 2016-10-12 at 1.11.19 PM.png

Physical exertion is required to stress the body and see how the athlete reacts – do they get onset of symptoms with a treadmill test or a bike test? At CCMI their RTP guidelines are a little more detailed and has 3 more steps. For example, in their RTP guidelines step 3 allows an athlete to return to a half day of school/work with restrictions. It is important to not only stress return to sport, but also return to daily life, which the general guidelines do not make much mention of.

Stay tuned for follow up posts that will discuss Post Concussion Syndrome, Second Impact Syndrome, and Physical Therapy interventions for the concussed athlete.


Thomas, D. G. MD, MPH et al Benefits of strict rest after an acute concussion: A Randomized Trial. PEDIATRICS 135(2); 2015

McCulloch, K. L. et al Development of Clinical Recommendations for Progressive Return to Activity After Military Mild Traumatic Brain Injury: Guidance for Rehabilitation Providers. J. Head Trauma Rehabil 30(1); 56-67

Concussion series, Part 1: Pathophysiology

Over the past few years concussions have become quite the “buzz word” in sports. Many years ago, no one really cared about concussions, and then all of a sudden, we’ve gone to the other extreme – everyone who gets hit has a concussion.

Concussions are a very serious topic. It is a mild traumatic brain injury (mTBI). Back in the day, the scale of brain injury would be: concussion, mild TBI, moderate TBI, severe TBI. Now concussions and mTBI should be, and are, interchangeable. That is because concussions ARE a form of brain injury. Many people believe that in order to sustain a concussion you need to have Loss of Consciousness or be hit in the head. In the above video, the hit was clean shoulder to shoulder, and Toews was conscious. But Toews sustained a concussion in that play. Loss of consciousness is also not a predictor of how severe the concussion is, nor will it dictate the length of recovery for the athlete.

It is not just a physical syndrome (headaches, nausea, vomiting, dizziness etc…) but is it a metabolic syndrome as well – it is an energy mismatch in the brain, leading to a large ATP deficit. The old theory/hypothesis of why concussions happened is the “coupe/contrecoupe” theorem shown below.

concussion1.png In this hypothesis, it states that the brain impacts the front of the skull and then impacts the back of the skull, creating two sites of injury. However, it has actually been shown that concussions are more widespread throughout the brain that just that. The new hypothesis is that concussions are “acceleration/deceleration” injuries that create shearing of the neuronal axons.


In the above image, shearing causes damage to the axons and also results in the energy mismatch that the literature has shown. When an athlete (really, any one in general too) experiences a concussion, action potentials are firing constantly at first (excitatory phase) and then when all of the ATP is used up, they become fatigued and lethargic (spreading depression phase).

If we all think back to physiology 101 (It been a long time since I’ve taken that class, and it was a memory I’d like to forget, haha), the concentration gradient inside a resting cell is as follows: K+ high inside, Na+ and Ca+2 high outside the cell. When there is shearing of the neuronal axons, there is also an resultant deformation of the cell membrane, leading to opening of ion channels and the ions flow down their respective gradients. This creates action potentials and causes the release and increase of Excitatory Amino Acids (EAAs): most notably, Glutamate. In order to restore the ion concentration balance to its resting state, we need activation of the Na+/K+ pumps – requires a lot of ATP. The release of glutamate triggers the activation of N-methyl-D-aspartate (NMDA) leading to an influx of calcium into the cell. Ca+2, however, has an affinity for the mitochrondria and when there is a large influx of it into the cell, it creates dysfunction within the electron transport chain – reduces the cell’s ability to create ATP, furthering the energy crisis.screen-shot-2016-09-27-at-9-12-58-am

In the above image, you can see the influx of calcium as well as NMDA in the middle of the cell body. An interesting point that has been made in the literature is that Mg+2 fits into one of the NMDA receptors like a plug. It’s been hypothesized that if you are sufficient in your body’s Mg+2 levels, then it can control how much calcium influxes into the cell and may decrease your recovery time. Many of the physical signs and symptoms can be derived from the underlying pathophysiology described above (headaches, fatigue, dizziness, inability to focus etc..).

That was a lot of physiology in one post. Take some time to wrap your head around the information. One of the big points I will be making in this series is that you have to recover physically AND metabolically to be considered 100% recovered from a concussion. However, many will not show signs and symptoms around day 8-10, but research has shown they are still not metabolically recovered – you will still be at risk for second impact syndrome and return to play at this point may further delay your recovery.


Giza, C., Hoda, D. The neurometabolic cascade of concussion. J of Athletic Training. 2001;36(3):228–235

Giza, C., Hoda, D. The new neurometabolic cascade of concussion. Congress of Neurological Surgeons. 2014;75(4):524-533

Signoretti, S. et al The Pathophysiology of concussion. American Academy of Physical Medicine and Rehabilitation. 2011;3: S359-S368

Clinical Anecdotes: Treating Complaints of Chest Pain


***This post will mark the start of a new segment – Clinical Anecdotes. While research is very important, it takes years and years to generate good research. It is always going to be somewhat behind – I say this meaning that since it takes a long time to generate good and reliable data for literature, by the time something has been validated, many times it is only confirming something that has been going on in the clinic for the past few years. For example, I see “new” research out quite a bit that states exercise is good for your heart health, exercise can help in the diabetic population etc…. But I would argue that this is nothing new. I’m not starting or engaging in an argument about this. This segment is meant to focus on clinical pearls of treatment to help guide your practice. ***

Recently in the clinic I had two athletes come in, both with c/o chest pain, what has helped them took a few visits to figure out but both have now greatly reduced pain levels.

Case 1:

28 year old male with primary c/o chest pain with dips at the gym. Pt presents with thoracogenic scoliosis (R sided convexity). Pin point pain with dips only (bench press was ok) and c/o pain at bottom of dip and pain that lingered – 8/10 at worst. No pain at rest.

Case 2:

18 year old female with c/o thoracic pain that was constant, referred into her neck, and when she retracted her shoulder blades, she had pain in her back as well as her chest that would cause her to cough, pain was 7/10 at worst. Pt’s posture is poor (severe forward head posture with poor stability and control in cervical spine). PMHx of high school rower and track and field sprinter.

The above only describes a limited background. In Case 2, she was cleared by her pediatrician of all other internal medical conditions as well as cleared chest X rays, no co-morbidities identified.

Both had improvement with Graston Technique for soft tissue mobilization. Both had poor posture and, therefore, started on posture correction and neuromuscular re-education for that. Both had complained of pain in a general bilateral chest pain that was also tender to palpation over the anterior shoulder. However, 2 muscles (on top of many others, i.e. pecs had already been addressed through multiple sessions with minimal improvement) were key in their treatment; Serratus Anterior and Latissimus Dorsi. In both cases, when the Lats and SA were released with Graston and soft tissue manual release techniques, both had significant pain reduction: Case 1 had an in session reduction to 1/10 pain with dips 3 sets of 5, and Case 2 had verbal reports of being able to sleep through the night and 4/10 pain with no pain in her neck anymore on her next visit. 

With both you can see how they might be experiencing general chest pain on the lateral and anterior sides due to the muscles’ pain referral pattern. I will also note that these were not the only symptoms seen in these patients, only a snapshot.

While their pain and symptom reduction was not due to SA and Lat release alone (both had a few sessions of NMR and postural retraining without the focus on SA and Lats), they have continued to improve and are able to tolerate increased activity with lower pain levels as well as improved their overall mobility.

Treating the competitive volleyball player series, Part 3: Lower Body Assessment

It’s fairly obvious that the shoulder is one of the more commonly injured joints, but just as obvious should be that the knees of a volleyball player are just as beat up. The impact alone, overtime, is enough to wear down a volleyball player’s knees. Both overuse and traumatic injuries can occur in volleyball to the lower extremities.

In volleyball, it is common for a blocker to land on the opposing hitter’s foot as seen below:

The rule is that you cannot land with a whole foot on the side of the dividing line. However, there is a bit of “no man’s land” where if part of your foot goes under the net, it is not called as a fault. This can be dangerous because having even part of your foot under the net can create a hazardous situation and lead to ankle sprains. I have an entire topic series devoted to lateral ankle sprains, here.

ACL injuries also occur often, more common in the women’s game. Mostly due to weakness in hips and decreased balance/proprioception. Biomechanically, many girls often land on 1 leg after an approach, and with decreased stability from their core and hips, there is an increased valgus moment at the knees:

As I mentioned in the first part of this series, many things are out of the athlete’s control, as in the above vide (first 30 seconds shows the ACL injury occurring). The set was pushed too far out and the hitter was reaching behind her, attempting to adjust to the set, resulting in her landing on 1 foot. Now, am I advocating for landing on 2 feet, always? Not necessarily. It is always better to land on 2 feet than 1. However it happens quite often due to the set location, and in the men’s game it is seen quite a bit as well – In the 2016 Olympics, #2 Aaron Russell an outside hitter for the United States often landed on 1 leg following a hit. The difference is neuromuscular control and overall strength. When treating athletes, don’t be quick to judge biomechanics (especially elite level athletes). Recognize that there are many situations that the athlete cannot control in game settings. It is our job, as rehab professionals, to make sure that their bodies are ready to adapt to any situation during matches. Once you have accounted for all aspects out of the control of the athlete, identify what their deficits are and improve their neuromuscular control/asymmetrical strength pattern so that they are able to adapt during a game safely.

When it comes to overuse injuries, many seen in volleyball are forms of tendonitis/tendonopathy, most notably patellar tendonitis/tendonopathy – also known as jumper’s knee. And it’s named rightfully so, first described and seen in athletes who engage in high repetitions of eccentric quad loading. It’s part of the biomechanics of landing from a jump – eccentric quad contraction to decelerate knee flexion; you’d never want to land straight legged and “jam” the tibiofemoral joint. With patellar tendonitis, it has been shown that it is the proximal end of the patella that becomes irritated and thickened when seen under imaging.

When examining these athletes, knowing what movements reproduce their pain will be key in providing the most effective and efficient treatment. Pain can be reproduced in patellar tendinopathy with resisted knee extension (more so in short sitting). Ascending and descending stairs may be painful, sitting for long periods of time and then standing up, as well as hopping/jumping can all lead to reproduction of symptoms.

Initially, depending on the severity and acuity of the patient’s symptoms, you will want to limit and even completely avoid all activities that require jumping and running. This will decrease the amount of impact on the athlete’s joints and allow for some much needed rest. During this phase, you will want to focus on strengthening of the patient’s hip and core (including eccentric quad control), improve joint mobility around the hip and tibiofemoral joints, as well as manual therapy to the patellar tendon (I prefer Graston or any type of IASTM).

It will also be crucial to note the athlete’s feet and observe whether or not their arches collapse. This can alter their biomechanics up the chain, leading to increased medial valgus stress on the tibiofemoral joint. Orthotics and instrinsic strengthening of the foot can help mediate this situation.

At some point in your rehab (I say this because depending on the athlete’s level of fitness and acuity of injury, I sometimes introduce squat progressions early on or later in the plan of care), you will want to re-train the athlete how to squat again – this is very important for return to sport due to the squat jump required during blocking. I will have a post detailing the importance of the squat and form in a later post – for now, I want to share a progression for the overhead squat that I like to use with my athletes.

The above progression starts with the client in quadruped, rocking back and forth working on maintaining spinal neutral – especially in lumbar spine. Then the client is progressed to tall kneeling, working on core and hip stability – all while maintaining lumbar neutral (make sure their lower lumbar spine does not go into flexion). Finally the exercise is progressed into standing with TRX suspension for external feedback and increased lower trap activation overhead. In all 3 parts of the progression, TheraBand can be tied around the client’s knees so that they are required to push against the resistance.


Rath, E. et al. Clinical signs and anatomical correlation of patellar tendinitis. Indian J Orthop. 2010 Oct-Dec; 44(4): 435–437

Rutland, M. et al. Evidence Supported Rehabilitation of Patellar Tendinopathy. NAJSPT. 2010 Sep; 5(3): 166–178.

Treating the competitive volleyball player series, Part 2: Shoulder Impingement Assessment

Congratulations to TEAM USA on their BRONZE medal and TEAM CHINA on their GOLD medal yesterday. Not the outcome that TEAM USA wanted, but it is still a medal and everyone played their hearts out. TEAM CHINA showed that they had the grit to grind it out against a very tough SERBIAN team.

While there can be a plethora of shoulder injury diagnoses in volleyball players, the most common would be overuse of the shoulder leading to impingement (of either form, subacromial or posterior/internal impingement). Front row attackers (hitters) have the highest risk of shoulder injuries due to the high number of repetitions (Top NCAA Division 1 hitters can reach up to 1,600 swings in a season, with an average of 40-50 swings  match*). *This number may not be accurate due to variability in number of sets and points in each set (3 vs. 4 vs. 5 set matches) – it also depends on if the team heavily relies on one athlete for offense or not.

The pathology of subacromial impingement is that the tendon of the supraspinatus muscle is “pinched” under the coracoacromial arch – the supraspinatus muscle passes inferior and anterior to this arch and when the shoulder is flexed in a neutral position, this muscle/tendon is jammed against the inferior portion of the coracoacromial arch. This can also irritate the subacromial bursa, leading to increased pain.

Posterior, or internal, impingement is when the posterior/superior aspect of the labrum is impinged on the underside of the supra and infraspinatus muscles; mostly secondary to laxity in the anterior capsule in overhead athletes.

In most literature, the pathology will focus on the glenohumeral joint and the immediate surrounding/involved structures. However, much of the pathology stems from elsewhere – thoracic spine, cervical spine, costovertebral joints, scapulothoracic “joint” etc… For example, if the client’s thoracic spine is hypomobile or “stuck” in extension, this will induce a relative “anterior tilt” of the scapula (posterior/inferior rotation of the costovertebral joint). If you were to only work on the glenohumeral joint, you’d get no where in your treatment because the CAUSE is NOT the GH joint, but the lack of mobility in the thoracic spine.

costovertebral extensionposture comparison

As you can see from the above image, a flattened T spine (middle image) can also predispose a client to forward head/rounded shoulder posture, thereby increasing the risk of shoulder impingement and muscle imbalances. In this situation, the client’s posture will increase pec minor and major compensation in an overhead athlete due to increased activation while trying to stabilize overhead and during follow through.

Lower traps and serratus anterior may be inhibited or dysfunctional in this posture. Lower trap inhibition reduces overall AROM in flexion – the lower traps are responsible for the final 10-15deg of flexion through inferior stabilization of the scapula, allowing room for GH joint to continue into flexion. If the scapula was not stabilized inferiorly, it would get in the way in the terminal degrees and cause pain and impingement. Lower traps would also act as a counterforce to the pec minor muscle in this situation. Serratus anterior is responsible for upward rotation of the scapula as well as improving congruency between the scapula and the rib cage. If inhibited, can lead to poor congruency and may lead to increased dominance of pec minor/major as well as winging of the scapula.

Another aspect that should be investigated is the SC/AC joint. Often neglected in shoulder rehab, but the SC joint is required to glide inferior and rotate posterior during shoulder elevation. The clavicle is the one bony connection of the scapula to the thorax. If the proximal end of the clavicle does not glide and rotate properly, it will negatively impact the AC joint at the distal end. This, ultimately, leads to poor gliding between the acromion and clavicle – decreasing overall shoulder flexion.

While subacromial impingement is the more talked about form of impingement, Internal/posterior impingement is quite common in the overhead athlete such as baseball pitchers and volleyball players. Any athlete that goes through a similar motion to the “throwing arc” is at risk for developing posterior impingement. This is when there is anterior laxity (or instability) and posterior shoulder pain due to pinching between the underside of the supra/infraspinatus and the posterior capsule/labrum.

Athletes will typically present with Glenohumeral Internal Rotation Deficit (GIRD), where they will have excessive external rotation and lack shoulder internal rotation. This is due to the requirements of their respective sport. In volleyball, if the setter sets the ball to the middle many aspects can go wrong and can lead to the middle hitter compensating to reach for the ball: 1. If the middle hitter’s approach and take off is in front of the hitter, often times the set will be behind the hitter and therefore, in order to hit the ball, they will be reaching way behind them, increasing anterior GH stress. 2. If the setter’s location is off and the set drifts off the net, the hitter will be in the same situation as #1. In both cases, there will be increased anterior capsule stress which can lead to laxity over time. However, only one of these situations is controllable by the hitter (#1).

In many cases, many therapists may give the “Sleeper Stretch”. This is because many believe that the posterior capsule is “tight” and that stretching it will help. In one study conducted by Borsa et al, it was shown that, in fact, the opposite it true – there isn’t “tightness”, but rather laxity in the posterior capsule in many cases. Therefore, the sleeper stretch is not a good idea. It also places the shoulder into further “impingement” if you think about it.

However, deficits in internal rotation can also be traced back to the thoracic spine – if you think about it, you need a bit of CONTRALATERAL thoracic spine rotation to reach up your back (L rotation for R IR up the back). In Treating the Overhead Athlete series, Part 4 I go over sidelying rib cage mobility. This exercise is a good one to give as a home program so that the athlete mobilizes their rib cage and T spine into contralateral rotation.
The above link is a video of Foluke Akinrawdewo, 2012 Olympic Silver Medalist/2016 Olympic Bronze Medalist/3x First Team All-American during her time at Stanford University. She is a great Middle Blocker and in the above video she is hitting a “slide” where the middle takes off one foot -like a lay up in basketball – behind the setter. It may appear that she is putting her shoulder into further impingement or hurting it.This is a common issue for volleyball hitters. Due to the dynamic nature of the sport and the high number of variables, there is never a black and white answer. As a MIDDLE hitter, Akinrawdewo has to commit to her approach and take off – it is very hard for her to adjust her approach speed and step length once she commits to a play. The setter (Alisha Glass in the above video – 3 time NCAA D1 Champion at Penn State, First Team All American) is taught to put up a hittable ball – in this case against 2 blockers, she cannot/should not put the ball too tight to the net. The ball also can drift off it’s trajectory mid set and the hitter will need to adjust their ARM to hit the ball (cannot adjust their approach very easily from the middle due to the speed of the game).

That was a lot of volleyball jargon. I am in no way criticizing Alisha Glass or Foluke Akinrawdewo – they understand the mechanics of their game as well. This is a snapshot into some of the problems of treating an athlete.  The main point and take away is that when/if you’re treating a volleyball player, DON’T JUMP TO CONCLUSIONS! This is actually very important when treating any athlete. You can try to correct their approach and arm swing, but realize that a lot of it is out of the athlete’s control due to the speed of the game and the number of variables involved. It is out job as sports physical therapists to make sure that out athletes can adapt to any situation during a game.


Escamilla, R. F. et al. Optimal Management of Shoulder Impingement Syndrome. J Sports Med. 2014; 5: 13–24.

Paine, R. et al. The Role of the Scapula. Int J Sports Phys Ther. 2013 Oct; 8(5): 617–629.

Manske, R. C. et al. Shoulder Posterior Internal Impingement in the Overhead Athlete. Int J Sports Phys Ther. 2013 Apr; 8(2): 194–204.

Borsa, P. A. et al. Mobility and Stability Adaptations in the Shoulder of the Overhead Athlete. Sports Medicine. 2008 Jan; 38(1): 17-36

Biomechanics of the Thorax


Treating the competitive volleyball player series, Part 1: An Introduction

Who’s been hyped up for the Olympics this year? I live for every 4 years (well, really every 2 because of the winter Olympics). Finally, other sports other than American Football, Basketball, Baseball, and Hockey will be featured for 2 weeks, and we get to see history being made.

This will be the first series of many to address athletes of specific sports. For those who don’t know me, I played volleyball in college and have coaching experience at the high school and collegiate levels – currently coaching at a local private school in Boston. USA volleyball is on the hunt for the ever elusive Olympic Gold, as they’ve finished with a silver medal at each of the last two Olympics, falling to 2 time defending champion and this year’s host, Brazil. So naturally, I am biased and picked volleyball as the first sport to address. However, having treated major league and collegiate baseball players and played soccer and ran track and field, you can expect these sports to be represented in the near future as well.

Volleyball players fall under the umbrella of “Overhead Athlete”, so if you would like more background on that, please refer to my 4 part series of “Treating the overhead athlete“. Naturally, volleyball players will present with shoulder injuries including but not limited to impingement, rotator cuff tear, labral tear, and scapular dyskinesia. However, due to the dynamic nature of the sport, lower body injuries also occur at a high rate including, but not limited to, ACL tears, ankle sprains, patellar tendinitis (jumper’s knee), ankle sprains, and patellofemoral pain syndrome (PFPS).

There are 6 basic skills involved in volleyball: serve receive forearm passing (bump, off of a serve), overhead passing (setting), hitting (spike), blocking, digging (a forearm pass that happens when you pass a hit), and serving. There are several positions in volleyball, and the athlete’s risk of injury is correlated to their position; setter, outside/right side hitter, middle blocker, and libero (back row specialist in the different color jersey).

Libero Dive
middle hitter slide
Middle Hitter – Slide
outside hitter
Outside Hitter
Setter jump setting

Front row players (hitters/middles/setters) have the highest rate of injuries. Middle and outside hitters not only put their shoulders at risk due to high repetitions, but upon landing, the impact on their joints (femoralacetabular, tibiofemoral, talocrural/subtalar) are at risk for injury. Setters may not have the high incidence of shoulder injuries as hitters, but they certainly can develop impingement and scapular dyskinesia due to their overhead arm position. And since setters on many teams play all the way around, they will be required to block at the net and are at risk for developing lower extremity pain/injuries.

Defensive players don’t usually develop upper extremity injuries, but can develop overuse injuries and tendinitis in their knees due to being constantly in a squat position. Hip injuries can also develop such as acetabular impingement, PFPS, and jumper’s knee. Not to mention, diving on the ground can lead to knee and hip bruises.

In the following 2 posts, I will divide the injuries into upper and lower extremity as well as dissect the injuries that develop, including WHY, and how you can assess your athlete.

Featured Professional: Ramez Antoun, PT, DPT, SFMA,PNF

ramez headshot

A few weeks ago I had the opportunity to connect with a fellow physical therapist in the Boston area, Dr. Ramez Antoun, PT, DPT, SFMA, PNF. Dr. Antoun is a graduate of UMASS Lowell’s DPT program as well as Kaiser Permanente’s Proprioceptive Neuromuscular Facilitation (PNF) fellowship in Vallejo, CA. He is SFMA and Dry Needling certified and is currently pursuing his COMT for manual therapy through the Institute of Orthopedic Manual Therapy (IOMT). He is the founder of NEUROPEDICS, a cash based physical therapy service – currently based in Somerville, MA:

Below is a highlight of the interview I had with Dr. Antoun:

JC: I know you’ve written on the PNF philosophies in your blog, which can be found here: But could you highlight some of these PNF philosophies?

RA: If you’ve read the book “Start with WHY” by Simon Sinek, he talks about the golden circle and how the core is the WHY statement (the why we do what we do), the outer ring is the HOW (how we do what we do), and the outermost ring is the WHAT (what products we will use, dumbbells, kettlebells etc…). As residents of PNF, we are introduced to philosophies.

The first philosophy of PNF is that every living thing has potential – this is rooted in neuroplasticity research. The brain is constantly able to make new connections, new patterns, new associations, which is one of the things we have to truly believe in when rehabbing [clients], because from a neurological standpoint, we have very debilitated [clients] (strokes/TBI) who are paralyzed and believing they can’t walk again, and that innate belief that you can create changes based, on neuro plasticity, that they can walk again, is the first stepping stone of PNF – going into treatment with a positive attitude. This leads me to philosophy number 2, which is treating the whole person. The whole human being encompasses the emotional (i.e. using positive language), the physical (i.e. biomechanical interventions), and the intellectual (i.e. educating the client). The third philosophy is always start with what the person can do – so a positive approach. We’re trained as therapists and trainers to look for weaknesses or impairments and highlight those when we’re talking through an evaluation process, but in PNF, first comment on what you see what’s good. For example: I see that your right shoulder moves really well, especially into upward rotation. The left side, not as good, but we can work with that. Rather than “Oh, that L side is tight, what’s going on there?” To me, the client is already coming to us broken down; a piece of their identity was already taken away from them. So one of the things I can do for them on initial contact is to be positive. The fourth philosophy is movement always needs to be purposeful and leading towards a functional goal. So our exercise program/progression should show a sense of progression back to functional. So I think 4×4 matrix (SFMA): supine/prone à quadruped à kneeling à standing.

JC: I completely agree with everything you’ve touched upon. Being positive. I don’t think that is something talked about enough in PT school. What was it like to go through the PNF residency in Vallejo, CA and how was this philosophy (#2) integrated?

RA: So the residency is 9 months, and it is split into 3 phases: 3month resident, 6month resident, 9month resident. You know how in PT school you always had a strength and problem list when evaluating/treating patients? When ever we did patient demos or working with a patient, they would force to always write down the positives, even within a treatment. In PT school, when a client doesn’t move the way you want them to, you say “No, not like that”. One time I was co-treating with my mentor, and she said, “That’s assuming that that movement is bad”. But when dealing with a neurological population, every movement needs to be considered beautiful, because if they couldn’t do that, then that would be paralysis. Instead of saying no, articulate what movement they did. For example, if you wanted them to reach up over 90 and they reached down below 90 articulate it “Good, you were able to reach down at this angle, now lets try to reach upward overhead”. That was huge, just being able to change my vocabulary and trying to not say “NO”.

JC: That’s a great philosophy, and along the lines of “any movement is better than no movement”.

RA: The only time to say no (and this can be applied to all populations) is when the movement is deemed unsafe and it was going to harm them. This brings us to the principle of “Protect before you correct” from Functional Movement Systems. For example, if someone is doing a lift, and his or her lumbar spine goes into flexion at the bottom, then “No, that is not how we load the spine”. There still is a framework of right and wrong, we still have to respect biomechanical movement. But nonetheless, we shouldn’t be quick to jump into giving negative feedback.

JC: I don’t like the segregation in the PT world. We have distinct settings that we practice in (acute care, inpatient rehab, ortho, sports etc…), but at the end of the day, our goal is to get the client in front of us to move better in the safest way possible. However, I feel that many therapists don’t see it that way, and think, “I’m an ortho therapist I don’t know what to do with a stroke patient”. I don’t like this separation.

RA: There is definitely overlap. There is a whole renaissance of where neuro and ortho are starting to blend together. And there’s a blend of the concepts in the sports world; neuro muscular control, neuro developmental postures, actually can make people move better than in isolation. But it hasn’t been like that. If you go back in history – guys like Maitland, Kaltenborn, Mulligan, Maggie Knott etc…. – They all hung out. They all influenced each other. I don’t know what made that message lost, that the neuro and ortho aspects need to be separated. But I think that they are starting to be marketed again, together.

JC: I completely agree, again. I’m not sure how the curriculum was at Umass Lowell, but at Emory, we were introduced to acute care, ortho, neuro, all separately and in isolation from each other.

RA: I think that it needs to be that way, initially. But by third year, maybe introducing the concept through a course like “Neuro for the orthopedic therapist” might be helpful. I don’t know if we can do ortho for the neuro therapist, but in the PNF residency in Vallejo, there were many therapists who had completed orthopedic training – if we had a patient who couldn’t get into a certain position due to tone or joint restrictions, then they would perform joint mobs. Then we’d follow it up with more neuro-based techniques, rolling etc…

JC: I felt very fortunate that while I was at Emory I had a professor (Dr. Baudo) – who has influenced my clinical reasoning and treatment philosophies a lot – whose big principle was segmental innervation. She would say, “If I have an athlete with an ankle sprain, why am I mobilizing L4/L5/S1? Because what do you think innervates the ankle? L4-5/S1.” So for me, a lot of diagnoses come back to the spine. If I can get one facet joint to move a little better, it could free up any tension on the underlying nerve.

RA: From a biomechanical aspect I might explain it like that. From a sensorimotor perspective I might explain it as stimulating the mechanoreceptors at that particular level, which can send feedback into the central nervous system to get an improved output from the brain for the dermatomal distribution. For patients, I explain it with the following visual explanation: Think about watering a plant. The pump is the spine, the hose is the nerve, the water is the electrical signal, and the plant is the muscle. If the pump isn’t working right, the plant isn’t going to get great water (poor water pressure). If we keep obsessing about why the end of the hose isn’t spitting out water and never look at or check out the pump to see if it’s working, how are we going to expect to help the plant grow? Go to the source of the problem.

Hope you guys enjoyed this interview. Please check out more of Dr. Antoun’s work on Facebook/Instagram at Neuropedics Physical Therapy and Sports Medicine Consulting.

Lateral Ankle Sprain series, Part 2: No Such Thing As A Minor Ankle Sprain

With all of the hype surrounding the upcoming Olympics, I felt like this was a great time to bring in some real life examples. This past week wrapped up the US Gymnastics and Track & Field trials – and what an exciting week it’s been. So far between Gymnastics, Track & Field, and Swimming it seems like in order to make the US Olympic team you have to start breaking some records.

Given that we are on the ankle sprain series, I wanted to draw everyone’s attention to the 200m Finals of the Track and Field Trials on July 10. Below is a video of the finals heat, many top contenders in the field vying for 1 of 3 spots on the Olympic roster. In lane 5, is Allyson Felix, the reining 200m Olympic champion from 2012. Prior to the 200m qualifiers, Felix had already qualified for Rio in the 400m, winning the 2016 trials a few days ago. Coming into the trials this year, Felix has been dealing with an ankle injury to her R leg after a misstep in a training session back in late April – forcing her to pull out of a couple meets in May and June. In an interview with her coach following the injury, he said “(The injury) is 80 percent better in less than a week”. I’m not sure that a grade 2 ankle sprain is 80% better in less than 7 days (some public education may be needed for this coach). Felix, herself, said “The speed wasn’t there” for her in the 200m trials.

If you’ve been keeping up with the news, you’ll know that Felix missed making the Olympic team for the 200m by .01s (what a photo finish), still running a blistering 22.50s. Take a look at the video below (excuse the woman yelling in the background):

The slow-motion play back begins at about 4:35. If you pay attention to Felix (in all blue, lane 5) as she’s pushing towards the finish line, you’ll notice that she does not get the same push with her R leg as she does with her L leg, she has asymmetrical strides bilaterally, and her hamstring prematurely contracts on her R side reducing her quad contraction that she needs for her push (leading to less hip extension as well).

Following an ankle injury, there is a change in neuromuscular activation and firing due to the body’s mechanism of protection. Peroneal activation is delayed, glute med activation is impaired, increased MTrPs develop in the  lateral gastrocs, increased activation of hamstrings. I’m assuming that with Felix being a high profile athlete, she’s getting/gotten some of the best rehab since her injury, but this just goes to show that even 2 months out, she is STILL dealing with the residual effects of an ankle sprain – grade 2.

Friel et al. found that not only is ipsilateral hip abductor weakness noted following an inversion ankle sprain, but that plantarflexion ROM is also limited on the involved side. This also means that the force that can be generated from the involved side is significantly less. As you can tell from the above video, that is exactly what happened to Allyson Felix in the 200m finals.

How many of you are reading this thinking: “She missed it because the other girls were faster” or “it was just bad luck”? Just a week ago, she blew away the competition in the 400m with a time of 49.68s. She had the speed for the 400m, however after 3 rounds in the 400m and 2 rounds in the 200m trials, by the time the 200m finals came around, she could no longer compensate and hide her ankle injury and it’s residual impairments.

On the flip side, she has been dealing with injuries (like most athletes) for a good part of her career, may also have chronic ankle instability. In 2010 she had to pull out of a meet due an ankle injury. She tore her hamstring in 2013 during the 200m event. Who’s to say that these past injuries did not contribute to her “misstep” 2 months ago?

Felix missed Rio in the 200m by .01s not simply because she didn’t have the speed. She didn’t have the most efficient movement pattern down the stretch. From the start, she was placing a lot of pressure on her R ankle – it’s her first “pull” step out of the blocks (she pushes off with her L). Down the stretch, she was not able to make the final push with her glutes and quads/gastroc-soleus, and the asymmetry of her stride decreased the amount of force she could generate.

For those who think ankle sprains don’t affect your performance, even months/years down the line: Allyson Felix missed the Olympic roster by .01s …. all because of an ankle sprain.


Hertel, J. Functional anatomy, pathomechanics, and pathophysiology of lateral ankle sprains. Journal of Athletic training. 2002;37(4):364–375

Friel, K et al. Ipsilateral hip abductor weakness after inversion ankle sprain. J Athl Train. 2006; 41(1): 74–78.





Lateral Ankle Sprain series, Part 1: An Introduction to Anatomy of the Ankle

It might seem odd to jump from the shoulder/overhead athlete in one topic series to lateral ankle sprains at the other end of the body in the very next, but I promise there is a connection – there always is. Many overhead athletes rely on the hip opposite their dominant side for power generation and stability – L hip (stance hip) for R handed pitchers, L hip adduction in R handed javelin throwers etc… Therefore, if the opposite hip is important, then so too is the opposite ankle. After all, the contralateral hip relies on the ankle to remain upright. 

Lateral ankle sprains are among the most common in sports injury. The ankle joint is comprised of three separate articular surfaces: the talocrural, subtalar, and distal tibiofibular joints. The talocrural joint is the articulation between the dome of the talus and the distal ends of the tibia and fibula, while the subtalar joint comprises of the anterior and posterior articulations of the talus and calcaneus, and distal ends of the tibia and fibula join together to form the final piece of the ankle in a syndesmotic joint.

The talocrural joint sits on an oblique axis and is the hinge joint that is responsible for dorsiflexion. This joint is crucial during weight bearing, as it allows any torque in the lower leg (internal/external rotation) to be transmitted to the foot (supination/pronation). The subtalar joint, an articulation between the calcaneus and talus is responsible for rear foot eversion/inversion and also participates in this force transfer. The subtalar joint is made up of two separate joint cavities and therefore, 2 separate joints, the anterior subtalar joint (talocalaneonavicular) and the posterior subtalar joint. The sinus tarsi and canalis tarsi separate the anterior and posterior components. Due to the location of the sinus tarsi, it is vulnerable to overuse injuries and ankle sprains, resulting in sinus tarsi syndrome – impingement of fatty tissue.

The distal tibiofibular joint makes up the last piece of the ankle joint. The tibia and fibula have two articulations, one distally and one proximally, and are connected along their shafts by a syndesmosis. Due to two points of contact between the tibia and fibula, as therapists, we need to address both in an ankle sprain. In normal dorsiflexion ROM, the fibula should glide superiorly and a little posteriorly. Most commonly, the distal tibiofibular joint can be anterolaterally shifted in chronic ankle injuries, reducing overall ROM in dorsiflexion – this is also due to reduced ligamentous stability from the anterior talofibular ligament (ATFL). Therefore, assessment of symmetry bilaterally of the fibula position following a lateral ankle sprain is paramount.

The main ligaments involved in stabilizing the ankle include the ATFL, posterior talofibular ligament (PTFL), calcaneofibular ligament (CFL) – all responsible for lateral stability – and the deltoid ligament – for medial stabilbity. The former three are more commonly injured due to their role in lateral stability and the prevalence of lateral ankle sprains, however the deltoid ligament can be pinched during grade 3 lateral ankle sprains.

Aside from rehabilitating the site of pain and addressing joint mobility/strength/proprioception deficits locally, it is vital to search up the chain for impairments – namely, the glutes/hip (including adductors) and anywhere along the lateral – including the peroneals and TFL – and functional lines. We are all familiar with the functional relationship between the glutes-lumbosacral fascia-lats (aka. Hip to contralateral shoulder relationship), however that is only on the posterior side, but there exists a similar relationship anteriorly. This relationship links the adductors and the contralateral lateral sheath of the rectus abdominis and pectoralis major.

When treating an athlete with an ankle sprain it is important to note not only the site of pain but to also address the core and hips higher up in the chain. This is due to the alterations in motor recruitment during gait following an ankle injury – antalgic gait often leads to mild Trendelenburg gait pattern and reduced activation of hip stabilizers in single limb stance secondary to pain. In the previous topic series, I’ve discussed how important it is for overhead athletes, and the demands of their sport, to have functional glute and core strength – it generally is a good idea to assess in any athlete. In one study it was also shown that any individual with a history of ankle sprains have reduced glute function. In the following segments I will address some manual interventions including taping and neuromuscular interventions, and return to sport testing.


Hertel, J. Functional anatomy, pathomechanics, and pathophysiology of lateral ankle sprains. Journal of Athletic training. 2002;37(4):364–375

Kobayashi, T. Fibular Malalignment in individuals with Chronic Ankle Instability. JOSPT. 2014; 44(11): 872-878


Featured Professional: Nicole Canning, PT, DPT

Dr. Nicole Canning, PT, DPT is our first featured professional on #NotYourAveragePhysio. She was a classmate of mine while at Emory University and is also the author of the blog: Check it out! Dr. Canning is also a former NCAA D1 soccer player at St. Johns University in Queens, NY, and is also a soccer coach with experience in strength and conditioning as well. Recently I’ve had the opportunity to catch up with her and pick her brain a little:
JC: Where do you currently work and what population do you treat?
NC: I currently work at Competitive Athlete Training Zone (CATZ) Physical Therapy Institute in Pasadena. Since we are also attached to a Sports Performance Center, I see mostly youth, high school, and collegiate athletes, as well as active adults. I also see a small mix of general orthopedic cases.
JC:What are your top treatment philosophies when treating athletes?
NC: My main priority is getting the athletes I treat back onto their respective field/court as safely and quickly as possible, making them a better athlete in the process, and preventing future injury. My two biggest philosophies are promoting efficient movement, and education.
At CATZ, we draw primarily from the Gray Institute and the philosophy of Applied Functional Science. Essentially in this philosophy, movement in all three planes (sagittal, frontal, and transverse) is addressed, with respect to ground reaction forces, center of mass, gravity, momentum, reaction, and relevance, in order to enhance functional movement. For example, when I am working with an athlete, I need to know what movements are specific to his/her sport, what internal and external drivers of movement are utilized, what types of movement do they need to be able to react to, etc. I then look at how they are currently moving and performing these tasks, figure out where the dysfunction is occurring, and then address those impairments in a sport-specific, movement-based, and meaningful way for each individual.
I also like to draw from the Strength and Conditioning world when prescribing exercises for my athletes. Since many of these athletes are currently working, have worked, or will eventually work with a Strength and Conditioning Coach, I believe it is helpful to incorporate those principles as well, and tie it in with whatever pathology or impairments a given individual presents with. I also think it’s important to understand periodization when working with athletes, especially with college athletes. It’s imperative to understand how you need to challenge them differently based on what point of their season (or off-season) they’re in. The Strength and Conditioning world has also helped me in my prescription of exercise dosage. There are different rep and set variables to work with based on what you are trying to achieve. I don’t think I can truly do my job to the best of my ability unless I incorporate essential Strength and Conditioning principles.
Another philosophy I tend to get on my soap box about is the mental/emotional aspect of treating athletes. Competitive athletes possess a very different mentality than the general population. They will over train, play through pain, and do whatever they feel they need to do in order to stay at the top of their game. It’s crucial to understand that in order to help it work for the patient and their rehabilitation rather than working against them.
Finally, the most important thing I do for my patients is education! My goal is to never see my patients again (as a patient) once they have returned to their sport. I educate them on how to maintain ideal movement, how to prevent future injuries, and how to listen to and respect their bodies when they need rest.
JC: What are your clinical interests?
NC: Although I love treating any and all athletes, my main clinical interest is in treating conditions of the lower extremity. I particularly enjoy treating patients with ACL injury because I can take the athlete and basically build them back up from scratch. Aside from gaining range of motion and improving strength and neuromuscular control, I can also take a look at what impairments may have put them at risk of that ACL tear in the first place, and then address those risk factors to decrease the risk of re-injury, or injury to the contralateral side. With patients with ACL injury, you get to literally teach them how to walk, climb stairs, squat, run, jump again. What better way to address dysfunctional movement and inefficient movement patterns and teach the athlete ideal movement instead?
JC: How has your background as an NCAA D1 soccer player helped you in treating athletes?
NC: The ways in which my background as an NCAA D1 soccer player helps me treat athletes are countless! Probably the biggest aspect it helps me with is the mental/emotional facet of treating athletes. Not only do I have insight into the mental and emotional roller coaster that goes along with being a competitive athlete (especially one sidelined with an injury), but I feel that it also helps my patients to connect with me and feel more comfortable when they learn that I was once in their shoes and, to some extent, can understand what they’re going through. This helps me understand when I can push them a little harder, and when I need to back off a bit and allow them to experience success. I think generally, there’s a high level of mutual respect and understanding between my patients and me, and when a patient truly believes that you’re the Physical Therapist who’s going to get them better, and help them become a better athlete, then you’ve already won half the battle.
JC: I know you conducted research, and presented a platform talk at CSM 2015, on implementation of ACL injury prevention programs, can you tell me a little more about that project?
NC: Yes, as a female soccer player, I have always been interested in ACL Injuries. Also, aside from being a Physical Therapist, I have been coaching youth soccer for nearly 10 years now. While I was in PT school, I noticed that many of the research articles I read had great ways of helping to identify and reduce risk factors for ACL tears. Actually, considering how common ACL tears are among female soccer players, I was surprised at how much research I was finding on the topic, especially in the past 5-10 years. This made me wonder how there could be so much research on preventing ACL injuries, and yet the number of ACL injuries per year kept increasing. I realized that there is a huge gap between clinical research and its actual implementation into the population it addresses. I also realized that Physical Therapists, Orthopedic Surgeons, Professional and Collegiate Strength and Conditioning Coaches and ATC’s all have access to this information, but by the time an athlete gets to any of these people, it is often too late. This information is staying at the collegiate and professional levels and has no way of being accessed by youth athletes. I find this to be extremely surprising and important because nearly every researcher, MD, PT, ATC, Coach, S&C Coach will tell you that this stuff needs to be introduced and implemented while the athlete is still developing and growing. I decided to delve a little more deeply into where this breakdown of information was occurring, why it wasn’t being implemented, and how to bridge that gap between clinician/researcher and youth soccer player so that the research can be utilized in a meaningful way.
Thank you to Dr. Nicole Canning PT, DPT for taking the time to chat. Hope you all enjoyed this new segment!