Rather than start a new topic series on the last day of the year, I’ve decided to close out 2016 by reflecting on what I’ve been able accomplish in 2016. While many regard this past year as a terrible year (i.e. deaths of some of my favorite, and very prominent, celebrities including Carrie Fisher and Prince), 2016 did have its moments. For starters, the #NotYourAveragePhysio was brought to you all in 2016, and I was given the opportunity to work with the Boston Blades as their head Physical Therapist (the season’s not over yet, if you’re in the Boston area and would like to catch a game, please email me or message me on FB).
I’d like to take this time and reflect on my top 5 posts from the past year:
Lateral Ankle Sprain series, Part 3: Manual Interventions – This post garnered a lot of attention over the summer and I was very excited about this post because while in school I didn’t know how to treat an ankle sprain with manual techniques very well. I was very excited to share a few manual techniques that I like to use and have achieved good clinical results. Give them a try in the new year, 2017!
Overhead Athlete series, Part 4: Treatment Interventions – This was another post I was very excited about. One of my clinical interests is treating the overhead athlete and often times I find that therapists and other healthcare professionals forget that the shoulder is, more times than not, the site of pain but NOT the cause of pain. The treatment interventions in this post demonstrate how important the Thoracic spine and Scapulothoracic connection is (obviously there’s aspects involved like the C-spine and AC/SC joints, but there wasn’t room to fit EVERYTHING in one post –> maybe another time I will tie it all together).
Breaking Down the Initial Evaluation, Part 3: Static Postural Assessment – LE – Going along the lines of finding the cause of pain, this post (and series) does just that! Never accept that the site of pain is the source of pain without having evaluated and assessed other contributing factors clinically (though more times than not, you’ll find that the source of pain is NOT the site of pain). There are times where I do treat the site of pain but more on that another time. 99% of the time, I find the source of pain and treat there rather than focusing on where my client says they are in pain. We have to start treating more holistically in 2017!
Featured Professional: Ramez Antoun, PT, DPT, SFMA, PNF – This was an interview I did with Dr. Antoun who is owner of Neuropedics in Boston, MA. I had so much fun conducting this interview and picking his brain – the entire interview was 3 hours long, I only included a snippet of it. There are some definite clinical pearls in this interview and I love his treatment philosophy!
Concussion series, Part 1: Pathophysiology – Last but not least, this post allowed me to articulate all of the training I had underwent through Complete Concussion Management Institute (CCMI) in Canada for treatment/management/diagnosis of concussions. It’s the hot topic buzzword in sports these days, and PT school definitely does not go over all of the intricacies and details of a concussion.
I’d like to also announce that in 2017, I will be adding a new segment to the blog answering YOUR questions. So please, FB message/email me any questions you may have regarding sports physical therapy, treatment, evaluation, or even a tough case you may have in the clinic!
May 2017 bring more professional development and topic series to you all!
Many of you know that this year I’ve been fortunate enough to be working with the Boston Blades in the Canadian Women’s Hockey League (CWHL) – a professional women’s hockey team/league – as their primary therapist for the season. It’s been a very exciting season so far, and it’s very rewarding to utilize some skills with the team (i.e. lots of taping) that I wouldn’t have the luxury of using in the clinic as much. I’ve also learned so much on the job just from observing. I can’t stress enough how crucial it is to be able to refine your observation skills as a physical therapist – even more so as a SPORTS PHYSICAL THERAPIST. It is paramount in our field to be able to pick up on the nuances and subtle movement patterns and be able to hone in on what is causing an athlete’s dysfunction, fast! It’s even more critical when you’re not as familiar with the sport at hand – which was my case starting the season.
My specialty area for treatment when it comes to sports and athletes – while I do treat athletes of all sports, my true expertise lies in overhead athletes such as baseball/softball players and volleyball players. Having gone to undergrad in Maine, I’m familiar with hockey (attending many Bowdoin v. Colby hockey games back in the day), but I’ve never ice skated before, let alone play hockey. However, through plenty of observation and research, I’ve come to understand movement/strength patterns necessary for the elite hockey player to be successful.
Hockey players are always in a hip hinged position that requires plenty of control from their core. Without a strong core, their posture will become compromised and the athlete will end up loading in a flexed spinal position that can lead to low back pain. For anyone who knows me, you’ll know that I consider the glutes as an important part of supporting the deep core muscles. Glutes are important for stability in the frontal plane as well as required for push off while skating (posterolateral movement – hip abduction with extension). This allows the athlete to project themselves forward on the ice. However, often times, the athlete will become quad dominant and will compensate with knee extension more than hip extension – staying in the hip hinged position and increasing stress on the low back while keeping the glutes in a lengthened state.
Hockey players don’t only develop LE dysfunction, but they can also develop increased UE (bilateral) dysfunction as well. They are constantly in a rounded and protracted position of the scapula. Depending on which hand they shoot with – their top UE is excessively internally rotated and their bottom hand is excessively protracted relative to neutral. This creates muscular imbalances when compared side to side (dominant Latissimus dorsi and Serratus Anterior, under-active RTC, rhomboids, and lower trap). Goalies are a separate category all on their own due to the demands of their position – this post serves as a general guide for screening hockey players.
A screen I really like, and am a bit biased towards, is the Selective Functional Movement Assessment (SFMA). It really does capture everything in one screen! What I’ve found through screening the hockey players is that most have poor scapular control (sometimes accompanied by cervical ROM deficits) with excessive winging in the Medial Rotation Extension (MRE) pattern and Dysfunctional Non-painful (DN) in LRF. Muscular imbalances arise from the upper traps (hyperactive due to overuse during bracing), increased pec major/minor and lat activation, and under-active lower traps and RTC – often leading to impingement patterns. Of course, T spine is always involved with scapular control issues. In lower extremities, players often have decreased glute recruitment overtime, decreased SLS balance, decreased hip mobility into IR/ER/flexion, and DN of overhead deep squat (ODS).
As I mentioned in the series on treating the competitive volleyball player, it’s not enough to just correct these dysfunctional patterns or tell the athlete to avoid those positions – you have to understand the demands on the sport and why the athlete has now assumed these postures and developed painful or high risk movement. As this was very surface presentation of screening a hockey player – it should help point you in some areas that need to be assessed – performing your own assessment and drawing your own conclusions is just as important because every athlete is different. I hope this post can help any therapist unfamiliar with the sport of hockey and guide them towards problem areas as a starting point.
Parts 1 and 2 discussed the pathophysiology and return to play guidelines for a concussed athlete. But what happens if the athlete’s symptoms don’t go away, and it’s been a month or more? The ICD-10 definition of Post Concussive Syndrome (PCS) states that in order to be diagnosed with PCS, the athlete must experience at least 2 or more symptoms for a span of at least 4 weeks (i.e. headaches, dizziness, nausea etc…).
Post concussive syndrome can be tricky because most often times, you will need to not just treat the physical symptoms of the athlete, but you have to address the psychosocial aspect as well. While many studies have shown that while physically an athlete can show no signs or symptoms as soon as a week (some recover as fast as 8 -15days), through magnetic resonance spectroscopy we’ve found that metabolically, it could take up to 30 days to fully recover. In many cases the athlete will have been told by someone, prior to seeing you, that they should rest until they are symptom free because it could further damage their brain. In Part 2, you’ll remember that in return to play/work/life guidelines, step 1 is brain rest and step 2 is light activity. Under most usual circumstances you need to be in a stage for 24 hours symptom free before progressing. However I did place an asterisk next to step 1 because you do not want your athlete in this stage of more than 3-4 days, though sometimes up to 14 days max.
If an athlete comes to your clinic 3-4 weeks out from their concussion still symptomatic, and they’ve been on brain rest for this entire time, you’ll want to start them on some light activity to increase their hear rate.Aerobic exercise via bike and treadmill have been proven to help PCS athletes and non-athletes recover and become symptom free. Prolonged rest for an athlete can lead to deconditioning and metabolic deficits: which from Part 1 you’ll remember that a concussion is ultimately a mismatch in energy and is a metabolic syndrome of the brain. You do not want your athlete to become anxious and fear that looking at a screen will cause more damage (especially since they are a few weeks out from the initial injury) – fear avoidance behavior should be avoided. Consistently reassure the athlete and provide a timeline of how they’re improving towards their goals. Utilize positive language. If you haven’t please check out my interview with Dr. Ramez Antoun, PT, DPT who explains why language is so important and why it is often overlooked.
It is also interesting that studies have shown that if you exercise too soon (within the first week of recovery) you run the risk of doing more harm than good, but aerobic exercise starting between 14-21 days after injury has shown to improve cognitive function.
Aside from the physical symptoms similar to whiplash (suboccipital/upper trap/levator/SCM tightness, hypomobility in cervical spine etc…) you will want to also address any visual tracking/vestibular deficits they may still have. Think back to your Neurorehabilitation courses in PT school (shout out to all of the wonderful neuro inpatient rehab therapists out there). You will want to assess for any nystagmus and saccadic eye movement, re-train smooth pursuit, as well as use X1 and X2 activities to retrain the VOR. Dix-Hall pike and CRT roll maneuvers are examples of great for assessing and treating any vestibular deficits that made still be lingering (assess properly for specific vestibular deficits so that you can pick the correct treatment approach). Many outpatient PTs will often forget about the vestibular/visual tracking systems due to focus on manual therapy any joint/soft tissue restrictions, but these systems can ALSO contribute to any lingering symptoms.
Another very important topic, when discussing concussions, is Second Impact Syndrome. Second impact syndrome is when an athlete, prior to full metabolic AND physical recovery of a previous concussion, sustains a second concussion. In an athlete recovering from a concussion, there is metabolic deficits in the brain, disruption of the blood brain barrier, as well as diffuse axonal injuries that contribute to their symptoms. However, if an athlete recovers physically (but has not fully healed metabolically), they will run the risk of serious damage if a second hit is sustained. There will be an additive effect in second impact syndrome and can lead to increased intracranial pressure and decrease cerebral perfusion, leading to increased edema and swelling of the white matter.
Many athletes will argue they feel better and unless you have objective tests to run, you will have nothing prevent the athlete from going back in. This is why baseline testing is so crucial and important in contact sports. Having objective data to compare before and after injury will allow you as the clinician/therapist to make a better judgement on whether or not the athlete should be allowed to return to play. Asymmetries or cognitive scores lower than their baseline could indicate delayed metabolic healing. However, it’s better to be on the conservative side if you are unsure – athletes have died in the past due to Second Impact Syndrome (google Rowan’s Law, an athlete in Canada who died after sustaining a second hit prior to full recovery. Now, in Canada, you must be cleared by a trained medical professional in order to return to play to prevent Second Impact Syndrome).
While sometimes I think that the media can go a bit crazy and over report certain things, concussions are to be taken very seriously. This is not to say that you have to suspect that every little hit is a concussion, but you need to be vigilant if you’re covering a sport on the sidelines as well as if an athlete comes to your clinic. There is not enough education to the public at this moment about the severity of concussions and parents and athletes need to be informed. Concussions should not be brushed off as something minor, they are a form of brain injury and you only get 1 brain – make sure to take care of it!
**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.
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.
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
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.
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.
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
***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.
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.
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.
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.
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.
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 4I 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
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).
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.
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: http://www.neuropedicspt.com/
Below is a highlight of the interview I had with Dr. Antoun:
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.