sportEX Medicine Journal Issue 65 - July 2015

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ISSUE 65 July 2015 ISSN 1471-8138


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n research reviews n shock-wave therapy n longitudinal Mcl sprain

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n putting concussion guidelines into action


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contents July 2015 issue 65


publisher/editor ToR DAvIES art editor DEBBIE AShER sub-editor ALISon SLEIgh PhD Journal watch BoB BRAMAh subscriptions & advertising +44 (0) 845 652 1906 CoMMISSIonIng EDIToRS AnD TEChnICAL ADvISoRS Tim Beames - MSc, BSc, MCSP Dr Joseph Brence, DPT, CoMT, DAC Simon Lack - MSc, MCSP Dr Markus W Laupheimer MD, MBA, MSc in SEM, MFSEM (UK), M.ECoSEP Dr Dylan Morrissey - PhD, MCSP Dr Sarah Morton - MBBS Brad neal - MSc, MCSP Dr nicki Phillips - PhD, MSc, FCSP

Jul 2015

Every month hundreds of papers are published within the realm of sports and exercise medicine and as a practicing clinician, despite our best intentions, it is impossible to remain continually up to date. As a result, to remain “current� and evidence-based can sometimes feel beyond reach. My name is Dr Sarah Morton, and I am the new commissioning editor for a section revolving around translating research into practice. This section is about bringing the literature together and presenting it to you as a practicing clinician, in a way that we hope will help you use the information to guide your practice. We will aim to incorporate the latest guidelines, the definitions and expert opinions all together in one place. Every other month we will invite an author with a special interest in the field or topic being discussed to develop a suitable article. The first article in this series is the Concussion in Sport article on page 26. Literally as we go to press today it was announced that Queensland Rugby player James Ackerman, a 25 year old father of two, had died following a head injury sustained after a tackle which took place in the first 5 minutes of a match a few days earlier. It illustrates the huge significance of this area of sports medicine and reinforces my belief in the importance of this project. I look forward to your comments and feedback as we move forward. dr sarah Morton, Mbbs and sporteX commissioning editor

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4 Journal watch 8 Research reviews 10 shock-wave therapy 13 Mcl injury case study

The latest key research from this quarter Pain syndromes

Benefits and mechanisms

18 fai part 2 26 concussion in sport 33 social watch

Biomechanics, diagnosis, mechanisms and clinical management Putting the guidlines into action Practical resources from the social networks

Diagnosis and management of longitudinal MCL sprains

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State-of-the-art anterior cruciate ligament tearS: a primer for primary care phySicianS. Salzler m, nwachukwu bu, rosas S, nguyen c, law ty, et al. the physician and Sportsmedicine 2015;43(2):169–177 Everything you need to know about the current state of anterior cruciate ligament (ACL) injury and rehabilitation. This article is an overview with current epidemiologic data, basic anatomy and physiology, clinical presentation, physical examination findings, imaging modalities and treatment options. According to the authors, after reading this short article, a medical care provider should understand ACL injuries and their appropriate management.

sportEX comment Trouble is that most of you can’t read it unless your institution pays $1,671., or your company pays $3,309. for a journal subscription or you pay $52 just for this ‘short article’. We have no problems with writers or publications making money but we are drawing the line at silly money. To prove that we are not being cheapskates we paid a tenner for the study into the effect of massage on rat tendons.

Similar clinical outcome outcomeS but more healthcare uSe in Shoulder impingement patientS following corticoSteroid injection compared with phySical therapy. foster ne. evidence-based medicine 2015;doi:10.1136/ebmed-2015-110171 This is a commentary on ‘One-year outcome of subacromial corticosteroid injection compared with manual physical therapy for the management of the unilateral shoulder impingement syndrome’ by Rhon DI, et al., Annals of Internal Medicine 2014;161(3):161–169. This study looked at 104 patients with who had been referred to physical therapy and who had at least a score of 20 on the Shoulder Pain and Disability Index. They randomly split into a physical therapy group who received treatment twice a week for 3 weeks and were given a home exercise programme or to a group who received a subacromial corticosteroid injection of 40mg of triamcinolone acetonide in up to three injections over 12 months plus pendulum exercises. Patients and treatment providers were not blinded to treatment but those assessing outcomes were. Other outcomes included global rating of change and pain intensity and all outcomes were assessed at 1, 3, 6 and 12 months. The two groups were similar at baseline and there was a 96% follow-up rate at 12 months. There were no statistically significant differences in the changes in shoulder pain and disability between groups at any time point. There were also no between-group differences in global rating of change or pain intensity. Both groups improved, on average, over time. Both groups demonstrated approximately 50% improvement in pain and disability at 1 month follow-up and this improvement was maintained at 12 months. However, patients in the physical therapy group proceeded to have significantly fewer visits to their primary care physician for shoulder pain.

sportEX comment This only surfaced because it’s a commentary on a previous piece of work which we missed but it is an important one so it is worth citing the commentary and the original work on the grounds of credit where it due is. Previous trials have also shown that adding an injection to a package of exercise and manual therapy does not provide superior pain and function outcomes at 12 weeks so this study further supports the view that effective care for shoulder impingement should be a physical therapy programme tailored to targeting strength and range of movement if for no other reason than the fact that over time there are less visits to the doctor so it is going to be cheaper in the long run.


literature review to juStify the uSe of autologouS blood injectionS in the treatment of lateral epicondyle tendinopathy. reid d, clough a. international musculoskeletal medicine 2015;37(1):33–38 All the usual databases were searched, which revealed three case study reports, four randomised controlled trials (RCTs) and two meta-analyses. The conclusion was that there is no level 1 evidence for efficacy, but there is no evidence of harm either.

sportEX comment ‘No evidence of harm’ will do us. If all else fails, it is worth a try. sportEX medicine 2015;65(July):4-7


journal watch maSSage may initiate tendon Structural changeS – a preliminary Study. andrzejewski w, Kassolik K, dziegiel p, pula b, et al. in vivo 2015;29(3):365–369 This study was conducted on fifty Buffalo strain rats, randomly divided into two equal groups. Both groups were subjected to physical training on a running track for 10 weeks. Running was for 10min on the first day and increased by 5min every day, until it reached 30min at the end of the first week. Speed was 0.3m/s in the first week, followed by an increased speed of 0.5m/s in the remaining period of the training. (If only it was so easy in humans). One group received massage using an algometer head (Digital Algometer Pain Diagnostic Gage; Wagner Instruments, Greenwich,

Sixteen patients (9M, 7F; aged 18–50 years) took part in a crossover study with different interventions on alternate days. They were measured for pain, pressure pain threshold and pain-free grip strength before being taped. The tape protocol was athletic tape applied in a diamond box pattern according to McConnell’s reloading procedure with four strips of none elastic, adhesive-backed sports tape laid distally to proximally in a diamond shape with traction force on the soft tissues towards the lateral epicondyle and perpendicular to the line of the tape. Alternatively, Kinesio tape used for treatment of muscle and

CT, USA) of 0.5cm2 in area, with a constant compression power of 9.81N (1 kg), using spiral movements along the tendon of the long flexor muscle of the digits for 5min, at the plantar surface of 1cm2 of each rear leg. The results showed that there was an increase in the percentage of collagen fibres in tendons with the smallest diameter (≥100nm) in the massage group at week 3, followed by a decrease in weeks 5 and 7 and a subsequent repeated increase in week 10. No significant differences were observed for either group in the number of collagen fibres based on

fibre diameter (101–200nm, 201–300nm and 301–400nm).

sportEX comment We keep telling you that regular massage is beneficial. This study shows that long-term massage during training may initiate structural changes. OK, this is rats and, by the way, we understand that animal studies are sometimes needed but we don’t need the graphic details of their dispatch that the authors of this paper chose to share with us. In fairness they were anaesthetised. Now let’s have some long-term human studies.

effect of KineSio taping verSuS athletic taping on pain and muScle performance in lateral epicondylalgia. goel r, balthilaya g, reddy rS. international journal of physiotherapy research 2015;3(1):839–844 fascia correction was applied from insertion to origin to inhibit extensor capi radialis brevis (ECRB) muscle function. For fascia correction the base of the fascia correction was applied in front of the pain point. The fascia was pulled towards the free direction. The tape ends were affixed without tension. Further measurements were taken immediately after taping and after 30min. The results showed significant pain reduction and increase in grip strength after both the taping techniques but no statistically significant differences for any outcome measure between the two taping techniques The immediate pain reduction was more after athletic taping (21%) than Kinesio taping (10%) which corresponded to an immediate increase in pain-free grip strength 14.5% more after athletic taping against an increase of 9.7% for the Kinesio tape. Thirty minutes later both the outcome measures gave similar percentage changes.

sportEX comment There is a lot wrong with this study not least of which is the low number of participants and the fact that that they only measured 30min after taping. A longer time period would have been interesting especially since some of the sufferers had the problem for over 2 years. It only gives a slight nod towards the reasons for the pain decrease: dispersed stresses generated by muscle contraction for the athletic tape and a reduction in mechanical stress on free nerve endings within the fascia through fascia unloading for the Kinesio tape. What it does show, however, is that whatever the underlying mechanism of the pain there is little difference between the two tape types and both create a window of diminished pain that could be used for a manual therapy treatment.



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doeS a temporary leg length diScrepancy have an influence on upper body poSture and lower jaw poSition in competitive athleteS? ohlendorf d, himmelreich m, mickel c, groneberg da, Kopp S. Sportverletzung Sportschaden 2015;doi:10.1055/s-0034-1399215 [epub ahead of print] Thirty-four competitive athletes (2F, 32M) who had no signs of temporomandibular dysfunction were scanned with a 3D back scanner in order to assess upper part of the body posture before and after the intervention which was to induce the leg-length discrepancy using wooden panels measuring 1 and 3cm thick placed unilaterally under the foot. In particular the position of the condylar process of the mandible was noted. Analysis showed a change in the height

of the shoulder girdle and pelvis. The biggest changes can be observed in the area of the height of the pelvis in the transverse plane. The position of the condyle in space changes significantly.

sportEX comment Unless you speak German you can only get the abstract of this study. It shows how alterations at one end of a kinetic chain can have a profound effect elsewhere. Leg length

is always worth checking – apparently leg-length asymmetries appear to be the third most common cause of running injuries and occur in 60 to 90% of the population. If you want to know more about leglength problems, check out ‘Detecting and treating leg length discrepancies’ by Caselli M, et al., Podiatry Today 2002;15(12).

match play performance characteriSticS that predict poSt-match creatine KinaSe reSponSeS in profeSSional rugby union playerS. jones mr, west dj, harrington bj, cook cj, et al. bmc Sports Science, medicine & rehabilitation 2014;6:38 Data was obtained from four European Cup games about 28 professional Rugby Union players (15 forwards, 13 backs), with blood samples collected 2h pre-, and 16 and 40h post-match which were subsequently analysed for the levels of creatine kinase (CK). The CK was identified as a marker of muscle damage. Relationships between changes in CK concentrations and number of physical contacts and high-speed running markers, derived from performance analysis and global positioning system were assessed. Moderate and moderatelarge effect-size correlations were identified between contact statistics and changes in CK post-match in forwards and backs. Moderate

emg Spectral differenceS among the quadricepS femoriS during the Stretch reflex. beck tw, Simmons jl, defreitas jm. muscle & nerve 2015;doi:10.1002/ mus.24625 [epub ahead pf print]


effect-size correlations were found between measures of high-speed running and sprinting, and changes in CK post-match within the backs.

sportEX comment The damage correlation from tackles is obvious but the relationship between the backs’ high-speed running and muscle damage is an interesting find. The authors’ plan was to increase understanding of recovery from game-induced muscle damage so that markers can be used to tailor individual recovery strategies. Could this mean the end of the dreaded ice bath or more of them? Watch this space.

Sixteen healthy subjects (mean age 21.2 ± 2.8 years) were given a tendon tap reflex test of the leg extensors as surface EMG signals were detected from the vastus lateralis (VL), rectus femoris (RF), and vastus medialis (VM) muscles of the dominant thigh. All EMG signals were processed with a wavelet analysis, and the resulting spectra were decomposed with non-parametric spectral decomposition. The results showed that the spectra for the VL had significantly more highfrequency power than those for the RF and VM, with similar spectral shapes for the RF and VM. There is speculation that the findings could have been due to differences in the width of the innervation zone, or the fibre type composition of the muscles.

sportEX comment This is a standard neurological test for the stretch reflex. This study suggests that the reflex transmission is not equal between the quadriceps muscles. Although the authors speculate about two possible reasons, their preference is on the reason being a different fibre type. Could this be a reason for muscle imbalance and patella tracking problems. Further research please.

sportEX medicine 2015;65(July):4-7


t effect of additional anKle and midfoot mobilizationS on plantar faSciitiS: a randomized the controlled trial. Shashua a, fletcher S, avidan l, ofir d, et al. journal of orthopaedic & Sports physical therapy 2015;45(4):265–272 Fifty patients aged 23–73 years with plantar fasciitis were randomly assigned to either an intervention or control group. Both received eight treatments, twice a week, consisting of stretching exercises and ultrasound. In addition, the intervention group received mobilisation of the ankle and midfoot joints. Dorsiflexion (DF) range of motion was measured at the

beginning and at the end of treatment. The results were evaluated by three outcomes: the numeric pain rate scale (NPRS), lower extremity functional scale (LEFS) and algometry. No significant difference was found between groups in any of the outcomes. Both groups showed a significant difference in NPRS and LEFS. Both groups significantly improved in DF range of motion with

no difference between groups.

sportEX comment What this suggests is that the relationship between plantar fasciitis and reduced dorsiflexion is due to soft tissue not the joints.

the immediate effect of atlanto-axial high velocity thruSt techniqueS on blood flow in the vertebral artery: a randomized controlled trial. erhardt j, windsor ba, Ketty r, hoekstra c, et al. manual therapy 2015;20(4):614–622 Twenty-three healthy participants (14F, 9M; mean age 40, range 27–69 years) were randomly assigned to two groups: an intervention group (n = 11) received high velocity thrusts (HVT) to the atlanto-axial segment (MANIP group) whilst a control group (n = 12) was held in the pre-manipulative hold position. Colour-flow Doppler ultrasound was used to measure VA3 haemodynamics. Primary outcome measures were peak systolic (PSV) and end diastolic velocities (EDV) of three cardiac cycles measured at neutral, pre-HVT, post-HVT, post-HVT-neutral positions. Visually, EDV were lower in the

MANIP group than in the control group across the four measurements. However, there were no significantly different changes between the MANIP and control groups for any measurement variable.

sportEX comment The high velocity thrusts to the atlanto-axial joint segment do not appear to affect the haemodynamics of the suboccipital portion of the vertebral artery during or immediately following HVT in healthy subjects. Hope that ‘healthy subjects’ is not a key word.

e exerciSe, education, manual-therapy and taping compared to education for patellofemoral oSteoarthritiS: a blinded, randomiSed clinical trial. crossley Km, vicenzino b, lentzos j, Schache ag ag, et al. osteoarthritis and cartilage. 2015; doi:http://dx.doi. org/10.1016/j.joca.2015.04.024 [epub ahead of print]

improving the radial nerve neurodynamic teSt: an obServation of tenSion of the radial, te median and ulnar nerveS during upper limb poSitioning. manvell j, manvell n, Snodgrass Sj, reid Sa. manual therapy 2015; doi:10.1016/j. math.2015.03.007 [epub ahead of print]

This was a randomised, participant and assessor-blinded clinical trial involving 92 people aged ≥40 years with symptomatic and radiographic patellofemoral osteoarthritis (OA). They were divided into a group who received physiotherapist delivered patellofemoral joint targeted exercise, education, manual-therapy and taping, or an education only group. Both had eight sessions over 12 weeks. Outcomes measured at 3 months and at a 9-month follow-up were patient-perceived global rating of change, pain visual analogue scale (VAS) and an activities of daily living (ADL) subscale of the knee injury and osteoarthritis outcome score (KOOS). The results were that 81 people (88%) completed the 3-month followup. The exercise, etc., programme resulted in more people reporting improvement (20/44) than the OA-education group (5/48) and greater pain reduction. No significant effects on ADL were observed. At 9 months there were no significant effects for self-report of improvement, pain or ADL

Tension of the radial, median and ulnar nerves was measured simultaneously using three buckle force transducers during seven upper limb positions in the axilla of ten embalmed whole body human cadavers (N = 20 limbs). The position that produced the most tension in the radial nerve was a composite consisting of scapular depression, shoulder internal rotation, elbow extension, forearm pronation and wrist flexion with the addition of shoulder abduction 40° and extension 25° plus wrist ulnar deviation and thumb flexion. Additionally, the composite position demonstrated the greatest difference in tension between the radial and median and radial and ulnar nerves.

sportEX comment Long term there doesn’t seem to be a difference but short term there is. That may be sufficient to get the sporty OA patella people through their next game.

sportEX comment This is basically the ‘upper limb neurodynamic test 2b’ (ULNT2b). And this study proves that on cadavers at least it does produce tension in the radial nerve. But, is it the same in live specimens and the million dollar question is that when you do it with a real body is it the stretched fascia causing the pain?


Brought to you By

Nxt Gen Institute of Physical Therapy

our regular research reviewer, physical therapist Joseph Brence, reviews research looking into (i) chronic widespread pain and (ii) complex regional pain syndrome.

Psychosocial variables are associated with the develoP develoPment of chronic widesP widesPread Pain BY Dr Joseph Brence DpT, coMT, DAc


hronic widespread pain (CWP) is a complex diagnosis, defined as pain on left and right sides of the body, above and below the waist, and in the axial skeleton (1). this diagnosis is often considered a challenge for many to treat because of contributing variables being multifactorial in nature, and often a combination of those in biological, psychological and social domains. In 2011, Smart et al. published a paper (2) examining a mechanisms-based classification of musculoskeletal pain. In this article, he describes one contributory mechanism, central sensitisation (or central hyper-excitability), as having: n Pain disproportionate to the nature and extent of injury or pathology n Disproportionate, non-mechanical, unpredictable pattern of pain provocation in response to multiple/ non-specific aggravating/easing factors n A strong association with maladaptive psychosocial factors (eg. negative emotions, poor selfefficacy, maladaptive beliefs and pain behaviours, altered family/work/social life, medical conflict) n Diffuse/non-anatomic areas of pain/ tenderness on palpation.

It is suspected that CWP is a result of central sensitisation, but there is a lack of good evidence to indicate risk factors associated with the development of CWP. A recent paper published in Pain (3), set out to examine the number of people without CWP, who would develop it within an 11-year window, and how variables such as anxiety, depression, alcohol use, smoking, difficulty sleeping, and body mass index (BMI) are associated with the risk of developing CWP. this study included individuals who participated in the Nord-trøndelag health Study from 1995 to 1997 and again in 2006–2008 (huNt2 and huNt3, respectively). From the data collected during this time, researchers included 28,327 (out of 65,233 initial participants) who completed both portions of the study. the study consisted of the completion of ‘the huNt health surveys’, which included several questionnaires and clinical tests. An initial survey, which was a self-report questionnaire relating to questions about pain, was filled out at home before attending a physical examination. the second questionnaire, consisting of follow-up questions to the first survey, was administered after a clinical examination. out of the initial cohort,

THE AUTHOR Dr Joseph Brence D DpT, coMT, DAc Dr Joseph Brence DPT, COMT, DAC is a physical therapist and clinical researcher from Pittsburgh, PA, USA. He is also a fellowship candidate with Sports Medicine of Atlanta, GA, USA. Joseph’s primary clinical interests involve a better understanding of the neuromatrix and determining how it applies to physical therapy practice. He is currently involved in a wide range of clinical research projects investigating topics such as the effects of verbalising of pain, the effects of mobilising v. manipulating the spine on body image perception and validation of an instrument which will assess medical practitioners’ understanding of pain. Clinically, Joseph treats a wide range of painful conditions in multiple settings including complex regional pain syndrome, fibromyalgia and chronic fatigue syndrome. Joseph also runs the Forward Thinking PT blog


approximately 19,000 individuals, without CWP during huNt2, were assessed for the development of CWP by huNt3. After the 11-year followup, the researchers found 12% of the participants ended up developing CWP. out of these 12%, they found the following variables as being associated risk factors: n Anxiety and depression n Former and current smoking n BMI <18.5kg/m2 and BMI ≥25kg/m2 n Sleeping problems. It was further found that high to moderate alcohol usage was associated with a reduced risk of CWP. overall, this study highlights the important relationship that appears to exist between psychosocial variables and pain. After tracking a very large cohort for 11 years, these researchers found non-musculoskeletal variables to be associated with the risk of developing CWP. For the practising clinician, we must understand the importance of assessing for these variables, when our patients present in pain. Although the variables may or may not be contributory to the patients’ current complaints, they could contribute to much more disabling conditions down the road. References 1. Wolfe F, Smythe hA, et al. the American College of rheumatology 1990 criteria for the classification of fibromyalgia. report of the Multicenter Criteria Committee. Arthritis and Rheumatism 1990;33:160–172 2. Smart KM, Blake C, Staines A, et al. the discriminative validity of “nociceptive” “peripheral neuropathic” and “central sensitization” as mechanisms-based classifications of musculoskeletal pain. The clinical Journal of Pain 2011:27;655–663 3. Mundall I, gråwe rW, et al. Psychosocial factors and risk of chronic widespread pain: An 11-year follow-up study–The HUNT Study. Pain 2014;155;1555–1561.

sportEX medicine 2015;65(July):08-09

ReSeARcH Review

Complex regional pain syndrome: what have we learned? A s we begin to understand more about pain science and neurophysiology, we still continue to struggle to understand certain painful diagnoses. one of these conditions, complex regional pain syndrome (CrPS), baffles many clinicians because of a true lack of understanding of its pathophysiology, as well as a lack of a gold reference standard for diagnosis (1). Because of this, it is important that we take a look at our current understanding of the condition, as well as some of the research that is being performed to understand it better. CrPS, is suspected to involve multiple systems resulting in severe pain; changes of the bones, joints, and skin; excessive sweating; tissue swelling; and hypersensitivity to light touch. Many clinicians believe CrPS involves the central nervous system, autonomic nervous system, and immune system because of the gamut of signs and symptoms involved. But because the actual mechanisms behind CrPS are yet to be completely understood, many are unsure of what to look for to make a diagnosis.

The BuDApesT criTeriA for crps A 2010 article in Pain set out to validate the Budapest Criteria for CrPS (2). this was performed because the authors suspected the International Association for the Study of Pain (IASP) diagnostic criteria had low specificity, which could result in over-diagnosis. the Budapest Criteria for CrPS includes: 1. Continuing pain, which is disproportionate to any inciting event 2. Patients must report at least one symptom in three of the four following categories: n sensory: hyperesthesia and/or allodynia n Vasomotor: temperature asymmetry and/or skin colour changes and/or skin colour asymmetry

n sudomotor/oedema: oedema and/or sweating changes/ asymmetry n Motor/trophic: decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin) 3. Patients must display at least one sign at time of evaluation in two or more of the same categories listed in point 2. 4. there is no other diagnosis that better explains the signs and symptoms.

In this paper, the authors evaluated 113 individuals with CrPS-1 and 47 individuals with non-CrPS neuropathic pain. they then compared the diagnostic accuracy using both guidelines and found the IASP guidelines to have high diagnostic sensitivity (1.0) but poor specificity (0.41). these findings replicated those in previous works (hence why a more definitive diagnostic schema is important). When using the Budapest criteria, the sensitivity stayed high (0.99) and the specificity also improved (0.68). this finding should help clinicians have more definitive guidelines in making a diagnosis of CrPS.

iMAgerY inTerVenTions for crps As the ability to diagnose CrPS is being refined, there is a significant amount of research being performed on how to intervene once diagnosed. From a physiotherapy perspective, there is a lot of work being done by two research groups in Australia, BodyinMind and the Neuro orthopaedic Institute (NoI), on the topic of graded Motor Imagery (gMI). gMI, as described by the NoI group, “is a rehabilitation process used to treat pain and movement problems related to altered nervous systems by exercising the brain in measured and monitored steps which increase in difficulty as progress is made” (3). In essence, this

series of interventions influence portions of the brain responsible for pain and movement. A 2013 case study, published in the Clinical Journal of Pain, assessed changes in fMrI findings after an individual with CrPS performed gMI for 6 weeks (4). the gMI programme consisted of three sequential, 2-week phases: n phase 1: Left/right discrimination. this was performed by discriminating between left- or right-sided pictures of hands on a computer program. n phase 2: Movement imagery. the individual imagined movements to match those seen on an image. n phase 3: Mirrored movements. the individual performed movements with the intact hand while observing it in a mirror to create the illusion that the affected limb was moving. the results of this study demonstrated subjective reductions in pain with associated marked changes in the areas of discriminative pain processing within the brain. to cut a long story short: not only did the patient have less pain, but there were neuro-anatomical variations as well.

conclusion overall we still have a significant amount to learn about CrPS, but it appears we are on the right track. Diagnostic criteria appear to be improving and less invasive interventions, such as gMI, are showing good promise. references 1. reinders MF, geertzen Jh, Dijkstra Pu. Complex regional pain syndrome type I: use of the International Association for the Study of Pain diagnostic criteria defined in 1994. The clinical Journal of Pain. 2002;18:207–215 2. harden rN, Bruehl S, et al. Validation of proposed diagnostic criteria (the “Budapest Criteria”) for complex regional pain syndrome. Pain 2010;150(2):268–274 3. Neuro orthopaedic Institute. Graded Motor imagery rehabilitation process . 4. Walz AD, usichenko t, et al. graded motor imagery and the impact on pain processing in a case of CrPS. The clinical Journal of Pain 2013;29(3):276–279.


Shock-wave therapieS for SportS injurieS introduCtion Extracorporeal shock-wave therapy (ESWT) is an increasingly popular treatment approach in the management of many soft tissue conditions. The literature and general media are full of reports of benefits in tendon and ligament conditions in particular, much of which can be difficult to interpret. It is important for the clinician to have a comprehensive understanding of the physiological basis for ESWT, current treatment systems, and the current evidence base for its use in musculoskeletal injuries.

extraCorPoreal shoCk-wave theraPy: definitions Shock waves are three-dimensional pressure pulses of microsecond duration with peak pressures of 35–120MPa. ESWT in its true sense, and the form that has been well researched, involves focused shock waves. These are concentrated into small focal areas of 2–8mm diameter to optimise the therapeutic effects and minimise effects on adjacent tissues (1). Many of the physical effects of focused-EWST (f-ESWT) are related to the energy delivered to a focal area. The concentrated shock-wave

This article discusses the possible benefits and mechanisms of effect of extracorporeal shock-wave therapy (ESWT). The terminology is also clarified, making it easier for the reader to interpret the literature on this subject. By Professor Cathy sPeed BMedsCi, diP sPorts Med, Ma, Phd, frCP, ffseM energy per unit area, the energy flux density, (EFD, in mJ/mm2), is a typical descriptor of shock-wave ‘dosage’ (2). There remains no consensus as to the definition of ‘high and ‘low’ energy ESWT, but as a guideline, low energy ESWT is EFD ≥0.12mJ/mm2, and high energy is >0.12mJ/mm2 (3). Focused shock waves can be generated by electrohydraulic, electromagnetic or piezoelectric mechanisms [Table 1, (4)]. The method of generation of the shock wave influences its waveform characteristics, focal area and tissue penetration and, therefore, its effects on tissue. All f-ESWT systems use focused reflectors to concentrate the shock waves on the target. Another form of treatment that is now commonly available is described as ‘radial shock-wave therapy’. However, these systems do not generate shock waves but

taBle 1: exaMPles of eswt and radial systeMs. [Speed CA. A systematic review of shockwave therapies in soft tissue conditions: focusing on the evidence. British Journal of Sports Medicine 2014;48:1538–1542 (4)]


type of system

system (manufacturer)

Focused ESWT – electromagnetic

Epos™ Ultra (Dornier, Germany), Sonocur™ systems (Siemens, Erlangen, Germany)

Focused ESWT – electrohydraulic

OssaTron® (HealthTronics, USA) Orthospec™ (Medispec Ltd, USA)

Focused ESWT – piezoelectric

Piezoson™ (Wolf, Germany)

Radial pulse therapy (radial ‘shock’-wave therapy)

Doloclast™ (EMS, Switzerland)

rather they deliver ballistic energy to a tissue, which does not have the characteristics of medical shock waves. Their description as shock waves adds to confusion in interpreting the literature. Such a treatment may be better termed radial pulse therapy (RPT) (4) or ballistic therapy. Some studies of ‘low energy ESWT’ are in fact referring to the use of RPT (5,6). The increasing popularity of radial ‘shock’wave systems is predominantly related to their lower cost.

Physiology of eswt The proposed mechanisms for benefit of f-ESWT on musculoskeletal tissue include direct effects on tissue calcification, alteration of cell activity through cavitation, acoustic microstreaming, alteration of cell membrane permeability, and effects on nociceptors through hyperstimulation, blocking the gate control mechanism (1–3, 7). f-ESWT also results in activation of stem cells (8) and tenocytes (9). Collagen production is enhanced although initially after treatment there is collagen disorganisation before upregulation occurs and, hence, there is a rationale for restricting exercise in the immediate post-treatment phase. There is also evidence that f-ESWT decreases inflammatory mediators in musculoskeletal tissue. Such effects are seen with both low and high sportEX medicine 2015;65(July):10-12

current trendS in SportS Medicine


energy f-ESWT, although there appear to be some differences in effect between the doses. Therefore, the evidence suggests that f-ESWT has a regenerative and tissue repairing effect (10–13). This process takes some time (at least 6 weeks after completion of treatment) and the expectations of the clinician and the patient in this respect must be managed. Radial pulses are not focused and it has been demonstrated that they do not have a penetrating effect on tissue but, rather, act superficially (8). The mechanisms of action of RPT on musculoskeletal tissues are as yet unclear. No direct comparison of f-ESWT with RPT has been performed, although a study design for such a trial in patella tendinopathy has been published (14).

evidenCe for Benefit A recent systematic review of shockwave therapy in musculoskeletal conditions by the author identified 23 methodologically adequate studies on the subject (4). There is evidence for benefit of f-ESWT and of RPT in a number of soft tissue musculoskeletal conditions, and evidence that both treatment modalities are safe. There is evidence that f-ESWT is effective in the treatment of plantar fasciitis, calcific tendinitis, and that RPT is effective in plantar fasciitis. Where benefit is seen with f-ESWT, it appears to be dose dependent, and greater success is seen with higher-dose regimes. There is low level evidence for lack of benefit of lowdose f-ESWT and RPT in non-calcific

rotator cuff disease and mixed evidence in lateral epicondylitis. Both treatments offer an alternative to surgery in the management of recalcitrant conditions. While the focus to date has been on the use of shock waves in only chronic cases recalcitrant to other medical interventions, its use in advance of some treatments (eg. steroid injections), or as an adjunct to others (eg. platelet rich plasma injection) should be considered, given the proposed mechanisms of action (at least in f-ESWT), its non-invasive characteristics and excellent safety record. References 1. Auge BK, Preminger GM. Update on shock wave lithotripsy technology. current opinion in urology 2002;12:287–290 2. Wess O, Ueberle F, et al. Working group technical developments – consensus report in high energy shock waves in medicine. In: Chaussy C, Eisenberger F, Jocham D, Wilbert D (eds). High energy shock waves in medicine. thieme 1997. ISBN 9783131048318. 3. Siebert W, Rose C, Lübbers C. Die laserassistierte Capsular-Shift-Operation (LACS) bei multidirektionaler Schulterinstabilität. video presentation at the 44th annual meeting of the association of South German orthopaedic practitioners 1996, Baden Baden, Germany 4. Speed CA. A systematic review of shockwave therapies in soft tissue conditions: focusing on the evidence. British journal of Sports Medicine 2014;48:1538–1542 5. Gleitz M. Myofascial syndromes and trigger points. Shock wave therapy in practice. Level10 books 2011. ISBN 978-3981383959 6. Rompe JD, Nafe B, et al. Eccentric loading, shock-wave treatment, or a wait-and-see policy for tendinopathy of the main body of tendo Achillis: a randomized controlled trial. american journal of Sports Medicine 2007;35:374–383 7. Speed CA. Extracorporeal shock-wave therapy in the management of chronic softtissue conditions. journal of Bone & joint Surgery (Br) 2004;86:165–171 8. Raabe O, Shell K, et al. Effect of

extracorporeal shock wave on proliferation and differentiation of equine adipose tissue-derived mesenchymal stem cells in vitro. american journal of Stem cells 2013;2:62–73 9. Leone L, Vetrano M, et al. Extracorporeal shock wave treatment (ESWT) improves in vitro functional activities of ruptured human tendon-derived tenocytes. pLoS one 2012;7:e49759 10. Chao YH, Tsuang YH, et al. Effects of shock waves on tenocyte proliferation and extracellular matrix metabolism. Ultrasound in Medicine and Biology 2008;34:841–852 11. Han SH, Lee JW, et al. Effect of extracorporeal shock wave therapy on cultured tenocytes. foot & ankle international 2009;30:93–98 12. Bosch G, de Mos M, et al. The effect of focused extracorporeal shock wave therapy on collagen matrix and gene expression in normal tendons and ligaments. equine veterinary journal 2009;41:335–341 13. Notarnicola A, Moretti B. The biological effects of extracorporeal shock wave therapy (eswt) on tendon tissue. Muscles, ligaments and tendons journal 2012;2(1):33–37 14. Cleveland RO, Chitnis PV, McClure SR. Acoustic field of a ballistic shock wave therapy device. ultrasound in Medicine and Biology 2007;33:1327–1335.

Th AuThoR ThE PRoFESSoR CAThY SPEED BMedSci, Dip PR Sports Med, MA, PhD, FRCP, FFSEM Professor Cathy Speed BMedSci, Dip Sports Med, MA, PhD, FRCP, FFSEM ((university of Suffolk) is a consultant in Rheumatology, Sport & Exercise Medicine. She is based at The Fortius Clinic, London, and at the Cambridge Centre for health and Performance in Cambridge. She is also a senior physician for the English Institute of Sport. Cathy is a consultant in Rheumatology, Sport & Exercise Medicine.



key Points n extracorporeal shock-wave therapy (eswt) is an increasingly popular treatment for many soft tissue conditions; however, the literature can be difficult to interpret. n shock waves are three-dimensional pressure pulses of microsecond duration. n eswt in its true sense involves shock waves that are concentrated (ie. focused-ewst (f-eswt)] into small areas to optimise therapeutic effects. n a typical descriptor of shock-wave ‘dosage’ is the shockwave energy per unit area, or energy flux density (efd) in mJ/mm2. n ‘radial shock-wave therapy’ does not deliver true shock waves and is better termed radial pulse therapy (rPt). n f-eswt has direct effects on musculoskeletal tissues, such as altered calcification, cell activity and cell membrane permeability. n f-eswt enhances collagen production, following an initial disorganisation and upregulation phase. n the regenerative and tissue repairing effects take some time, so the expectations of the patient must be managed.


n Can the terms focused extracorporeal shock-wave therapy (f-ESWT) and radial shock-wave therapy be used interchangeably? If not, why not and what other term would be better to use? n Are the effects of f-EWST dose dependent, and if so which dose seems to be more effective? n What conditions seem to benefit from f-EWST? n What are the suggested mechanisms of benefit of DISCUSSIONS f-EWST?

Want to share on Twitter? hERE ARE SoME SuggESTIonS tweet this: Extracorporeal shock-wave therapy in its true sense involves focused shock waves. tweet this: The method of generation of the shock wave influences its waveform characteristics and therefore its effects on tissue. tweet this: The evidence suggests that f-ESWT has a regenerative and tissue repairing effect. tweet this: f-ESWT benefits musculoskeletal conditions such as plantar fasciitis and calcific tendinitis.

sportEX medicine 2015;65(July):10-12

msk diagnosis, treatment and rehabilitation - case study

A cAse sTudY of A lonGiTudinAl MediAl collATeRAl liGAMenT spRAin This case study presents the insights gained from the presentation and treatment of a longitudinal sprain of the medial collateral ligament (MCL) of the knee in a professional footballer. MCL sprains are usually transverse and longitudinal sprains present with subtle differences. This article describes the differences in the common signs and symptoms and clinical testing to allow readers to make a differential diagnosis in their own practice. BY AshleY Jones Bsc, MssT And RichARd Moss Msc, GsR

inTRoducTion Ligament sprains are the most commonly presented knee injury (1) and the medial collateral ligament (MCL) is the most commonly injured ligament

Figure 1: MCL ligament (highlighted) and semi-membranosus muscle. (Primal Pictures)

to be responsible for assisting in the control of rotational movement and forces of the knee joint (3). In contrast, the superficial bundle is suggested to be primarily responsible for the control of valgus (medial) stress (4) (Fig. 1). The collateral ligaments form part of the knee ligament complex that traditionally comprises the two collateral ligaments, the two cruciate ligaments of the anterior cruciate ligament (ACL) and the posterior cruciate ligament (PCL),

lcl - lateral collateral ligament All - anterolateral ligament (discovered 2013) pop - popliteal tendon lfe - lateral femoral epicondyle pfl - popliteofibular ligament GT - Gerdy’s tubercle

Š2014 Primal Pictures Ltd

Mcl ligament

within the knee complex of young athletes (2). The collateral ligaments of the knee are strong longitudinal bands of fibrous tissue that run across the medial and lateral aspects of the knee joint from the distal femur to the proximal tibia on the medial aspect and distal femur to the head of the fibula on the lateral aspect. The MCL consists of two bands of ligamentous fibres, the deep bundle and the superficial bundle. The deep bundle of fibres is suggested

Figure 2: Lateral ligaments of the knee (Image credit: University of Leuven)


LIGAMenT sPrAIns Are The MosT CoMMonLy PresenTed knee Injury

and the knee joint capsule. This area of anatomy has recently been publicised by the proposed existence of the additional ligamentous band on the lateral aspect of the knee in the form of the anterolateral ligament (ALL) (5) (Fig. 2). The MCL is often additionally associated with a wide variety of other musculoskeletal knee conditions, such as ACL injury (6). The most common mechanism of injury for the ligamentous structure is excessive valgus stress and external rotation being exerted on the knee during high contact sports

The CLInICAL AssessMenT oF A PATIenT wITh A susPeCTed MCL sTrAIn Is CoMMonLy done usInG A vALGus sTress TesT AT 30° knee FLexIon Figure 3: Typical mechanism of medial collateral ligament injury. (R. Moss, 2015)

VAlGus sTRess

such as football, rugby, ice hockey or dynamic high velocity sports such as skiing (Fig. 3) (7). The MCL originates from the medial epicondyle of the femur, passing inferiorly and anteriorly across the knee joint line to insert into the medial condyle and shaft of the tibia (8). during dynamic knee kinematics, when the joint is positioned in 25° of flexion, the MCL provides 78% of valgus-restraining force compared with 57% of restraining force being provided during full extension (9).

cAse sTudY A 22-year-old male professional footballer suffered a contact injury to the medial aspect of his right knee 35 minutes into a competitive match in the english Football League. The exact mechanism of injury was a legal block tackle, where the player’s flexed knee was subjected to a significant external

excessive valgus stress produced by the force of the opposing player. The player immediately had pain on the medial aspect of their right knee and had difficulty when bearing full weight on the right leg. on clinical assessment he additionally presented with pain on performance of the valgus stress test of the right knee, specifically located on the proximal third of the MCL with no degree of abnormal laxity present when tested against the uninjured contralateral limb. The player was immediately removed from the field of play and conservatively treated with ice therapy every 2 hours for 10 minutes with the limb also immobilised and non-weight-bearing using a pair of elbow crutches. The injured knee was initially taped using an elasticated adhesive bandage in order to control the initial excessive inflammatory responses to injury. The initial diagnosis was MCL sprain. Twenty-four hours post-injury the presentation included significant swelling on the medial aspect of the knee tracing the anatomical position of the MCL. The patient also reported pain on palpation of the right medial knee joint line. The ongoing management of the injury used cryotherapy (in the form of ice), compression (using Tubigrip) and elevation. The patient was advised to increase joint mobility, working up to the onset of pain in both knee flexion and extension. Initially, gravity-

TABle 1: TYpicAl siGns And sYMpToMs of A MediAl collATeRAl liGAMenT spRAin. (r. Moss, 2015) Typical sign

Typical symptoms

Little visible swelling on the medial aspect of the knee.

Pain during flexion and extension of the knee (final 10°).

heat on palpation of the MCL.

sensation of medial knee laxity when bearing full weight.

Lack of range of movement in knee flexion and extension.

Medial laxity and pain during cutting or lateral change-of-direction movements.

symptomatic gain when bearing full weight.

Patient may report hearing an audible ‘pop’ during the mechanism of injury.

MCL, medial collateral ligament


sportEX medicine 2015;65(July):13-17

msk diagnosis, treatment and rehabilitation - case study

TABle 2: TYpicAl siGns And sYMpToMs foR The diffeRenTiATion of lonGiTudinAl And TRAnsVeRse MediAl collATeRAl liGAMenT sTRAins. (r. Moss, 2015) signs and symptoms

longitudinal Mcl tears

Transverse Mcl tears


no laxity on valgus stress in comparison to asymptomatic side.

Laxity present on valgus stress in comparison with the asymptomatic side.

swelling location

Located on the proximal 1/3 of the MCL.

Located close to/mirroring the medial joint line of the knee.

weight-bearing pattern

Pain present during the early stages of healing with little/no laxity.

Pain present during the early stages of healing with apparent laxity and apprehension compared to the asymptomatic limb.


Pain present on palpation of the medial femoral condyle as well as proximal 1/3 of the MCL.

Pain on the medial joint line.

eliminated exercises on a polished surface were prescribed. The patient was also advised to continue using the crutches for the next 3–5 days, or as symptoms allowed. Before the injury the player had no previous history of knee injuries, was otherwise fit and well and no medication or pharmacological interventions were being used. regular follow-up assessment took place twice a day and a reduction in the inflammatory symptoms was observed in comparison with the contralateral uninjured limb. however, there was no reduction in the pain level experienced by the patient during palpation of the right medial knee joint line. It was also evident that the patient had a lack of passive and functional active range of motion compared to the contralateral uninjured limb, particularly when performing knee flexion. Magnetic resonance imaging (MrI) was taken 4 days after the onset of injury to aid the diagnostic clinical reasoning of the injury and to give an indication of the injury severity to enable the formulation of an estimated recovery time. upon interpretation, the images suggested that the patient had suffered a partial longitudinal tear to the proximal third of the MCL with no other associated soft tissue or bony damage. The recovery time agreed between the multidisciplinary medical department members was 8–10 weeks because of the uncommon, and therefore uncertain, nature of the injury. The joint was immobilised and non-weight-bearing for a further 5 days using elbow crutches, followed by encouragement to increase the weight bearing on the limb under

guidance from the club physiotherapist. over the following 4 weeks, the player was subjected to intense therapeutic treatment and rehabilitation sessions, showing promising signs of healing at an accelerated rate compared to a typical transverse partial tear to the MCL. The club physiotherapist performed daily objective testing of the injured limb, conducting a structured protocol agreed by the club medical department to assess and monitor changes in both pain and laxity of the right knee. during this ongoing clinical assessment of the player, it was notable that that there was an apparent lack of excessive joint laxity when tested using the valgus stress test and a passive force was placed upon the injured ligamentous structure. A further follow-up radiological investigation using MrI was conducted 4 weeks after the onset of injury, which suggested a thickening of the proximal third of the MCL while still showing evidence of a partial longitudinal tear in the same region of the ligament. The patient demonstrated no apparent excessive laxity on objective clinical assessment at this point and also experienced no significant pain or discomfort. Also, a full active knee range of motion was present and the player reported no apparent symptoms when bearing full weight. After the results were interpreted and discussed by the medical department it was decided that the player would begin straight-line running in order to promote optimal conditions for tissue healing and to continue progression

along the rehabilitation programme through progressive loading of the healing structures. The player made a full recovery from injury and, to date, has not suffered any recurrence of medial knee injury. There have also been no other structural injuries surrounding the knee in question, with the player completing the remaining 6 months of the football season. The medical team within the professional club advised the player to continue an individual knee-strengthening programme in order to minimise the risk of any recurrence of the injury.

ApplicATion To clinicAl pRAcTice The traditional presentation of an MCL strain commonly seen in sporting and non-sporting contexts is as a transverse tear in the ligamentous fibres that cross the medial knee joint line. with injury incidence rates being suggested to be 7.60 per 1000 person years and with male athletes 1.42 times more likely to sustain the injury than female athletes (10), the accuracy of the diagnosis used to inform subsequent injury treatment management is paramount. Patients suffering from a strain to the MCL will typically present following a mechanism of injury that would include an excessive valgus force being applied to the lateral aspect of a distally fixed limb; commonly it is also associated with a position with a degree of knee flexion that creates a relatively unstable joint structure by unlocking the screw-home mechanism of the knee joint. The symptoms 15

The MedIAL CoLLATerAL LIGAMenT Is oFTen AddITIonALLy AssoCIATed wITh A wIde vArIeTy oF oTher MusCuLoskeLeTAL knee CondITIons

online if you have a current subscription, login at https:// to view this video or download the mobile apps which are free to subscribers with online access. Video 1: Testing the medial collateral ligament of the knee. (A. jones and r. Moss, 2015)

reported by patients will largely depend upon the severity of the damage that has been sustained; however, typically these will include pain on the medial aspect of the knee that can often by specifically located to the site of the sprain on the ligament. This pain is found in conjunction with a feeling of instability, particularly with sidestepping and twisting (lateral femoral rotation) actions or reported when standing from a sitting position. The typical observational signs displayed by an MCL strain, again corresponding with the severity of the damage sustained, may include visible oedema, heat and erythema focused around the medial joint line of the knee (Table 1). The clinical assessment of a patient with a suspected MCL strain is commonly differentiated using a valgus stress test at 30° knee flexion compared against the clinical outcome observed at 0° knee flexion [sensitivity = 86–96% (11,12)] which is used to detect excessive ligament laxity created by a lack of longitudinal ligamentous fibre integrity (video 1). In order to assess the nature of the laxity exhibited at the presenting joint, bilateral testing of the contralateral limb should be conducted to account for individual differences in normal joint laxity. In order to differentiate between a suspected transverse sprain and a possible longitudinal sprain of the MCL of the knee in a clinical setting, the key clinical differences that could be observed are shown in Table 2.

conclusion with the prevalence of MCL injury reported by Gage et al. (1), particularly within sporting populations (2), the importance of accurate and reliable diagnosis is vital in informing its subsequent investigation, management and rehabilitation. The discrete differences in presentation of a partial longitudinal tear in the proximal third of the MCL of the knee, in comparison 16

with the traditional and more common transverse tearing of the ligamentous fibres must be recognised to maximise the application of therapeutic modalities and minimise the negative impact of injury upon sporting performance. The reliable and popular objective assessments for such conditions have been shown to have potential limitations, as the apparent lack of medial laxity, when under passive valgus stress, would traditionally suggest a lack of damage to the MCL (13). however, this case study demonstrates the potential presence of MCL damage. The most important clinical differences in presentation between a traditional transverse MCL strain and a potential longitudinal MCL strain are the presentation of atypical MCL strain pattern of signs and symptoms with the addition of an atypical lack of excessive laxity on passive valgus stress and the patient’s description of their pain being more likely to be located over the medial femoral condyle rather than the typical medial knee joint line.

fuRTheR ResouRces 1. Lundblad M, walden M, et al. The ueFA injury study: 11-year data concerning 346 MCL injuries and time to return to play. british Journal of sports medicine 2013;47(12):759–762 ( 2. For information about crutches see the website ( 3. youTube video review of medial ligament injuries of the knee by sports Injury Clinic ( 4. Brukner & khan’s Clinical sports Medicine online (

References 1. Gage B, McIlvain n, et al. epidemiology of 6.6 million knee injuries presenting to united states emergency departments from 1999 through 2008. academic emergency medicine 2012;19(4):378–385 2. swenson d, Collins C, Comstock r. epidemiology of knee injuries among us high school athletes, 2005/06-2010/11. medicine & science in sports & exercise 2013;45(3):462–469 3. Indelicato P. Isolated medial collateral ligament injuries in the knee. Journal of the american academy of orthopaedic surgeons 1995;3(1):9–14 4. warren L, Marshall j. The supporting structures and layers on the medial side of the knee: an anatomical analysis. Journal of bone and Joint surgery 1979;61(1):56–62 5. Claes s, vereecke e, et al. Anatomy sportEX medicine 2015;65(July):13-17

msk diagnosis, treatment and rehabilitation - case study

of the anterolateral ligament. Journal of anatomy 2013;223(4):321–328 6. Frobell r, Cooper r, et al. Acute knee injuries, Chapter 32, p652. In: Brukner P, khan k. (eds) Brukner & khan’s Clinical sports Medicine, 4th edn. mcgraw–hill s education 2011. IsBn 978-0070998131 (£78.23). Buy from Amazon 7. schein A, Matcuk G, et al. structure and function, injury, pathology, and treatment of the medial collateral ligament of the knee. emergency radiology 2012;19:489–498 8. Palastanga n, Field d, soames r. The lower limb, Chapter 3, p340. In: Anatomy and human movement, 4th edn. butterworth heinemann 2012. IsBn 978-0702053085 (£46.79). Buy from Amazon 9. Grood e, noyes F, Butler d. Ligamentous and capsular restraints preventing straight medial and lateral laxity in intact human

cadaver knees. Journal of bone and Joint surgery (am) 1981;63:1257–1269 10. roach C, haley C, et al. The epidemiology of medial collateral ligament sprains in young athletes. the american Journal of sports medicine 2014;42(5):1103–1109 11. harilainen A. evaluation of knee instability in acute ligamentous injuries. annales chirurgiae et gynaecologiae 1987;76:269–273 12. Garvin G, Munk P, vallet A. Tears of the medial collateral ligament: magnetic resonance imaging findings and associated injuries. canadian association of radiologists Journal 1993;44:199–204 13. Palmer M, epler M. knee, Chapter 13, p325. In: Fundamentals of musculoskeletal assessment techniques, 2nd edn. lippincott williams and wilkins 1998. IsBn 9780781710077 (£38.70). Buy from Amazon

THE AUTHORS ASHlEy JOnES BSc, MSST A Ashley is a practising sports therapist having graduated from the University of Huddersfield in 2008. During this time his experience has mainly been in professional football where he was head of academy medical services for a football league club for 5 years. Having recently made the transition into full time lecturing, Ashley currently delivers on the BSc Sports and Exercise Therapy course at leeds Beckett University. Ashley also delivers Emergency Aid courses for the Football Association and works within a Sports Injury clinic, when he has the time! Ashley is currently studying towards an MSc in Football Rehabilitation, with research interests being injury-based audits and treatment protocols adopted within professional football. RIcHARD MOSS MSc, GSR R Richard is a graduate sport rehabilitator (GSR) and certified strength and conditioning coach ((cScS). He graduated from the BSc (Hons) Sport Rehabilitation course at the University of Salford PGcE from the University of northampton in 2006, achieving his PG in 2009 and his MSc in Sports Injuries from Manchester Metropolitan University in 2011. He is currently Senior lecturer in Sports Therapy at leeds Beckett University, as well as being a member of the Executive committee of his governing body, BASRaT, in the role of Accreditation Officer. Richard has also worked practically across a variety of sports ranging from youth to professional levels.

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The reLIABLe And PoPuLAr oBjeCTIve AssessMenTs For suCh CondITIons hAve Been shown To hAve PoTenTIAL LIMITATIons KeY poinTs n The common presentation of medial collateral ligament (Mcl) sprains normally includes a transverse sprain. n Mcl injury incidence rates are suggested to be 7.60 per 1000 person years. n Male athletes are thought to be 1.42 times more likely to sustain the injury than female athletes. n Although transverse sprains to the Mcl are more common, the absence of valgus laxity does not discount a longitudinal sprain and should therefore be considered. n diagnosis of a longitudinal sprain to the Mcl suspected by critical reasoning based upon patient assessment findings can be confirmed using imagery. n The most important difference in presentation between transverse and longitudinal Mcl strains are atypical strain pattern signs and symptoms and atypical lack of excessive laxity on passive valgus stress plus the position of pain over the condyle.

n MCL injuries are common, but are they all the same? n Can imaging alone diagnose the injury DISCUSSIONS

and what role do clinical testing skills play? n why is accurate identification of the injury important?

want to share on Twitter? HERE ARE SOME SUGGESTIOnS Tweet this: The most common mechanism of MCL injury is excess valgus stress & external rotation of the knee in high contact sports. Tweet this: optimal tissue healing and rehabilitation requires progressive loading of the healing structures. Tweet this: In longitudinal MCL sprains, pain is more likely to be located over the medial femoral condyle.


Femoroacetabular impingement mechanisms, diagnosis and treatment options using postural restoration®: part 2 This article is Part 2 in a series about femoroacetabular impingement (FAI). The author describes the biomechanics of lumbo-pelvic-femoral dysfunction in relation to FAI as well as methods of diagnosis. This will allow the reader to apply Postural Restoration Institute® clinical assessment skills when diagnosing conditions such as FAI. By JAson mAsek mA, PT ATc cscs PRc

FAI mechAnIsms Introduction




Figure 1: (a) Pincer impingement, (b) cam impingement and (c) mixed impingement. (J. Masek, 2014)


Femoroacetabular impingement (FAI) is recognised as an anatomical discrepancy between the proximal femur and the acetabulum, which may increase the risk of intraarticular hip pathology, including labral tears (1,2) and contribute to the development of groin pain (3). FAI can occur on the acetabular side of the hip, termed ‘pincer impingement’, the femoral side of the hip, termed ‘cam impingement’, or it can occur on both the acetabulum and the proximal femur, termed ‘mixed impingement’ (Fig. 1). In pincer-type FAI, acetabular retroversion is the principle abnormality (4), causing an anterosuperior overhang of the acetabular edge, leading to conflict with the femoral neck upon flexion and internal rotation (3,5,6). Camtype FAI occurs when there is an abnormal femoral head–neck offset (7), or increased bone formation at the femoral head–neck junction. These bony changes are typically anterior and lateral, which causes impingement when the hip is brought into positions requiring large amounts of flexion. Hip muscle strength and hip range of motion (ROM) have been examined in people with labral pathology (8)

and with FAI (9,10,11). These studies all demonstrate reductions in hip muscle strength and hip joint ROM in those with pathology. As the majority of FAI lesions and associated hip pathology occur in the anterior and superior regions of the hip (12), the loads associated with these regions of the hip require consideration. Reduced hip internal rotation, flexion and abduction ROM have been reported in people with symptomatic FAI (10). Given the known strength and ROM impairments associated with FAI, it is not surprising that alterations in normal movement patterns are commonly observed in individuals with FAI. Analysis of functional movement patterns is an essential component of the initial clinical assessment, and findings usually dictate the course of clinical management. However, despite the importance of movement analysis, very little has been published in this area. Although FAI has been characterised, the underlying cause of the observed bony abnormalities has not been determined. The patterns of impairment in the cam and pincer impingements differ considerably and require different pathomechanical explanations. FAI is intuitively a dynamic concern whereby pathology results from abnormal motion of the femur sportEX medicine 2015;65(July):18-25

msK diagnosis, treatment and rehabilitation

relative to the acetabulum and/or the acetabulum relative to the femur. Part One of this series discussed patterns of asymmetry and positional influences of the pelvis as it relates to FAI (13). Part Two of this series reviews traditional FAI biomechanics used by the orthopaedic literature and discusses the proposed biomechanical mechanisms of FAI as described by the Postural Restoration Institute. Objective findings associated with FAI and findings to direct clinical management are also discussed.

FAI and retroversion Evidence suggests that altered position of the innominate plays a role in FAI incidence and progression, and recent studies are beginning to isolate specific mechanical factors that may be of particular importance. The position of the pelvis influences acetabular orientation, in particular pelvic tilt in the sagittal plane (14). Acetabular retroversion has been suggested as a factor leading to FAI (15). Acetabular retroversion has been described as a posterolaterally orientated acetabular opening with reference to the sagittal plane, which is seen as the crossover sign (COS) on standard radiographs (Fig. 2). The COS as seen on a standard anteroposterior (AP) radiograph indicates the presence of acetabular retroversion (4,16). Abnormalities of the acetabulum associated with impingement include excessive cover of the head as seen in acetabular retroversion (4,15). In these hips the femoral neck that is normal impinges against an over-covering acetabulum, resulting in contact between the femoral neck and the acetabular rim. This mechanism has been termed pincer impingement (3,6). Acetabular retroversion has recently been suspected of being an important factor in the development of FAI and hip osteoarthritis (17). Furthermore, changes in acetabular orientation can occur with alterations in pelvic tilt (anterior/ posterior) and pelvic rotation (left/ right). Specifically, changes in anterior and posterior pelvic tilt and with pelvic rotation suggest that the two innominate bones are rotated differently in individuals with sacroiliac dysfunction (17). Cibulka et al. (18) also suggest that

the difference in muscle strength of hip rotators is dependent upon the position that the hip rotator muscle is tested in and the type of hip rotation symmetry or asymmetry that is present. Before muscle testing or strengthening the hip rotator muscles, the presence of joint rotation asymmetries and the effect of joint positioning must be considered. Anterior pelvic tilt and/or acetabular retroversion influences ROM and impingement of the hip. Ross et al. (19) looked at the effect of changes in pelvic tilt on ROM and impingement of the hip. With regard to an anterior pelvic tilt there was a significant loss of 6–9° of hip internal rotation and subsequently an increase in FAI. In contrast, an increase in posterior pelvic tilt resulted in greater hip internal rotation, less impingement and more hip flexion. The results of the study have several clinical implications with regard to pelvic position and FAI. Individuals with limited hip internal rotation may have an increased anterior pelvic tilt; therefore, while assessing hip ROM, pelvic position should be considered. FAI symptoms may be reduced by opposing an anterior pelvic tilt.

FAI and labral tears The differentiation between impingement and labrum tears may be difficult. Both have similar aetiology, although possibly the association of a click or locking may indicate a tear rather than impingement. Conversely, impingement may be a precursor to a labrum tear. It is generally accepted that most labral tears occur in the anterior, anterior-superior, and superior regions of the acetabulum. Fitzgerald noted a 92% incidence of anterior or anterosuperior location of tears in 55 active adult patients reporting a slipping or twisting injury with catching-type pain (20). Seldes et al. (21) found 74% of tears to be in the anterosuperior location, with Byrd (22) also reporting the majority of the lesions occurring at the anterosuperior portion. The repetitive rubbing between the femur and acetabulum is known to cause damage to the anterior aspect of the acetabular labrum and the underlying articular cartilage (6). Seldes et al. found labral lesions to

be a common occurrence. In a study of 55 hips, the author found 96% to have gross labral tears (21). McCarthy explored 54 acetabulae and found 93% to have at least one labral lesion (23,24). Byers et al. investigated 365 hips, finding that 88% of the patients had labral lesions (25). Structural abnormalities occur in combination with labral tears and FAI. Nearly 90% of individuals with labral pathology have an underlying structural abnormality with regard to the femur and/or acetabulum (26,27). Nearly 73% of patients with FAI also had concurrent labral tears (28,29) and 86–94% of labral tears occur anteriorly (29,30). Hyperextension combined with femoral external rotation is the injury pattern most commonly associated with the presentation of acetabular labral tears (31). It is thought that the labrum takes on a weight-bearing role at the extremes of motion with excessive forces leading to tearing (20). Furthermore, sports involving repetitive twisting motions and movements to end-range hyperflexion, hyperextension and abduction are at greater risk (32).







Figure 2: Acetabular retroversion has been described as a posterolaterally orientated acetabular opening with reference to the sagittal plane, which is seen as the crossover sign (COS) on standard radiographs. (J. Masek, 2014)


Figure 3: Left anterior chain (AIC) pattern. With the tendency for anterior tilt and forward rotation of the left hemi-pelvis, the position of the pelvic girdle orients the pelvic girdle to the right causing a shift in one’s centre of gravity to the right. The pelvic girdle is directed into a stance-like AF IR position on the right and AF ER position on the left. (J. Masek, 2014)

Left AIc pattern The relationship between an underlying postural pattern of asymmetry of the lumbo-pelvic-femoral complex has been discussed in the Part 1 (13). For this reason it deserves some general considerations and review as it relates to FAI and its associated pathomechanics. Examination of one’s posture may reveal an increased lumbar lordosis or pelvic obliquity that may account for hip impingement (7,15). Therefore, if the pelvis is more anteriorly rotated, the greater the risk for impingement (15). The presence of asymmetry throughout the pelvic girdle, as described by Hruska, is known as the ‘left anterior interior chain’ (left AIC) pattern (33–35). This pattern calls attention to the tendency for anterior tilt and forward rotation of the left hemi-pelvis. The position of the pelvic girdle orients


the pelvic girdle to the right causing a shift in one’s centre of gravity to the right. The pelvic girdle is directed into a stance-like AF IR (acetabularfemoral internal-rotation) position on the right and AF ER (acetabular-femoral external-rotation) position on the left (Fig. 3). This predominant position orients the sacrum and spine to the right. due to the lack of sufficient left AF IR, secondary to the inadequate activation of the left acetabular-femoral/ femoral-acetabular (AF/FA) rotators, compensatory activity throughout the frontal and transverse planes of the thorax and consequently the right upper extremity will occur. The typical left AIC pattern involves a pattern of pelvic, spinal and diaphragmatic orientation towards the right with compensation usually occurring above the diaphragm (usually T8/T9) rotating the spine back to the left (33–35). Individuals who have acquired a left AIC pattern lose the ability to perform active AF IR on the left and active AF ER on the right (Fig. 4). This leads to compensatory activity of the femur as it relates to acetabular position. With regards to a left AIC non-compensatory patterned pelvis, the femurs would orientate themselves inwardly on the left and outwardly on the right secondary to the passively orientated position of the respective acetabulum (Fig. 4b). In other words, the left acetabulum is rotating forward on an internally rotated positioned femur and compensatory femoral external rotation on an inwardly orientated positioned acetabulum has to occur for forward progression. likewise, the


right acetabulum is rotating backward on an externally positioned femur and compensatory femoral internal rotation on an outwardly orientated positioned acetabulum also has to occur for forward progression (Fig. 4a). The left hemi-pelvis has become positioned anteriorly in the sagittal plane, abducted in the frontal plane, and externally rotated in the transverse plane. left lumbo-pelvic-femoral musculature such as the hamstrings, left gluteus medius, and left ischiocondylar adductor, have lost their optimal mechanical advantage/leverage to correctly function. The reverse is true on the right. The right hemi-pelvis has become positioned posteriorly in the sagittal plane, adducted in the frontal plane, and internally rotated in the transverse plane. From a Postural Restoration® perspective it is the intent to restore the left hemi-pelvis into a state of left AF IR and the right hemi-pelvis to a state of right AF ER. Along with restoring pelvic position, femoral compensatory activity is reduced so that normal femoral internal rotation on the left and femoral external rotation on the right (Fig. 4c).

FAI and Postural Restoration® The Postural Restoration Institute® has proposed two common types of hip impingement: anterosuperior acetabular-femoral impingement (ASAF); and anteromedial femoralacetabular impingement (AMFA) (34). Comparisons are similar to the traditional cam and pincer types used in traditional orthopaedic literature. With regards to Postural Restoration®,


Figure 4: (a) Right hemi-pelvis positioned posteriorly, adducted, and internally rotated with right compensatory femoral internal rotation. Left hemi-pelvis positioned anteriorly, abducted and externally rotated with left compensatory femoral external rotation. (b) Right hemi-pelvis positioned posteriorly, adducted, and internally rotated with right femur orientated outwardly. Left hemi-pelvis positioned anteriorly, abducted and externally rotated with left femur orientated inwardly. (c) Right hemi-pelvis positioned anteriorly, abducted and exteranally rotated with right compensatory femoral external rotation. Left hemi-pelvis positioned posteriorly, adducted, and internally rotated with left compensatory femoral internal rotation. (J. Masek, 2014)


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ASAF is similar to the cam type of impingement and usually occurs on the left side. AMFA, however, is similar to pincer type and usually occurs on the right side. The Postural Restoration Institute® differentiates the types of impingements with regards to the side of the respective hemipelvis, mechanisms, diagnosis and management of the aforementioned types of impingement. Furthermore, it is not unlikely to have a mixed type of impingement that could occur on either the right or left side. Anterosuperior acetabular-femoral impingement (ASAF) ASAF is most often seen on the left side when the individual attempts to ‘shift’ or pull their femur into the acetabulum with the ischiocondylar adductor. Contributing factors include an anteriorly rotated, forwardly positioned left innominate with laxity of the iliofemoral and pubofemoral ligament structures. Often times these individuals present with, and are not limited to, long and weak adductors, overactive FA external rotators and abductors, weak AF extensors, and overactive FA hip flexors (tensor fascia latae) acting as femoral-acetabular internal rotators. Common clinical findings are: positive left adduction drop test (Fig. 5); positive or negative left extension drop test (Fig. 6); and increased left seated femoralacetabular external rotation (Fig. 7). An individual with a left AIC pattern will demonstrate an anterior tilt and forward rotation of the left hemipelvis. As a result of this position, the individual will usually demonstrate weakness and lengthening of specific muscles in all three planes on the left and right side. Individuals with a left AIC pattern will usually demonstrate decreased left FA IR secondary to acetabular position. The patient’s left femur or leg is abducted if in a left AIC pattern or left AF ER position. This is noted when the individual is placed in a seated position with the legs directly in front of the examiner. The left femur will hit the posterior inferior rim of the acetabulum upon FA IR. Because of the acetabularfemoral position (AF ER) on the left side, the individual must compensate

by recruiting the femoral-acetabular (FA) external rotators to orientate the femur towards midline to ambulate (Fig. 3) (33–35). The joints of the lumbo-pelvicfemoral complex are also stabilised by a dense system of ligaments. The femoroacetabular joint is reinforced by the strong spiral iliofemoral, ischiofemoral and pubofemoral ligaments. The iliofemoral ligament is made up of two bands resembling a ‘y’ that prevent hyperextension of the femoroacetabular joint. Furthermore, the lateral band of iliofemoral ligament limits adduction, whereas the medial band of iliofemoral ligament limits lateral rotation. The pubofemoral ligament tightens during extension and abduction of the femoroacetabular joint (the pubofemoral ligament prevents excessive abduction of the hip joint). It appears logical that if ligaments are compromised secondary to compensatory activity, the femoroacetabular joint will become unstable and if the muscles are compromised secondary to compensatory activity, pelvic-femoral dysfunction will result. Thus an individual may present with a compromised iliofemoral and pubofemoral ligament secondary to compensatory external rotation of the lumbo-pelvic-femoral complex. Because of the flexed, abducted, and externally rotated left hemi-pelvis there is accompanying extension, adduction and internal rotation weakness. This occurs as a result of passive internal orientation of the femur secondary to the acetabular position and/or as a result of compensatory activity of the external rotators to orientate the femur towards midline. The lower extremity on the contralateral side of the rotated pelvis would most likely demonstrate external rotational weakness secondary to the orientation of the acetabulum on the femur. left anterosuperior acetabularfemoral impingement usually occurs in the stance phase of gait, when the support limb is placed in adduction and internal rotation. due to the fact that the left hemi-pelvis is in a state of flexion, abduction, and external rotation, there is a recurring contact between the anterior femoral head– neck region and the anterior aspect

Figure 5: Positive left-side adduction drop test. (J. Masek, 2014)

Figure 6: Positive left-side extension drop test. (J. Masek, 2014)

Figure 7: Increased left-side seated femoral acetabular external rotation (FA ER). (J. Masek, 2014)

of the acetabular rim and/or labrum during extreme hip flexion and internal rotation movements during this phase. These findings are consistent with Mason (31) in which he postulates that femoral external rotation is the injury pattern most commonly associated with anterior hip pathology in that this may be due to a slight subluxation and subsequent glide of the femoral head onto the anterior acetabular labrum. Anteromedial femoral-acetabular impingement (AMFA) AMFA is often seen on the right side. A left AIC patterned individual with a right AF IR positioned acetabulum will demonstrate impingement of the right femur on the acetabulum upon femoralacetabular compensatory internal rotation. Contributing factors include an anteriorly rotated, forwardly positioned left innominate, right posterior capsular instability, weak inferior gluteus maximus, and laxity of the ischiofemoral ligament and tightness of the adductor musculature on the right. Common clinical findings include: decreased right FA ER (Fig. 8), increased FA IR (Fig. 9) and decreased right passive FA abduction (Fig. 10). 21

due to the extended, adducted and internally rotated right hemi-pelvis there is accompanying flexion, abduction and external rotational weakness secondary acetabular-femoral orientated position. This occurs as a result of the passively external orientated appearance of the femur secondary to the acetabular position. Therefore, compensatory activity of the internal rotators occurs to orientate the femur towards midline because of the acetabular position of the right hemi-pelvis. Thus, the right femur will ‘impinge’ on the anterior, superior and medial acetabular rim upon FA ER (Fig. 3). Right anteromedial femoralacetabular impingement usually occurs in the stance phase of gait, when the support limb is placed in adduction and internal rotation and is preparing for the swing phase of gait. due to acetabular position of the right hemi-pelvis and the inability for the femur to abduct and externally rotate impingement will most likely result during the late stance phase of the gait cycle and/or early swing phase. In summary, many individuals suffer from hip impingement as a Figure 8: Decreased right-side FA ER. (J. Masek, 2014)

Figure 9: Increased right-side FA IR. (J. Masek, 2014)

Figure 10: Decreased right-side passive abduction. (J. Masek, 2014)


result of poor acetabular position and from compensatory femoralacetabular activity secondary to acetabular position. Often, even the slightest deviations result in poor distribution of forces to the lumbopelvic-femoral complex, which in turn leads to strain patterns as the pelvic girdle compensates for these forces in the least favourable way. These adaptive firing patterns may occur as a result of improper lower extremity pathomechanics, which influence further compensations.

FAI dIAgnosIs gait One of the easiest ways to determine if an individual is in pain is to watch the way they move. And perhaps the most commonly observed and universal movement pattern is gait. From a subtle loss of trunk rotation or pelvic translation to a gross loss of reciprocal gait, a dynamic assessment of walking is a very valuable. The hip plays an important role in normal walking and running and, thus, gait is usually significantly affected by hip pathology. The restoration of normal gait function is essential to the overall treatment plan. There are two phases in the normal gate cycle: the stance phase, when the foot is on the ground; and the swing phase, when the foot is moving forward. Most hip problems become noticeable in the stance phase (36). Peak acetabular pressure (throughout the acetabulum) has been observed during terminal stance (37). The hip moves in a combination of three basic planes: flexion and extension, abduction and adduction, and external rotation and internal rotation. The pelvis rotates in the transverse plane during the gait cycle. The pelvis rotates forward on the swing side, whereas it rotates backward on the stance side. That is, as the right limb swings forward, the right hemipelvis also moves forward so that the pelvis rotates to the left. during stance for the right limb, the pelvis rotates to the right. during swing and stance phases of gait both the femur and pelvis should be rotating on each other simultaneously. Some of this rotation is AF IR and some is AF ER. Stance

phase can be divided into two halves. The first half begins just after heel contact as the body’s centre of mass is moving forward, toward the foot that just contacted the ground. The body is essentially shifting its centre of gravity over the supporting lower extremity as the pelvis, femur and tibia are all rotating internally in the transverse plane. This is a normal gait cycle called AF IR; the acetabulum is rotating internally over the femur. AF IR motion continues until midstance where the hemi-pelvis is in a maximum amount of AF IR position. After midstance the pelvis, femur and tibia reverse their direction and begin to externally rotate as the centre of mass starts moving toward the other leg which is still in swing phase. External rotation occurs until toe-off. This is a normal cycle of gait called AF ER (Fig. 4). yang et al. (38) suggests that during normal human gait there is interdependence between the movements of the thorax, lumbar region and pelvis. Furthermore pelvic rotation dictates trunk rotation in the transverse plane during gait and pelvis dysfunction would magnify the disruption of coordination between the thorax, lumbar spine and pelvis contributing to inefficient gait. Kennedy et al. demonstrated differences in gait characteristics between those with and without FAI, and showed that those with FAI exhibited reduced frontal plane ROM at the hip joint and the pelvis (39). Hunt et al. recently reported that individuals with FAI walked significantly slower and displayed decreased peak extension, adduction, and internal rotation angles (11). This is consistent with PRI findings suggesting the inability to reciprocate from AFIR to AFER as well as adduction to abduction in the frontal plane. Hunt shows that previous opinions about gait are incorrect (11). The study compared the gait of healthy controls to those with FAI hypothesising that gait abnormalities would resolve after surgery. Gait measurements were obtained both preoperatively and postoperatively. The study found that pre-surgical gait abnormalities did not automatically resolve after surgery. Furthermore, surgical patients did not only retain their old faulty, painful sportEX medicine 2015;65(July):18-25

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gait patterns, but also adopted new deficiencies that resulted after surgery, such as those arising from scar tissue, soft tissue pathology, neuromuscular patterning, or loss of arthrokinematic motion in the hip. Hunt’s study highlights the significance of early intervention for physical therapy with both operative and non-operative individuals. Although the patients in the study who underwent FAI surgery did exhibit decreased pain, non-optimal preoperative gait patterns that persisted postoperatively most likely pre-disposed these individuals for re-injury or related comorbidities to the lumbo-pelvic-femoral complex such as pelvic pain, back pain or sacroiliac joint dysfunction.

special tests Strength and ROM deficits as a result of altered pelvic and hip position are a common finding associated with FAI. Furthermore, Cibulka et al. (18) suggest that before muscle testing or strengthening the hip rotator muscles, the presence of joint rotational asymmetries and the effect of joint positioning must be considered. Therefore, the Postural Restoration Institute® has formulated a series of assessments using a triplanar examinational approach in attempt to quantify pelvic position in all three respective planes. Clinical experience has demonstrated that this battery of assessments provides useful information that allows specific management considerations for FAI. Sagittal plane limited sagittal pelvic ROM occurs in individuals with FAI. Attempts to increase hip flexion and internal rotation not compensated for by the increased motion through one or both hemi-pelvis(es) may also result in secondary strain/injury to the lumbar spine in attempt to cover the acetabulum over the femoral head with an anterior pelvic tilt. limited hip extension flexibility has been proposed as one possible cause of increased anterior pelvic tilt and lumbar lordosis (40). This is commonly assessed clinically using the extension drop test. Extension drop test For this test, the subject will sit at

the end of a table and roll backwards on the table while holding both knees to their chest. This position ensures that the pelvis is posteriorly rotated and the spine is flexed. The examiner holds one hip in maximum flexion while the limb to be measured is slowly lowered towards the table in a relaxed position. A positive test is indicative of the inability of the respective hip to extend horizontally level with the table. Furthermore the inability to extend one or both hemi-pelvis(es) is indicative of an anterior pelvic tilt or a forwardly rotated hemi-pelvis (Figs 6 & 11). Passive straight leg raise The hamstrings are directly involved in the movements of the hip and knee joints. This group performs an important role in the anteroposterior pelvic tilt, indirectly affecting lumbar lordosis. Therefore, altered length and/ or flexibility of the hamstrings may produce significant postural deviations and affect the functionality as well as position of the hip joint and lumbar spine. The passive straight leg raise can be considered as an objective measurement of flexibility and/or length of the hamstrings (41), possibly possessing clinical validity (42). To perform the passive straight leg raise place the subject in a supine position on a table or floor with both legs extended with their lower back and sacrum being flat against the table or floor. Slowly raise one leg, asking the subject to keep their knee loosely extended throughout the movement. Continue to raise the leg until firm pressure and or resistance is felt. From a postural restoration standpoint, when each respective leg is raised, they should not exceed and/or be limited to 90°. If the individual exceeds 90° this would most likely suggest overstretched hamstrings and possible lumbar and/or hip pathology. If the individual is limited, this suggests that when the clinician lifts the leg for the passive straight leg raise the hamstring becomes taut at an earlier point than it should because the muscle is already pre-lengthened due to the position of the pelvis (anterior pelvic tilt). In other words, the leg won’t go as far because it’s already being stretched before it even moves. Positionally, the

Figure 11: Negative right-side extension drop test (J. Masek, 2014)


Figure 12a: Passive straight leg raise showing (a) 60–70° flexion with the left leg and (b) 90° on right. (J. Masek, 2014)


tightness may be felt in the hamstrings but the hamstring is not shortened – it is lengthened and it may be related instead to the position of the pelvis or anterior pelvic tilt on the respective hemi-pelvis (Fig. 12). Frontal and sagittal plane Adduction drop test (Ober’s test) This test assesses the individual’s ability to extend and adduct the femoroacetabular joint. lay the individual on their side with the lower leg and hip flexed (90°). Then passively abduct and extend the individual’s upper leg, with the knee flexed to 90°. Slowly lower the upper limb, if a contracture is present, the leg will remain abducted and not fall to the table. Moreover, this test suggests that the contact of the posterior inferior femoral neck on the posterior inferior rim of the acetabulum does allow the femur to adduct; possibly secondarily to an anteriorly


Figure 13: Negative right adduction drop test. (J. Masek, 2014)

Figure 14: Increased left passive abduction. (J. Masek, 2014)

rotated, forward hemi-pelvis that is usually seen on the left in a left AIC patterned individual. An adduction drop test (Ober’s test) may indicate a lumbo-pelvic-femoral complex that is in a sub-optimal position. This clinical reasoning would suggest that traditional clinical reasoning regarding the Ober’s test (that a positive test indicates short muscle requiring passive stretching) may need to be reconsidered (Figs 5 & 13) (43). Frontal plane Passive abduction raise test The patient lies on his or her side with their bottom knee and hip flexed at 70–90°. Their top knee and hip will remain straight (0° of hip flexion). Passively stabilise the patient’s innominate with one hand as the other hand passively moves their leg into abduction. Standing behind the patient usually provides more examiner biomechanical comfort in lifting the leg. Patients with tight right intercostal walls and short and strong right adductors will demonstrate limited passive abduction when compared to the other side. usually the examiner will feel lateral buttressing of the femoral head on the lateral superior acetabulum as the femur is abducted. When right thoracic abduction or side bending occurs, discontinue the test. A positive test is indicated by a restriction on one or both sides that does not allow sufficient abduction. This is usually seen on the right side especially if left adduction drop test is positive in a left 24

AIC oriented individual (Figs 10 & 14). Transverse plane Range of motion In an impinged hip, the contact between a widened femoral neck, an abnormally shaped or oriented acetabulum, or both typically results in decreased ROM of the joint. Specifically, motions requiring hip flexion in combination with adduction and internal rotation, such as getting into a low vehicle, are most frequently affected in those with FAI and result in the most consistent reports of pain (3). Individuals with FAI develop a reduction in functional ROM leading to high impaction loads at terminal ranges. These increased forces result in compensatory effects on bony and soft tissue structures within the femoroacetabular joint (hip joint) and respective hemi-pelvises. These structural mechanics lead to abnormal stress and asymmetric loads between the femoral head and the acetabulum. dynamic factors may contribute to hip pain as abnormal stress and contact between the femoral head and acetabulum rim occur with hip motion (44). Individuals with left anterosuperior acetabular-femoral impingement usually demonstrate decreased left FA IR and increased left FA ER (Fig. 7). Anteromedial femoral-acetabular impingement (AMFA) is often seen on the right side. Common clinical findings include: decreased right FA ER (Fig. 8), and increased FA IR (Fig. 9).

summARy Optimal alignment of the femur and its position in relation to the acetabulum has marked clinical implications in regards to the lumbo-pelvic-femoral complex. likewise, the acetabulum’s position has clinical implications as well. It is the author’s opinion that the acetabulum orientation has a greater impact on clinical decision making than activity that appears positionally oriented but actually is compensatory in nature. What becomes essential is to match the clinical signs and symptoms to the structural or biomechanical abnormalities in order to arrive at a possible explanation for the cause and pathomechanics of the particular musculoskeletal disorder in question. The better we understand and appreciate the underlying causes

and mechanism of FAI, the better we will be prepared to develop more progressive interventions for this common condition. In Part Three of this series I will propose management considerations for FAI using Postural Restoration®.

online References Owing to space limitations in the print version, the references that accompany this article are available at the following link and are also appended to the end of the article in the web and mobile versions. Click here to access the references

FuRTheR ResouRces 1. Hruska clinic website http://www. 2. Postural Restoration Institute website Th AuThoR ThE JAson mAsek mA, PT J ATc cscs PRc AT Jason Masek completed his degree in Physical Therapy from Des Moines university-osteopathic Medical Center in Des Moines, Iowa, uSA. he received his athletic training experience from the university of Nebraska-Lincoln and the university of Minnesota. Jason currently practices at the hruska Clinic™ Restorative Physical Therapy Services in Lincoln, Nebraska, uSA. Jason has developed a strong background in sports medicine and athletic injuries with an emphasis in manual physical therapy. he is a member of the National Athletic Trainers Association, the National Strength & Conditioning Association. Jason has earned the designation of Postural Restoration Certified (PRC) as a result of advanced training, extraordinary interest and devotion to the science of postural adaptation, asymmetrical patterns and the influence of polyarticular chains of muscles on the human body as defined by the Postural Restoration Institute® in Lincoln, Nebraska, uSA. sportEX medicine 2015;65(July):18-25

msK diagnosis, treatment and rehabilitation

n Name and describe the two types of femoroacetabular impingement described by the Postural Restoration Institute®. n What is the left AIC chain pattern and what are the mechanical factors that relate to FAI? n does pelvic asymmetry cause FAI?


Want to share on Twitter? hERE ARE SoME SuggESTIoNS Tweet this: With the strength and ROM impairments in FAI, it is not surprising that abnormal movement patterns are commonly seen. Tweet this: Anterior pelvic tilt and/or acetabular retroversion influences ROM and impingement of the hip. Tweet this: A left AIC pattern causes weakening of specific muscles in all three planes on the left and right side. Tweet this: Gait analysis is a valuable tool in FAI assessment. Tweet this: Biomechanical assessment of FAI needs to be done in all three planes.

key PoInTs n cam and pincer impingements differ considerably and require different pathomechanical explanations. n AsAF is similar to the cam-type impingement as it relates to PRI. n AmFA is similar to the pincer-type impingement as it relates to PRI. n Pelvic asymmetry and acetabular orientation have a profound effect on femoral compensations. n The position of the pelvis, in particular pelvic tilt in the sagittal plane, is an important factor. n The presence of pelvic asymmetries and the effect of acetabular position/orientation must be considered before muscle testing or strengthening. n The typical left AIc pattern involves a pattern of pelvic, spinal and diaphragmatic orientation towards the right, with compensation usually occurring above the diaphragm (usually T8/T9) rotating the spine back to the left. n gait is a normal mechanical process in daily function. Therefore, normal gait mechanics allows one to assess abnormal movement patterns as it relates to FAI. n gait abnormalities do not automatically resolve after surgery, suggesting that the mechanical issues present before surgery have not been resolved. n The Postural Restoration Institute® has formulated a series of assessments using a triplanar examinational approach.

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Femoroacetabular impingement mechanisms, diagnosis and treatment options using postural restoration®: part 2


References 1. Beck M, Kalhor M, et al. Hip morphology influences the pattern of damage to the acetabular cartilage. Femoroacetabular impingement as a cause of early osteoarthritis of the hip. Journal of bone & Joint surgery (br) 2005;87:1012–1018 2. Philippon MJ, Weiss dR, et al. Arthroscopic labral repair and treatment of femoroacetabular impingement in professional hockey players. american Journal of sports medicine 2010;38:99–104 3. Ganz R, Parvizi J, et al. Femoroacetabular impingement: a cause for osteoarthritis of the hip. clinical orthopaedics and related research 2003;417:112–120 4. Siebenrock KA, Schoeniger R, Ganz R. Anterior femoro-acetabular impingement due to acetabular retroversion: treatment and peri-articular osteotomy. Journal of bone and Joint surgery (am) 2003;85-a(2):278–286 5. Husson Jl, Mallet JF, et al. Applications in hip pathology. orthopaedics & traumatology: surgery & research 2010;965:s10–s16 6. Beck M, leunig M, et al. Anterior femoroacetabular impingement: mid-term results of surgical treatment. clinical orthopaedics and related research 2004;418:67–73 7. Ito K, Minka MA, et al. Femoroacetabular impingement and the cam-effect. A MRI-based quantitative anatomical study of the femoral head-neck offset. Journal of bone & Joint surgery (br) 2001;83:171–176 8. yazbek PM, Ovanessian v, et al. Nonsurgical treatment of acetabular labrum tears: a case series. Journal of orthopaedic & sports physical therapy 2011;41:346–353 9. Casartelli NC, Maffiuletti NA, et al. Hip muscle weakness in patients with symptomatic femoroacetabular impingement. osteoarthritis and cartilage 2011;19:816–821 10. Nussbaumer S, leunig M, et al. validity and test-retest reliability of manual goniometers for measuring passive hip range of motion in femoroacetabular impingement patients. bmc musculoskeletal disorders 2010;11:194–204 11. Hunt MA, Guenther JR, Gilbart MK. Kinematic and kinetic differences during walking in patients with and without symptomatic femoroacetabular impingement. clinical biomechanics 2013;28(5):519–523 12. Allen d, Beaulé PE, et al. Prevalence of associated deformities and hip pain in patients with cam-type femoroacetabular impingement. Journal of bone & Joint surgery (br) 2009;91:589–594 13. Masek J. Femoroacetabular impingement mechanisms, diagnosis and treatment options using Postural Restoration: part 1. sporteX medicine 2015;64:10–18 14. ul Islam S, dandachli W, Witt J. Pelvic tilt and acetabular orientation: can the effect


be quantified? the bone & Joint Journal 2013;95-b(supp 1):227 15. Reynolds d, lucas J, Klaue. Retroversion of the acetabulum: a cause of hip pain. Journal of bone and Joint surgery (br) 1999;81b:281–288 16. Myers SR, Eijer H, Ganz R. Anterior femoroacetabular impingement after periacetabular osteotomy. clinical orthopaedics and related research 1999;(363):93–99 17. Cibulka M. Sacroiliac joint dysfunction as a reason for the development of acetabular retroversion: a new theory. physiotherapy theory and practice 2014;30(4):249–253 18. Cibulka MT, Strube MJ, et al. Symmetrical and asymmetrical hip rotation and its relationship to hip rotator muscle strength. clinical biomechanics 2010;25(1):56–62 19. Ross JR, Nepple JJ, et al. Effect of changes in pelvic tilt on range of motion to impingement and radiographic parameters of acetabular morphologic characteristics. american Journal of sports medicine 2014;42(10):2402–2409 20. Fitzgerald RH Jr. Acetabular labral tears diagnosis and treatment. clinical orthopaedics and related research 1995;311:60–68 21. Seldes RM, Tan v, et al. Anatomy, histologic features and vascularity of the adult labrum. clinics in orthopedics 2001;382:232–240 22. Byrd JW. labral lesions: an elusive source of hip pain case reports and literature review. Journal of arthroscopy and Joint surgery 1996;12:603–612 23. McCarthy J, Noble P, et al. Anatomy, pathologic features and treatment of acetabular labral tears. clinics in orthopedics 2003;406:38–47 24. lewis Cl, Sahrmann SA. Acetabular labral tears. physical therapy 2006;86(1):110–21 25. Byers Pd, Contepoi, CA, Farkas TA. A post mortem study of the hip joint. annals of the rheumatic diseases 1970;29:15–31 26. dolan MM, Heyworth BE, et al. CT reveals a high incidence of osseous abnormalities in hips with labral tears. clinical orthopaedics and related research. 2011 mar;469 (3):831–838 27. Wenger dE, Kendell KR, et al. Acetabular labral tears rarely occur in the absence of bony abnormalities. clinical orthopaedics and related research 2004;426:145–150 28. Kang C, Hwang dS, Cha SM. Acetabular labral tears in patients with sports injury. clinics in orthopedic surgery 2009;1(4):230–235 29. McCarthy JC, Noble PC, et al. The Otto E. Aufranc Award: The role of labral lesions to development of early degenerative hip disease. clinical orthopaedics and related research 2001;393:25–37

30. Mintz dN, Hooper T, et al. Magnetic resonance imaging of the hip: detection of labral and chondral abnormalities using noncontrast imaging. arthroscopy 2005;21(4):385–393 31. Mason JB. Acetabular labral tears in athletes. clinics in sports medicine 2001;20:779–791 32. Schmerl M, Pollard H, Hoskins W. labral injuries of the hip: A review of diagnosis and management. Journal of manipulative and physiological therapeutics 2005;28(8):632 33. Hruska RJ. Myokinematic Restoration. An integrated approach to treatment of lower half musculoskeletal dysfunction. postural restoration institute course manual 2014 34. Hruska RJ. Advanced Integration. postural restoration institute course manual 2014 35. Hruska RJ. Impingement and instability. postural restoration institute course manual 2014 36. Balderston R, Rothman RH, et al. The hip, pp234–236. lea & Febiger 1992. ISBN: 978-0812113020. Buy from Amazon 37. Krebs dE, Robbins CE, et al. Hip biomechanics during gait. Journal of orthopaedic & sports physical therapy 1998;28(1):51–59 38. yang yT, yoshida y, et al. Interaction between thorax, lumbar, and pelvis movements in the transverse plane during gait at three velocities. Journal of applied biomechanics 2013 Jun;29(3):261–269 39. Kennedy MJ, lamontagne M, Beaulé PE. Femoroacetabular impingement alters hip and pelvic biomechanics during gait: Walking biomechanics of FAI. gait & posture 2009;30(1):41–44 40. Schache AG, Blanch Pd, Murphy AT. Relation of anterior pelvic tilt during running to clinical and kinematic measures of hip extension. british Journal of sports medicine 2000;34 (4):279–283 41. Gajdosik Rl, Rieck MA, et al. Comparison of four clinical tests for assessing hamstring muscle length. Journal of orthopaedic & sports physical therapy 1993;18(5):614– 618 42. Gajdosik Rl. Passive extensibility of skeletal muscle: review of the literature with clinical implications. clinical biomechanics 2001;16:87–101 43. Tenney HR, Boyle Kl, deBord A. Influence of hamstring and abdominal muscle activation on a positive Ober’s test in people with lumbopelvic pain. physiotherapy canada 2013;65(1);4–11 44. Hammoud S, Bedi A, et al. The recognition and evaluation of patterns of compensatory injury in patients with mechanical hip pain. sports health 2014;6(2):108–118.

sportEX medicine 2015;65(July):18-25

ConCussion in sport puTTInG ThE GuIdElInES InTo ACTIon Concussion in sport has received a lot of attention in recent years, particularly within the media, and the pressure put on clinicians to get it right is immense. Within sport there are so many interested parties, the patient, the coach, the team and the fans, that assessing concussion can be difficult. This article brings together the resources and evidence available to help you put current guidelines into practice. It also points you in the right direction to find any more information that you might want. By Dr Sarah Morton MBBS

IntroDuctIon Concussion has had a lot of publicity recently within the media, although this is not a new area of concern. Back in 2013, concussion hit the headlines in rugby when George Smith, an Australian rugby player, was allowed to continue playing despite what appeared to be obvious concussion to the public watching on TV (Video 1). Indeed the England full back Mike Brown diagnosed the concussion online (Fig. 1) – although he himself has recently said he was tempted to lie over his own concussion (Video 2) to avoid missing

Twitter comments from July 2013 regarding George Smith’s concussion. (Twitter, 2013)


games in the 2015 Six nations (1). And Mike Brown was not the only victim of concussion during the Six nations. George north, the Welsh winger, has also received a lot of media attention for being knocked out twice within the same match (Video 3). despite going off for concussion checks initially, north returned to the field of play and was knocked unconscious again bringing about a lot of media interest, including Brian Moore stating that the Welsh Rugby union should be punished for the handling of the situation (2). The Welsh Rugby union later admitted that if they had seen the initial incident they would not have allowed him to return to the field of play (3). dr Jamie Roberts, one of north’s team mates, believes the fallout from this incident will make the game safer (3). however, to make matters worse, north has subsequently been knocked out again, this time in a club match. Such is the publicity now surrounding concussion that the sports pages are full of stories such as the fact that George north has been ordered to take 1 month off rugby (4). And it is not only the rugby pages that are full of stories. There have been high profile stories regarding Fernando Alonso suffering concussion in a F1 practice crash (5), Audley harrison ending his boxing career due to head injuries (6) and within nFl (national

Football league) the cost from head injuries have been rising (7, 8). Back in 2013, Barry o’driscoll, the exInternational Rugby Board Medial officer resigned because of concussion stating: “My views on suspected concussion in rugby are well known and documented within the IRB [now known as World Rugby]. They were the reason for my resignation. The 5-minute assessment of a player who has demonstrated distinct signs of concussion for 60 to 90 seconds and usually longer, is totally discredited. There is no scientific, medical or rugby basis for the safety of this process. This experiment, which is employed by no other sport in the world, is returning the player to what is an extremely brutal arena.” So what does this mean for us as clinicians today? how are we supposed to support our patients and make the correct decision for them, especially under such intense scrutiny from the media, and, as a result, the general public?

DefInItIon of concuSSIon The Zurich 2012 Concussion Consensus statement defined concussion as ‘a brain injury’ that is ‘a complex pathophysiological process affecting the brain, induced by biomechanical forces’ (9). It reports that concussion is a functional disturbance without any changes seen by standard imaging sportEX medicine 2015;65(July):26-32

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taBle 1: SIgnS anD SyMPtoMS of concuSSIon aS laID out By the ZurIch conSenSuS 2012.


[S. Morton 2015, sourced from McCrory p, et al., 2013 (9)] examples Symptoms Symptoms

Somatic eg. headache Cognitive eg. ‘feeling like a fog’ Emotional eg. labile

Physical signs Physical signs

loss of consciousness loss of memory

Behavioural changes Behavioural changes cognitive impairment cognitive impairment Sleep disturbance Sleep disturbance


Video 1: The George Smith vs Richard Hibbard headclash (Courtesy of YouTube user Rugbydump Clips).

Slowed reaction times unable to sleep

techniques. The American Medical Society for Sports Medicine also laid out a similar definition for concussion in 2013: “concussion is defined as a traumatically induced transient disturbance of brain function” (10). Both statements, therefore, agree that concussion is a shortterm condition that does not result in structural brain damage. however, it is also recognised that it is a spectrum and concussion is likely to be the mild end of the brain injury spectrum (11). There is, therefore, limited need for any brain imaging, unless other diagnoses are suspected, for example an intracranial haemorrhage or a skull fracture (9). There is some indication that functional magnetic resonance imaging can be used to correlate symptoms with the likely recovery time (9). however, although imaging may be useful for a research situation, this is unlikely to add useful information to your clinical examination and/or management. The signs and symptoms of concussion, as defined by the Zurich Consensus, are laid out in Table 1 (9). Although it is helpful to outline these signs and symptoms there are many overlaps with other conditions. It should also not be forgotten that there are nICE (The national Institute for health and Care Excellence) guidelines for head injury that place importance on assessing whether the head injury is low or high risk for a clinically important brain injury and/or a cervical spine injury, something that should not be forgotten (12). The guidelines for requiring a computed tomography (CT) head scan within 1 hour are clearly outlined as: GCS (Glasgow Coma Scale – see Table

If you have a current subscription, login at to view this video, download the mobile app which is free to subscribers with online access or use the links below where provided.

2) less than 13 on initial assessment, GCS less than 15 2-hours post-injury, suspected open, depressed or basal skull fracture, post-traumatic seizure, focal neurological deficit and more than one episode of vomiting (12). Therefore, examination is crucial and should include the following as a bare minimum: a careful examination of the head to look for signs of basal skull fracture (such as panda eyes) and any obvious depressed fractures and a full neurological examination including upper limbs, lower limbs and the cranial nerves. Although this is possible in an A&E setting, it is appreciated that these checks cannot be realistically performed pitch side. The decision, therefore, is whether or not the player is safe to play on and not whether a CT scan is required (although as a sign of severity on the injury spectrum, if any of those criteria are met the decision is easily made – take your patient off the pitch and take them to hospital immediately). If there are concerns about the mechanism of injury then the full examination should be performed when the player is off the pitch.

Video 2: Mike Brown collides with Andrea Masi, England v Italy, 14th Feb 2015 (Courtesy of YouTube user RBS 6 Nations).

Video 3: George North knocked out twice against England | Six Nations 2015. (Courtesy of YouTube user Rugby Riot).

PItch-SIDe aSSeSSMent anD evaluatIon pitch-side evaluation testing has been improving over the past few years. The Standardised Assessment of Concussion Tools (SCAT) is now in its 3rd edition


and is supported by the majority of large sporting bodies (13). SCAT testing combines various concussion measures including the Maddocks Questions and the Balance Error Scoring System (10). SCAT3 has been developed for all athletes aged 13 and over; there is a separate child SCAT3 for anyone under the age of 13. A pdF is available from the British Journal of Sports Medicine which outlines exactly how to proceed through the test (Further resources 1). It includes details for both the examiner and the athlete. It is aimed at medically trained professionals only – there is a separate Sport Concussion Recognition Tool for the general public (13). World Rugby (formerly the International Rugby Board (IRB)) initially developed a pitch Side Concussion Assessment Tool (pSCA) to try and establish a multi-modal assessment (14). Interestingly it was developed for pitch-

taBle 2: glaSgow coMa Scale. [S. Morton 2015, sourced from Teasdale & Jennett, 1974 (18)] Score 4 3 2 1

Behaviour Eye opening

response Spontaneously To speech To pain no response

Best verbal response

orientated to time/place/person Confused Inappropriate word Incomprehensible sounds no response

5 4 3 2 1

Best motor response

obeys commands Moves to localised pain Flexion withdrawal from pain Abnormal flexion to pain (decorticate) Abnormal extension to pain (decerebrate) no response

6 5 4 3 2 1

taBle 3: MaDDockS ScorIng SySteM uSeD In Both Scat anD PSca toolS. [S. Morton 2015, sourced from SCAT3 (13), Fuller et al., 2015 (14) and SCAT2 (15)] Question


side use rather than on the pitch use (14). This initially corresponded with the introduction of the 5-minute concussion assessment reversible substitution in Rugby union, where a player could leave the pitch for up to 5 minutes to be assessed and if they are found not to have concussion following that assessment they can return to the field of play within that 5 minutes. The pSCA included the Maddocks score (Table 3), a tandem balance test and symptomatic questions as well as judgements to be made by the team doctor. A pdF of the test is available - see Further resources 2. The test also includes the use of the SCAT2 (the forerunner of SCAT3 in use of athletes aged 10 and above – see Further resources 1) post- match and comparing it to the baseline SCAT2 score to that player (see below for baseline cognitive testing) (14,15). A recent pilot study of the pSCA tool showed a sensitivity of 84.6% and specificity of 74% for identifying players who later went on to be confirmed as having concussion (14). This suggests that it is a useful tool, although the authors of the study do recognise more work is needed around standardising the assessment post-match and training medical professionals as to how to undertake the test (14). Since 2014 World Rugby has used the head Injury Assessment Tool (hIA), a development from the pSCA (Further resources 3). It still includes the Maddocks score (Table 3), the tandem balance test and symptomatic questions but now also includes some short term memory questions. The introduction of the hIA corresponded to the concussion substitution time being increased to 10 minutes. A pocket SCAT is available as it is

returnIng to Play neuropsychological testing is being used more and more for professional athletes at regular intervals to establish a baseline cognitive function (9). From this, testing can be done following concussion and at regular intervals after this during the recovery period until the patient returns to their baseline, as was mentioned above with the use of SCAT2 testing post-match in the pSCA tool (9,14). however, this should not be the sole determinant in when a patient should return to play and should be used alongside clinical examination. Also, when neuropsychological testing is not available it is very important to use examination to aid your decision. The flowchart shown in Figure 2 is recognised as the return-to-play protocol (9). Rest is defined as complete physical and cognitive rest (9). Indeed The Football Association (FA) goes further to include no playing of video games or similar during that period of 24 hours’ rest (9). light aerobic exercise is defined as ‘gentle activity that increases the heart rate to no more than 70% of predicted maximum heart rate’, for example swimming, walking or cycling on an exercise bike (9). Sport-specific exercise includes activities that are beginning to become more similar to


At what venue are we today? Which half is it now? Who scored last in the match?

recognised that carrying the full version onto the pitch is not always practical. There are also numerous apps available now to assess concussion using your phone, although it is difficult to evaluate the quality of these. It may be that this is an area for future development as it is likely that the peer-reviewed development of an app would be well received by the medical profession.

No activity

Light aerobic activity

Sportspecific exercise

Noncontact training drills

Fullcontact practice

Return to play

What team did you play last game? did your team win the last game?


Figure 2: The graduated return-to-play protocol as according to the November 2012 Zurich International Conference on Concussion. [S. Morton 2015, sourced from McCrory et al., 2013 (9)]

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U19 and below

Clearance by HCP recommended Clearance by doctor

2 weeks’ rest symptom free GRTP 24 hours per stage Earliest RTP = 19 days

Minimum 7 days’ rest + symptom free

Return to academic studies Clearance by doctor recommended

GRTP 48 hrs per activity stage

Earliest RTP = 23 days

Clearance by doctor

Figure 3: RFU guidance for return to play for rugby players without access to full-time medical staff. GRTP, graduated return to play (as described in Fig. 2); HCP, healthcare professional; RTP, return to play. [RFU (17)]

those in the sport player, for example running drills (9). At this stage there is no head impact (9). non-contact training drills continue with no head impact but can include more complex drills that allow the athlete to perform to a higher level and to increase their cognitive load (9). ‘Full-contact practice’ equates to normal training regimes, under close supervision of the medical and coaching teams.

It is estimated that it should take 1 day to move between each step, but players should not move on until the medical/coaching staff are happy (9). however, this is not a definite and it is very much guided by you as the clinician and the patient. This means that the minimum time for a player to return to the pitch is 7 days (9). If the player experiences any symptoms when progressing up the protocol

then they must return to the previous asymptomatic level and stay at that for at least another 24 hours (9). Return to play on the same day has been discredited and the 2012 Consensus statement unanimously agreed that no player should return on the day (9). This is due to the literature suggesting that pitch-side testing is unlikely to fully establish the extent of any neuropsychological deficits and formalised testing is required (9). The FA recommends that players should have neuropsychological testing, either with a SCAT3 test or similar, before returning to play (16). The FA recommends that SCAT3 testing should be carried out every 48 hours following the injury until the athlete returns to the pitch. At the return-to-play stage they should be at their baseline profile and progression should have been seen during the return-to-play process (16). The English Rugby Football union (RFu) has developed different advice for their players who do not have access to a full-time medical professional, as seen in Figure 3 (17). This means that the earliest return to play for an adult is 19 days and for under 19s is 23 days; these are,

MeDIcal PractItIoner IntervIew (S. Morton, 2015)

Dr abosede ajayi, consultant in emergency Medicine & Sports Physician, chief Medical officer for British Diving 1. how do you feel the management of concussion has changed over recent years? I feel it has become more structured and objective in assessment, management and diagnosis. There has been a shift to recognising that loss of consciousness is not the only cause, nor indeed head injury, but head impulse has a role in the aetiology. Additionally formalising assessment for subtle cognitive symptoms using SCAT3 and other tools has helped manage symptoms and return to play. high profile incidents (eg. Serge Betsen – Rugby World Cup 2007, and several football players at Football World Cup 2014) have highlighted the issue beyond sports physicians. 2. how would you suggest managing a patient pitch side with concussion? use the International Rugby Board pitch Side Concussion Assessment (pSCA) to assess. There should be mandatory

removal if diagnosed using pSCA or if any loss of consciousness, problems with balance or/and cognition, etc., identified prior to using the pSCA tool. 3. What is the advice you give to players regarding return to play? There should be a step-wise return to play based on symptom progression. The player has to be symptom free prior to return to training. There needs to be a progressive increase in training load with reassessment of symptoms at each stage. If symptoms recur the player has to have time off until fully resolved. In the absence of previous baseline neuropsychometric testing then there needs to be a mandatory 3-week stand-down for all players. otherwise this can be brought forward if he successfully completes phased return to play with no symptoms but a minimum of a 10-day stand-down usually applies.

4. how does the literature fit with both your management and returnto-play advice? how best can we translate the literature on concussion into evidence based practice? observational studies and pragmatic studies support the use in terms of diagnosis and initial management. There is limited robust level 1 or 2 evidence on concussion management. Much data from young athletes in uSA nCAA (national Collegiate Athletic Association) system is emerging. There is a need to look beyond to non-nCAA sports and other age groups to improve all of this. 5. Where is the literature lacking and what would you like to see happen in the future relating to concussion? long-term data on multiple concussion and need/benefit of longer stand-down times for each recurrence has to be investigated further.


therefore, the guidelines for the majority of rugby players within the uK (17). The RFu recommends that during the rest period players should gradually reintroduce reading, watching television, playing computer games and driving (17). The RFu also recommends regular assessment of the concussion during the graduated return-to-play process using the pocket Concussion Recognition Tool. As above, they recommend taking 24 hours per stage, or 48 hours if under 19. The RFu outlines that it is a player’s (or parent’s) responsibility to gain official medical clearance before returning to play. If a player has access to a doctor during training then the RFu has developed a Return to play pathway in

MeDIcal PractItIoner IntervIew (S. Morton, 2015) Dr Ian Beasley, head of Medical Services for the fa 1. how do you feel the management of concussion has changed over recent years? We have refined our management, and defined it more clearly. What has changed more is the education process for all, including the public. 2. how would you suggest managing a patient pitch side with concussion? Any suspicion, they are taken from the field of play and not allowed to return. 3. What is the advice you give to players regarding return to play? Follow Zurich RTp guidelines, at least 6 days for adult players, longer for youth players. 4. how does the literature fit with both your management and return-to-play advice? how best can we translate the literature on concussion into evidence-based practice? It is straight forward and all written down. The difficulty is adhering to it, and on occasion the help of a ‘second opinion’ is required to reinforce the need to follow the advised pathway. 5. Where is the literature lacking and what would you like to see happen in the future relating to concussion The RTp guidelines do not have hard and fast evidence to back them up as yet, and lots of work is being done on this at present. The link between sports-related concussion and degenerative brain disease in later life has yet to be elucidated. In football, we need to understand heading and its effects on the brain.



Clearance by doctor Clearance by doctor


2 weeks’ rest symptom free GRTP 24 hours per stage

Minimum 7 days’ rest + symptom free

Earliest RTP = 6 days

Whole RTP process supervised by the doctor within a structured concussion management programme

GRTP 24 hours each stage Earliest RTP = 12 days

Return to academic studies

Clearance by doctor Clearance by doctor

Figure 4: RFU guidelines for return to play in 7 days for rugby players with access to full-time medical staff. [RFU (17)]

an Enhanced Care Setting which does allow a 7-day return to sport (Fig. 4). To be able to complete the enhanced care setting the player must have baseline psychometric testing available and/or a baseline SCAT3 assessment. This allows serial testing to be completed following the concussion during the return-to-play programme (17). As can be seen in our Medical practitioner Interviews and with the information above, a minimum of 7 days before return to play is very much a guide and people and professional body’s opinion on the length of time to return to play differs. Therefore, it is most important that you as the clinician believe the player to be safe to return to play.

of topics are available. Aside from the advice for healthcare professionals there is also separate advice available for players, parents, coaches and match officials ( 4. The Irish Rugby union has a similar webpage with concussion guidelines for the domestic game ( including videos available aimed at different groups. 5. World Rugby has videos available online, including ‘Concussion in rugby: Recognise and Remove’ ( 6. The FA advice is also available online: head injuries in professional football (

reSourceS avaIlaBle

Concussion is likely to remain a difficult area of medicine to treat. however, there are resources out there for medical professionals to use, and potentially develop further. As a pitch-side medical professional the challenge is increased tenfold with the additional pressures of the environment, team and coach. It is therefore important to remember that the patient is the number one priority and to use the structured assessments available will normally guide your management.

There are numerous other resources available to medical professionals. 1. England Rugby has its own webpage Concussion – headcase ( especially for Concussion and healthcare professionals. From this there are links through to assessment tools and the consensus statements discussed above. 2. The RFu has Return to play after concussion guidelines ( as discussed above (17). 3. The RFu website also has a link to the presentations from the Fourth International Consensus Conference on Sports Concussion held in Zurich in 2012 ( Simply click on the presenters’ names and videos and power point presentations on a range


References 1. Kitson R. England’s Mike Brown admits he was tempted to lie over concussion ( the Guardian 2015 2. Moore B. WRu deserve punishment for George north concussion treatment in Wales’s defeat to England in Cardiff ( the telegraph 2015 sportEX medicine 2015;65(July):26-32

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3. Baldock A. Six nations 2015: George north concussion row will help make game safer, says Jamie Roberts ( the independent 2015 4. Simon n. northampton wing George north ordered to rest for at least a month after suffering third concussion in four months against Wasps ( mail online 2015 5. Weaver p. Fernando Alonso did suffer

concussion in crash, admits Ron dennis ( the Guardian 2015 6. Audley harrison calls time on boxing career over health fears ( the Daily express 2015 7. Cornwell R. Concussion in sport crisis deepens as nFl star quits at 24 over fears of brain damage ( irish independent 2015

8. Scholfield d. Rugby concussions soar by 59 per cent, says report ( the telegraph 2015 9. McCrory p, Meeuwisse Wh, et al. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, november 2012. British Journal of sports medicine 2013;47:25–258 10. harmon KG, drezner JA, et al. American

MeDIcal PractItIoner IntervIew (S. Morton, 2015) Dr Mike england MBBS MSc(SeM) MfoM MfMlM ffSeM(uk) Medical Director rfu game Development and Director rfu Injured Players foundation 1. how do you feel the management of concussion has changed over recent years? The management of concussion in sport has been developing over the last decade as scientific understanding has developed, mainly influenced by the International Concussion in Sport Conferences and their Consensus Statements, the last of which was published in 2013 and included the concerns raised around neurodegenerative disorders, including chronic traumatic encephalopathy (CTE). The head Injury Assessment (hIA) introduced by World Rugby in international games and adopted by elite rugby competitions around the world, including in England in the premiership, was created in response to these developments in understanding. There is no doubt, however, that the media interest over the last 18 months has shone a spotlight on this issue, and that has helped significantly in raising awareness. What is often not recognised by the media is that the RFu had been working on this issue long before they became interested; CogSport testing was introduced in premiership Clubs 13 years ago to help manage their return to play, and the RFu introduced it’s first community game awareness campaign in 2007. lessons were learnt from this campaign and our latest awareness and education programme ‘don’t be a headcase’ was launched in January 2013. This programme continues to develop and is generally recognised as the leading and most comprehensive resource available in uK. It is now used by a range of sports and

allied health care organisations. At the end of 2014, premiership Rugby, the Rugby players Association and the RFu introduced mandatory online education for all premiership coaches, players and referees. We are seeing a cultural change in the game in the way concussion is perceived and managed, with a move to a more cautious approach generally. What is interesting is I am now hearing healthcare professionals working in this field in the nhS advocating that ‘health should follow sport’s lead’ and learn from us how to better manage mild traumatic brain injury whether it is from sport or from everyday incidents such as falls and road traffic collisions. 2. how would you suggest managing a patient pitch side with concussion? In principle it is a simple message; Recognise and Remove, and If in doubt Sit Them out. We should not, however, forget general first aid/immediate care procedures and if a more serious injury, e.g. airway or neck injury, is suspected then that must be managed appropriately as a priority. The pitch Side Recognition Tool is a useful aide-memoire. 3. What is the advice you give to players regarding return to play? Follow the published guidelines for your sport. In Rugby union these are made available as part of our don’t be a headcase programme and for the professional game through their hIA protocols. The overriding principle is to ensure full recovery before return to play. In practice this involves resting the body and brain until symptom free, then following a Graduated Return to play

(GRTp) protocol, and we recommend gaining medical clearance before return to contact training and playing. We also recommend a more cautious approach with children and a return to studies before return to play. 4. how does the literature fit with both your management and returnto-play advice? how best can we translate the literature on concussion into evidence based practice? There is still a lack of high quality evidence in these areas, and that presents challenges. Within rugby we work hard to base our management on evidence where it exists, incorporate the International Consensus guidance, but also use uK-based independent experts to scrutinise our own guidance and procedures. 5. Where is the literature lacking and what would you like to see happen in the future relating to concussion? As highlighted in a number of systematic reviews the literature is lacking in many areas, despite the explosion in published articles on concussion in the academic literature in recent years. My understanding is that concussion was considered ‘out of scope’ in the recently published nICE head Injury Guidelines because of the lack of evidence. I would like to see awareness continuing to grow, continued work on the prevention of head injuries, and the nhS develop services and clear care pathways for mild traumatic brain injury (which includes concussion). This would support the development of the evidence needed on best practice in management.


Medical Society for Sports Medicine position statement: concussion in Sport. British Journal of sports medicine 2013;47:15–26 11. helmy A, Agarwal M, hutchinson p. Concussion and sport. BmJ 2013;347:f5748 12. national Institute for health and Care Excellence (nICE) 2014. head injury: triage, assessment, investigation and early management of head injury in children, young people and adults ( 13. SCAT3™. Sport Concussion Assessment Tool – 3rd Edition ( British Journal of sports medicine 2013;47:259 14. Fuller GW, Kemp Sp, decq p. The International Rugby Board (IRB) pitch Side Concussion Assessment trial: a pilot test accuracy study. British Journal of sports medicine 2015;49:529–535 15. SCAT2. Sport Concussion Assessment Tool 2 ( British Journal of sports medicine 2009;43:i85–55 16. The Football Association. head injuries in professional football ( 17. English RFu. Return to play after concussion ( 18. Teasdale G, Jennett B. Assessment of coma and impaired consciousness: a practical scale. the Lancet 1974;304(7872):81–84.

further reSourceS 1. pdF of SCAT3 tool. British Journal of sports medicine 2013;47:259 (ref. 13) 2. pdF of World Rugby (IRB) pSCA tool. Fuller et al., British Journal of sports medicine 2015;49:529–535 (ref. 14) 3. pdF of head Injury Assessment (hIA)

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THE AUTHOR DR SARAH MORTON MBBS Dr Sarah Morton MBBS is an academic foundation year one doctor at Hillingdon Hospital. She completed her medical degree at Imperial College. Her intercalated degree was in Sports and Exercise Medicine at Queen Mary University of London. Since then she has published papers on risk factors in patellar tendinopathy, low back pain in cricketers and high-volume image-guided injections. She was awarded the Helal and Harries Sports and Exercise Medicine prize in 2014 for her work on risk factors in patellar tendinopathy. She continues her research in this around her on-call sessions, even occasionally managing to make it to a cricket or rugby match or play a game of netball herself. Sarah is commissioning editor for the Translational Research Review channel under the Physical Therapy category of the website.

key PoIntS n concussion is a common sports injury and you should be on the lookout for it. n If you have any suspicion surrounding an incident that it might be concussion take the worst-case scenario – remember players do not have the same motivations as you (the clinician) on the pitch or in the clinic, whatever age they are. n you have to use your experience as a medical practitioner to advise players accordingly, whether that is to come off the pitch now or to not play this weekend. n Do not be swayed by the coach, player or parent – you are the expert! this applies to both taking a player off the pitch and allowing a player to return to the pitch, whether now or in a week or a month. n use the guidelines and resources available to help you with your assessment. n Pitch-side testing has developed to include the Scat3 and IrB PSca tool. n return-to-play guidelines suggest a minimum of one week before returning to play, but again you are the expert and should use the guidelines accordingly. n If in doubt ask your colleagues for advice. Medicine is very much a team game and if you don’t feel you are experienced enough to make the decision ask someone to help you.



tweet this: There is no scientific, medical or rugby basis for the safety of 10-minute assessment for concussion. tweet this: Rugby union has introduced a reversible substitution to allow a 10-minute concussion assessment. tweet this: Return to play requires a minimum of 7 days and must be guided by the clinician and patient. tweet this: Concussion is a shortterm condition that does not result in structural brain damage


n do you feel that pitch-side assessment tools are sufficient for making a through medical assessment? Is the 10 minutes allowed in Rugby union sufficient time to decide whether a player is concussed? n If you had been the medical professional witnessing George north’s injury would you have allowed him to return to play? Can you empathise with the medical team allowing him to return or do you believe there is no justification? n Where would you like to see more research in concussion? do we understand enough the long-term consequences of concussion? like the uSA are the compensation bills going to start rising over the next 20 years?

continuing education Multiple choice questions This article also has a certificated elearning test which can be found under the elearning section of our website. For more information on how to access the test click this link

this quiz is aCCessiBLe


With a suBsCription that inCLuDes onLine aCCess to this JournaL.

sportEX medicine 2015;65(July):26-32

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8 weeks post-launch

By tor Davies, founDer of sporteX anD

current state of play

new opportunities for content bundles

most of the work that’s taken place has done so behind the scenes however there’s a few cool changes that have recently taken place which will improve your experience on the site itself.

the new site allows us to bundle articles together in a completely customised content package which you could use for a number of reasons. the most obvious ones are a handful of articles for a continuing education purpose for clinics or CPD providers looking for additional content. other applications might be to map to a syllabus to provide complimentary resources, or for an association or membership body wanting to provide additional value for money to members, or to a product provider/supplier wanting to provide a valueadd to high priority customers or as part of a marketing conversion campaign. the resources could be purchased either by you under a group subscription or provided for sale individually to the individuals themselves. the content can consist of anything we have published in the past or to our sub-categories under which we will publish new content on an ongoing basis. Basically we can create a content package that is mapped specifically to the outcome you want. We can even set up scheduled emails to trigger when you want your content recipients to be notified of the availability of the content, for example scheduled to coincide with the delivery of a course or as part of a marketing campaign. if you would like to discuss any of these opportunities, just drop me an email (( with an outline of what you want to achieve and we can explore what might fit best.

1. The Padlock the unlocked Padlock symbol shows against any content that you have access to. it appears all over the site, wherever you happen to be (note that you do have to be logged in first otherwise it doesn’t know who you are or what you have access to!). if you’ve logged in and don’t see any padlocks and think that you should, just drop us an email to 2. The Quizzes Until about 2 days before we sent the journals to print, there was no way to find articles that specifically had a continuing education quiz attached to them (not something i’d realised until a couple of my eagle eyed subscribers pointed it out to me at CoPA last week - thank you, you see your feedback does matter!). So we’ve just fixed that! You can now isolate articles which have quizzes using the ‘Quick Links’ box in the right hand panel on the Home page. You can also use this link

so what’s next on s

3. Favourite articles We snuck this one in quietly but it’s the start of big things to come when we bring a more ‘social’ approach to the site in the coming months. if there’s an article you’d like to store in your Favourites section, just click the star and whenever you want to re-access it, you’ll find it under the Favourites section in your Account area (by the way this is also one of elements factored into the author royalty equation so the authors will love it too!).


t be honest i was hoping to launch the next phase to of this site with this July issue but things have just taken longer than i rather ambitiously hoped! that said, i’m even more pleased with the outcome than i had expected so i’m not complaining. the next phase involves creating a social network around the context of our content. By the time you read this journal, the tech development will be underway and should be much simpler than the foundation work that we’ve built to date. this platform has been built completely from scratch based on the direction that sporteX has taken which has been entirely driven by our subscribers. i would like nothing more than for you to start getting involved in giving feedback about how you feel the site is developing and what you’d like to see more (or less) of. Please go to this article online and use the Comments section to get involved. You’d be amazed at how motivating that is for both myself and my developer!

sportEX dmedicine 2015;65(July):34

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