sportEX Medicine Journal Issue 58 - October 2013

ISSUE 58 Oct 2013 ISSN 1471-8138

promoting

excellence in

highlights

sports

n latest research news n research analysis

n the brain: movement & Pain Part 2

medicine n acute soft tissue injury and P.r.i.c.e

n sPrint-related hamstring injuries

To purchase tickets visit http://spxj.nl/APPI13

contents ocTober 2013 issue 58

Welcome

publisher/editor Tor Davies Bsc tor@sportex.net art editor DeBBie asher debbie@sportex.net sub-editor alison sleigh Journal watch BoB BraMah subscriptions & advertising support@sportex.net +44 (0) 845 652 1906 Technical aDvisors steve aspinall lynn Booth Joanne elphinston helen Millson Dr Dylan Morrisey Prof graham smith Joan Watt Dr nick Webborn Prof greg Whyte Paula clayton

Bsc (BasraT), Msc McsP, Msc BPhty Ma, McsP McsP, McsP, Msc PhD FcsP, srP McsP, srP MrcgP, Dip sports Med, Msc PhD, Bsc (hons) Msc, MsMa

is published by centor publishing Ltd 88 Nelson road Wimbledon, sW19 1hX Tel: +44 (0)845 652 1906 Fax: +44 (0)845 652 1907 www.sportex.net

oct 2013

it’s been a busy but good year. Despite the economic doom and gloom, you, our subscribers have kept us moving forward in these difficult times, enabling us to invest in making our relatively new continuing professional education modules, accessible on most mobile tablets. no longer do you have to be on a laptop or desktop computer, now you can just log in to our (also new) mobile-optimised website on your tablet or smartphone, and complete your elearning wherever you are (and the certificates will be stored against your account). however, as much as i love being able to launch these new techie developmernts, our new sales and marketing director has hauled me (not exactly kicking and screaming) from behind the nerdy computer, to remind me what it is i’m actually trying to achieve through sporteX. as a result we’ve seen many of you at coPa, The sMa annual conference, exercise is Medicine in cardiff, and even a couple of you in the Us at the american orthopedic society for sports Medicine. it has been reinvigorating! While i confess that i enjoy the nerdy side of the job, like anyone who chose physical therapy as a profession (at least originally), i’m a people-person at heart and i’d forgotten how good it is to hear directly from you, what you find useful about the journals. it reminds me why i started sporteX. My dream is the same now as it was 14 years ago. We’re here to transform the ever-expanding research base into good solid practical application and help make your lives a bit easier.

Tor davies, physio-turned publisher and sporteX founder tor@sportex.net

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4 Journal watch 7 research analysis 10 The brain and pain part 2 The latest key research

Two detailed reviews of recent research on low back pain and claudication issues a follow-up to the previous article describing the constant process of neuroplastic remodelling

coNTeNTs 16 acute soft tissue injury 20 hamstring injury

could a new treatment acronym, Police, be more effective than Price? sprint-related hamstring injuries - the current state of play

To FiNd ouT More abouT sporTeX visiT

DISCLAIMER While every effort has been made to ensure that all information and data in this magazine is correct and compatible with national standards generally accepted at the time of publication, this magazine and any articles published in it are intended as general guidance and information for use by healthcare professionals only, and should not be relied upon as a basis for planning individual medical care or as a substitute for specialist medical advice in each individual case. To the extent permissible by law, the publisher, editors and contributors to this magazine accept no liability to any person for any loss, injury or damage howsoever incurred (including by negligence) as a consequence, whether directly or indirectly, of the use by any person of any of the contents of the magazine.

Copyright subsists in all material in the publication. Centor Publishing Limited consents to certain features contained in this magazine marked (*) being copied for personal use or information only (including distribution to appropriate patients) provided a full reference to the source is shown. No other unauthorised reproduction, transmission or storage in any electronic retrieval system is permitted of any material contained in this publication in any form.

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online

CLICK ON RESEARCH TITLES TO GO TO ABSTRACT

SHOuLdER pAIN ANd mOBILITy dEfICITS: AdHESIvE CApSuLITIS. Kelley mJ, Shaffer mA, et al. Journal of Orthopaedic & Sports physical Therapy 2013;43(5):A1–A31 Frozen shoulder, also known as adhesive capsulitis, refers to a condition where the shoulder becomes painful and stiff. Although it sometimes occurs following trauma the cause is more often idiopathic.

Other conditions increase risk factors including diabetes and thyroid disease. It affects between 2% and 5% of the population at some point in their lives, and typically occurs in adults between 40 and 65 years of age. Sufferers usually experience an initial period of pain at rest, and severe pain with movement. This leads to a progressive loss of motion and limited function of the shoulder over several months. Often in the ‘freezing’ phase comes a time when there is less pain but greater difficulty performing activities of daily living. Eventually, the condition starts to ‘thaw’ and shoulder motion and function gradually return. The condition can last up to 18 months. The treatment guidelines published here include the use of heat, electrical stimulation for pain, joint mobilisation, neuromuscular re-education, and patient education.

sportEX comment This is an excellently researched piece of work. It highlights the need for a true diagnosis to ensure there are no underlying conditions getting lost under the ‘frozen’ umbrella and then it sets out treatment guidelines based on the irritability of the presentation. It comes with a shorter version of the report to use as a patient information handout. This is exactly sportEX’s sort of research!

dOSE–RESpONSE EffECTS Of mEdICAL ExERCISE THERApy IN pATIENTS WITH pATELLOfEmORAL pAIN SyNdROmE: A RANdOmISEd CONTROLLEd CLINICAL TRIAL. Østerås B, Østerås H, et al. physiotherapy 2013;99(2):126–131 Forty-two patients (40 finished the study) with patellofemoral pain syndrome (PFPS) were assigned at random to an experimental group or a control group. Both received 3 treatments per week for 12 weeks. The experimental group received high-dose, high-repetition medical exercise therapy, and the control group received low-dose, low-repetition exercise therapy. The groups differed in terms of number of exercises, number of repetitions and sets, and time spent performing aerobic/global exercises.

Outcome measures were pain and function measured using a step-down test and the modified Functional Index Questionnaire (FIQ).

At baseline, there were no differences between the groups. After the interventions, for all outcomes the intervention group scored better.

sportEX comment Beast ‘em to get ‘em better.

WALKING vERSuS RuNNING fOR HypERTENSION, CHOLESTEROL, ANd dIABETES IABETES mELLITuS RISK REduCTION. Williams pT, Thompson pd. Arteriosclerosis, Thrombosis, and vascular Biology. 2013;33:1085–1091 The data for this study came from the National Runners’ (n=33 060) and Walkers’ (n=15 945) Health Study. Baseline expenditure (metabolic equivalent hours per day [METh/d]) was compared with self-reported, physician-diagnosed conditions during a 6.2 years follow-up. Running significantly decreased the risks for incident hypertension by 4.2%, hypercholesterolemia by 4.3%, diabetes mellitus by 12.1% and coronary heart disease (CHD) by 4.5% per METh/d. The corresponding reductions for walking were 7.2%, 7.0%, 12.3% and 9.3%.

sportEX comment The METh/d thing means that for the equivalent energy expenditure the walkers have to keep going for longer, but what it really means is that you don’t have to kill yourself to not kill yourself.

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sportEX medicine 2013;58(October):4-6

JOURNAL WATCH

Journal Watch C COmpARISON Of ACTIvE STRETCHING TECHNIquE IN mALES WITH NORmAL ANd LImITEd HAmSTRING fLExIBILITy. Ayala f. Sainz de NOR Baranda p. et al. physical Therapy in Sport 2013;14(2):98–104 Using unilateral passive straight leg-raise test (PSLR) 138 males were categorised according to hamstring flexibility and assigned to one of 2 groups: normal hamstring flexibility (>80°) or limited hamstring flexibility (<80°). In each group, participants were randomly distributed into one of 2 treatment subgroups: (a) control or (b) active stretching in which they performed stretches of 180s on 3 days a week for 12 weeks. Measurement was hip flexion passive range of motion (HF-PROM) determined through the PSLR test. Both stretching subgroups significantly improved their HF-PROM from baseline. The control subgroups did not.

sportEX comment Nothing here we didn’t know but sometimes it is nice to have the proof.

ACTIvATION Of THE GLuTEuS mAxImuS ANd HAmSTRING muSCLES duRING pRONE HIp ExTENSION WITH KNEE fLExION IN THREE HIp ABduCTION pOSITIONS. Kang S-y, Jeon H-S, et al. manual Therapy 2013;18(4):303–307 Thirty healthy subjects participated in this study to investigate the influence of hip abduction position on the electromyography (EMG) amplitude and onset time of the gluteus maximus (GM) and hamstrings (HAM) during prone hip extension with knee flexion (PHEKF) exercise. Surface EMG signals were recorded in 3 hip abduction positions:

0°, 15° and 30°. GM EMG amplitude was greatest in the 30° hip abduction position, followed by 15° and then 0° hip abduction during PHEKF exercise.

HAM EMG amplitude at 0° hip abduction was significantly greater than at 15° and 30° hip abduction. Additionally, GM EMG onset firing was delayed relative to that of the HAM at 0° hip abduction. The GM

EMG onset occurred earlier than the HAM in the 15° and 30° hip abduction positions.

sportEX comment If you want to fire the gluts, 30° hip abduction is the optimum.

T THREE-dImENSIONAL KINEmATIC COmpARISON Of TREAdmILL ANd AN OvERGROuNd RuNNING. Sinclair J, Richards J, et al. Sports Biomechanics 2013; doi:10.1080/14763141.2012.759614 Twelve participants ran at 4.0m/s in both treadmill and overground conditions. Angular kinematic parameters of the lower extremities during the stance phase were collected at 250Hz using an eight-camera motion analysis system. Hip, knee, and ankle joint kinematics were quantified in the sagittal, coronal, and transverse planes. Hip flexion at footstrike and ankle excursion to peak angle were found to be significantly reduced during treadmill running with a significantly greater peak ankle eversion.

sportEX comment Treadmills are useful for research as you can control more variables and they are even more useful when there is a foot of snow on the ground or the heavens have rent asunder, but as this shows they do change running biomechanics.

www.sportEX.net

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online

CLICK ON RESEARCH TITLES TO GO TO ABSTRACT

RuNNERS WITH ANTERIOR KNEE pAIN uSE A GREATER pERCENTAGE Of THEIR AvAILABLE pRONATION RANGE Of mOTION. Rodrigues p, TenBroek T, Hamill J. Journal of Applied Biomechanics 2013;29(2):141–146 The headline grader in this study is the fact that 24% of runners will sustain an injury that stops them running for 7+ days. The most frequent injury is anterior knee pain (AKP).

Nineteen healthy runners and 17 with AKP had their passive pronation range of motion (ROM) measured using a custom-built device and a motion capture system. Dynamic pronation angles during running were captured and compared with the available ROM. In addition, traditional pronation variables were evaluated. There were no significant differences in traditional pronation variables noted between healthy and injured runners but injured runners used significantly more of their available ROM, maintaining a THE SpLASH/ICpC INTEGRITy mARATHON IN IBAdAN, NIGERIA: INCIdENCE ANd mANAGEmENT Of INJuRIES ANd mARATHON-RELATEd HEALTH pROBLEmS. Ogwumike OO, Adeniyi Af. BmC Sports Science, medicine and Rehabilitation 2013;5:6 This study outlines the incidence of injuries, marathon-related health problems and delivery of physiotherapy at the maiden and second editions of the Splash 105.5 FM/ICPC Integrity Marathon in Ibadan city, south-west Nigeria in 2009 and 2010.

In both events, 16.3% and 17.2% of the runners respectively reported injuries with significant occurrence in first-time runners mostly at the finish line. The reported injury type and site were muscle cramps and the thigh (39.7% and 76.4% respectively). Heat exhaustion was reported by 42.8% of runners in 2009 and 56.3% in 2010.

sportEX comment Ok the races were in Africa so you expect heat but there is a big education issue here for first-time runners.

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4.21° eversion buffer, whereas healthy runners maintained a 7.25° buffer. It is thought that the excessive and/ or prolonged pronation keep the tibia internally rotated as the knee begins to extend, thus disrupting the ‘screw home’ mechanism and creating an overuse knee injury.

sportEX comment There are myriad reasons why runners get overuse injuries but this is suggesting that excessive and prolonged pronation can cause AKP. These days with gait analysis, proper relevant footwear in the short term and muscle strengthening in the longer term one of these reasons can be reduced if not eliminated.

pRENATAL ALCOHOL ExpOSuRE ANd CHILdHOOd BALANCE ABILITy: fINdINGS fROm A uK BIRTH COHORT STudy.

Humphriss R, Hall A, et al. BmJ Open 2013;3:e002718 Researchers looked at 6,915 children who participated in the Avon Longitudinal Study of Parents and Children. The kids had a balance assessment at age 10 which including walking on a beam and standing on one leg for 20 seconds. This was correlated against how much alcohol their mothers consumed during pregnancy. It recorded that 70% drank no alcohol, 25% drank between one to two and three to four glasses a week, and about 5% drank seven or more glasses per week. There was no evidence that alcohol consumed during pregnancy was detrimental to childhood balance. In fact, higher use of alcohol during pregnancy had some correlation with better balance outcomes. But, they also found a correlation with ‘social advantage’ meaning wealth and education and ‘social disadvantage’ meaning binge drinking and abstinence. Not surprisingly the rich kids did better and it could be social economic status that gives better results rather than the booze.

sportEX comment Question: Is drinking while you are pregnant bad for your child’s future athletic ability? Well, this study suggests it doesn’t make a difference but previous studies in animals and humans have shown that alcohol exposure is related to a decrease in the size of the cerebellum so best not take a chance. Sorry for building your hopes up.

sportEX medicine 2013;58(October):4-6

reSearch reviewS

Should a preScriptive clinical prediction rule drive our deciSion making proceSS in patientS with low back pain?

BY Joseph Brence DpT, coMT, DAc

Our regular research reviewer, physical therapist Joseph Brence, reviews research looking into (1) the effectiveness of clinical prediction rules in the decision making process for therapists treating patients with low back pain, and (2) whether fear of movement affects the daily functioning of those who suffer from claudication.

L

ow back pain is one of the most common reasons why patients seek physical therapy in an outpatient setting. A recent systematic review estimated that the 1-year incidence of first time low back pain ranges between 6.3 to 15.3%.

Recurrence rates range between 24 and 33% and it is the single leading cause of activity limitation and work absence worldwide. The rate of development of chronic low back pain has risen from 3.9% in 1992 to 10.2% in 2006 and the economic burden is tremendous (1,2). With all of this said, what can we, as physical therapists, do to intervene and prevent our patients from developing recurring or chronic issues? It is speculated that early intervention is key to management and in 2002, Flynn et al. published an article in the journal Spine which defined a clinical prediction rule (CPR) for clinicians to use to identify individuals who present clinically with low back pain who will respond favourably to manipulation (3). But despite the findings, is there enough substantiated evidence to say this is the answer? Let’s investigate further…

cLinicAL preDicTion ruLe originATion

IT Is my OPInIOn ThAT The CPR, desPITe hAvIng sOme ReseARCh TO suPPORT ITs PResCRIPTIve nATuRe, LIkeLy IdenTIFIes A suBgROuP OF IndIvIduALs WhO WOuLd ImPROve On An OsWesTRy, desPITe The mAnuAL InTeRvenTIOns used www.sportEX.net

The CPR originated out of a prospective, cohort study that followed a group of patients who presented to physical therapy with non-radicular low back pain. The researchers of this study administered a pain diagram, modified Oswestry disability questionnaire, fear-avoidance beliefs questionnaire (FABQ) and assessed a list of subjective and objective variables. The therapists then provided the same treatment to all patients for the first two sessions, which included a supine lumbar manipulation, pelvic tilting exercise, and education to maintain usual activity within limits of pain. (The side of lumbar manipulation was chosen based on the side of a positive standing flexion test. If this test was negative, the side of a painful sacral sulcus would be manipulated. If neither of these were positive, the patient’s subjective complaint of a more painful side would be manipulated.)

The results of this study indicated that of the 71 subjects who completed, 32 (45%) had successful outcomes from manipulation (20 subjects after one session and 12 after two).

From those who improved, 11 potential variables were identified to be consistent among the successes and these were then entered into a logistic regression. Five variables were retained in the final model and the clinical prediction rule was born! It 7

included: duration of symptoms <16 days, at least one hip IR >35°, hypomobility with lumbar spring testing, FABQ <19, and no symptoms distal to the knee.

Out of the 32 patients who had successful outcomes in this study, 6 were positive for all five variables and 14 had at least four present. success was measured as a reduction in the Oswestry score (mean 73% in success group; 14.6% in non-success) as compared to baseline.

cLinicAL preDicTion ruLe vALiDATion Following the publication of this study, a validation study soon followed (4). This study was a randomised controlled trial which compared a group of participants who received spinal manipulation with exercise to those who received exercise only. The inclusion criteria used were the same that was used

by Flynn et al. (3), and comparisons were later made in those who fitted the CPR v. those who did not. The authors found that outcomes from spinal manipulation were dependent on those who fitted the CPR (at least 4 out of the 5 variables) and that this resulted in a 92% success rate. The reduction in Oswestry scores was higher in the manipulation group than the exercise group. Again, when individuals fitted the CPR, the success from spinal manipulation was high.

oTher AssociATeD reseArch In 2008, hancock et al. performed an independent evaluation of the CPR (5). The design of this study was also a randomised controlled trial, but unlike the first two articles, this group took a slightly different approach. This study allowed the therapist to adjust the type of manual care applied and instead of simply performing a manipulation (a grade 5 thrust as defined in the first two studies), these researchers performed low (97%) to high grade (3%) techniques, based upon a patient response. This approach was used to maintain external validity and to assess the CPR’s ability to generalise to a more typical population.

Outcomes were also measured differently from the first two studies, and a Roland–morris disability questionnaire was applied rather than an Oswestry questionnaire. This article found that CPR did not generalise and performed no better than chance in identifying patients whom would benefit from lumbar manipulation. This study, in my opinion, overlooked one key point: the CPR was developed to predict a successful outcome on an Oswestry disability questionnaire. The authors on this study measured disability with a different tool. If one changes outcomes measured, the CPR will likely change.

Another study, published this month in Manual Therapy (6), assessed the clinical prediction rules influence on clinical decision making. A sample of 535 therapists was included and an assessment of their clinical decision making, based upon a fictitious patient, was analysed. The authors found that factors that lead to an increased likelihood to manipulate included: board certification, male gender (of the therapist) and increased attendance of manual therapy courses. Therapists who use the CPR (and those who do not) were found to avoid manipulation as the fictitious patient’s complaints became more sinister. This study found that the 8

use of Flynn’s CPR did not increase the likelihood for applying inappropriate or contraindicated treatments but did find that demographically, there is a subgroup more likely to apply it.

Finally, two independent systematic reviews (7,8) critically analysed the quality of the research performed in these studies and both found that the current body of evidence does not support direct application of the CPR. One of the reviews even concluded that the validation studies did not provide evidence that validated the CPR. Additional, better designed, validation studies with more rigorous methodology need to be conducted to support the generalisability of CPRs to clinical practice. so despite all of the excitement of the research above, a critical analysis states that more rigorous work must be done.

MY ThoughTs ABouT The cpr It is in opinion that the CPR, despite having some research to support its prescriptive nature, likely identifies a subgroup of individuals who would improve on an Oswestry scale, despite the manual interventions used. This rule demonstrates someone with very acute symptoms, low fear-avoidance, good hip mobility, no radicular symptoms, and some stiffness.

This opinion may differ with the findings in Childs’ validation article (4), but I suspect if we get our patients moving early on, it is scientifically plausible that we can limit the development of more centralised pain, psychosocial factors, etc. I also believe that within-and-between-session-patientresponse changes are very predictive and hold some plausible weight. I do believe that manual care does assist in outcomes (whether it be low or high grade) but more substantial research needs to be performed to determine if true manipulative (thrust) therapy is the ultimate treatment for individuals who fit this rule. references 1 1. Freburger Jk, holmes gm, et al. The rising prevalence of chronic low back pain. archives of internal medicine 2009;169:251–258 http://spxj.nl/15xotQt 2. hoy d, Brooks P, et al. The epidemiology of low back pain. best practice & research clinical rheumatology 2010;24:769–781 http://spxj.nl/1dnaO3B 3. Flynn T, Fritz J, et al. A clinical prediction rule for classifying patients with low back pain who demonstrate short-term improvement with spinal manipulation. Spine 2002;27:2835–2843 4. Childs Jd, Fritz Jm, et al. A clinical prediction rule to identify patients with low back pain most likely to benefit from spinal manipulation: a validation study. annals of internal medicine 2004;141:920–928 5. hancock mJ, maher Cg, et al. Independent evaluation of a clinical prediction rule for spinal manipulative therapy: a randomized controlled trial. european Spine Journal 2008;17:936–943 6. Learman k, showalter C, et al. does the use of a prescriptive clinical prediction rule increase the likelihood of applying inappropriate treatments? A survey using clinical vignettes. manual therapy 2012;17:538–543 7. haskins R, Rivett dA, et al. Clinical prediction rules in the physiotherapy management of low back pain: a systematic review. manual therapy 2012;17:9-21 8. may s, Rosedale R. Prescriptive clinical prediction rules in back pain research: a systematic review. Journal of manual and manipulative therapy 2009;17:36-45.

sportEX medicine 2013;58(October):7-9

reSearch reviewS

inTroDucTion Claudication, derived from the Latin word claudicare (to limp), is a symptom of progressive leg or back pain that occurs with ambulation and activity. This symptom affects millions of individuals worldwide and generally has two major origins: neurogenic and vascular. neurogenic claudication is most commonly associated with lumbar spinal stenosis. spinal stenosis is a resultant narrowing of the spinal column which causes pressure on the spinal cord, or narrowing of the opening in which spinal nerves leave the column. It is estimated that 85% of individuals with spinal stenosis have leg pain and 62% have a classic signs of claudication (1). vascular claudication is often secondary to peripheral artery disease. vascular claudication occurs not because of an adequate blood supply to muscles at rest but the inability for blood to meet the increased demand during muscle use. This often results in the sensation of cramping or pain. generally these sensations are resolved with rest.

A recent article published by Wood et al. set out to determine, compare and explain the differences in the degree of fear of movement/(re-)injury and activity avoidance in individuals with neurogenic claudication, vascular claudication and asymptomatic (2). We often understand the physical presentations of these disorders, but may not consider the secondary complications which affect the health and well-being of our patients.

MeThoDs This article was a prospective study which assessed multiple variables in 82 adults, between the ages of 55 and 90. These variables included: n Pain on a visual analogue scale n disability on the Quebec back pain disability scale n Physical functioning on a short-Form 36 n maximum ambulation distance (estimated by the participant) n kinesiophobia on the Tampa scale for dinesiophobia (Tsk) n depression on the Center for epidemiological studies depression scale.

www.sportEX.net

claudication may reSult in fear of movement/(re-)inJury and activity avoidance The measure of kinesiophobia was subscored to obtain (1) a somatic focus which determines the ‘fear of movement/(re-)injury’ and (2) ‘activity avoidance. This subscaling model has shown to be effective in determining fear and avoidance tendencies in people with various chronic pain conditions.

resuLTs Out of the 82 adults, it was found that individuals who suffer from neurogenic claudication appear to experience a higher degree of fear of movement/ (re-)injury and activity avoidance, as compared to their asymptomatic counterparts. In addition, it was found that these individuals also report a higher degree of activity avoidance than their vascular claudication counterparts (as well as a higher overall score of the Tsk). The vascular claudication group had significantly higher movement/(re-) injury and total Tsk scores, compared to the asymptomatic group.

There are a variety of speculations that may explain these results. First, the authors suspect that the ‘severity of illness’ may not have been equivalent between the two claudication groups.

One of the inclusion criteria for the neurogenic group was the previous ‘recommendation for surgery’. This criterion may have elicited a nocebo response and increased the perceptual severity as compared to the vascular claudication group. In addition, the spectrum of symptoms experienced by those with vascular claudication may not be perceived to be ‘as severe’. For example, vascular claudication may result in the mild sensation of cramping to critical ischemia. Another speculation is that of the co-morbid symptom of low back pain, which exists in those with neurogenic claudication. The authors

state that 87% of individuals with neurogenic claudication suffer from low back pain (secondary to the stenosis) and that this in and of itself, may increase kinesiophobia.

concLusion Overall, this study compared a group of individuals with claudication and found that kinesiophobia is a factor which impacts the daily functioning of those who suffer from it. It appears that those with neurogenic claudication have more overall fear and activity avoidance, and I recommend that the focus of our treatment in these patients, should begin by screening for and addressing those beliefs. references 2 1. Turner JA, ersek m, et al. surgery for lumbar spinal stensosi: attempted metaanalysis of the literature. Spine 1992:17;1–8 2. Wood dW, haig AJ, yamakawa ksJ. Fear of movement/(re)injury and activity avoidance in persons with neurogenic versus vascular claudication. the Spine Journal 2012;12:92–300.

ThE auThOr 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 versus 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 blog www.forwardthinkingpt.com.

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The brain, movemenT and pain PArT 2 by ben CormaCk FaFS

neuroplaStiCity Neuroplasticity is neither a positive or negative process. It is an ongoing process of the remodelling of both the physical structure and functional organisation of the brain. The brain is a plastic and changeable area. In the last 30 years the study of neuroplasticity has exponentially exploded especially in relation to pain, movement and skill acquisition. Before this our brains were thought to remain unchanged after our late teens. Instead they are actually dynamically modifiable throughout our lives.

The process of neuroplasticity is modulated by the actions that we perform on a daily basis and provide input to and output from the brain. This could be based around movement, language or even emotion.

A conservative estimate of our brain’s capacity is that it has around 120 billion neurons each capable of making approximately 10,000 synaptic connections. We use collections of neurons to create specific neural patterns associated with an action.

These have been referred to as ‘neurosignatures’ (1) or ‘neurotags’ (2).

As collections of neurons 10

Our brains are constantly being remodelled in response to our movement and pain experiences. This article seeks to highlight the neural mechanisms involved in this neuroplastic remodelling, as these processes are vital for therapists to understand. We will look at how we can start to target the cortical representations of the physical parts of the body within our cerebral cortex and the research, science and techniques behind the process. fire together within a pattern, the associated connections become stronger. Donald Hebb, the famous Canadian neuroscientist, described this process simply as ‘neurons that fire together, wire together’. This forms the basis of Hebbian learning. Hebbian learning dictates that simultaneous activation of neurons within a pattern leads to a pronounced increase in synaptic strength between the two neurons. These patterns have also been described as ‘engrams’: ”The general idea is an old one, that any two cells or systems of cells that are repeatedly active at the same time will tend to become ‘associated’, so that activity in one facilitates activity in the other.”

Hebb (3) The implications for our often-isolated joint-by-joint approach to treatment are obvious. If we never incorporate a joint into a function-related movement

pattern then we are not helping the brain form and strengthen the necessary patterns for movement success. By simply treating isolated joints we may never help the neurons within a cortical representation of the body part or joint ‘fire’ with neurons in other representations to increase the synaptic strength required for successful integrated movement. Many therapy techniques and rehabilitation exercises focus on a single area and in a single plane of movement, generally in the sagittal plane. Functional movement success may lie in the active integration into a motor pattern or varied motor patterns that involve increasing the size and connections of multiple representations through multispeed and multi-planar movement.

The physical process of neuroplasticity in the brain happens as: “Axon branches more active in releasing neurotransmitters persist at specific neuromuscular sportEX medicine 2013;58(October):10-15

evidence based pracTice

sites, whereas less active axon branches retract, resulting in the canonical elimination of polyneuronal innervation.” Hau et al. (4)

DiSinhibition In the first part of this article (sportEX medicine 2013;57:12–17) we talked about the memory recall model that autoassociates input with a specific pattern and then makes an output.

Allport explains this: “If the inputs to a system cause the same pattern of activity to occur repeatedly, the set of active elements constituting that pattern will become increasingly strongly interassociated.

That is, each element will tend to turn on every other element and (with negative weights) to turn off the elements that do not form part of the pattern.” Allport (5) An interpretation of Moseley and Butler’s take on Melzack’s ‘neurosignature’, redubbed the ‘neurotag’, looks at the failure to ‘turn off’ the unassociated elements described by Allport. We can have many neural patterns that share neurons and, as we previously discussed, each individual neuron is able to make around 10,000 connections with other neurons. Within a specific pattern the brain should be able to inhibit other connections not associated with the specific pattern that we want to recall. If we fail to inhibit connections that involve neurons associated with pain then every time we activate certain neurons involved in a neural pattern we may also activate the neurons associated with pain. This has been described as disinhibition. These neural patterns could be involved with visual, auditory or movement-based patterns. In this way many inputs could trigger a pain output. A neural pattern encompasses neurons in multiple brain areas. These can be associated with emotion, thought, memory, balance, vision and stress responses to name just a few (6). These complex patterns show how a sensory input may evoke many different outputs within brain and how we can start to associate movement with negative emotions such as fear and also stress responses.

The neurotransmitter GABA (gamma-aminobutyric acid) is an www.sportEX.net

inhibitory chemical that reduces the activity of the neuron to which it binds.

GABA neurons and receptors have been found in brain areas that coordinate perception and response to painful stimuli. GABA also regulates sensory processing at a spinal level. long-term depression (lTD) of inhibitory mechanisms such as GABA has been associated with pain sensitisation. This depression requires activation of excitatory neurotransmitter NMDA (N-Methyl-D-Aspartate) receptors (7).

Often a client’s pain association is with movement. As the patterns are constantly going through neuroplastic change this that means the less we move, the less sensory feedback we create. As we use sensory areas of our brain to dictate motor planning this may mean we start to move less into certain positions associated with pain and therefore we create less sensory feedback. Over time we create a mutual feedback loop of neural degradation that is plastically reinforced within the associated brain areas (8).

tweaking the ‘tag’ A treatment approach based on this view may be to subtly alter painful movements that have a specific ‘neurotag’. By changing the painful movement just enough we may elicit an alternative output, an output that does not contain pain.

An example of a painful movement could be lumbar pain when bending down to pick something up off the floor. We could alter the client’s leg position forward or back, the leg width or the rotation of the femur or foot. We could also alter the reach, reaching hand, amount of rotation of the spine or the bend of the knees. These subtle shifts may be enough to change the motor planning, output and proprioceptive input associated with pain. We may also reinforce positive associations with previously painful movement by not avoiding them altogether, but by instead altering the previously painful motor pattern.

The more chronic the pain, the less the

relationship we see with tissue damage (9) and may need a revised approach based around the brain rather than tissue-based pain mechanisms.

CortiCal mapS The best known brain areas studied in relation to neuroplasticity are the sensory and motor sections of the cerebral cortex.

Neuroplasticity within the visual and auditory cortex has also been studied.

Within our cerebral cortex we have representations of areas of our body that we use to sense, plan and carry out our movements. These representations have also been described as maps (10). They are a neuronal resource assigned to areas of the body to process information and perform tasks. The homunculus models give us a wonderful visual depiction of the amount of brain space dedicated to individual sections of the body. Our body parts are somatotopically organised so that neurons for adjacent body parts lie adjacent to one another within the cortex.

These representations provide our sensory and motor systems with an internal ‘map’ of our movement capabilities within external space. successful movement not only requires physiological capacity but also neurological capacity.

Does our current paradigm of the body support this?

Our cortical maps are constantly being neuroplastically reorganised, as are nearly all areas of the brain.

A famous study by Merzenich (11) in 1984 mapped the brain area for a monkey’s hand before amputating the third finger and then mapping the brain again 62 days later. He found that the brain areas mapped to the second and fourth finger had invaded the area previously associated with the third finger. The cortex had plastically reorganised to reallocate the available neuronal resource. Elbert (12) studied the representations of the right and left hands of violin players. He found the representations of the left hand (D1–D5) that operated the strings rather than the bow had an increased cortical representation in comparison

VArIABIlITy HAs BEEN CITED As A kEy FACTOr IN INjury PrEVENTION 11

to the less dextrously demanding bow operation. A similar study by Pascualleone (13) found the reading finger of Braille readers had an expanded cortical representation compared to non-reading finger. There is an amazing display of neural plasticity also associated with Braille. The visual cortex is normally activated by the lateral geniculate nuclei associated with vision, rather than other sensory systems. However, in the case of Braille reading, the visual cortex was activated by input from the tactile stimulation of the fingers (14).

Neuroplastic change in the sensory cortex has been associated with phantom limb pain. The brain space dedicated to the amputated limb remains but now receives sensory input from other sources such as the face and upper arm (9). The brain senses the input within the areas associated with the amputated limb. The motor output associated with this input is to touch or scratch the sensation in the limb that no longer physically exists.

Plastic changes within the cortex have been linked with pain (6, 15, 9).

Painâ&#x20AC;&#x2122;s impact on cerebral cortex is one of the most well studied areas of neuroplasticity. Flor et al. (16) found that with chronic low-back pain patients, the cortical back representation in the somatosensory cortex (s1) had invaded the lower leg representation and the extent of this expansion was closely associated with the chronicity of the pain. We see less well defined maps of people in chronic pain states (17). This reduced definition between representations has been described as smudging or blurring of the representations within the cortex. The worse the definition of the cortical map, the harder our premotor planning and motor execution part of the motor cortex will find it to plan and implement the movement (18).

Deafferentation (phantom limb pain) serves as a dramatic example of what can happen when we reduce input and the resultant plastic reorganisation of cortical representations. Although any underuse will create cortical changes, overuse of a specific skill or body part can also create problems such as focal dystonia. With focal dystonia we see poor definition of cortical representations, such as in chronic 12

pain, through expansion of the cortical representations because of overuse of the associated body part (19). It has been well documented in musicians where highly trained individuals lose the task-specific voluntary control of their movements. This has been said to be because of the imprecise firing of neurons in the cortex as a result of the failure of inhibitory mechanisms to silence the surrounding areas uninvolved in the skill (20,21). It is of interest to note that subtle shifts of context such as wearing a glove or using a modified plectrum have been employed by musicians to overcome this debilitating condition. Did they change the neurosignature/neurotag pattern associated with the condition as previously discussed in this article?

Balancing our representations with alternative movement may be a useful adjunct to any training programme for sports that require repetitive skills. Any movement that we use regularly, positive or negative, will be reinforced.

representations. We should be also thinking about the process of building and strengthening synapses as well as the muscular or cardiovascular systems. Feeding our cortical maps via movement is important when we consider the poor quality of movement and movement responses of chronic pain sufferers (18).

Figure 1: Move the foot into full dorsiflexion

impliCationS For the therapiSt This all means that the representations within our brains are shaped by both the afferent input and efferent output that we use to achieve a movement task. Our cortical maps need to be well defined, distinct from other representations and of a sufficient size to create healthy and precise movement.

The therapistâ&#x20AC;&#x2122;s interaction with a patient can be used to both assess a patientâ&#x20AC;&#x2122;s motor output that relies on these representations and also provide the movement task required to create a change within the representation.

The output that we ask the patient to perform will also stimulate the proprioceptive input.

We can guide the input both within a treatment and through homework that will alter the representations positively through a movement skill. Controlled movements in multiple planes and speeds will provide input that over time will change the movement hardware (the brain) so it can run a variety of software programs (movement patterns). This, however, needs to be actively patientdriven and performed with focus.

Quality movement practice at varied movement tasks will improve cortical

Figure 2: Move the foot into full plantarflexion

Figure 3: Move the foot into full adduction

Figure 4: Move the foot into full abduction sportEX medicine 2013;58(October):10-15

evidence based pracTice

reDeFining mapS: Variability anD SpeCiFiCity Variability has been cited as a key factor in injury prevention (22,23) as the ability for the individual to adapt to many challenges within a movement rather than rigidly adhering to a specific movement ideal. Deviation away from movement ideals such as pronation have been shown not to provide a definitive causative link to injury (24,25).

Pain and previous injury has been linked with decreased motor variability as the body seeks to create a safe predictability in movement (26,27).

Thomas Hanna, in his book Somatics, describes the process of motor impairment as ‘sensory motor amnesia’ or sMA. As we decrease the variability to protect injured or threatened tissue, so the sensory and motor neuronal hardware associated with good movement neuroplastically decreases (28). Overtime we ‘forget’ how to move into certain positions.

Through the process of decreased variability, previous pain could affect future movement, injury risk and pain.

We can seek to restore variability in movement by challenging the sensory and motor areas of the brain to create movement patterns that explore the full range of the joint. As we move through different positions at a joint we are assessing and challenging the body’s ability to create controlled motion in a variety of joint ranges, angles and speeds all requiring the stimulation of specific neurons and associated connections. In this way we are restoring the variability of movement.

The brain takes notice of a novel stimulus (29) and will adapt accordingly if the stimulus is prolonged. Without conscious involvement in the task we may fail to alter the predominant subconscious movement map associated with body segment.

A progression from having a varied and defined movement map is the ability to refine specific motor patterns required for movement tasks such as the specific motions at a joint and also the associated joints within a kinetic chain. An example of this would be the ability of the ankle and foot to go through the motions of pronation, a fairly universal movement for most of www.sportEX.net

FuNCTIONAl MOVEMENT suCCEss MAy lIE IN ACTIVE INTEGrATION the population. This is biomechanically defined at the subtalar joint as eversion, abduction and dorsiflexion. A wellrounded ankle rehabilitation programme may encompass movement capacity at the joint, specific pronation mechanics as well as specific pronation mechanics from a number of foot position, surfaces and inclines. How many injuries occur while away from our comfortable range or when reacting to an external stimulus not regularly encountered that requires rapid variability in movement?

ankle CirCle Challenge A movement drill, such as an ankle circle, could be used to restore motor skills, proprioceptive input and movement through a wide range of joint positions that may have been impaired by underuse or previous injury.

The concept behind an ankle circle is the controlled exploration of the joints movement capacity. The aim is to work just outside of the present sphere of movement of the joint so the motor and sensory systems are receiving

online

stimulation outside of their normal safe range.

A low-demand way to start could be in a seated position that reduces the need to balance in a standing position.

First explore the full range of available dorsiflexion (Fig. 1) and plantarflexion (Fig. 2). Then explore adduction (Fig. 3) and abduction (Fig. 4). The idea is to have the movement come almost exclusively from the ankle joint rather than the tibia as well. This will create dissociation at the target joint. Now go from a dorsiflexed position into an abducted position and then abducted to plantarflexed. This will create a semi circular motion. To complete the circle move from a plantarflexed to adducted position and then up to full dorsiflexion. you can then smooth this process out into a complete circle (Video 1). An interesting comparison is the ability to perform this motor challenge in both a clockwise and anticlockwise movement.

As they are different motor patterns, we often see a difference in the client’s ability to perform what is essentially the

if you have a current online subscription, login at www.sportex. net to view this video or download the mobile apps which are free to subscribers with online access.

Video 1: a tutorial for the ankle circle challenge to provide further support for its implementation

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THE MOrE CHrONIC THE PAIN THE lEss THE rElATIONsHIP WE sEE WITH TIssuE DAMAGE same range of motion. This highlights the difference between an anatomical capacity and a motor capacity. A left and right ankle comparison is also useful to assess motor ability between both ankles as they are controlled by different maps in the opposite side motor and sensory cortex.

For a successful treatment outcome the following points need to be considered: 1. Client education on why task is being performed.

2. Conscious concentration on stimulus and what is trying to be achieved.

3. Aim for a smooth, non-jerky motion.

4. Focus on parts of the circle that are not smooth and are difficult to move through.

5. If you or the client has to move fast to achieve the challenge then slow them down. The speed makes up for a lack of control.

6. People will want to use the visual system to help them with the movement. This can be used in the beginning but phased out as a progression, forcing them to use the proprioceptive system alone.

7. Another progression is to do the circle in a standing position adding in a balance challenge. This can also be done closed chain and in a gait like stance for more functional specificity.

DriVer anD the paSSenger The concept of the driver and the helpful passenger looks at the practitioner as a ‘guide’ (the helpful passenger) rather than in command (as the driver) of the patient’s body. In many therapy techniques we ‘drive’ the body while the patient passively allows him/herself to be manipulated. Although this does create change to afferent sensory feedback and local tissue, passive movement does not start to stimulate 14

brain areas involved within active movement and motor learning.

Mima et al. (30) looked at active versus passive finger motion and found stimulation in the primary and secondary sensory cortex with passive motion. However, active movement created stimulation in the primary sensorimotor cortex, premotor cortex, supplementary motor area, basal ganglia and cerebellum. These areas are all associated with motor learning and storage of motor patterns.

There is substantial evidence that the cerebellum, along with being a sensory integration and motor comparison centre (31), plays an essential role in motor learning both within the cerebellum itself and other brain structures (31–33).

Cortical changes have also been shown to be stronger when associated with learning about the experience and not just the sensory feedback involved.

Cortical representations can increase two to threefold within 1–2 days of the new sensorimotor skill being first acquired (34). Attention to the stimulus appears to be implicated in cortical change (35).

This would mean a conscious, concentrated and active patient-driven experience of movement may be needed to create cortical change in the motor and sensory areas.

A shift in focus of the therapist to a ‘helpful passenger’ who is able to guide the active and conscious motor learning process may create more neurological change than a ‘driver’ who passively creates change within the position of the structure.

ConCluSion We must start the paradigm shift of just seeing our patient interaction as being neurological rather than simply at a physiological level when dealing with movement and pain. This article has sought to highlight the mechanisms involved in this process and the specific brain areas and associated conditions involved with neuroplastic change within the cerebral cortex. We must be aware that we are all constantly plastically adapting to the sensory input and movement requirements we expose ourselves to.

We have the ability to positively shape client movement potential and experiences with our therapy techniques at a cortical level. This can be done by shifting the focus from being a ‘driver’ of the anatomy to being a ‘helpful passenger’, guiding movement and pain education. This puts ownership of movement back into the hands of the patient for long-lasting changes within the brain.

reFerenCeS Due to the large number of references accompanying this article, for space reasons, we’ve decided to publish them online. To view, please login to http://spxj.nl/1a2y9i9.

ThE AuThOr Th Ben is a movement and exercise specialist based in London. he is a fellow of Applied Functional Science (FAFS) having studied at the Gray Institute in the uS and is currently undertaking a medical neuroscience course with Duke university, North Carolina, uS. Ben is the founder of Cor Kinetic (www.cor-kinetic.com), which is a continued professional development (CPD) provider based around understanding the body in its functional context and the associated mechanics and neuroscience, especially functional movement’s impact on both pain and performance.

Cor Kinetic have worked with staff from many of the top teams in both premiership rugby and football both in house and on the CPD courses they run that also include physios and osteopaths from private practice and NhS.

sportEX medicine 2013;58(October):10-15

evidence based practice

Further reSourCeS 1. Cor-kinetic websitewww.cor-kinetic.com 2. Cor-kinetic blog http://bencormackpt.wordpress.com/ 3. The Neuro Orthopaedic Institute www.noigroup.com/ 4. Butler D. The sensitive nervous system. opTp 2006.

IsBN 978-0975091029. http://spxj.nl/14kd3Fw 5. Blakeslee s. The body has a mind of its own. random house, sept 2009.

IsBN 978-0812975277. http://spxj.nl/12v4XD7

DISCUSSIONS

www.sportEX.net

n Do we pay enough attention to the neurological factors involved in movement compared to the structural/physiological factors? n Is variability key to injury prevention? n Is Melzack’s ‘neuromatrix’ concept a valid model when dealing with chronic pain? n should therapists be drivers or helpful passengers?

continuing education Multiple choice questions This article also has an elearning test which can be found under the elearning section of our website.

Tests from April 2013 onwards can be done on most digital devices.

1. login to our website, click the Online Access button in the main menu bar and the go to the elearning section (you must be logged in).

2. Click on the quiz you wish to do. successful completion results in a stored certificate under the My Account area of our website.

This can be downloaded or printed at any time as evidence of continuing education for many national and international membership associations.

This quiz is accessible

free

wiTh a subscripTion ThaT includes online access To This journal.

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The brain, movemenT and pain PArT 2 references 1. Melzack r. Pain and the neuromatrix in the brain. journal of dental education 2001;65(12):1378–82 2. Butler D. What is a neuromatrix.

Neuromatrix training blog 2008; http://neuromatrixtraining.blogspot.co.uk/ 3. Hebb DO. The organization of behavior: a neuropsychological theory. Wiley & sons 1949. New edition: psychology press 2002. IsBN 978-0805843002 (Print £35.14, kindle £26.36). Buy from Amazon http://spxj.nl/16ugvmO 4. Hau jy, smear MC, et al. regulation of axon growth in vivo by activity based competition. nature 2005;434:1022–1026 5. Allport DA. Distributed memory, modular systems and dysphasia. In: Newman sk and Epstein r (eds) Current perspectives in dysphasia. churchill livingstone 1985.

IsBN 978-0443030390 6. Moseley l. A pain neuromatrix approach to patients with chronic pain. manual therapy 2003;8(3):130–140 7. Woolf Cj, salter MW. Neuronal plasticity: increasing the gain in pain. science 2000;288:1765–1769 8. Blakeslee s. The body has a mind of its own: how body maps in your brain help you do (almost) everything better. random house 2009. IsBN 978-0812975277 (Print £18.97, kindle £6.11). Buy from Amazon http://spxj.nl/12v4XD7 9. ramachandran Vs, Blakeslee s.

Phantoms in the brain: human nature and the architecture of the mind. fourth estate 1999. IsBN 978-1857028959 (Print £6.99).

Buy from Amazon http://spxj.nl/1dyWV0F 10. Buonomano DV, Merzenich MM. Cortical plasticity: from synapses to maps. annual review of neuroscience 1998;21:149–186 11. Merzenich MM, Nelson rj, et al. somatosensory cortical map changes following digit amputation in adult monkeys. journal of comparative neurology 1984224: 591–605 12. Elbert T, Pantev C, et al. Increased cortical representation of the fingers of the left hand in string players. science 1995;270(5234):305–307 13. Pascual-leone A, Torres F. Plasticity of the sensorimotor cortex representation of the reading finger in Braille readers. brain

1993;116( pt 1):39–52 14. sadato N, Pascual-leone A, et al.

Activation of the primary visual cortex by Braille reading in blind subjects. nature 1996;11;380(6574):526–528 15. Flor H. Cortical reorganisation and chronic pain: implications for rehabilitation. journal of rehabilitation medicine 2003;suppl.

41:66–72 16. Flor H, Braun C, et al. Extensive reorganization of primary somatosensory cortex in chronic back pain patients. neuroscience letters 1997;224:5–8 17. Vartiainen N, kirveskari E, et al. cortical reorganization in primary somatosensory cortex in patients with unilateral chronic pain.

The journal of pain 2009;10(8):854–859 18. Butler Ds. The sensitive nervous system. opTp 2006. IsBN 9780975091029 (Print £65.99). Buy from Amazon http://spxj.nl/14kd3Fw 19. Byl NN, Merzenich MM, jenkins WM. A primate genesis model of focal dystonia and repetitive strain injury: I. learning-induced dedifferentiation of the representation of the hand in the primary somatosensory cortex in adult monkeys. neurology 1996;47(2):508–520 20. Bara-jimenez W, Catalan Mj, et al.

Abnormal somatosensory homunculus in dystonia of the hand. annals of neurology 1998;44(5):828–831 21. Hallet M. Neurophysiology of dystonia: the role of inhibition. neurobiology of disease 2011;42:177–184 22. Davids k, Glazier P, et al. Movement systems as dynamical systems: the functional role of variability and its implications for sports medicine. sports medicine 2003;33:245–60 23. Glasgow P, Bleakley CM, Phillips. Being able to adapt to variable stimuli: the key driver in injury and illness prevention? british journal of sports medicine 2013;47:64–65 24. Hetsroni I, Finestone A, et al. A prospective biomechanical study of the association between foot pronation and the incidence of anterior knee pain among military recruits. journal of bone & joint surgery (br) 2006;88(7):905–908 25. Powers CM, Chen Py, et al. Comparison

of foot pronation and lower extremity rotation in persons with and without patellofemoral pain. foot and ankle international 2002;23(7):634–640 26. Hodges PW, Tucker k. Moving differently in pain: a new theory to explain the adaptation to pain. pain 2011;152(s):s90– s98 27. jacobs jV, Henry sM, Nagle kj.

People with chronic low back pain exhibit decreased variability in the timing of their anticipatory postural adjustments. behavioral neuroscience 2009;123:455– 458 28. Hanna T. somatics: reawakening the mind’s control of movement, flexibility, and health. da capo press 2004. IsBN 9780738209579 (Print £11.99). Buy from Amazon http://spxj.nl/187N2rk 29. Daffner kr, Mesulam MM, et al. regulation of attention to novel stimuli by frontal lobes: an event-related potential study. neuroreport 1998;9(5):787–791 30. Mima T, sadato N, et al. Brain structures related to active and passive finger movements in man. brain 1999;122(pt 10):1989–1997 31. kandel Er, schwartz j, jessell T. Principles of neuroscience (5th edn). mcGraw-hill medical 2000. IsBN 978-0838577011 (Print £52.79, kindle £79.41). Buy from Amazon http://spxj.nl/16mkQsX 32. Gilbert PF, Thach WT. Purkinje cell activity during motor learning. brain research 1997;128(2):309–328 33. Houk jC, Buckingham jT, Barto AG. Models of the cerebellum and motor learning. behavioral and brain sciences 1996;19(3):368–383 34. Blake DT, Merzenich MM. Changes of AI receptive fields with sound density. journal of neurophysiology 2002;88(6):3409– 3420 35. recanzone GH, schriener CE, Merzenich MM. Plasticity in the frequency representation of primary auditory cortex following discrimination training in adult owl monkeys. The journal of neuroscience 1993;13(1):87–103.

Acute soft tissue injury mAnAgement updAte Protection, rest, ice, compression and elevation, or PRICE, has been central to acute soft tissue injury management for many years. Although PRICE has many purported effects, the supporting scientific evidence has only recently been scrutinised. This article provides a compendium of the key messages from a recently developed set of clinical guidelines for the use of PRICE. This includes an overview of the scientific rationale for PRICE, practical advice for clinical implementation and suggestions that a new treatment acronym (POLICE) may be a better reflection of the current evidence base.

BY Dr chris BleakleY mcsP, PhD

T

he acronym PRICE (protection, rest, ice, compression and elevation) has been central to acute soft tissue injury management for many years. Its purported effects include: reduced tissue damage and oedema, analgesia and a faster return to function. The Association of Chartered Physiotherapists in Sport and Exercise Medicine (ACPSEM: Physios in Sport UK) previously examined the quality of the evidence base for using PRICE (1). A recent update (2) found a significant increase in the volume of research in this area (with over 250 relevant studies); however, much of the evidence base was comprised of basic scientific studies and observational evidence, rather than clinical evidence. The absence of high quality clinical research means that we are sometimes challenged

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to incorporate basic scientific theory into clinical practice. This review will provide an update on the scientific rationale for PRICE and its constituent components, and practical advice for clinical implementation.

ProTecTion, resT or movemenT Few can argue with the importance of protection in the early stages after injury. The rationale is to prevent rebleeding and re-rupture at the injury site. Practically, protection is guided by the nature of injury and may involve modified weight-bearing, taping, bracing or casting. Tissue support can also maximise patient comfort and confidence. Advising rest after an injury is less definitive and risks misinterpretation. Rest is commonly construed as a passive treatment sportEX medicine 2013;58(October):16-19

Literature review

approach devoid of movement or exercise. This can be deleterious as even short periods of unloading will produce adverse changes in muscle strength, tissue morphology, biomechanical properties and tensile strength.

There is growing evidence that early and progressive tissue loading is superior to rest. Loading usually involves progressive weight-bearing in conjunction with therapeutic exercise.

Traditionally, the rationale for introducing loading has been to restore mobility, strength and function after injury.

Although these goals remain important, contemporary evidence suggests that inducing mechanical load on healing tissue can also have an important biological effect. The underpinning mechanism is mechanotransduction, whereby mechanical loading prompts cellular responses that promote tissue structural change (3). During recovery from injury, this can involve (through upregulation of gene expression) the synthesis of key proteins associated with tissue healing (4,5).

The best practitioners are able to find a balance between loading and unloading during tissue healing.

Stressing tissues too aggressively after injury causes further damage. But, too much emphasis on unloading may be harmful and inhibits recovery. The secret is to find the ‘optimal loading’; this means replacing rest with a balanced and incremental rehabilitation programme where early activity promotes better recovery (6).

The benefits of optimal loading are probably best exemplified during muscle recovery. Muscle fibres have a capacity for regeneration; their satellite cells have the potential to proliferate and differentiate to eventually form new myofibres after injury. However this process is largely dependent on the induction of mechanical loading during the recovery process (7,8). Muscle tissue that is stress shielded throughout recovery will be compromised by fibrosis and is less likely to show regeneration of new fibres. An important caveat in the early stages is that muscle fibres around the injury site tend to work anaerobically until revascularisation is complete, so initially optimal loading should be of www.sportEX.net

short duration with longer rest periods.

Early static activation and mobilisation should progress to concentric and eccentric challenges. In general, the nature and intensity of mechanical loading should be case specific, progressive and reflect the unique mechanical stresses of the injured tissue.

ice Ice remains a stable component of acute injury management. Its basic premise is to cool injured tissue to achieve various therapeutic effects including reductions in pain and tissue damage and enhanced function. There is now a glut of research examining the effects of topical cooling on skin temperature (2). Unsurprisingly, it is clear that ice reduces superficial tissue temperature and induces analgesia.

Cooling skin temperature to less than 15°C is an important threshold for maximising analgesia. This can be readily achieved clinically using a 10 minute topical application of crushed ice (2). Side effects such as skin burns and nerve palsies are generally rare unless cooling interfaces are less than 0°C (this is often the case with commercial ice packs), excessive external compression is employed or the patient falls asleep (turning a 10 minute treatment into a 40 minute treatment!).

A common supposition is that ice decreases inflammation. There is evidence from animal models to suggest that ice can have a consistent effect on important cellular and physiological events associated with inflammation after injury. This includes cell metabolism, white blood cell activity within the vasculature, and potentially apoptosis – all of which were reduced (9). However, promising lab-based research doesn’t always translate into a clinical setting. The effect of ice on inflammation, swelling and function in a human model remains equivocal. To date only one study has examined the effectiveness of ice on recovery from acute muscle tear, with disappointing results (10). A fundamental problem is that muscle tissue cannot be readily cooled; therefore it is often difficult to reach the large temperature thresholds needed to reduce cellular

THE ABSEnCE OF HIgH qUALITy CLInICAL RESEARCH MEAnS THAT wE ARE SOMETIMES CHALLEngED TO InCORPORATE BASIC SCIEnTIFIC THEORy InTO CLInICAL PRACTICE metabolism. This is often compounded in clinical situations associated with high levels of body fat, deep tissue injury or insulating barriers at the cooling interface (such as post-surgical dressings). Clinicians should consider that in some clinical scenarios, coldinduced benefits may be limited to analgesia.

comPression anD elevaTion Oedema is a cardinal sign of acute inflammation after soft tissue injury.

Although some components of inflammation are essential for healing to progress (11), prolonged oedema is

ICE REMAInS A STABLE COMPOnEnT OF ACUTE InjURy MAnAgEMEnT

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COnTEMPORARy EvIDEnCE SUggESTS THAT InDUCIng MECHAnICAL LOAD On HEALIng TISSUE CAn ALSO HAvE An IMPORTAnT BIOLOgICAL EFFECT. THE UnDERPInnIng MECHAnISM IS ‘MECHAnOTRAnSDUCTIOn’

A FUnDAMEnTAL PROBLEM IS THAT MUSCLE TISSUE CAnnOT BE READILy COOLED. THIS MEAnS THAT In SOME CLInICAL SCEnARIOS, COLD-InDUCED BEnEFITS MAy BE LIMITED TO AnALgESIA

may depend on the magnitude of compressive pressure, the duration of application and whether this is applied intermittently or continuously.

High pressure, continuous compression such as a cohesive bandage applied under full stretch, will be best at preventing bleeding (eg. immediate pitch side management of an injury). As time post-injury progresses our focus should change from preventing frank bleeding to preventing excessive oedema formation; this requires much lower pressures as we only need to exceed the interstitial pressure at the injury site (15–30mmHg may suffice, however, this will vary based on the site of injury). The device must also conform to the shape of the injured body part.

A bad example of this is Tubigrip (a tube shaped device fitted on an L-shaped limb) which seems to create pressure peaks in the wrong areas and is not clinically effective (14). On the contrary, the popular approach of using horseshoe felt/pads (U- or L-shaped pads fitted around the ankle malleolus) conforms to the shape of the ankle and may even shunt oedema away from the pressure/pain sensitive injury site.

Enhancing venous outflow and lymphatic drainage should be a feature throughout recovery. Although uniform compressive pressures will decrease the size of the vessel and increase blood flow, they do not create much of a pressure gradient.

To do this most effectively, devices need to induce a graduated pressure (ie. compressive forces are higher distally than proximally). The final piece of the puzzle is to choose between continuous or intermittent pressures.

In the absence of injury, venous and lymphatic flows are maintained by the intermittent contraction and relaxation of the surrounding musculature (musculovenous pump), and intermittent pressure changes within the thoracic cavity. Pragmatists would therefore suggest that the best way of enhancing venous outflow and lymphatic drainage is to exercise (yes, we are back to optimal loading and not rest).

Perhaps the most revolutionary approach to enhance vascular and lymphatic function post-injury is the use of ‘kinesio tape’ or similar brands.

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sportEX medicine 2013;58(October):16-19

an unwanted by-product. It leads to increased tissue pressures causing pain, movement restrictions and muscle inhibition (arthrogenic muscle response) (12). Oedema forms when fluids accumulate within the interstitial space; this is really the aggregate effect of leaky capillaries, higher hydrostatic pressures within the vasculature and an altered osmotic gradient after injury (because of extravasation of cells from the vasculature into the interstitial space). If we can restore the pressure gradients at the capillary bed, we can prevent or limit the extent of oedema.

Most practitioners try to achieve this using at least one of these (sometimes contradictory) approaches: elevation, external compression, or taping.

The physiology underpinning elevation is pretty clear cut. Elevating your ankle decreases the gravitational force exerted on the column(s) of blood between the heart and foot thereby decreasing the hydrostatic pressure within the vasculature.

Although the optimal duration or angle of elevation remains contentious, common sense would suggest elevating for as long as possible after injury. Surprisingly there are few clinical studies in this area. The temporary effects of elevation should also be considered as tissue volumes quickly return to baseline when the injured limb is replaced into a gravity-dependent position. This is known as the ‘rebound effect’ and is most pronounced in distal body segments, such as ankles (13). A graduated return to standing after elevation is perhaps most logical.

Remember, early therapeutic exercise may be most comfortable and effective when undertaken in an elevated position.

There is some suggestion that elevation and compression should not be used simultaneously. Indeed a small number of studies have reported that when used together, they actually increase tissue girth after injury (1,2).

Elevation alone is probably enough to reduce hydrostatic pressure after injury; therefore, any additional external squeezing force maybe superfluous.

Elevation’s preventative approach (preventing the fluid from leaving the vessel in the first place) also seems much more logical than compression’s reactive approach (squeezing the fluid back in). However, although elevation probably trumps compression (at least when it comes to normalising tissue pressures), spending all day in an elevated position is not only impractical, but it doesn’t align with the concept of optimal loading.

As athletes are likely to spend a considerable amount of time walking, loading and exercising, compressive devices are an essential adjunct.

Clinical studies into compression are lacking, and much of its rationale is extrapolated from research relating to deep venous thrombosis prophylaxis and lymphoedema management. It is clear however that the effects of compressive devices are dose dependent. Indeed, their exact physiological effect (preventing bleeding, preventing oedema, venous shunting, lymphatic drainage)

LiterAture review

Although clinical evidence is lacking, the customary ‘crop circle’ bruising pattern that this tape leaves on the skin suggests a mechanistic action beyond placebo. The idea of microscopically ‘lifting’ the skin to clear lymphatic channels is akin to ‘anti-compression’ and is indicative of the current uncertainty in this field of study.

FuTure research Rest is a redundant phrase for the majority of soft tissue injuries. Replacing rest with ‘optimal loading’ gives us P.O.L.I.C.E. (protection, optimal loading, ice, compression and elevation); another neat acronym which better reflects the current evidence base (2). Specifically it includes the key concept of ‘mechanical loading’ which is one of the most powerful tools at a practitioner’s disposal. we should, however, be cognisant of the limitations associated with treatment acronyms. Although they can be used to enhance patient recall and compliance, they should not be used as a formula for treatment.

POLICE should be a stimulus to a new field of research. There is no ‘one size fits all’ approach to injury management; each constituent of POLICE will have a unique dose-dependent response. A number of mechanobiology research groups are undertaking significant work to further understand how healing tissues respond to mechanical stimulus.

Their key challenge is to quantify what is ‘optimal’ in terms of the dosage, nature and timing of mechanical loading after various injuries and how this can be best incorporated into clinical practice. references 1. Kerr KM, Daley L, Booth L for the Association of Chartered Physiotherapists in Sports and Exercise Medicine (ACPSM). guidelines for the management of soft tissue (musculoskeletal) injury with protection, rest, ice, compression and elevation (PRICE) during the first 72 h. chartered society of physiotherapy, 1998.

2. Bleakley CM, glasgow PD, et al.

Management of Acute Soft Tissue Injury Using Protection Rest Ice Compression and Elevation: recommendations from the Association of Chartered Physiotherapists in Sports and Exercise Medicine (ACPSM).

ACPSM 2011. http://spxj.nl/1chtZIy 3. Khan KM, Scott A. Mechanotherapy: how physical therapists’ prescription of exercise promotes tissue repair. British journal of www.sportEX.net

sports medicine 2009;43:247–52 4. Bring DK, Reno C, et al. joint immobilization reduces the expression of sensory neuropeptide receptors and impairs healing after tendon rupture in a rat model. journal of orthopaedic research 2009;27:274–80 5. Martinez DA, vailas AC, et al. Temporal extracellular matrix adaptations in ligament during wound healing and hindlimb unloading.

American journal of physiology: regulatory, integrative and comparative physiology 2007;293(4):r1552–r1560 6. Bleakley CM, glasgow P, MacAuley DC. PRICE needs updating, should we call the POLICE? British journal of sports medicine 2012;46:220–221 7. Best TM, gharaibeh B, Huard j. Stem cells, angiogenesis and muscle healing: a potential role in massage therapies?

British journal of sports medicine 2013;47:556–560 8. järvinen TA, järvinen TL, et al. Muscle injuries: optimising recovery. Best practice & research clinical rheumatology 2007;21:317–331 9. Bleakley CM, Davison gw. Cryotherapy and inflammation: evidence beyond the cardinal signs. physical therapy reviews 2010;15:430–435 10. Prins jC, Stubbe jH, et al. Feasibility and preliminary effectiveness of ice therapy in patients with an acute tear in the gastrocnemius muscle: a pilot randomized controlled trial. clinical rehabilitation 2011;25:433–441 11. Scott A, Khan KM, et al. what do we mean by the term “inflammation”? A contemporary basic science update for sports medicine. British journal of sports medicine 2004;38:372–380 12. Palmieri RM, Ingersoll CD, et al.

Arthrogenic muscle response to a simulated ankle joint effusion. British journal of sports medicine 2004;38:26–30 13. Tsang KK, Hertel j, Denegar CR. volume decreases after elevation and intermittent compression of postacute ankle sprains are negated by gravity-dependent positioning. journal of Athletic training 2003;38:320–324 14. watts BL, Armstrong B. A randomised controlled trial to determine the effectiveness of double Tubigrip in grade 1 and 2 (mild to moderate) ankle sprains. emergency medical journal 2001;18:46– 50.

Th AuThOr ThE Dr Chris Bleakley (BSc, PhD, MCSP, S SrP) is a Physiotherapist and Lecturer at the ulster Sports Academy, university of ulster. he is the Education and research Officer for the Association of Physiotherapists

online if you have a current online subscription, login at www.sportex.net to view these digital extras or download the mobile apps which are free to subscribers with online access. client advice handout CLIENT ADVICE HANDOUT

Immediate

treatment of injuries

WHY IMMEDIATE TREATMENT IS IMPORTANT

requirements and subsequent influx of blood.

The ice helps constrict the blood vessels thereby limiting bleeding and reducing the accumulation of unnecessary tissue protein.

How: Crushed ice wrapped in a damp towel or cloth is best (ice cubes can be wrapped in the cloth and smashed against a wall to crush them).

Alternatively ice in a plastic bag, a frozen gel pack, or a packet of frozen peas is a cheap and practicalsubstitute. A damp towel must be placed between the ice and the skin to avoid ice burn.

When and duration: The sooner ice can be applied the better. Ice should be applied for between 20–30 minutes every 3–4 hours. If the area is very bony such as the elbow, reduce this time to around 10 minutes. Do not return to activity immediately as the ice will have an analgesic ‘numbing’ effect.

The success of injury healing can be boosted by appropriate, effective and timely action particularly in the early stages of an injury (ie. the first 72 hours).

Any ‘soft tissue’ is subject to injury including ligaments (which join bones to bones), tendons (which join muscles to bones) and to muscles themselves. The immediate reaction of the body to injury is similar irrespective of the soft tissue structure and is known as an inflammatory reaction.

Injuries can be caused by overstretching, bruising or crushing. A strain describes overstretching of a muscle, while a sprain describes overstretching of a ligament or tendon.

THE INFLAMMATORY REACTION Tissue injury usually involves damage to small blood vessels that results in bleeding at the site of injury. This bleeding leads to the four main signs of inflammation: 1. Heat – chemicals released from the damaged tissue causes dilation of surrounding blood vessels to bring healing agents to the area. The result is more blood and therefore heat 2. Redness – is due to the increase in blood to the area 3. Pain – is caused by the chemicals released from the injured tissues as well as the increased tissue pressure from the fluid acting on nearby nerve endings 4. Swelling – is the result of this accumulation of extra fluid.

This inflammatory reaction is necessary as it is part of the natural healing process. However the body tends to overreact to sudden traumatic injury and as a result more inflammatory fluid accumulates than is necessary for healing. This fluid contains a protein that turns into replacement ‘scar’ tissue. If too much is allowed to form it may prevent thestructure returning to normal function with reduced flexibility and increased risk of re-injury.

POLICE PROTOCOL Anyone experiencing an injury should benefit from the following recommendations which should be carried out immediately and for up to 3–5 days after injury. These are remembered by the acronym POLICE (until now

20

58MD16-19PRICEBleakley_proofed AS_2.indd 20

COMPRESSION

Aim: To protect the injured tissue from undue stress that may disrupt the healing process and/or cause further injury.

How: This could include splinting or bandaging by a medical professional or simply rest, slings or crutches. Complete immobilisation isn’t usually necessary or desirable. Make sure the method of protection can accommodate swelling.

When and duration: Immediately and for 3–5 days depending on injury severity.

Aim: Compression limits an unnecessary accumulation of inflammatory fluid and ultimately over-production of scar tissue.

How: Simple off-the-shelf compression bandages such as Tubigrip™ and adjustable neoprene supports are best for self-application. The area should be compressed a minimum of six inches above and below the site of injury. It should be flexible enough to accommodate initial swelling and continue to apply pressure as this reduces.

The application of bandages and strapping is best left to a medical practitioner. Loosen the compression if you feel pins and needles around the compressed area.

When and duration: As soon as possible following injury and continue for the first 72 hours.

OPTIMAL LOADING

ELEVATION

Aim: Too much rest slows down recovery. Early and gentle work of the injured muscle actually stimulates tissue healing.

How: Start gently, but use progressive exercise to work up to normal levels of strength and movement. Be careful not to do too much too soon as this could cause further damage.

When and duration: Rest for a minimum of 24 hours after injury, then begin a progressive loading programme for as long as needed, depending on injury severity.

Aim: To lower the blood pressure and therefore help limit bleeding and encourage drainage of fluid through the lymphatic system.

How: Using pillows, foot stools, slings etc.

When and duration: As soon as possible following injury and for the first 72 hours.

referred to as PRICE where the R for rest has been replaced by OL for optimal loading.).

PROTECT

ICE Aim: Ice is used to limit the body’s overreaction by reducing the temperature of the injured tissue and therefore the energy

When following POLICE is also important to avoid HARM, hence the saying ‘Give POLICE and avoid HARM’.

AVOID H – Heat (eg. hot bath, sauna) A – Alcohol R – Running M - Massage sportEX medicine 2013;58(October):16-20

11/09/2013 12:50

n which treatment acronym do you think is a better reflection of the current evidence base? PRICE or POLICE? DISCUSSIONS what are the limitations of each? n what does optimal loading mean to you as a practitioner? what is the underpinning mechanism for optimal loading and how can this be best exploited? n what are the most important factors when choosing an effective compressive device to manage an acute ankle sprain? How might this change throughout the recovery period? n which components of POLICE would have most therapeutic effect when managing a 2-day-old, deep hamstring strain? n After a muscle injury, some practitioners choose to apply kinesio tape and compressive wrap concomitantly. why might this be ineffective?

This article is based on a document published by Physios in Sport (ACPSEM) which can be purchased from their website in both summary and full versions. For more information visit http://spxj.nl/18nmP32

19

cLient Advice HAndout

Immediate

treatment of injuries

WhY immeDiaTe TreaTmenT T is imPorTanT

requirements and subsequent influx of blood.

The ice helps constrict the blood vessels thereby limiting bleeding and reducing the accumulation of unnecessary tissue protein. how: Crushed ice wrapped in a damp towel or cloth is best (ice cubes can be wrapped in the cloth and smashed against a wall to crush them).

Alternatively ice in a plastic bag, a frozen gel pack, or a packet of frozen peas is a cheap and practicalsubstitute. A damp towel must be placed between the ice and the skin to avoid ice burn.

When and duration: The sooner ice can be applied the better. Ice should be applied for between 20–30 minutes every 3–4 hours. If the area is very bony such as the elbow, reduce this time to around 10 minutes. Do not return to activity immediately as the ice will have an analgesic ‘numbing’ effect.

The success of injury healing can be boosted by appropriate, effective and timely action particularly in the early stages of an injury (ie. the first 72 hours).

Any ‘soft tissue’ is subject to injury including ligaments (which join bones to bones), tendons (which join muscles to bones) and to muscles themselves. The immediate reaction of the body to injury is similar irrespective of the soft tissue structure and is known as an inflammatory reaction.

Injuries can be caused by overstretching, bruising or crushing. A strain describes overstretching of a muscle, while a sprain describes overstretching of a ligament or tendon.

The inFlammaTorY reacTion ion Tissue injury usually involves damage to small blood vessels that results in bleeding at the site of injury. This bleeding leads to the four main signs of inflammation: 1. heat – chemicals released from the damaged tissue causes dilation of surrounding blood vessels to bring healing agents to the area. The result is more blood and therefore heat 2. redness – is due to the increase in blood to the area 3. Pain – is caused by the chemicals released from the injured tissues as well as the increased tissue pressure from the fluid acting on nearby nerve endings 4. swelling – is the result of this accumulation of extra fluid.

This inflammatory reaction is necessary as it is part of the natural healing process. However the body tends to overreact to sudden traumatic injury and as a result more inflammatory fluid accumulates than is necessary for healing. This fluid contains a protein that turns into replacement ‘scar’ tissue. If too much is allowed to form it may prevent thestructure returning to normal function with reduced flexibility and increased risk of re-injury.

Police ProTocol Anyone experiencing an injury should benefit from the following recommendations which should be carried out immediately and for up to 3–5 days after injury. These are remembered by the acronym POLICE (until now

20

comPression c omP om Pression

aim: To protect the injured tissue from undue stress that may disrupt the healing process and/or cause further injury. how: This could include splinting or bandaging by a medical professional or simply rest, slings or crutches. Complete immobilisation isn’t usually necessary or desirable. Make sure the method of protection can accommodate swelling.

When and duration: Immediately and for 3–5 days depending on injury severity.

aim: Compression limits an unnecessary accumulation of inflammatory fluid and ultimately over-production of scar tissue. how: Simple off-the-shelf compression bandages such as Tubigrip™ and adjustable neoprene supports are best for self-application. The area should be compressed a minimum of six inches above and below the site of injury. It should be flexible enough to accommodate initial swelling and continue to apply pressure as this reduces.

The application of bandages and strapping is best left to a medical practitioner. Loosen the compression if you feel pins and needles around the compressed area.

When and duration: As soon as possible following injury and continue for the first 72 hours.

oPTimal loaDing

elevaTion

aim: Too much rest slows down recovery. Early and gentle work of the injured muscle actually stimulates tissue healing. how: Start gently, but use progressive exercise to work up to normal levels of strength and movement. Be careful not to do too much too soon as this could cause further damage.

When and duration: Rest for a minimum of 24 hours after injury, then begin a progressive loading programme for as long as needed, depending on injury severity.

aim: To lower the blood pressure and therefore help limit bleeding and encourage drainage of fluid through the lymphatic system. how: Using pillows, foot stools, slings etc.

When and duration: As soon as possible following injury and for the first 72 hours.

referred to as PRICE where the R for rest has been replaced by OL for optimal loading.).

ProTecT

ice aim: Ice is used to limit the body’s overreaction by reducing the temperature of the injured tissue and therefore the energy

when following POLICE is also important to avoid HARM, hence the saying ‘give POLICE and avoid HARM’.

avoiD h – Heat (eg. hot bath, sauna) a – Alcohol r – Running m - Massage sportEX medicine 2013;58(October):16-20

Sprint-related hamString injurieS The currenT sTaTe of play

BY Colm DalY mCSP, mSC

IntroDuCtIon Hamstring injury is the most common injury seen in sports that involve sprinting accounting for 6â&#x20AC;&#x201C;26% of all injuries seen in football, rugby, Gaelic games, cricket, track sprinting and Australian football (AFL) (1-7). There is little doubt that hamstring injury is a major rehabilitation challenge with high recurrence rates across multiple sports (8). With this article, we will explore the numerous risk factors, such as inadequate rehabilitation, increasing age, strength imbalances and biomechanical asymmetries. We will highlight recent progress that has been made on injury prevention and show how the absence of cohesive clinical recommendations creates a rehabilitation challenge. Recent muscle injury classifications by Chan et al. and Mueller-Wohlfahrt et al. will be explored (9,10). These have given us a better basis on which to understand the complexity of hamstring muscle injury,

Hamstring injury is a major problem for sports involving high-speed running. This article will explore how common the problem is, how often it recurs and what work has been done on risk factors and their moderation. Further, recent advances in diagnostic classifications and rehabilitation will be outlined.

SpRinT-ReLATeD HAMSTRinG injuRy RiSk iS pReDoMinAnTLy ConFineD To THe biCepS FeMoRiS (LonG HeAD) 20

especially when one considers the range of possible structures that can be injured or contribute to pain in the hamstring area. Finally, recent promising rehabilitation publications are described to give an immediate clinical takeaway.

an anatomICal anD PhYSIologICal overvIew The hamstring complex comprises three muscles â&#x20AC;&#x201C; medially the semitendinosus and semimembranosus, and laterally the biceps femoris. The latter is comprised of a biarticular long head and uniarticular short head, each with separate innervations from the tibial and common peroneal nerves respectively.

The biceps femoris (long head) and semitendinosus form a common tendon originating at the ischial tuberosity of the pelvis, whereas the semimembranosus passes deep to this tendon, inserting more superiorly and laterally on the same tuberosity. Distally, the long tendon of the semitendinosus wraps around the medial aspect of the knee,

and, along with sartorius and gracilis, forms the pes anserinus insertion on the anteromedial aspect of the tibia.

The semimembranosus inserts along the medial tibial condyle, communicating with the popliteal region. Laterally, the distal biceps femoris inserts onto the fibula, joining with fibres of the lateral collateral ligament and fascia of the lower leg (Figs 1,2).

During high-speed running, the hamstrings are almost constantly active, contracting concentrically to pull the leg posteriorly through stance and acting eccentrically to slow the forward moving limb at the end of swing (11,12). Although the muscle complex as a whole is active within both the concentric and eccentric phases, the largest contribution comes from the biceps femoris (13). Although this is somewhat speculative, the joint wrapping anatomical arrangement of the distal hamstring insertions suggests that they may also act in the transverse (rotation) plane around the knee joint (14). Altered sportEX medicine 2013;58(October):20-26

literature review

hamstring synergy may therefore lead to changes in rotary control of the knee joint and possibly expose the athlete to increased ligamentous and articular injury risk. in the context of this article, sprint-related hamstring injury risk is predominantly confined to the biceps femoris (long head) (15). A growing body of research points to the terminal swing phase of sprinting as the moment when the biceps femoris is likely to injure.

At this moment the hip is flexed and the knee is nearing terminal extension.

The lengthening biceps femoris is acting eccentrically to slow tibia down in preparation for foot contact. The risk of injury lies in the combination of a lengthened muscle generating high eccentric forces. When these forces exceed the maximum tolerable level of strain within the sarcomeres, the muscle fibres tear (11,16-19).

Carl Askling has highlighted an alternative, non-sprint-related mechanism of hamstring muscle injury. This stretching-type injury involves the proximal tendon of the semimembranosus and is often seen in dance. in sport, as in dance, this injury tends to occur at extreme, forced hip flexion combined with knee extension, such as during a slide tackle or high kick. The much more proximal site of injury appears to be associated with a more difficult and prolonged rehabilitation (15).

InCIDenCe Hamstring injury occurs commonly in sports that involve sprinting. in english premiership football, hamstring injury accounted for 12% of all injuries over two seasons (1). The high incidence of hamstring injury in football is confirmed by ekstrand et al. who monitored european professional football across the 2001–2009 seasons and found that hamstring injuries accounted for 37% of all muscle injuries (20). in the 2002/03 and 2003/04 english premiership rugby seasons, a hamstring injury incidence of 5.6 per 1000 player-hours was recorded during matches, with backs sustaining this injury more often than forwards (incidence 8.6 v. 3.0 per 1000 player-hours)(2). in cricket, hamstring injury accounted for 11% of all injuries over 5 seasons (5), whereas in Gaelic games hamstring was the most www.sportEX.net

common injury over four seasons in football (24%) and accounted for 16.5% (95% Ci 11.8 to 21.8) of injuries over one season in hurling (3,4). in track athletics, 14% of injuries that occurred involved the hamstring (7), and in Australian rules football hamstring injuries account for, on average (10 seasons), six new injuries per club per season (6).

HAMSTRinG injuRy iS THe MoST CoMMon injuRy Seen in SpoRTS THAT invoLve SpRinTinG

reCurrenCe previous injury is the greatest risk factor for hamstring injury accounting for a two- to sixfold increase in risk (21). Re-injury rates of 13.9–63.3% over two subsequent seasons exist across multiple sports (8). in football, a hamstring injury has been reported to increase reinjury risk by 11.6 fold (oR; 95% Ci 3.5-39) during the following season (22). Aside from Australian rules football (where rates have dropped from 45% to 12%) (6) the rates of re-injury have remained static for 30 years. This suggests that there are risk factors associated with previous injury which are persistent despite rehabilitation. Due to the lack of prospective data in this area, it is difficult to discern if such factors exist before the initial injury or are present as a result of the injury itself.

unDerStanDIng rISk faCtorS Whether a risk factor exists as a result of an injury, pre-dates an injury or exists in the absence of any injury, the recognition and amelioration of such factors is key in reducing (re-) injury rates. it is increasingly recognised that risk factors in hamstring injury are complex and multifactorial (21).

This challenges the conditioner and/ or clinician to consider multiple and often complex inter-related issues when designing injury prevention and/ or rehabilitation programmes. For an excellent overview of the risk factors in hamstring injury the reader is directed to the review by opar et al. (23).

The following risk factors will now be discussed in more detail: n exposure n Age n Scar formation n Strength asymmetry n Fatigue n biochemical factors and neuroinhibition.

© Primal Pictures 2013

Figure 1: Biceps femoris muscle in isolation

online

animation

If you have a current subscription, login at www.sportex.net to view this material or download the mobile apps which are free to subscribers with online access.

Biceps femoris

Semitendinosus Semimembranonosus

© Primal Pictures 2013

Figure 2: Muscles that make up the hamstrings

21

exposure A fundamental reality of sprint-related hamstring injury is that these injuries relate to speed. There is a threshold to muscle fibre force tolerance. in the case of the biceps femoris this is inherently linked to running speed. The faster we run, the more energy is being absorbed by the biceps femoris during terminal swing. in sport, it is the sprinters who sustain this injury (eg. the backs in rugby union). As we push the performance boundaries and our fast runners become faster, they will get closer and closer to muscle fibre failure. An obvious concept (although perhaps alien to readers of this publication), is that maybe the most effective way to reduce hamstring injury risk is to run slower!

age increasing age has been highlighted as a risk factor in hamstring injury (8,23).

This fact is true even when other confounding factors such as previous injury are considered. it is not currently clear why athletes display up to a fourfold increased risk of hamstring injury as they progress into their midtwenties. Suggested reasons include natural age-related reductions in muscle volume, but it seems less likely that this would apply to elite level 24-year-old athletes. Another possible explanation is in the tentative links between hamstring muscle dysfunction and lower lumbar degenerative changes. As highlighted within the Munich consensus injury classification (see below), there is growing recognition of the potential for neuromuscular dysfunction originating at the spinal level. perhaps tethering of the nerve root or maladaptive postural control linked to spinal dysfunction could have a bearing on hamstring function.

These links however, require further investigation and remain speculative.

Scar formation Silder et al. have reported a proliferation of scar tissue in the region of the musculotendinous junction following injury, leading to increased levels of strain in adjacent muscle fibres during eccentric contractions (24).

Should these levels of strain exceed the mechanical limits of these fibres an injury is likely to occur. Although it is accepted that prevention is most 22

definitely better than cure, early and effective post-injury rehabilitation may be key in minimising excessive, and function limiting scar formation. However, early rehabilitation must also be considerate of the potential vulnerability of the injury site and care must be taken to ensure any loading protocols are non-injurious.

Strength asymmetry pre-season asymmetries in knee flexor strength as well as imbalances in hamstring/quadriceps peak torque (H:Q ratio) have been suggested as potential predictors of subsequent hamstring injury in American and association football, AFL and track athletics. However, a number of authors have found no association between asymmetry and injury risk [see opar et al. (23)]. Studies examining H:Q ratios are similarly conflicting, although an increase in peak quadriceps concentric torque on the injured limb appears to be associated with increased risk (25).

This finding illustrates the complexity in examining for strength imbalances/ deficits in hamstring injury prevention. it is well accepted that lumbo-pelvichip control has a bearing of hamstring muscle function (26,27). Therefore, future studies should examine for deficits in strength in these regions. it appears that athletes who have returned to sport following hamstring injury have persistent eccentric weakness of their hamstrings when compared to the uninjured leg measured using isokinetic dynamometry (28). This weakness is present despite these athletes having pain-free function and having returned to their sport unhindered.

Although this data is based on a rather homogenous group (n=28) of recreational athletes this information builds on similar findings by Lee et al. who report a decrease in eccentric hamstring peak torque which occurred at shorter hamstring lengths on the injured side (29). Again this data is based on isokinetic analysis of a small group of previously injured athletes (n=14) from a range of sports. nevertheless, addressing hamstring eccentric weakness after injury has become a major component of modern rehabilitation strategies and has led to

clear reductions in re-injury rates (see below).

fatigue Hamstring injuries tend to occur late in each half of european football games and have recently been associated with games congestion within ueFA competitions (30,31). both factors suggest that fatigue and injury are associated. This may be related to inherent physiological consequences within the muscles or more systemic effects. Fatigue has been shown to lead to increases in knee extension and decreases in hip flexion during running (32). in addition, fatigue appears to lead to a selective loss of eccentric hamstring torque generation capability (33,34). Further research is required to confirm these findings.

Biomechanical factors and neuroinhibition Deficits in lumbo-pelvic-hip control and flexibility have been identified as potential risk factors in hamstring injury (21).

Running with increased peak anterior pelvic tilt, hip flexion and knee extension would theoretically lead to increase peak strain on the biceps femoris during terminal swing. indeed increased activity of the gluteus maximus and external oblique have, at least theoretically be shown to reduce peak biceps femoris strain (35,36). brughelli et al. have reported asymmetrical running patterns in athletes with prior injury (37).

Rehabilitation programmes which address postural control have been shown to be superior to those that donâ&#x20AC;&#x2122;t in terms of injury recurrence (26). persistent reductions in muscle activity levels in previously injured biceps femoris have also been demonstrated (28). perhaps the most recent development in the area of hamstring injury risk is the proposed idea of persistent neuroinhibition following injury.

Fyfe et al. postulate that the cumulative effect of pain, inadequate early rehabilitation, muscle atrophy, eccentric weakness and shorter functional muscle lengths may lead to attempts at rehabilitation being in vain (38). This hypothesis requires further evaluation but, once again, this theory re-iterates the absolute necessity of getting early rehabilitation right. sportEX medicine 2013;58(October):20-26

literature review

taBle 1. muSCle InjurY ClaSSIfICatIon SYStem BaSeD on SIte of leSIon [aDaPteD from Chan et al. (9)].

1. Proximal mtj 2. muscle

A. proximal

a. intramuscular

b. Middle

b. Myofascial

C. Distal

c. Myotfascial/perifascial d. Myotendinous e. Combined

3. Distal mtj MTJ, musculotendinous junction.

taBle 2: munICh ConSenSuS muSCle InjurY ClaSSIfICatIon SYStem [aDaPteD from mueller-wohlfahrt hw, et al. (10)].

Type A: indirect muscle injury/disorder functional

Type b: Direct muscle injury

Structural

1. overextension 3. partial muscle tear A. Fatigue-induced A. Minor b. Delayed-onset b. Moderate muscle soreness 4. (Sub)total tear 2. neuromuscular (including subtotal or A. Spine-related complete muscle tear b. Muscle-related or tendinous avulsion)

InjurY ClaSSIfICatIon DeveloPmentS Recent literature reflects the growing realisation that not all hamstring injuries are related to muscle fibre injury. in an anatomical environment composed of neural, perifascial, myofascial, myotendinous and tendinous structures, there is much potential for painful dysfunction, both locally and via neural and myofascial referral. A number of recent papers have recommended an update to the injury classification terminology, which until recently has following the basic Grade 1–3 model.

Chan et al. propose a more detailed description of injury location suggesting that such differentiation may be of prognostic value (Table 1)(9).

The proposed muscle injury classification system termed the Munich consensus (10) refers to structural injuries using a classification broadly in line with the Grade 1–3 system (Table 2). The Munich consensus classification also includes a useful reference to non-structural muscle disorders including those related to overexertion or neuromuscular aetiology. These disorders are reported to be distinct from structural injuries in that they have, www.sportEX.net

Contusion Laceration

for the most part, negative MRi findings with a distinct spinal or local aetiology.

An early prospective study has highlighted the prognostic value of the Munich ‘structural’ sub-classification in predicting recovery times but indicated that the ‘functional’ sub-classification has less value in this regard.

Finally, Malliaropoulos et al. report a functional classification system specific for hamstring injuries based on measures of active range of motion at 48 hours after injury (Table 3)(39).

This classification is predictive of return to full activity in track athletes with significant differences in recovery time between each grade. These measures are taken with the injured athlete lying supine with hips and knees flexed to 90°. The athlete actively extends their

opTiMiSinG ReCoveRy FRoM boTH An injuRy AnD FunCTionAL peRSpeCTive iS key.

ReCenT LiTeRATuRe ReFLeCTS THe GRoWinG ReALiSATion THAT noT ALL HAMSTRinG injuRieS ARe ReLATeD To MuSCLe FibRe injuRy

taBle 3: arom funCtIonal ClaSSIfICatIon [aDaPteD from mallIaroPouloS et al. (39)]. functional classification

arom deficit

Grade i

<10°

Grade ii

10–19°

Grade iii

20–29°

Grade iv

>30°

AROM, active range of motion.

Figure 3: Position of goniometer for measuring the active straight leg raise (39). Photo courtesy of Katy Sheffield, Solihul College, UK.

23

ReCenT LiTeRATuRe ReFLeCTS THe GRoWinG ReALiSATion THAT noT ALL HAMSTRinG injuRieS ARe ReLATeD To MuSCLe FibRe injuRy Box 1: mrI ImageS ShowIng DIfferent hamStrIng InjurIeS anD ShowIng how the ClaSSIfICatIon SYStem BY Chan et al. woulD Be uSeD (9).

Sagittal Bf

knee and a measure is made with a goniometer. The deficit between injured and uninjured side is recorded (Fig. 3). each of the three injury classification systems outlined provides a valuable contribution to the previous simplistic diagnostic approach to hamstring injury. Future research is required to explore the prognostic value of such methods and identify optimal associated rehabilitation protocols. it is important to note that the three systems outlined are mutually complementary and an overall diagnostic consensus would be welcomed. examples of different hamstring injuries and how they would be classified using the system suggested by Chan et al. (9) can be seen in box 1.

what IS oPtImal rehaBIlItatIon?

Image 1: Sagittal MRi image showing a tear of the biceps femoris classified as a Grade ii 2.b.b injury. oedema and haemorrhage of the muscle or MTj extending to the fascial planes of the biceps femoris can be seen.

myotendinous involvement

optimise hamstring lengthening mechanics

Image 2: Axial MRi image showing an injury at the musculotendinous junction (MTj) with myotendinous involvement – classified as a Grade i or ii 1.d injury.

Intramuscular

myofascial fluid

image 3: Axial MRi image of a myofascial tear of the MTj, with myotendinous involvement and the presence of myofascial fluid classified as a Grade i or ii 1.c/d injury.

MRi images kindly provided by o. Chan, Queen Mary university of London, uk.

24

There is little doubt that a premature return to sporting activity and associated inadequate rehabilitation are major risk factors for re-injury. optimising recovery from both an injury and functional perspective is key. This is likely to comprise of three main elements: optimise hamstring lengthening mechanics; address postural control deficits; restore sport specific function.

Addressing eccentric strength deficits is paramount in hamstring injury prevention and rehabilitation. There is now strong evidence that eccentric strengthening reduces hamstring injury and re-injury rates. The most well known, and arguably most easily achieved, method for gaining enhanced eccentric strength is the nordic lunge (video 1). The evidence of the effectiveness of this exercise is compelling. peterson et al. have shown that there is a 70% reduction in hamstring (re-)injury rates when their 10 week nordic protocol is implemented and followed in football (40).

This protocol is not without its critics particularly with regard to the single joint, uniplanar nature of the exercise (21,41). The nordic lunge is not an easy exercise. perhaps this is reflected in the poor levels of compliance recorded in some

research papers (42,43). Finally, many commentators anecdotally report high levels of delayed-onset muscle soreness after completion of this programme. it is this author’s opinion that this argument is somewhat redundant – peterson and colleagues specifically describe a very gradual build-up of repetitions which is likely to allow adequate time for athletes to become accustomed and therefore reduce the likelihood of DoMS (40). nevertheless, as described by Silder and colleagues, this form of exercise should only be introduced when postinjury healing has been well established so as to avoid iatrogenic injury (27).

address postural control deficits The role of lumbo-pelvic-hip control in hamstring injury is now well established, although further confirmatory research in this area would be welcomed. A recent publication by Silder and colleagues (27) builds on prior contributions (26,44) in highlighting the value of early and systematic targeting of postural control during rehabilitation. The ‘postural agility and trunk stability’ (pATS) protocol, initially proposed and tested by Sherry and best (26) represented a sea-change in rehabilitation design in hamstring injury and a move away from traditional stretching and strengthening methods. incorporating multidimensional pelvic control work (video 2) and especially combining eccentric hamstring loading using exercises such as the 3-dimensional bridge and single leg ‘y’ touch (video 3) is likely to enhance rehabilitation greatly. For a more comprehensive overview of similar exercises the reader is directed to the papers mentioned above, as well as Heiderscheit et al. (41).

restore sport specific function This goal involves several aspects, many of which maybe unique to the athlete’s sport. The therapist/conditioner should consider the sport specific demands of the athlete’s sport and incorporate such elements into rehabilitation. Silder et al. outline a combined eccentric loading and running protocol which they show to be equally as effect as the pATS protocol in preventing re-injury (27). The use of controlled exposure to sprinting in early- to mid-stage rehabilitation is sportEX medicine 2013;58(October):20-26

literature review

welcome as it replicates closely the exact form of activity when the injury causing dysfunction is likely to occur. The reader is directed to this excellent paper for further direction, including a detailed protocol design.

Successfully addressing neuroinhibition following hamstring injury is a challenging task. Askling and nilsson describe a similar test which they suggest can be used as a final outcome measure to clear an athlete to return to sport (45). The Askling H-Test is a measure of insecurity and range in an active, high-speed, straight leg raise using a specially built device. notably, when used as pre-requisite test for return to sport clearance, early indications suggest that ensuring the athlete has achieved bilateral symmetry may lead to a marked reduction in reinjury rates.

ConCluSIon Hamstring injuries are common and challenging injuries to treat. The growing recognition that the aetiology of hamstring injury is complex and multifactorial has led to the emergence of refinement of injury prevention and rehabilitation methods. Although the evidence is still in its infancy, the incorporation of appropriate and effective eccentric strengthening, lumbo-pelvic hip control protocols and sport specific drills (including running) into (p)rehabilitation may give the clinician/conditioner enhanced and potentially more effective means of achieving optimal outcome for their athletes. references 1. Woods C, Hawkins RD, et al. The Football Association Medical Research programme: an audit of injuries in professional football analysis of hamstring injuries. British journal of Sports medicine 2004;38(1):36–41 2. brooks jH, Fuller CW, et al. epidemiology of injuries in english professional rugby union: part 1 match injuries. British journal of Sports medicine 2005;39(10):757–766 3. Murphy jC, Gissane C, blake C. injury in elite county-level hurling: a prospective study. British journal of Sports medicine 2010;46(2):138–142 4. Murphy jC, o’Malley e, et al. incidence of injury in Gaelic football: a 4-year prospective study. american journal of Sports medicine 2012;40(9):2113–2120 5. orchard j, james T, et al. injuries in Australian cricket at first class level 1995/1996 to 2000/2001. British journal

www.sportEX.net

of Sports medicine 2002;36(4):270–274; discussion 5 6. orchard jW, Seward H, orchard jj.

Results of 2 decades of injury surveillance and public release of data in the Australian Football League. american journal of Sports medicine 2013;41(4):734–741 7. bennell kL, Crossley k. Musculoskeletal injuries in track and field: incidence, distribution and risk factors. Australian journal of Science and medicine in Sport 1996;28(3):69–75 8. de visser HM, Reijman M, et al. Risk factors of recurrent hamstring injuries: a systematic review. British journal of Sports medicine 2011;46(2):124–130 9. Chan o, Del buono A, et al. Acute muscle strain injuries: a proposed new classification system. Knee Surgery, Sports traumatology, arthroscopy 2012;20(11):2356–2362 10. Mueller-Wohlfahrt HW, Haensel L, et al.

Terminology and classification of muscle injuries in sport: the Munich consensus statement. British journal of Sports medicine 2013;47(6):342–350 11. Chumanov eS, Heiderscheit bC, Thelen DG. Hamstring musculotendon dynamics during stance and swing phases of high-speed running. medicine & Science in Sports & exercise 2011;43(3):525–532 12. Thelen DG, Chumanov eS, et al. Simulation of biceps femoris musculotendon mechanics during the swing phase of sprinting. medicine & Science in Sports & exercise 2005;37(11):1931–1938 13. Chumanov eS, Wille CM, et al. Changes in muscle activation patterns when running step rate is increased. gait & posture 2012;36(2):231–235 14. Lynn Sk, Costigan pA. Changes in the medial-lateral hamstring activation ratio with foot rotation during lower limb exercise. journal of electromyography & Kinesiology 2009;19(3):e197–205 15. Askling CM, Malliaropoulos n, karlsson j.

High-speed running type or stretching-type of hamstring injuries makes a difference to treatment and prognosis. British journal of Sports medicine 2012;46(2):86–87 16. Heiderscheit bC, Hoerth DM, et al. identifying the time of occurrence of a hamstring strain injury during treadmill running: a case study. Clinical Biomechanics 2005;20(10):1072–1078 17. Schache AG, Wrigley Tv, et al. biomechanical response to hamstring muscle strain injury. gait & posture 2009;29(2):332–338 18. Thelen DG, Chumanov eS, et al. Hamstring muscle kinematics during treadmill sprinting. medicine & Science in Sports & exercise 2005;37(1):108–114 19. Thelen DG, Chumanov eS, et al. neuromusculoskeletal models provide insights into the mechanisms and rehabilitation of hamstring strains. exercise and Sport Sciences reviews 2006;34(3):135–141 20. ekstrand j, Hägglund M, Waldén M. epidemiology of muscle injuries in professional football (soccer).

online video 1: nordic lunge exercise (http://spxj.nl/1dChPnx).

Courtesy of Colm Daly

video 2: Dynamic and core stability: the pelvis (http://spxj.nl/1afjmdu).

Courtesy of Bob wood

video 3: Y touch exercise (http://spxj.nl/1dChPnx) Courtesy of Colm Daly

american journal of Sports medicine 2011;39(6):1226–1232 21. Mendiguchia j, Alentorn-Geli e, brughelli M. Hamstring strain injuries: are we heading in the right direction? British journal of Sports medicine 2012;46(2):81–85 22. Arnason A, Sigurdsson Sb, et al. Risk factors for injuries in football. american journal of Sports medicine 2004;32(1 Suppl):5S–16S 23. opar DA, Williams MD, Shield Aj. Hamstring strain injuries factors that lead to injury and re-injury. Sports medicine 2012;42(3):209–226 24. Silder A, Thelen DG, Heiderscheit bC. 25

effects of prior hamstring strain injury on strength, flexibility, and running mechanics.

Clinical Biomechanics 2010;25(7):681–686 25. Freckleton G, pizzari T. Risk factors for hamstring muscle strain injury in sport: a systematic review and meta-analysis.

British journal of Sports medicine 2013;47(6):351–358 26. Sherry MA, best TM. A comparison of 2 rehabilitation programs in the treatment of acute hamstring strains. journal of orthopaedic & Sports physical therapy 2004;34(3):116–125 27. Silder A, Sherry MA, et al. Clinical and morphological changes following 2 rehabilitation programs for acute hamstring strain injuries: a randomized clinical trial. journal of orthopaedic & Sports physical therapy 2013;43(5):284–299 28. opar DA, Williams MD, et al. knee flexor strength and bicep femoris electromyographical activity is lower in previously strained hamstrings. journal of electromyography & Kinesiology 2013;23(3):696–703 29. Lee Mj, Reid SL, et al. Running biomechanics and lower limb strength associated with prior hamstring injury. medicine & Science in Sports & exercise 2009;41(10):1942–1951 30. ekstrand j, Hägglund M, Waldén M. injury incidence and injury patterns in professional football: the ueFA injury study.

British journal of Sports medicine 2011;45(7):553–558 31. bengtsson H, ekstrand j, Hägglund M. Muscle injury rates in professional football increase with fixture congestion: an 11-year follow-up of the ueFA Champions League injury study. British journal of Sports medicine 2013;47(12):743–747 32. pinniger Gj, Steele jR, Groeller H. Does fatigue induced by repeated dynamic efforts affect hamstring muscle function?

medicine & Science in Sports & exercise 2000;32(3):647–653 33. Small k, Mcnaughton L, et al. The effects of multidirectional soccer-specific fatigue on markers of hamstring injury risk. journal of Science and medicine in Sport 2010;13(1):120–125 34. Greig M. The influence of soccer-specific fatigue on peak isokinetic torque production of the knee flexors and extensors. american journal of Sports medicine 2008;36(7):1403–1409 35. Chumanov eS, Heiderscheit bC, Thelen DG. The effect of speed and influence of individual muscles on hamstring mechanics during the swing phase of sprinting. journal of biomechanics 2007;40(16):3555–3562 36. Chumanov eS, Thelen DG, et al. Anterior pelvic tilt increases hamstring stretch during sprinting. medicine & Science in Sports & exercise 2006;38(5):S265–S626 37. brughelli M, Cronin j, et al. Contralateral leg deficits in kinetic and kinematic variables during running in Australian rules football players with previous hamstring injuries. journal of Strength and Conditioning research 2010;24(9):2539–2544 38. Fyfe jj, opar DA, et al. The role of neuromuscular inhibition in hamstring strain injury recurrence. journal of electromyography & Kinesiology 2013;23(3):523–530 39. Malliaropoulos n, isinkaye T, et al.

Reinjury after acute posterior thigh muscle injuries in elite track and field athletes. american journal of Sports medicine 2011;39(2):304–310 40. petersen j, Thorborg k, et al. preventive effect of eccentric training on acute hamstring injuries in men’s soccer: a cluster-randomized controlled trial. american journal of Sports medicine 2011;39(11):2296–2303 41. Heiderscheit bC, Sherry MA, et al.

continuing education Multiple choice questions This article also has an eLearning test which can be found under the eLearning section of our website.

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Hamstring strain injuries: recommendations for diagnosis, rehabilitation, and injury prevention. journal of orthopaedic & Sports physical therapy 2010;40(2):67–81 42. engebretsen AH, Myklebust G, et al. prevention of injuries among male soccer players: a prospective, randomized intervention study targeting players with previous injuries or reduced function. american journal of Sports medicine 2008;36(6):1052–1060 43. Gabbe bj, branson R, bennell kL. A pilot randomised controlled trial of eccentric exercise to prevent hamstring injuries in community-level Australian Football. journal of Science and medicine in Sport 2006;9(1–2):103–109 44. Heiderscheit bC, Sherry MA, et al.

Hamstring strain injuries: recommendations for diagnosis, rehabilitation, and injury prevention. journal of orthopaedic & Sports physical Therapy 2010;40(2):67–81 45. Askling CM, nilsson j, Thorstensson A. A new hamstring test to complement the common clinical examination before return to sport after injury. Knee Surgery, Sports traumatology, arthroscopy 2010;18(12):1798–1803.

further reSourCeS See the physical Solutions (uk) web-site for additional training and information resources (http://www.physical-solutions. co.uk/).

ThE AuThOr Th Colm Daly is a sports physiotherapist and is studying for a PhD at Queen Mary university of London. his research aims to explore the biomechanical features associated with prior hamstring injury particularly in relation to high-speed running in elite sport. having worked in elite Gaelic games over several years, Colm completed his MSc (Sports and Exercise Medicine) in 2012. he started his PhD studies soon thereafter and continues to practise clinically in London at Physiotherapy London (physiotherapy-specialists.co.uk) and The London Independent hospital (bmihealthcare.co.uk/lih).

n When and why is the biceps femoris most likely to be injured during sprinting? n How can we ensure that we achieve DISCUSSIONS sport specific rehabilitation in athletes following hamstring injury? n What are the key modifiable risk factors in hamstring (re-)injury, and how can we go about addressing them?

sportEX medicine 2013;58(October):20-26

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