SPORTING ANKLES and how to care for them

diagnosis • treatment • rehabilitation • prevention

SPORTING ANKLES and how to care for them

SPORTING ANKLES and how to care for them

© Green Star Media Ltd 2015 A CIP catalogue record for this book is available from the British Library. Published by P2P Publishing Ltd Registered office: 33-41 Dallington, London, EC1V 0BB Tel: 0845 450 6402 Registered number: 06014651

ISBN: 978-1-905096-98-5

Publisher Jonathan A. Pye Editor Jane Taylor Designer Charlie Thomas

The information contained in this publication is believed to be correct at the time of going to press. Whilst care has been taken to ensure that the information is accurate, the publisher can accept no responsibility for the consequences of actions based on the advice contained herein. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise without the permission of the publisher. Contributors

Mark Alexander is sports physiotherapist to the Australian Olympic Triathlon team, lecturer/coordinator of the Master in sports physiotherapy programme at La Trobe University, Melbourne, and managing director of BakBalls, a self-treatment device for back pain

Nick Cullen is a consultant orthopaedic surgeon with a special interest in disorders of the foot and ankle, based at the Foot and Ankle Unit, Royal National Orthopaedic Hospital, Stanmore, UK

Sean Fyfe is a physiotherapist, strength and conditioning coach and elite tennis coach

Nick Grantham is a strength and conditioning coach who has worked with elite athletes for the past 10 years, including Olympic and Paralympic finalists and many sports professionals

David Joyce is injury and performance consultant at Galatasaray Football club in Turkey. An Australian physiotherapist, he has worked for the English Premier League, the English Institute of Sport and the English Rugby Premiership. He teaches on the MSC in sports physiotherapy at the University of Bath

Trevor Langford is a sports therapist for Middlesbrough Football Club Youth Academy and Senior Squad

Ulrik Larsen is a an APA sports physiotherapist, practice principal with Optima Sports Medicine in Brisbane, Australia, and founder of Rehab Trainer

Ryan Shulman is a medical practitioner and former sports physiotherapist

Scott Smith is a manipulative physiotherapist working at Albany Creek Physiotherapy in Brisbane

Darren Stanborough is a sports physiotherapist and sports scientist working in the English Premier League with Fulham Football Club

Lauren Young is a trainee at the Whittington Hospital and Watford General Hospital in the UK. Her main interests are emergency medicine and sports injuries CONTENTS 7 Editorial

9 Ankle anatomy at a glance

13 c hronic instability Some ankles just keep rolling over. Here’s the latest evidence as to why – David Joyce

19 t ight and troubled Poor ankle flexibility can set off a chain reaction of biomechanical problems for sportspeople – Trevor Langford

29 Just a simple sprain? Ankle injuries are rarely straightforward, as this cautionary tale shows – Scott Smith

33 t ough love in a bucket A nasty but highly effective treatment for minor ankle sprains – Mark Alexander

37 Definitely not a simple sprain (I) If you know it’s serious, take it seriously, or risk putting paid to your sporting passion – Ulrik Larsen

47 Definitely not a simple sprain (II) Syndesmosis injuries are not common, but they need careful and patient management – Ryan Shulman

53 Decline and falls How a single injury can turn into an ongoing nightmare – Lauren Young

59 t ough athlete, tough challenge Dodgy ankles felled this mountain runner. But meticulous rehab put her back on track – Sean Fyfe

67 Knock-on damage For one professional footballer, an ankle sprain turned into groin strain – Darren Stanborough

71 A dangerous dance This most graceful artform can wreak havoc on feet and ankles – Nick Cullen

79 Wonderful water You may not be able to weight-bear but you can still stay fit and get going on that crucial rehab – Nick Grantham

PEAK PERFORMANCE sporting ankles From the editor

t’s the easiest thing in the world to turn an ankle. And one of the most common sports injuries of all. Which is probably why we are all guilty of under-playing the consequences. After the initial searing pain, we limp Ihome, reach for the pain-killers, chuck the frozen peas on the swollen ankle, put the foot up for an hour or two, and hobble around for a couple of days. Then we tend to resume business as usual. If we’re lucky, we get away with it. But, as this book describes, ankles are complicated structures and ankle injuries tend to be trickier than we assume. Even the simple sprains can leave strange legacies that will dog us – reduced balance, repeat incidents, new pain in other places – perhaps for years after. And too often, what we assume to be simple sprains turn into more complicated injuries that need highly specialised care. Read on, and take heed. You will learn how complex the ankle is, how easy it is to misdiagnose or simply to miss altogether the true problems. You will find practical advice on emergency treatment and effective rehab – even if you are confined to crutches. Once you have read the cautionary tales and the advice from our team of experts, you will, hopefully, never again lightly dismiss your ankle injury. And that may save you your sporting career.

Jane Taylor Editor

page 7

PEAK PERFORMANCE sportiNG ANKles

Main movements of the ankle

Dorsiflexion Plantarflexion

Eversion Inversion

pAGe 9 PEAK PERFORMANCE sportiNG ANKles

Ankle and foot bones

Right foot

Main ankle joints and ligaments

Left foot

pAGe 10 PEAK PERFORMANCE sporting ankles

The main soft tissues around the ankle

Lateral (outer side) view

Medial (inner side) view

page 11

CHRONIC INSTABILITY

Some ankles just keep on rolling over. Here’s the latest thinking on why Sprains to the lateral ligaments of the ankle are responsible for more time lost from sports participation than any other injury, and the rate of recurrence has been reported to be as high as 80%(1). The reasons why these rates are so high are still somewhat mysterious. Landing from a jump on to an opponent’s shoe in netball, and reaching for a wide volley in tennis are examples of commonly reported mechanisms of ankle injury. In these kinds of situations, the lateral (outer-edge) ligaments may be exposed to a stretching force that exceeds their tensile strength. The mechanism of recurrent ankle sprains is not thought to be dramatically different from that of an initial sprain. The question then, is: why do some people go on to suffer chronic ankle instability? Below, we look at some of the mechanical and functional control issues among athletes that may help us to get closer to answering that question.

Mechanical instability Mechanical ankle instability refers to repeated episodes of ‘giving way’ because of structural abnormalities within the ankle complex. Commonly described causes are:

Pathological ligamentous laxity While it is the talocrural joint that is primarily implicated in lateral ankle sprains, as many as four out of five people with such sprains may also have subtalar joint instability(2 ) (see illustrations, page 10). Despite the fact that injured ankle ligaments generally heal well, laxity (looseness) can persist at any joint in the ankle complex. After an acute injury, a loss of

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the normal collagen pattern and altered joint mechanics during the tissue repair phase may result in the ligaments healing in a lengthened position. This may leave the ankle complex mechanically unstable. There really is no such thing as a simple ankle sprain.

Abnormalities in joint movement A restriction in the dorsiflexion movement after a sprain is thought to limit the ankle’s ability to reach a fully close-packed (stable) position during standing, leaving the ankle complex precariously exposed to repeated inversion (turning inwards) stresses. It has also been suggested that those with chronic ankle instability are more prone to develop an anterior subluxation (partial displacement) of the fibula at the lower tibiofibular joint(3). The alteration in fibular movement may mean that the peroneal muscles no longer have a firm base from which they can act to stabilise the ankle dynamically.

Synovial inflammation and degenerative joint changes Traumatic or degenerative osteochondral lesions, synovitis and synovial tissue hypertrophy have all been found in people with chronic ankle instability and all may cause impingement in the talocrural and subtalar joints. Research cannot yet tell us, however, whether these changes are cause or effect: whether they structurally predispose the individual to ankle instability, or are a response to altered loading from repeated ankle sprains.

Functional instability Some people may have no structural impairment, yet they still roll their ankles. ‘Functional’ ankle instability is said to occur when the individual repeatedly feels their ankle ‘giving way’ without a specific mechanical cause(8). The contributing factors include:

Impaired proprioception

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There is strong evidence that chronically functionally unstable athletes demonstrate proprioceptive deficits, such as: ●●errors in detecting ankle positions prior to ground contact, ●●failure to accurately replicate passively positioned joint angles; ●●an inability to set appropriate muscle force levels to provide joint stability prior to landing from a jump.

It seems that these proprioceptive deficits impair the athlete’s ability to prepare the ankle to accept and transfer load during challenging athletic tasks such as changing direction or landing from a jump.

Muscle weakness There has been a great deal of research into strength deficits among those with chronic ankle instability. The current prevailing thought is that, while strength is an important consideration during ankle rehabilitation, lack of strength is not clearly related to chronic instability(4). The clinical significance of this apparent lack of association is that muscle strength should not be used as the only benchmark for a return to sport.

Postural control The body’s postural control system aims to maintain postural equilibrium during all activities. There is evidence to suggest that the body modifies its postural control motor patterning after repeated ankle sprains, in an effort to preserve balance. Quite what the stimulus is for these alterations remains unclear. In days gone by, we used to think that an ankle sprain had the potential to damage the mechanoreceptors located within the injured ligament. However, repeated studies have failed to show that the loss of postural control is, after all, due to a loss of these sensory organs. Clearly, other areas of the postural control system must be examined, and it appears possible that the precise reasons for the loss of postural control with chronic ankle instability are unique to each different athlete.

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Altered movement strategies Neuromuscular control, according to one elegant definition, is: ‘the unconscious activation of dynamic restraints occurring in preparation for and in response to joint motion and loading for the purpose of maintaining and restoring functional joint stability.’ (5)

An athlete’s ability to pre-emptively stabilise the ankle joint before ground contact is vital to avoid excessive joint movement upon contact. We are beginning to appreciate the importance of preparatory muscle activity during dynamic tasks. The time it takes for the ankle to reach maximum inversion is much less than the time it takes for the central nervous system to react to this perturbation and generate force in the peroneals to resist the wobble. The peroneal muscles seem to be less well adapted to provide reactive stability than they are in the preparatory setting of ankle posture. It seems that those with chronic ankle instability may have lost their anticipatory muscle action(6). Statistical extrapolation of this finding suggests that such individuals are likely to suffer a sprain every 100,000 steps (or, on average, about once every three months). It appears, therefore, that altered motor control strategies are preventing individuals with chronic ankles from achieving a stable close-packed position of the ankle joint during dynamic tasks, predisposing them to further episodes of instability. It is reasonable to assert that those athletes involved in twisting and jumping, or sports involving variable terrain, are most at risk.

Conclusion Chronic instability may be the product of an interaction between mechanical and functional factors. Yet, despite burgeoning research into this area, the precise nature and interaction of all the contributing factors is still unclear. The best we can say is that floppy-ankled sportspeople are left with little choice but to alter their motor control patterns to compensate for their mechanical failings in order to maintain function and performance. For example, those with chronic

page 16 PEAK PERFORMANCE sporting ankles instability seem to decrease the amount of knee flexion they deploy when landing from a jump(7). They also appear to reduce how much they allow their ankle to dorsiflex after landing. It is as though the brain believes that by making the joint rigid, it is making it safer. Which of course is wrong: this strategy only serves to make the ankle ‘brittle’ and less able to attenuate landing forces – ending up in further injury. Chronic ankle instability is a multi-dimensional problem and there is still some way to go before we understand the exact nature of the interactions between altered joint mechanics and functional control patterns. David Joyce References 1. Yeung, M. S., Chan, K. M., So, C. H., & Wuan, W. Y. (1994). An epidemiological survey on ankle sprains. British Journal of Sports Medicine, 28, 112-116 2. Meyer, J. M., Garcia, J., Hoffmeyer, P., & Fritschy, D. (1986). The subtalar sprain: a roentgenographic study. Clinical Orthopaedics & Related Research, 226, 169-173 3. Kavanagh, J. (1999). Is there a positional fault at the inferior tibiofibular joint in patients with acute or chronic ankle sprains compared to normals? Manual Therapy, 4, 19-24 4. Kaminski, T. W. (2006). The relationship between muscle strength deficits and chronic ankle instability. Paper presented at the 3rd International Ankle Symposium, Dublin 5. Riemann, B. L., & Lephart, S. M. (2002). The sensorimotor system, part I: The physiologic basis of functional joint stability. Journal of Athletic Training 37, 71–79 6. Konradsen, L. & Hojsgaard, C. (1993). Pre-heel-strike peroneal muscle activity during walking and running with and without an external ankle support. Scandinavian Journal of Medicine and Science in Sports 3, 99-103 7. Gribble, P. A., & Robinson, R. H. (2006). Chronic ankle instability creates knee joint alterations during a dynamic stability task. Paper presented at the 3rd International Ankle Symposium, Dublin 8. Hertel, J. (2006). Overview of the aetiology of chronic ankle instability. Paper presented at the 3rd International Ankle Symposium, Dublin

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page 18 INFLEXIBILITY

Tight ankles spell trouble for sportspeople. Poor flexibility can set off an unwelcome chain reaction

You don’t have to have had an ankle injury to have tight ankles. But for sportspeople or athletes it is very common that after even a minor injury, let alone surgery or a longer immobilisation of an ankle joint, the result is a less flexible ankle. In particular, there is a risk of reduced movement in ‘dorsiflexion’ (flexing the foot by pulling the toes up towards the leg). If this is not rehabilitated properly, it can place greater biomechanical demands on the body during sport that increase the risk of the athlete developing an overuse injury. Dorsiflexion is something we all tend to take for granted in daily life and in sport. Lunging, ascending and descending stairs, squatting and getting into and out of a car all require it. In running, active dorsiflexion is essential to achieve heel strike at the terminal stage of the swing phase, while a maximum passive dorsiflexion angle is required during mid-stance phase, to transfer load ready for toe push off (6). In sports with multidirectional movement patterns (eg, tennis, football, rugby and hockey), the athlete must dorsiflex effectively into both inversion and eversion, so as to transfer load and direction. At the catch of the rowing/sculling stroke, maximal passive dorsiflexion enables the rower to exploit knee and hip flexion, thereby optimising lower limb power output and function.

Reasons for restriction If an athlete has restricted dorsiflexion, then to fully execute a movement, the lower limb will need to compensate at other joints. If there is a disparity between joints at the rear-foot/

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How to measure dorsiflexion

by Mark Palmer A lack of dorsiflexion has been implicated in predisposing a number of injuries: l Reduced ankle dorsiflexion range was associated with patellar tendinopathy in volleyball players l Restricted ankle dorsiflexion was a risk factor for lower- extremity overuse injuries in 450 naval trainees l Reduced dorsiflexion was implicated in the development of patellofemoral pain syndrome in runners l Reduced ankle dorsiflexion in the front leg of fast bowlers was associated with a significantly increased risk of injury in cricketers l Soldiers with reduced dorsiflexion had 4.6:1 odds of developing a metatarsal stress fracture l Reduced dorsiflexion range was associated with ankle sprain in children and PE students l Ankle dorsiflexion range of movement was significantly associated with sustaining a lower extremity injury in recreational Aussie Rules players

For full evidence base, see references at the end of this chapter. Test: the ankle dorsiflexion lunge Weight-bearing mostly through the (front) test leg, the player moves their foot back as far as possible, while still being able to dorsiflex with the heel on the ground so the knee touches the wall in front. The foot should point directly ahead and the knee should move directly over this. The distance from great toe (the end of the big toe) to wall is measured. Score 0 for normal; 1 for abnormal or 2 for very abnormal.

page 20 PEAK PERFORMANCE sporting ankles ankle (the first point of ground contact) during load-bearing activities, this can have a significant effect not just on the lower limb but throughout the kinetic chain.

It is important to identify whether limited movement is related to: ●●a mechanical restriction into the joint, ●●posterior chain tightness, or ●●joint stiffness

Mechanical restriction into the joint If an athlete has no history of ankle ligament injury, but does have a ‘mechanical block’ limiting their dorsiflexion, a talotibial osteophyte (bony growth) may show up on x-ray, indicating anterior impingement syndrome. This may be related to recurring microtrauma to the anterior talocrural joint capsule, common in kicking sports as a result of the repetitive kicking action, but also common in ballet dancers(1,9). If an anterior osteophyte is causing symptoms including pain or discomfort, this should be investigated further (1).

Posterior chain tightness Restricted dorsiflexion will generally result in the athlete excessively pronating in order to complete a movement. If the restriction is related to tightness of muscles and soft tissues throughout the ‘posterior chain’, this can affect how the talus sits in relation to the calcaneus (8) (see illustrations, page 10) . A therapist can work out the position of the calcaneus by the direction of pull on the Achilles tendon as it inserts slightly lateral to the midline of the calcaneus (8). This type of posterior chain tightness can result in both increased plantarflexion and eversion, forcing the subtalar joint to pronate. Both plantarflexion and eversion apply force medially on to the talus, and downward and medially to the navicular, which can result in a loss of height of the medial longitudinal arch (MLA) – a collapsed arch. The MLA is supported by a complicated network of soft

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tissues, including the plantar fascia, tibialis posterior and the calcaneo-navicular ligament. A collapsed medial arch can elongate the plantar-fascia, increasing the stress on it and thereby the athlete’s risk of developing painful plantar fasciitis. An elongated plantar fascia can then increase tension back into the posterior chain, making unwanted hyperpronation more likely. So it is essential to work out exactly why the posterior chain of muscles is tight.

Joint stiffness If the reduced dorsiflexion is caused by stiffness within the ankle joint, then posterior chain tightness could result anyway, because of the compensations that will occur at the subtalar joint. The tibialis posterior not only functions to support the MLA, but also works to decelerate pronation during stance (10). Compensatory pronation therefore could potentially lead to tibialis posterior tendon injury – although we still don’t have definitive research on this (10). Dysfunction of the posterior tibialis tendon can cause the MLA to collapse, resulting in flat foot(7). If, after immobilisation, the ankle inverters are not stimulated, the ability of posterior tibialis to control eversion will decreased, which can accentuate pronation at the subtalar joint. Excessive pronation can also increase the pressure through the various forefoot and toe joints, causing hallux valgus deformity (bunions) and metatarsalgia(10). A review of the effects of foot-arch height on running biomechanics established that low-arched runners were more susceptible to lower leg medial stress injuries(10). It indicated that low-arched runners presented more frequently with posterior tibialis and anterior knee pain (with two of the most common injuries being patellar tendinopathy and medial knee pain). In contrast, high-arched runners presented more with lateral-related injuries. Both low- and high-arched runners were prone to plantar fasciitis. Sportspeople who suffer recurring ankle ligament injury tend to show strength deficits in hip abductors and extensors (3). In addition, it seems that those with recurrent ankle sprains had on

page 22 PEAK PERFORMANCE sporting ankles average a 3-degree deficit in dorsiflexion on Poor alignment their bad side (2). In some cases the reduced hip abductor muscle activity will be related to these biomechanical compensations; in others it will be the result of not having included specific hip abduction exercises in the rehab programme. During immobilisation or a period of non weight bearing, the hip abductors lose their effectiveness in controlling medial-femoral rotation during load-bearing. This results in the knee tending to turn inwards on the tibia, producing an exaggerated quadriceps angle (Q angle). The diagram (right) shows this combined effect. Note the weakness in hip abductors, evidenced by the pelvis tilting laterally (positive Trendelenburg sign). A key aspect of rehabilitation of the injured ankle should therefore be gluteal activation.

Following the chain... In this situation, one outcome of the increased Q angle is a tight iliotibial band – which blends with the peroneal longus. The ITB tightness results because, in the absence of abductor strength, the tensor fascia lata starts to dominate at the hip. This adds to the valgus force at the knee joint, further reducing stability during biomechanical loading. But it doesn’t end there: where the tight ITB inserts on to the patella and the lateral tibia (at Gerdy’s tubercle), its pull will accentuate the lateral rotation of the tibiofemoral joint. The ensuing lateral pull on the patella can lead to patellofemoral dysfunction. So in cases of anterior knee pain, you should also take a look at what is going on at the ankle joint and at the strength of the hip muscles. A fundamental cause of medial collateral ligament (MCL) and anterior cruciate ligament (ACL) injury is the increased valgus force that comes from an increased Q angle on landing

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with poor control of hip abductors (4). Hewett et al assessed the landing valgus knee joint angle in females (who are reported to be more susceptible than males to ACL injury). One possible explanation relates to females generally having a wider pelvis(5). But increased valgus force combined with excessive pronation because of restricted dorsiflexion may also contribute to ACL injury.

Conclusion An athlete who suffers chronic anterior knee pain, recurring soft-tissue injury or injury to the medial structures of the lower limb should check out whether their ankle dorsiflexion is adequate. The compensations for tightness through the ankle don’t just stop at the knee and hip but continue to the sacroiliac joint, the lumbar spine and beyond. Clearly, a reduction of only a few degrees of dorsiflexion can have a significant effect on biomechanical loading throughout the kinetic chain.

Trevor Langford References 1. Brukner P, Khan K (2001). ‘Clinical Sports Medicine’. (revised 2nd Ed). McGraw Hill. Australia. 2. Drewes LK, McKeon PO et al (2009). ‘Dorsiflexion deficit during jogging with chronic ankle instability’. Journal of Science and Medicine in Sport. 12 (6): 685-687. 3. Friel K, Mclean N et al (2006). ‘Ipsilateral Hip Abductor Weakness After Inversion Ankle Sprain’. Journal of Athletic Training. 41 (1): 74-78. 4. Hewett TE, Myer GD et al (2005). ‘Biomechanical Measures of Neuromuscular Control and Valgus Loading of the Knee Predict Anterior Cruciate Ligament Injury Risk in Female Athletes’. The American Journal of Sports Medicine. 33 (4): 492-501. 5. Lewis T (2000). ‘Anterior Cruciate Ligament Injury in Female Athletes: Why are women so vulnerable?: Literature review’ Physiotherapy. 86 (9): 464-472. 6. Novacheck TF (1998). ‘The biomechanics of running’. Gait and Posture. 7: 77-95.

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7. Pomeroy GC, Pike RH et al (1999). ‘Current Concepts Review: Acquired Flatfoot in Adults Due to Dysfunction of the Posterior Tibialis Tendon’. Journal of Bone and Joint Surgery. 81: 1173-1182. 8. Stovitz SD, Coetzee JC (2004). ‘Hyperpronation and Foot Pain’. Steps towards Pain Free feet. The Physician and Sports Medicine. 32 (8). 9. Tol JL, Van Soest AJ et al (2002). ‘Relationship of the kicking action in soccer and anterior ankle impingement syndrome’. The American Journal of Sports Medicine. 30: 45-50. 10. Williams DS, McClay IS et al (2001). ‘Arch structure and injury patterns in runners’. Clinical Biomechanics. 16: 341-347.

Ankle injury evidence base 1. Kiesel, K, Plisky, PJ, Voight ML. Can Serious Injury in Professional Football be Predicted by a Preseason Functional Movement Screen? NAJoSPT. 2007, Aug 2(3). 2. Woods C, Hawkins R, Hulse M et al. The Football Association Medical Research Programme: an audit of injuries in professional football-analysis of preseason injuries. Br J Sports Med. 2002 Dec;36(6):436-41; discussion 441. 3. Sheppard C, Hodson A. Injury Profiles in Professional Footballers. The Football Association Medical and Exercise Science Department Newsletter. 2006 Nov; Issue 17. 4. Dennis RJ, Finch CF, McIntosh AS et al. Use of field-based tests to identify risk factors for injury to fast bowlers in cricket. Br J Sports Med. 2008 Jun;42(6):477-82. Epub 2008 Apr 7. 5. Murray E, Birley E, Twycross-Lewis R et al. The relationship between hip rotation range of movement and low back pain prevalence in amateur golfers: an observational study. Phys Ther Sport. 2009 Nov;10(4):131-5. 6. Vad VB, Bhat AL, Basrai D et al. Low back pain in professional golfers: the role of associated hip and low back range-of-motion deficits. Am J Sports Med. 2004 Mar;32(2):494- 7. 7. Verrall GM et al. Hip joint range of motion restriction preceeds chronic groin injury. J Sci Med Sport. 2007 Feb (28). 8. Ibrahim A, Murrell G A C, Knapman P. Adductor strain and

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hip ROM in male professional soccer players. J Orthop Surg 2007 15(1). 9. Van Dillen LR, Bloom NJ, Gombatto SP et al. Hip rotation range of motion in people with and without low back pain who participate in rotation-related sports. Phys Ther Sport. 2008 May;9(2):72-81. 10. Sigward SM, Ota S, Powers CM. Predictors of frontal plane knee excursion during a drop land in young female soccer players. J Orthop Sports Phys Ther. 2008 Nov;38(11):661-667. 11. Muscle flexibility as a risk factor for developing muscle injuries in male professional soccer players. A prospective study. Am J Sports Med. 2003 Jan-Feb;31(1):41-6. 12. Witvrouw E, Bellemans J, Lysens R et al. Intrinsic risk factors for the development of patellar tendinitis in an athletic population. A two-year prospective study. Am J Sports Med. 2001 Mar-Apr;29(2):190-5. 13. Gabbe BJ, Bennell KL, Finch CF, et al. Predictors of hamstring injury at the elite level of Australian football. Scand J Med Sci Sports 2006;16:7–13. 14. Gabbe BJ, Finch CF, Bennell KL et al. Risk factors for hamstring injuries in community level Australian football. Br J Sports Med. 2005;39(2):106-10. 15. Malliaras P, Cook JL, Kent P. Reduced ankle dorsiflexion range may increase the risk of patellar tendon injury among volleyball players. J Sci Med Sport. 2006 Aug;9(4):304-9. Epub 2006 May 2. 16. Kaufman KR, Brodine SK, Shaffer RA et al. The effect of foot structure and range of motion on musculoskeletal overuse injuries. Am J Sports Med. 1999 Sep-Oct;27(5):585-93. 17. Lun V, Meeuwisse WH, Stergiou P et al. Relation between running injury and static lower limb alignment in recreational runners. Br J Sports Med. 2004 Oct;38(5):576-80. 18. Hughes LY. Biomechanical analysis of the foot and ankle for predisposition to developing stress fractures. J Orthop Sports Phys Ther. 1985;7(3):96-101. 19. Tabrizi P, McIntyre WM, Quesnel MB et al. Limited dorsiflexion predisposes to injuries of the ankle in children. J

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Bone Joint Surg Br. 2000 Nov; 82(8):1103-6. 20. Willems TM, Witvrouw E, Delbaere K et al. Intrinsic risk factors for inversion ankle sprains in male subjects: a prospective study. Am J Sports Med. 2005 Mar;33(3):415-23. 21. Gabbe BJ, Finch CF, Wajswelner H et al. Predictors of lower extremity injuries at the community level of Australian football. Clin J Sport Med. 2004 Mar;14(2):56-63. 22. Noehren B, Davis I, Hamill J. ASB clinical biomechanics award winner 2006 prospective study of the biomechanical factors associated with iliotibial band syndrome. Clin Biomech. 2007 Nov;22(9):951-6. Epub 2007 Aug 28. 23. Leetun DT, Ireland ML, Willson JD et al. Core stability measures as risk factors for lower extremity injury in athletes. Med Sci Sports Exerc. 2004 Jun;36(6):926-34. 24. Hewett TE, Myer GD, Ford KR et al. Biomechanical measures of neuromuscular control and valgus loading of the knee predict anterior cruciate ligament injury risk in female athletes: a prospective study. Am J Sports Med. 2005 Apr;33(4):492-501. Epub 2005 Feb 8. 25. Brophy RH, Chiaia TA, Maschi R et al. The core and hip in soccer athletes compared by gender. Int J Sports Med. 2009 Sep;30(9):663-7. Epub 2009 Jul 7. 26. Engebretsen AH, Myklebust G, Holme I et al. Intrinsic risk factors for acute ankle injuries among male soccer players: a prospective cohort study. Scand J Med Sci Sports. 2009 Jun 23 (epub ahead of print).l 27. McHugh MP, Tyler TF, Tetro DT et al. Risk factors for noncontact ankle sprains in high school athletes: the role ofhip strength and balance ability. Am J Sports Med. 2006 Mar;34(3):464-70. Epub 2005 Oct 11. 28. McGuine TA, Greene JJ, Best T et al. Balance as a predictor of ankle injuries in high school basketball players. Clin J Sport Med. 2000 Oct;10(4):239-44.

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page 28 THE SIMPLE SPRAIN

You always hope it’s just a simple sprain. But ankle injuries are rarely straightforward, as this cautionary tale shows

I recently treated Fraser, a promising young Australian Rules football player who had sustained an innocuous inversion sprain of the ankle – the most common kind when the ankle rolls outwards. I saw him quite soon after the incident and it looked as though the rehabilitation process would be short and straightforward. I was confident enough about this to tell the coaching staff that Fraser would soon be back on the training paddock, ready for the upcoming final series. As it turned out, I got it completely wrong. A few weeks passed; Fraser’s range of movement returned to his ankle, and he was able to complete stationary balance drills and strengthening exercises. But he couldn’t hop on the bad leg or run without lateral ankle pain. I started to think that this rehab might take a little longer than anticipated. Fraser had an MRI scan on the ankle, which revealed swelling over the anterior talo-fibular (ATFL) ligament, but no other significant findings. There were no ruptured ligaments or torn tendons. He was sent to see a sports physician to seek further explanation as to why the injury was taking so long to heal. The sports physician thought the player should adopt a ‘wait and see’ approach, sitting out the rest of the season and starting to train again in the short off-season. This advice did not go down well with the athlete or the coaching staff. Six weeks later, when I next saw Fraser, he still could not hop on the leg pain-free, so was still unable to do any running. He still had swelling over the ATFL, but had full range of motion

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with no laxity (looseness) in any of the supporting ligaments. It was then that I tried a different treatment technique, a posterior glide of the fibula at the lateral malleolus. I also mobilised the head of the fibula, which was very stiff. I taped the fibula in a posterior direction, and Fraser was able to hop pain-free for the first time in 19 weeks. It was a miracle. Or maybe not: Brian Mulligan, the legendary New Zealand physio, has provided the physiotherapy profession with numerous manual techniques to help correct joint immobilities and subluxations. This is but one of the invaluable treatment techniques he prescribes(1). I saw Fraser again 10 days later and he was up to running 1.5km without pain; he was also positive that he would complete his rehabilitation before pre-season training. The intriguing thing about all this was that I had already attempted Mulligan’s posterior glide two months earlier, with no result – no reduction in pain nor increase in function. So why did tape and the manual gliding of the fibula belatedly help, and why had it not helped at an earlier stage? The answer lies in the anatomy of the anterior ankle. Irritation in the lower edge of the inferior tibio-fibular ligament and the front of the anterior talo-fibular ligament can thicken these ligaments, setting up a series of knock-on effects. The irritated and thickened tissue becomes vulnerable to getting pinched between the tibia and talus as the foot is dorsiflexed. The ligaments may also begin to rub on the joint capsule of the ankle, which can inflame the synovial lining of the capsule, causing synovitis. Finally, the inflamed ligaments can form too much scar tissue along the front and side of the ankle joint, creating a small mass of tissue called a meniscoid lesion. Dorsiflexing the ankle can trap the tissue between the edge of the ankle joint, causing pain, popping, and a feeling that the ankle will give way and not support body weight. The tape helps to offload the fibula or move the pressure away from the antero-lateral surface of the ankle. Fraser was able to load the ankle with running and hopping, with little, if any soreness.

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However, my first attempt at this treatment, had, I believe, been too early, when the area was probably still too inflamed to respond positively. The joint capsule in particular is extremely sensitive to irritation. Only when the stuctures had all calmed down was it possible to move forwards in the rehab. When treating acute ankle sprains, health professionals are taught to encourage the client to regain ankle dorsiflexion as early as possible, because research shows that the sooner the person regains this movement, the sooner they will be back to normal function. In the past I have stirred up many clients’ pain by making them do repeated dorsiflexion exercises, or by mobilising the anterior ankle joints. Now I am being much less aggressive about pushing my clients to regain this dorsiflexion, as sometimes this can clearly lead to more irritation – slowing rather than speeding recovery. There was nothing unusual about Fraser’s ankle injury in terms of the cause – it was just a lot of damage to a very sensitive part of the ankle joint. I believe the moral of this short story is that the therapist needs to add up all the information presented by the client and treat them without using a pre-determined recipe. By thinking anatomically and being flexible in treatment approach, the therapist is more likely to find the best treatment options to help their client recover faster. Scott Smith Reference 1. Brian Mulligan. ‘Manual therapy – NAGS, SNAGS, MMMs etc’ (5th ed) 1995. Wellington Plane View Press

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page 32 EMERGENCY TREATMENT

Tough love in a bucket: this unpleasant but highly effective treatment will speed recovery from minor ankle sprains

This article explains how to manage a nasty ankle sprain immediately after it happens. The regime I outline below has been used in elite sport for years but doesn’t feature outside of this rarefied setting. I suspect the reason is simple: it is extremely uncomfortable! But it works: I have seen athletes on crutches after sustaining diagnosed Grade 2 / 2+ ankle sprains (see box overleaf for grading definitions), who were able to walk without crutches with only a minimal limp after their first session of this therapy, and who were back training after three to four days, albeit with a lot of tape support. An ankle sprain produces internal bleeding, inflammatory processes, pain and swelling. The brain also gets involved, producing muscle inhibition and a reduction in proprioception, which usually forces the injured athlete to limp in an effort to reduce pain. By numbing the ankle and tricking the brain into allowing the ankle to move through a normal range of movement without pain, I believe we can minimise the detrimental effects of ankle sprains.

The 25-minute cryo-kinetic ice bath regime By icing the ankle in an ice bath, strictly following the protocol outlined below, I believe you will be able to ●●limit the bleeding by reducing the micro-circulation, and ●●trick the brain and hence the muscles into thinking that the ankle isn’t that badly injured, so normal function can be restored more rapidly than you would otherwise expect.

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How ankle sprains are graded for severity Sign/symptom Grade I Grade II Grade III Ligament tear None Partial Complete

Loss of functional ability Minimal Some Great

Pain Minimal Moderate Severe

Swelling Minimal Moderate Severe Ecchymosis (purple bruising from bleeding Usually not Common Yes under the skin)

Difficulty weight bearing None Usual Almost always source: Wexler RK; The injured ankle. Am Fam Physician. 1998 Feb 1;57(3):474-80. [abstract] Precaution! 1. Any vascular conditions (such as Reynaud’s disease) or diabetes will be adversely affected by this cold treatment. Do not undertake it 2. If you experience severe unremitting pain during this process (rather than extreme discomfort that settles after 4-5 minutes), it is possible you have suffered an ankle fracture, so cease icing immediately. And if you suspect you have fractured your ankle, don’t attempt this technique until after an x-ray has excluded any fractures.

The ice-bucket protocol 1. Use a bucket (rectangular is best) that can easily accommodate the injured foot 2. Fill with cold water and enough ice to make the water really cold. How cold? I’m not aware of any research that states an optimal temperature, but I suggest 12-15°C 3. Check precautions and contraindications of ice applications (see, eg, www.sportsinjuryclinic.net/cold_therapy/ coldtherapy_contraindications.php) before you start treatment 4. Sit on a chair with injured foot and ankle (up to mid shin) in the iced water for 10 minutes. It is normal to feel pain from the cold but this should abate after 5 minutes, as the foot and ankle go numb

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5. After 10 minutes stand up, with your foot still in the bucket, and perform 2 minutes of mini squats, keeping the range within what pain permits (ie, don’t push into pain) 6. Sit again for 2 minutes with your foot stationary in bucket 7. Stand and perform 2 minutes of small calf raises, again within pain limits (ie, the calf raises should not cause pain) 8. Sit for 2 minutes 9. Stand and repeat the 2 minutes of mini-squats 10. Sit for 2 minutes 11. Stand and repeats the 2 minutes of calf raises 12. Sit for 1 minute, totalling 25 minutes of cryo-kinetic icing.

Perform this regime every two to three hours for the first two days after the injury. In elite sport, injured athletes will even set their alarms and ice a couple of times, late at night and early morning (eg, 12pm and 3am) to minimise swelling and maximise recovery speed. For the averagely active person who also has a day job, I would get them to do this regime as soon as possible after the injury and then, for the first two to three days, once a day towards the end of the day when they’re back from work and have settled down for the evening. I have even had success with this technique on chronic swollen ankles that had been sprained four to six weeks previously. After one to two sessions in the bucket, the swelling was minimal and range of movement improved dramatically.

Caution! ●●only exercise within pain limits, to avoid making tissue damage worse ●●only take as much weight on the injured foot as you can tolerate within pain levels, but aim to progress the amount of weight-bearing during the ice sessions ●●this regime is supplemental to, not a replacement for, the other RICE principles (rest, ice, compression, elevation), so it is vital that you continue with compression and elevation between ice sessions. Mark Alexander

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Evidence / good reading l Knobloch K et al (2006): Microcirculation of the ankle after Cryo/Cuff application in healthy volunteers. Int J Sports Med. 2006 Mar: 27(3):250-5. l Bleakley C et al (2004): The Use of Ice in the Treatment of Acute Soft- Tissue Injury, a Systematic Review of Randomized Controlled Trials. Am J Sports Med Jan: 32: 251-261

page 36 PEAK PERFORMANCE sporting ankles SERIOUS SPRAINS I

A badly turned foot, if ignored, can put an end to your sporting passion. Here’s what to watch out for The chances are that anyone who has done any kind of weight- bearing sport has had a sprained ankle. But there is a vast difference between mild sprains and moderate to severe lateral ankle sprains that actually damage the ankle. With these, incorrect care can easily turn a recovery time from 3-4 months into a 12-18 month epic. What are the signs and symptoms that distinguish a sprained ankle that is damaged? Only by identifying these features can we undertake the crucial early management, and predict which sprains will require longer time frames for recovery. I am not talking here about mild ankle sprains that will always get better regardless of what is done to them – most athletes will ‘walk them off’ because there is no real damage to the ankle. Nor will I discuss medial ankle sprains, or acute forefoot/mid-foot injuries. And finally, I will not be looking at the obviously severe injuries that need orthopaedic referral: fractures of tibia and/or fibula, talar dome and ankle dislocations. Usually these will be picked up in the emergency department of the local hospital. If the injury happens on the field, the severity of pain would be enough to convince anyone to summon an ambulance and immediate x-rays! So what does that leave? Precisely the tricky sprains in which damage to the ankle is unlikely to show up positive on X-ray. Commonly these injuries have a history of having occurred with some heavy weight-bearing and twisting force; they produce significant swelling, pain, lack of normal range of movement; and the individual will be unable to walk and/or run

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The chances are that anyone who has done any kind of weight- bearing sport has had a sprained ankle. But there is a vast difference between mild sprains and moderate to severe lateral ankle sprains that actually damage the ankle. With these, incorrect care can easily turn a recovery time from 3-4 months into a 12-18 month epic. What are the signs and symptoms that distinguish a sprained ankle that is damaged? Only by identifying these features can we undertake the crucial early management, and predict which sprains will require longer time frames for recovery. I am not talking here about mild ankle sprains that will always get better regardless of what is done to them – most

Scenario 1: you’re running at speed with the ball and step heavily off your left foot to move quickly to your right. But the ground doesn’t feel quite like you thought it would. In a split second your foot has rolled underneath your leg, resulting in a feeling of more than one ‘crack’ followed shortly afterwards by a searing pain that envelops your whole foot and leaves you writhing in agony on the ground. Scenario 2: while contesting the ball among a few other players you jump as high as you can to reach it. You land while you are twisting around, catching the edge of another player’s shoe, and causing your foot to land on the ground on its outside edge. The crunch that you feel is nauseating and soon so is the pain. Both these situations will very likely result in damage to bone, joint, ligament, tendon, or nerve that will require profound rest for complete healing to take place. How long and to what degree the rest needs to be enforced depends on the all-important diagnosis.

athletes will ‘walk them off’ because there is no real damage to the ankle. Nor will I discuss medial ankle sprains, or acute forefoot/mid-foot injuries. And finally, I will not be looking at

page 38 PEAK PERFORMANCE sporting ankles the obviously severe injuries that need orthopaedic referral: fractures of tibia and/or fibula, talar dome and ankle dislocations. Usually these will be picked up in the emergency department of the local hospital. If the injury happens on the field, the severity of pain would be enough to convince anyone to summon an ambulance and immediate x-rays! So what does that leave? Precisely the tricky sprains in which damage to the ankle is unlikely to show up positive on X-ray. Commonly these injuries have a history of having occurred with some heavy weight-bearing and twisting force; they produce significant swelling, pain, lack of normal range of movement; and the individual will be unable to walk and/or run without pain and aggravation. A typical situation is that an athlete will have been given an all-clear on x-ray but then will still be in pain a few weeks later, and feeling very frustrated as they’d expected to be back on the field within two to four weeks. The most common mistake that clinicians, coaches and athletes make is to under-rate the severity of damage and return to activity too early. The fatal assumption is that when the X-ray is negative, then the damage can’t be too bad…. Wrong! Let’s paint a couple of painful pictures to help us understand how a damaged ankle sprain happens. The first few days is the critical phase for diagnosis because it immediately determines the management and time frames for full recovery. The athlete should see a soft-tissue therapist or their regular physio for an assessment, and get their answers to the following questions: ●●Are further investigations warranted? ●●Do you need to refer the athlete to a specialist? ●●Do they need a cast or crutches? ●●Roughly how long will their rehabilitation take?

Without a good working diagnosis, none of these questions can be answered.

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The crucial first week While there isn’t any hard evidence to back this up, the issue of whether the athlete can reasonably weight-bear during the first week seems to be critical in establishing whether any of the four ‘nasties’ discussed below has occurred. This is because for the foot not to be able to stand simple weight-bearing implies that the weight-bearing surface and/or the stability mechanisms of the ankle must have been severely compromised. This, therefore, is the first key diagnostic and management judgement: if it is painful to weight-bear on the foot in the first week, significant damage has occurred. The athlete needs to be non-weight bearing, on crutches, to the level that ensures there is no pain. The option of soft-casting the ankle to hold it still will often need to be considered to achieve complete immobilisation. Any negative secondary effects of non-weight bearing for a week will be far outweighed by further damage caused by painful weight bearing. From non-weight bearing, the athlete will need to move cautiously through the following progressions: ●●partial weight-bearing to… ●●full weight bearing to… ●●walking to …. ●●transitional drills to … ●●running

Delay each new step rather than re-aggravate the symptoms. Use the water for rehab to practise each successive stage to reduce body weight and rehearse technique. There are four main types of primary damage that may in isolation or in combination prevent reasonable weight bearing in the first week.

1. Osteochondral defect (OCD) This is damage to the surface chondral layer of the bone; the damage may be simple bruising, through to a displaced segment of cartilage. It may occur on the talar dome, the

page 40 PEAK PERFORMANCE sporting ankles inferior tibial surface (‘tibial plafond’), or the medial fibular surface in the lateral gutter of the ankle. The damage to various parts of the bony surfaces is commonly the result of the twisting force of landing, which causes the talus to invert and medially rotate in the tight angular ankle joint.

Signs ●●usually there is no obvious sign on initial X-ray, but closer inspection or re-X-ray may reveal disruption to the joint margins. ●●significant pain on weight bearing ●●the medial and lateral anterior talar dome, anterior tip of tibia or fibula will be very tender to touch ●●swelling all around joint ●●CT or MRI scan should tell all ●●if sufficiently disrupted, this may require surgical referral. Recovery time frame: three to six months

2. Bone stress short of fracture Signs ●●not visible on X-ray; bone scan will confirm but is not really necessary ●●extreme tenderness on medial / lateral malleolus or along shaft of tibia or fibula will confirm diagnosis ●●may be positive to squeeze or stress tests (where the bone is gently stressed as if you were trying to bend a stick). Recovery time frame: will heal by itself with sufficient rest over two to six weeks, depending on severity

3. Lateral ankle ligament tear leading to gross instability This is significant tearing (Grade II), through to complete rupture (Grade III) of the anterior talo-fibular (ATFL) and/or calcaneo-fibular (CFL) ligaments. Complete rupture of the lateral ligament complex requires immediate orthopaedic referral for stabilisation surgery.

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Signs ●●the most common result of a plantar-flexion/inversion sprain, rarely occurs in isolation from bony injury. ●●talocrural joint demonstrates instability, leading to overloading of capsular and/or ligamentous structures and later possibly synovitis (thickened and inflamed capsule) ●●athlete will probably be unable to weight-bear for initial period because of likely bony structure damage ●●trial taping for diagnostic purposes: stirrups and heel locks can artificially stabilise the lateral ankle complex and help to diagnose a pure instability problem. Recovery time frame: three to six months, depending on other damage

4. Tibio-fibular ligament / syndesmosis damage leading to instability Also known as ‘high ankle sprain’ (see following article on p45). Can be very nasty, requiring orthopaedic referral to prevent long-term arthritic changes . The fibula will usually fracture laterally as well, preventing further damage along the line of the syndesmosis.

Signs ●●landing with twisting is very likely to stress and drive the tibia and fibula apart, causing a tear of the ligament and syndesmosis (in addition to damage to other structures above) ●●palpation of the anterior shin between tibia and fibula will show tenderness; medial/lateral stress test holding the calcaneum will reveal gapping and laxity between tibia and fibula. ●●with significant instability, separation of tibio-fibular articulation is likely to be seen on a weight bearing (heel pressure) X-ray, compared with other side ●●it may be useful at a later stage to re-X-ray in weight bearing at end-of-range dorsiflexion (if that was not possible at the outset because of pain) to detect any ongoing instability of the tibio-fibular complex compared with other ankle. With luck it may show up negative at the three-month stage with fibrosing

page 42 PEAK PERFORMANCE sporting ankles and scar tissue doing a sufficient job of holding it together. ●●tibio-fibular compression taping may help with stabilising in the early weight-bearing phases. Recovery time frame: absolutely critical to prevent weight bearing on foot for up to three or four weeks with a more conservative progression through partial to full weight bearing. In total, allow six to eight months to return to sport.

Continued pain at 4 to 8 weeks If things are not going well, or you are noticing new symptoms, consider the following secondary damage issues. These may not clearly manifest until the worst of the pain, swelling and disability has receded, but they need to be addressed in their own right as part of the mid- to late-stage rehabilitation process. These are the most common ones:

1. Talo-crural joint hypomobility / restriction This leads to capsular synovitis / lateral impingement of fibula and talus in the lateral gutter.

Signs ●●a very common side effect of any ankle sprain; it is critical to maintain maximum mobility to promote the best rate of healing. ●●if the talus cannot posteriorly glide during weight bearing, it will cause on-going impingement of anterior bony structures ●●after the acute phase, the therapist should perform manual posterior glides of talus and undertake dorsiflexion testing at a wall to establish the extent of dorsiflexion deficit and the sites of restrictions (based on points of pain). Never stretch forward in weight bearing to improve dorsiflexion, as this risks aggravating the damaged structures. ●●fibrosis and thickening of the posterior capsule responds well to manual loosening procedures. Deep tissue massage of uninjured soft tissues (especially calf) is very useful in the acute phase. The use of seat-belts in the mid to late stages of rehab can help to force the various bones to glide in normal ways

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again to gain final degrees of dorsiflexion – this should be done by an experienced physiotherapist.

2. Peroneal tendinopathy Signs ●●damage of the peroneal muscles and tendons is possible, but would not prevent normal weight bearing initially. Static muscle testing, especially in dorsiflexion, will show up pain and weakness (there could be a tear in the muscle belly). ●●treat as any muscle injury through to full return to function. ●●restricted or fibrosed peroneus longus can prevent normal dorsiflexion at later stages of rehab; massage and stretching is the answer. ●●the peroneal tendon can sublux from a torn tendon sheath posterior to the lateral malleolus, leading to chronic clicking and pain that may require surgery.

3. Reflex sympathetic dystrophy Also known as ‘complex regional pain syndrome’ or Sudeck’s atrophy. A relatively uncommon condition of burning pain, pins and needles or numbness, on-going and excessive swelling, often spreading up the whole shin, and discoloration of the foot and/or leg. It arises from a disturbance in the sympathetic nervous system that controls the blood flow and sweat glands to the limb. The neural disturbance may have its origins in over-stretching of nerve tissue during the ankle sprain, changing the way the nerve impulses are sent and causing a short circuit or overactivity. Signs ●●the risk of developing this may increase with too aggressive a rehabilitation strategy – go slow! ●●keep this diagnosis (even in ‘mild’ forms) at the back of your mind if strange things are happening to the ankle that are really slowing down the return to function. ●●look for positive neural signs and paresthesia (numbness, pins and needles). ●●continue to work on range of movement and pain relief.

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Personally I find deep tissue massage/ trigger-point release to gastrocnemius and soleus muscles is critical for mobility gains. Acupuncture has occasionally worked wonders for pain relief. ●●can severely delay return to function, from three to 12 months ●●adverse neural tension testing, done by a physiotherapist, can determine what level of nerve tethering or dysfunction is present.

4. Proprioceptive deficit Reams of research and knowledge have been developed to aid understanding of how a severe disruption to the normal functioning of a joint or body part can then create long term damage to the brain-body connection to that body part. The brain’s ability to be aware of and to co-ordinate reflexes at the injured ankle can set up a chain of injuries elsewhere through the lower limbs unless the proprioceptive deficit is corrected through an exercise programme.

Signs ●●do this test on yourself if you have ever badly injured an ankle or knee joint: in a completely dark room, stand on each leg in turn. Note the significant challenge of standing easily on the previously injured leg! ●●proprioception in every damaged ankle will have been moderately to severely affected; this will need to be addressed during the mid- to late stages of rehabilitation.

Conclusion Once there is clarity about the nature and severity of damage to structures, the injured sportsperson and their therapist will be able to develop time frames for recovery and get on with managing the injury and beginning an exercise programme. More often than generally acknowledged, a period on crutches can be critical for the initial phase of healing, and to prevent side-effects such as on-going instability, long-term swelling and ankle thickening, and even reflex sympathetic dystrophy.

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Getting the rest and healing phases right will help to minimise the time you will need to take out of your sport, and you will be safeguarding the long-term wellbeing of your ankle.

Ulrik Larsen

page 46 SERIOUS SPRAINS II

Syndesmosis injuries of the ‘high ankle’ are uncommon, but need prompt diagnosis and careful handling

All sports therapists will be used to the regular appearance in their clinics of the classic ankle injury: the plantar-flexion inversion injury (turning the ankle inwards as you land on the foot), which results in the lateral (anterior talofibular or ATFL) ligament sprain. The frequency of this sprain – which accounts for up to 15% of all sports-related injuries – is largely explained by the inherent weakness of the anterior talofibular ligament and the bony anatomy of the lateral ankle. Less frequently a sportsperson will appear with a ‘high ankle sprain’ – a diagnosis that is easy to miss. However, the ramifications for rehabilitation are significant, with longer recovery times, and on occasion the need for surgical treatment. High ankle sprain describes an injury to the syndesmosis (ligamentous articulation) between the two lower leg bones, tibia and fibula (see illustrations, page 10). Injury to this structure often occurs together with injuries to the deltoid ligament and associated fractures of the medial and/or lateral malleoli (the bony prominences at the ankle end of tibia and fibula).

Anatomy The ankle is composed primarily of three joints: the talocrural; the inferior tibiofibular, and the subtalar (see page 10). Each joint is maintained by a joint capsule, ligament and the dynamic stability of muscles and their associated tendons.

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The talocrural joint is the articulation between the tibia and the talus (maintained on either side by the medial and lateral malleoli). This joint provides plantarflexion and dorsiflexion (point and flex movements). The subtalar joint is the articulation between the talus and the calcaneus. These two bones pivot on one another in an attempt to regulate stable foot position on uneven surfaces by providing inversion and eversion (inwards and outwards turning movements). The inferior tibiofibular joint is the articulation between the bottom end of the tibia and fibula. This articulation is supported by the syndesmosis and allows for a small amount of rotational and translation (sliding) movements. The major ligaments making up the syndesmosis are the anterior and posterior inferior tibiofibular ligaments and the interosseous tibiofibular ligament, which is continuous with the interosseous membrane between the tibia and fibula.

How a syndesmosis sprain occurs A lateral ligament injury happens as a result of a plantarflexion / inversion force that puts the anterior talofibular ligament (ATFL) under stress. Injury to the syndesmosis complex happens with an external rotation force to a dorsiflexed or hyperdorsiflexed ankle. These injuries have most commonly been reported in American football, soccer, rugby and skiing. Examples of how this injury occurs include a football player being struck on the outer thigh, leg or trunk while their foot is planted. This causes internal rotation of the leg against the foot (see illustration opposite). Another common situation occurs in skiing: if the front tip of the outside ski catches in snow, the foot is forced into an externally rotated position (see illustration opposite), while the boot holds the ankle in a dorsiflexed position. Initial external rotational forces cause the talus to twist and force itself laterally against the fibula. This creates a force that draws apart the fibula and tibia, placing the structures of the

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How syndesmosis injury occurs

syndesmosis under tension. If the force is great enough, the anterior tibiofibular ligament ruptures. As the force increases, more of the ligamentous structures that make up the syndesmosis will fail. Occasionally all of the ligaments can rupture and the interosseous ligament and membrane can tear, causing a separation of the tibia and fibula, though this is rare in isolation. The force required to disrupt these structures is usually strong enough to fracture the fibula and rupture at least part of the deltoid ligament.

Assessment Individuals with this injury will typically avoid heel-to-toe walking, as the heel strike causes an axial load through the talus, separating the tibia and fibula. It also necessitates movement into a painful dorsiflexed position. The far end of the anterior tibiofibular ligament will be painful to touch, and also more proximally, indicating interosseous membrane damage. The degree to which tenderness extends along the interosseous membrane has been related in one piece of research to the number of days that an affected athlete has missed from competition1. Medial tenderness is typically greater than that over the lateral malleolus. Range of movement will usually be limited with minimal swelling. Ligament stress tests should always

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assess the lateral and medial structures, as these can also be involved.

Management High ankle sprains take significantly longer to rehabilitate than a simple lateral ankle sprain. Table 1 below summarises a typical treatment strategy. More serious injuries, in which a fracture has occurred, or where x-ray demonstrates significant instability, usually need to be stabilised surgically.

Tests for high ankle sprain Tests specific to ‘high ankle sprains’ include: l external rotation stress test (Kleiger test). A positive test reproduces pain over the outer front section of the distal syndesmosis and indicates injury. Reproduction of medial ankle pain may indicate involvement of the deltoid ligament l the squeeze test (Hopkins test) is probably more sensitive in significant injuries and may not be as good in more subtle injuries – it should not be used in isolation. (Alonso2 found that diagnosticians were able to use the external rotation stress test with greater reliability than the squeeze test to determine syndesmosis injury) l the cross leg test is a variation of the squeeze test. Signs of a positive test mirror those of the squeeze test l because of the bony anatomy of the ankle, simple dorsiflexion creates a distraction (separation) force across the syndesmotic ligaments. The talus is wider at the front than at the back. The plantarflexed ankle places minimal stress on the syndesmosis, but moving the ankle into dorsiflexion forces the wider front portion of the talus into the ankle mortise, creating a separation force between the tibia and the fibula, which stresses the ligaments holding them together at the syndesmosis

Magnetic Resonance Imaging (MRI) is very accurate in the diagnosis of syndesmosis injury, but will frequently show up aberrations that may not be the cause of symptoms. It is also expensive, so while it may be appropriate for elite athletes who need definitive diagnosis and possibly prompt surgical referral, a clinical diagnosis is generally all that is needed for non-elite athletes who are not bound by a strict competition schedule.

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Table 1: Syndesmosis injury treatment schedule Phase/ Goals Intervention Criteria

Acute phase l Minimise pain and l Rest, ice, compression, and elevation (first week) swelling (RICE), electrotherapy, cryotherapy l Maintain passive l Stabilise: casts, splints, braces, heel raise, range of movement taping within limits of pain l Non-weight bearing with crutches

Sub-acute l Eliminate pain and l Gait: partial weight bearing without pain phase (1 to 2 swelling l Simple standing (two-legged) balance weeks) l Restore passive range exercises on eg, towels with gradual increase of movement in weight bearing l Gait re-education l Gentle calf massage and stretching l Strengthening with resistance bands l Stationary bike l Early proprioception exercises

Advanced l Restore full pain-free l One-leg balance training in plantar flexion phase (2 to 5 active range of eg, on heel raise weeks) movement l Strengthening with calf raises, squats, l Normal gait lunges l Proprioception l Proprioception exercises, wobble board, re-education trampette, Swiss ball l Early sideways movements, figure of 8, straight line walk/run

Final phase (5 l Return to pre-injury l Fast cutting, running, jumping to 9 weeks) function l Plyometric movements: hopping on uneven surface, single leg hop on/off mini-tramp l Sport-specific training

Conclusion High ankle sprains are an uncommon but serious form of ankle injury among sportspeople. It is really important to consider this possibility at the time of the injury as a delay in diagnosis will leave the injured ankle exposed to significant longer term problems, such as early onset osteoarthritis or chronic ankle instability and pain. Ryan Shulman

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References 1 Nussbaum ED, Hosea TM et al. Prospective evaluation of syndesmotic ankle sprains without diastasis. Am J Sports Med 2001;29:31–5. 2 Alonso A, Khoury L et al. Clinical Tests for Ankle Syndesmosis In jury: Reliability and prediction – of Return to Function. Journal of Orthopaedic & Sports Physical Therapy Volume 27 (4): 276-284.

page 52 A CAUTIONARY TALE

If only Lauren Young had read all the preceding advice, much misery might have been avoided

In June 2005, while running down a dimly lit country lane, I inverted my left ankle in a 30cm hole in the road. I went down and within seconds the pain arrived, like a hot poker being driven through the side of my ankle. I tried to stand, but couldn’t put any weight on my left foot. Friends called an ambulance. I cried, not just because of the throbbing pain, but also at the thought of having to rearrange my life for several weeks. My ankle was swelling spectacularly; the paramedics placed it in a splint and gave me some much needed nitrous oxide to inhale for pain relief. Injury was a new experience: throughout an active sporting life, playing club and county hockey as goalkeeper, and playing for my university first team, I had never had ankle problems. The hospital took x-rays; I was told there was no fracture. My left ankle was immobilised in a below-knee temporary plaster cast. I was put on crutches, instructed not to weight- bear until my follow-up appointment, and prescribed paracetamol and codeine for pain management. Two weeks later, and after a second set of x-rays were clear, I was placed in a weight-bearing cast and told that ‘simple sprains like this get better by themselves’. I started to weight bear, initially with gritted teeth and tears – but I assumed that the severe pain was normal at three to four weeks post-injury. I had asked why it was that the pain had subsided in my ankle joint but remained in my midfoot area, and was reassured that it would settle by itself. Over the next three weeks my foot

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swelled up so much that I needed two changes of cast, and a third when the swelling eventually settled. After five weeks of immobility, the cast was removed and I was asked to organise my physiotherapy. My ankle gave way repeatedly at first, requiring me to buy and use a stirrup brace for walking. My physio assured me this instability would improve with time. I still couldn’t drive or resume my all- important cash-generating summer job as a waitress; and I was heavily dependent on my parents for every-day activities. I progressed through eight sessions of massage, stretching, muscle strengthening and balance exercises, using a resistance band and wobble board. At the final session the physio manipulated my ankle: I lay face down, grimacing with pain as my ankle was wrenched in all directions. I was then discharged and told that the giving-way would resolve and I should get back to hockey. I never did get back to hockey. I wore the brace for another two months; I continued dutifully doing all my rehab exercises. Gradually my anxiety about re-injuring my ankle faded and I managed to get back to walking without the brace, and even to running on a treadmill – but not outside. I was reluctant to run for a bus, and wearing heels was out of the question.

A repeating pattern Over the next three years I sustained a series of inversion injuries to my left ankle, about three or four a year. Each time I pulled out the brace again, and after each occurrence I noticed my proprioception getting worse. My ankle started to swell up more and more in the evenings and with each incident I was taking longer to recover. I tried lace-up braces, neoprene supports, strapping, taping on to my skin and orthotics; nothing was as supportive as the hard plastic stirrup braces with air cells that I’d used initially. Up until July 2008 my right ankle had remained uninjured, but while walking across a campsite in the dark one night, I tripped and twisted that side, too. At the time I was in the Australian outback, hundreds of miles from the nearest

page 54 PEAK PERFORMANCE sporting ankles hospital, so was extremely relieved when I realised I could weight bear on it. My well-rehearsed RICE routine wasn’t possible on a trekking holiday, so I hobbled my way through the rest of the trip with a basic elastic support and analgesia. One month later, back in London, I started my first job as an orthopaedic foundation doctor. When my consultant asked why I was limping on his ward round, I explained and was promptly sent for x-ray. There was no fracture, but the ATFL was probably ruptured, and I provided much entertainment as the orthopaedic junior doctor in an Aircast boot for the next four weeks. In October 2008, dodging a speeding car, I yet again inverted my left ankle, in plantar flexion initially, then dorsiflexion as I planted my foot. The pain was so intense I stood shaking at the other side of the road, unable even to touch my foot to the ground. I couldn’t believe I had reinjured my left ankle so soon after my right. When I arrived at the emergency room, my ankle was huge and I knew this time it was really bad. I was given morphine and admitted to my own ward for analgesia and elevation. The x-ray showed a proximal navicular fragment fracture, but no other bony injury. The next morning I saw my consultant, this time as a patient. I was placed in a full below-knee cast, non-weight bearing, and discharged home. I returned to work with difficulty four days later. At my two-week fracture clinic follow-up, I found weight bearing hard, the pain was still awful and my entire lateral foot, sole and ankle were deep purple, with bruising going up to the back of my knee. I had tenderness over my lateral and medial malleoli, which would remain for 10 weeks. I had pain when squeezing the tibia and fibula together (the squeeze test) and tenderness over my fibula head which I had put down to the cast rubbing, but the bruising around it meant I had probably also fractured the fibular head. I also had a positive anterior drawer test and talar tilt test. Because of the continuing pain, I was sent for MRI, which showed:

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●●complete ATFL and CFL ruptures ●●deltoid ligament tear ●●bone bruising of medial malleolus and parts of the talus bone ●●injured talocalcaneal ligament ●●navicular avulsion fracture, with areas of chondral damage.

The MRI also showed that I had some anatomical anomalies: an accessory inferior ATFL, known as a Bassett’s ligament, and a low lying peroneus brevis muscle. A Bassett’s ligament can cause anterolateral ankle pain because of ligamentous impingement after ankle sprains (1), and may well have been the cause of my ankle pain since my original injury in 2005. I was told that the medial ligaments would probably heal completely without problem, but that lateral ligament damage can lead to further problems in a minority of cases. At four weeks I was put into an Aircast boot for another month, and told that the bone bruising would take months to heal. I underwent further physiotherapy, initially on the right ankle while the left was in a cast, and then on both. As before I worked on my muscle strength, proprioception and flexibility, but this time also did gluteus medius strengthening. I had two separate courses of intense physiotherapy and again tried strapping and bracing for my left ankle. All these measures failed to correct the instability. It took six months for the pain to settle to a ‘background’ level in the left ankle; after a day on my feet the ankle would always be swollen and uncomfortable. I continued to invert the ankle even when walking on flat surfaces, and found the feeling of instability very unpleasant. I had subconsciously become extremely anxious about my ankles: I wouldn’t run at all, I wore stirrup braces for even the most sedate country walks, never wore heels and would cross cobblestones only with great caution. I saw my consultant again, this time to discuss surgical options. At first this seemed a drastic step, but we decided that I had failed all conservative treatment and it really was the only option. We also discussed the right ankle, in which anterior

page 56 PEAK PERFORMANCE sporting ankles impingement had started to cause me to externally rotate my hip whenever I went down stairs. MRI of the right ankle showed lateral gutter synovitis and confirmed an ATFL rupture. It also showed a Bassett’s ligament, like the left ankle, which could be the reason for the impingement.

The operation I underwent a single operation under general anaesthetic, for both ankles. My consultant opted to reconstruct my left lateral ankle ligaments, removing the inflamed soft tissue that was causing anterolateral impingement. I also had loose cartilage removed to prevent further chondral damage. On the right ankle, I had arthroscopy to remove soft tissue causing anterior impingement and resection of Bassett’s ligament.

Reflections Looking back over my four years of ankle problems, I have wondered whether I could have avoided surgery. After the initial injury in 2005 I had believed the repeated inversion injuries to be just a ‘weak ankle’. I hadn’t sought medical attention and had assumed that my left ankle would remain troublesome. I think it comes down to a combination of unlucky anatomy (bilateral Bassett’s ligaments), unlucky repeat injuries and passive acceptance of having to just live with my ‘weak ankle’ – something that surely many other people also assume. Lauren Young Reference 1. Bassett FH III, Gates HS III et al (1990) Talar impingement by the anteroinferior tibiofibular ligament. J Bone Joint Surg 72A:55– 59

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page 58 COMPLEX INJURY REHAB

Even the toughest athlete can be undermined by their dodgy ankles. But meticulous rehab can put you back on track

Mel loves mountain running. Much of her week revolves around training, getting ready for the long run at the weekend, and ultimately the big competition. I first saw her about six weeks out from a race called the Kokoda Challenge, a 96km team race. She was struggling with two complaints. The first, and lesser, was repeated ankle sprains on both legs; the second was chronic iliotibial band (ITB) problems, again on both sides. Although these are clearly two different issues, they are not entirely separate, as we shall see. Mel was always running on uneven, rocky ground and would roll her ankles several times during every training and competition run. On assessment, she demonstrated laxity on both ankles in the anterior talofibular ligament (ATFL, the most commonly strained ligament of the ankle). There was no joint effusion or pain, just increased plantar flexion and inversion and increased joint movement on the ATFL anterior draw test. Her proprioception was, to put it mildly, terrible. When balancing on one foot, she would lose balance immediately upon closing her eyes. She was unable to balance on the ball of her foot on one leg, and couldn’t hold balance on one leg when using any balance device such as a wobble board or BOSU ball. The immediate aim was to stop her rolling her ankles, to prevent long term joint damage and, importantly, to decrease the risk of a serious acute ankle injury – a risk that is clearly

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inherent in the nature of her sport. We needed to retrain Mel’s proprioception. And now to Mel’s ITB problems. She had been suffering from lateral knee pain for about a year. She had been battling through the pain in training; it would come on after different distances, but would usually start when she was going downhill. Because she’d had this problem for a long time and past treatment had not been successful, she had an MRI scan; this revealed irritation of the under-surface of the ITB and some very mild bony inflammation at the lateral femoral condyle. In consultation with the sports doctor, we decided that a cortisone injection would be appropriate. This would permit Mel to carry on doing some running and create a window for some rehab work. Mel, however, was not keen on the idea, preferring to try rehab alone first. Upon assessment, she had only mild tensor fascia lata (TFL), hip flexor and ITB tightness, which we treated with soft tissue massage, trigger points and stretching. But these measures didn’t really target the underlying problem. Mel was able to carry on running and doing her rehabilitation but with the continued deficit in her range of movement. In 1994 Bullock-Saxton et al (1) demonstrated the significant difference in patterns of muscle activation around the hip among those who had previously suffered a severe ankle sprain, with delayed activation of gluteus maximus on the previously injured side and changes in the local perception of vibration on both sides. On testing, Mel’s gluteus maximus activation was very poor. In prone hip extension (lying face down), gluteus maximus activation was almost non-existent and she struggled with any other hip extension-dominant exercise. And she was finding single leg stance exercises difficult not merely because of her lack of proprioception but also because of poor gluteus medius function, which could be seen in isolated hip abduction in side lying, and single leg stance drills. To sum up the picture thus far, Mel, who was trying to compete in endurance mountain races, had:

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●●chronic ATFL laxity ●●ITB friction syndrome confirmed by MRI ●●poor proprioception ●●poor gluteus maximus and medius function, and ●●anterior and lateral tightness.

Running into trouble Her running gait reflected this lot perfectly. She ran with a very long stride length. Her heel strike occurred way out in front of her hip (instead of underneath it), constantly putting gluteus maximus into a lengthened position. This was making it more difficult for the muscle to contract and extend the hip. So Mel was pulling herself along with her hip flexors and rotating her pelvis with a rather forceful hip extension so that she could propel her body forwards at heel strike. Because of her long stride length, she crossed her midline by a large degree, ramping up the demand on her already weak gluteus medius. It was not surprising that in stance phase her pelvis exhibited considerable lateral tilt. It is worth mentioning that elite runners also tend to drift across the midline, because they, too, run with a long stride. The difference is that their greater stride length comes from their powerful propulsion through each stride; heel-strike remains firmly under the hip. Not only does a running gait such as Mel’s lead to injury, it is also very inefficient. Because her stance phase was very long, any elastic energy stored from the initial ground contact was lost, causing her to have to work harder to transfer energy with every stride. This is why elite runners tend not to have a heel- toe running pattern: they are moving so efficiently that a heel- toe pattern would cause them to spend too long on the ground and therefore lose too much energy. A key aim of all runners – from track to marathon – should be to decrease ground contact time, in order to increase efficiency and hence speed.

The rehab Mel didn’t want to stop running, despite pleas, because running

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was more than just exercise for her. As with many people, it was her solitude and stress relief. So we had to prioritise proprioception, to try and improve this before she suffered a serious ankle injury. We started with low-level balance exercises, such as: ●●balancing on one foot with eyes closed for 2 sec at a time ●●single leg balancing with small heel raises, using support as needed.

We progressed this to: ●●increasing the time and height of the heel raises ●●single leg balancing while throwing a ball.

We further progressed to: ●●single leg knee bends with eyes closed ●●hopping drills, eg, on-the-spot, around cones, in patterns, hopping then holding balance on the ball of the foot.

As Mel improved, we were able to introduce external devices to overload the proprioceptive system: a soft mat, wobble board and Bosu ball. Other high level exercises included: ●●balancing on wobble board while throwing and catching a ball ●●single leg knee bends on the BOSU ball. There are two important goals with proprioceptive training. Firstly, to improve the function of the proprioceptive system with progressively more difficult activities; and secondly (especially important in Mel’s case, as she was running long distances on uneven ground), to increase the endurance of the neuromuscular system. We started her on low level activation drills for her gluteus maximus and gluteus medius. For the glute max, she had to lie prone and simply practise squeezing left and right glutes together and then isolating each side. This progressed to prone hip extension, concentrating on first isolating glute max contraction while maintaining neutral pelvis and spine. Mel also did single leg bridge exercises (see illustration opposite top), again concentrating

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Single leg bridge

initially on squeezing the glute max and then extending the hip, but not arching the lumbar spine. We encouraged her to concentrate on feeling as though she was activating her gluteus maximus in walking and in particular on stairs. For gluteus medius activation, we used clams (side-lying with hips flexed to 30 degrees, heels together and lifting top knee apart without the pelvis moving, (see illustration below) and side-lying hip abduction with a straight leg. Once Mel had completed these, she progressed to standing drills, starting with squats. First we used double leg squatting to boost gluteus maximus strength bilaterally, then single leg squats to add an emphasis on gluteus medius, so as to stabilise the pelvis and knee.

Side lying clam

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We later introduced the more technically demanding Romanian deadlifts (RDLs). These, I believe, are the best way for athletes to strengthen the gluteus maximus (see www. pponline.co.uk/encyc/weight-training-the-romanian- deadlift-41777 for a full briefing on RDLs). Mel finally progressed to single leg RDLs, a very challenging exercise. Gluteus medius endurance bilaterally was worked on with ‘crab walks’. This involves looping a flex-band around the ankles in standing, assuming a semi- squat and widening the stance, then taking small sideways shuffling steps with one foot, then the other, while maintaining the tension on the band. This burns the gluteus medius muscles; it can be progressed by increasing the number of steps or using a stronger band. I usually start people with 10 steps out and 10 steps the other way x2 for a single set.

Not any old exercises… We tailored all the above strengthening exercises to suit Mel’s specific sporting needs. She had to have exceptional endurance in all those key muscles we were targeting if she was going to maintain an efficient gait throughout an event. Her programme was therefore designed to reflect this, using lower weights but higher reps (starting at 15), and more than the standard three sets. These extra repetitions had the added benefit of helping her hard-wire the beneficial motor patterns more rapidly. It also meant she had to work very hard indeed on her rehab. Particularly during the late-stage rehab, the sessions were extremely arduous. But then, she wasn’t trying to do what might be considered normal for a 43-year old woman. One bonus was that because the later sessions were so tough, she needed to take adequate recovery time, which limited her to a maximum of three sessions a week. Mel became technically very competent and strong; she continues regularly to perform her exercises as maintenance.

Running form The running technique re-education was quite simple. We concentrated on shortening her stride and getting her to feel as

page 64 PEAK PERFORMANCE sporting ankles though her heel strike was back under her body and not straying over the midline. Next, Mel had to feel like she quickly propelled her body over her foot, to produce a decrease in her ground contact time. We cued her to feel her gluteus maximus contracting as she extended her hip. As she had good body awareness, this worked well for her. I also encouraged her to connect up the feeling she was getting in the gym rehab work with how her gluteals were working in her running. As you can imagine, to achieve this entire programme before the 96km Kokoda run was impossible, and Mel knew it. But she wanted to try anyway. As expected, she didn’t make it and her knees were a problem. But at least she had stopped rolling her ankles. After letting her knees settle, she put her head down and worked hard at her rehabilitation. She also started running again, with the pain improving and still no rolling of the ankles. Gradually, as she got better and better, the pain diminished. Mel had a favourite 18km training loop she liked to do regularly and she began running that pain-free – which she hadn’t been able to do for 12 months. In fact, she came to physio after one weekend hugely excited because she had beaten her personal best by 10 minutes on her 18km training loop. But the real test was yet to come: a 50km mountain run. This took place about three months after the Kokoda event. Mel ran strong and pain-free. She was pumped. So was I, actually.

Sean Fyfe

Reference 1. Bullock-Saxton. J, Janda V, Bullock M. ‘The influence of ankle sprain injury on muscle activation during hip extension.’ Int J Sports Med 1994; 15: 330-334

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page 66 KNOCK-ON DAMAGE

For this professional footballer, an ankle sprain turned into groin strain

As a northern hemisphere physiotherapist working with professional footballers, I started back at pre-season training in early July with a few hectic weeks of screening, physical testing and training. It was with relief that I stepped on the plane to Portugal for our pre-season training camp without a single player in the treatment room. As luck would have it, during the first training session in this different environment one of our strikers inverted his left ankle. Immediately my mind started racing as to why it had happened: was it the new, unfamiliar training surface? Or the heat and associated fatigue? Had we fallen short in our injury prevention training? Or was it just bad luck? The answer is impossible to know, but a combination of the above is likely. Matt, the 18-year-old striker, said he’d felt a sudden sharp pain followed by an intense throbbing. His range of movement (both active and passive) was limited, he was unable to weight- bear and by the time we got him to the treatment room was already developing swelling around the ankle. Matt expressed extreme displeasure at my palpating anywhere around the ankle joint, but particularly around the ATFL (anterior talofibular ligament) and the distal posterior fibula, around and above the lateral malleolus. His high anxiety and discomfort limited my ability to conduct a detailed examination but I had enough concern to request an X-ray to exclude a fracture. Thankfully fracture was ruled out and so we began the process of standard ankle rehabilitation. Within about a week, we were able to get Matt back on the

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grass, lightly jogging without any discomfort. His ankle still had a diffuse effusion (swelling) laterally and the joints (subtalar and talocrural joints) were certainly stiffer compared to his non-injured ankle, so we continued the rehab with daily joint mobilisations (often preceded by warm bathing), continued strengthening, range of movement and proprioceptive exercises, followed by football-specific work on the grass. At approximately two weeks post-injury we felt confident for Matt to go back into full training with continued pre-session ankle mobilisation and taping. At this point, he was getting no pain with any functional training or palpation, but his ankle did still appear slightly ‘puffy’ and stiffer to mobilise compared to the other side. Two days after recommencing full training, Matt re-presented to the treatment room with gradual onset right- sided groin pain. Biomechanical assessment highlighted patterns of movement dysfunction, many of which we had already noted on pre-season screening. He revealed excellent local muscle strength around the groin, albeit with a level of discomfort upon activation, but very poor muscle control around his trunk and pelvis. For instance, on a single leg squat, on both left and right legs, Matt’s knees drifted medially towards his midline, he flexed through his spine and hips, and generally lost his balance the lower he went. This highlighted control weaknesses in and around the hips and low back that needed to be improved to allow better injury-free function with higher training loads. We had seen similar patterns of dysfunction, weaknesses and lack of control during the pre-season period in many of the players and all had been involved in generic core stability, strengthening and balance control classes to help to address these issues. Given the rapid onset of Matt’s groin pain so soon after return to full training, it would be fair to consider that his recent ankle injury had contributed to his new symptoms. But we reasoned that the bigger influence was likely to have been poor pelvic control, leading to overload of the adductors, especially as he had returned from his ankle rehab to a higher

page 68 PEAK PERFORMANCE sporting ankles intensity of training. Matt’s poor pelvic control is not unusual in a physiologically developing athlete. Experience has taught us that during phases of sudden growth, young players undergo periods of poor co-ordination and joint control. This is probably because the skeleton develops at a faster rate than soft tissues, so the myofascial system, which controls movement and stabilises the joints, struggles to do its job efficiently. This can place undue stress on joints and/or soft tissue structures which can easily present as dysfunction, pain or injury. Preventive therapies look to minimise and correct any dysfunction, with the aim of preventing injury in developing athletes. We set to work on Matt’s individualised programme, focusing on the specific aspects relevant to this groin injury. The most significant features included isometric holds in inner range (muscle shortened), mid range and outer range (muscle lengthened) positions in all of the stabilising muscles of the pelvis and trunk (iliacus, psoas, glutes, abdominals and back extensors). Secondly Matt worked to improve movement dissociation; he would move one part of his body while focussing to keep another area still. For instance, he would stand in a single-leg, bent-knee position on his right leg, and rotate his upper trunk to the left while maintaining the exact level of knee flexion and preventing this bent knee from turning inwards when the trunk rotated (which requires good activation of gluteus medius). As the next two weeks passed, Matt made improvements in his pelvis and trunk control. But this seemed to make little difference to the pain he continued to report as we again tried to phase his return to training. It was at this point that we more closely analysed Matt’s running gait and observed an asymmetry. He ran with a reduced stride length and an associated decreased weight-bearing phase on his left leg. When we tested his straight leg raise for hamstring flexibility, it was significantly reduced on the left side and he had a posterior pelvic rotation on the left, which was probably secondary to the tight hamstrings.

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The previously injured left ankle was stiff and had significantly reduced dorsiflexion compared to how it had been just before his return to training. This would be the consequence of tightness through his posterior chain (calf, hamstrings, glutes), which would have caused a pulling down on his ischial tuberosity and a posterior pelvic rotation on the same side. Any torsion within the pelvis will naturally put certain soft tissue structures under more tension, which in this scenario was, we believed, his right adductor muscles. We commenced an intensive week of therapy to balance the soft-tissue systems left to right, consisting of daily ankle joint mobilisation, soft tissue release work using heat, acupuncture, trigger point therapy and massage of the left posterior chain. We also prescribed dynamic (kicking motion) hamstring flexibility exercises alongside static calf stretches for both gastrocnemius and soleus. This regime improved Matt’s straight leg raise and consequentially corrected his left posterior pelvic rotation. Over the next week he was successfully reintroduced into training with a normalised gait pattern and stride length. His groin discomfort seems to have gone on permanent vacation and Matt continues with his individualised control exercises and ankle mobilisations several times a week to ensure this remains the case. This case study reminds us how one injury can so readily lead to another and also how a relatively simple injury can become greatly complicated in the presence of pre-existing circumstances. In this instance, Matt’s age, the fact that he is still developing, his prior weakness and associated lack of control all impacted on the knock-on effects of his ankle injury. While we have to be mindful of the effect any injury can have on the body, in a sport such as football, we must always give consideration to other possible pre-existing factors to ensure that return to full fitness is completed as quickly, safely and successfully as possible.

Darren Stanborough

page 70 DANCE INJURIES

Dancers can wreak havoc on their feet and ankles, as this tour of the damage reveals

Dancers put high stresses through their feet and ankles, often at the extremes of the range of movement of certain joints. Among female dancers in particular, the vulnerability of the foot and ankle is frequently compounded by the risk of injury as a result of the ‘female triad’ (nutritional deficiencies, amenorrhea and osteopenia). Up to 40% of all dance injuries occur to the foot and ankle. Injuries may be acutely traumatic or chronic overuse. Chronic injuries may result from repetitive fatigue or impingement syndromes. Early recognition of symptoms and prompt treatment will help to speed the dancer’s return to performance, and can be career-saving.

Acute trauma High level dance generates large forces within the skeleton, usually the result of the body’s deceleration from jumps and twists; ballet also requires remarkably fine-tuned balance. It is the combination of loss of balance and large force that causes many acute injuries among dancers.

Ankle sprains Ankle sprains are common. They result from dancers working for hours a day in positions that predispose to sprains. The most common cause is loss of balance when landing from a jump. The anatomical location of injury depends on the ankle position during impact. The talus is wider at the front and narrower at the back,

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making the joint potentially unstable in plantar flexion. However dancers rarely sprain the ankle when in full plantar flexion, such as at full pointe, as the ankle is stable in an anatomically ‘locked’ position. In full pointe it is the midfoot that is most frequently injured, however when the hindfoot unlocks, with just a few degrees of dorsiflexion off full pointe, the ankle becomes incongruent again, predisposing it to ligament injury. In dorsiflexion the ankle again becomes stable. The most frequently injured ligament is the anterior talofibular ligament (ATFL), followed by the calcaneofibular (CFL). Sprains are graded 1 to 3 in increasing severity. Grade 1 sprains are the most common, representing partial tears of the lateral ligament, with lateral (outer edge) pain and swelling. Weight bearing is comfortable and tests (inversion and anterior drawer) will show no increased laxity. These injuries do not need immobilisation, but a RICE (rest, ice, compression, elevation) regime and early rehabilitation with peroneal and proprioceptive exercises. The dancer can expect to return to dance within three to four weeks. Grade 2 injuries involve a tear of the ATFL, with lateral swelling, a positive anterior drawer and negative inversion test. Weight bearing is uncomfortable. These ankles need to be immobilised for three weeks, followed by rehabilitation. The dancer should expect to take up to eight weeks before they return to dance. Grade 3 injuries involve rupture of the entire lateral ligamentous complex and in essence are a kind of ankle dislocation; fortunately this is an uncommon pattern of sprain in dance. The dancer will have marked swelling and find weight bearing difficult because of pain; anterior draw and inversion tests will show gross instability. The optimal management of Grade 3 injuries is controversial: some propose surgical repair, others immobilisation in a pneumatic walker (lightweight immobilising boot), allowing sagittal plane movement only, for four to six weeks, followed by peroneal strengthening and proprioceptive rehabilitation. A return to dance may take 12 weeks.

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Grade 2 and 3 sprains can mimic fractures, so x-ray is advisable when a dancer is unable to weight-bear or has tenderness over the malleoli.

Chronic sprains Pain, swelling or instability may persist after a sprain, which can be a result of:

Chronic ankle instability This may be rotational or varus (inward-tilting). Varus instability is often compensated for by proper peroneal training. Rotational instability is very difficult to correct with rehabilitation. Dancers notice rotational instability when performing ‘inside turns’.

Persistent pain Anterolateral impingement can be caused by an incarcerated lateral ligament, synovitis or meniscoid type lesions. It often requires arthroscopic cleaning out. Pain may be exacerbated by peroneal weakness, so an appropriate peroneal rehabilitation programme is essential. Longitudinal tears of the peroneal tendon, or peroneal subluxation, are often linked to persistent outer-edge ankle pain, swelling and clicking. Ultrasound or MRI scan are very good at showing subluxation and tears; these generally need surgical repair. Osteochondral defects of the talar dome occur during ankle sprains and fractures. They can cause persisting pain, intermittent swelling, clicking and locking. Osteochondral lesions are best diagnosed on MRI scan and are treated initially with arthroscopic cleaning out and drilling. Resistant lesions are treated with chondral or osteochondral transplant.

Hindfoot injuries Hindfoot sprains and dislocations are often misdiagnosed as ankle sprains. They involve injuries to the interosseous and cervical ligaments, or dislocations of the subtalar or

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calcaneocuboid joints Hindfoot dislocations frequently produce stiffness or ongoing instability. These injuries may present with persistent instability or pain and swelling in the sinus tarsi (‘sinus tarsi syndrome’).

Midfoot injuries These occur as a result of loss of balance in the en pointe position. They cause midfoot swelling and tenderness. Chronic midfoot injuries also occur, associated with ‘sickling’ (excessive supination). Weight bearing x-rays of the foot may show diastasis (separation) of the Lisfranc joint; stress x-rays or CT scan should also be considered as the deformity may be subtle. Undisplaced injuries or those with mild laxity may be immobilised in a plaster cast, displaced injuries are treated operatively to close and fix the gap.

Fractures Ankle Ankle fractures are uncommon in dancers. Stable fractures may be treated in a plaster cast; displaced or unstable fractures are treated surgically to prevent problems with bone healing and allow early rehabilitation.

Fifth metatarsal base Dancers are susceptible to fractures of the fifth metatarsal. These may be avulsion type fractures of the base or occur at the metaphyseal-diaphyseal junction. Suspected fifth metatarsal fractures should be investigated with plain x-ray. Many are treated symptomatically in a pneumatic walking boot, but displaced intra-articular fractures and those at the metaphyseal-diaphyseal junction should be surgically fixed.

Chronic overuse injuries Stress fracture Stress fractures are caused by repeated loading of a bone. Dancers have a high incidence of osteopenia in which their bones are weaker and more prone to a type of stress fracture

page 74 PEAK PERFORMANCE sporting ankles known as insufficiency fracture. Stress fractures can occur in any bone in the lower limb. They initially present as pain after activity, but with time pain can be experienced during normal activity and at rest, and night pain is quite common. The dancer may find it hard to pinpoint the source of pain and frequently there are few clinical findings – x-rays for instance can show as normal, especially within two weeks of onset. It is therefore important to keep this injury in mind, as early diagnosis will minimise recovery time for the dancer. The most common stress fracture among dancers is to the base of the second metatarsal. The area will be tender to palpation. MRI or bone scan should be performed in those with negative or equivocal x-ray results. Most of these fractures heal with conservative treatment, which should involve immediate rest and immobilising the foot in a pneumatic walker, returning to dance once the patient is pain free. Other stress fractures are managed similarly. However, navicular stress fractures (which are fortunately relatively uncommon), require more stringent immobilisation in a below-knee cast if the fracture extends into cortical bone. Complete fractures and those remaining symptomatic after immobilisation should be surgically fixed.

Flexor hallucis longus (FHL) dysfunction Among dancers the FHL tendon is particularly susceptible to injuries. In some dancers, when the foot is in extreme ankle dorsiflexion, the muscle belly of the FHL will impact on the fibro-osseous canal of the tendon. Repeated impaction may cause medial (inner side) ankle pain. Alternatively the FHL tendon can become entrapped along its course, resulting in stenosing tenosynovitis and partial tears and nodules. The nodules can produce triggering of the great toe. FHL tendinosis is frequently found in association with posterior impingement syndromes (see below). In addition to its role as a flexor of the great toe (big toe), the FHL is a dynamic stabiliser of the medial foot and ankle,

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especially in plantar flexion. Repetitive activity such as en pointe or sickling in abduction may cause the tendon to become inflamed. Initial treatment is RICE and rehabilitation, with a graduated return to activity, restricting plié and pointe work. Where conservative management fails, surgical decompression of the FHL sheath may be appropriate.

Achilles tendinosis Achilles tendinosis is common in dancers, with overuse being a significant factor. It is not usually an inflammatory condition other than in the early stages. The dancer places heavy demands on the tendon during en pointe and plié. Mechanical contributors are overpronation and tight heel cords. Dancers usually present with local tenderness over the Achilles tendon, occasionally with swelling. Initial treatment is rest, ice and physiotherapy; a heel raise can be used but should be discarded as soon as possible to avoid further calf contracture. Rehabilitation should progress through concentric and eccentric strengthening and stretching exercises. Orthotic management for overpronation can be useful but often proves impractical in dance footwear. Steroid injections should be avoided: this is not an inflammatory condition and these injections can predispose to tendon rupture. Surgical cleaning out may be needed if conservative management fails.

Sesamoid disorders Large forces pass through the sesamoids during dance, notably when rolling through on demi or full pointe, so dancers are prone to injuries including fracture arthritis and ‘sesamoiditis’. Sesamoid injuries can result in prolonged disability. Dancers complain of pain in the plantar aspect of the ball of the foot. Pain is worse on passive dorsiflexion and resisted plantar flexion. Treatment is symptomatic and can require extended periods away from dance. Work in demi pointe should initially be

page 76 PEAK PERFORMANCE sporting ankles restricted and an offloading U-shaped pad should be worn. Steroid injections can be useful. Sesamoidectomy can be considered in resistant cases but should be regarded as a last resort, as it may prevent a return to high level dance.

Impingement syndromes The extremes of plantar and dorsiflexion that certain dance positions require can lead to impingement syndromes of the front and rear ankle joints. In anterior impingement, the source of pain may at first be hard to pinpoint, usually occurring during plié. There may be restriction to dorsiflexion and it may be mistakenly diagnosed as tight heel cords – the prescribed stretching regimes for such injuries may in this case exacerbate the problem. Anterior spurs (osteophytes, bony prominences) may develop after prolonged impingement or can result from ankle sprains. Examination may reveal anterior ankle tenderness, especially in dorsiflexion. Lateral ankle x-rays in maximal dorsiflexion show tibiotalar contact. The dancer should take anti-inflammatories, use a small heel raise when not dancing, and avoid provocative positions. Arthroscopic clear-out of osteophytes is performed if conservative treatment fails, but spurs do tend to recur over a few years. In posterior impingement, also known as ‘talar compression syndrome’, the dancer will feel pain at the rear of the ankle, especially in the demi and en pointe positions. The pain can prevent the dancer from achieving these positions. There maybe posterior swelling, tenderness and crepitus (grinding). Rapid dorsiflexion from a plantar flexed position reproduces the symptoms. Posterior impingement may be soft tissue or bony. Bony impingement results from a prominent posterior process of talus, an accessory posterior ossicle ‘os trigonum’ (these can be associated with FHL tendinosis), or occasionally a prominent calcaneus. Ankle instability can also cause posterior impingement.

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Treatment in the early stages involves restriction of relevé and en pointe, proprioceptive work and anti-inflammatory medication. Ultrasound-guided injection may help settle symptoms. Surgical excision of the os trigonum or prominent posterior process may be appropriate.

Nick Cullen

Further reading 1. Tom Faciszewski, Robert T. Burks et al. ‘Subtle Injuries of the lisfranc joint.’ JBJS 1990. 72-A;10. 1519-22. 2. William G Hamilton. ‘Stenosing tenosynovitis of the flexor hallucis longus tendon and posterior impingement upon the Os Trigonum in ballet dancers.’ Foot & Ankle, 3:74-80. 3. William G Hamilton. ‘Sprained Ankles in Ballet dancers.’ Foot & Ankle,1982, 3.2; 99-102 4. William G Hamilton, Mark J Geppert et al. ‘Pain in the posterior aspect of the ankle in dancers: Differential diagnosis and operative treatment.’ JBJS. 1996. 78-A; 10. 1491-99. 5. William T Hardaker, Susan Margello et al. ‘Foot and Ankle injuries in theatrical dancers.’ Foot & Ankle. 1985, 6;2. 59-69. 6. Bernard Kleiger. ‘Anterior tibiotalar impingement syndromes in dancers’ Foot & Ankle.1982. 3;2 69-73. 7. George J Kolettis, Lyle J Micheli et al. ‘Release of the flexor hallucis longus tendon in ballet dancers.’ JBJS. 1996. 78-A; 9 1386-90. 8. Jim Macintyre, Elizabeth Joy. ‘Foot and ankle injuries in dance’ Clinics in sports medicine. 2000. 19;2 351-66. 9. Martin J O’Malley, WG Hamilton et al. ‘Stress fractures at the base of the second metatarsal in ballet dancers.’ Foot & Ankle International, 17:89-94, 1996. 10. Ryan AJ. ‘The epidemiology of dance injuries’, in Ryan AJ and Stephens RE (eds), Dance medicine – a comprehensive guide. Chicago, Pluribus press, 1987. 11. Torsten Wredmark, Carl A Carlstedt et al. ‘Os Trigonum syndrome: A clinical entity in ballet dancers.’ Foot & Ankle,1991, 11.6 ; 404-06.

page 78 POOL-BASED REHAB

While you are off your feet, wonderful water will keep you fit and speed your rehab. Here’s how

I discovered the wonders of pool-based rehab and training when I started working at the Sports Injury and Rehabilitation centre in Lilleshall, central England in the late 1990s. I soon started to include a wide range of pool-based training in my athletes’ programmes. Since that time I have learnt a great deal about how water workouts can improve body alignment, aerobic and anaerobic fitness, flexibility, strength and overall balance and coordination, and I still use the pool with my athletes for training, recovery and rehabilitation. Below I set out some of the applications and drills I have found invaluable over the years.

Key properties of water Buoyancy is the term used to describe a fluid force that always acts vertically upwards. It enables the water to support the body, which is particularly useful during rehabilitation from injury. You can also increase your buoyancy with the aid of floatation devices such as belts and vests. Hydrostatic pressure in a fluid increases with depth, and is applied over the surface of any object immersed in the fluid(3,4). This turns out to be another valuable property in rehabilitation: the increased pressure on the body can be used to reduce swelling and allow the athlete to exercise an injured limb without the risk of aggravating swelling. Fluid dynamics (flow): When an object such as a human hand moves slowly through water, there is little apparent disturbance around the hand. As the speed of movement increases, waves

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and eddies are created (3,4). Two different types of flow exist: ●●laminar, characterised by smooth layers of fluid molecules flowing parallel to one another; ●●turbulent, characterised by a mixing of the layers of fluid molecules.

In pool training, we can alter the fluid dynamics to change the intensity of the training session. If you maintain a streamlined shape, you will produce minimal disruption to flow. But when you adopt an unstreamlined shape or use an unstreamlined object such as a float, you will disturb flow and increase drag, which ups the intensity of the movement. Depth: There is an inverse relationship between water depth and the amount of body weight supported by the musculoskeletal system. When you stand on the bottom of the pool immersed up to your neck, your body is bearing about 8% of its weight. Drop the water level to around mid chest and the body bears 28% to 35% of its weight, increasing to 47% to 54% at waist height(5). So by changing the level of the body in the water you can increase or decrease loading on the musculoskeletal system, which is very useful for rehab and injury prevention. Bear in mind, though, that if you are bouncing up and down, lifting arms above your head etc, the loading values will increase proportionate to the amount of the body out of the water.

Effective water workouts Cardiovascular training Deep water running is a good alternative to land-based running(2,6). In a joint study, researchers from England and Tasmania compared the effectiveness of deep water running and road running in improving maximum oxygen uptake in a group of 20 untrained young women. Both training programmes produced similar and substantial improvements in VO2max, and the researchers concluded that deep water running, in common with other aerobic activities, offers

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Aqua jogging

significant cardiovascular benefits when performed at an appropriate frequency (three to five days a week), intensity (60% to 75% of maximum heart rate) and duration (20 to 60 minutes) (1).

Aqua jogging / running (see illustration above) The two terms tend to be used interchangeably. Although I believe the two adapted techniques outlined below give more bangs for your buck, ‘standard’ aqua jogging is a good training technique, so here are the basic rules on form: ●●Maintain almost upright body position, with just a slight forward lean from the pelvis (5 to 10 degrees) ●●Keep trunk ‘tight’ ●●Bring the knees to approximately 90 degrees and simply push the foot straight down behind you (avoid a bicycling movement). ●●Pull the arms forward and back with no lateral movement, keeping the hands relaxed and thumbs pointing up.

I frequently hear coaches and athletes argue that standard aqua jogging is too easy to provide an adequate workout. It is

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true that this kind of running in deep water doesn’t really create a lot of disruption to the flow. So I increase the level of challenge and the athletes I work with happily accept that these sessions are as tough as anything they undertake on dry land. You can progress or alter the intensity of these drills by: ●●using fins on feet ●●using a 2:1 ratio of feet to hands (two leg drives to each arm drive) or vice versa ●●attaching floats to arms or legs (beware excessive build up of lactate in the muscles) ●●using bungees attached to the side of the pool to add variety or as a tool for interval work

Drill 1: Flexed position running A whole-body exercise similar to running. Unlike standard aqua jogging, when performing this drill the body will be almost horizontal. This technique is particularly useful for games players (hockey, rugby etc) who adopt a flexed position. You will get increased activation around the gluteals, hip flexors and hamstrings.

Technique: ●●Work in deep water where your feet cannot touch the ground ●●Once in the water, lower your hips so you maintain a forward lean from the pelvis of about 45 degrees ●●Keep trunk ‘tight’ ●●Reach straight forwards to full extension with one arm, then pull your arm back with palm leading. Bend your arm as you pull back, until approx 90 degrees at elbow, then continue pulling through to your hip. ●●Bring opposite knee forward towards your chest (keep toes pulled up so foot is flexed) while pushing the other leg straight back until fully extended. Keep toes/foot flexed until the bottom of the leg drive, when the foot may plantar-flex. ●●Maintain hip, knee and ankle alignment (avoid using a ‘breast-stroke’ leg movement, especially when fatigue starts to set in).

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Upright running

Drill 2: Upright running (see illustration above) This form of aqua running is predominantly used for recovery specific to upright running musculature, cadence development and maximal resistance work. It also helps improve flexibility and range of movement, which has particular benefits for slow runners who shuffle along with a short stride length. We’ve also found that our horizontal jumpers returning from injury like this technique because the large range of movement helps to stop them from ‘tightening up’ during their rehabilitation.

Technique: ●●Maintain almost upright body position, with just a slight forward lean from the pelvis (5 to 10 degrees) ●●Keep trunk ‘tight’ ●●Reach straight forward with one arm. Pull arm back with palm leading (scoop action), until the elbow bends to approx 90 degrees. Continue to pull through to your hip ●●Bring opposite knee forward towards your chest (keep foot flexed), extend the leg forwards. Once fully extended in front of the body, pull leg straight back through the water, aiming to keep the leg as straight as possible. Point toes (plantar-flex) at the bottom of the leg drive ●●Maintain hip, knee and ankle alignment

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Drill 3: Cross-country ski running (Fig illustration opposite) In this drill the legs remain straight throughout and the major movement comes from the pelvis, rather than the knee, which creates much greater gluteal contraction. This is a great drill for warming up and provides increased gluteal function and pelvic control. Good for lower limb recovery.

Technique: ●● Maintain almost upright body position, with just a slight forward lean from the pelvis (5 to 10 degrees) ●● Keep trunk ‘tight’ ●● Adopt an ‘opposition position’, extending your right arm and left leg forward at the same time ●● Keeping both arms and legs straight, begin to ‘scissor’ walk ●● You should aim to swing your arms and legs an equal distance in front and behind the line of your body ●● Keep hands relaxed with thumbs pointing up. If you want to increase the intensity you can turn your hands to form a paddle, flex each foot as it drives forwards, and point it pushing back.

Table 1: Anaerobic training, sample session This session uses a flexed running position no of distance lengths (25m pool) % VO2 max rest comment 2 25m 60 none Warm-up

6 12.5m 12.5m 80 70 30 sec after every length

6 25m 80 length 1 = 40sec length 2 = 30sec length 3 = 20sec length 4 = 30sec length 5 = 40sec,

8 12.5m 12.5m 70 100 30sec after every length 6 15m 10m 90 50 None Recovery intervals 2 25m 50 none Warm down, use any preferred swim stroke

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Cross-country ski running

Strength and power training Pool based plyometrics can be excellent for strength and power development. While I’ve had some interesting conversations (arguments) with coaches who don’t believe you can develop power in the pool, my own experience suggests otherwise and there is even some research to back me up(7, 8). This is great news for anyone looking for a low-risk power-based training tool. I’ve also used this very successfully with athletes returning from injury. Research has shown that on dry land the musculoskeletal system is subjected to minimum impact forces of three to five times bodyweight when landing during plyometric drills such as depth jumps. For this reason, most high intensity land-based plyometric drills are out of bounds for athletes returning to fitness. But plyometric training in water allows them to slot back into the training programme early. A 70kg male performing a plyo drill in a pool will reduce the impact forces from a range of 210kg to 350kg to a range of 35kg to 57kg. You can change the intensity level simply by changing the level of the water. The water provides support as the athlete’s body moves downwards, and resistance as the athlete explodes upwards or moves sideways. As water-based strength and power training is still very underdeveloped, there seem to be no hard and fast rules. The Ohio University team(8) suggests

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adopting the same training principles as on dry land (volume, intensity, frequency).

Control, stability and balance The pool is a great environment for all three aspects of fitness, and is particularly useful during the initial stages of rehab. In general, deep-water work will involve open kinetic chain movements and shallow water training will involve predominantly closed chain movements. You can develop control, stability and balance in a number of ways. Here are some ideas.

Floatation devices If you place a float under a limb it will create upward pressure on the limb, providing a controllable proprioceptive challenge. This can be increased by changing the size, shape or density of the float. Sample exercise: in deep water, stand on a float (not touching the pool floor) with knees bent, straighten up and try to maintain your balance. Repeat. This is a great drill for improving control, stability and proprioception around joints.

Current By working against a current, you can increase the proprioceptive challenge to the joint and the need to control and stabilise the body. For an even greater challenge, increase turbulence.

Depth By increasing or decreasing the depth of immersion you will alter the proprioceptive demands. The more fully the body is immersed in the water, the greater the stability as increased hydrostatic pressure acts upon the body’s joints.

Surface area You can increase the surface area of the feet and hands using fins and mitts, which will intensify the proprioceptive demands

page 86 PEAK PERFORMANCE sporting ankles placed upon the proximal joints. Sample exercise: if you have rolled your ankle and you want to regain strength and proprioception, sit on the side of the pool with legs dangling in the water. Place a float underneath the injured foot and use the foot to keep the float balanced.

Conclusion The pool is a fantastic and versatile training environment. As well as its many benefits for rehab work, it offers a unique opportunity for athletes involved in high impact sports such as running, basketball, football, rugby or netball to train in a no-impact or low-impact setting. Nick Grantham

References 1 Davidson K (2000). ‘Deep Water Running Training and Road Running Training Improve V02 max in Untrained Women.’ Journal of Strength and Conditioning Research. 14 (2): 191-195 2 Dowzer CN, Reilly T (1998). ‘Deep Water Running.’ Sports Exercise and Injury. 4: 56-61 3 Grimshaw P, Burden A. Instant Notes in Sport and Exercise Biomechanics (2006) 4 Hall SJ. Basic Biomechanics (4th Ed) (2004) 5 Harrison RA, Bulstrode S. ‘Percentage weight bearing during partial immersion in the hydrotherapy pool.’ Physiother Practice 1987;3:60-63. 6 Loupias JP, Golding LA. ‘Deep Water running: a Conditioning Alternative’ (ACSM’s Health and Fitness Journal 2004, 8 (5) 5-7 7 Martel GF, Harmer ML et al (2005). ‘Aquatic Plyometric Training Increases Vertical Jump in Female Volleyball Players.’ Medicine and Science in Sports and Exercise. 37(10): 1814-1819 8 Miller MG, Berry DC et al (2001). ‘Recommendations for implementing an aquatic plyometric programme’ Strength and Conditioning Journal. 23 (6): 28-35.

page 87 Notes