Management of Iliotibial Band Syndrome in Athletes: By Katrina Egan

 

Management of Iliotibial Band Syndrome in Athletes

Introduction

Iliotibial Band Syndrome (ITBS) or inflammation of the iliotibial band appears to result from the repetitive friction of the iliotibial band tendon on the lateral femoral epicondyle.  It was first described by Colson and Armour in 1975 and later in more detail by Renne, Orava, Noble and Sutker et al (Aronen et al 1993).

Iliotibial band syndrome occurs primarily in long distance runners, however it has been well documented in cyclists and military recruits, as well as american football players, weight lifters and skiers.  It is not recognised as commonly affecting athletes in sprint running or multidirectional sports such as rugby, netball or basketball.  In surveys of long distance runners, it is one of the most common injuries reported (Orchard et al, ’96).  The incidence of ITBS relative to all overuse injuries that effect runners ranges from 1.6 – 12% (Messier et al, ’95).  At the Sports Medicine Clinic at the Marine Corps Depot in San Diego, ITBS is one of the most common knee problems (Aronen et al “93).

The characteristic feature of this injury is the onset of pain, during activity, that is well localised to the lateral femoral condyle.  The pain usually progresses rapidly and soon keeps the athlete from continuing activities (Lindenburg ’84).

In a paper by Messier and Pittala in 1988 titled “Etiologic Factors Associated with Selected Running Injuries”, they defined ITBS as inflammation of the iliotibial band as it passes over the lateral femoral condyle and/or inflammation at the insertion on Gerdy’s tubercle.  It is important to note that this inflammation is secondary to overuse.

The objective of this assignment is to provide the reader with a detailed understanding of what exactly ITBS is, the anatomy and pathophysiology involved with this condition, and some of the causative and biomechanical features.  From here a specific clinical presentation of ITBS will be illustrated, describing the benefits and shortcomings of certain tests such as Ober’s test, and introducing some new tests.  Differential diagnosis and the use of further investigative tools such as plain x-rays, MRI’s and ultrasound scans will be discussed.

The emphasis of the assignment will then be on the management of this condition, once accurately diagnosed, including conservative, cortisone injections and surgical procedures.  And how this relates to the serious athlete, as compared to the weekend warrior!

As with all overuse injuries, ITBS is a great frustration to the runner or cyclist that is in training for a specific event or series of events.  It is very important that the sports physiotherapist recognises this syndrome from the initial consultation and assessment so that the strict conservative treatment protocol can begin immediately.  It is essential that the sports physiotherapist takes into account the psychological implications an overuse injury like this has, and plans to maintain the cardiovascular fitness of the athlete during the rehabilitation phase through cross training.

Anatomy and Function

 

The iliotibial band is formed proximally at the level of the greater trochanter by the coalescence of the fascial investments of the tensor fasciae latae, the gluteus maximus muscle and the gluteus medius muscle.  The ITB is connected to the linea aspera of the femur, via the intermuscular septum, until the supracondylar tubercle of the femur, just proximal of the lateral condyle.  Distally, the ITB thickens and inserts on the anterolateral aspect of the tibia, into the tubercle known as Gerdy’s tubercle.  At the level of the lateral femoral condyle, the ITB contacts the lateral femoral epicondyle and the inserting fibres of the lateral collateral ligament of the knee (Muhle et al, ’99 and Messier et al, ’95).

Due to this strong attachment of the iliotibial band to the linea aspera via the lateral intermuscular septum, the iliotibial band is effectively attached directly to the femur (Mercer et al, ’98).  McMinn (1994) suggested that this attachment of the ITB to the femur form the gutter behind the bulging vastus lateralis.

Following a detailed dissection, Kaplan (1958), described the ITB as a tense ligament stretched between the iliac crest and the lateral surface of the tibia intimately connected with the lateral intermuscular septum and fixed longitudinally to the femur.  Kaplan suggests that because of the complexity of its attachments the ITB does not represent a tendon of either tensor fasciae latae or of gluteus maximus.

A very recent article describing a new clinical test for the ITB, as published in the New Zealand Journal of Sports Medicine, by Bloomfield and Watson, from Narrabeen, Sydney, have described a iliopatellar band.  They have cited an article by Terry et al, 1986, from the American Journal of Sports Medicine, which describes the ITB dividing into two functional components;

  1. The iliotibial tract ( band )
  2. The iliopatellar band ( ligament )

This division is described as being above the level of the knee, and in the formation of an inverted Y.  No other article reviewed in the preparation of this assignment mentioned this anatomical phenomenium.  It is suggested that this iliopatellar ligament blends with (and perhaps forms the bulk of) the lateral retinaculum when inserting at the lateral aspect of the patella.  Its function is to provide a restraint to medial subluxation of the patella and anatomically connect the anterior aspect of the ITB and femur to the patella.

In 1996 Simon Rouse published a review paper in Physiotherapy, titled “The role of the Iliotibial Tract in Patellofemoral Pain and Iliotibial Band Friction Syndrome”.  The purpose of this article was to investigate critically the role of the iliotibial tract in patellofemeral pain syndrome.  Rouse looked at both the Kaplan paper of 1958, which he describes as the most complete investigation of the iliotibial tract, the 1986 paper by Terry et al, and a further paper by Terry et al in 1993.  In summary, Kaplan provides no evidence to support the theory the patella is pulled laterally by the iliotibial tract, while neither of Terry’s articles provide strong evidence to suggest the iliotibial tract does pull the patella laterally.

A second anatomical disagreement within the literature with regards to the iliotibial band, is whether or not a bursa exists.  A very recent article, (1998), in the Journal of Ultrasound Medicine, reported on a case of a 39-year-old female runner.  This woman developed pain during a 10km race, and at the clinical exam six hours after the race she was diagnosed as having ITBS.  This women then went on to have an MRI, (only 6hrs post race), where findings were consistent with an acute tendinitus, plus a “presumed fluid filled collection, located deep to the tendon and probably corresponding to an iliotibial bursitis”.  The authors, Bonaldi et al, go on to say that the bursa is located between the femoral condyle and the deep portion of the ITB.

Muhle et al (1999), have described the MRI findings of 16 ITBS patients and MR arthrographic findings of 6 cadaveric knees.  They recognise that previous studies have shown that ITBS is related to an inflamed bursa, however, state that their results were derived from close correlation of the results of MRI and microscopic examination in cadavers and show no bursa beneath the ITB.  They found in all specimens, a thin layer of fatty tissue between the ITB and the lateral femoral epicondyle.  This paper suggests that well-defined fluid collections are more likely to arise from chronic inflammation beneath the ITB with formation of a secondary, or adventitious, bursa, rather than from inflammation of a primary bursa.

In a third article titled “Magnetic Resonance Imaging of Iliotibial Band Syndrome”, by Evan et al, (1994), seven patients with ITBS were MRI’ed and five of those were found to have fluid deep to the ITB.  The authors also dissected 10 disease free cadaveric knees and demonstrated a potential space beneath the ITB.  They then stated that this “bursa” is in an area anatomically consistent with the focal fluid collection seen on the MRI scans of patients with ITBS.

Reading the literature, it would be difficult to categorically state whether a bursa exists or not in the normal knee between the ITB and the femoral condlye.  The evidence suggests that there is space for this bursa, and given the function of bursa to reduce friction between anatomical structures, it would make sense that there was a fluid filled sac in this region.  There is, however, very good evidence in the literature to suggest that in the ITBS afflicted knee, there is an inflammation of a bursa deep to the band.  This bursa may either be primary or secondary as a result of the inflammation.

Evans, in 1979, described the function of the band as a ligament between the lateral femoral condlye and the lateral tibia, stabilising the knee joint.  He felt that because it crossed both the hip and knee joint, the band had differing effects on the knee according to various hip positions.  He suggested that the ITB locks the knee into extension and contributes to pelvic slouch by action on the hip, achieving maximum stability with minimal effort during standing.

Going back to Kaplan’s article from 1957, he is willing to agree with a small role of stability in the knee, but presents a strong case that the ITB does not transmit any extensor action to the knee.  He electrically stimulated ITB’s, with patients under a GA and found no action on the knee joint, regardless of the hip or knee position.  This concept is further supported by the fact that excision of substantial parts of the ITB does not affect the knee.

The ITB is involved in four actions of the lower extremity.  It is a primary abductor of the hip, contributes to internal rotation of the hip when the hip is flexed 30 degrees, and, depending on its relation to the lateral femoral epicondlye, is an accessory in leg flexion and extension.  When the knee is less than 30 degrees of flexion the band is situated anterior to the epicondyle and assists extension.  When the knee is in greater than 30 degrees flexion, the band is posterior to the epicondlye and it assists flexion (Aronen et al, ‘93).

Causative Factors

 

It is the friction caused by the ITB sliding over the lateral epicondlye during repeated flexion and extension that presumably results in inflammation and pain during sporting activities such as running and cycling.  As an athlete runs, flexion takes place at the hip and knee.  At approximately 30 degrees of knee flexion, the ITB passes over the lateral epicondlye and friction is produced.  During weight bearing activities, compression and friction forces increase and pain occurs (Cernohous et al, 2000).  ITBS can develop in cyclists, so full weight bearing is not essential, but is a likely contributor.

There is disagreement within the literature as to whether there are some anthropometric, biomechanical and training factors that may predispose an athlete to suffer from ITBS.  A few of the more commonly attributed abnormalities include: an organically prominent lateral femoral condyle, a tight ITB, genu varum posture of the affected knee, exaggerated forefoot pronation, inappropriate footwear, training variables such as hills, increased mileage, crowned roads and often cited is that of leg length discrepancy.

A paper that specifically investigated this, by Messier et al, in 1995, seems to have the most reliable and tested data.  In their study they compared 70 non injured runners with 56 ITBS afflicted runners.  The significant findings of this study were:

  • Weekly mileage was significantly greater and running experience significantly less in the injured runner.
  • Injured runners also had more cycling within their training regimes than the non injured runners.  This cycling may exacerbate the ITB.
  • Training on crowned roads was nearly identical between groups.
  • Body height discriminated between the two groups with the control group being taller, and heavier.
  • Leg length discrepancies are similar between noninjured runners and ITBS runners.
  • The injured group generated less peak torque and performed less work than the control group.  This reduced strength in the injured runner was bilateral.
  • This study found there was little difference in the rearfoot motion between groups.
  • Normalised maximum braking forces were significantly attenuated in the ITBS group.  These forces decelerate the body immediately after heel strike.

The authors concluded that the two most significant discriminators, weekly mileage and maximum braking force were effective variables in predicting whether a runner was likely to be injury free, yet were poor predictors of ITBS.  The most useful results clinically were that some previously conceived risk factors were in fact not an issue i.e. crowned roads, rear foot action and leg length, and the potential risk factors for ITBS are training volumes, height and weight, strength and force variables.

Errors in training were noted in 42% of the 52 cases reported by McNicol et al, 1981.

Barber and Sutker, in 1992 reviewed case histories of 19 athletes with ITBS.  They concluded that ITBS is most often described in high mileage runners i.e. 32-64 kms per week, and have maintained this distance for several months.  It was felt this intensity of stimulus is required to set up an overuse injury of this nature.  They found that a common factor was a significant change in the training schedule, usually starting 2-3 weeks prior to the onset of symptoms.  Excessive use of one pair of shoes and change of running surfaces were also noted.

Lindenburg felt that it was possible that both excessive and inadequate ankle joint pronation contributed to ITBS.  This agreed with Subotnick’s view that internal rotation of the tibia as a result of subtalar joint pronation increases tension in the ITB.

A majority of these studies looked at runners and the biomechanics of running.  Many of these predisposing factors are invalid in a non weight-bearing situation such as cycling.  In cycling, with each pedaling cycle, the ITB is pulled anteriorly on the down stroke and posteriorly on the upward stroke.  Knee flexion and extension occur approximately 4800 times an hour, so the ITB is especially susceptible to repetitive irritation (Holmes, 1994).  Excessive pronation while pedaling, perhaps as a result of the cleat position, excessive hill work and increased mileage have also been indicated in ITBS in cyclists.

Clinical Presentation and Diagnosis

 

Barber and Sutker’s paper reported on 19 athletes with ITBS.  Symptoms included pain aggravated by repetitive knee movement, as with running or cycling.  The discomfort would appear after a constant distance was covered.  Walking generally didn’t aggravated symptoms, however up and down stairs and running down hills often aggravated the pain.  Aronen, from the Marine Corps stated that people with ITBS usually describe an insidious onset of discomfort over the lateral aspect of the knee while running.  In his experience the discomfort increases as they continue to run.  The pain may stop while walking, but will return with the resuming of running. 

Objectively there was localised tenderness to palpate at the lateral femoral condyle, and / or Gerdy’s tubercle on the anterolateral aspect of the tibia.  Pain can sometimes be elicited at the lateral femoral epicondyle by flexing and extending the knee in a varus stress (Lutter 1985).

There was nil tenderness noted at the joint line, the popliteal tendon, the lateral collateral ligament or the anterior lateral fat pad.  Functional tests such as jogging on the spot, hopping and squatting did not cause discomfort.  There was no intra-articular effusion or ligamentus laxity (Barber and Sutker, 1992).  In athletes with severely inflamed ITB’s they will walk with the knee fully extended to avoid having the tendon rub on the lateral femoral epicondyle.

In addition to the above clinical presentation, Meisser and coworkers agreed an injury existed when the symptoms caused an athlete to miss a work out, reduce mileage or prompt a visit to a medical practitioner.  They added to the objective signs a tightness of the ITB.  This sparks a debate within the literature.  That is, is ITB tightness an entity and how reliable and valid are the current procedures we utilise to test this?

Dr Susan Mercer, from Otago University had a paper published in the New Zealand Sports Medicine Journal in 1999, challenging the validity of the Ober’s Test, and it’s relevance to ITBS.  She cited numerous authors, who postulated that a tight ITB was the cause of excessive frictioning in ITBS, and who went on to claim stretching of this ITB played an important role in the treatment of this syndrome.

Ober first described his test in 1936 and his objective was to assess the degree of hip abductor contracture in patients with sciatica, and subsequently used for assessing hip abductor contractures following poliomyelitis.  Dr Mercer did an extensive literature review and found no evidence validating the Ober’s test for assessing ITB tightness.  Due to the attachment of the ITB to the femur, questions are asked regarding the development of distal tightness in the ITB leading to pathologies around the knee joint.  This is further questioned when there is no apparent interest in whether the knee is flexed or extended during the Ober’s test.  She concluded that there is no convincing biological evidence to suggest that tightness of the ITB distal to its proximal femoral attachment occurs, and we continue to use this test only because of convention.

Dr Paul Bloomfeild, from the Sydney Academy of Sport has proposed a new test to evaluate the effect of the ITB and iliopatellar ligament on the medial glide of the patella and patellofemeral joint mechanics.  This test is well described and validated in the New Zealand Sports Medicine, autumn 2000 issue.  This seems more relative to patellofemoral problems and not ITBS as such.

The differential diagnosis for ITBS should include early degenerative joint disease, a cystic or torn lateral meniscus, lateral capsular sprains, lateral tibial or femoral condyle osteonecrosis, stress reactions, pseudogout, chondromalacia and popliteus tendinitis (Barber and Sutker, 1992).

Further Diagnostic Tools

 

Magnetic Resonance Imaging (MRI), has been useful in demonstrating objective evidence of ITBS, and is helpful when a definite diagnosis is essential.  Ekman et al demonstrated that patients with ITBS had a significantly thicker ITB over the lateral femoral epicondlye as compared with a control group.  They also noted the presence of fluid deep to the ITB in five out of seven cases.  One of the patients was followed up 12mnths later and the MRI scan demonstrated a significant reduction in the bursal fluid.  This patient had returned to activities.  These authors concluded that ITBS was a problem of the tendon and the underlying bursa.

A more recent paper reporting on the findings of MRI in ITBS, by Muhle et al, 1999, indicated normal width in the ITB of ITBS patients, however, they noted that this contrast as compared with Ekman’s findings may be due to the stage of the pathology.  That is that a more chronic condition may have developed a thickening of the ITB.  Muhle et al also felt the bursa was secondary to the condition, and the tendon had a circumscribed fluid collection around its distal portion.

With the expensive nature of MRI testing, Bonaldi et al, 1998 suggest that perhaps other imaging techniques should be investigated, particularly if follow up tests are recommended.  They reported the use of ultrasonography in ITBS.  It is important to note this was a report of one acute patient.

The ultra sound scan demonstrated focal thickening, peritendinous odema, poorly defined tendon borders and a fluid filled collection deep to the tendon – suggesting an iliotibial bursa.  Following conservative treatment, at day 14 a further scan was undertaken, demonstrating decreased thickening of the tendon, decreased peritendonous odema, and the disappearance of the adjacent bursa.  This study showed that ultrasound provided the same findings as a MRI but at a reduced cost.

Injury Management

In the planning of an appropriate treatment programme it is important to first establish the stage at which the injury is in, and therefore the irritability of the condition.  This will become evident following a detailed subjective examination.  An athlete may present with an acute, sudden onset inflammatory response, an insidious acute onset or a progressive chronic condition.

In the acute condition the initial treatment focus will be on the reduction of pain and inflammation.  As a result of reading the current literature, a sound, evidence and experience based treatment regime could be as follows:

First 3 days

  • immobilising the knee, with the use of a ridged brace and using crutches
  • icing the knee 3-4 times a day
  • taking NSAID’s and analgesics
  • pulsed ultrasound

 

Additional aspects for athletes

  • Explain the condition to the athlete, giving attention to the need to reduce activities to result in decreasing inflammation.  Give the athlete a firm indication of how this injury will progress and some potential time lines.  Better to be slightly on the conservative side.
  • In this initial stage, while conducting he subjective assessment, some causative factors may be identified, and therefore steps to combat these may be given consideration.
  • Be sensitive to the psychological implications this injury has on an athlete depending on the timing within the competitive season.
  • Initiate discussion with the athlete and coach regarding planning of cross training able to be continued during this phase i.e. within an immobiliser, thus preventing flexion / extension of the knee.  The purpose of this cross training would be to maintain strength, endurance and flexibility of the athlete except the injured knee.  This could be achieved through weight training, upper body ergs, exercises such as chin-ups, dips, abdominals, press-ups etc.
  • Begin training identified intrinsic factors that may be contributing such as weak hip abductors and external rotators, and poor pelvic stability. 
  • Visualisation sessions are important, particularly with highly skilled sports.
  • Discuss nutritional aspects such as reducing carbohydrate input while reducing aerobic activities, and ensuring good nutritional habits to provide the body with the best environment for healing.

 

This initial regime has been well used by the Marine Corps clinic, with great success.  If after 3 days the athlete is still experiencing pain, a 4th day is recommended.

Following this initial phase, athletes are then encouraged to begin a controlled return to activity. 

Return to Activity Phase (Day 4 – 18-20)

  • Resume walking normally, and activities of daily living
  • Continue course of NSAID’s
  • Ice after running
  • Pulsed ultrasound
  • Localised soft tissue  massage of the distal portion of the ITB
  • Progress training of identified intrinsic biomechanical factors, such as correcting muscle imbalances.
  • Run for a distance, until they experience tightness, not discomfort.  (It has been documented that tightness is experienced prior to discomfort).  Once they reach this point, STOP running, and do not continue that day.
  • Potential implicated extrinsic factors should be address prior to the running.  These would include correct footwear and flat running surface.

 

Additional for Athletes

  • Progress aspects as mentioned in initial stages.  Be aware that the athlete will be getting frustrated with not training properly for numerous days now, and may be inclined to do more than they should given the acute pain has subsided.  Stress the importance of not pushing through the pain as this will result in further time off training.

 

Full return to training

  • At this stage, after 2-3 weeks of the previously outlined treatment regime, the athlete should be progressing towards training volumes and intensities as prior the injury.  The athlete will require a graduated programme, for both physical adaptation and mental confidence.

 

Complications

If at this satge the athlete is not progressing significantly following the conservative management, a more aggressive stance maybe required.  It is suggest that the next step would be a cortisone injection into the bursa underlying the ITB (Aronen, 1993).  There is good evidence in the literature that correctly placed and timed cortisone injections are beneficial in the treatment of such conditions (Targett, 1998).  A study by Blair et al, 1999, showed cortisone injections were of significant benefit in reducing short term pain and improving range of movement in the impinged shoulder.  The cortisone was injected into the sub acromial bursa.  It is recommended that the conservative management regime for ITBS be started again following the injection.  All intrinsic and extrinsic factors need to be corrected.

Failing a maximum of 2-3 injections the athlete would then need to consider surgical management. 

The syndrome responds well to conservative treatment in most cases, so surgery is only rarely needed (Martens et al 1989).  The surgical procedure described by Martens et al was as follows; the knee is held in 30 degrees of flexion and a lateral longitudinal incision over the lateral epicondyle, exposing the posterior part of the ITB.  A triangular piece with the base posteriorly located is resected.  The lateral femoral epicondyle is, after resection free at 60 degrees of knee flexion.  The resected triangle is about 2cm at its base and 1.5cm in height. 

Post surgery, the leg is put in a splint with the knee in extension for 1 week, then weight bearing is allowed.  The athlete will most likely regain sporting activities 3-4 weeks post op.  Martens suggested that no intensive rehabilitation programme was necessary since there was no pre-op muscle wasting and a short post op inactivity phase.

However, in a study by Holmes, 1993, he encouraged indoor cycling for 15 mins on day 3 post op, and this was gradually increased as tolerated in the first week post op.  He discouraged any hill work for cyclists for about 4-6 weeks post surgery.

Summary

 

It would appear that ITBS is a common injury primarily amongst runners and cyclists, and less frequently with other athletes also.  The literature would suggest that a significant predisposing factor in the development of ITBS is that of high mileage, or intense training.  This makes it an injury susceptible to the elite athlete, whom will be training quite specifically for an event.  As a sports physiotherapist, dealing with high performance athletes our greatest responsibility to the athlete with regards to this injury is early and correct diagnosis.  There is no getting around that the athlete must rest the inflicted leg, and this rest needs to take place sooner rather than later.  The resting and rehabilitation in order to alleviate the pain is quite specific, and has very good outcomes.  But it is the early detection that is important to the athlete so they can begin the resting phase immediately, and thus reduce the overall rehabilitation time. 

As an elite athlete it is imperative that a good understanding of the condition is known, and the consequences of continued training is explained.  It is also of extreme importance that training is continued in alternate forms, for both physical and psychological needs of the athlete.

It is very interesting to note the detailed anatomy of the ITB as described earlier in this assignment, which enlightens us into the tests and stretches we have previously performed.  There is very strong evidence to suggest that Ober’s test and stretching of the ITB has poor scientific base, and the clinician using these methods is doing so under convention rather than anatomical understanding.

ITBS is a common injury that will respond very well with conservative management as guided by the sports physiotherapist.  It is a great opportunity to assist an otherwise debilitated athlete, into a return to training is a relatively short time frame.  It is essential to work with the athlete’s support team, which could include coach, psychologist, and dietician and strength trainer.

References

 

  1. Aronen, J. et al.  Practical, Conservative Management of Iliotibial Band Syndrome.  The Physician and Sportsmedicine, Vol. 21, No. 6, June, 1993.
  2. Barber, A. and Sutker, A.  Iliotibial Band Syndrome.  Sports Medicine.  14 (2): 144-148, 1992.
  3. Bloomfield, P. and Watson, A.  A New Clinical Test: The Iliotibial Band/Lateral Retinaculum Test Description and Reliability Study.  New Zealand Journal of Sports Medicine.  Vol. 28, No. 1, 2000.
  4. Bonaldi, V. et al.  Iliotibial Band Friction Syndrome: Sonographic Findings.  Journal of Ultrasound Medicine.  Vol. 17, 1998.
  5. Cernohous, S et al.  Iliotibial Band Friction Syndromewww.csuchico.edu/phed/atc/Projects/Itband/ITBFS.html
  6. Ekman, E. et al.  Magnetic Resonance Imaging of Iliotibial Band Syndrome.  The American Journal of Sports Medicine, Vol. 22, Np.6, 1994
  7. Lindenburg, G. et al.  Iliotibial Band Friction Syndrome in Runners.  The Physician and Sportsmedicine, Vol. 12, No. 5, May, 1984.
  8. Martens, M. et al.  Surgical Treatment of the Iliotibial Band Friction Syndrome.  The American Journal of Sports Medicine, Vol.17, No. 5, 1989.
  9. Mercer, S. et al.  Stretching the Iliotibial Band: an Anatomical Perspective.  New Zealand Journal of Physiotheraphy.  Vol.26, No.2, 1998.

10.  Messier, S et al.  Etiology of Iliotibial Band Friction Syndrome in Distance Runners.  Medicine and Science in Sports and Exercise.  Feb, 1995.

11.  Messier, S. and Pittala, K.  Etiologic Factors Associated with Selected Running Injuries.  Medicine and Science in Sports and Exercise.  Vol 20, No.5, 1998.

12.  Muhle, C. et al.  Iliotibial Band Friction Syndrome: MR Imaging Findings in 16 Patients and MR Arthrographic Study of Six Cadaveric Knees.  Radiology, July, 1999.

13.  Murphy, B. et al.  Iliotibial Band Friction Syndrome: MR Imaging Findings. Radiology, Nov, 1992.

14.  Newsham, R. and Mercer, S.  Ober’s Test – Is it a Valid Test of Iliotibial Band Tightness?  New Zealand Journal of Sports Medicine.  Vol. 27, No. 3, 1999.

15.  Orchard, J. et al.  Biomechanics of Iliotibial Band Friction Syndrome in Runners.  The American Journal of Sports Medicine, Vol. 24, No.3, 1996.

16.  Rouse, S.  The Role of the Iliotibial Tract in Patellofemeral Pain and Iliotibial Band.  Physiotherapy, Vol. 82, No. 3, March 1996.

17.  Schwellnus, M. et al.  Anti-inflammatory and Combined Anti-inflammatory / Analgesic Medication in the Early Management of Iliotibial Band Friction Syndrome.  South African Medical Journal, Vol 79, May, 1991.

18.  Targett, S.  Cortisone Injections in Sports Injuries.  New Zealand Journal of Sports Medicine. Vol. 224, No.2, 1996.

Katrina Egan… M.HSc (Hons)

Based in Mooloolaba Sunshine Coast Queensland Australia

Katrina is a NZ trained physio holding a Masters degree. She is one of the few qualified Manipulative Physiotherapists on the beautiful Sunshine Coast in Australia.

Still a strong All Blacks New Zealand Rugby supporter, (we will forgive her for that!!) Katrina enjoys what the coast offers, paddling and swimming regularly with the Maroochydore SLSC. As a former international athlete (1992 World Surf Ski Champion), a national kayak coach and a recent finisher of the Coolangatta Gold, Katrina has a very good understanding of the athletic body and the need to keep training. Kat’s passion is her two dogs, Mana and Kia. Her canine and physio interests combined in completing a Level 1 Canine Physio course last year, and she is very happy to exchange ideas about your four legged family members.

As the practice principal Kat leads with enthusiasm and an excellent hands-on approach. After 20 years in the profession she has the experience and knowledge to assist everyone. Katrina also has a great network of other professionals that she is also happy to refer you to if necessary

www.johnhartfitness.com

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