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ITBS = Iliotibial Band Syndrome

Iliotibial band syndrome (ITBS) is a common cause of lateral knee pain in the athletic population. ITBS is notably prevalent in runners and is considered the 3rd most common running injury and the 2nd most common knee injury in runners. There is still no consensus on the exact cause of the condition and as a result there is still much to learn about the complexities of the syndrome (Strauss, 2011). If not managed wisely this overuse condition can become quite stubborn. As such prevention should be the key focus. However, if onset occurs, early evidence based treatment approaches need to be implemented.

Before we look at why the ITB gets painful or dis functional we first have to understand what and where the ITB is and what it does. The ITB is not simply a thickened fascia structure on the outside of the thigh; its anatomy and structure is in fact complicated. Very briefly, the ITB is a thickening of the lateral fascia lata and cannot be separated from it. It originates from the pelvis, attaching onto the front tip of the pelvic bone (the anterior superior iliac spine) and the hip capsule and crosses both the hip and the knee joints. The fascia lata is furthermore attached to the periosteum of the sacrum and the length of the femur bone. (Antonio, 2013). Various muscle partly insert into the ITB and will arguably affects its functioning. These include the Tensor Fascia Lata (TFL) muscle (a powerful hip flexor), some fibers of Vastus lateralis (the outer part of the quadriceps muscle group), and a portion of the Bicep femoris muscle which is one of the hamstring muscles (Antonio, 2013). From the back of the leg up to three quarters of the muscle fibers of Gluteus maximus (Gmax), the strong buttock muscle, attach onto it (Louw, 2014). The Gmax is of particular interest, as it attaches onto the back musculature via the thoracolumbar fascia (Antonio, 2013), which could aid with force distribution between the lumbar spine and knee. Considering the amount of fibres of the Gmax muscle that attach onto the facisa lata and ITB, it should be considered that the ITB acts as a tendon of insertion to the Gmax muscle and should be a key focus of possible intervention (Antonio, 2013).

The primary function of the ITB is considered to be providing passive lateral knee stability during single limb loading, preventing excessive varus loading. It also passively resists hip adduction and internal rotational forces (Fairclough, 2006; Lutz, 2015; Baker, 2011). The Gluteus medius (Gmed) muscle has mostly been considered to be the primary muscle responsible for resisting hip adduction during limb loading. Research however has indicated that the forces that the gluteus medius is required to resist, are considerably more than its metabolic capacity (Fairclough, 2006). Considering the attachments of the Gmax, TFL as well as vastus lateralis onto the ITB, a contraction of these muscles during limb loading would tension the ITB in order to resist the hip adduction forces and as such help the Gmed muscle.

Research has also looked into the elastic energy storage capacity of the ITB and found that the tension created in the ITB by the contraction of muscles during fast running is up to 7J of energy. This has led to the believe that the elastic energy storage capacity of the ITB could play a role in improving running economy (Eng et al, 2015). As one can see the ITB is a complicated structure that plays an important role in the human body while running. But when the training load you apply to this structure is more than what it can handle, pain will transpire.

Key take home points:

What does the ITB do:

-Supports/protects the outside of your knee joint, more specifically forces that push the knee out (varus strain).

-Protects the inside of your knee by limiting forces that pulls your knee over the midline of the body (abduction/internal rotation).

-Disperse and transfer forces that results from impact through the lower leg (i.e. running and jumping) to the femur, pelvis and back. Thus helping with shock absorption.

- It improves running economy by storing and releasing elastic energy.

Symptoms of ITBS.

Generally people that have ITBS presents with the following symptoms.

-Pain on the outside of the knee that is aggravated by running or cycling.

-The pain generally starts at about the same time/distance into the activity.

- The pain can be sharp and debilitating and is often made worse by longer training sessions, downhill running or on cambered courses.

-There might also be swelling on the outside of the knee and it is generally painful when applying pressure to the outside of the knee.

-Repeated knee flexion and extension in standing may reproduce the pain.

-In cases where the ITB has been irritated more acutely, i.e. by continuing training irrespective of pain, symptoms might be more severe affecting walking, stair climbing and simply straightening the knee after having it bent for a while.

What is the most common causes ITBS

Iliotibial band pain often develops following a rapid change in your training. More readily a rapid increase in training volume, i.e. distance or duration of training. A rapid change in training intensity by increasing the speed for example is generally not associated with the onset of ITBS. Less frequently the training terrain can also cause the onset of ITBS symptoms, specifically when when a runner had to race or train on a cambered surface .

What is the actual pathology, what is happing in and around the ITB that causes pain.

By convention, it has been believed that ITBS is an irritated tendon caused by tightness of the structure, resulting in painful rubbing over the outside bony prominance of the knee. For this reason it has commonly been called iliotibial band friction syndrome (ITBFS). However, there is not much evidence in the literature for ITBS being caused by friction of the band and more recently it has been suggested that the irritated structure is probably not the band itself. Next we jump into common myths and misconceptions regarding ITBS.

3.1 Challenging Friction

It has been previously presumed that during activities involving repetitive knee flexion (such as running, cycling or hiking with a heavy backpack), the ITB repetitively shifts forwards and backwards over the lateral femoral condyle, causing friction and irritation of the structure itself. However this view has been recently challenged.

As previously mentioned, the ITB is not a distinct anatomical structure but merely a thickened zone within the lateral fascia lata. Thus, the ITB is not free to move relative to the femur. It is therefore suggested that AP gliding of the ITB, that has been thought to cause friction of the band and region itself, is therefore impossible. It is rather implied that the previously described friction component to the syndrome is more likely an illusion based on the cyclic tension shift in the ITB and tightening of the lateral fascia, exerting repetitive compression on the structures that lie deep to the ITB (Fairclough 2007).

3.2 Challenging inflammation of the ITB

A recent surgical case series study (Hariri, 2009) in which lateral surgical excisions of the bursa in the sub ITB space were removed, calls the notion of inflammation of the ITB itself into question when symptoms of the syndrome were relieved. The presence of a large, maladaptive cyst arising from the joint capsule itself has also been reported on (Costa, 2004) and this structural adaptation, perhaps a stress reaction, has been confirmed in anatomical reviews during lateral excisions of the knee synovium (Nemeth and Sanders, 1996).

On the other hand with MRI studies by Isusi et al (2007), they could not identify a bursa in the area, but rather signal changes from the soft tissues immediately below (that is deep to) the ITB. They also found an osseous reaction or sub-chondral osseous erosion of the lateral condyle, without evidence of inflammation or thickening of the band itself. There is in fact, little evidence that pathological changes take place in the iliotibial band within this condition (Hariri, 2009).

Therefore, it is suggested that two different subtypes of ITBS exist, the first of which involves irritation of a cyst, bursa, or synovial recess at the lateral knee. A second theory would be pain arising from compression of the connective tissues, especially the adipose tissue, that underlie the portion of the band between the lateral epicondyle and the knee joint line. This adipose tissue is highly innervated, vascular and contains Pacinian Corpuscles. The Pacinian Corpuscles are highly sensitive to pressure increases and relay information that plays a role in proprioception. It is speculated that an abnormal increase in pressure will cause hypertrophy of the Pacinian Corpuscles, which could play a role in the increase in pain sensitivity observed in the patients presenting with ITBS.

3.3 Challenging ITB tightness

It is a reasonable argument to link tightness of the ITB with the syndrome, since presumably a tighter band would lead to greater compression of the underlying tissues with each gait cycle, which is routinely assessed using the Ober test. However, no study to date has actually correlated a positive Ober test with the syndrome itself. This suggests that a so called 'tight ITB' is not necessarily a risk factor for the condition (Devan, 2004). In fact, runners with ITBS that had so called 'looser' iliotibial band exhibited increased strain at the knee during running, that is, it elongated more rapidly when subject to an external load (Noehren 2007). Falvey (2010) also discovered that only 2mm of stretch deformity could be achieved to the ITB and that we should remember the incredibly high tensile strength of the band when thinking about stretching it out.

It has been suggested that tightness of this tendon-like structure is possibly not the issue but more likely the mechanism of tightening up, perhaps inappropriately, against the knee at various phases (20 – 30 degrees) of the gait cycle (Choi, 2007). This brings into light two questions with regards to treatment approaches. Firstly, the normal response of an athlete slowing down the pace of their running in order to relieve symptoms should be challenged as this could actually make the irritation worse when they spend more time within these flexion ranges. Secondly the notion of trying to stretch a structure with incredible high tensile strength should be reconsidered since its length is not correlated with the onset of symptoms of ITB. Additionally, it seems trying to increase the distensibility of the band could actually accentuate the symptoms of ITB syndrome. This will be discussed in depth in the management of this condition.

3.4 Contributing biomechanics

Proximally, it seems reasonable to associate the hip abductor weakness with ITBS since this might lead to an increased hip adduction angle during the stance phase of gait, or during pedal strokes for cyclists, consequently placing an increased strain on the ITB and thus a greater potential for it to compress the tissues underneath it (Noehren, 2007; Fredericson, 2000). The magnitude and timing of hip abductor activation during the gait cycle as well as the amount of hip adduction that occurs during the stance phase of gait still remain in question.

Locally at the knee, the ITB is most likely to compress its underlying structures with the knee flexed at about 20–30 degrees (Choi, 2007). The commonly held association of ITBS with running downhill may be due to the fact that downhill running results in a higher degree of knee flexion at heel strike. An additional subtlety in running biomechanics of an increased knee flexion angle during heel strike has been demonstrated (Miller et al, 2007 towards the end of an exhaustive run in runners with a history of ITBS. Internal rotation of the knee in landing, due to attachments to Gerdy’s tubercle and the iliopatellar ligament, has also been a factor discovered in runners who already had ITBS (Noehren et al 2007).

Distally, internal rotation of the tibia due to excessive rear foot eversion has also been suggested as a contributing mechanism due to the ITB attachment at Gerdy’s tubercle; however the mechanism behind this still remains unclear (Noehren, 2007). This brings into light the foot position and cleat angle of cyclists and how this could contribute to poor recruitment of gluteal muscles (important for power during standing pedal strokes) and thus added strain on the ITB. Additional biomechanical factors that have been linked to ITBS include increased landing forces, low hamstring strength when compared to the quadriceps strength on the same side, and genu recurvatum.

In summary, the biomechanics of the syndrome are multi-faceted and complex but during running the dysfunction seems to occur when the knee falls inwards during gait causing the hip to adduct and internally rotates. For cyclists, the angles at which the knee operates to the hip and foot should be investigated further.

  1. Physiotherapeutic management of Iliotibial Band Syndrome (ITBS)

There are a lot of theories around the cause of ITBS and as a result there are numerous current physiotherapeutic treatment options available, many of which still require much investigation. This section will outline and challenge some of the evidence based current practice of ITBS.

4.1 Rest

ITBS is classified as an overtraining syndrome due to the fact that it is caused by repeated micro trauma. The condition is caused without a single discrete incident occurring. Characteristic of an overtraining syndrome is the decline in performance as well as signs and symptoms that persist over extended periods. This leads to a change in the composition of the structures to adjust to the extended load. In the early stages (reactive stage), the soft tissue will respond well to periods of decreased loading in rest, and will regenerate to improve its structure and function. Structures presenting with symptoms in the late degenerative stage, will not regenerate as well in response to rest, as it has limited capacity for degenerative repair. In the latter stage, rest will only bring temporary relief and symptoms needs to be managed intermittently (Timpka et al, 2015).

There were no recommendations found on the amount of rest that is required for ITBS. It could be suggested that the rest period should depend on the severity of symptoms and the needs of the patient. If an athlete does not want to lose aerobic fitness has to rest, relative rest is recommended. In the case of ITBS, relative rest would imply physical activity that does not irritate the ITB and the underlying structures. This would entail exercises that do not require repetitive knee flexion in the ranges from 0° to 30° such as deep seated cycling and swimming freestyle

4.2 Anti-inflammatory modalities

As previously described, there is evidence to support irritation of the structures deep to the band and not the band itself and consequently, the injection of corticosteroids and oral administration of NSAIDS to treat what is believed to be an inflammatory condition is common practice however, on 20 cadaveric studies of the ITB (Falvey et al 2010) , no bursa was found present between the ITB and the underlying lateral femoral epicondyle with a clinical implication that anti-inflammatory treatment such as ultrasound, NSAIDS and cortico-steroid injections aimed at treating an inflamed bursa will not serve as treatment for ITB-syndrome.

4.3 Stretching

Some practitioners prescribe stretches for the ITB with the aim of lengthening the structure and thereby reducing the amount of friction and/or compression between the ITB and the underlying structures. Five cadaveric studies on ITB strain suggested that that the ITB is attached longitudinally to the full length of the femur results in reduced potential for physiological lengthening of the structure. It is a lateral thickening of the fascia those envelopes the thigh and its mobility can therefore be influenced by adhesions in the neighbouring soft tissues. The HIP stretch (hip flexion, adduction and external rotation, with added knee flexion) evoked the most strain in the ITB, however, no plastic deformation occurred during the application of the stretches. Clinically this means that the ITB as an entity cannot be stretched in order to achieve plastic deformation or lengthening. Soft tissue mobilizations of the fascia in the area may relieve symptoms in the ITB.

In 19 in vivo measurements of ITB displacement (Falvey, 2010), it was shown that there is minimal lengthening of the ITB during isometric contraction of the TFL. This suggests that in order to minimize the amount of excessive compression between the ITB and the lateral femoral epicondyle, the muscles attached to the ITB needs to be stretched. Soft tissue release of these muscles may also relieve the strain put on the ITB.

4.4 Abductor Strengthening

Noehren et al (2014) found that male runners with ITBS showed increased hip internal rotation and knee adduction during running. The subjects also showed decreased ITB length as tested with Ober’s test, as well as decreased hip external rotator strength. However, the difference between the groups in hip external rotator strength was not considered clinically relevant as there was a relatively large effect size, indicating that altered neuromuscular control could also be a contributing factor.

Fredericson et al (2000) investigated the effects of a 6 week hip abductor-strengthening program on 24 runners presenting with ITBS. The first two sessions consisted of the application of ultrasound with a corticosteroid gel. The subjects also had to stretch the ITB three times daily. The exercises consisted of pelvic drops and hip abduction exercises. The subjects started with 1 set of 15 repetitions, and had to build up to 3 sets of 30 repetitions over the course of 6 weeks. If the participants experienced no muscle soreness the following day, they had to increase the amount of repetitions by 5 per day. The subjects had to discontinue any aggravating activities during this time, and they were allowed to take anti-inflammatories until they were able to do their daily activities without pain. There was a very significant increase in the torque of the gluteal muscles in the affected limb after the 6 week period, and 22 of the 24 subjects were able to return to running by the end of this period.

4.5 Training errors and strategies

A systematic review by Strauss et al (2011) found some observational and retrospective studies that identified training errors that can affect the ITB and may contribute to the development of ITBS. These errors include rapid changes in training routine, over-striding, hill training and increased mileage. Running on a steep camber and excessive downhill running also may cause ITB symptoms. It is therefore very important for the Physiotherapist to educate the patient on the risk factors for developing ITB-symptoms, and if the patient already presents with the syndrome, to address the training errors.

There are many factors with regards to running form that may contribute to the development of ITBS. Daoud et al determined that runners who land on their forefoot, or forefoot-strike (FFS), are less inclined to over-stride and as a result there is less impact on the joints of the lower limb with more compliance to the impact forces during landing, as the energy that is transmitted through the limb at landing is absorbed by the muscles. These runners were found to sustain less stress injuries (of which ITBS is one of) than runners who rearfoot-strike (RFS). Consequently, FFS will aid in managing ITBS.

Additionally, in a study done by Chumanov et al (2012), 45 injury-free, recreational runners were examined. The runners were instructed to increase their running cadence by 5-10% of their preferred rate, and measurements were made on ground reaction forces and electro-myographic activity of lower limb muscles during running. The study found that there occurred pre-activation of the Gmax and Gmed muscles during the late swing phase in anticipation for landing. This implies that by increasing running cadence, specifically for runners suffering from ITBS, the hip abductors get activated prior to landing and will therefore prevent excessive hip and joint movement that may irritate the ITB.

4.6 Surgical interventions

Surgical interventions on the ITB can be divided into two categories: open surgery (that entailed literally cutting the band) and arthroscopic surgery (whereby irritated tissue underneath the ITB is excised). The advantages of the arthroscopic technique above the open surgery include that it allows for quicker recovery as it is less invasive than open surgery, and the procedure also allows for intra-articular investigation of the knee joint to identify other possible pathologies (Michels et al, 2008).

Michels et al (2008) conducted a study on 36 athletes who suffer from resistant ITBS. The participants underwent a standardized arthroscopic resection of the lateral synovial recess and after 3 months all the athletes were able to return to sport pain free. It is important to note that surgery is only recommended in chronic cases of ITBS that has not responded to conservative treatment.

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