Definition

The iliotibial band (ITB) is a dense fascia on the lateral aspect of the knee and hip. Traditionally, the gluteus maximus and tensor fascia lata were thought to be the proximal origin of the ITB. Further anatomic dissections have demonstrated that the gluteus medius also has direct and indirect contributions to the ITB (Fig. 69.1) [1]. Proximal attachment includes the iliac tubercle or iliac crest [2,3]. In the distal thigh, the ITB attaches to the linea aspera and the upper edge of the lateral femoral epicondyle [3,4]. According to Terry [5], after passing over the lateral femoral epicondyle, it separates into two components. The iliotibial tract of the distal ITB attaches to Gerdy tubercle of the anterolateral proximal tibia. The iliopatellar band of the ITB has aponeurotic connections to the patella and the vastus lateralis [5]. Other distal attachments include the biceps femoris, the lateral patellar retinaculum, and the patellar tendon [5,6]. An anatomic pouch can be found underlying the posterior ITB at the level of the lateral femoral epicondyle [7]. Controversy exists as to whether this pouch is a bursa, a synovial extension of the knee joint, or degenerative tissue [7,8]. Others have reported that a highly innervated fat pad overlies the lateral femoral epicondyle [9].

Iliotibial band syndrome (ITBS) or iliotibial band friction syndrome is an overuse injury typically referring to lateral knee pain as a result of impingement of the distal ITB over the lateral femoral epicondyle. Less commonly, ITBS may refer to hip pain associated with movement of the ITB across the greater trochanter. This chapter deals primarily with distal ITBS. The suspected pain generator in ITBS is as controversial as the anatomy around the lateral epicondyle. It has been postulated to be bursitis, synovitis, or irritation of the fat pad, posterior fibers of the ITB, or periosteum [3,6,9–12]. Although the anatomic pain generator may not be fully known, pain at the distal aspect of the ITB is thought to be caused by the fibers of the ITB passing over the lateral femoral epicondyle with knee flexion and extension [6,11].

Friction has been implicated as the most important factor in ITBS [8,11]. Maximum friction occurs when the posterior fibers of the ITB pass over the lateral femoral epicondyle at 20 to 30 degrees of knee flexion, the putative “impingement zone.” [8] Repeated knee flexion and extension, particularly with increased running mileage per week, creates friction and has been shown to predispose an individual to lateral knee pain [8,11]. Friction has been shown to play a role in cycling activities as well. Cycling-induced ITBS is thought to result from the repetitive activity of cycling, as less time is spent in the impingement zone than during running activities [11]. Other authors have theorized that pain is due not only to friction but also to compression of the fat pad between the ITB and the lateral femoral epicondyle. The compression of the fat pad was found to be greatest at 30 degrees of flexion, similar to previous reports, and increased with internal rotation of the tibia during knee flexion [6,9].

Several factors may increase the risk for development of ITBS. Although it has not been extensively studied, poor neuromuscular control appears to be an important modifiable risk factor for ITBS. Weakness of hip abductors has been implicated in ITBS [6]. However, difference in strength of hip abduction was not found in a study of 10 runners with ITBS compared with controls [13]. Specifically, neuromuscular control is needed to attenuate the valgus–internal rotation vectors at the knee after heel strike. If appropriate control is not available, the ITB may have an abrupt increase in tension at its insertion site [10,14,15]. Increased hip adduction and knee internal rotation have been noted in female runners, suggesting increased ITB strain as a mechanism of injury [15]. Increased foot inversion, maximum knee flexion, and knee internal rotation were noted during an exhaustive run in recreational runners with history of ITBS [16]. Peak rearfoot eversion, knee internal rotation angle, and hip adduction angle were increased in 35 female runners with history of ITBS compared with matched controls [17]. Contradictory results were found in a study of 18 runners with ITBS compared with controls. Results indicated decreased hip adduction in those with ITBS, although they were found to have a lack of “coordination” defined as earlier hip flexion and knee flexion [18]. Hamill and colleagues [19] noted that the strain rate of the ITB during stance phase was increased in female runners who developed ITBS compared with healthy age-matched controls, and Miller and coworkers [16] noted increased ITB strain in recreational runners with history of ITBS. Strengthening of the gluteus medius and tensor fascia lata, decelerators of the valgus–internal rotation vectors at the knee, has been shown to reduce symptoms of ITBS [10,20]. Lack of dynamic flexibility, particularly of the ITB, has been implicated with ITB injury susceptibility [6,15,21,22]. No research study to date, though, has revealed a correlation between ITB tightness and ITB injury. Theoretically, however, tightness of the ITB or its constituent muscles increases impingement of the ITB on the lateral femoral epicondyle [8]. Other risk factors that may be attenuated with proper shoe wear or foot orthoses include excessive foot-ankle pronation and supination [6,16]. Training errors, such as rapid changes in training routine, hill training, striding, and excessive mileage, have also been highlighted as increasing the risk of ITBS [6,12]. Increased ground reaction force, as with running in old shoes, may also increase frictional forces at the knee and exacerbate symptoms [8]. Intrinsic or nonmodifiable factors, such as bone malalignment or a wide distal ITB, may contribute to the development of ITBS [22,23]. Finally, repeated direct trauma to the lateral knee, particularly with soccer goalies, appears to be injurious to the ITB impingement area [23].

Symptoms

Symptoms of ITBS occur typically at the lateral femoral epicondyle but may emanate from the distal attachment of the ITB at Gerdy tubercle on the tibia [6,12]. ITBS is the most common cause of lateral knee pain in runners [6]. Individuals present with sharp or burning lateral knee pain that is aggravated during repetitive activity. This pain may radiate up into the lateral thigh or down to Gerdy tubercle [24]. Runners often describe a specific, reproducible time when the symptoms commence [25]. Pain usually subsides after a run; however, in severe cases, persistent pain may cause restriction in distance [26,27]. Runners also note more pain with downhill running because of the increased time spent in the impingement zone [8]. Paradoxically, runners state that faster running and sprinting often do not produce pain. Fast running allows the athlete to spend more time in knee angles greater than 30 degrees [8]. Cyclists present with rhythmic, stabbing pain with pedaling. Specifically, they complain of pain at the end of the downstroke or the beginning of the upstroke. Bikers with improper saddle height and cleat position may experience greater symptoms [28,29].

ITBS symptoms may also occur as a lateral snapping hip. An external or lateral snapping hip occurs as the ITB rapidly passes anteriorly over the greater trochanter as the femur passes from extension to flexion [30]. Athletes, particularly dancers, sometimes experience an audible painful snap on landing in poor turnout (decreased external rotation at the hip) and with excessive anterior pelvic tilt [31].

Physical Examination

Physical examination begins with a screening examination of the joints above and below the site of injury. Hip girdle examination includes an assessment for joint range of motion, asymmetries [32], muscle strength (particularly hip abductors) [10], and lumbopelvic somatic dysfunctions [33]. The modified Thomas and Ober tests are used to assess flexibility of the ITB and related musculature at the hip and knee (Figs. 69.2 and 69.3) [6,12,34].