Treatment Protocols

Chapter Eight

Treatment Protocols As demonstrated throughout this book, the human body is remarkably well-designed to handle the forces associated with walking and running. In fact, contrary to popular belief, long distance running does not cause degenerative changes in our joints, and may even protect us from developing osteoarthritis. The long-held belief that the amplified impact forces associated with running would accelerate the development of osteoarthritis was disproved in a 25-year study by Chakravarty et al. (1). By comparing tibiofemoral joint space on serial x-rays taken between 1984 and 2002 on 45 runners and 53 age-matched controls, the authors confirmed that running altered neither the severity nor prevalence of knee osteoarthritis. In a detailed meta-analysis of the literature evaluating the progression of knee arthritis and exercise, Bosomworth (2) confirms that not only does running not accelerate the development of knee osteoarthritis, it may be protective: his meta-analysis confirmed that aging runners present with reduced rates of lower extremity disability and all-cause disability.

Although a significant body of literature confirms that running does not cause osteoarthritis, epidemiologic studies prove that runners are much more likely to develop a wide range of musculoskeletal injuries, including sprains, strains and fractures. In a thorough review of the literature, van Mechelen et al. (3) report that the annual injury rate for runners is somewhere between 37% and 56%. This is consistent with research by Lysholm and Wiklander (4), who followed 60 runners for 12 months and reported 39 of the 60 athletes developed 55 injuries. The authors reported that sprinters were most likely to be injured (with hamstring injuries being prevalent), followed by middle distance runners (who complained of backache and hip problems) and lastly, long distance runners, who presented with a greater frequency of foot injuries.

As noted by van Mechelen et al. (3), 50 to 75% of running injuries are overuse in nature and the most common cause for injury is exceeding the mileage limits we were designed to tolerate. Several studies show the potential for injury dramatically increases when we run more than 35-40 miles per week (5,6). This number makes perfect sense when you consider the early hominids had foraging distances of only 8-9 miles per day (7). Moreover, because the metabolic cost of running was so high, our ancestors rarely ran as their preferred form of travel was walking and when necessary, a hybrid pendular style shuffle jog (refer back to figure 3.10). The impulsive form of running that we

are so fond of was extremely rare among our ancestors (8).

The reason for this is simple: if the early hunter-gatherers ran the high mileage common among modern long distance runners, we would not have survived as a species because the metabolic cost of travel would have been so high we would have lacked the energy necessary to care for our children (8). The infrequent use of impulsive running in our hominid ancestors explains why the knee, the body’s best shock absorber, is by far the most frequently injured joint while running: it was designed to manage the 2-fold increase in force associated with walking and shuffle jogging, not the 5-fold application of force associated with impulsive running.

Because we were not designed for impulsive running long distances, the best way to prevent injury is to run less than 35-40 miles per week. Of course, this is not always possible because in order to run faster, even recreational athletes run more than 60 miles per week, and it is common for professional runners to run between 120 and 150 miles per week. Unfortunately, running high mileage can have a detrimental effect on our musculoskeletal system, as an MRI study of runners’ knees performed before and after a marathon revealed significant cartilage proteoglycan and collagen breakdown, particularly in the patellofemoral and medial tibiofemoral joints (9). The authors note that because the biochemical changes in the articular cartilage were present even after 3 months of reduced activity, the runners were at higher risk for degeneration. This may explain why the meta-analysis of exercise and arthritis performed by Chakravarty et al. (1) found that although moderate exercise did not predict knee osteoarthritis, elite athletes were shown to be at increased risk for developing degenerative joint changes.

To maximize the beneficial effect of training while minimizing weekly mileage (and hence, our potential for injury), experts at Furman University (10) developed a training approach that allows for improved performance with minimal strain on the musculoskeletal system.

Because faster runners do not have the luxury of running reduced mileage, alternate methods of cross-training are recommended.

Should an injury develop, a thorough biomechanical exam should identify the specific problems with strength, flexibility, proprioception and/or bony alignment that might be responsible for producing the injury, and the appropriate treatment protocol initiated. Identifying the 345

Human Locomotion: The Conservative Management of Gait-Related Disorders cause is essential, as once injured, reinjury rates among runners can be as high as 70% (3). This is consistent with research confirming the best predictor of future injury is prior injury (5,11). To assist the practitioner in prescribing the best possible treatment protocols, the following section reviews treatment options for a few of the more common gait-related injuries. Obviously, this list is not meant to review all possible treatments and/or injuries, it merely provides a review of the more effective biomechanical treatment interventions.

Achilles Tendinitis Despite its broad width and significant strength, the Achilles tendon is injured with surprising regularity. In a study of 69 military cadets participating in a 6-week basic training program (which included distance running), 10 of the 69 trainees suffered an Achilles tendon overuse injury (12). The prevalence of this injury is easy to understand when you consider the tremendous strain runners place on this tendon. For example, during the push-off phase of the running cycle, the Achilles tendon is exposed to a force of 7 times body weight. This is close to the maximum strain the tendon can tolerate without rupturing (13). In addition, when you couple the high strain forces with the fact that the Achilles tendon significantly weakens as we get older, it is easy to see why this tendon is injured so frequently.

Achilles tendon overuse injuries are divided into several categories: insertional tendinitis, paratenonitis and non-insertional tendinosis. As the name implies, insertional tendinitis refers to inflammation at the attachment point

of the Achilles on the heel. This type of Achilles injury typically occurs in high-arched, inflexible individuals, particularly if they possess a Haglund’s deformity (see Fig. 4.45). Because a bursa is present near the Achilles attachment, it is common to have an insertional tendinitis with the retrocalcaneal bursitis. Until recently, the perceived mechanism for the development of insertional tendinitis seemed straightforward: the individual possessing a high arch and tight gastrocnemius/soleus creates an increased tensile strain in the posterior aspect of the Achilles tendon when the ankle is maximally dorsiflexed during late midstance/early propulsion. Although logical, recent research has shown that just the opposite is true (14).

By placing strain gauges inside different sections of 6 cadaveric Achilles tendons and loading the tendons with the ankle positioned in a variety of angles, researchers from the University of North Carolina discovered the posterior portion of the Achilles tendon is exposed to far greater amounts of strain (particularly as the ankle was dorsiflexed) while the anterior aspect of the tendon, which is the section most frequently damaged with insertional tendinitis, was exposed to very low loads. The authors suggest that the lack of stress on the forward aspect of the Achilles tendon (which they referred to as a tension shielding effect) may cause that section to weaken and eventually fail. As a result, the treatment of an Achilles insertional tendinitis should be to strengthen the anterior aspect of the tendon. This can be accomplished by performing the eccentric load exercise illustrated in figure 8.1. It is particularly important to work

Fig. 8.1. Insertional Achilles tendinitis protocol. While standing on a level surface, the subject maximally plantarflexes both ankles (A) and slowly lowers the involved leg (B). Three sets of 15 repetitions are performed daily with enough weight to produce fatigue.

346

Chapter Eight Treatment Protocols that causes it to project directly into the Achilles tendon.

This addition often pushes into the back the Achilles insertion causing chronic inflammation, particularly if a Haglund’s deformity is present. Treatment in this situation is to look for sneakers that do not contact the Achilles insertion. A simple alternative is to cut off the upper back section of the heel counter so it no longer touches the tendon. It is also important to avoid heavy motion control sneakers when treating Achilles tendon injuries because their inherent stiffness increases the length of the lever arm from the ankle to the forefoot, thereby increasing strain on the Achilles tendon.

The second type of Achilles tendon overuse injury is paratenonitis. This injury represents an inflammatory reaction in the outer sheath of cells that surround the tendon.

The first sign of this injury is a palpable lump that forms a few inches above the Achilles attachment. Treatment for Achilles paratenonitis is to reduce the swelling with frequent ice packs. Night braces are also effective with paratenonitis because tissues immobilized in a lengthened position heal more rapidly (17). If the paratenonitis worsens, it may eventually turn into a classic Achilles noninsertional tendinosis. This injury involves degeneration of the tendon approximately 2-4 cm above the attachment on the heel. Because this section of the tendon has such a poor blood supply, it is prone to injury and tends to heal very slowly.

Unlike paratenonitis, non-insertional tendinosis represents a degenerative noninflammatory condition.

Apparently, repeated trauma from overuse causes fibroblasts to infiltrate the tendon, where, in an attempt to heal the injured regions, they begin to synthesize collagen.

In the early stages of tendon healing, the fibroblasts manufacture almost exclusively type 3 collagen, which assists in the repair process but is relatively weak and inflexible compared to the type 1 collagen found in healthy tendons. As healing progresses, greater numbers of fibroblasts appear and collagen production shifts from type 3 to type 1. Unfortunately, the tendon is frequently unable to adequately remodel and a series of small partial ruptures begin to form that can paradoxically act to lengthen the tendon. An asymmetrical increase in the range of ankle dorsiflexion on the side of the injured Achilles tendon is a clinical sign indicative of advancing tendinopathy.

Although the classic treatment for Achilles tendinosis is 6 weeks of rest (which theoretically allows the fibroblasts more time to remodel), a randomized controlled trial by Silbernagel et al. (18) reveals that tendinopathy patients who continue to exercise but monitor pain by not allowing tendon discomfort to exceed 5 on a scale of 10 do just as well as a non-exercising tendinopathy control group, even at the 12-month follow-up. The authors emphasize that a training regimen of continuous but pain-monitored tendonloading physical activity represents a valuable option for patients with Achilles tendinopathy.

the Achilles tendon with the ankle maximally plantarflexed, because this position places greater amounts of strain on the more frequently damaged anterior aspect of the tendon.

When lateral insertion injuries occur in individuals with cavovarus feet, an effective treatment protocol is to incorporate valgus wedges. If a plantarflexed first ray is associated with the cavovarus foot, a sub-1 balance should be incorporated. In contrast, if an Achilles injury occurs in an individual who pronates excessively throughout stance phase, varus posts and/or orthotics should be considered.

In an interesting EMG study of orthotics and muscle activation patterns in individuals with and without Achilles injuries, Wyndow et al. (24) confirmed that individuals with Achilles injuries are more likely to present with a premature cessation of soleus muscle activity, while the lateral gastrocnemius stays active for a prolonged period.

The authors state the asymmetrical tendon tension created by the altered muscle activation pattern could cause or perpetuate an Achilles tendon injury. When muscle activity was reevaluated when the Achilles injured group wore orthotics, muscle activation patterns became more symmetrical, resulting in a more even transfer of force throughout the Achilles tendon.

Even though heel lifts are frequently prescribed to treat this injury, recent evidence suggests that when used on individuals with reduced ranges of ankle dorsiflexion, heel lifts actually increase EMG activity in the medial gastrocnemius and tibialis anterior muscles (15). Because this is consistent with prior research suggesting that heel lifts may increase strain on the Achilles tendon (16), the routine prescription of heel lifts for the treatment of Achilles tendon disorders needs to be reconsidered.

Rather than accommodating tightness in the gastrocsoleus complex with heel lifts, a better approach is to lengthen these muscles with gentle stretches. This can be accomplished with both straight and bent knee stretches to lengthen the gastrocnemius and soleus muscles, respectively. Because overly aggressive stretching can damage the insertion by pulling on it too vigorously, the stretches should be performed with mild tension and held for 35 seconds. They should be repeated every few hours and best results occur when deep tissue massage is performed prior to stretching. An alternate method to stretch the gastrocsoleus is to have the patient stand on a slant board for extended periods. The slant board should be angled to produce a mild stretch and adjusted as the range of ankle dorsiflexion increases. If calf inflexibility is extreme and does not respond to stretching, a night brace should be prescribed.

An important consideration in the treatment of insertional Achilles tendinitis relates to the forward pitch of the sneaker’s heel counter (this is the back upper portion of the sneaker that touches the Achilles tendon). Over the past few years, many sneaker manufacturers have added a forward angulation to the upper portion of the heel counter 347

Human Locomotion: The Conservative Management of Gait-Related Disorders Several biomechanical factors may make an individual prone to developing non-insertional tendinosis.

In the study of military recruits by Mahieu et al. (12), the recruits developing Achilles injuries presented with weaker ankle plantarflexors and excessive ankle dorsiflexion (measured off weight-bearing with a standard goniometer).

When this combination is present, an effective treatment protocol is to prescribe heavy load eccentric exercises (Fig. 4.222). In an important study comparing 3-dimensional movement patterns between runners with and without Achilles tendinopathy, Williams et al. (25) determined that compared to controls, runners with Achilles tendinopathy moved through the gait cycle with reduced ranges of peak knee internal rotation and reduced external tibial rotation moments. The authors state that because tibial excursion angles were the same, the decrease in peak knee internal rotation was most likely the result of the femur being internally rotated relative to the tibia. Because internal femoral rotation simultaneously displaces the lateral gastrocnemius origin anteriorly and the medial gastrocnemius origin posteriorly, the medial side of the gastrocnemius muscle is placed under greater strain. The increased muscle strain is transferred into the Achilles tendon during the latter half of stance phase, potentially resulting in injury.

The reduced external rotation moment discovered in this study is also significant, and the authors claim it is most likely associated with underlying weakness of the tibialis posterior muscle. This could result in injury to the Achilles tendon because the medial side of the gastrocsoleus complex is forced to assist with eccentric control of transverse plane tibial rotation during early stance. Because the Achilles tendon lacks the lever arm afforded tibialis posterior (Fig. 3.16), compensation for a weakened tibialis posterior muscle would greatly increase the workload placed on the gastrocsoleus complex, which in turn would increase tensile strain placed on the Achilles tendon. Given the results of this study, comprehensive management of Achilles tendinopathy should include exercises to strengthen the hip external rotators and tibialis posterior (the exercise illustrated in Fig. 4.221 is especially helpful).

Besides aggressive strengthening exercises, another effective method for improving Achilles tendon function is deep tissue massage. As described by Hammer (19), this type of massage can be augmented with tools designed for use with the Graston technique (referred to as “instrumentassisted soft tissue mobilization�). The theory is that aggressive massage induces microtrauma that stimulates fibroblasts to accelerate repair of tissues in the extracellular matrix (e.g., collagen, elastin, and proteoglycans). To test this theory, researchers from the Biomechanics Lab at Ball State University (20) surgically damaged the Achilles tendons of different groups of rats. In one group, an aggressive deep tissue massage was performed for 3

minutes on the 21st, 25th, 29th and 33rd day post injury.

Another group served as a control. One week later, both groups of rats had their tendons evaluated with light and electron microscopy. Laboratory results revealed that tendons receiving deep tissue massage showed increased fibroblast proliferation that the authors claimed would create an environment favoring tendon repair. The ability of deep tissue massage to accelerate healing was also confirmed in an animal study by Loghmani and Warden (21). Fibroblast repair associated with controlled microtrauma may also occur following extracorporeal shock wave therapy, in which high frequency sonic vibrations mechanically stimulate an injured Achilles tendon. Because of comparable outcomes between shock wave therapy and heavy load eccentric exercises in the treatment of non-insertional Achilles tendinosis (22), shock wave therapy should only be considered after conventional methods have failed.

Regardless of whether the Achilles injury is insertional or non-insertional, an important method for lessening stress on the Achilles tendon is to strengthen the flexor digitorum longus muscle. Because this muscle works synergistically with the soleus muscle to decelerate the forward motion of the leg during late midstance, it may significantly lessen strain on the Achilles tendon by decelerating elongation of the tendon. Figure 4.218 illustrates the simple home exercise necessary to strengthen this muscle. It is also important to emphasize calf endurance exercises since decreased endurance has been correlated to Achilles tendinopathy (26). This is especially true following surgical repair of Achilles tendon ruptures (27).

In addition to toe and endurance exercises, gait changes should be recommended in which the patient is instructed to shorten the length of stride, land on the heel during the contact period and deliberately plantarflex the toes during the propulsive period. Emphasizing a rearfoot contact point is essential because forefoot strike patterns result in increased rearfoot eversion excursions and eversion velocities during early stance phase (28,29), which would place unnecessary strain on an injured Achilles tendon.

Conscious plantarflexion of the toes during the latter half of stance allows flexor digitorum longus and flexor hallucis longus to assist in distributing tensile strains away from the Achilles tendon. It is possible to evaluate the degree in which the digital flexors are participating in load sharing by observing wear patterns present on the insole: When the digital flexors are strong, well-defined indents form beneath the tips of the toes. Conversely, when the digital flexors are weak, there are no indents beneath the toes and excessive wear is present in the center of the forefoot only.

The last factor to consider when treating Achilles tendon injuries is that cortisone injections into either the bursa or tendon should be avoided. In an important study published in the Journal of Bone and Joint Surgery (23), 348

Chapter Eight Treatment Protocols cortisone was shown to lower the stress necessary to rupture the Achilles tendon and was particularly dangerous when done bilaterally.

Metatarsalgia and Metatarsal Stress Fractures A frequently overlooked cause for metatarsalgia and metatarsal stress fractures is ankle equinus. The limited range of ankle dorsiflexion associated with this condition forces the heel to leave the ground prematurely during late midstance, thereby driving the forefoot into the ground with excessive force. As demonstrated by DiGiovanni et al. (31), tension in the gastrocnemius muscle alone is responsible for the symptoms associated with ankle equinus. Because of this, it is essential that conservative treatment address the gastrocnemius contracture. This can be accomplished with the straight knee stretch illustrated in figure 4.130 along with recommendations for sleeping with a night brace.

While ankle equinus secondary to gastrocnemius contracture may increase ground-reactive forces centered beneath the forefoot, the metatarsals are also prone to injury if the digital plantarflexors are weak. As demonstrated by Ferris et al. (32), strong digital plantarflexors effectively distribute pressure away from the metatarsal heads to the tips of the toes, while also lessening bending strains in the metatarsal shafts (see Fig. 3.38). These muscles can be strengthened with the exercises illustrated in Fig. 4.218. In addition to distributing pressure by strengthening the toes, other effective methods for treating metatarsalgia include incorporating metatarsal pads and/or toe crests (Fig. 6.24 and 6.25). In recalcitrant cases of metatarsalgia, an alternate method of treatment is to incorporate a Morton’s platform beneath the first metatarsal head. Because the first metatarsal is twice as wide and 4 times as strong as the neighboring metatarsals, it is better able to tolerate the redistribution of pressure away from the painful neighboring metatarsal heads. This addition is especially helpful when pain is centered beneath the second metatarsal head. Although it was originally believed that elevating the first metatarsal head during propulsion would produce functional hallux limitus, a kinematic study by Nawoczenski et al. (33) has shown that this is not the case. The only contraindication for a Morton’s extension is hypermobility of the first ray, which can be evaluated by measuring the thumb radius index (Fig. 4.98).

As with all propulsive period injuries, metatarsalgia and metatarsal stress reactions may also be treated by having the individual reduce the length of stride and avoid a forefoot contact point. Although they may be useful for increasing tone in the digital flexors while walking, individuals prone to metatarsal injury should not wear minimalist sneakers while running, as the resultant switch to a forefoot strike pattern may result in reinjury. This is especially true for individuals with narrow forefeet, since they may lack the surface area necessary to distribute ground-reactive forces associated with use of barefoot type sneakers.

Sesamoiditis The word sesamoid is Latin for “sesame seed,” and these small bones are located inside specific tendons where they improve mechanical efficiency by pulling the tendon farther away from the joint’s axis of motion. Although the classic example of a sesamoid bone is the patella, the tibial and fibular sesamoid bones located in the flexor hallucis brevis muscle are extremely important during locomotion, since forces centered beneath the hallux are great and the improved mechanical advantage afforded flexor hallucis brevis by these small bones is invaluable.

The most common cause for sesamoid injury is the rigid plantarflexed first ray and accommodating this deformity with a 2-5 long metatarsal post is an effective way to reduce pressure on these bones (Fig. 4.72). It is also possible that a hypermobile subtalar joint allows for excessive propulsive period pronation that increases ground-reactive forces centered beneath the sesamoid bones. That being the case, either custom or over-the-counter orthotics may be appropriate. An orthotic made with an excessively elevated medial longitudinal arch may occasionally be helpful, since it allows for a redistribution of pressure away from the sesamoids onto the medial arch. Of course, because of the risk of iatrogenic injury associated with excessive buttressing of the arch, this approach should be used as a last resort.

Though rarely discussed, an invaluable method of treating sesamoiditis is to perform deep tissue massage on the flexor hallucis brevis muscle before performing a series of gentle hold-relax stretches. In a study of the body’s largest sesamoid bone, the patella, researchers confirmed that the best predictor of chronic retropatellar pain is tightness in the quadriceps muscle (30). The increased tension in the quadriceps muscle may cause the patella to track abnormally in the intercondylar groove, resulting in chronic discomfort. The pain associated with chronic sesamoid injury frequently increases tension in flexor hallucis brevis, which may be responsible for producing increased compression of the sesamoids in their grooves.

The stretches should not be performed if they produce discomfort and fracture of the sesamoid bones should be ruled out before performing any stretches to increase hallux dorsiflexion. To ensure adequate distribution of pressure away from the sesamoids, sneakers with wellcushioned forefeet should always be considered. Because they frequently produce a transition to a forefoot strike pattern, minimalist sneakers should be avoided and the patient should be encouraged to make ground contact on the posterolateral aspect of the heel.

349

Skipping forward

(a section of this chapter is not shown)

Chapter Eight Treatment Protocols pressure readouts. By the seventh week of basic training, 22 cadets from the control group developed medial tibial stress syndrome, compared to only 2 in the orthotic group.

While the exact mechanism is uncertain, the fact that orthotic intervention significantly lessens the potential for developing medial tibial stress syndrome confirms that this condition is somehow related to abnormal biomechanics.

Whether exaggerated pronation leads to medial tibial stress syndrome by excessively tractioning the flexor digitorum longus muscle (straining the muscle-tendon junction) or by internally rotating the tibia thereby damaging the tibial cortex is unknown.

In addition to orthotic intervention, conservative care should include strengthening exercises for the deep and superficial calf muscles. It is especially important to strengthen the flexor digitorum longus muscle. Although calf inflexibility is not related to the development of medial tibial stress syndrome, once the injury has occurred, the deep posterior calf musculature stiffens, potentially perpetuating this injury. Night braces are recommended if the patient complains of leg pain when getting out of bed. The efficacy of the night brace is improved by wedging a towel or a piece of foam beneath the toes. Because several studies have correlated excessive hip rotation with the development of medial tibial injury, aggressive strengthening exercises for the hip internal and external should be prescribed. It is important to strengthen gluteus maximus and tibialis posterior with closed kinetic chain exercises, since these muscles may restore the coupled motions of subtalar supination/tibial external rotation during early propulsion.

Although unproven, failure of these muscles to rotate the leg externally during the propulsive period may lead to a twisting of the tibia, potentially resulting in medial tibial stress syndrome.

Because the development of medial tibial stress syndrome has been associated with high weekly mileage and faster running, a modest reduction in distance and speed should be encouraged. Neoprene calf wraps are helpful when returning to sport and taping the medial leg may enhance proprioception. Since running on asphalt and other hard surfaces increases the preactivation of shock absorbing muscles, patients with medial tibial stress syndrome should be encouraged to run on soft trails. Because individuals developing medial tibial stress syndrome often present with reduced bone strength, it is important to evaluate dietary factors such as daily intake of vitamin D, calcium, magnesium and daily protein intake (less than 30 gms of protein per day has been associated with reduced bone healing). Finally, while NSAIDs are routinely prescribed for the management of this condition, an award-winning study by Cohen et al. (113) confirms that nonsteroidal anti-inflammatory drugs such as indomethacin and celecoxib can significantly reduce tendon-to-bone healing in laboratory animals, and regular use of these drugs should therefore be discouraged.

Stress Fractures In any given year, more than 1 in 5 runners will sustain a stress fracture (114). In the US alone, as many as 1,920,000 runners develop stress fractures annually (115).

While stress fractures occasionally result from various nutritional/endocrine disorders that result in inadequate bone formation, it is more likely that various biomechanical factors cause an otherwise healthy bone to fracture. For example, as previously discussed, the metatarsal shafts are more prone to fracture when the gastrocnemius muscle is tight and/or the digital flexors are weak. Rather than attempting to strengthen an already strong bone, treatment in this situation should be to lengthen the gastrocnemius and strengthen the flexor digitorum longus and brevis muscles. The lateral metatarsal shafts are also more likely to fracture in cavovarus foot types because the foot in this situation is maintained in an inverted position throughout stance phase, which distributes a greater amount of stress to the lesser metatarsals. A valgus post placed proximally to the metatarsal shafts may distribute pressure away from the lesser metatarsals, perhaps lessening the potential for reinjury.

As related to the navicular, an interesting pilot study by Agosta and Morarity (116) found that limited ankle dorsiflexion was associated with the development of navicular stress fractures, most likely because the early heel lift associated with gastrocnemius contracture produced a “jamming� of the distal talus into the navicular acetabulum. Although further research is needed to confirm their findings, the fact that 45% of individuals suffering navicular stress fractures do not return to sport (117) suggests that improving gastrocnemius flexibility should always be considered.

Even though it supports only one sixth body weight, the fibula is more likely to fracture in individuals with excessive rearfoot eversion. As demonstrated by Wang et al. (118), subtalar pronation tilts the talus laterally, transferring a greater percentage of ground-reactive forces into the fibula. This is problematic when present in individuals with toe-out gait patterns, which have also been shown to increase force transfer through the fibula (118).

Fibular stress fractures may also occur in cavovarus foot types between the origins of the peroneus brevis and longus muscles. Because the peroneal muscles perform different actions during the gait cycle (peroneus brevis stabilizes the rearfoot against excessive inversion during midstance, while peroneus longus stabilizes the medial forefoot during propulsion), the bony interface between these two muscles is subjected to a shear force that may result in stress fracture/reaction. A similar biomechanical event occurs in rowers when the anterolateral ribs fracture at the bony interface between the origins of the external abdominal oblique and the serratus anterior muscles (119).

Apparently, tension generated in neighboring muscles may be sufficient to crack the interfacing bone.

367

Human Locomotion: The Conservative Management of Gait-Related Disorders By far, the most common site for stress fracture is the tibia. In their 12-month study of 111 track and field athletes, Bennell et al. (120) noted that 46% of all stress fractures occurred in the tibia. A probable mechanism is that osteoblasts are simply unable to keep up with the microscopic damage associated with excessive impact loading and the end result is a stress fracture. This is particularly true in individuals presenting with narrow tibiae, a proven risk factor for developing tibial stress fractures (121).

In an interesting study of muscle volume and the development of stress fractures, Burne et al. (106) found that strength was important in preventing stress fractures and the authors determined that a 10 mm reduction in calf circumference resulted in a 4-fold increase in the incidence of tibial stress fracture. This is consistent with research demonstrating the muscles of the leg and thigh adjust to bony vibrations in the tibia by tensing prior to heel strike (122,123). An animal model suggests the long digital flexors play an important role in dampening bony vibrations while in vivo human studies suggest bicep femoris and the lateral gastrocnemius are important dampeners of impact forces (124).

In their evaluation of 3-dimensional motion in runners with and without a history of tibial stress fracture, Milner et al. (125) determined that runners with a prior tibial stress fracture attempt to absorb shock in the frontal plane rather than the sagittal plane: The injured runners possessed greater ranges of rearfoot eversion and hip adduction. The logical conclusion of this research is that since orthotics reduce the degree of calcaneal eversion during early stance, they should reduce the risk of tibial stress fractures. Although some research suggests custom molded orthotics may lessen impact forces traveling through the lower extremity (126), and improve the symmetry of frontal plane rearfoot and tibial rotation (127), research confirming they lessen the risk of tibial stress fracture has been inconclusive (128,129). Additionally, although orthotics have been proven to reduce calcaneal eversion, they have not been shown to correct the increased hip adduction found in the tibial stress fracture group. To be comprehensive, management of tibial stress fractures should include foot orthotics designed to lessen the degree/ velocity of calcaneal eversion, along with specific exercises to strengthen the gluteus medius/maximus muscles. This is especially important in individuals with flat feet, because lessening calcaneal eversion is more difficult with this foot type.

In addition to orthotics and exercises, tibial stress fractures should also be treated with gait modifications.

As demonstrated by Crowell et al. (115), a single session of real-time visual feedback training can successfully reduce impact loading during the early stance phase of gait. The authors emphasize that it may be possible to train individuals to run in a way that reduces the risk of stress

fracture. Since few private practitioners are able to provide feedback regarding tibial acceleration, the simplest method to lessen the risk of injury is to have the patient shorten his or her stride length. Even small reductions in the length of stride can appreciably lessen impact loads. Switching to a forefoot or midfoot strike pattern is a simple and effective method for reducing tibial impact forces (130).

While tibial stress fractures are associated with increased rearfoot eversion and hip adduction, the biomechanical causes of femoral stress fractures are less clear, and the most likely culprit may simply be overuse (131). Although unverified, weakness in gluteus maximus and TFL may play a role in the development of femoral stress fractures, since these muscles generate significant tension in the iliotibial band that, through extensive fascial connections to the entire femur, create a lateral compressive force that stabilizes the femur during stance phase (Fig. 8.18). The recently discovered extensive fascial connections between the ITB and the entire femur support this hypothesis (132) and until proven otherwise, femoral shaft fractures should be treated with tensor fasciae latae and gluteus maximus strengthening exercises.

Unlike femoral shaft stress fractures, femoral neck stress fractures have predictable biomechanical causes.

Because of the increased bending strains placed on the femoral neck, individuals with coxa varum and/or long femoral necks are prone to developing femoral neck stress fractures. Femoral neck stress fractures are classified as tension or compression stress fractures, depending upon the location of the crack (Fig. 8.19). This distinction is important, since tension stress fractures are more likely to produce a fracture requiring surgical fixation. The most common complaint signaling a possible femoral neck stress fracture is groin pain during single-leg stance.

Regardless of whether the femoral neck stress fracture is on the tension or compression side, treatment is to aggressively strengthen the hip abductors and external rotators. As explained by the paleoanthropologist Owen Lovejoy (133), these muscles create a compressive force along the femoral neck that lessens bending moments associated with walking and running (Fig. 3.22). Because these exercises may tighten the involved muscles, they should be prescribed with specific stretches.

The last stress fracture to be discussed occurs in the sacrum. Although rare in a general athletic population, sacral stress fractures are more frequently seen in high mileage long distance runners, particularly elite females returning to sport following pregnancy. A possible mechanism for the post-pregnancy prevalence of sacral stress fractures is that during the final trimester, the core muscles are weakened by abdominal distention, while the sacroiliac joints become hypermobile secondary to the hormone relaxin (which remains elevated as long as the mother continues to breastfeed). The combination of reduced muscle tone and joint laxity may predispose to sacral stress fracture 368

Chapter Eight Treatment Protocols

Fig. 8.18. Anatomy of the iliotibial band. Because the iliotibial band has an extensive fascial expansion that travels deep to attach to the posterior aspect of almost the entire femur (A), tension created in the gluteus maximus and TFL creates a compressive force (B) that prevents the femur from bending during single-leg stance (C).

Although the literature concerning sacral stress fracture describes protracted recoveries, clinical experience with dozens of elite long distance runners consistently reveals excellent outcomes with return to sport in less than 3 months. As with all stress fractures, the use of NSAIDs should be discouraged since they may have a negative effect on bone remodeling (134-136).

While most experts recommend the “10% rule� when returning to running following a stress fracture (i.e., the athlete increases mileage by 10% per week), this approach has been proven to not alter reinjury rates and should therefore be abandoned (137). Because conventional formulas typically used to predict recovery time for specific stress fractures do not work, (e.g., 6 weeks for a metatarsal stress fracture and 12 weeks for a femoral stress fracture), Matheson et al. (138) recommend the injured athlete wait until the damaged bone is pain-free for two weeks with daily activity before attempting a trial run.

To allow osteoblasts time to repair damage associated with the return to running, the athlete should run on alternate days, starting at 2 miles every other day. Because impact forces are related to stride length, the runner is typically told to run 1-2 minutes per mile slower than their usual training pace for the first 2 weeks. Runners with stress fractures in the tibia or femur should be encouraged to switch to a midfoot strike pattern, while runners with midfoot or forefoot stress fractures should be encouraged to land on their heels. Because athletes recover at different rates, it is important to increase weekly mileage on a caseby-case basis.

Fig. 8.19. Femoral neck bending forces. Superimposed body weight (A) causes the femoral neck to bend downward, creating tensile strains on the superior side (B), and compressive forces on the inferior side (C).

because it allows the normally rigid sacroiliac joint to shift excessively while running. Treatment in this situation is to strengthen the core musculature and mobilize the hips to restore horizontal flexion (this motion is limited in the latter stages of pregnancy).

369

Human Locomotion: The Conservative Management of Gait-Related Disorders Patellofemoral Pain Syndrome To help dissipate ground-reactive forces associated with running, the body places its largest sesamoid bone, the patella, inside the quadriceps tendon. Unlike the small oval sesamoid bones found elsewhere in the body, the patella is shaped like a plate (the word patella is Latin for small plate). By displacing the quadriceps tendon farther from the knee axis of motion, the patella improves the mechanical efficiency of the knee by as much as 50% (139), and its large surface area allows for enhanced pressure distribution. Because of this mechanically efficient design, the patellofemoral joint can easily manage the ground-reactive forces associated with walking and shuffle jogging. Unfortunately, the 5-fold increase in ground-reactive forces associated with impulsive running is not so easily managed, and as many as 1 in 4 runners will develop patellofemoral pain syndrome (140).

Despite the high prevalence, the exact cause for this condition has been enigmatic. Early research based on an off weight-bearing model of knee function suggested the most likely biomechanical cause for patellofemoral pain syndrome was a lateral shifting of the patella between the femoral condyles. The classic example of this occurs when a high Q-angle or weakness of the vastus medialis obliquus muscle (VMO) allows the patella to displace laterally into the lateral femoral condyle. As a result, various treatments were designed to correct faulty movement of the patella, with standard treatment programs emphasizing taping, soft tissue mobilization and quadriceps strengthening.

Unfortunately these treatment protocols have had mixed outcomes.

To evaluate patellofemoral mechanics in a weightbearing environment, Powers et al. (141) utilized dynamic MRI as subjects performed closed kinetic chain knee flexion. Surprisingly, these authors discovered the primary cause of lateral patellar displacement was not a shifting of the patella into the femoral condyle, but a shifting of the lateral aspect of the distal femur into the patella. Powers et al. (141) confirmed that rather than shifting into the stable lateral femoral condyle, the lateral femoral condyle rotates into the stable patella. Recent CT and functional MRI evaluations support this observation, confirming the most likely cause of patellofemoral pain during weight-bearing is abnormal motion of the femur, not altered motion of the patella (142,143).

Hip weakness has been cited as the most probable mechanism for the exaggerated internal femoral rotation.

In a 3-dimensional evaluation of runners with and without patellofemoral pain syndrome, Dierks et al. (144) proved that runners with weak hip abductors have greater ranges of internal femoral rotation during stance phase, and the degree of rotation increases when runners become fatigued.

Although the authors state that it is unclear whether hip weakness is a cause or an effect of patellofemoral pain syndrome, comprehensive conservative treatment should

include exercises that target these specific muscles.

In addition to manually testing for weakness, Crossley et al. (145) show that it is possible to assess hip abductor strength with the dynamic single-leg squat test (Fig. 8.20). Besides identifying people with hip abductor weakness, this test also predicts delayed recruitment times in the hip abductors and has excellent interrater reliability (145).

According to Tyler et al. (146), it is also important to evaluate strength of the hip flexors. In their evaluation of a patellofemoral pain treatment program including iliopsoas exercises and hip abduction stretches, the authors note 93% of successfully treated patients exhibited significant increases in hip strength and flexibility during a 6-week treatment regimen. Table 2 lists the specific protocol used in their study and Fig. 8.21 reviews the more common exercises used to isolate the hip abductors, external rotators and flexors.

Phase 1.

A) Off weight-bearing hip flexion, adduction, extension, and abduction performed while maintaining a neutral pelvis.

B) Stretches for hip flexors, hamstrings, quadriceps, and iliotibial band.

C) Manual therapy to restore flexibility to the medial/ lateral retinaculum.

D) Home exercises including single-leg balance, rock board, 4-inch step-ups (varying height of step, reps, and speed) and upper extremity reaches.

Phase 2. Begins when patient can minisquat to 45 degrees and perform pain-free step-ups with good form.

A) Continue off weight-bearing exercises and stretches.

Increase resistance with exercises.

B) Lower extremity reaches (e.g., star excursion exercises). Focus on weakest movements.

C) Step-downs: vary height of step, reps and speed.

D) Increase difficulty of balance exercises.

Phase 3. Begins when patient can perform 4-inch stepdowns with no pain and good eccentric control.

A) Continue home stretching.

B) Begin plyometric drills while maintaining proper form.

C) Begin lunges and incorporate return-to-sport drills such as crossover running and single-leg hop drills.

Return to activity clinical milestones: A) Vertical jump test (less than 20% normative data, adjusted for body size).

B) Pain-free vertical hop test.

C) Pain-free sport-specific test.

Table 2. Patellofemoral Rehabilitation described by Tyler et al. (146).

370

Guidelines

Chapter Eight Treatment Protocols

Fig. 8.20. The dynamic single-leg squat test. When the hip abductors are working properly, the lower extremity, pelvis, and spine remain well-aligned while stepping off a 4-inch platform (A). When the hip abductors are weak, the individual accomplishes the step-down by tilting the torso ipsilaterally (B), lowering the contralateral pelvis (C), or by valgus collapse of the ipsilateral leg (D). Modified from Crossley et al. (145).

Fig. 8.21. Alternate hip exercises. A and B) Thera-Band速 exercises performed by rotating body in all 4 directions (hamstring pull and hip abduction not illustrated); C) Piriformis exercise; D) Sidelying gluteus medius exercise; E) Standing hip abduction/external rotation; F) Lunge.

371

Human Locomotion: The Conservative Management of Gait-Related Disorders While hip strengthening has recently become the most important clinical goal in the management of anterior knee pain, a long-term finding in patellofemoral pain research is that individuals with retropatellar pain often present with delayed recruitment times of the vastus medialis obliquus muscle. This is especially true for individuals with patellae that are offset and tilted laterally (Fig. 8.22).

Although a variety of exercises have been recommended to isolate the vastus medialis obliquus muscle, the most clinically popular exercises, such as the open kinetic chain seated leg extension with toe-out and the standing wall press with adductor squeeze, have been proven to stimulate vastus lateralis with greater intensity, potentially worsening the muscle imbalance (147).

To isolate vastus medialis, the individual should practice palpating the vastus medialis obliquus while isometrically tensing their quadriceps. Repeating a 10-second contraction, 30 times per day is usually sufficient to selectively improve tone in the vastus medialis obliquus muscle. Once the vastus medialis obliquus can be effectively recruited, the patient should be instructed to perform long-step forward lunges without a stride (Fig. 8.23). As demonstrated by Escamilla et al. (148) this exercise produces significantly lower patellofemoral joint forces than conventional lunges. Three sets of 15 repetitions should be performed daily with enough resistance to produce fatigue. Each repetition should last 6 seconds with a 3-second eccentric phase and a 3-second concentric phase, and patient discomfort should be less than 3 on a scale of 1 to 10.

The next exercise typically recommended is to perform 3 sets of 15 lateral step-ups onto a 4-inch platform.

Lateral step-ups have been proven to place less stress on the knee (149) and produce higher levels of gluteus medius activity than conventional step-ups (150). The lateral step-

Fig. 8.23. The long-step forward lunge. The individual maintains the feet in a fixed position while raising and lowering the body. Drawn from a photograph in Escamilla et al. (148).

ups can be performed while holding weights, and as strength increases and pain decreases, the individual can switch to lateral step-downs. To lessen discomfort during the acute phase, protective taping or bracing is recommended. While it was originally believed that various taping positions could realign the patella in the trochlea groove, this concept has been abandoned (151,152).

By increasing cutaneous stimulation, taping and bracing may simply lessen pain by stimulating receptors that compete with the slower pain fibers. Reduced pain may allow for improved muscle recruitment patterns by blocking neurological inhibition.

According to Pal et al. (153), a vastus medialis obliquus specific strengthening protocol may not be necessary for all patients with patellofemoral pain syndrome, and isolating vastus medialis obliquus is likely to produce favorable outcomes only in patients with lateral patellar malalignment. Although exercises targeting the vastus medialis obliquus produce better shortterm outcomes in patellar tracking compared to standard short arc seated leg extension exercises, both exercise interventions produce similar long-term improvements in vastus medialis obliquus timing and activation (153). As a result, the simple progressive resistance open kinetic chain exercises may be recommended for patients with wellaligned patellae.

Patellofemoral pain syndromes may also be the result of inflexibility. As demonstrated by Witvrouw et al.

Fig. 8.22. Transverse plane patellofemoral joint alignment. A) Bisect offset index (BO) represents the percentage of the patella lateral to the midline of the femur.

B) The patellar tilt angle is formed by the lines joining the posterior femoral condyles and the transverse bisection of the patella. M=medial and L=lateral. Redrawn from Pal et al. (153).

372

Chapter Eight Treatment Protocols (154), inflexibility of the quadriceps muscle is a proven risk factor for the development of patellofemoral pain, and the muscular tightness should be corrected with the stretch illustrated in figure 4.140. The response to stretches should be evaluated with the test position illustrated in figure 4.128. The patient should be encouraged to use a massage stick or a foam roller directly over trigger points in the quadriceps muscle prior to stretching. Additionally, because the iliotibial band has a fibrous connection directly to the lateral aspect of the patella, inflexibility of the hip abductors should also be assessed, and tightness treated with the stretches illustrated in figure 4.138 and 4.139.

Since excessive pronation may allow the lower extremities to internally rotate through greater ranges of motion (displacing the lateral femoral condyle into the lateral patellar facet), controlling excessive pronation with orthotic intervention is a popular treatment protocol for managing patellofemoral pain syndrome. In an extremely thorough randomized controlled trial, Collins et al. (155) confirm that individuals with patellofemoral pain syndrome treated with prefabricated foot orthotics have significantly better outcomes compared to individuals treated with flat inserts. Although it is tempting to assume the orthotics are effective because they lessen pronation and hence internal rotation of the lateral femoral condyle into the patella, studies correlating improved outcomes with reduced ranges of pronation have found conflicting results: Sutlive et al.

(156) report that people who pronate through small ranges of motion are more likely to have successful outcomes when treated with orthotics, while the Vicenzino et al.

(157) note that individuals with greater midfoot mobility are more likely to have a favorable response to orthotic intervention.

More recently, Crossley et al. (158) found no correlation between excessive foot pronation and improved clinical outcomes following orthotic intervention. This is consistent with 2- and 3-dimensional studies confirming no correlation between patellofemoral pain and pronation (159,144). To add to the confusion, Bellchamber and van den Bogert (160) make the dogmatic claim that because power flow during walking moves from proximal to distal bony segments (i.e., movement of the foot is determined by movement of the tibia), the use of foot orthoses “may increase stress at the knee during internal rotation phase by creating a moment which opposes the motion induced by the proximal segments.� Because the authors observed erratic reversals in the direction of power flow when running, they claimed orthotics may occasionally be useful when treating knee pain in running athletes.

While the authors used rigorous scientific protocol to determine the intersegmental moments traveling through proximal and distal segments, the concept of power flowing in a specific direction should be viewed cautiously, since force does not flow through the body like water through a hose. If power does flow proximal to distal, then placing a

varus or valgus wedge beneath the foot would have no effect on motions in the knee or hip while walking. Lafortune et al. (161) confirm this is not the case, since their detailed in vivo study incorporating surgically implanted intracortical rods reveals that while walking, the addition of varus and valgus posts significantly affect lower extremity rotation patterns: varus posts lessen internal rotation while valgus posts increase internal rotation.

Even if their concept of power flow is correct, the graphs presented in their study show a clear power flow from proximal to distal segments during propulsion, but during the midstance period while walking and running, when knee flexion and retropatellar pressures are at their peak, the graphs demonstrate numerous brief periods in which power flows up the tibia from the foot, suggesting orthotic intervention might be helpful.

The main reason orthotic intervention produces such variable clinical outcomes when prescribed to alter pronation probably has nothing to do with the direction of force flow, and is most likely explained by arch related variation in the location of the subtalar axis. As demonstrated by Williams et al. (162), while people with low arches present with greater ranges of pronation during stance phase, they convert a much smaller percentage of frontal plane motion into tibial rotation. Conversely, individuals with high arches move through stance phase with smaller ranges of calcaneal eversion, but they convert a larger percentage of this motion into tibial rotation. The end result is that people with high and low arches move through the gait cycle with almost identical ranges of tibial rotation (162). This is consistent with a growing body of research showing a limited connection between arch height and patellofemoral pain syndrome.

This is not to say that orthotics should not be used in the management of this common disorder. Because orthotic intervention is associated with excellent outcomes in 25-40% of a patellofemoral pain population (155,163), the clinical challenge lies in identifying the individuals most likely to have favorable outcomes. To address this issue, Crossley et al. (158) performed a clinical prediction rules study and made the important observation that when individuals with patellofemoral pain report less discomfort when performing single-leg squats while wearing prefabricated orthotics, the potential that orthotic intervention will produce a marked reduction in symptoms after 12 weeks of regular use increases from 25% to 45%.

According to Crossley et al. (158), the patients most likely to respond to orthotic intervention typically claim the prefabricated devices make it easier to balance while performing the squat, and frequently report an increased ability to complete pain-free step-downs from a 20 cm high platform (the steps were performed at a rate of 48 steps per minute).

The final consideration in the nonsurgical management of patellofemoral pain syndrome relates to 373

Human Locomotion: The Conservative Management of Gait-Related Disorders against the lower pole of the patella, Lavagnino et al. (170) confirm the tendon is damaged by excessive tensile strain, not compressive impingement. By placing a cadaveric knee in a specially designed jig and calculating localized amounts of strain at specific angles of knee flexion, the authors determined the section of the tendon just anterior to the lower pole of the patella was subjected to the greatest degrees of tensile strain, particularly at 60° knee flexion (Fig. 8.24). This corresponds to the exact location of injury classically associated with patellar tendinopathy. At lower angles of knee flexion, the authors observed that tensile strains were distributed evenly throughout the tendon, explaining the low prevalence of tendinopathy in walkers and recreational joggers.

In an attempt to identify potential risk factors for the development of patellar tendinopathy, van der Worp (171) performed an extensive review of the literature and found some evidence suggesting that reducing body weight, increasing thigh flexibility and quadriceps strength, and incorporating orthotic devices to control excessive pronation might be effective methods for reducing risk of injury. However, the evidence correlating a lessened potential for injury with a specific treatment intervention was weak. As with patellofemoral pain syndrome, the ability of an orthotic to favorably modify symptoms associated with patellar tendinopathy is unpredictable. Furthermore, because patellar tendinopathy is primarily a sagittal plane injury, altering frontal and transverse plane motions with an orthotic is less likely to produce a favorable outcome.

Because of these reasons, an orthotic device should only be prescribed if the patient responds favorably to specific functional tests while wearing a prefabricated orthotic; e.g., jumping off a 12-inch platform.

the evaluation of alternate biomechanical factors that may increase the range of internal tibial rotation present during stance phase. The most common factor affecting tibial rotation is ankle equinus, in which an early heel lift causes the talus to adduct and plantarflex thereby twisting the tibia inward. It is also important to evaluate the integrity of the ankle ligaments following ankle sprain, because laxity of the anterior talofibular ligament significantly increases the transfer of calcaneal eversion into internal tibial rotation (164). Treatment of ankle laxity should include rock boards and closed kinetic chain exercises to stabilize the lower kinetic chain.

The biomechanical evaluation should also include measurements to rule out limb length discrepancies, since the long limb knee flexes through a larger range of motion (165) and is therefore more likely to develop retropatellar pain. Structural limb length discrepancies greater than 6 mm should be treated with the appropriate lift.

Manual therapies applied to the spine, hip, and knee should also be considered. In a recent randomized controlled trial, van den Dolder and Roberts (166) confirm that transverse friction massage and patellar mobilization produce significant reductions in a functional step-down task compared to a control group. Spinal manipulation should also be considered, since it may improve neural drive to the quadriceps muscle (167). Finally, because running amplifies ground-reactive forces 5-fold, overweight individuals should be encouraged to reduce body mass index, and even small reductions in weight may significantly lessen discomfort. In almost all situations, individuals with patellofemoral pain syndrome should walk and/or run with shorter stride lengths, and consider switching to mid or forefoot strike patterns, which lessens the transfer of ground-reactive forces through the knee by as much as 50% (168).

Patellar Tendinopathy Also known as jumper’s knee, patellar tendinopathy is a degenerative condition characterized by local tenderness of the patellar tendon at its origin on the lower pole of the patella. It is suggested that repetitive, rapid loading of the patellar tendon produces microscopic tearing within the tendon, leading to structural changes that weaken the tendon. Because stresses in the tendon are greater at higher angles of knee flexion, this injury is more prevalent in jumping sports, such as basketball and volleyball. Histological changes associated with patellar tendinopathy are similar to those seen in plantar fasciitis and lateral epicondylalgia, and include increased water and proteoglycan content, increased cross-link concentrations, neovascularization and tendon fascicle disorganization (169).

Although it was originally suggested that knee flexion produced microscopic tendon damage of the posterior aspect of the patellar tendon when it pinched

Fig. 8.24. Measuring tensile strain in the patellar tendon with a custom-made jig. Localized peak strain in the patellar tendon occurs at the lower pole of the patella when the knee is bent 60° (X). Redrawn from Lavagnino et al.

(170).

374

Chapter Eight Treatment Protocols In almost all situations, vigorous deep tissue massage of the quadriceps is useful, since it may improve elasticity of the quadriceps aponeurosis thereby decelerating the transfer of tensile strains into the patellar tendon. The patient should be encouraged to use foam rollers and/or massage sticks over the entire length of the quadriceps muscle.

To lessen pain during sport, compressive straps should be placed around the distal thigh. Although unproven with patellar tendinopathy, cadaveric evaluation of tendon forces in the elbow proves that a well-positioned brace will significantly reduce tendon loads (172). As demonstrated

by Takasaki et al. (172), the precise placement of the brace is important and greater reductions in tendon strain values occur when the brace is placed closer to the tendon.

According to Wadsworth et al. (173), braces work because they distribute forces generated by muscle contraction thereby reducing neurological inhibition.

Of all the proposed treatment protocols, increasing quadriceps strength has produced the most impressive outcomes. In an in depth study of the effects of heavy slow resistance training on patellar tendon fibril morphology and tendon mechanical properties, Kongsgaard et al. (169) used electron microscopes and ultrasonography to evaluate tendon biopsies removed from individuals with and without patellar tendinopathy before and after completing a 12-week exercise protocol incorporating heavy resistance training. The training sessions consisted of 3 weekly sessions in which 3 bilateral knee extension exercises were performed: squats, leg presses, and hack squats.

The subjects completed 4 sets of each exercise with a 2-3 minute rest between each set. During week one, the subjects performed the 4 sets with a 15 repetition maximum. (Note that repetition maximum refers to the maximum amount of repetitions an individual can lift a specific weight without stopping; e.g., a 10 repetition maximum is the amount of weight an individual can lift 10 times, but the person would be too fatigued to complete an 11th repetition.) During the second and third week, the same 4 sets were performed with a 12 repetition maximum. During weeks 4 and 5, the weight used were the 10 repetition maximum; during weeks 6, 7 and 8, an 8 repetition maximum was used; and finally, weeks 9 through 12 used a 6 repetition maximum.

All exercises were performed to 90° knee flexion and back again, incorporating equal eccentric and concentric components of muscular contraction. Each subject was told to spend 3 seconds descending, and 3 seconds ascending from each exercise (i.e., 6 seconds per repetition).

Before and after completing this rigorous training program, biopsies of tendons in patients with patellar tendinopathy were compared to biopsies of tendons taken from a healthy control group. All aspects of tendon morphology and mechanical properties were studied.

Surprisingly, when compared to the control tendons, the patellar tendinopathy tendons possessed similar mechanical

properties before and after the training program, explaining why athletes with this injury are able to perform at such high levels (albeit with considerable discomfort).

The most important finding from this study relates to tendon stiffness. At the start of the study, the tendinopathy patients possessed notably reduced fibril density, and the individual fibers appeared larger. By the end of the training protocol, tendon morphology normalized and the strength training produced an approximate 70% increase in fibril density with slight reductions in fibril area (Fig. 8.25).

These changes were responsible for significant reductions in tendon stiffness and swelling, explaining why the tendinopathy patients reported considerable reductions in pain.

The authors speculate that overuse may cause microrupture of specific areas of the patellar tendon resulting in “stress deprivation of adjacent tenocytes.� The stressed tenocytes elicit a catabolic response eventually resulting in reduced formation of new fibrils (hence the older, fatter, less populated fibril population). It is theorized that heavy slow resistance training results in augmented tenocyte activity, which in turn produces increased fibril density, as numerous small-sized fibrils appeared. The changes in fibril density occurred rapidly, and by week 12, there was no difference in fiber morphology between the patellar tendinopathy and the control group. Kongsgaard et al. (169) relate the reduced tendon stiffness to the increased production of new fibrils: Because the smaller fibrils have fewer cross-links between them, the tendon itself becomes more resilient, as fewer cross-fibrils allow greater flexibility. Since the mechanical properties were not affected by tendinopathy, the authors suggest that the only performance suppressing factor associated with tendinopathy may be the tendon pain.

While heavy load resistance training increases tendon flexibility and decreases pain, the weights used in this protocol are often extreme and may not be tolerated by less fit patients. To evaluate the effect of low load resistance training on a less athletic patient population, Kubo et al.

(174) evaluated tendon elasticity in middle-aged and elderly women before and after performing 50 squats daily

Fig. 8.25. Electron microscopy of tendon biopsies taken before (A), and after (B), a 12-week heavy resistance strength training program. Note the significant increase in small-sized fibrils following strength training.

375

Human Locomotion: The Conservative Management of Gait-Related Disorders for 6 months. No additional weights were used, and the subjects performed squats with body weight only. Using ultrasonography, the authors concluded that even low load resistance training significantly improves tendon elasticity.

Future research is needed to determine if the same results are possible without performing full squats, as this exercise is difficult for patients with chondromalacia patella even when using body weight alone, .

An alternate protocol is to have the patient with retropatellar pain perform the long-step lunges without strides as illustrated in figure 8.23. Rather than using high weights with lower repetitions, this exercise may be performed 50 times per day with each repetition lasting 6 seconds (a 3-second eccentric phase followed by a 3-second concentric phase). Although unproven, this protocol may be a viable alternative for patellar tendinopathy in patients with chondromalacia patella.

If symptoms persist despite resistance training, a trial of aggressive deep tissue massage performed at the site of the tendinopathy should be considered. Although unproven in patellar tendinopathy, deep tissue massage has been proven to accelerate healing in animal studies (175,176). If the patient continues to have discomfort, extracorporeal shock wave therapy should be considered as this intervention has proven effective in the management of chronic patellar tendinopathy (177). Surgical intervention should only be considered as a last resort, because outcomes are unpredictable (178).

band is a powerful stabilizer of the entire lower extremity.

Iliotibial band syndrome is common in runners, representing up to 12% of all running-related overuse injuries (180). The pain is often described as burning, and is reproduced clinically with Noble’s test, in which the examiner compresses the distal band against the lateral femoral condyle while the knee is flexed 30° (Fig. 8.26). It was originally suggested that iliotibial band syndrome was a sagittal plane injury in which the distal aspect of the iliotibial band shifted posteriorly as the knee flexed, snapping over the lateral femoral epicondyle at approximately 30° knee flexion. The repetitive friction was thought to create an inflamed bursa responsible for producing the pain.

In a thorough review of iliotibial band anatomy and function, Fairclough et al. (179) prove that the sagittal plane model is invalid. As illustrated in figure 3.30, what appears to be a forward/backward displacement of the band during knee flexion is actually an illusion created by alternating tensions generated by the tensor fasciae latae and gluteus maximus muscles. Using MRI, the authors conclusively prove the band does not snap back and forth, but is compressed into the lateral aspect of the femur as the knee is flexed, with peak compression occurring at 30° flexion. Fairclough et al. (179) claim the iliotibial band possesses two distinct sections: a lower ligamentous component that runs between the epicondyle and Gerdy’s

Iliotibial Band Compression Syndrome The iliotibial band is a powerful stabilizer of the entire lower extremity during the gait cycle. Proximally, the iliotibial band originates from fibers of the gluteus maximus, medius, and tensor fasciae latae muscles. It also receives reinforcement from a superficial layer of fascia attaching directly to the iliac crest. The strength of the iliotibial band is in large part derived from the fact that the majority of the gluteus maximus muscle attaches directly to the posteroproximal portion of the band.

Although frequently described as an isolated structure, the iliotibial band actually represents a lateral thickening of the circumferential layer of fascia that surrounds the thigh. As illustrated in figure 8.18, the iliotibial band is anchored via the intramuscular septum to the entire femoral shaft along the linea aspera, where it may play a role in lessening stance phase bending strains placed on the femur. Before attaching to the tibia at Gerdy’s tubercle, the iliotibial band sends a fibrous slip to the patella (which prevents medial displacement of the patella during knee flexion) and a more powerful slip directly to the femur. As demonstrated by Fairclough et al. (179), this fibrous slip approaches the femur at an oblique angle and consists of dense fibrous connective tissue devoid of elastic fibers.

Because it traverses the periosteum to attach directly into the femur, this rarely mentioned lower attachment of the

Fig. 8.26. Noble’s test. The examiner compresses the distal aspect of the ITB where it passes over the lateral femoral epicondyle (A). The hip is slightly flexed and adducted while the examiner flexes the knee. ITB syndrome typically produces discomfort over the epicondyle when the knee is flexed 30°.

376

Chapter Eight Treatment Protocols tubercle (which functions to limit internal tibial rotation), and a proximal tendinous component extending from the hip and attaching to the lateral femoral condyle through the dense fibrous band.

The authors claim the proximal component of the iliotibial band should be considered as a separate musculotendinous unit, suggesting the pain associated with an iliotibial band syndrome may be an enthesopathy in which tensile strain in the lower femoral attachment produces insertional bone pain (comparable to the bone pain associated with an insertional Achilles tendinitis). The authors also suggest the pain may result from repetitive compression of the highly innervated fatty tissue beneath the distal aspect of the iliotibial band. Contrary to the majority of published literature, Fairclough et al. (179) confirm the band itself is never inflamed, and there is no evidence of bursitis or inflammation in the distal part of the vastus lateralis muscle.

There are numerous biomechanical factors believed to be associated with the development of this syndrome.

Some authors feel the excessive pronation associated with flat feet may play a role, while others claim people with high arches are more likely to develop iliotibial band syndrome.

To identify biomechanical factors potentially responsible for the development of this common injury, Ferber et al. (181) performed 3-dimensional motion analysis of 35 runners with iliotibial band syndrome and compared rearfoot, knee and hip movements to 35 age-matched controls. Compared to the control group, the iliotibial band syndrome group exhibited significantly greater peak knee internal rotation and peak hip adduction angles, with no appreciable difference in peak rearfoot eversion angles.

In fact, runners with iliotibial band syndrome had slightly reduced rearfoot eversion angles compared to the control group, which is consistent with research suggesting this injury is more likely to happen in people with high arches (182). The authors state that because the band has a strong attachment to the distal femur, excessive hip adduction increases tensile strain along the entire band, while the exaggerated knee internal rotation increases torsional strain along the distal aspect of the band. The combination of increased tensile loading from the hip and torsional loading from the knee amplifies compression of the band against the lateral knee.

Because there was no difference in the angle of peak knee flexion, these authors concur with the research

by Fairclough et al. (179), questioning the validity of the sagittal plane theory in which the band snaps over the epicondyle as the knee flexes.

The detailed 3-dimensional kinematic analysis performed by Ferber et al. (181) suggests that strengthening the hip abductors and external rotators may play an important role in the management of iliotibial band syndrome. This is consistent with research by Fredrickson

et al. (183), who demonstrated that a 6-week program of hip abductor exercises produced a 51% increase in muscle strength, and completely resolved symptoms in 22 of 24 runners.

This does not imply that evaluation of the foot and ankle is not important in the management of iliotibial band syndrome. In certain situations, excessive pronation may amplify the degree of internal tibial rotation and/or valgus collapse of the knee, and varus posts and/or orthotics should be considered. It is also possible that iliotibial band syndrome results from hypopronation, since several 2- and 3-dimensional studies have shown that runners developing iliotibial band syndrome are more likely to move through smaller ranges of rearfoot eversion during early stance (184,185). Perhaps hypopronation results in iliotibial band syndrome because the individual with a rigid rearfoot is forced to absorb shock with excessive frontal plane motion of the hip, which greatly increases tensile strains placed on the band. If reduced ranges of subtalar pronation are present, valgus posts placed beneath the lateral heel may be an effective treatment intervention. Interestingly, runners with iliotibial band syndrome are also more likely to strike the ground with rearfoot inverted excessively, which may represent a compensatory movement strategy to improve shock absorption (181).

While the clinical efficacy of exercises and/or orthotics may play an important role in the management of this condition, it is also essential to evaluate hip abductor flexibility, since tightness in the tensor fasciae latae, gluteus medius, and gluteus maximus muscles may increase tensile strain on the band. Tension in these muscles may be so great that they cause the band to snap over the greater trochanter when the hip moves from flexion to extension.

The snapping of the band is palpable during physical examination and it may result in chronic lateral hip pain.

In an extremely detailed cadaveric study of the effect of stretching on the iliotibial band and proximal muscles, Falvey et al. (186) surgically implanted strain gauges into the iliotibial bands of 20 fresh cadavers and evaluated the effect of 3 different stretches on lengthening the band.

They also evaluated elasticity of the tensor fasciae latae/ iliotibial band aponeurosis with ultrasonography while athletes performed maximum voluntary contractions of the hip abductor musculature. Their detailed analysis confirmed that the iliotibial band itself is extremely rigid and resistant to stretch, since it lengthened less than 0.2% with a maximum voluntary contraction. Because of the extreme inflexibility of the fascial component of the iliotibial band, the authors emphasize that current treatment protocols focusing on reducing tension in the band are inappropriate, since they are treating the “symptoms of the condition rather than the cause.� The authors state that to be effective, tension in the muscular component of the band must be reduced with soft tissue therapies such as massage or dry needling of myofascial trigger points.

377

Human Locomotion: The Conservative Management of Gait-Related Disorders In order to lessen tension throughout the entire band, it is important to stretch both the gluteus maximus and the tensor fasciae latae muscles, since failure to do so would result in continued tightness in the posterior and anterior aspects of the band, respectively. Evaluating inflexibility is especially important with structural limb length discrepancies, and the iliotibial band is usually tight on the side of the long limb. As a result, it is often necessary to accommodate discrepancies greater than 8 mm with the appropriately sized lift.

Medial Knee Pain The two gait-related factors responsible for the development of medial knee pain are varus collapse, which creates a compressive force that damages the medial tibiofemoral joint, and valgus collapse, which creates tensile strain that stresses the supporting ligaments (Fig. 8.27).

Valgus collapse of the knee is prevalent in athletic young females, and may result from hip weakness/ delayed muscular recruitment times and/or various biomechanical factors, such as femoral anteversion and excessive pronation. In addition to stressing the medial collateral, the posterior oblique, and the anterior cruciate ligaments, valgus collapse may also strain the pes anserine muscle group, potentially resulting in chronic tendinitis/ bursitis (Fig. 8.28). While the development of pes anserine bursitis/tendinitis is often attributed to factors such as excessive pronation, obesity and/or knee instability, Alvarez-Nemegyei (187) confirms that the presence of a valgus knee either alone or in combination with collateral instability is the most important risk factor associated with the development of pes anserine tendinitis/bursitis.

Given the recalcitrant nature and the severity of the resultant medial knee injuries, it is important to identify all possible causes responsible for the valgus collapse and initiate the appropriate treatment. For example, an individual with ankle equinus and anteverted hips typically responds best to stretches and various manual techniques to restore ankle motion along with gluteus medius and maximus exercises to protect against excessive internal femoral rotation. Conversely, an individual with a hypermobile midfoot and genu valgum responds best to a varus posted orthotic with appropriate arch elevation, along with strengthening exercises for peroneus longus and the hip abductor/external rotator musculature.

In all situations, treatment of valgus collapse should include the agility drills discussed in chapter 4 (see Table 1 on page 157). Because they have been proven to lessen valgus collapse in jumping athletes (188), varus posts are often prescribed regardless of foot type. When used on individuals with excessive pronation, it is important to evaluate post efficacy with 2-dimensional motion analysis.

Because individuals with flat feet have a tendency to pronate excessively in spite of the varus post, it is often necessary

Fig. 8.27. Knee alignment. Varus collapse creates a compressive load at the medial knee (A), while valgus collapse creates a tensile strain that can damage the restraining ligaments (B).

Fig. 8.28. The pes anserine muscle group.

378