A New Approach To Adult-Acquired Flatfoot

Ask experienced DPMs what pathology has seen the most dramatic increase in prevalence over the last 20 years and, aside from plantar heel pain, they will tell you it is posterior tibial tendon dysfunction (PTTD). Currently, most authorities have dropped the description PTTD in favor of “adult-acquired flatfoot.” This is due to increased recognition of the fact that a rupture or attenuation of the posterior tibial tendon cannot itself lead to the deformity and disability that one sees in older adults with progressive flatfoot deformity. Significant ligamentous rupture occurs as the flatfoot deformity progresses. These ligaments include the spring ligament, the superficial deltoid ligament, the plantar fascia and the long and short plantar ligaments. Evaluating and recognizing various levels of ligamentous rupture is critical for treating the adult-acquired flatfoot (AAF). However, clinical staging of patients with AAF continues to rely on a system proposed by Johnson and Strom in 1989 before researchers recognized the role of ligamentous rupture in the pathology.1 In 1996, Myerson recognized the presence of a deltoid ligament rupture in late stage AAF and proposed adding a stage IV to the original classification when one sees valgus deformity of the ankle.2 With these things in mind, I would like to propose a revised classification system for the different stages of AAF. Building upon a previous discussion of PTTD pathomechanics, I believe this simple classification system can help facilitate appropriate decision-making when it comes to choosing conservative and surgical treatment options for AAF.3 When Patients Initially Present With AAF Prevailing opinion recognizes the presence of a preexisting flatfoot in nearly all patients with a symptomatic, progressive AAF. There is also a strong correlation with obesity, hypertension and diabetes among patients with AAF, making them poor surgical risks. The condition affects females more than males with 60 being the average age for the onset of symptoms. In the adult acquired flatfoot, symptoms have an insidious and usually unilateral onset. While patients may present with a progressive flatfoot deformity secondary to acute trauma or neuropathic conditions, for the purposes of this article, we’ll focus on the more common idiopathic, progressive and symptomatic AAF. Patients with AAF can initially present with various levels of pain, deformity and disability. Keep in mind that significant pain and edema can often obscure an accurate clinical examination. Often, immediate treatment of the acute symptoms will be necessary before you can proceed with a more thorough diagnostic work-up. In these situations, patients with AAF are treated no different than an athlete who has an acute ankle sprain. The combination of PRICE (protection, rest, ice, compression and elevation), which is commonly used for athletic injuries, is just as relevant in treating patients who have painful symptoms of AAF. For the immediate treatment of the acute symptoms of tenosynovitis, tendon rupture or ligament rupture in the patient with AAF, I recommend immobilization with a walking boot. Alternatively, one can employ an Unna Boot or wrap the foot and ankle with tape, but these options are not as protective. These measures can usually alleviate symptoms within several weeks. At this point, one may proceed to a subsequent detailed examination without the interference of significant pain or antalgic gait patterns. Pertinent Pointers On The Clinical Exam Evaluating static stance is the most critical part of examining the patient with a suspected progressive AAF deformity. In less than a minute, an experienced clinician can detect the telltale signs of a foot that has undergone attenuation or rupture of the posterior tibial tendon and/or key ligaments of the hindfoot. Since the majority of posterior tibial tendon rupture cases present unilaterally, comparing the symptomatic foot to the asymptomatic foot can give you insight into the severity of the pathology. First, evaluate the malleolar position from a dorsal view of the foot. In most cases, you will see an obvious asymmetry in which the symptomatic foot will have an noticeable internally rotated position of the malleoli, demonstrated by anterior displacement of the fibular malleolus and posterior displacement of the medial malleolus. From this same dorsal view of the feet in static stance, compare the medial and lateral borders. In the progressive symptomatic AAF, the medial bulge of the talonavicular joint and the lateral concavity of the calcanealcuboid joint will appear more extreme on the symptomatic side. Proceed to evaluate the position of the rearfoot from the posterior view. Both feet will demonstrate a valgus heel, but the symptomatic foot will show various extremes of medial displacement of the distal tibia and talus, relative to the calcaneus and forefoot. This medial displacement of the rearfoot will cause an apparent tibial varum deforminty. These findings are consistent with closed chain pronation-subluxation of the midtarsal joint. From this posterior view, you can measure the alignment of the tibia relative to the calcaneus. One should measure this rearfoot angle with the patient in a relaxed position and in a corrected, neutral position of the subtalar joint. This allows you to assess the relative flexibility of the disorder. The flexibility of the deformity and to what degree one can reduce the deformity can be important parameters in choosing between surgical procedures or appropriate ankle foot orthosis correction. While the patient is standing, ask him or her to perform the single heel rise test. While holding one foot off the floor, the patient should raise up on the ball of the other foot, lifting the heel off the floor. When the posterior tibial tendon is weak or ruptured, you will note that the midtarsal joint is significantly unstable. The normal rigid lever of the entire arch of the foot is now shortened into two segments intersecting at the midfoot. The force of the calf muscles will cause a plantarflexion moment to the midtarsal joint rather than the metatarsalphalangeal joints. A shortened lever distal to the insertion of the Achilles will prohibit lifting of the heel off the ground, despite full strength of the gastroc-soleus. What You Should Look For During The Off-Weightbearing Exam The off-weightbearing exam (open chain) should include all standard biomechanical protocols including range of motion and muscle testing. One should make comparisions between the symptomatic foot and asymptomatic foot. Keep in mind that testing the strength of the posterior tibial muscle/tendon can be misleading due to recruitment of the anterior tibial muscle. In order to minimize inversion of the foot by the anterior tibial muscle, one should push against the plantar-medial portion of the first metatarsal head while instructing the patient to invert the foot from a plantarflexed and everted ankle position. While the patient is non-weightbearing, evaluate heel cord tightness with the patient’s knee flexed and extended. This is an important pre-surgical criteria and also determines the need for an ambitious stretching program during the conservative treatment period. Almost all authorities agree that the heel cord is the single most deforming force in the progression of the adult acquired flatfoot deformity. Another subtle yet effective measure of activity of the posterior tibial muscle is the supination lag test described by Abboudi and Kupcha.4 In this test, the patient is seated on the edge of the exam table with both feet hanging in the air in a plantarflexed ankle position. Then you would instruct the patient to bring the soles of the feet together in the direction of supination of the subtalar joints. In the case of an attenuation or rupture of the posterior tibial tendon, the affected foot will “lag behind” the normal foot and show a loss of inversion curvature on the dorsum of the foot. Testing For Ligamentous Integrity In The Hindfoot: What You Should Know Assessing ligamentous integrity in the hindfoot is crucial in the clinical exam of the patient with AAF. As the flatfoot deformity progresses, there is potential for attenuation or rupture of the spring ligament, the superficial and deep deltoid ligaments, the plantar fascia as well as the long and short plantar ligaments. Currently, there are no reliable clinical tests for determining loss of integrity of any of these specific structures. However, we do know that the ligaments of the hindfoot are responsible for movement transfer between the foot and the leg. Specifically, inversion of the foot is coupled to external rotation of the leg. When the major hindfoot ligaments are ruptured, this coupling is lost and the foot literally becomes mechanically disconnected from the leg. Performing the Hubscher maneuver or the Jack test allows you to determine mechanical coupling between the foot and the leg. With the patient in a weightbearing postion, passively dorsiflex the patient’s hallux to end range of motion. This dorsiflexion of the hallux causes plantarflexion of the first ray, supination of the subtalar joint and external rotation of the tibia. When the plantar fascia, spring ligament and superficial deltoid ligaments have been attenuated, passive dorsiflexion of the hallux results in no movement transfer between the foot and the leg. In other words, you will not see external rotation of the tibia. A second test, presumed to be linked to rupture of the posterior tibial tendon as well as the plantar ligaments, is the first metatarsal rise test described by Hintermann.5 In this test, the patient is fully weightbearing on both feet and you proceed to invert the heel of the symptomatic foot in a varus direction. When there is a dysfunction of the posterior tibial tendon, you will see the first metatarsal rise off the ground as you proceed to invert the heel. In the normal foot, supination of the rearfoot raises the height of the medial arch and the forefoot will remain plantigrade due to tensioning of the intact plantar ligaments. With absent or lax plantar arch ligaments, inversion of the heel causes no arch raise and the forefoot simply inverts with the rearfoot as one unit. Others may argue that the first metatarsal rise test identifies a forefoot suppinatus deformity that almost always accompanies a moderate to severe AAF. Prolonged ambulation on a valgus heel requires the forefoot to invert to remain plantigrade. Prolonged inversion of the forefoot, caused by ground reaction forces against an everting rearfoot, will lead to attenuation and adaptation of the ligaments supporting the medial column of the foot. When the foot is brought into a corrected position (i.e. out of calcaneal eversion), this adapted forefoot inverted deformity (suppinatus) becomes immediately apparent. All the debate aside, one can employ the first metatarsal rise test to identify ligamentous attenuation and the resultant forefoot deformity, which one must consider when planning surgical interventions. What is critical again in this test is determining to what degree you can reduce the deformity. One should press down on the first metatarsal to determine if you can fully correct the suppinatus. Recognizing a non-reduceable varus deformity of the forefoot is critical in planning surgical procedures for AAF. Key Recommendations For Diagnostic Testing Radiographic evaluation of the AAF requires weightbearing AP and lateral views of the foot as well as weightbearing AP views of the ankle. Obtaining comparison views of the contralateral foot are helpful but significant differences may not be obvious. Radiographic criteria for working up the AAF deformity have been well described in the literature.2,6-8 With severe stages of AAF, the AP ankle view will show valgus tilt of the talus in the ankle mortise as well as impingement between the calcaneus and the fibula. Occasionally, a stress fracture of the fibula will result from this chronic valgus force of the calcaneus. Further diagnostic testing involving ultrasound and magnetic resonance imaging may be of questionable value in the initial evaluation of the patient with symptomatic AAF. Determining the extent of rupture or tendinopathy may not necessarily dictate variations in the treatment regimen. Clinical testing as described above may be just as helpful in directing an initial conservative treatment program. When these measures fail, further testing with ultrasound and MRI can then be very helpful in making surgical decisions. Researchers have recently shown that ultrasound is more sensitive and specific than MRI for diagnosing longitudinal tears of the posterior tibial tendon.9 The advantages of using ultrasound testing include the convenience of office-based exams and the ability to conduct the exam for a static and dynamic condition. Choosing Appropriate Conservative Care After evaluating and staging the severity of pathology, one must decide on an appropriate course of treatment. In the majority of cases, conservative care is the choice for initial management of symptoms and disability. Since most surgical interventions for any stage of AAF are significant in scope and potential disability, conservative measures are almost always preferred given the multiple medical problems commonly seen in the patient population with AAF.10 The compilation of clinical findings in the aforementioned tests enables you to classify the deformity into one of four stages, based upon a revision of the widely accepted Johnson and Strom classification.1 This classification originally had only a few clinical guidelines to determine staging. The revision separates Stage I from Stage II, based upon the presence of ligamentous rupture. Specific clinical tests are used to classify the severity of the pathology. In Stage I AAF, you may or may not see a noticeable structural change in the foot. Both feet will have a flatfoot deformity, but the patient can still raise the heel on the symptomatic foot without difficulty. The primary symptom is tenosynovitis of the posterior tibial tendon. Short term immobilization (two to six weeks) with a rigid walking boot or pneumatic walking boot will usually reduce the symptoms. Patients can subsequently wear a rigid functional foot orthosis with stable footwear. Numerous orthotic enhancements have been suggested to control the severe pronation forces that occur among patients with any stage of AAF. Most podiatric orthotic labs have a so-called “PTTD Package” orthotic design, which would include a deep heel cup, medial heel skive and medial and lateral flanges designed to control severe pronation. A Review Of Stage II Clinical Findings In Stage II AAF, one will note attenuation of the posterior tibial tendon, which is accompanied by a visible change in foot structure alignment with loss of one or more critical ligaments in the hindfoot. However, the hallmark of this deformity is the fact that it is still flexible and can be reduced. When performing the clinical exam of patients with Stage II AAF, one will see the following key findings: • The patient will have difficulty or be unable to independently raise his or her heel. • The inversion strength of the posterior tibial tendon will be at least one grade weaker than contralateral side. • The rearfoot can be manually inverted to a vertical position in stance, but the first metatarsal will rise off the ground. This constitutes a positive first metatarsal rise test. • One can reduce the first metatarsal rise (i.e. forefoot suppinatus), producing a neutral forefoot to rearfoot relationship. You should see this reduction in both the weightbearing and non-weightbearing assessment. • The Hubscher maneuver will detect loss of ligamentous integrity. Activation of the windlass causes no movement transfer to the tibia. • You may note an absence of degenerative changes in the rearfoot complex and no valgus tilt of ankle mortise on standing radiographs. Treatment Considerations For Stage II AAF These tests confirm rupture of the posterior tibial tendon as well as loss of ligamentous integrity of the rearfoot. This loss of ligamentous integrity found in Stage II AAF will inhibit the efficacy of standard orthotic therapy. Hintermann has shown that the foot becomes mechanically disconnected from the leg when the spring ligament, the deltoid and the subtalar interosseous ligaments are severed.11,12 Foot orthotics rely on ligament integrity to redirect ground reaction forces to the ankle and leg. Employing ankle-foot orthoses (AFOs) enables you to apply three point force systems above and below the ankle-rearfoot complex, which is necessary for the successful treatment of intermediate to advanced stages of AAF. Since 1996, over 20,000 patients with AAF have been treated with the podiatric AFO (Richie Brace®). A podiatric AFO differs from a traditional AFO in that it includes a balanced functional foot orthotic footplate. In addition, the podiatric AFO has limb uprights oriented to control ankle rotations in the transverse and frontal planes as opposed to posterior shell AFOs that are designed to control dropfoot and other sagittal plane conditions. Podiatric AFOs are fabricated on corrected models that are created from negative casts of the patient’s foot and lower leg. The traditional neutral suspension casting technique is recommended in order to capture contours of the heel as well as the medial and lateral arches. In addition, one must manually reduce the forefoot suppinatus deformity in order to ensure optimal functioning of the first ray. As with any orthotic therapy, appropriate footwear prescription is critical. Running shoes with motion control characteristics, such as medial posting, reinforced heel cup and stiff shank construction, are recommended. Alternatively, high top leather oxford orthopedic footwear with adjunctive pedorthic modifications (medial sole wedge and flare) can be extremely effective in augmenting orthotic therapy for AAF. Physical therapy can be an important adjunctive treatment of Stage II AAF. Strength deficits and loss of range of motion can be significantly improved with four to eight weeks of supervised, hands-on therapy. In addition, older patients with AAF demonstrate significant loss of balance and proprioception, which can also be improved with rehabilitation. When Patients Have Stage III AAF In Stage III AAF, the deformity becomes rigid and you can see arthritic changes on radiographs. You will note the following findings during the clinical exam of these patients: • The patient cannot independently raise his or her heel. • The patient has a positive supination lag test. • The first metatarsal rise test is positive and the varus deformity cannot be reduced. • One cannot bring the rearfoot to a vertical position in stance. • Radiographs will demonstrate arthritic changes in the calcaneal-cuboid joint, subtalar joint and/or the talonavicular joint. • One can see impingement of the calcaneus on the fibula on the AP ankle X-ray. Whether the patient demonstrates the above Stage III or Stage IV findings, one’s approach to conservative treatment should be more aggressive in terms of restricting ankle and rearfoot motion. With this in mind, one should consider using a gauntlet style AFO (Arizona AFO®). This combination of a polypropylene and leather device can maintain foot-ankle-leg alignment similar to a well-molded cast. In a recently published study, researchers reported impressive outcomes in the treatment of 20 patients with various stages of AAF.13 Ninety percent of the patients reported statistically significant improvement of symptoms. The long term results of AFO therapy in patients with Stages II and III AAF have not been reported. Anecdotally, there have been many reports from practitioners stating that up to 30 percent of patients with Stage II AAF only require an AFO for six to 12 months. They note that these patients remain asymptomatic without the AFO for months or years thereafter as long as they wear traditonal foot orthoses and proper shoes. When Conservative Treatment Fails Despite the reported success with AFOs in treating intermediate and late stage AAF, a percentage of patients will become surgical candidates. When patients still have symptoms after three months of immobilization and three subsequent months of AFO therapy, one may want to consider surgical options. Furthermore, documented progression of the deformity both clinically and radiographically would warrant the consideration of surgery. Over the past 10 years, there appears to be a trend toward a more unified opinion about the surgical approach to patients with AAF. Ten years ago, it would not be unusual to hear experts advocate arthrodesis of one or more joints of the hindfoot as the procedure of choice for treating Stage II AAF. Perhaps this was a response to the disappointing results of the solitary flexor digitorum longus tendon transfer procedure which had gained popularity in the ‘80s.14 Currently, there appears to be a reluctance to fuse any major joint of the rearfoot when it comes to treating Stage II AAF. A survey of 104 academic orthopedic foot and ankle surgeons on their preferred surgical approach to flexible Stage II AAF was published last year.15 Only 12 percent of the respondents stated they would use an arthrodesis procedure of any of the major hindfoot joint. Eighty-eight percent favored other bony procedures including the medializing calcaneal osteotomy, a calcaneal lengthening osteotomy or a medial column stabilization involving arthrodesis of the navicular cuneiform joint or the first metatarsal-medial cuneiform joint. Most preferred a combination of procedures including a medializing calcaneal osteotomy with a posterior tibial tendon augmentation.15 With this trend in mind, it is easy to apply our clinical examination system to the selection of general categories of surgical procedures. We have identified tests for the early Stage I AAF foot with no structural change or tendon rupture. Surgical consideration should focus on debridement of the posterior tibial tendon when conservative care fails. Our tests for determining the degree that the deformity can be reduced can also differentiate those patients needing arthrodesis and those who do not. Generally, for patients who have a Stage II AAF that can be reduced, one can proceed with a medializing calcaneal osteotomy or lateral column lengthening and/or a medial column stabilization with posterior tibial tendon augmentation as well as spring ligament repair. Arthrodesis of one or more joints of the hindfoot is favored in Stage III AAF in which rigidity and arthritis are key findings. O’Malley has shown that the talonavicular fusion most accurately reduced the deformity in experimental AAF models.8 Wulker has confirmed that a talonavicular fusion acts almost like a triple arthrodesis in eliminating motion in the remaining joints of the hindfoot.16 However, many would consider the potential negative effects of such a rigid fusion on an older patient population and the deleterious effects of force transmitted to the ankle and knee.17,18 In Conclusion Much has been learned from the significant research conducted over the past 10 years on the pathomechanics of the AAF. There appears to be more agreement today among practitioners regarding operative and non-operative strategies for treating this challenging disorder. Selecting appropriate treatment requires a careful evaluation of the patient and determination of the extent of pathology. Accurate staging of the AAF deformity is critical in determining which treatment intervention is most appropriate. Dr. Richie is President-Elect of the American Academy of Podiatric Sports Medicine. He is also an Adjunct Associate Professor of Biomechanics at the California School of Podiatric Medicine at Samuel Merritt College. Editor’s Note: For a related article, see “Current Concepts In Flatfoot Surgery,” in the October 2003 issue or check out the archives at www.podiatrytoday.com.
 

References:

References 1. Johnson KA, Strom DE: Tibialis posterior tendon dysfunction. Clin Orthop 239:196-206, 1989. 2. Myerson MS: Adult Acquired Flatfoot Deformity. J Bone and Joint Surg 1996; 78A: 780-92. 3. Richie DH. Clearing Up the Confusion about Posterior Tibial Tendon Dysfunction. Podiatry Today 14(12): 38-44, 2001. 4. Abboud J, Kupcha P: Supination lag as an indication of posterior tibial tendon dysfunction. Foot and Ankle 19:570, 1998. 5. Hintermann B, Gachter A: The first metatarsal rise sign: A simple, sensitive sign of tibialis posterior tendon dysfunction. Foot and Ankle 17:237, 1996. 6. Weil Jr LS, Benton-Weil W, Borrell AH, Weil Sr LS: Outcomes for surgical correction for stages 2 and 3 tibialis posterior dysfunction. Jour Foot and Ankle Surg 37:467,1998. 7. Lombardi CM, Dennis LN, Connolly FG, Silhanek AD: Talonavicular joint arthrodesis and Evans osteotomy for treatment of posterior tibial tendon dysfunction. Jour Foot and Ankle Surg 38:116, 1999. 8. O'Malley MJ, Deland JT, Kyung-Tai L: Selective hindfoot arthrodesis for the treatment of adult acquired forefoot deformity: An in vitro study. Foot and Ankle 16:411, 1995. 9. Rockett MS, Waitches G, Sudakoff G, et al.: Use of ultrasonography versus magnetic resonance imaging for tendon abnormalities around the ankle. Foot and Ankle Int 1998: 19 (9): 604-12. 10. Holmes GB Jr, Mann RA: Possible epidemiological factors associated with rupture of the posterior tibial tendon. Foot and Ankle 13:70, 1992. 11. Hintermann B, Nigg BM, Cole GK: The influence of selective arthrodesis on movement transfer between calcaneus and tibia in vitro. Clin Biomech 9:356-361, 1994. 12. Hintermann B, Nigg BM, Cole GK, Sommer C: The transfer of movement between tibia and calcaneus. Clin Biomech, 9:349-355, 1994. 13. Augustin, et.al: “Nonoperative treatment of adult acquired flatfoot with the Arizona brace.” Foot and Ankle Clinics N America 8 (2003) 491-502. 14. Michelson J, Conti S, Jahss M: Survivorship analysis of tendon transfer surgery for posterior tibial tendon rupture. Orthop Trans 16:30, 1992. Abstract. 15. Hiller L, Pinney SJ: Surgical treatment of acquired flatfoot deformity: What is the state of practice among academic foot and andkle surgeions in 2002? Foot and Ankle Int 2003: 24 (9): 701-705. 16. Wulker N, Stukenborg C, Savory KM: Hindfoot motion after isolated and combined arthrodeses: Measurements in anatomic specimens. Foot and Ankle Int 2000: 21 (11): 921-927. 17. Deland JT, Page AE, Kenneally SM: Posterior calcaneal osteotomy with wedge: Cadaver testing of a new procedure for insufficiency of the posterior tibial tendon. Foot and Ankle 20:290, 1999. 18. Kitaoaka HB, Patzer GL: Subtalar arthrodesis for posterior tendon dysfunction and pes planus. Clin Orthop 345:187, 1997. Additional References 19. Mueller TJ: Acquired flatfoot secondary to tibialis posterior dysfunction: Biomechanical aspects. J. Foot Surg. 30:2, 1991. 20. Johnson KA: Tibialis posterior tendon rupture. Clin Orthop 177:140-147, 1983. 21. Conti S, Michelson J, Jahss M: Clinical significance of magnetic resonance imaging in preoperative planning for reconstruction of posterior tibial tendon ruptures. Foot and Ankle 13:208, 1992. 22. Mosier SM, Lucas DR, Pomeroy G et al: Pathology of the posterior tibial tendon in posterior tendon insufficiency. Foot and Ankle 19:520, 1998. 23. S. Ferra JJ, Rosenberg GA: Nonoperative treatment of posterior tibial tendon pathology. Foot and Ankle Clinics 2:261, 1997. 24. Astion DJ, Deland JT, Otis JC, Kenneally S: Motion of the hindfoot after simulated arthrodesis. J Bone Joint Surg 79-A:241-245, 1997. 25. Thordarson DB, Schmotzer H, Chan J, Peters J: Dynamic support of the human longitudinal arch. Clin Orthop 316:165-172, 1995. 26. Sangerozan BJ, Mosca V, Hansen ST: Effect of calcaneal lengthening on relationships among hindfoot, midfoot, and forefoot. Foot and Ankle 14:136, 1993. 27. Cooper PS, Nowak MD, Shaer J: Calcaneo-cuboid joint pressures with lateral column lengthening (Evans) procedure. Foot and Ankle 18: 200, 1997. 28. Deland JT, Otis JC, Kyung-Tai L, Kenneally SM: Lateral column lengthening with calcaneo-cuboid fusion: Range of motion in the triple joint complex. Foot and Ankle 16: 729, 1995. 29. Myerson MS, Corrigan J, Thompson F: Tendon transfer combined with calcaneal osteotomy for treatment of posterior tibial tendon insufficiency: A radiologic investigation. Foot and Ankle 16:712, 1995. 30. Deland JT, Anoczky SP, Thompson FM: Adult acquired forefoot deformity at the talonavicular joint: Reconstruction of the spring ligament in an in vitro model. Foot and Ankle 13:327, 1992. 31. Pomeroy GC, Manolis A: A new operative approach for forefoot secondary to posterior tibial tendon insufficiency: A preliminary report. Foot and Ankle 18:206, 1997. 32. Harper MC, Tisdel CL: Talonavicular arthrodesis for the painful adult acquired forefoot. Foot and Ankle 17:658, 1996. 33. Kitaoka HB, Zong Ping L, Kai-Nan A: Effect of the posteiror tibial tendon on the arch of the foot during simulated weightbearing: Biomechanical analysis. Foot and Ankle 18:43, 1997. 34. Hintermann B, Nigg BN, Sommer C: Foot movement and tendon excursion: An in vitro study. Foot and Ankle 15: 386, 1994.