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Posterior Tibial Tendon Dysfunction

Table of Contents

1. Biomechanical and Clinical Factors Related to Stage I Pages 776 - 784

Posterior Tibial Tendo Dysfunction

2. Foot Kinematics During a Bilateral Heel Rise Test in Pages 593 – 603

Participants with Stage II Posterior Tibial Tendon Dysfunction

776 | october 2011 | volume 41 | number 10 | journal of orthopaedic & sports physical therapy

[ research report ]

Posterior tibial tendon dysfunction (PTTD) is a progressive and debilitating condition that is estimated to affect nearly 5 million people in the United States.7 In the early stages (stage I) of the condition, PTTD is a common running-related injury.31

While the aetiology of PTTD has not been established, it is considered multifactorial in nature and has generally been related to progressive alterations in arch structure, muscular strength, and gait biomechanics.

Few studies have been conducted to understand how arch structure may play a role in the progressive nature of PTTD.4,15,24 Williams et al36 conducted a

TT STUDY DESIGN: Case control.

TT OBJECTIVES: To investigate differences in arch height, ankle muscle strength, and biomechani-cal factors in individuals with stage I posterior tibial tendon dysfunction (PTTD) in comparison to healthy individuals.

TT BACKGROUND: PTTD is a progressive condition, so early recognition and treatment are essential to help delay or reverse the progression. However, no previous studies have investigated stage I PTTD, and no single study has measured static anatomi-cal structure, muscle strength, and gait mechanics in this population.

TT METHODS: Twelve individuals with stage I PTTD and 12 healthy, age- and gender-matched control subjects, who were engaged in running-related activities, participated in this study. Measure-ments of arch height index, maximum voluntary ankle invertor muscle strength, and 3-dimensional rearfoot and medial longitudinal arch kinematics

during walking were obtained.

TT RESULTS: The runners with PTTD demonstrated significantly lower seated arch height index (P = .02) and greater (P = .03) and prolonged (P = .05) peak rearfoot eversion angle during gait, compared to the healthy runners. No differences were found in standing arch height index values (P = .28), arch rigidity index (P = .06), ankle invertor strength (P = .49), or peak medial longitudinal arch values (P = .49) between groups.

TT CONCLUSION: The increased foot pronation is hypothesized to place greater strain on the pos-terior tibialis muscle, which may partially explain the progressive nature of this condition. J Orthop Sports Phys Ther 2011;41(10):776-784, Epub 12 July 2011. doi:10.2519/jospt.2011.3545

TT KEY WORDS: foot kinematics, gait, tendinopathy

1Research Associate, Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada. 2Postdoctoral Fellow, Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada. 3Clinical Assistant Professor, Division of Podiatric Surgery, University of Calgary, Calgary, Alberta, Canada; Adjunct Assistant Professor, Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada. 4Associate Professor, Faculties of Kinesiology and Nursing, University of Calgary, Calgary, Alberta, Canada; Director, Running Injury Clinic, Calgary, Alberta, Canada. This study received ethical approval from the Conjoint Health Research Ethics Board of the University of Calgary. Address correspondence to Dr Reed Ferber, Faculty of Kinesiology, 2500 University Drive NW, University of Calgary, Calgary, Alberta, Canada T2N 1N4. E-mail: [email protected]

MELISSA RABBITO, MSc, CPedC1 • MICHAEL B. POHL, PhD2 • NEIL HUMBLE, DPM3 • REED FERBER, PhD, CAT(C)4

Biomechanical and Clinical Factors Related to Stage I Posterior

Tibial Tendon Dysfunction

retrospective analysis of running inju-ries in runners with high and low plan-tar arch and reported that the low-arch group had a 3-fold higher incidence of

stage I PTTD compared to the high-arch group. Dyal et al4 also reported that a lower arch height was associated with the symptomatic PTTD foot compared to the uninvolved foot. In contrast, Shibuya et al30 reported that radiographic and MRI scans of patients with PTTD at various stages showed damage to the spring ligament, with a lower arch height only present in patients with stages III and IV PTTD. Thus reduced arch height may be a predisposing factor related to stages III and IV PTTD, while a more typical arch height would be expected in stage I PTTD. Moreover, stage I PTTD is char-acterized by tendon inflammation, with no change in foot shape, while stage II PTTD is characterized by the tendon’s elongation and dysfunction, as the foot develops adult acquired flatfoot disor-der.13 Thus it can be hypothesized that no differences in arch shape would be expected for patients with stage I PTTD, and, consequently, other factors, such as reduced ankle muscle strength, should be considered.

There is a paucity of research regard-ing differences in ankle invertor muscle strength for individuals with PTTD. Alva-rez et al1 reported significant concentric and eccentric ankle invertor strength re-ductions for the involved compared to the uninvolved ankle. Following a 10-week

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journal of orthopaedic & sports physical therapy | volume 41 | number 10 | october 2011 | 777

strengthening program, the PTTD group exhibited a 58% increase in strength, concomitant with significant reductions in pain. Houck et al8 also reported that patients with PTTD exhibited 30% re-duced ankle invertor strength compared to age-matched controls. However, while these 2 studies indicate that ankle in-vertor strength may be associated with PTTD, the individuals with PTTD in the aforementioned studies were at stages II to IV of the condition, and no study has investigated individuals with stage I PTTD for potential differences in ankle invertor strength. Because stage I PTTD involves mild swelling to the tendon and pain upon palpation, it is reasonable to hypothesize that reduced force output would be present in these individuals.

Few studies have investigated dif-ferences in gait biomechanics for indi-viduals with PTTD. Ness et al23 reported increased rearfoot eversion throughout stance in patient with PTTD compared to controls; however, all their study’s pa-tients with PTTD had failed conservative treatment and were scheduled for opera-tive intervention. Tome et al32 also report-ed that individuals with stage II PTTD demonstrated significantly greater peak rearfoot eversion and a lower medial lon-gitudinal arch (MLA) angle during walk-ing. Finally, Houck et al9 investigated patients with stage II PTTD and reported increased rearfoot eversion compared to controls. Thus, increased rearfoot ever-sion is present in individuals with stages II to IV PTTD when walking; however, no studies have investigated whether increased rearfoot eversion is present in stage I of the condition. Because PTTD is a progressive condition, identifying if potentially contributing factors related to static foot structure, ankle invertor muscle strength, and gait biomechan-ics may be present in individuals with stage I PTTD could lead to interventions aimed at early detection and prevention of PTTD progression.

The purpose of this study was to in-vestigate differences in arch height, ankle muscle strength, and kinematic factors in

individuals presenting with stage I PTTD in comparison to healthy individuals. Compared to the control group, we hy-pothesized that the PTTD group would demonstrate (1) no differences in static arch height, (2) decreased ankle inver-tor muscle strength, and (3) greater and prolonged peak rearfoot eversion and lower peak MLA during the stance phase of walking.

METHODS

Subjects

Subjects were recruited through the Running Injury Clinic at the University of Calgary and

various sports medicine clinics, includ-ing local practitioners such as pedor-thists, podiatrists, and medical doctors. All subjects were actively involved in running and running-related sports and provided informed, written consent. The study protocol was approved by the Con-joint Health Research Ethics Board of the University of Calgary.

A Canadian certified athletic thera-pist, who is also a Canadian certified pedorthist, screened potential subjects through a clinical assessment that in-cluded a detailed history, differential diagnosis for other tendinopathies and musculoskeletal injuries, muscle strength testing, and manual palpations. Several steps were taken to differentiate between individuals with stages I and II PTTD. Typically, individuals with stage I PTTD exhibit signs of tendinopathy without postural changes in the foot, whereas those with stage II PTTD exhibit tendon

elongation, acquired flatfoot deformity, and fixed rearfoot deformities.13 More-over, with stage I PTTD, individuals gen-erally exhibit pain superior and posterior to the medial malleolus, whereas those with stage II PTTD exhibit pain near the distal insertions of the tendon. Thus a clinical examination of passive rearfoot eversion and midfoot mobility was con-ducted and location of pain was evalu-ated to initially screen potential subjects. Once selected, potential subjects were screened according to specific inclusion and exclusion criteria.11,13,14

Each subject was required to meet the following inclusion criteria to qualify for the PTTD group: (1) mild swelling and/or tenderness posterior to the medial mal-leolus, (2) pain posterior and/or superior to the medial malleolus, aggravated by recreational activity, (3) pain that had been present for at least 3 weeks, and (4) participation in recreational running or walking a minimum of 3 times per week and 30 minutes per session. Subjects were excluded from the PTTD group if they met any of the following exclusion criteria: (1) previous surgery on the af-fected foot, leg, or knee; (2) osteoarthritis in the knee of the affected side; (3) fixed rearfoot deformities; (4) recurrent ankle sprains on the affected side; (5) ligament tears or boney abnormalities of the af-fected foot; (6) a physical or medical condition that contraindicated the test-ing protocol; (7) pregnancy; or (8) flexor hallucis longus or flexor digitorum longus tendinopathy.

In total, 15 individuals with PTTD presented for consideration, 3 of which

TABLE 1 Demographic Data

Abbreviations: BMI, body mass index; PTTD, posterior tibial tendon dysfunction.*Values are mean SD unless otherwise specified.

PTTD (n = 12) Control (n = 12) P Value

Age, y 30.3 7.9 28.5 8.6 .30

Weight, kg 65.7 11.5 68.9 12.8 .26

Height, cm 168.2 10.8 170.1 7.8 .32

BMI, kg/m2 23.2 3.4 23.7 2.8 .37

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[ research report ]

were excluded from the study, 1 due to incorrect location of pain (presentation of lateral ankle pain), another who met all the inclusion criteria but whose data were deemed unusable after processing, and a third due to multiple confound-ing injuries, including plantar fasciitis and metatarsalgia. Based on a 0-to-10 visual analog scale, with 0 representing no pain and 10 extreme pain, the PTTD group reported an average pain score of 5 during running activity and 3.5 during activities of daily living. The visual analog scale has been established as a reliable and valid measure of self-reported pain.29 No individuals with stage II PTTD were screened, most likely because the sample was recruited primarily from sports med-icine clinics, which typically see patients involved in recreational sports that de-mand a level of activity limited by stage II PTTD.11,13,14

Control subjects (9 females and 3 males) were matched to individuals with PTTD (9 females and 3 males), based on age, gender, and body mass index (BMI), and screened by the same exclusion cri-teria as those used to screen the PTTD group. There were no statistical differ-ences between groups for the variables listed in TABLE 1 and other demographic variables.

StructureArch height index (AHI) was measured using a custom-built arch height index measurement system2 (FIGURE 1). Two boards were placed under the foot, 1

under the calcaneus and 1 under the forefoot, to allow the midfoot to achieve maximum deformation. AHI was defined as the ratio of dorsum height at 50% of total foot length, divided by the foot length from the back of the heel to the head of the first metatarsal (truncated foot length).35 Seated AHI was obtained with the subject seated, hips and knees flexed to 90°, and approximately 10% of total body weight on the foot. Standing AHI was obtained with the subject stand-ing, with equal weight on both feet. Arch rigidity index (ARI) is defined as the ratio of standing AHI divided by seated AHI.27 AHI and ARI were deemed appropriate measurements of static foot structure, as their reliability has been previously demonstrated.2,35

Additionally, and to better understand the anatomical structure of the foot, go-niometric measurement of passive rear-foot range of motion was obtained. With the subjects in a prone position, the calcaneus was passively and maximally everted by the therapist (FIGURE 2). The mean SD passive and maximal rearfoot eversion for the subjects with PTTD was 6.5° 3.1° and 4.8° 2.0°, respectively. Pilot testing was conducted on 7 control subjects, and the test-retest reliability for the measurement of passive rearfoot eversion was r = 0.94.

StrengthTo assess the strength of the ankle inver-tor muscles, the subjects were seated on the ground, with their knee fully extend-ed and their foot in a plantar-flexed and inverted position (FIGURE 3). They were instructed to use only their ankle inver-tor muscles to produce a force against the stationary force dynamometer (Lafayette Instruments, Lafayette, IN). During the contraction, the investigator palpated the tibialis anterior tendon to ensure that this muscle was not being recruited. The movements of subtalar inversion and forefoot adduction were based on strength testing, as described by Kend-all et al,12 to best isolate the ankle inver-tor muscles. Four trials of ankle invertor maximum voluntary isometric contrac-tion were collected and the average of these 4 trials was recorded. Force mea-surements from the dynamometer were normalized to body mass.10 Pilot testing, using the aforementioned 7 control sub-jects, indicated a test-retest reliability for ankle invertor strength of r = 0.86.

BiomechanicsThree-dimensional walking data were collected using an 8-camera motion analysis system (Vicon Motion Systems Ltd, Oxford, UK). All subjects were bare-foot and fitted with 9-mm retroreflec-tive markers, adhered to the skin at the anatomical landmarks of the tibia, fibula, and foot (FIGURE 4). A standing calibra-tion of 1 second was obtained with the feet 0.30 m apart and pointing directly forward. Following the standing calibra-

FIGURE 1. Arch height index measurement system. (A) Adjustable sliders were used to measure total foot length, (B) truncated foot length, (C) and dorsal height at 50% of total foot length.

FIGURE 2. Measurement of maximal passive rearfoot eversion range of motion.

FIGURE 3. Strength testing of the tibialis posterior muscle using a strap and dynamometer.

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tion, the subjects were provided a 1-min-ute warm-up walk on the treadmill at 1.2 m/s–1. Following the familiarization peri-od, marker trajectory data were captured at a rate of 120 Hz.

Ten continuous footfalls of the walk-ing trial were selected for analysis. Raw marker trajectory data were filtered us-ing a fourth-order low-pass Butterworth filter at 12 Hz. Anatomical coordinate systems were created for the shank and rearfoot using Visual 3D software (C-Motion Inc, Germantown, MD). Only the stance phase of gait was analyzed, and all kinematic data were normalized to 100 data points. Stance phase was defined as initial heel contact to toe-off and these events were identified using the veloci-ties of the superior calcaneal and hallux markers.38

Cardan angles were used to calculate 3-dimensional angles for the rearfoot and shank. Rearfoot eversion was expressed as frontal plane motion relative the shank segment. The MLA was calculated in a manner similar to the method used by Tome et al.32 The MLA was defined as the angle subtended by 2 lines, one from the marker on the medial aspect of the calcaneus (MCAL) to the navicular tuber-osity and the other from the head of the first metatarsal (D1MT) to the navicular

tuberosity (FIGURE 5).Custom LabVIEW software (National

Instruments Corp, Austin, TX) was used to calculate discrete kinematic variables of interest, which included peak rearfoot eversion, peak MLA, and the time of peak rearfoot eversion.

Statistical AnalysisAn a priori power analysis was conducted using kinematic rearfoot data previously published.23,32 Individuals with stage II PTTD, compared to healthy controls, had a significant difference in rearfoot ever-sion angle (PTTD, 10.4° 4.5°; control, 5.4° 3.6°). Using these values, the fol-lowing calculation was used to estimate the required number of subjects to ade-quately power this study: n = [2 SD2 (Za + Zb)

2]/2, where SD is the pooled standard deviation, Za is the z score of alpha (.05), Zb is the z score of beta (.80), and is the dif-

ference between the 2 means.33 Applying this calculation gives an estimation of 10 subjects per group, with a statistical signif-icance of 0.05. Thus 12 subjects per group was considered appropriate for the study.

The following biomechanical variables obtained during walking were compared between the PTTD and control groups: (1) peak rearfoot eversion, (2) eversion excursion, (3) time to peak rearfoot ever-sion, and (4) peak MLA. The following anatomical and strength variables were compared between groups: (1) seated AHI, (2) standing AHI, (3) ARI, (4) pas-sive rearfoot eversion range of motion, and (5) ankle invertor strength. Because the biomechanical and strength vari-ables were associated with directional hypotheses, independent 1-tailed t tests were employed. Because no differences in static arch height were hypothesized, in-dependent 2-tailed t tests were employed. All comparisons were conducted using an alpha of .05, in SPSS, Version 17 (IBM Corporation, Armonk, NY) software.

RESULTS

Structure

The PTTD group demonstrated significantly lower seated AHI (PTTD, 0.36 0.01; control, 0.38

FIGURE 4. (A) Posterior and (B) medial view of marker placement. The markers at the tibial tuberosity and head of the fibula are not pictured. Abbreviations: BLSH, bottom lateral shank; BMSH, bottom medial shank; D1MT, distal first metatarsal head; HLX, hallux; ICAL, inferior calcaneus; LCAL, lateral calcaneus; MCAL, medial calcaneus; MMAL, medial malleolus; NAV, navicular tuberosity; SCAL, superior calcaneus; SUST, sustentaculum tali; TLSH, top lateral shank; TMSH, top medial shank.

FIGURE 5. Medial longitudinal arch angle calculation.

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[ research report ]

0.02; P = .02), no significant differenc-es in standing AHI (PTTD, 0.34 0.01; control, 0.35 0.02; P = .28), and no differences in ARI (PTTD, 0.92 0.02; control, 0.90 0.04; P = .06) values, as compared to healthy controls (TABLE 2).

StrengthThere was no difference in ankle invertor strength between the 2 groups (PTTD, 1.00 0.41 N/kg; control, 0.99 0.35 N/kg; P = .49).

BiomechanicsThe PTTD group exhibited significantly greater rearfoot eversion (6.0° 4.6°; P = 0.03) compared to controls (2.9° 2.6°) and significantly greater time to peak eversion (45.8% 8.1%; P = .05) com-pared to controls (38.1% 12.9%) (TABLE

3, FIGURE 6). There were no between-group differences in rearfoot eversion excursion (PTTD, 6.6° 2.9°; control, 5.9° 1.5°; P = .24) or peak MLA (PTTD, 12.5° 8.0°; control, 13.0° 9.4°; P = .49) (TABLE

3, FIGURE 7).FIGURE 6 shows the PTTD rearfoot in-

version/eversion curve to be in a more everted position throughout the stance phase of gait as compared to that of the control group. Therefore, to better un-derstand the significantly greater peak eversion between groups, we conducted a post hoc analysis of rearfoot angle at heel strike and found that the PTTD group landed in significantly less inver-sion (0.1° 2.5°; P = .01) compared to controls (3.9° 2.7°). In addition, there was a significant positive correlation be-tween rearfoot angle at heel strike and peak rearfoot eversion angle for both the PTTD (r = 0.81; P = .02) and control (r = 0.86; P = .01) groups.

DISCUSSION

The purpose of this study was to investigate differences in arch height, ankle muscle strength, and

biomechanical factors in patients with stage I PTTD in comparison to healthy individuals. While PTTD is considered a progressive condition, most studies 8-10,24,32 have focused on stage II of the

condition in subjects who were predomi-nately overweight and relatively seden-tary women, as opposed to patients with stage I PTTD who were generally young-er and active. To our knowledge, no study has investigated these factors for stage I PTTD.

The PTTD group demonstrated a lower arch height in a seated position but no differences in standing AHI mea-surements or ARI, compared to controls. Because the differences in seated AHI were minimal and no other structural dif-ferences were measured between PTTD and controls, these findings support our hypothesis and indicate that there were no differences in static foot measures be-tween groups. Moreover, the AHI values for both the PTTD and control groups fall within the normative SD value of 0.34 0.03 for a group of 100 rec-reational runners reported by Butler et al,2 suggesting overall typical static arch height measures.

Shibuya et al30 also reported no dif-ferences in talar declination angle, or Meary’s angle, between individuals with stage I PTTD and healthy controls, as measured using radiographs. However, these authors did not measure AHI, so comparisons are difficult. Both Neville et al24 and Houck et al8-10 measured AHI in individuals with stage II PTTD and found significantly lower values than in healthy controls. Therefore, the results of the current study suggest that arch structure, while perhaps not a contribut-ing factor in stage I PTTD, may be more apparent in later stages of the condition.

In contrast to our hypothesis, there were no differences in ankle invertor strength between the 2 groups. These results are in contrast to the findings of Alvarez et al1 and Houck et al,10 who re-ported that individuals with PTTD exhib-ited significantly reduced ankle invertor strength compared to healthy controls. However, these authors investigated per-sons with a mean age of 50 and 61 years, respectively. Our subjects were classified as having stage I PTTD, were 30 years old on average, and were regularly ac-

TABLE 2 Static and Strength Measurements*

Abbreviations: AIS, ankle inverter strength; AHI, arch height index; ARI, arch rigidity index; PTTD, posterior tibial tendon dysfunction.*Values are mean SD unless otherwise specified.


AHI seated 0.36 0.01 0.38 0.02 .02

AHI standing 0.34 0.01 0.35 0.02 .28

ARI 0.92 0.02 0.90 0.04 .06

AIS, N/kg 1.00 0.41 0.99 0.35 .49

TABLE 3 Biomechanical Variables*

Abbreviations: MLA, medial longitudinal arch; PTTD, posterior tibial tendon dysfunction.*Values are mean SD unless otherwise specified.


Peak eversion, deg 6.0 4.6 2.9 2.6 .03

Eversion excursion, deg 6.6 2.9 5.9 1.5 .24

Time to peak eversion, percent stance 45.8 8.1 38.1 12.9 .05

Peak MLA, deg 12.5 8.0 13.0 9.4 .49

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tive in either running, exercise walking, or running-based sports for a minimum of 30 minutes per day, 3 times per week. Thus the similarities in ankle invertor muscle strength between the PTTD and controls in the current study seem rea-sonable, considering that both groups were involved in regular physical activ-ity and those with PTTD exhibited only minor swelling and pain to the posterior tibialis region.

In support of our hypothesis, the PTTD group exhibited greater peak eversion while walking, compared to the control subjects, which is similar to the findings of previous studies involv-ing stages II to IV PTTD.9,23,28,32 More-over, those with PTTD demonstrated approximately 4° less inversion at heel strike compared to controls, and a sig-nificant positive association was found between rearfoot angle at heel strike and peak rearfoot eversion angle. These data suggest that the PTTD group exhibit al-tered rearfoot kinematics throughout the entire stance phase of gait. It is possible that greater rearfoot eversion is associat-ed with early identification of the PTTD; however, prospective studies are neces-sary to answer this question.

Interestingly, when calculated with respect to the amount of passive maxi-mal rearfoot eversion, the PTTD group utilized 92% of their available rearfoot range of motion, reaching a peak ever-sion value of 6° out of 6.5° of available range of motion. In contrast, the control group used only 60% of their available eversion range of motion, reaching 2.9° out of a possible 4.8°. These results are similar to those reported by Youberg et al,37 in which healthy subjects used 68.1% of their available passive rearfoot eversion range of motion while walking. Thus the results of the current study sug-gest that individuals with stage I PTTD exhibit atypical and excessive pronation mechanics. While speculative, these data also suggest that they may be at risk for ligamentous damage, which is consistent with the progressive nature of PTTD.

Although both groups reached the

peak eversion in the first half of stance, the PTTD group reached peak eversion at 45.8% of the stance phase as compared to 38.1% of stance for the control group. These findings are in contrast to the data by Tome et al,32 who reported that indi-viduals with PTTD reached peak eversion earlier in the stance phase compared to controls. Thus, we postulate that the in-creased rearfoot eversion measured in the present study places greater strain on the posterior tibialis muscle, which may partially explain the progressive na-ture of this condition. While no strength deficits were found in the PTTD group, other elements of muscle control, such as improper activation timing,6,21,22 lack of eccentric control,17,18,25,26 and atypical fiber recruitment,16 may contribute to the altered rearfoot eversion. Future re-search is necessary to better understand the interrelationship of muscle function and biomechanical movement patterns.

Because the posterior tibialis muscle is a major invertor and stabilizer of the MLA, we also expected a greater MLA value (lower arch) in those with PTTD

while walking. However, no differences in MLA angle between the groups were measured, which is consistent with the finding of no difference in standing AHI between groups and no differences in strength. These results are in contrast to those of Tome et al,32 who measured the difference between standing MLA, normalized to subtalar neutral position, as compared to the peak MLA value in gait. Because we did not obtain MLA values in a subtalar neutral position, we are not able to directly compare our re-sults to those of Tome et al.32 In addition, the present study was limited, in that the vertical height of the medial calcaneal marker from the plantar surface was not standardized, which might have masked between-group differences.

The biomechanical results of the cur-rent study provide support for PTTD be-ing a progressive condition. For example, the stage I PTTD group exhibited a 3.1° increase in rearfoot eversion compared to controls, whereas Tome et al32 reported that patients with stage II PTTD dem-onstrated a 6.2° increase compared to

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FIGURE 6. Representative rearfoot eversion patterns for posterior tibial tendon dysfunction (orange) and controls (blue, shaded area is standard deviation) during the stance phase of gait. Positive values indicate rearfoot inversion, negative values eversion.

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[ research report ]

controls. Moreover, while discrete values were not reported, Ness et al23 provided data showing that an approximately 10° increase in rearfoot eversion throughout the stance phase of gait could be ob-served in individuals with stage II PTTD compared to controls. Thus, increases in frontal plane rearfoot kinematics appear to be associated with PTTD severity. In-terestingly, a strong positive association was found between rearfoot angle at heel strike and peak rearfoot angle in the cur-rent study. Ness et al23 reported a similar eversion offset throughout stance. These results suggest that individuals with PTTD exhibit altered rearfoot kinemat-ics throughout the stance phase of gait, regardless of stage I or II of the condition. Moreover, the lack of differences in MLA between groups for the present study and a reported 8° change in MLA for stage II PTTD32 suggest that stage I PTTD may not involve midfoot or forefoot changes in walking kinematics, whereas these factors may be apparent in stage II and beyond.5,7,34 Thus, PTTD progression may

be best understood by rearfoot kinematic measures during stage I, whereas altered midfoot and forefoot kinematics may play a role in stage II and beyond.19,20 Fi-nally, the results of the current study also suggest that patients with stage I PTTD exhibit similar arch structure and ankle invertor strength as compared to healthy controls and that these variables may not be associated with early identification of the condition.5,34 In contrast, individuals in the more severe stages of the PTTD progression generally exhibit marked dif-ferences in arch height, strength, and gait kinematics.20,24

Several limitations are acknowledged. First, this study did not include the clas-sically defined PTTD demographic of sedentary women over the age of 40, who are diabetic or obese.13,14 However, the use of a younger, more active popu-lation is supported by previous research demonstrating PTTD that is a common injury among runners.31,36 It is also pos-sible that stage I PTTD is distinct and only associated with tendon overload

due to the altered rearfoot mechanics re-ported in the current study. In contrast, tendon overload in stages II to IV PTTD may be associated with other factors, such as obesity, altered MLA and rear-foot mechanics, as well as neuromotor and muscular strength deficits. Second, due to the placement of markers directly on the skin, participants had to under-go the biomechanical analysis barefoot, and foot kinematics have been shown to be different between barefoot and shod gait.3 Third, the examiner responsible for determining inclusion/exclusion cri-teria, data collection, and analysis of the data was not blinded to group allocation. However, a different clinician initially screened all patients over the phone, and all subjects were assigned a research number to blind the examiner during statistical analysis and to help minimize potential bias. As well, the present inves-tigation was designed as a case control study; yet we sought to theorize about the interrelationships between variables. In addition, we powered the study based only on potential differences in rearfoot eversion. Thus future research, involving multiple covariates, with a sample size calculated considering a variance inflator factor, is necessary to better understand the multifactorial nature of biomechani-cal, strength, and structural factors for patients with PTTD.

CONCLUSION

The results of the current study suggest that runners with stage I PTTD are likely to present with nor-

mal inversion ankle muscle strength, sig-nificant differences in rearfoot pronation during walking gait, and no differences in foot posture as compared to healthy controls. The increased foot pronation is hypothesized to place greater strain on the posterior tibialis muscle, which may partially explain the progressive nature of this condition. Future investigations should be directed towards assessing the effects of rehabilitation programs for in-dividuals in the early stages, to shed light

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FIGURE 7. Representative medial longitudinal arch (MLA) patterns for posterior tibial tendon dysfunction (orange) and controls (blue, shaded area is standard deviation) during the stance phase of gait. Values closer to 0 indicate arch deformation.

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on the clinical and biomechanical factors that can be altered to prevent PTTD pro-gression. t

KEY POINTSFINDINGS: Runners with stage I PTTD exhibited significant differences in rearfoot pronation during walking gait, along with normal inversion ankle muscle strength and foot posture, as compared to healthy controls.IMPLICATION: The increased foot prona-tion is hypothesized to place greater strain on the posterior tibialis muscle, which may partially explain the progres-sive nature of this condition.CAUTION: This study involved a group of healthy runners that does not repre-sent the classic PTTD demographic of middle-aged, sedentary women with diabetes and obesity, which are often identified as primary risk factors.

ACKNOWLEDGEMENTS: This work was support-ed in part by research grants from the Alberta Innovates: Health Solutions and the Olympic Oval High Performance Fund at the Uni-versity of Calgary, and through a charitable donation from SOLE Inc.

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2. Butler RJ, Hillstrom H, Song J, Richards CJ, Davis IS. Arch height index measurement system: establishment of reliability and normative values. J Am Podiatr Med Assoc. 2008;98:102-106.

3. De Wit B. Biomechanical analysis of the stance phase during barefoot and shod running. J Biomech. 2000;33:269-278.

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8. Houck JR, Neville C, Tome J, Flemister AS. Foot kinematics during a bilateral heel rise test in participants with stage II posterior tibial ten-don dysfunction. J Orthop Sports Phys Ther. 2009;39:593-603. http://dx.doi.org/10.2519/jospt.2009.3040

9. Houck JR, Neville CG, Tome J, Flemister AS. Ankle and foot kinematics associated with stage II PTTD during stance. Foot Ankle Int. 2009;30:530-539. http://dx.doi.org/10.3113/FAI.2009.0530

10. Houck JR, Nomides C, Neville CG, Samuel Flemister A. The effect of Stage II posterior tibial tendon dysfunction on deep compart-ment muscle strength: a new strength test. Foot Ankle Int. 2008;29:895-902. http://dx.doi.org/10.3113/FAI.2008.0895

11. Johnson KA, Strom DE. Tibialis posterior tendon dysfunction. Clin Orthop Relat Res. 1989;196-206.

12. Kendall FP, McCreary EK, Provance PG, Rodgers MM, Romani WA. Muscles: Testing and Function with Posture and Pain. 5th ed. Baltimore, MD: Lippincott, Williams, & Wilkins; 2005.

13. Kohls-Gatzoulis J, Angel JC, Singh D, Haddad F, Livingstone J, Berry G. Tibialis posterior dysfunction: a common and treatable cause of adult acquired flatfoot. BMJ. 2004;329:1328-1333. http://dx.doi.org/10.1136/bmj.329.7478.1328

14. Kohls-Gatzoulis J, Woods B, Angel JC, Singh D. The prevalence of symptomatic posterior tibialis tendon dysfunction in women over the age of 40 in England. Foot Ankle Surg. 2009;15:75-81. http://dx.doi.org/10.1016/j.fas.2008.08.003

15. Kong A, Van Der Vliet A. Imaging of tibialis pos-terior dysfunction. Br J Radiol. 2008;81:826-836. http://dx.doi.org/10.1259/bjr/78613086

16. Kulig K, Burnfield JM, Requejo SM, Sperry M, Terk M. Selective activation of tibialis posterior: evaluation by magnetic resonance imaging. Med Sci Sports Exerc. 2004;36:862-867.

17. Kulig K, Lederhaus ES, Reischl S, Arya S, Bash-ford G. Effect of eccentric exercise program for early tibialis posterior tendinopathy. Foot Ankle Int. 2009;30:877-885. http://dx.doi.org/10.3113/FAI.2009.0877

18. Kulig K, Reischl SF, Pomrantz AB, et al. Non-surgical management of posterior tibial tendon dysfunction with orthoses and resistive exer-cise: a randomized controlled trial. Phys Ther. 2009;89:26-37. http://dx.doi.org/10.2522/ptj.20070242

19. Michaud T. Foot Orthoses and Other Forms of Conservative Foot Care. Philadelphia, PA: Lip-pincott Williams & Wilkins; 1997.

20. Mosier SM, Pomeroy G, Manoli A, 2nd. Patho-anatomy and etiology of posterior tibial tendon dysfunction. Clin Orthop Relat Res. 1999;12-22.

21. Murley GS, Buldt AK, Trump PJ, Wickham JB. Tibialis posterior EMG activity during barefoot walking in people with neutral foot posture. J Electromyogr Kinesiol. 2009;19:e69-77. http://dx.doi.org/10.1016/j.jelekin.2007.10.002

22. Murley GS, Menz HB, Landorf KB. Foot posture influences the electromyographic activity of selected lower limb muscles during gait. J Foot Ankle Res. 2009;2:35. http://dx.doi.org/10.1186/1757-1146-2-35

23. Ness ME, Long J, Marks R, Harris G. Foot and ankle kinematics in patients with poste-rior tibial tendon dysfunction. Gait Posture. 2008;27:331-339. http://dx.doi.org/10.1016/j.gaitpost.2007.04.014

24. Neville C, Flemister A, Tome J, Houck J. Comparison of changes in posterior tibialis muscle length between subjects with posterior tibial tendon dysfunction and healthy controls during walking. J Orthop Sports Phys Ther. 2007;37:661-669. http://dx.doi.org/10.2519/jospt.2007.2539

25. Pohl MB, Rabbito M, Ferber R. The role of tibi-alis posterior fatigue on foot kinematics during walking. J Foot Ankle Res. 2010;3:6. http://dx.doi.org/10.1186/1757-1146-3-6

26. Pomeroy GC, Pike RH, Beals TC, Manoli A, 2nd. Acquired flatfoot in adults due to dysfunction of the posterior tibial tendon. J Bone Joint Surg Am. 1999;81:1173-1182.

27. Richards CJ, Card K, Song J, Hillstrom H, Butler R, Davis IM. A novel arch height index measurement system (AHIMS): Intra- and inter-rater reliability. Toledo, OH: American Society of Biomechanics; 2003.

28. Ringleb SI, Kavros SJ, Kotajarvi BR, Hansen DK, Kitaoka HB, Kaufman KR. Changes in gait associated with acute stage II poste-rior tibial tendon dysfunction. Gait Posture. 2007;25:555-564. http://dx.doi.org/10.1016/j.gaitpost.2006.06.008

29. Scott J, Huskisson EC. Graphic representation of pain. Pain. 1976;2:175-184.

30. Shibuya N, Ramanujam CL, Garcia GM. As-sociation of tibialis posterior tendon pathol-ogy with other radiographic findings in the foot: a case-control study. J Foot Ankle Surg. 2008;47:546-553. http://dx.doi.org/10.1053/j.jfas.2008.08.010

31. Taunton JE, Ryan MB, Clement DB, McKenzie DC, Lloyd-Smith DR, Zumbo BD. A retrospec-tive case-control analysis of 2002 running injuries. Br J Sports Med. 2002;36:95-101.

32. Tome J, Nawoczenski DA, Flemister A, Houck J. Comparison of foot kinematics between subjects with posterior tibialis tendon dysfunc-tion and healthy controls. J Orthop Sports Phys Ther. 2006;36:635-644. http://dx.doi.org/10.2519/jospt.2006.2293

33. Vincent WJ. Statistics in Kinesiology. 2nd ed. Champaign, IL: Human Kinetics; 2009.

34. Wapner KL, Chao W. Nonoperative treatment of posterior tibial tendon dysfunction. Clin Orthop Relat Res. 1999;39-45.

35. Williams DS, McClay IS. Measurements used

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MORE INFORMATIONWWW.JOSPT.ORG@

to characterize the foot and the medial longi-tudinal arch: reliability and validity. Phys Ther. 2000;80:864-871.

36. Williams DS, 3rd, McClay IS, Hamill J. Arch structure and injury patterns in runners. Clin Biomech (Bristol, Avon). 2001;16:341-347.

37. Youberg LD, Cornwall MW, McPoil TG, Hannon

PR. The amount of rearfoot motion used during the stance phase of walking. J Am Podiatr Med Assoc. 2005;95:376-382.

38. Zeni JA, Jr., Richards JG, Higginson JS. Two simple methods for determining gait events during treadmill and overground walking using kinematic data. Gait Posture.

2008;27:710-714. http://dx.doi.org/10.1016/j.gaitpost.2007.07.007

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journal of orthopaedic & sports physical therapy | volume 39 | number 8 | august 2009 | 593

[ RESEARCH REPORT ]

abnormal kinematics during a heel risetask.41 The normal combined action of theposterior tibialis and triceps surae mus-

cles is thought to produce ankleplantar flexion with inversion dur-ing a heel rise task.15,23,33 Clinically, an

1Associate Professor, Ithaca College-Rochester Campus, Department of Physical Therapy, Center for Foot and Ankle Research, Rochester, NY. 2Assistant Professor, SUNY UpstateMedical Center, Department of Physical Therapy, Syracuse, NY. 3Associate Professor, Department of Orthopedic Surgery, University of Rochester Medical Center, Rochester, NY.The University of Rochester Research Subjects Review Board and The Ithaca College All College Review Board for Human Subjects Research approved the protocol for this study.The authors are grateful for support from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (grant 1R15ARO54507-01A1). Address correspondence to DrJeff Houck, Ithaca College, Rochester Campus, 1100 South Goodman Street, Rochester, NY 14620. E-mail: [email protected]

JEFF HOUCK, PT, PhD¹ PT, PhD² MS¹ MD³

Foot Kinematics During a Bilateral HeelRise Test in Participants With Stage IIPosterior Tibial Tendon Dysfunction

abnormal heel rise test is observed whenthe individual cannot perform a heel riseor performs the heel rise with hindfooteversion (fails to invert on rising), sug-gesting that the posterior tibialis mus-

cle no longer is acting to invert thehindfoot.22,29 Although there areanecdotal descriptions of abnor-mal kinematics of the foot in indi-

viduals with PTTD,22,29 there are noquantitative studies that examine foot

kinematics during a heel rise task.A variety of in vivo foot kinematic

methods have been proposed to measureabnormal movements in individualswith foot problems.18,27,31,37-39 For exam-ple, some have proposed measuring 3 of5 metatarsals of the forefoot separately,27

while others treat all the metatarsals as asingle forefoot segment.31,38 In vivo stud-ies of skin-mounted and bone-mountedmarkers define skin artifact errors andinfluence this segmentation. Errors intracking the movement of the calca-neus, representing the hindfoot, are low(average across a gait cycle, 2.6°),32

supporting the widespread use of thehindfoot relative to the tibia to measurehindfoot inversion/eversion and ankleplantar flexion/dorsiflexion.18,27,31,37-39

Measurements of forefoot motions varyconsiderably, depending on segmenta-tion.18,27,31,37-39 Measurements of the first

he heel rise test is used to assess foot and ankle muscle functionfor individuals with a wide spectrum of conditions, but, inparticular, foot conditions.4,9 Specifically, the heel rise test isrecommended for individuals with posterior tibial tendon

dysfunction (PTTD).30,34 Weakness of the posterior tibialis muscle isthought to contribute to the inability to perform a heel rise task or

Experimental laboratory studyusing a cross-sectional design.

To compare foot kinematics,using 3-dimensional tracking methods, during a bi-lateral heel rise between participants with posteriortibial tendon dysfunction (PTTD) and participantswith a normal medial longitudinal arch (MLA).

The bilateral heel rise test iscommonly used to assess patients with PTTD;however, information about foot kinematics duringthe test is lacking.

Forty-five individuals volunteeredto participate, including 30 patients diagnosedwith unilateral stage II PTTD (mean SD age,59.8 11.1 years; body mass index, 29.9 4.8 kg/m2) and 15 controls (mean SD age, 56.5 7.7years; body mass index, 30.6 3.6 kg/m2). Footkinematic data were collected during a bilateralheel rise task from the calcaneus (hindfoot), firstmetatarsal, and hallux, using an Optotrak motionanalysis system and Motion Monitor software. A2-way mixed-effects analysis of variance model,

with normalized heel height as a covariate, wasused to test for significant differences between thenormal MLA and PTTD groups.

The patients in the PTTD groupexhibited significantly greater ankle plantar flexion(mean difference between groups, 7.3°; 95%confidence interval [CI]: 5.1° to 9.5°), greater firstmetatarsal dorsiflexion (mean difference betweengroups, 9.0°; 95% CI: 3.7° to 14.4°), and less halluxdorsiflexion (mean difference, 6.7°; 95% CI: 1.7°to 11.8°) compared to controls. At peak heel rise,hindfoot inversion was similar (P = .130) betweenthe PTTD and control groups.

Except for hindfoot eversion/inversion, the differences in foot kinematics inparticipants with stage II PTTD, when compared tothe control group, mainly occur as an offset, notan alteration in shape, of the kinematic patterns.J Orthop Sports Phys Ther 2009;39(8):593-603.doi:10.2519/jospt.2009.3040

ankle, flat foot, medial longitudi-nal arch, posterior tibialis

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594 | august 2009 | volume 39 | number 8 | journal of orthopaedic & sports physical therapy

[ RESEARCH REPORT ]stance phase of walking, followed by ris-ing after 70%.19,31,39 This kinematic pat-tern was the same for the PTTD group.However, for the individuals with PTTD,this foot kinematic pattern occurredrelative to a lower MLA position.31,39

In contrast to the ligament and musclechanges noted above, other passive sup-porting structures, such as the plantarfascia, are typically less affected in indi-viduals with PTTD.1,8,12 Preservation ofthe plantar fascia in a pronated foot maybe important for the transfer of Achillestendon force to the metatarsal heads10,14

and raising the MLA during late stancethrough the windlass mechanism.19 Thelack of involvement of the plantar fasciain many patients with PTTD may explainwhy rising of the MLA during late stancewas preserved even in participants withseverely abnormal foot posture.18,31,39

During a heel rise task, the foot kine-matics associated with PTTD may takeadvantage of similar mechanisms.

Theoretically, the inability to performa heel rise test may occur from failure tostabilize the midfoot, resulting in a flex-ible foot or lever during the test. Lesshindfoot inversion may lead to less bonystability in the midfoot,2 contributing todorsiflexion of the first metatarsal relativeto the hindfoot. Posterior tibialis muscleweakness may lead to decreased hindfootinversion and the inability to heel rise, orhindfoot eversion during the heel rise.16,41

This has led to the current clinical rec-ommendations to focus on the presenceof hindfoot eversion at peak heel rise asa sign of advancing PTTD.22,29 However,abnormal MLA lowering reflected by firstmetatarsal dorsiflexion may be equallyimportant as a clinical sign. Currently, nodefined variables from the forefoot havebeen identified for use clinically whenevaluating a heel rise task. A current clin-ical guideline26 suggests that both unilat-eral and bilateral heel rise tests be usedin individuals with PTTD; however, theinterpretation focuses on the presence ofhindfoot eversion not midfoot stability.A description of in vivo foot kinematicsprovides a basis for understanding foot

movement during a heel rise test and thepotential for development of more de-fined clinical criteria for both the forefootand hindfoot.

The purpose of this study was to com-pare foot kinematics of the hindfoot, firstmetatarsal, and hallux in patients withstage II PTTD (PTTD group), comparedto individuals with a normal MLA height(control group). The primary hypothesiswas that participants with stage II PTTDwould demonstrate greater hindfootplantar flexion, hindfoot eversion, andfirst metatarsal dorsiflexion, comparedto those in the control group, duringthe heel rise task. Hallux dorsiflexionwas expected to be lower in participantswith stage II PTTD compared to thosein the control group. The secondary hy-pothesis was that the range of movement(ROM) from standing to peak heel rise,measured using 3-dimensional motionanalysis techniques, would not differ be-tween patients with stage II PTTD andthose in the control group. Previous stud-ies noted that the kinematic patterns overthe stance phase of walking for individu-als with PTTD were essentially similarto those in control subjects (eg, normalarch rising/lowering, normal hindfooteversion/inversion), but offset towarda pronated foot posture. Therefore, theROM, during the heel rise task, was ex-pected to be similar for each kinematicvariable between the participants withPTTD and controls.

total of 30 participants with

stage II PTTD and 15 controls vol-unteered for this study. Participants

with unilateral PTTD were referred by anorthopaedic surgeon and were clinicallyclassified as stage II. The stage II PTTDclassification required participants tohave 1 or more signs related to PTTD,including (1) tenderness to palpation ofthe posterior tibial tendon, (2) swellingof the posterior tibial tendon sheath, and(3) pain during single-limb heel rise. In

metatarsal have the advantage of beingsensitive to changes in the height of themedial longitudinal arch (MLA).17,39 Fur-ther, an in vitro study estimated low (lessthan 2.3°) bone-tracking errors spe-cific to the first metatarsal.40 Trackingfirst metatarsal relative to the hindfootsegment, while not providing specificinformation about joint movement (eg,talonavicular or calcaneocuboid joints),does identify individuals with a pronat-ed foot posture17 and PTTD.39 Further,in vitro studies have demonstrated astrong relationship (r2 = 0.85) betweenfoot kinematic measurements and pos-terior tibialis tendon length using thehindfoot and first metatarsal.11 Given thelarge changes in foot posture document-ed in previous studies of walking,31,39 thechanges in foot movements associatedwith PTTD are expected to be muchlarger than measurement errors.

Studies of walking trials suggest thatthe current clinical focus on hindfootkinematics during the heel rise test maybe less significant than first metatarsalkinematics. Ness et al31 and Tome et al39

noted significantly greater hindfoot ever-sion, first metatarsal dorsiflexion, andfirst metatarsal abduction during walk-ing. The mechanisms that are thought tocontribute to this offset in foot kinemat-ics during walking include (1) failure toinvert the subtalar joint,2 (2) decreasedligamentous support (eg, spring anddeltoid ligaments),1,8,12 and (3) decreasedmuscular control.41 Because in vivo footkinematic methods are not specific to ajoint (eg, talonavicular or calcaneocuboidjoints), the specific mechanisms at playare not revealed by these methods. Never-theless, the differences between controlsand individuals with PTTD were reflec-tive of a shift in foot kinematics towarda more pronated foot (greater hindfooteversion, first metatarsal dorsiflexion,and first metatarsal abduction), but nota change in the shape of the kinematicpattern. For example, for the individu-als in the control group, foot kinematicpatterns for the MLA showed a loweringof the arch during the first 70% of the

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addition, the individuals with PTTD wererequired to have 1 or more signs of flexi-ble flatfoot deformity, including excessivenonfixed hindfoot valgus deformity dur-ing weight bearing and/or excessive firstmetatarsal abduction. Excessive hindfootvalgus and first metatarsal abductionwere based on visual comparisons be-tween the involved and uninvolved side.Because the inclusion criteria relied onside-to-side comparisons, all participantsin the PTTD group were required to haveunilateral involvement. Participants wereexcluded if their foot pain prevented themfrom ambulating greater than 15 m.

The control participants were as-ymptomatic and required to fall into therange of age, gender, and body mass in-dex (BMI) of the first 15 participants ofthe PTTD group ( ). Control par-ticipants were admitted if they had nohistory of foot and ankle problems and anarch height index comparable to a previ-ous study of healthy participants.5,43 Thearch height index is described as the ratioof dorsum height at 50% of foot length,divided by the foot length from the heelto the base of the first metatarsal head.5,43

Greater values indicate a higher MLA. A

normal arch height index was defined asequal to or greater than an average ( SD)value reported in a previous study (0.34

0.03).5 Because this study includedparticipants both with and without flat-foot, values equal to or above the averageare theorized to be more representativeof how clinicians define a normal MLA.All participants were informed of the ex-perimental procedures and signed a con-sent form approved by The University ofRochester and Ithaca College Institution-al Review Boards.

A 5-segment foot kinematic model, thatincluded the tibia, calcaneus (hindfoot),first metatarsal, second to fourth meta-tarsals, and hallux, was used to mea-sure foot movement.17 The kinematicsof the second to fourth metatarsal seg-ment were measured but not utilized inthis study. To track movement, sets of 3infrared-emitting diodes (IREDs) weremounted on rigid thermoplastic plat-forms. The platforms were then attachedusing double-sided adhesive tape to theskin over each boney segment of interest( ). Six infrared cameras (Optotrak

Motion Analysis System; NDI, Waterloo,Ontario, Canada), synchronized withforce plate (model 9286; Kistler Group,Winterthur, Switzerland), were usedto collect kinematics (60 Hz) and force(1000 Hz) data with the Motion Monitor,Version 7.24 software (Innsport TrainingInc, Chicago, IL). Anatomically basedcoordinate systems were established foreach segment using digitized boney land-marks consistent with a previous study.17

The resulting segment x-axes for the firstmetatarsal and hallux were aligned withthe shaft of the first metatarsal and hal-lux, respectively. The vertical axes werethe perpendicular to a plane formed bythe x-axis and an arbitrary point at thesame height as the distal first metatarsaland hallux digitized points. This has theeffect of aligning the first metatarsal andhallux coordinates systems with the sag-ittal-plane orientation of the first meta-tarsal (ie, declination angle) and hallux.The tibia vertical axis was aligned witha vector from the lateral malleolus to thefibula head. The tibia anterior/posterioraxis was perpendicular to a plane formedby the y-axis and medial malleolus. Thehindfoot segment x-axis was aligned witha line from the posterior heel to the tip ofthe second metatarsal. The y- and z-axesfor the hindfoot were aligned with thelaboratory reference frame. The poste-rior heel digitized point, tracked relative

Picture of the placement of the infraredlight-emitting diodes used to track the tibia,calcaneus, first metatarsal, and hallux.

Subject Characteristics*

Abbreviation: PTTD, posterior tibialis tendon dysfunction.* Data are means SD, with the exception of involved side and gender.† Involved side: control group assigned proportional to PTTD group.‡ Between-group difference using an independent t test.

P ‡

Age (y) 56.5 (7.7) 59.8 (11.1) .316

Height (cm) 164.9 (7.3) 168.3 (9.9) .194

Mass (kg) 83.0 (10.8) 85.4 (17.5) .643

Body mass index (kg/m2) 30.6 (3.6) 29.9 (4.8) .658

Involved side† R, 5; L, 10 R, 12; L, 18

Gender M, 1; F, 14 M, 9; F, 21

Static foot posture

Foot length (cm) 24.55 (1.02) 24.95 (4.50) .648

Truncated foot length (cm) 18.37 (0.92) 19.80 (1.83) .01

First metatarsal height (cm) 6.98 (0.41) 6.14 (0.61) .01

Arch height index 0.38 (0.03) 0.31 (0.02) .01

Heel rise performance

Heel height (m) 0.11 (0.01) 0.12 (0.02) .660

Normalized heel height (%) 59.3 (8.2) 54.0 (10.4) .093

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[ RESEARCH REPORT ]metatarsal head intermittently lifted offthe ground, which clinically reflects fore-foot varus. To assure that the zero posi-tion is not influenced by this foot posture(ie, is similar between subjects), an ad-justment to the first metatarsal positionwas calculated in all subjects. The ad-justment calculated the angle of the firstmetatarsal segment as if the head wereon the floor. The details of this methodare published in a previous study.17 Thegoal of achieving a common first meta-tarsal position when in STN is supportedby an equal average first metatarsal angle(declination angle), in the laboratory co-ordinate system, between participants inthe control group (mean SD, –25.1°3.3°) and the PTTD group (mean SD,–25.1° 5.6°) in this study. Between-session reliability collected on 6 partici-pants using the described foot kinematicmethods and procedures resulted in astandard error of the measurement ofless than 2.0° for all variables, similar topublished studies.17,35,36

Once the STN position was estab-lished, participants completed the heelrise task. At a comfortable pace, partici-pants were instructed to rise up on theirheels and return to the starting positionrepeatedly. During each repetition, par-ticipants were encouraged to rise up ashigh as they could. Participants stoppedonce they completed at least 5 heel risesover a 5- to 15-second interval (range,5-8 repetitions) to minimize discomfortand achieve peak performance (peakheel height). Finally, participants wereallowed fingertip-to-fingertip contactwith an examiner, to assist with balanceduring the heel rise task. Only bilateralheel rise tasks were performed, becausemany participants with PTTD are unableto perform a single heel rise task.

Because of the lack of controls on theheel rise task, vertical ground reactionforce was assessed in a subset of partici-pants, to understand the influence of “fin-gertip” support and compensations withthe opposite limb. To assess if load fromside to side was equivalent, the verticalground reaction force (normalized to sub-

to the hindfoot, was used to estimate heelheight. Kinematic data were smoothedusing a fourth-order, zero-phase-lag But-terworth filter with a cut-off frequency of6 Hz. To calculate relative joint angles, aCardan angle z-x-y sequence of rotationswas used as suggested by Cole et al.6

The joint angles calculated included thehindfoot with respect to the tibia (hind-foot inversion/eversion and ankle plan-tar flexion/dorsiflexion), first metatarsalwith respect to the hindfoot (first meta-tarsal plantar flexion/dorsiflexion), andhallux with respect to the first metatarsal(hallux plantar flexion/dorsiflexion). Theerrors associated with this approach areexpected to be similar to studies com-paring bone- and skin-mounted mark-ers, which were reported as 2.3° forthe first metatarsal40 and 2.6° for thecalcaneus.32

As shown in previous studies, the defi-nition of neutral or zero position of thefoot joints strongly affects the measure-ment of foot kinematics.17,35,36 Surpris-ingly, determining the subtalar neutral(STN) position has repeatedly shownadequate between- and within-sessionreliability.17,35,36 Consistent with thesestudies, the STN position was adopted tostandardize the neutral alignment of thefoot.17,39 In brief, from a relaxed standingposture participants were asked to movetheir hindfoot into eversion and inver-sion, resulting in the raising and lower-ing of their arch. The examiner manuallypalpated the talonavicular joint until themid position was judged to have beenachieved. The participant was asked tohold this position, while a 1-second trialwas collected. This procedure was repeat-ed 2 times. The mean of 2 STN trials wasthen used as the zero joint position for allfoot kinematic angles. Because the goal isto describe foot kinematic angles from acommon zero or reference foot posture,both the hindfoot and forefoot are ex-pected to be in a similar position whenin STN. However, when participants withPTTD were placed into STN, the first

ject body mass) was assessed bilaterallyin a subset of 16 participants with PTTDand all those in the control group. Thesummed right and left vertical ground re-action force was at least (lowest values)89% and 83% of body weight at peak heelrise for the control and PTTD groups, re-spectively. The average near body weightvalues were 98% and 96% for the controland PTTD groups, respectively, whichsuggests that the effect of the “fingertip”support during the heel rise was mini-mal. The participants with PTTD appliedfrom 28% to 50% (average SD, 40%8%) of their body weight on the involvedside, while those in the control group ap-plied 37% to 58% (average SD, 49%5%) of body weight on the measured side.Because of an unexpected prevalence forthe involved side to be the left in the in-dividuals with PTTD, the left side wastested as the involved side in 10 and theright side in 5 individuals in the controlgroup. Data suggest subtle compensationwith the uninvolved side (average, 9% ofbody weight) in the PTTD group.

Heel height was measured in thePTTD and control participants to deter-mine if overall performance was similarbetween groups. Heel height was expect-ed to show a dependence on truncatedfoot length (distance from back of heel tofirst metatarsal head). Therefore, a priorinormalized heel height was anticipated asa covariate to adjust for differences in footkinematics attributable to foot length.

The ankle plantar flexion/dorsiflexiondata were used to identify the start andend of a heel rise cycle ( ). Eachheel rise cycle was interpolated to 100%cycle at 1% intervals (101 points). For eachsubject the 3 trials with the highest peakankle plantar flexion angle were selectedand averaged to gain a representative pat-tern for each subject. Time normalizationto percent cycle allowed for participantswith diverse speeds, and hence, heel risecycle time to be averaged. The heel risecycle was subsequently divided into 2phases, the preparation phase and heel

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normalized heel height and sagittal-planekinematic variables supported using nor-malized heel height as a covariate. Pair-wise comparisons between groups werepursued in the case of a significant inter-

rise phase ( ). The preparationphase on average ( SD) ended at 32%6% of the heel rise cycle, determined byvisually assessing each pattern. To assessthe primary hypothesis, foot kinematicangles at the mid point of the prepara-tion phase (specific to each subject) andpoint of peak ankle plantar flexion wereanalyzed ( ). To address the sec-ondary hypothesis, the ROM for eachfoot kinematic angle was the differencebetween the foot kinematic angle at themid point of the preparation phase andangle at peak ankle plantar flexion.

The first purpose of this investiga-tion was to compare 4-foot kinematicvariables, including hindfoot eversion/inversion, ankle plantar flexion/dorsi-flexion, first metatarsal plantar flexion/dorsiflexion, and hallux plantar flexion/dorsiflexion angles between participantswith PTTD and controls. A 2-way mixed-model analysis of variance (ANOVA) wasused to individually assess each foot kine-matic variable across groups (PTTD andcontrol) and cycle points (preparationand peak heel rise). Group was treatedas a fixed variable and cycle points as arepeated measure. Data were first ana-lyzed for an interaction effect to deter-mine differences between groups specificto either the preparation or the peak heelrise cycle point. The presence of an in-teraction would signal a change in shapeof the kinematic pattern for that variable.In the absence of interaction, main effectfor groups was analyzed to determine anoffset in angular positions between the2 groups. The presence of a main effectwould indicate an offset in angular valuesbut similarity of the kinematic patternsbetween groups. To assess ROM acrossfoot kinematic variables, a 2-way ANOVAwas performed, using group (PTTD andcontrol) by kinematic variable (hindfooteversion/inversion, ankle plantar flexion/dorsiflexion, first metatarsal plantar flex-ion/dorsiflexion, and hallux plantar flex-ion/dorsiflexion). Similarly, group was afixed factor and foot kinematic variablewas a repeated factor. For each analysis,heel height normalized to truncated foot

length was used as a covariate to controlfor differences in heel rise performance.Significant Pearson correlation coeffi-cients (r values ranged between 0.56 to0.67, for all variables P .05) between

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Preparatory Phase Heel Rise Phase

Representative trial of ankle plantar flexion/dorsiflexion relative to time. The points used to determinethe start and end of the heel rise are identified. The prepatory and rising phases were also distinguished basedon ankle angle. Data were taken at 15% of the heel rise cycle and at peak ankle plantar flexion. Plantar flexion isnegative.

Variables Evaluated During the Heel Rise Task

Abbreviation: PTTD, posterior tibialis tendon dysfunction.* Data are mean (SD) degrees.† Main effect difference between groups using normalized heel height as a covariate.‡ Based on 2-way (group by portion of heel rise) mixed-model ANOVA.§ Significant difference (P .05) between groups at preparation.

P † P ‡

Ankle plantar flexion (–)/dorsiflexion (+)

Preparation 8.5 (3.2) 0.2 (3.9)

Peak heel rise –22.1 (7.7) –18.4 (5.6) .001 .407

First metatarsal plantar flexion (–)/dorsiflexion (+)

Preparation 3.6 (2.7) 13.5 (7.7)

Peak heel rise –18.2 (5.9) –4.9 (14.9) .001 .590

Hallux plantar flexion (–)/dorsiflexion (+)

Preparation –3.6 (3.5) –7.2 (6.7)

Peak heel rise 40.1 (6.7) 28.3 (14.2) .01 .362

Hindfoot eversion (–)/inversion (+)

Preparation –2.2 (1.9) –9.1 (3.1)§

Peak heel rise 5.9 (3.2) 3.8 (4.6) .001 .034

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[ RESEARCH REPORT ]

0 10 20 30 40 50 60 70 80 90 100

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Hindfoot

Plantar flexion

Dorsiflexion

First metatarsalHallux

Plantar flexion

Dorsiflexion

Control PTTD

% Heel Rise

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% Heel Rise

A

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Ankle Plantar Flexion/Dorsiflexion

First Metatarsal Plantar Flexion/Dorsiflexion

Hallux Plantar Flexion/Dorsiflexion

The average ( SD, shown for 1 direction) sagittal plane angles for (A) hindfoot dorsiflexion/plantar flexion, (B) first metatarsal dorsiflexion/plantar flexion, and (C)hallux dorsiflexion/plantar flexion are shown across the heel rise cycle for the participants with posterior tibial tendon dysfunction (PTTD) and controls.

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height showed a mean difference betweengroups for the preparatory phase of 7.1°(95% CI: 5.3° to 8.9°) greater hindfooteversion. However, at the peak heel risepoint, the amounts of hindfoot inversionwere similar (P = .130) for the PTTDand control groups (mean difference be-tween groups adjusted for normalizedheel height, 1.6°; 95% CI: –1.1° to 4.3°).A post hoc analysis revealed that 7 of 30(23%) participants with PTTD failedto invert, while all but 1 of the controls(6.7%) achieved some amount of hindfootinversion. A Fisher exact test suggestedthat the proportions of participants whofailed to achieve hindfoot inversion inboth groups were not significantly differ-ent (P = .243).

The range-of-motion (ROM) valuesacross cycle points were only significantlydifferent for hindfoot inversion/eversion( ). Using normalized heel heightas a covariate, there was a significant in-teraction between group and ROM (P =.033). Pairwise comparisons revealed thathindfoot inversion ROM in the PTTD

groups, 6.7°; 95% CI, 1.7° to 11.8°). A posthoc analysis revealed that 15 of 30 partici-pants (50%) with PTTD failed to achievefirst metatarsal plantar flexion at peakheel rise, while all of the controls (100%)achieved some amount of first metatarsalplantar flexion at peak heel rise. A Fisherexact test confirmed that the proportionsof participants that failed to achieve firstmetatarsal plantar flexion in the PTTDgroup was statistically higher than for thecontrol group (P .001).

The hindfoot inversion/eversion kine-matics depended on both the group andcycle point of the heel rise task (signifi-cant interaction effect). Hindfoot inver-sion/eversion kinematic angles at specificcycle points are provided in , andthe overall kinematic patterns are pro-vided in . The data analyzed withnormalized heel height as a covariateshowed that the hindfoot inversion atthe preparatory phase of heel rise for thePTTD group was significantly greatercompared to the control group (P .001).The data adjusted for normalized heel

action for all of the ANOVA models. Analpha level of .05 was used for all statisti-cal tests.

he sagittal-plane foot kine-

matics were significantly differ-ent between the PTTD and control

groups across the heel rise cycle points(main effect). Foot kinematic angles atspecific cycle points are provided in2, and the overall kinematic patterns areprovided in . When using normal-ized heel height as a covariate, the averagedifference between groups, across cyclepoints, differed from the data shown in

and . The data adjustedfor normalized heel height showed thatthe PTTD group used greater ankle plan-tar flexion (adjusted mean differencebetween groups, 7.3°; 95% confidenceinterval [CI]: 5.1° to 9.5°), greater firstmetatarsal dorsiflexion (adjusted meandifference between groups, 9.0°; 95% CI:3.7° to 14.4°), and lower hallux dorsiflex-ion (adjusted mean difference between

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HindfootInversion

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PTTD

% Heel Rise

Control

Hindfoot Inversion/Eversion

The average ( SD, shown for 1 direction) frontal-plane angle for hindfoot relative to the tibia is shown across the heel rise cycle for the participants with posteriortibial tendon dysfunction (PTTD) and controls.

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[ RESEARCH REPORT ]

he new findings of this study

suggest that abnormal kinematics inindividuals with stage II PTTD occur

in both the hindfoot and forefoot duringa heel rise task. Previous studies focus-ing on walking revealed that forefoot ab-normalities were common in individualswith PTTD.18,31,39 This study confirms thatsimilar abnormal kinematics occur duringa heel rise task. Except for hindfoot inver-sion/eversion, differences in kinematicswere primarily the result of offsets towarda flatfoot posture (greater ankle plantarflexion, first metatarsal dorsiflexion, andhallux plantar flexion in the participantswith PTTD), not differences in the shapeof the foot kinematic patterns ( ).This offset in pattern is consistent withthe current view that static foot posturemay predict dynamic foot movement.31

The exception was hindfoot inversion,which depended on the heel rise cyclepoint. Although participants with PTTDstarted (preparation phase) in more hind-foot eversion than controls, they achieveda similar hindfoot inverted position ascompared to controls at peak plantar flex-ion ( ). This finding contrasts withcurrent clinical observations that hindfooteversion at peak plantar flexion during aheel rise is a typical sign of PTTD.22,29 Thefocus on first metatarsal movement mayexpand the interpretation of the heel risetest in patients with PTTD.

The heel height achieved in this studyis reflective of heel rise performanceacross groups, which is similar (2). The low ankle plantar flexion anglesreported from tracking the calcaneus asthe hindfoot segment are different thanclinical definitions. Clinical definitions ofankle plantar flexion use a single foot seg-ment, including the metatarsals, not justthe calcaneus. An estimate of the clini-cal assessment of ankle plantar flexioncan be derived from the truncated footlength (heel to first metatarsal head) andheel height achieved. For example, ankleplantar flexion angle is approximately31° (controls: 30.9° = tan–1[0.11/0.184];

normalized heel height was 5.2° (95%CI: 2.3° to 8.1°). All other ROM variableswere similar between groups ( ).

group was significantly greater than thatin the control group (P = .001). The meandifference between groups adjusted for

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Hindfoot Inversion First MetatarsalPlantar Flexion

Ankle Plantar Flexion Hallux Dorsiflexion

PTTDControl

The average ( SD) range of motion (ROM) values for hindfoot inversion, first metatarsal plantar flexion,ankle plantar flexion, and hallux dorsiflexion are shown for the participants with posterior tibial tendon dysfunction(PTTD) and controls. *Indicates statistical significance.

A B

Tibia

Hallux First metatarsal

Hindfoot

Hallux First metatarsal

Hindfoot

Tibia

Ankle plantar flexion

First metatarsal plantarflexion 100%

Hallux dorsiflexion

Lower hallux dorsiflexion

First metatarsalplantar flexion 50%dorsiflexion 50%

Greater ankleplantar flexion

Control PTTD

A schematic sagittal plane representation of the foot illustrates the findings. (A) Control participantsused a combination of ankle plantar flexion, first metatarsal plantar flexion, and hallux dorsiflexion to achieve peakheel rise. (B) The participants with posterior tibial tendon dysfunction (PTTD) used greater ankle plantar flexion, avariable amount of first metatarsal plantar flexion, and lower hallux dorsiflexion to achieve peak heel rise.

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ment alone does not fully account forplantar fascia behavior via the windlassmechanism. Unexpectedly, in this study,despite achieving comparable hindfootinversion, first metatarsal dorsiflexionwas markedly higher in participants withPTTD compared to controls. Alterationsin joint axes of rotation, as noted for thefirst metatarsal by Glasoe et al,13 may be atplay in altering the normal hindfoot-fore-foot coupling demonstrated by Blackwoodet al2 in vitro. Despite equivalent firstmetatarsal plantar flexion ROM acrossgroups, the PTTD group was influencedby approximately 50% of the participantswho failed to plantar flex their first meta-tarsal beyond the STN position (). In contrast, all the individuals in the

control group achieved some amount offirst metatarsal plantar flexion beyond theSTN position. This offset toward greaterfirst metatarsal dorsiflexion relative to theSTN position may indicate altered jointaxes and soft tissue support.18,31,39 Furtherresearch investigating mechanisms otherthan hindfoot inversion on first metatar-sal kinematics seem warranted.

Clinically, this study demonstrates thatdocumenting the ability to heel rise andnoting the existence of hindfoot eversionat peak heel rise ignores the more com-monly occurring abnormal dorsiflexionof the first metatarsal. Many participantswith PTTD started in a hindfoot evertedposition, yet achieved hindfoot inver-sion at peak heel rise. This may indicatea functioning posterior tibialis muscle at50% body weight for the bilateral heelrise. Although not common, failure to in-vert the hindfoot may indicate a more se-vere weakness.22,29 A single-limb heel risetest may show greater differences in footkinematics because the load is increasedfrom 40% to 50% body weight to close to100%. If first metatarsal plantar flexionoccurs during the test, this supports theidea that mechanisms within the foot arefunctioning despite starting from a flat-foot posture. Failure of the first metatar-sal to achieve plantar flexion may indicate

first metatarsal plantar flexion occurredrelative to a lower MLA position in par-ticipants with PTTD compared to the con-trols ( ). Given the foot kinematicmethods, it is difficult to precisely identifyat which joint the first metatarsal plantarflexion ROM took place. However, forparticipants with PTTD, higher plantarflexion of the talonavicular, naviculocunei-form, or first metatarsal cuneiform jointsis a possibility.3 The fact that the firstmetatarsal plantar flexion ROM occurswhen the foot is increasing weight-bear-ing forces suggests increasing MLA heightduring high load. This finding is consis-tent with studies using a kinetic model ofthe foot that suggested a power generationof the medial foot at push-off during walk-ing.27 Periods of power generation suggestthat active mechanisms are responsible.27

The first metatarsal plantar flexion ROM,therefore, may be the result of (1) musclecontrol of the intrinsic muscles,24 (2) flex-or hallucis longus muscle,20,21 (3) Achillestendon forces acting through the plantarfascia,10 and/or (4) some combination ofthese actions, which are retained in indi-viduals with PTTD.

The potential influence of the plantarfascia on raising the MLA is suggested byhallux dorsiflexion. The participants withPTTD in this study used approximately 7°less hallux dorsiflexion compared to thecontrol participants. However, the totalhallux ROM was similar across groups( ). Previous studies have suggest-ed that, as hallux dorsiflexion increases,so does the MLA.19 Magnetic resonanceimaging studies demonstrate infrequentinvolvement of the plantar fascia in par-ticipants with PTTD in contrast to con-sistent abnormal signal (as an indicationof soft tissue damage) found in the springand deltoid ligaments.1,8,12 Therefore, ris-ing of the MLA, even in participants thathave a low MLA, may be an indicationof an intact windlass mechanism via theplantar fascia. Because only the move-ment of the hallux was collected in thisstudy, the influence of the lateral 4 digitson the plantar fascia was not taken intoaccount. It is possible that hallux move-

PTTD: 31.2° = tan–1[0.12/0.198]), whentaking truncated foot length and heelheight into account. However, the co-variate analysis was used to adjust fordifferences in performance (normalizedheel height) within the PTTD group,which had the effect of reducing the dif-ferences in foot kinematics across groups.However, even when taking into accountdifferences in normalized heel height,the participants with PTTD used differ-ent ankle and foot kinematics during theheel rise task.

In this study, ankle plantar flexionwas an offset toward greater plantarflexion in participants with PTTD. Au-thors argue that the triceps surae mus-cle is shortened in participants withhindfoot plantar flexion due to greatercalcaneal plantar flexion observed onradiographs.9 The data from this studyconfirm that participants with PTTD usegreater ankle plantar flexion relative tothe STN position than participants witha normal MLA ( 7°). This shift towardhigher ankle plantar flexion may shortenthe triceps surae, resulting in a shift inthe force-length relationship and func-tionally weaker muscle.9 Despite thepossibility of functionally weaker plantarflexors, the participants with PTTD onaverage achieved similar normalized heelheights as controls. Increasing the loadon the plantar flexors, as is done during asingle-limb heel rise, may further reduceheel rise performance (normalized heelheight). Independent of ankle plantarflexor weakness, ineffective boney con-tact and/or muscle control to stabilizethe midfoot (measured in this study asfirst metatarsal dorsiflexion) may con-tribute to reduced heel rise ability.2

Separation of the foot into the hindfootand first metatarsal segments provides in-sight into how the increase in height of theMLA contributed to the clinical definitionof ankle plantar flexion of approximately31°. The PTTD group used equal ankleplantar flexion ROM and first metatarsalplantar flexion ROM as controls to achievea similar heel height ( ). Althoughthe ROM was the same between groups,

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[ RESEARCH REPORT ]eral heel rise test. Except for hindfooteversion/inversion, the foot kinematicdifferences between the participantswith stage II PTTD and those in thecontrol group mainly occurred as off-sets. The amount of motion that tookplace between the preparation phase ofheel rise and peak heel rise was simi-lar between groups, suggesting thatMLA raising and lowering occurredsimilarly in both groups, though overa different range of joint movement.The one exception was for hindfooteversion/inversion. Despite the hind-foot achieving an inverted position atpeak heel rise, the first metatarsal rela-tive to the calcaneus was significantlymore dorsiflexed, which suggests thatfirst metatarsal movement in individu-als with PTTD may be less dependenton hindfoot movement.

Failure of the hindfoot toinvert is uncommon during a bilat-eral heel rise test in individuals withstage II PTTD. Failure to achievefirst metatarsal plantar flexion oc-curred in 50% of subjects with stageII PTTD. Except for hindfoot inver-sion, foot kinematic ROM is normalin participants with stage II PTTD.Differences in foot movement are at-tributable to offsets in standing pos-ture, in this case quantified using theSTN position.

During a bilateral heelrise test, MLA kinematics may bemore sensitive than hindfoot kine-matics in identifying abnormal footmovement in individuals with stageII PTTD.

The results are specific to theseverity (stage II) of PTTD, definition of“normal” MLA, and the foot kinematicmethods used.

ACKNOWLEDGEMENTS: The authors wouldlike to acknowledge the efforts of Can-dace Nomides, Jen Churey, and KellyVan Vlack, who assisted with data pro-cessing.

ods differ in their approach to segment-ing the foot and defining foot kinematicangles which make comparisons acrossstudies difficult.7,25,27,31,37,44 The size of thebones and soft tissue over the mid foot(eg, tendons) make measuring motionat these joints difficult to do using skin-mounted markers. Some studies compar-ing bone- mounted and skin-mountedmarkers suggest low average errors (lessthan 3°) for the hindfoot and first meta-tarsal.32,40,42 The foot kinematic data re-ported in this study should be viewed withrespect to these errors. Because it is notpossible to blind study participants to thePTTD condition, there is the potential forbias in establishing STN positions acrossgroups. The similarity of first metatarsalangles across groups (approximately 25°)suggests that equivalence in foot positionwas achieved; however, without blinding,bias is not completely eliminated. Thefoot loading was lower (approximately9% body weight) in the subjects withPTTD, which might have masked somedifferences in foot kinematics. This is across-sectional study, which does not al-low establishing of cause-and-effect rela-tionships. Therefore, inferences made inthe discussion related to cause-and-effectrelationships are speculative. This sampleis large for studies of participants withPTTD.31,38,39 Nevertheless, larger samplesare desirable. The designation of stage IIPTTD was dependent on clinical evalua-tion methods that have not been assessedin terms of validity. Future studies mayconsider the reliability and validity ofstaging PTTD. Finally, the definition of anormal MLA used for the control groupwas based on a sample of 100 subjects.5

Alternative definitions of normal MLAmay change the comparisons betweengroups.

ndividuals with PTTD are more

likely to display abnormal firstmetatarsal dorsiflexion as com-

pared to abnormal hindfoot eversionat peak plantar flexion during a bilat-

failure of coupling between the hindfootand forefoot and/or loss of muscle con-trol. Clinical methods that do not rely onmovement analysis techniques would bebeneficial to grade hindfoot and forefootcontrol during a heel rise test and war-rant future research.

Because the alterations in foot move-ment are primarily offsets as opposed toalterations in kinematic patterns, footposture may predict abnormal MLA ki-nematics. With the exception of hind-foot inversion/eversion, the abnormalkinematic patterns associated with theparticipants with PTTD were offsets,without changes in the shape of the footkinematic patterns. A previous study ofparticipants with a variety of foot pos-tures, but none associated with PTTD,found that the longitudinal arch anglemeasured in standing was similar tothe same angle measured during walk-ing (r = 0.97).28 Given this, measures offoot posture may reflect the offsets thatare observed during movement if simi-lar relationships hold in individuals withPTTD. Recent studies appear to supportsuch an association.18,31,38,39 For example,a study that failed to use a correction oroffset to align foot segments in partici-pants with PTTD suggested similar footkinematic angles compared to controls.38

In contrast, studies that used radio-graphs18,31 or the STN position39 to alignfoot segments documented offsets in footkinematics, not alterations in the shapeof foot kinematic patterns. Therefore,the offsets, measured statically, appearresponsible for the measured alterationsin foot kinematic patterns. Consideredtogether, these studies suggest that clini-cal measurements of foot posture (eg,with radiographs or standardized mea-sures) may predict foot kinematics dur-ing movement in individuals with PTTD,similar to a previous study of people freeof foot pathologies.28

The limitations of this study are associat-ed with the foot kinematic methods, studydesign, and sample. Foot kinematic meth-

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[ RESEARCH REPORT ]

@ WWW.JOSPT.ORG

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