Relationship of plantar-flexor peak torque and dorsiflexion range of motion to kinetic variables during walking.

Research investigating human walking often has been focused on kinematic variables, which describe motion without regard to the forces that cause the motion. Kinetics is the study of forces that cause movement.[1,2] Understanding kinetic variables, such as moments and power, may assist in understanding the mechanical causes of movement and how these movements might best be enhanced.[2]

A joint moment has been described as a measure of the net effect of all agonist and antagonist muscle activity that causes rotation at a given joint.[1,3] Clinicians often use an isokinetic dynamometer to measure joint movements or peak torque as an indicator of muscle performance.[4]

A link-segment model can be used to estimate joint moments during a functional activity, such as walking.[1-3,5] We are aware of no studies that have compared the peak moments measured on an isokinetic dynamometer with peak moments measured during walking. Strong relationships between these measures would enhance the validity of using isokinetic dynamometers to predict moments during functional activities such as walking.

Power is a kinetic variable that reflects the rate of work performed at a given joint, and can be calculated by taking the product of the moment and the joint angular velocity.[3,5] Power will be positive when the moment and angular velocity have the same direction. A positive power typically indicates the muscle is generating mechanical energy (concentric contraction), whereas a negative power usually indicates muscle is absorbing mechanical energy (eccentric contraction).[5]

Limitations in ankle moments and power during walking have been identified in several patient populations and are believed to contribute to various gait deviations.[6-9] In a study children with spastic hemiplegia secondary to cerebral palsy, Olney et al[7] found that the ankle plantar flexors produced just over a third of the positive work (integral of power) for the affected limb instead of the two thirds that is usually observed.[7] In a study of adult patients with hemiplegia, the affected ankle produced lower ankle plantar-flexor moments and power than the unaffected side, and ankle power at both sides was strongly related (r=.83, P<.001) to gait speed.[8] Winter et al[9] reported decreases in ankle power in elderly subjects (mean age=68 years, SD=3.9, range=62-78) compared with younger subjects (mean age=24.6 years, SD=2.2, range=21-28), which were believed to result in shorter step lengths and increased periods of double support. Winter[1] also reported that the ankle moment is an important contributor to the overall support moment, a summation of the ankle plantar-flexor moment, the knee extensor moment, and the hip extensor moment. During the latter portion of the stance phase (70%-100%), the ankle plantar-flexor moment contributes the greatest portion of any of the lower-extremity joints to the support moment. If this support moment is limited because of a limited ankle moment, overall support may be compromised.

Mueller et al[6] report that patients with diabetes mellitus (DM) and peripheral neuropathies showed less ankle motion, moments, and power compared with age-matched control subjects. These limitations were believed to contribute to lower walking speed and stride length. Although the patients with DM and peripheral neuropathies showed decreased plantar-flexor peak torque (PFPT) measured with an isokinetic dynamometer and decreased ankle mobility measured with a goniometer, the relationship between these measures and gait variables was not described.

The primary purpose of our study was to determine the relationship of PFPT and dorsiflexion range of motion (ROM) to peak ankle moments and power during the late stance phase (70%-100%) of walking in subjects without DM and in subjects with DM and associated peripheral neuropathies. Because the plantar-flexor muscles are primarily active during the late stance phase,[10] we hypothesized that PFPT would contribute most to ankle moments and power during the late stance phase of walking. We also hypothesized that ankle dorsiflexion ROM would have a relationship with ankle moments during the late stance phase. We speculated that adequate ankle dorsiflexion ROM is necessary to allow the superincumbant body weight to rotate over the foot during the late stance phase (Fig. 1).

A correlation between the variables PFPT and dorsiflexion ROM and the variables ankle moments and power during walking would provide some evidence for treating these variables with the goal of improving gait deviations such as decreased stride length, walking speed, and overall stability.

Patients with DM and peripheral neuropathies were chosen as subjects because they could provide a wide range of values for PFPT and dorsiflexion ROM.[6,11] In addition, their gait characteristics have been described in detail previously.[6]

A secondary purpose of this study was to determine whether other factors related to grouping subjects with DM or without DM (such as sensory deficits) would make a contribution to ankle moments or power during walking. This information would help to identify limitations of using patients with DM and peripheral neuropathies as a representative group of patients with limited PFPT and dorsiflexion ROM.

A tertiary purpose was to determine the contribution of subject weight and walking speed to ankle moments or power during walking. Consideration of these variables would be important for appropriate interpretation of results and for identifying the need for control of the variables in future investigations.

Methods

Patients with DM and peripheral neuropathies were recruited from past and present patients of the Diabetic Foot Center at Washington University School of Medicine and Barnes Hospital (St Louis, Mo). Criteria for patient selection were that the patient had been diagnosed with DM; have a history of neuropathic plantar ulcer; be unable to sense a 5.07 Semmes-Weinstein monofilament on the plantar aspect of the foot; and be able to walk independently without pain, an ankle-foot orthosis, or an assistive device (ie, walker or crutches). A history of a neuropathic ulcer and an inability to sense a 5.07 Semmes-Weinstein monofilament were the criteria for determining the existence of severe peripheral neuropathy.[11-13] Age-matched subjects without DM were recruited from university employees and outpatients in well elderly and cardiac rehabilitation programs. Eligibility criteria for subjects without DM were a negative history of DM, neurological disease, or orthopedic problem and an ability to ambulate independently without pain, an anklefoot orthosis, or an assistive device. There were 9 subjects with DM and peripheral neuropathies and 10 subjects with no history of DM (Tab. 1). The mean age of the subjects with DM was 57.9 years (SD=14.1, range=35-75), and the mean age of the subjects without DM was 56.8 years (SD=11.3, range=37-68). In the DM group, the mean duration of diabetes was 21.0 years (SD=6.4, range=14-35). There was no significant difference (P>.05) in age, weight, height (t test), or gender (chi-square test) between the groups.

Table 1. Subject Characteristics

                           Group
                           With         Without      All
Characteristic             Diabetes     Diabetes     Subjects

n                              9           10           19
Age (y)
  x                           57.9         56.8         56.4
  SD                          14.1         11.3         12.3
  Range                    35-75        37-68        35-75
Gender
  F                            2            2            4
  M                            7            8           15
Weight (kg)
  x                           93.7         83.9         88.5
  SD                          14.3         24.3         20.3
  Range                    63.2-112.9   59.1-146.7   59.1-146.7
Height (m)
  x                            1.82         1.75         1.78
  SD                           0.10         0.05         0.09
  Range                    1.62-1.93    1.68-1.83    1.62-1.93
Diabetes
Type I/type II                  5/4
Duration of diabetes (y)
  x                            21.0
  SD                            6.4
  Range                        14-35
Duration of diabetes (y)   63.2-112.9   59.1-146.7   59.1-146.7

Procedure

All subjects signed an informed consent form prior to testing. All measurements were taken a minimum of two times during the same session to determine test-retest reliability. Reliability of all measures was good, as evidenced by intraclass correlation coefficients (ICC[2,k])[14] of [greater than or equal to].84 (Tab. 2).

To measure dorsiflexion ROM, subjects were positioned prone with the hip and knee extended on a firm treatment table with the tested foot and ankle protruding over the end of the table. A standard plastic goniometer with the scale marked in 2-degree increments was used. The axis of the goniometer was placed over the lateral malleolus, with one arm aligned with the head of the fifth metatarsal head and the other arm aligned with the head of the fibula. We palpated the subtalar joint and attempted to keep it in neutral during testing. The tester passively dorsiflexed the ankle, and then the subject was asked to actively dorsiflex the ankle. The greater angle of dorsiflexion was used as dorsiflexion ROM.[13] The intrarater ICC of .97 was similar to the value of .96 determined in a previous study assessing reliability of ankle goniometric measures in a group of patients with diabetes.13

Plantar-flexor peak torque was measured next. Each subject was placed supine on the Lido Active isokinetic table(*) with the knees extended and the right foot secured to the footplate by two Velcro[R] straps.(dagger) The axis of the dynamometer was aligned with the axis of the ankle joint (at the distal border of the lateral malleolus). To stabilize the leg further during testing, a strap was secured over the right thigh. Subjects were tested at a velocity of 60[degrees]/s, which is comparable to the average angular velocity observed at the ankle joint during the stance phase of walking.[5(pp250-252)] During walking, however, ankle angular velocity varies, whereas the isokinetic device maintains a constant speed. Subjects were allowed several sub-maximal practice contractions to become acquainted with the resistance and speed of movement. The foot was placed in a position of maximum dorsiflexion, and the subject was instructed to push as hard and as fast as possible through the full ROM. This procedure was repeated four times. The highest value was taken as the PFPT.[4] After a 2-minute rest, the test was repeated. The intrarater ICC value was .99.

Gait Testing

During gait testing, subjects wore shorts and their own shoes. The heels of the subjects' shoes were [less than or equal to]2.54 cm ([less than or equal to] in). Retroreflective markers were placed on the skin over the head of the fifth metatarsal, the ankle (distal lateral malleolus), the knee at the lateral femoral condyle, the greater trochanter of the hip, and the mid-superior iliac crest directly superior to the greater trochanter of the hip. Footswitches,(double dagger) secured to the plantar surface of the forefoot (at the first metatarsal head) and the rear foot (at the posterior lateral heel), were used to determine initial contact (heel-strike) and toe-off during ambulation and to verify synchronization of video and force platform data.

An ExpertVision[TM] system(double dagger) was used for video analysis. The video camera,(sections) sampling at 60 fields per second, and an attached spotlight were placed 6 m to the side of the walkway, perpendicular to the anterior-posterior axis of the force platform. The raw coordinate data were smoothed using a fourth-order Butterworth filter with a cutoff at 6 Hz.[9]

Data were collected as subjects walked normally across a 6.8-m walkway. A 60X120-cm AMTI LG6-2-1 force platform,(parallel) embedded at floor level midway down the walkway, sampled the force data at 60 Hz. Subjects were allowed to practice walking on the walkway with the footswitches secured to their feet for two to three trials. When the subjects reported they were accustomed to walking on the walkway, data were collected. Ten trials were recorded for each subject. Subjects were allowed to rest as needed.

Data Analysis

To calculate moments of force at the ankle, knee, and hip, a standard two-dimensional link-segment model of the lower limb was developed for the foot, shank, and thigh segments.[5] Power throughout the stance phase was calculated by determining the product of the moment and the angular velocity. Values were calculated for every 0.0167 second (60-Hz sampling frequency) of the stance phase. For each kinematic and kinetic variable of walking, a mean of the first three trials of complete data was used to enhance reliability.[15] The peak values of ankle moment and power during terminal stance (70%-100% of stance) were selected for analysis. As indicated in Table 2, ICC values for peak ankle moment and peak ankle power were .84.

Table 2. Reliability (ICC(a)) for Intrarater
Agreement for
Variables Used in
This Study

Measure                           ICC

Ankle ROM(b) (goniometer)         .97
Plantar-flexor peak torque         99
Walking speed                     .98
Plantar-flexor peak moment
  during walking                  .84
Peak ankle power during walking   .84

(a) ICC=intraclass correlation coefficient (2,k).[14]
(b) ROM=range of motion.

Hierarchical multiple regression analysis was used to determine the contribution of the subject characteristics to ankle plantar-flexor peak moment and power measurements during walking.[16] Ankle plantar-flexion peak moment and power during the late stance phase of walking (70%-100% of stance) were the dependent variables for each analysis. Because muscle performance is believed to be the primary factor contributing to a joint moment or power,[5] PFPT was entered as the first independent variable. Dorsiflexion ROM, group (with DM or without DM), subject weight, and walking speed were entered next. Group (with DM or without DM) was analyzed because other aspects of the disease process in diabetes (eg, sensory loss) may influence postural stability and moments about the ankle.[17]

Results

Moments

Means and standard deviations for all variables for the group with DM, the group without DM, and all subjects are shown in Table 3.

[TABULAR DATA OMITTED]

Plantar-flexor peak torque accounted for 40% of the variance of ankle plantar-flexor peak moment during walking (r=.63, P=.002, Tab. 4). No other variable accounted for as much variance in ankle moments as did PFPT.

[TABULAR DATA OMITTED]

Dorsiflexion ROM was entered next into the analysis and did not show a contribution to the ankle plantar-flexor peak moment (squared semipartial correlation, [sr.sup.2]=.03, P>.05). There was, however, high redundancy between PFPT and dorsiflexion ROM (r=.78, P<.001, Fig. 2).

The addition of group (with DM or without DM) did not make a contribution to ankle moments during walking after PFPT and dorsiflexion ROM were entered into the multiple regression analysis ([sr.sup.2]=.03, P>.05, Tab. 4).

The addition of subject weight made a contribution (130%) to ankle plantar-flexor peak moment variance ([sr.sup.2] =.13, P=.03, Tab. 4). The combination of PFPT, dorsiflexion ROM, group, and subject weight accounted for 59% of the variance in ankle moments during walking (Tab. 4).

After PFPT, dorsiflexion ROM, group, and subject weight were entered into the analysis, the addition of walking speed contributed no unique variance ([sr.sup.2]=.05, P>.05).

Power

Plantar-flexion peak torque accounted for 53% of the variance of peak ankle power during walking (r=.72, P<.001, Tab. 5). Dorsiflexion ROM, group (with DM or without DM), weight, or walking speed did not add a contribution (all P>.05). As noted, there was considerable redundancy between the variables. Besides the high correlation between PFPT and dorsiflexion ROM (r=.78, P<.001), there was a correlation between PFPT and walking speed (r=.48, P<.05), dorsiflexion ROM and ankle power (r=.72, P<.001), and ankle power and walking speed (r=.48, P<.05, Tab. 6).

[TABULAR DATA OMITTED]

Discussion

Consistent with our primary hypothesis, PFPT made the greatest contribution to explaining the variance of the plantar-flexor peak moment (r=.63, [R.sup.2]=.40) and power (r=.72, [R.sup.2]=.53) during the late stance phase of walking. The plantar-flexor muscles are the primary muscle group active during this portion of walking[10] and supply the primary force for the ankle moment and power.

Although dorsiflexion ROM did not make a contribution to the ankle moment or power during walking in the hierarchical multiple regression analysis, there was a strong correlation (r=.78, P<.001) between PFPT and dorsiflexion ROM (Tab. 6, Fig. 2). There also was a strong correlation between dorsiflexion ROM and ankle power (r=.72, P<.001, Tab. 6). The large amount of redundancy between PFPT and dorsiflexion ROM and the order of entry into the regression analysis (ie, PFPT before dorsiflexion ROM) appear to be the primary reasons why dorsiflexion ROM did not make a contribution to explaining the variance of ankle power during walking.

As illustrated in Figures 1 and 2, plantar-flexion moments and dorsiflexion ROM appear to be interdependent.

(*) Loredan Biomedical Inc, 2121-B Second St, Ste 107, PO Box 1154, Davis 95616. (dagger) Velcro USA Inc, 406 Brown Ave, Manchester, NH 03108. (double dagger) Motion Analysis Corp. 3650 N Laughlin Rd, Santa Rosa, CA 95403. (sections) NEC Corp. NEC Bldg, 33-1, Shiba 5-chrome, Minato-ku, Tokyo 108, Japan (distributed by NEC Corp, Broadcast Equipment Dept, 1555 W Walnut Hill Ln, Irving, TX 75038). (parallel) Advanced Mechanical Technology Inc, 151 California St, Newton, MA 02158. ankle dorsiflexion ROM appears to allow the necessary moment arm to produce an ankle plantar-flexion moment, as explained in our primary hypothesis (Fig. 1). We speculate that increasing dorsiflexion ROM allows for an increase in the external dorsiflexion moment and necessarily increases the requirement for the internal (muscle-generated) plantar-flexion moment control during walking (Fig. 1a). Decreasing dorsiflexion ROM decreases the potential for the external dorsiflexion moment and necessarily decreases the requirement for the internal plantar-flexor moment control during walking (Fig. 1b).

Besides limiting the requirement for an internal plantar-flexor moment, limitations in ankle dorsiflexion ROM can contribute a large portion to the internal plantar-flexion moment during walking. Siegler et al[18] reported that the equinus deformity in a patient with hemiparesis contributed 21% of die total ankle moment. Tardieu et al[19] also found a contribution to the internal ankle moment from plantar-flexion contractures in children with cerebral palsy. This contribution appears to occur by passive resistance to stretch of the structures surrounding a joint during the latter portions of the stance phase.[18,19] Limited dorsiflexion ROM is a common finding in persons with limited plantar-flexion muscle strength, including elderly people and patients with DM, cerebral palsy, and hemiplegia.[6,11,18-20] We hypothesize that decreased dorsiflexion ROM can be a compensation for decreased plantar-flexion muscle strength to maximize ankle moments during walking. Additional research is needed to test this hypothesis.

According to our analysis, group (with DM or without DM) accounted for no variance of ankle moments or power beyond that accounted for by PFPT. Differences between the subjects with DM and the subjects without DM appeared to operate through PFPT. A potential limitation of using patients with DM and associated peripheral neuropathies as a population of patients with limited ankle strength and mobility is that other factors of DM may influence ankle moments besides PFPT and dorsiflexion ROM. As mandated by the criteria for admission to our study, the group of subjects with DM and associated peripheral neuropathies had severe, sensory neuropathy. Somatosensory deficits in this population may influence gait characteristics.[17,21] If somatosensory deficits influenced ankle moments during walking in this study, however, we would have expected an effect due to group (with DM versus without DM) in our hierarchical multiple regression analysis. We did not analyze sensory deficits, however, and additional research is needed to study the specific efects of peripheral neuropathies and somatosensory deficits on gait.

In addition to PFPT, weight made a contribution (13%) to the plantar-flexor peak moment during walking. Subjects with greater mass will, logically, require greater internal joint moments to control the mass than subjects with less mass. These findings support the recommendations made by some investigators that moments should be "normalized" by weight.[22]

Walking speed did not make a contribution to predicting ankle moments or power after PFPT and dorsiflexion ROM were considered (Tabs. 4, 5). In this group of subjects, there was a correlation (r=.48) between PFPT and walking speed. We speculate that plantar-flexor muscle weakness limits ankle moments, ankle power, and walking speed. Therefore, walking speed added no unique contribution to ankle moments or power during walking beyond that predicted by PFPT. Our findings are in agreement with reports from Perry et al[23] and Bohannon,[24] who found a high correlation between plantar-flexor torque and walking speed in patients with post-polio syndrome (r=.55) and patients with cerebrovascular accident (r=.47). The relationship between PFPT and walking speed was trivial when we examined only subjects without DM (Tab. 6, bottom portion below main diagonal, r=.09). The subjects without DM appeared to have a reserve of plantar-flexor muscle performance available that they could use to generate ankle moments and speed during walking, whereas the subjects with DM and associated peripheral neuropathies did not.

Clinical Implications

The isokinetic measure of PFPT provided a prediction of ankle moments and power measured during walking. Isokinetic devices are available in many rehabilitation facilities and are widely used by clinicians. At the current time, measuring joint moments or power during walking requires a gait laboratory with substantial equipment and personnel. Our results provide some evidence for using an isokinetic device to identify subjects with muscle weakness that is related to decreased moments and power during walking. The mean PFPT of the subjects with DM (X=55.3 N-m) was more than 3 standard deviations lower than the mean PFPT of the age-matched control group subjects (X=90.2 N-m, SD=11.1 N-m). Based on these and other data,[6,23,24] we expect that subjects tested with methods described in this study with PFPT less than 2 standard deviations below the mean of the group without DM (X=68 m) would show gait deviations of decreased step length and walking speed. This hypothesis requires verification in a prospective study.

Despite the relationship between these measures, however, only 400% and 53% of the variance of ankle moments and power during walking was accounted for by the measures of PFPT on an isokinetic device. Isokinetic devices can be used to measure joint moments in non-weight-bearing positions, and these measures may provide a general indication of a patient's ability to generate moments during a functional activity such as walking. These measures, however, cannot predict specific joint moments or power during walking according to our data.

Ankle moments and power are known to be limited during walking in patients with DM and peripheral neuropathies,[6] cerebral palsy,[7] and hemiplegia[8] and in elderly persons.[9] Decreased moments and power at the ankle are believed to contribute to gait deviations, including decreased step length and walking speed. In our opinion, limited ankle moments and their accompanying limitation of the overall support moment may also contribute to the increased incidence of falls and injuries reported in patients with DM and peripheral neuropathies.[21] When possible, increasing plantar-flexor muscle strength and dorsiflexion ROM may improve ankle moments during walking and reduce these gait deviations. Additional research is needed to test this hypothesis.

Increasing ankle moments in an attempt to decrease gait deviations may not be desirable for all patients. Although step length and walking speed may increase in some patients, increasing the push-off and resultant ankle moment during walking can result in increased vertical and anterior-posterior forces on the forefoot.[6,25] Increased forefoot forces and pressures are believed to contribute to ulcers in patients with neuropathies.[11,17,20] Therefore, decreasing ankle plantar-flexion moments during the latter portion of the stance phase may be indicated in patients with peripheral neuropathies who are susceptible to forefoot ulcers.[28]

Limitations of the Study

This study analyzed variables only at the ankle, and walking is clearly a function and integration of movement throughout the entire body. This study was part of a larger project that analyzed the gait characteristics of patients with DM and peripheral neuropathies compared with age-matched control group subjects.[6] The focus of this study was to determine how specific measures were related to specific kinetic variables measured during walking. Analysis of whole body movements, or even movements of an entire lower extremity, was beyond the scope of this study.

Another limitation of this study is that walking occurs in three dimensions, whereas we considered only movement and forces in the sagittal plane. The foot was considered a rigid segment and the ankle a hinge joint. Although these assumptions may introduce some error, we were most interested in the sagittal plane, because this is the plane of progression. Additional research using a three-dimensional model would be interesting to document basic gait deviations in the frontal and transverse planes. Other limitations to using the link-segment model include reliance on previously published anthropometric data and correct placement of reflective markers on anatomical landmarks. These limitations have been discussed in detail elsewhere.[5,6,8]

There also are certain limitations in the statistical analysis. Although compared with other biomechanical studies 19 subjects is a relatively large number for analysis of kinetic variables using the link-segment model, it is a relatively small number for statistical analyses. A larger sample may have shown a contribution of dorsiflexion ROM and weight to ankle power, even after the contribution of PFPT had been accounted for. Additional research on another sample should be conducted to confirm these results.[16] Our results were consistent with the a priori hypotheses, and they do fit into a logical theoretical framework that increases our confidence in the findings.[16]

In addition, there was considerable redundancy between the variables of PFPT, dorsiflexion ROM, and walking speed (Tab. 6). Redundancy in independent variables makes inference more difficult than if variables are independent.[16] With this limitation in mind, inferences were made with a logical rationale, and supported, as much as possible, by the statistical analysis.

Conclusion

Plantar-flexor peak torque measured with an isokinetic dynamometer was related to ankle moments and power measured during walking using a link-segment model. There also was a high correlation between PFPT and dorsiflexion ROM. In view of these findings, we believe that, when possible, increasing PFPT and dorsiflexion ROM may help to decrease gait deviations such as decreased step length and walking speed. When increasing PFPT is not possible, such as in patients with severe muscle or neurological disease, the natural occurrence of limited dorsiflexion ROM may help to maximize ankle moments during walking.

References

[1] Winter DA. Overall principle of lower limb support during stance phase of gait. J Biomech. 1980;13:923-927. [2] Winter DA. Biomechanics of normal and pathological gait: implications for understanding human locomotor control. Journal of Motor Behavior. 1989;21:337-355. [3] Elftman H. Forces and energy changes in the leg during walking. Am J Physiol. 1939; 125;339-356. [4] Fugl-Meyer AR, Gustafsson L, Burstedt Y. Isokinetic and static plantar flexion characteristics. Eur J Appl Physiol. 1980;45:221-234. [5] Winter DA. Biomechanics and Motor Control of Human Movement. 2nd ed. New York, NY: John Wiley & Sons Inc; 1990. [6] Mueller MJ, Minor SD, Sahrmann SA, et al. Differences in the gait characteristics of patients with diabetes and pelipheral neuropathy compared with age-matched controls. Phys Ther. 1994;74;299-313. [7] Olney SJ, MacPhail HA, Hedden DM, Boyce WF. Work and power in hemiplegic cerebral palsy gait. Phys Ther. 1990;70:431-438. [8] Olney SJ, Griffin MP, McBride ID. Temporal, kinematic, and kinetic variables related to gait speed in subjects with hemiplegia: a regression approach. Phys Ther. 1994;74:872-885. [9] Winter DA, Pada AE, Frank JS, Walt SE. Biomechanical walking pattern changes in the fit and healthy elderly. Phys Ther. 1990;70:340-347. [10] Sutherland DH, Cooper L, Daniel D. The role of the ankle plantar flexors in normal walking. J Bone Joint Surg [Am]. 1980;62:354-363. [11] Mueller MJ, Diamond JE, Delitto A, Sinacore DR. Insensitivity, limited joint mobility, and plantar ulcers in patients with diabetes mellitus. Phys Ther. 1989;69:453-462. [12] Proceedings of a consensus development conference on standardized measures in diabetic neuropathy: clinical measures. Diabetes Care. 1992:15;1081-1083. [13] Diamond JE, Mueller MJ, Delitto A, Sinacore DR. Reliability of a diabetic foot evaluation. Phys Ther. 1989;69:797-802. [14] Lahey MA, Downey RG, Saal FE. Intraclass correlations: there's more than meets the eye. Psychol Bull. 1983;93:586-595. [15] Mueller MJ, Norton BJ. Reliability of equipment to measure kinematics of rearfoot motion: a technical report. Phys Ther. 1992;72: 731-737. [16] Cohen J, Cohen P. Applied Multiple Regression/Correlation Analysis for the Behavioral Sciences. 2nd ed. Hillsdale, NJ: Lawrence Erlbaum Associates Inc; 1983. [17] Cavanagh PR, Simoneau GG, Ulbrecht JS. Ulceration, unsteadiness, and uncertainty: the biomechanical consequences of diabetes mellitus. J Biomech Suppl. 1993;26:23-40. [18] Siegler S, Moskowitz GD, Freedman W. Passive and active components of the internal moment developed about the ankle joint during human ambulation. J Biomech. 1984; 17: 647-652. [19] Tardieu C, Lespargot A, Tabary C, Bret MD. Toe-walking in children with cerebral palsy: contributions of contracture and excessive contraction of triceps surae muscle. Phys Ther. 1989;69:656-662. [20] Delbridge L, Perry P, Marr S. Limited joint mobility in the diabetic foot: relationship to neuropathic ulceration. Diabet Med. 1988;5: 333-337. [21] Cavanagh PR, Derr JA, Ulbrecht JS, et al. Problems in gait and posture in neuropathic patients with insulin-dependent diabetes mellitus. Diabet Med. 1992;9:469-474. [22] Winter DA. Foot trajectory in human gait: a precise and multifactorial motor control task. Phys Ther. 1992;72:45-56. [23] Perry J, Mulroy SJ, Renwick SE. The relationship of lower extremity strength and gait parameters in patients with post-polio syndrome. Arch Phys Med Rehabil. 1993;74:165-169. [24] Bohannon RW. Strength of lower limb related to gait velocity and cadence in stroke patients. Physiotherapy Canada. 1986;38:204-206. [25] Mueller MJ, Sinacore DR, Hoogstrate S, Daly L. Hip and ankle walking strategies: effect on peak plantar pressures and implications for neuropathic ulceration. Arch Phys Med Rebabil. 1994;75:1196-1200.

MJ Mueller, PhD, PT, is Assistant Professor, Program of Physical Therapy, Washington University School of Medicine, Box 8502, 660 S Euclid Ave, St Louis, MO 63110 (USA) ([e-mail]). Address all correspondence to Dr Mueller.

SD Minorm, PhD, PT, is Assistant Professor, Program in Physical Therapy, Washington University School of Medicine.

JA Schaaf, PhD, is Research Associate and Lecturer, Department of Mechanical and Aeronautical Engineering, University of California, Davis, CA 95616.

MJ Strube, PhD, is Professor of Psychology, Washington University.

SA Sahrmann, PhD, PT, is Associate Professor, Program in Physical Therapy, Washington University School of Medicine.

This study was supported by a grant from the Foundation for Physical Therapy Inc.

This article was submitted October 31, 1994, and was accepted March 31, 1995.