Archives of Physical Medicine and Rehabilitation
Volume 90, Issue 5 , Pages 819-826, May 2009

Changes in Passive Mechanical Properties of the Gastrocnemius Muscle at the Muscle Fascicle and Joint Levels in Stroke Survivors

  • Fan Gao, PhD

      Affiliations

    • Rehabilitation Institute of Chicago, Chicago, IL
    • Department of Physical Medicine and Rehabilitation, Northwestern University, Chicago, IL
    • Department of Health and Kinesiology, University of Texas at Tyler, Tyler, TX
    • ,
  • Thomas H. Grant, MD

      Affiliations

    • Department of Radiology, Northwestern University, Chicago, IL
    • ,
  • Elliot J. Roth, MD

      Affiliations

    • Rehabilitation Institute of Chicago, Chicago, IL
    • Department of Physical Medicine and Rehabilitation, Northwestern University, Chicago, IL
    • ,
  • Li-Qun Zhang, PhD

      Affiliations

    • Rehabilitation Institute of Chicago, Chicago, IL
    • Department of Physical Medicine and Rehabilitation, Northwestern University, Chicago, IL
    • Department of Orthopaedic Surgery, Northwestern University, Chicago, IL
    • Department of Biomedical Engineering, Northwestern University, Chicago, IL
    • Corresponding Author InformationReprint requests to Li-Qun Zhang, PhD, Rehabilitation Institute of Chicago, Ste 1406, 345 E Superior St, Chicago, IL 60611

Article Outline

Abstract 

Gao F, Grant TH, Roth EJ, Zhang L-Q. Changes in passive mechanical properties of the gastrocnemius muscle at the muscle fascicle and joint levels in stroke survivors.

Objectives

To investigate the ankle joint–level and muscle fascicle–level changes and their correlations in stroke survivors with spasticity, contracture, and/or muscle weakness at the ankle.

Design

To investigate the fascicular changes of the medial gastrocnemius muscle using ultrasonography and the biomechanical changes at the ankle joint across 0°, 30°, 60°, and 90° knee flexion in a case-control manner.

Setting

Research laboratory in a rehabilitation hospital.

Participants

Stroke survivors (n=10) with ankle spasticity/contracture and healthy control subjects (n=10).

Interventions

Not applicable.

Main Outcome Measurements

At the muscle fascicle level, medial gastrocnemius muscle architecture including the fascicular length, pennation angle, and thickness were evaluated in vivo with the knee and ankle flexion changed systematically. At the joint level, the ankle range of motion (ROM) and stiffness were determined across the range of 0° to 90° knee flexion.

Results

At comparable joint positions, stroke survivors showed reduced muscle fascicle length, especially in ankle dorsiflexion (P≤.048) and smaller pennation angle, especially for more extended knee positions (P≤.049) than those of healthy control subjects. At comparable passive gastrocnemius force, stroke survivors showed higher fascicular stiffness (P≤.044) and shorter fascicle length (P≤.025) than controls. The fascicle-level changes of decreased muscle fascicle length and pennation angle and increased medial gastrocnemius fascicle stiffness in stroke were correlated with the joint level changes of increased joint stiffness and decreased ROM (P<.05).

Conclusions

This study evaluated specific muscle fascicular changes as mechanisms underlying spasticity, contracture, and joint-level impairments, which may help improve stroke rehabilitation and outcome evaluation.

Key Words: Contracture, Muscle spasticity, Rehabilitation, Stroke

List of Abbreviations: ACSA, anatomical cross-sectional area, ROM, range of motion

 

SPASTICITY, CONTRACTURE, and muscle weakness are commonly observed after stroke and are major sources of disabilities poststroke. Clinically, the phenomenon of footdrop is associated with an increase in the tone of the calf muscles. Muscle tone may result from both reflex and nonreflex changes and is usually accompanied with increase of passive joint/muscle stiffness.1 In the spastic lower limb, it is not clear how hypertonia at the ankle joint is related to changes in the biomechanical properties of the plantar flexor muscles.2, 3, 4, 5, 6, 7 A better understanding of changes in muscle architecture and its association with joint biomechanical properties could help us gain insight into mechanisms underlying spasticity/contracture and provide guidance to the rehabilitation of patients poststroke. The changes in the mechanical properties may be associated with changes in skeletal muscle architecture, such as muscle fascicle length, pennation angle, and muscle thickness. Muscle architecture plays a significant role in normal muscle function and is closely related to the mechanical properties of the joint.8 Recent studies based on a biomechanical model suggested that an increase in ankle joint stiffness could be attributed to shortened calf muscles.2 However, there has been little experimental evidence evaluating muscle architecture and joint stiffness in the same patients with ankle spasticity/contracture.

Ultrasonography has been used in studying muscle and tendon function in healthy populations in vivo and noninvasively.9, 10, 11 However, only a few ultrasonic studies have been conducted to examine hypertonic muscles in patients with neurologic disorders, with mixed results reported and with a lack of study on lower limb muscle architecture poststroke. Shortland et al12 reported no difference in muscle fascicle length between children with spastic diplegia and healthy children, suggesting muscle architecture changes do not contribute to contracture in the patients, while Cheatwood et al13 reported significantly shorter muscle fascicle length in the group of children with spastic cerebral palsy. Li et al14 found that the fascicle length of spastic brachialis muscle on the affected side was significantly shorter than that on the unimpaired side. The differences in gastrocnemius muscle architecture were also studied in children with cerebral palsy, and fascicle length of spastic muscle was significantly shorter than that in nonparetic muscle of healthy children.15, 16, 17

The purpose of the this study was to investigate, in vivo and noninvasively, the biomechanical changes of the medial gastrocnemius muscle at both the joint level (characterized by the ROM, stiffness, resistance torque at controlled position) and the muscle fascicle level (characterized by the muscle fascicle length, pennation angle, muscle thickness) at ankles in both stroke survivors with spasticity/contracture and healthy control subjects. We hypothesized that there are significant differences in these biomechanical properties at the fascicle and joint levels between the 2 groups, and changes at the joint level are correlated to those at the fascicle level.

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Methods 

Participant Selection 

A convenience sample of 10 chronic stroke survivors (at least 1 year poststroke; age, 54.7±11y; weight, 84.5±15.5kg; height, 176±5.3cm; shank length, 39.4±1.0cm) with ankle spasticity/contracture were recruited. The Modified Ashworth Score18 was measured at the ankle (2.57±0.58). In addition, the following criteria were used: the subjects were not involved in any other studies that could potentially affect the test results, and subjects could walk independently without walking aid and sit on a chair for 2 hours. Ten age-matched and sex-matched healthy subjects (age, 56.6±20.7y; weight, 87.1±17.6kg; height, 177.3±3.7cm; shank length, 38.6±1.2cm) without any neurologic or muscular disorders served as controls. All subjects gave informed consent approved by the institutional review board.

Experimental Setup 

A custom knee-ankle joint test device was used to investigate the biomechanic properties of the biarticular medial gastrocnemius muscle. The motor at the knee was fixed rigidly to a frame anchored to the ground, and a leg linkage was mounted to the knee motor through a 6-axis JR3 force sensor.a The ankle motor was mounted at the distal end of the leg linkage, and a footplate was mounted to the ankle motor through another 6-axis force sensor. The ankle motor and footplate could be adjusted along the leg linkage so that the ankle and knee motors were aligned with the ankle and knee flexion axes, respectively (fig 1).

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  • Fig 1. 

    (A) Experimental setup. The knee-ankle evaluation device consists of 2 motors and a linkage between. The JR3 force/torque sensors were mounted on the motor shaft at both joints to measure the joint torques/forces. With the knee flexion axis aligned with the knee motor, the ankle motor can be adjusted along the leg linkage to align it with the ankle flexion axis. (B) Longitudinal ultrasonic images of the medial gastrocnemius muscle at rest. The skin is on the top of the image, and the left side corresponds to proximal. The muscle tendon junction represented the musculo-tendon (muscle aponeurosis) junction. α and β are the posterior and anterior pennation angles, respectively. The medial gastrocnemius muscle tendon junction was taken as the distal reference point.

Experimental Protocol 

A brief medical history including the date of stroke, ambulatory status, use of ankle-foot orthosis, use of antispasticity drugs, and current therapy was documented for each stroke survivor. The leg length (from the lateral femoral epicondyle to the lateral malleolus19) and foot height (from the bottom of foot to the lateral malleolus) were measured to align the knee and ankle with the experimental device.

Subjects were seated upright with the thigh and trunk secured using Velcro straps. The leg and foot were attached to the leg linkage and footplate, respectively (see fig 1). Four knee positions, starting from full extension with an increment of 30° of flexion, were tested. At each knee position, the ankle flexion angle was systematically varied between 20° dorsiflexion and 45° plantar flexion, with increments of 10° in dorsiflexion and 15° in plantar flexion relative to 0° of ankle flexion. The knee and ankle motors were locked at each of the target positions. At each knee position, the subject was asked to relax with the ankle at the resting position. The corresponding ankle resting angle and torque were recorded. In addition, the resistance torque at 0° dorsiflexion was measured. At each of the knee and ankle positions, the subject was asked to relax, and the knee and ankle torques and angles were recorded for 2 seconds. Because some stroke survivors had reduced ROM, the experiment was conducted within the comfort limits of each subject.

Ultrasonic images of the medial gastrocnemius muscle were collected using a 14-MHz high-resolution matrix probe.b LOGIQView, a technique of extended field of view, was used to overcome the limited field of view and register the muscle images covering the full fascicle lengths. A previous study has shown the reliability of ultrasound technique for measuring muscle architecture,20 and the accuracy of extended field of view has been reported to be better than 5%.21 The probe was placed perpendicular to the skin and moved smoothly along the middle line of the medial gastrocnemius throughout its length (see fig 1). All scans were conducted by an experimenter with experience in ultrasonic measurements. The scan was repeated 3 times, and the averaged values of these measurements across scans were used in further analysis.

Data Analysis 

The torque signal at each joint was low-pass–filtered with fourth-order Butterworth filter (5Hz cutoff frequency) and averaged across the 2-second period. Ankle joint stiffness was calculated as the change of ankle joint resistance torque over the change of ankle joint angle (K=Δτ/Δθ) across the ROM. In this study, the ankle joint stiffness was quantified between different ankle positions reaching steady state instead of during continuous dynamic movement. The muscle fascicle length,22 as indicated by the line between the aponeuroses, was measured at 5cm proximal to the muscle-tendon junction (see fig 1B). In addition to the absolute fascicle length, its normalization to the lower-leg length was also calculated for the individual subjects. The pennation angle was defined as the angle between the fascicle and the aponeurosis both posteriorly and anteriorly (see fig 1B). For simplicity, we focused on the anterior pennation angle. Muscle thickness was measured at 5cm proximal from the muscle-tendon junction (see fig 1B). Measurements including joint resistance torque, joint stiffness, muscle fascicle length, and pennation angle were interpolated across the ankle flexion using the shape-preserving piecewise cubic method (by using interp1 function in MATLAB with option pchipc).

The gastrocnemius contribution to the ankle passive resistance torque was estimated as the difference of the passive ankle resistance torque between full knee extension and 90° knee flexion. The calculation was done in the range of 20° plantar flexion to 15° dorsiflexion. With the gastrocnemius moment arm for ankle plantar flexion obtained from SIMM,d the passive resistance force of the gastrocnemius was determined and related to the measured medial gastrocnemius fascicle length. The moment arm was not normalized for individual subjects because there were no significant differences in body height for either stroke survivors (P=.15, t test) or healthy controls (P=.74, t test) compared with the body height used in SIMM (175cm, height of an average man). Furthermore, assuming the passive force sharing between the lateral and medial heads of gastrocnemius to be proportional to the ACSA with the medial and lateral gastrocnemius ACSAs at 10.20 and 6.53cm2, respectively,23 the passive medial gastrocnemius force was determined as 61% of the total passive gastrocnemius force. It was assumed that the passive tension of the gastrocnemius muscle was negligible at 90° knee flexion because it had been reported that the passive tension was close to 0 with 10° plantar flexion and greater than 50° knee flexion.24 The corresponding medial gastrocnemius fascicular force was scaled by 1/cos(θpennation), with θpennation the pennation of medial gastrocnemius fascicles. The medial gastrocnemius fascicular stiffness was determined as the slope of the medial gastrocnemius fascicular force and fascicular length relationship.

Statistical Analysis 

Repeated-measures analysis of variance was used to analyze the response variables (fascicle length, pennation angles, muscle thickness, joint stiffness, ROM) with respect to each factor (subject population, ankle position, knee position). The significance level was set at .05, and adjustments were made if a violation of sphericity was found (Huynh-Feldt adjustment if the sphericity estimate >0.75, Greenhouse-Geisser otherwise). The Student t test was used for comparison of the variables between groups. The Pearson correlation coefficient was used to quantify associations among the variables, and the Spearman rank correlation was used to test the monotonic trend (eg, if one variable is increased, the other follows). Correlations between the muscle architecture measures (medial gastrocnemius fascicular stiffness, fascicle length, pennation) and the joint-level variables (passive resistance torque, joint stiffness, ankle dorsiflexion ROM) were evaluated.

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Results 

Biomechanic Changes at the Joint Level 

Decreased passive ankle range of motion in stroke survivors 

Under comparable joint torques (5Nm in dorsiflexion and 3Nm in plantar flexion), stroke survivors showed reduced ROM compared with healthy controls. With knee flexion of 30°, the ankle positions ranged from –34.1±4.8° to –3.1±4.1° and from –37.7±4.8° to 13.5±6.9° for stroke survivors and healthy control groups, respectively. The ROM difference became significant as the ankle was dorsiflexed. The ankle positions ranged from –31.2±7.9° to –6.4±5.1° and from –35.3±6.5° to 6.5±5.3° with the knee fully extended for stroke survivors and healthy control groups, respectively. Across the different knee flexion angles, patients poststroke showed a larger ankle resting angle (more into plantar flexion) than the healthy controls (P=.006). At full knee extension, the ankle resting positions of the stroke and healthy groups were –18.2±6.6° and –13.6±3.9°, respectively. With the knee flexed from 30° to 90°, the resting positions changed from 19.5±5.2° to 17.5±4.6° and from 12.7±3.5° to 13.1±5.2° for the stroke and control groups, respectively. Although the medial gastrocnemius spans both knee and ankle, the ankle resting position was not significantly affected by the knee position (P=.841).

Increased ankle stiffness in stroke survivors 

Ankle stiffness changed with both ankle (P<.001) and knee flexion (P<.001). Stroke survivors exhibited higher ankle stiffness than healthy controls, especially in dorsiflexion (fig 2; P<.05). At 0° dorsiflexion and full knee extension, for example, the stiffness was .24±.08 and .72±.28Nm/° for the control and stroke groups, respectively. Ankle stiffness ranged from .076 to .75Nm/° and from .17 to 1.46Nm/° for the control and stroke groups, respectively. Ankle stiffness was highest at extreme dorsiflexion and lowest around the ankle resting position (see fig 2).

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  • Fig 2. 

    Passive stiffness at the ankle joint for both healthy subjects (dark line) and patients poststroke (gray line) at 4 knee positions: (A) full knee extension, (B) 30° knee flexion, (C) 60° knee flexion, and (D) 90° knee flexion. *Significant differences between the 2 populations with P<.05 (t test). Abbreviations: DF, dorsiflexion; PF, plantarflexion.

Biomechanic Changes at the Muscle Fascicle Level 

Muscle fascicle length 

As a biarticular muscle, the medial gastrocnemius muscle fascicle length varied with both ankle (P=.001) and knee flexion (fig 3; P=.001, both groups combined), and a significant interaction between the knee and ankle flexions was also observed (P≤.001). The fascicle length increased monotonically as the ankle dorsiflexed but decreased as the knee flexed (P≤.001; see fig 3). For instance, for stroke survivors, the muscle fascicle length increased from 32.0±8.1mm to 58.8±10.7mm as the ankle moved from 45° plantar flexion to 15° dorsiflexion with the knee at full extension, while it decreased from 51.4±8.4mm to 34.2±7.0mm as the knee flexed from full extension to 90° flexion with the ankle at the neutral position.

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  • Fig 3. 

    Muscle fiber lengths of both healthy subjects (dark line) and stroke survivors (gray line) at 4 knee positions: (A) full knee extension, (B) 30° knee flexion, (C) 60° knee flexion, and (D) 90° knee flexion. *Significant differences between the 2 populations with P<.05 (t test). Abbreviations: DF, dorsiflexion; PF, plantar-flexion.

Although the 2 groups showed similar trends, stroke survivors had significantly shorter muscle fascicles compared with healthy subjects across the ankle ROM, especially with the ankle dorsiflexed (see fig 3; P<.05). Medial gastrocnemius fascicle length depended on both knee and ankle positions, and significant interaction between the 2 joints was observed (P<.05). With the knee fully extended, for example, the fascicle length of stroke survivors was shorter than that of healthy controls across the range of 45° plantar flexion to 15° dorsiflexion. However, the difference diminished as the knee was flexed. Similar results were observed for normalized muscle fascicle lengths. Stroke survivors showed significantly shorter normalized muscle fascicle length than healthy controls, especially with the ankle dorsiflexed (P<.05).

Pennation angle 

The pennation angle decreased monotonically as the ankle moved from plantar to dorsiflexion and increased as the knee flexed from full extension to 90° flexion (P=.001). For instance, for control subjects, the pennation angle increased from 19.5±2.6° to 27.4±5.1° as the knee flexed from 0° to 90° flexion with the ankle at 0° dorsiflexion (fig 4). The pennation angle ranged from 17.1±2.4° to 41.4±7.8° and from 14.2±4.0° to 37.1±6.4° for the healthy and stroke groups, respectively.

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  • Fig 4. 

    The relationship between the medial gastrocnemius fascicle length and the passive gastrocnemius force (thick line) and the medial gastrocnemius fascicle force (gastrocnemius force × 0.610 / cos(θpennation); thin line) for the stroke and control groups (the group average with 1-sided SE was shown for both fascicle length and muscle/fascicle force). The medial gastrocnemius fascicle length was determined at full knee extension with ankle between 20° plantar flexion and 15° dorsiflexion.

Stroke survivors showed smaller pennation angles than healthy controls, especially at more extended knee positions (P≤.049; fig 5). For instance, the pennation angles with the ankle at 0° dorsiflexion and at 30° of knee flexion were 22.1±3.1° and 17.5±3.9° for the controls and stroke survivors, respectively. The differences decreased as the ankle approached extreme dorsiflexion.

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  • Fig 5. 

    Anterior pennation angles of both healthy subjects (dark line) and stroke survivors (gray line) at 4 knee positions: (A) full knee extension, (B) 30° knee flexion, (C) 60° knee flexion, and (D) 90° knee flexion. *Significant differences between the 2 populations. P<.05 (t test). Abbreviations: DF, dorsiflexion; PF, plantarflexion.

Muscle thickness 

With the knee extended and/or the ankle dorsiflexed, the medial gastrocnemius became tighter, and muscle thickness decreased. As the knee was flexed, the change in muscle thickness with ankle dorsiflexion also increased. For instance, for healthy control subjects, as the ankle moved from 15° dorsiflexion to 45° plantar flexion, the muscle thicknesses increased from 10.0±3.7 to 15.0±3.1mm, 9.8±4.0 to 14.7±2.8mm, 10.7±3.2 to 16.2±2.5mm, and 10.9±2.6 to 17.6±3.5mm at 0°, 30°, 60°, and 90° knee flexion, respectively. The muscle thickness for stroke survivors was slightly smaller than that of healthy controls. However, the differences were significant only at extreme ankle dorsiflexion and knee extension.

Passive force and fascicle length relationship 

At comparable levels of medial gastrocnemius fascicular force, ranging from 20 to 80N, the medial gastrocnemius fascicular stiffness (slope of the medial gastrocnemius fascicular force and medial gastrocnemius fascicular length relationship) was significantly higher for stroke survivors than controls (P≤.044; see fig 4). For example, at 50N medial gastrocnemius fascicular force, the slopes were 12.4±4.7 and 6.5±3.6N/mm for the stroke and control groups, respectively. Similarly, the gastrocnemius force and medial gastrocnemius fascicle length curve of stroke survivors had significantly steeper slope than that of controls at comparable levels of gastrocnemius force (P≤.044). In addition, at comparable gastrocnemius passive tension levels ranging from 30 to 130N, stroke survivors had significantly shorter medial gastrocnemius fascicle length than controls (P≤.025). For instance, the medial gastrocnemius muscle fascicle lengths were 48.1±13.4 and 65±15mm for the stroke and control groups, respectively, at 80N gastrocnemius passive tension (P≤.001; see fig 4).

Relationship Between Changes at the Joint and Fascicle Levels 

The joint and fascicle level variables were correlated. The ankle ROM showed a moderate negative correlation with the muscle fascicle length (r=–.286; P<.01), pennation angle (r=.304; P<.01) and medial gastrocnemius muscle fascicle stiffness (r=–.151; P<.05) at full knee extension. Joint stiffness showed a negative correlation with muscle fascicle length (r=–.20; P<.01) and a positive correlation with medial gastrocnemius fascicular stiffness (r=.51; P≤.001). Significant correlations were observed between the variables evaluated within the fascicle or joint level. At the fascicle level, muscle fascicle length was correlated with pennation angle (r=–.46; P≤.001). At the joint level, the resistance torque and joint stiffness were correlated (r=.66; P≤.001), and the 2 variables were both correlated with the ankle ROM negatively (r=–.69, P≤.001; and r=–.38, P≤.001, respectively).

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Discussion 

Biomechanic changes at the ankle joint are associated with spasticity/contracture in stroke survivors, including reduced ROM and increased resistance and stiffness at the ankle. However, the corresponding changes at the muscle fascicle level and the correlations between changes at the 2 levels have not been investigated together in the stroke population. In this study, we use ultrasonography combined with biomechanical measurements to evaluate in vivo muscle fascicle as well as joint properties and correlate the pathologic changes at the joint level with the underlying changes at the muscle fascicle level.

The current study examined biomechanic changes at the joint level with more complete knee-ankle positions than previous studies on healthy subjects.2, 4, 7 In the current study, 4 knee positions ranging from full extension to 90° flexion were evaluated, while previous studies usually involved only 1 knee position,4, 7 and 1 study measured changes in gastrocnemius fascicle length as a function of knee and ankle position without reporting the absolute fascicle length.25 Our results agreed well with previously reported results at comparable leg positions.2, 4, 7 For instance, the ankle joint stiffness measured at 10° dorsiflexion with 90° knee flexion for stroke survivors was 0.6±0.4Nm/° in the current study and 0.5±0.4Nm/°,7 0.44Nm/°,2 and 0.5±0.4Nm/°4 in previous studies.

In this study, muscle architecture was compared between stroke survivors and healthy subjects quantitatively. In general, measurements of muscle architecture in healthy subjects agreed well with previously published data.10, 20, 25, 26, 27, 28 In this study, the medial gastrocnemius fascicle length of healthy control changed from 28 to 78mm across the ankle and knee positions. The results on medial gastrocnemius fascicle length normalized to the lower-leg length also showed similar results. Arampatzis et al26 reported a range from 37 to 67mm across 6 ankle and knee angle combinations with the ankle position between 20° plantar flexion and 10° dorsiflexion. The larger range of fascicle length in our study may arise from the larger range of ankle and knee positions (ankle position between 45° plantar flexion and 15° dorsiflexion). Because of the lack of published data, direct comparisons could not be made for the results on stroke survivors.

Muscle force is transmitted to the tendon at a pennation angle with muscle force scaled according to the cosine of the pennation angle.9, 23, 29 It has been reported that hypertrophy of muscles involves an increase in pennation angle.9 In contrast, the smaller pennation angles in stroke survivors observed in this study indicated muscle atrophy poststroke. Furthermore, considering the muscle fascicle length may be reduced poststroke, the decreased pennation angle suggests higher fascicular tension under the passive condition, which may be associated with the increased tone of the calf muscles in stroke.

Functional impairments at the joint level are closely related to the changes in muscle architecture properties. The higher medial gastrocnemius fascicle stiffness, joint stiffness in dorsiflexion, and reduced ROM at controlled resistance torques in stroke survivors were associated with shortening of muscle fascicles as demonstrated by the significant correlations between the 2 sets of variables. It has been shown that the number of sarcomeres in series in a muscle is highly adaptable to changes in muscle length.30, 31, 32 Patients poststroke often develop footdrop, which may be a result of shortened plantar flexors fascicles. As shown in figure 4, stroke survivors had significantly higher gastrocnemius muscle and medial gastrocnemius fascicular stiffnesses, indicating an underlying mechanism for the increased joint stiffness. This was consistent with an in vitro study by Friden and Lieber,33 who showed that the spastic muscle cell is stiffer and shorter than the normal control. Similarly, through modeling analysis, Svantesson et al34 showed that muscle stiffness was significantly higher in the affected leg than the nonaffected leg of stroke survivors. In addition, in this study, a significant correlation (r=.855; P<.001) was observed between the Modified Ashworth Score and ankle joint stiffness.

Study Limitations 

There were limitations with the present study. First, the fascicle length and pennation were determined 5cm from the muscle tendon junction. Although it has been shown that there is marked uniformity in fascicle length throughout a muscle,35, 36 some studies reported heterogeneity of pennation angles37 and fascicle lengths38 along the length of muscle. Thus, the relationships between joint angles and fascicle arrangement might differ in different portions of a muscle. In this study, we chose the location of 5cm from the muscle tendon junction to obtain a representative measurement and kept it consistent across the subjects. Second, the measured medial gastrocnemius pennation angle was assumed to be the same for the lateral gastrocnemius. However, the lateral head may have smaller pennation.10 To distribute the tension between the lateral and medial heads, we assumed that the tension was proportional to the ACSA, which represented an approximation for the 2 populations. It would be interesting to see whether the ACSA and passive tension ratio of medial head to lateral head is altered because of stroke. Last, the sample size in the current study was relatively small, although significant differences in biomechanical properties were still observed.

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Conclusions 

The present study found that compared with healthy subjects, stroke survivors showed simultaneous changes at the fascicle and joint levels, including decreased length and reduced pennation angle of the muscle fascicles, and decreased ROM and increased stiffness in dorsiflexion at the joint. Biomechanic changes at the fascicle and joint levels were correlated to each other, and the changes at the joint may originate from the muscle fascicles. Clinical symptoms of spasticity/contracture may be closely related to changes in muscle architecture, including shortening of muscle fascicles and reduction of pennation angle. In vivo evaluation of both muscle and joint properties may serve as a quantitative tool in stroke rehabilitation and outcome evaluation.

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  • a JR3 Inc, 22 Harter Ave, Woodland, CA 95776.
  • b GE LOGIQ-9, PO Box 414, Milwaukee, WI 53201.
  • c MathWorks Inc, 3 Apple Hill Dr, Natick, MA 01730.
  • d MusculoGraphics Inc, 3617 Westwind Blvd, Santa Rosa, CA 95403.

 Supported by the National Institutes of Health (grant nos. HD044295 and HD043664).

 No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit on the authors or on any organization with which the authors are associated.

PII: S0003-9993(09)00078-1

doi:10.1016/j.apmr.2008.11.004

Refers to erratum:

  • Correction

    Archives of Physical Medicine and Rehabilitation September 2009 (Vol. 90, Issue 9, Page 1643)

Archives of Physical Medicine and Rehabilitation
Volume 90, Issue 5 , Pages 819-826, May 2009

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