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Quadriceps Femoris and Hamstring Muscle Function in a Person With an Unstable Knee

ME Maitland, PhD, PT, is Associate Professor and Physical Therapist, Sport Medicine Centre, University of Calgary, 2500 University Dr NW, Calgary, Alberta, Canada T2N 1N4 (maitland{at}acs.ucalgary.ca). Address all correspondence to Dr Maitland
SV Ajemian, is Customer Service Engineer, Motion Analysis Corp. Mr Ajemian was a student at the McCaig Centre for Joint Injury and Arthritis Research, University of Calgary, when this case report was written
E Suter, PhD, is Adjunct Assistant Professor, Human Performance Laboratory, University of Calgary

Submitted October 9, 1997; Accepted August 6, 1998

	Abstract

 
Background and Purpose. The purpose of this case report is to describe the evaluation, treatment, and short-term outcome for an individual with chronic, progressively worsening instability of the knee during gait associated with anterior cruciate ligament (ACL) insufficiency. Case Description. The patient was a 34-year-old man who sustained bilateral ACL injuries. Subsequently, an autograft reconstruction of the left knee ACL was performed. Eight months post-reconstruction, the left knee was unstable despite bracing. Gait analysis and tests to determine the presence of muscle inhibition were performed prior to and after 12 weeks of training. Isometric torque of the knee extensors and flexors was measured with the knee in 90 degrees of flexion. A training program primarily consisted of electromyographic biofeedback during thigh muscle exercises, balance exercises, and gait. Outcomes. Muscle inhibition decreased and maximal isometric knee flexion and extension torques increased during the 12-week training period. Gait analysis demonstrated a 50% decrease in the maximum knee extensor moment and an increase in walking speed. Discussion. Selected gait variables, torque production, and muscle inhibition may change in a person with an unstable knee. The measurement of variables that have previously been documented as mechanisms of knee instability during walking allows for the selection of a specific treatment approach.

Key Words: Anterior cruciate ligament • Electromyography • Gait analysis • Rehabilitation

	Introduction

Top Abstract Introduction Case Description Outcomes Discussion Conclusion References

 
Knee stability during walking following anterior cruciate ligament (ACL) injury is the result of passive connective tissue tension, learned motor patterns, and muscular responses to mechanical stimuli.¹ Because the ACL is the primary connective tissue constraint to anterior translation of the tibia on the femur, increased tibiofemoral joint laxity was found with passive displacement tests² and isolated quadriceps femoris muscle contraction.³ During gait, a person with an ACL-deficient knee may also respond to external forces by using muscles for stability.

There is evidence that muscular control of knee joint stability is impaired following an ACL injury.^4–6 Hamstring muscle contractions in response to postural perturbations, for example, were found to be slower,⁴ postural sway during one-leg standing was found to be greater,⁵ and the threshold to detect passive motion of the knee joint was found to be decreased⁶ in subjects with ACL deficiencies compared with uninjured subjects. Disability in people following an ACL injury may be caused by changes in muscular control.⁷

Persistent muscle weakness has been attributed to patients' inability to voluntarily activate the muscles.⁸ Researchers have described associations between the inability to control the activity of the quadriceps femoris muscles and pain,⁸ joint effusion,⁹ immobilization,¹⁰ and altered joint receptor function.⁷ We are not aware of any studies in which the influence of other potential sources of muscle inhibition, such as psychological and emotional aspects, are documented.

The evaluation of knee dysfunction in people with possible problems in motor control presents a challenge. Lorentzon et al¹¹ used tomography to measure thigh muscle cross-sectional area in conjunction with isokinetic testing in subjects with ACL deficiencies. They found a 5% decrease in quadriceps femoris muscle cross-sectional area and a 25% decrease in knee extensor peak torque at 30°/s compared with the uninjured side. Lorentzon et al¹¹ concluded that limited activity of the quadriceps femoris muscle was the most important factor in producing the torque deficits. These authors, however, did not report whether the percentage of muscle deficit was gravity corrected. Therefore, their use of percentages should be viewed with caution. Snyder-Mackler et al¹² stimulated the femoral nerve during maximal voluntary isometric contractions in subjects with ACL injuries and in subjects without ACL injuries. They found that electrical stimulation of the femoral nerve produced an increase in torque above that obtained with a maximum volitional effort in the subjects with subacute ACL injuries compared with subjects without ACL injuries. In both protocols,^11,12 the maximum volitional activity of the knee extensor muscles was measured relative to the estimated maximum muscular force. The authors^11,12 provided potential methods for evaluating a patient's level of muscle inhibition.

The ability of physical therapy interventions to enhance force production in muscles of people with unstable knees remains controversial.¹¹ Whether muscle inhibition can be modified, in our view, would depend in part on the inhibitory mechanisms involved. Some researchers^11,12 have questioned the effectiveness of "strengthening" exercises for patients with muscle inhibition, assuming that muscle inhibition is a potentially unmodifiable and overwhelming mechanism of thigh muscle dysfunction. Other experts recommend muscle stimulation, electromyographic (EMG) biofeedback, and other methods to overcome muscle inhibition.⁸ The purpose of our case report is to describe the evaluation, treatment, and short-term outcome for a patient with chronic instability of the knee during walking.

	Case Description

Top Abstract Introduction Case Description Outcomes Discussion Conclusion References

 
Patient

The patient was a 34-year-old man who had bilateral knee pain and who reported "giving way" of the left knee as a consequence of a motor vehicle accident (MVA). There were no fractures as a consequence of the MVA. His left knee problems limited his ambulation to short distances. He had a previous history of left ACL deficiency from a soccer injury sustained 4 years prior to the MVA. The diagnosis by the orthopedic surgeon following the MVA was bilateral ACL-deficient knees and left knee osteoarthritis. Ten months after the MVA, he underwent a patellar tendon autograft reconstruction of his left ACL.

Eight months post-reconstruction, he was reviewed by a multidisciplinary group because of left knee instability. During walking, the left leg demonstrated observable anterior instability of the tibia on the femur, and the left tibia visibly subluxated anteriorly with every step. Although there was no known traumatic injury to the hamstring or quadriceps femoris muscles, the patient did not appear, based on our observations, to contract the thigh muscles in an appropriate sequence during gait. The consensus of the surgeons at rounds was that the patient was not a candidate for a revision of his ACL reconstruction and that the patient should seek physical therapy directed at muscular coordination.

Modified KT2000

The KT2000 Knee Ligament Arthrometer^* has been used to quantify the passive displacement of the anterior tibial tubercle relative to the patella (representative of the femoral position) during the application of anterior and posterior forces to the tibia.² The patient was positioned supine with the knee supported at an angle of approximately 20 degrees, and the force-displacement measurement device was attached to the lower extremity. The analog output of the KT2000 was stored on a computer disk, and the force-displacement curve was used to quantify the displacement and stiffness of both knees.¹³ We measured passive displacement at 135 N because this measure has been found to be the most sensitive in detecting differences between left and right sides.¹⁴ The reliability of measurements obtained with the KT2000 was found to be .94 (intraclass correlation coefficient) for subjects with ACL-deficient knees.¹⁵ The passive knee instability measure provided an indication of the integrity of the ACL reconstruction of the left knee. We hypothesized that the instability of the left knee during walking was related to inability of the reconstructed connective tissue to constrain anterior translation of the tibia on the femur, and we were interested in determining whether differences in passive constraints between the patient's 2 unstable knees could account for differences in stability during walking.

Force-displacement plots during anterior translation of the tibia demonstrated passive laxity of both knees (Fig. 1). At 135 N of force, the anterior displacement was 21 mm for the right knee and 22 mm for the left knee. The mean normal anterior displacement at 135 N of force has been reported to be 6 mm.¹⁶

View larger version (22K): [in this window] [in a new window] Figure 1. Modified KT2000 force-displacement test results for left anterior cruciate ligament (ACL)-reconstructed knee and right ACL-deficient knee. Both knees exhibited a similar passive instability. A theoretical plot for a representative, uninjured knee is presented for comparison.

Assessment of Muscle Inhibition

The assessment of muscle inhibition, in our opinion, can theoretically allow for the discrimination between muscle weakness caused by changes within the muscle and muscle weakness caused by insufficient activation of a muscle. Muscle inhibition was estimated using the interpolated twitch torque technique.²³ Bipolar surface EMG electrodes were placed on the vastus lateralis muscle. Carbon-rubber surface stimulation electrodes were placed over the femoral nerve distal to the inguinal canal and over the distal mid-quadriceps femoris muscle. The patient was positioned on a KinCom dynamometer (Kinematic Communicator 125 AP). Stimulation of 240 V for 0.8 milliseconds was applied with a Grass S88 muscle stimulator equipped with a subject isolation unit.^|| Electrical stimulation was applied at rest (resting twitch torque) and during maximal isometric quadriceps femoris muscle contractions (interpolated twitch torque). Before testing, the patient was familiarized with the test situation, and a series of near-maximal practice contractions were performed. Three trials at 2 knee joint angles (90° and 30° of knee flexion) on both lower extremities were performed before and after the 12-week training period. Muscle inhibition (expressed as a percentage) was calculated by the following equation:

The percentage of muscle inhibition prior to treatment was far greater (Table) than for a group of subjects without knee instability.²³ The mean muscle inhibition of the quadriceps femoris muscle determined for a group of 10 volunteers was found to be 10% at 30 degrees of knee flexion and 12% at 90 degrees.²³

View larger version (15K): [in this window] [in a new window] Figure 2. Surface electromyographic activity (EMG) of hamstring muscle of the left lower extremity during walking.

View larger version (18K): [in this window] [in a new window] Figure 4. Mean ankle joint moment (A) and knee joint moment (B) of 5 trials during one step cycle measured before and after the training period. Duration of gait is normalized to stance phase, and moment is normalized to body weight-meters (BWm). Posttreatment plantar-flexion moments increased in amplitude (A) and knee extension moments decreased (B), as compared with pretreatment values.

View larger version (17K): [in this window] [in a new window] Figure 3. Mean ground reaction forces of 5 trials during one step cycle measured before and after a 12-week training period. The gait cycle is normalized to the duration of stance, and the force is normalized to body weight (BW). Following the training period, vertical ground reaction force was separated more distinctly into 2 peaks (panel A, circle). Both the anterior and posterior peak forces of the anteroposterior ground reaction force increased in amplitude (panel B, circles). The medial component of the mediolateral ground reaction force became evident (panel C, circle).

View larger version (17K): [in this window] [in a new window] Figure 5. Mean knee joint angle for 5 trials before and after training period. Duration of the step cycle is normalized to stance phase. The knee flexed early in the stance phase (circle).

The Shuttle modified less press was chosen as an exercise device because the knee joint angle could be controlled between 5 and 60 degrees (Fig. 6). Zero to 66 degrees of knee flexion is considered to be the normal range of motion for humans during walking and stair climbing.¹ We also believed that forces applied to the lower extremity could be controlled by the patient at a level at which the knee position could be maintained with this device. The apparatus also permitted easy setup for EMG biofeedback and visual feedback. The patient was in a supine position on the modified leg press and performed 1- and 2-legged presses while observing the position of his knee in a mirror and monitoring activity levels of the quadriceps femoris and hamstring muscles with EMG biofeedback (Fig. 6).

View larger version (127K): [in this window] [in a new window] Figure 6. Electromyographic biofeedback training during closed-chain exercise on the Shuttle leg press.

Gait training on a treadmill at 2 km/h with bilateral upper-extremity support and a mirror was used to encourage symmetrical lower-extremity motion and endurance. The patient was instructed to contract the hamstring muscles prior to the onset of weight bearing.

	Outcomes

Top Abstract Introduction Case Description Outcomes Discussion Conclusion References

 
Patient's Report

The patient remarked that he was able to walk with increased confidence. He stated that his knee was more stable. The knee pain, however, was not resolved.

Isometric Torque Production

Maximal isometric torque production by the extensors and flexors of both knees increased throughout the 12-week training period (Fig.7). Right knee extension isometric torque at 90 degrees of knee flexion increased by 119%, right knee flexion torque increased by 79%, left knee extension torque increased by 209%, and left knee flexion torque increased by 117%.

View larger version (21K): [in this window] [in a new window] Figure 7. Maximal isometric peak knee extensor torque and peak knee flexor torque at 90 degrees of knee flexion measured periodically during the training period.

Gait Analysis

The assessment of treatment outcome was based, in part, on comparisons with previously published graphics of the gait variables.^25,26 Our analysis also considered reports proposing theories of adaptive and maladaptive compensation patterns in subjects with ACL injuries.^1,27

The patient's average self-determined walking speed during gait assessment was 0.54 m/s prior to the training program and 0.67 m/s after the training program. Rectified and smoothed hamstring muscle EMG during gait (Fig. 2) demonstrated a distinct activation prior to heel-strike and during the initial portion of the stance phase at the posttraining assessment.

Ground reaction forces for the left lower extremity, averaged over 5 trials before and after treatment, are depicted in Figure 3. Our patient demonstrated some improvement in the separation of the deceleration phase and the acceleration phase of the vertical ground reaction force after treatment (Fig. 3A). The mean (± standard deviation) anterior ground reaction force increased from the pretreatment assessment (0.043±0.013 of body weight [BW]) to the posttreatment assessment (0.084±0.007 BW). The mean posterior ground reaction force also increased from the pretreatment assessment (0.103±0.025 BW) to the posttreatment assessment (0.124±0.011 BW). The medial peak ground reaction force (Fig. 3C) was negligible before treatment, (0.002±0.002 BW) but was distinct after treatment (0.020±0.008 BW).

Mean left ankle and knee joint moments measured before and after treatment are illustrated in Figure 4. Ankle plantar-flexion moments were increased after treatment (0.078±0.055 BW) compared with before treatment (0.028±0.038 BW), indicating that more of the propulsive forces were generated through the ankle (Fig. 4A). The mean knee extension moment (Fig. 4B) was reduced in the posttraining trials (0.059±0.033 BW) compared with the pretraining trials (0.125±0.022 BW).

Mean knee joint angle measurements obtained during the stance phase of gait are illustrated in Figure 5. Pretreatment measurements showed that the knee joint flexion angle increased abnormally early before toe-off (50% of stance phase). After treatment, the knee joint angle was maintained for a longer duration during the stance phase (80% of stance phase).

	Discussion

Top Abstract Introduction Case Description Outcomes Discussion Conclusion References

 
The patient described in this case report had bilateral ACL-deficient knees. Although the passive knee instability was comparable for both sides, only the left tibia displayed anterior displacement with each step during the stance phase of gait. The patient demonstrated instability of the left tibiofemoral joint during gait that had been progressive over time. The case history presented here describes an approach to the evaluation and treatment of a patient with muscle inhibition and gait abnormalities. We focused on inpatient measurements because we did not expect changes in function to occur during the period of the study.

Ideally, assessment of the causes of knee instability should lead to appropriate treatment procedures, but there does not appear to be a clear cause of the unilateral tibiofemoral instability in this case. Anterior translation of the tibia is known to be related to the anterior component of the ground reaction force. The quadriceps femoris muscle has been shown to produce an anteriorly directed force on the tibia when it contracts at between 30 and 0 degrees of knee flexion.²⁸ The adaptations of gait observed in our patient, that is, reduction in knee extension moment, decreased anterior ground reaction force, and increased knee flexion, all caused a decrease in anterior shear at the tibiofemoral joint, which should have resulted in a decreased anterior translation of the tibia relative to the femur. Despite these adaptations, instability during walking remained to some extent. Knee stability may also be affected by the contact surface geometry, including congruity, radius of curvature, and anteroposterior tilt, relative to the direction of the applied forces.²⁹ Radiographs were difficult to interpret in this regard, and the mechanics of surface geometry in our patient remain unclear.

Another possible mechanism for unilateral instability during walking may be motor control deficits. Disruption of walking mechanics caused by ACL injury may require alternative muscle activity patterns during locomotion. Left thigh muscle activity during gait appeared, based on observation, to be sporadic and not timed to the gait cycle. This observation was confirmed by EMG analysis. Peak knee extension moment, which occurred at a knee flexion angle of between 14 and 38 degrees, was unopposed by coordinated activity of the hamstring muscles. Over the 12-week training period, volitional muscle activity was improved, as demonstrated by isometric torque measurements and a decrease in muscle inhibition. Gait assessment demonstrated increased weight shifting onto the left lower extremity, activity of the hamstring muscles during touchdown, and a decreased net knee extensor moment. These findings suggested to us improved motor control. An observed decrease in knee extension moment after training as a result of hamstring muscle activity may have resulted in reduced anterior shear of the tibia on the femur. We believe that these findings warrant further investigation to determine whether the altered gait patterns typical of individuals with ACL deficiencies¹ may be a consequence of muscle inhibition and muscle weakness.

The relationship between knee flexor and extensor peak torque measurements and knee function during walking remains controversial. Some authors³⁰ have reported a relationship between torque and ratings of knee symptoms during activities obtained with a questionnaire, whereas other authors³¹ have disputed a relationship between function and measured torque. In general, there is little evidence that a linear relationship exists. The peak isokinetic knee extensor and flexion torque deficits following ACL reconstruction have been found to have a wide range.¹⁵ Our report documents a case in which initially the left knee extensors and flexors failed to regain the ability to produce a torque. The injured knee extensor torque was only 52% of that of the uninjured knee for this patient. Increasing the knee extensor torque without improving hamstring muscle activity during gait may increase instability in the standing position because of the unopposed active drawer effect on the tibia.²⁷

The use of braces is another method of decreasing instability. Several brace designs were used by this patient, but they did not achieve the desired effect of stabilizing the anterior displacement of the tibia relative to the femur. The degree of anterior tibial subluxation during the stance phase of gait while wearing any of the braces was comparable to that observed without a brace. This observation would lead us to believe that the best stabilization effect was achieved by the onset of hamstring muscle activity prior to the onset of quadriceps femoris muscle activity at heel-strike during the stance phase of gait. There is evidence that certain individuals with ACL deficiencies may successfully compensate for ACL-related knee instability.³² In some cases, the hamstring muscles assumed the role of joint stabilizer in patients with ACL deficiencies.⁷ Ciccotti et al³³ described mechanisms where the vastus lateralis, biceps femoris, or tibialis anterior muscle may protect the unstable knee.

The patient remarked that he noticed improvements in his ability to walk on level ground and on stairs. Single-leg stance was considerably easier. He also reported that he believed the improvements in torque production carried over to everyday activities. The knee gave out less often, and he felt more confident in his ability to get around.

Despite the patient's reports of improved gait and our measurements of gait, force production, and muscle inhibition, the patient had continued complaints of pain and residual instability of the left knee. Tibiofemoral and patellofemoral joint osteoarthritis and meniscal degeneration are well-documented sequelae of the ACL injury that would have had an impact on the patient's pain and function.³⁴ Co-contraction of the quadriceps femoris and hamstring muscles may increase internal joint loads, whereas the calculated net internal moments are decreased. Consequently, pain may be increased by muscle co-contraction, and increased joint loads have been implicated in the onset and progression of osteoarthritis.³⁵

	Conclusion

Top Abstract Introduction Case Description Outcomes Discussion Conclusion References

 
A patient with unilateral observable knee instability during walking was the focus of this case report. Both of the patient's knees had comparable passive laxity due to ACL injury, but only one knee exhibited instability during walking. The protocol described in this case report was used to assess some of the potential mechanisms contributing to the unilateral instability, such as muscle activity, range of motion, and forces and moments calculated during walking. In addition, muscle torque and muscle inhibition were assessed. In view of the absence of reliability for the measures we used on the type of patient in our study, our observations must remain tentative. The physical therapy focused on methods to improve mechanisms associated with active joint stability. This case report indicates that selected gait variables, torque production, and muscle inhibition may be improved with treatment. Research is needed, however, to determine whether the treatment affects function and disability level.

	Acknowledgments

 
The ability to carry out this case report was the result of collaboration and sharing of resources between departments and laboratories. We are very grateful for the eager cooperation of the McCaig Centre for Joint Injury and Arthritis Research. Equipment used for this project was generously provided by funding from The Western Orthopaedic Arthritis Research Foundation, ATCO & Canadian Utilities, and Trans Canada Pipeline.

	Footnotes

 
^* MEDmetric Corp, 7542 Trade St, San Diego, CA 92121-2412.

Dataq Instruments, B220 –150 Springside Dr, Akron, OH 44333.

Lumex, PO Box 9003, Ronkonkoma, NY 11779-0903.

Chattanooga Group Inc, PO Box 489, Hixson, TN 37343.

^|| Grass Instruments, Astromed Industrial Park, West Warwick, RI 02893.

^# Kistler Instruments Corp, 75 John Glenn Dr, Amherst, NY 14228-2171.

^** Motion Analysis Corp, 3617 Westwind Blvd, Santa Rosa, CA 95403.

Enraf-Nonius Delft, Röntgenweg 1, PO Box 453, 2600 AL Delft, the Netherlands.

Contemporary Design Corp, PO Box 5146, Glacier, WA 98241.

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