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N Am J Sports Phys Ther. 2008 November; 3(4): 234–241.
PMCID: PMC2953341

Biomechanics of Multi-ligament Knee Injuries (MLKI) and Effects on Gait

Mark V. Paterno, PT, MS, SCS, ATCa and Timothy E. Hewett, PhD, FACSMb

Abstract

Stability at the knee joint is provided by both the static structures, including the ligaments and joint capsule and the coordinated activation of dynamic structures surrounding the joint. These dual stabilizers allow for functional movements, such as gait, to occur safely, effectively, and efficiently. In the presence of a multi-ligament knee injury (MLKI) an absence of static stability can result in an increased reliance on the dynamic knee stabilizers. If sufficient stability is not provided, the potential for an increase in abnormal movements in the knee joint can result. These potential gait alterations that may be associated with a MLKI can result in abnormally high stresses on healing tissues and potentially high shearing forces on articular cartilage, resulting in early breakdown. Early recognition of gait abnormalities and an appropriate implementation of a gait re-training program to control abnormal forces in a patient following an MLKI or a surgical intervention for a MLKI are critical for successful long-term outcomes.

Keywords: Gait, knee, biomechanics, multi-ligament knee injury

INTRODUCTION

The knee joint, comprised of the tibiofemoral and patellofemoral joints, is a complex and dynamic structure and functions as the mobile point of the two longest levers in the body.1 Therefore, the neuromuscular components of the knee must control large magnitude torques imposed by the environment in order to provide adequate stability of a highly mobile joint. The required stability is created in the joint from both static and dynamic stabilizers. Passive stability is created from the ligamentous and capsular structures surrounding the knee. Dynamic stability is provided by the muscular contractions occurring around the joint during movement. Compromise of either the static or dynamic stabilizers of the knee will likely result in impaired movement, functional deficits, and potentially both short and long-term disability.

Walking (gait) is a functional movement that requires effective and efficient knee joint stability via both passive and dynamic joint restraints. Injury to any of the static stabilizers of the knee places an increased burden on the remaining ligamentous structures to provide stability during functional activities such as walking. In the case of a multi-ligament knee injury (MLKI), increased joint laxity in the absence of effective static ligamentous restraints can result in excessive demands on the dynamic stabilizers of the knee and lead to excessive or abnormal motion in the knee joint. These altered movement patterns can increase tensile stress on healing tissues and ultimately deter healing in the patient, both post-injury and post-surgically.14 In addition, this altered repetitive abnormal movement may place abnormally high stress on the articular cartilage of the knee, which could result in premature breakdown of the cartilaginous tissues. Hence, the physical therapist's ability to recognize and correct altered gait in a patient following a MLKI is critical to ensure that the knee joint is not subjected to altered movement patterns and abnormally high forces to the joint.

BIOMECHANICS OF THE KNEE

A discussion of the implications of normal and pathologic gait on the knee joint should begin with an understanding of the role of the static stabilizers of the knee. Static stability in the knee is provided by the four primary ligments of the knee: anterior cruciate ligament (ACL), posterior cruciate ligament (PCL), medial collateral ligament (MCL), and the lateral collateral ligament (LCL). Understanding each ligament's individual contribution to the stability of the knee joint in both unloaded and loaded positions will help the clinician better appreciate their role in normal gait, and how gait will potentially be altered in the absence of one or more of these ligaments in the case of a patient with MLKI.

The cruciate ligaments are the primary static restraints to anterior and posterior translation of the knee joint. The medial and lateral collateral ligaments provide frontal plane stability to the knee, as they are the normal primary static restraints to valgus and varus movement at the joint, respectively. During a normal gait cycle, these ligaments will control frontal plane forces imposed on the knee. The amount of ligamentous stability provided by each of these ligaments is defined by three underlying properties. These properties include the attachment location of the ligament, the “just taut” length of the ligament, and the stiffness properties of the ligament. The anatomic location of the ligament attachment on the tibia and femur create the functional length of the ligament and help to determine their primary restraint function. Slight anatomic variations in the location of the ligament attachment can potentially alter the laxity of the knee joint in multiple planes. The “just taut” length of the ligament dictates the maximum amount of translation or motion in the joint prior to the ligament beginning to resist movement in that plane. Finally, the stiffness of the ligament will dictate how much motion is available after the ligament reaches its slackening end point and is stressed beyond that limit, the “just taut” length, but prior to failure.1,2

The knee can be biomechanically described as having three axes of rotation and six degrees of freedom.2,3 Along each axis and plane, the knee possesses the ability to rotate and translate, respectively, which allows for a total of twelve motions. About the X-axis and in the sagittal plane, the knee has the ability to rotate into flexion and extension and translate in an anterior and posterior direction. About the Y-axis and in the frontal plane, the knee has the ability to rotate in abduction and adduction and translate in a medial and lateral direction. Finally, about the Z-axis and in the transverse plane, the knee has the ability to rotate into internal and external rotation and translate into distraction and compression. Each of these six motions is needed to execute a normal gait cycle. Compromise or limitations created by MLKI can result in stereotypically altered gait patterns.

NORMAL GAIT

Prior to discussion of abnormal gait mechanics caused by MLKI, an understanding of normal gait mechanics is essential for the determination and differentiation of abnormal from normal gait mechanics. The walking gait cycle can be sub-divided into distinct events that together describe the normal cycle of gait. Typically, a gait cycle is described as beginning at initial contact on one foot and ending when that foot completes a full stride and immediately prior to the next initial contact. Each gait cycle can be sub-divided into eight categories. The first five components of the gait cycle include initial contact, loading response, mid-stance, terminal stance, and pre-swing.4 Together these components make up the stance phase of gait, which comprises approximately 60% of a gait cycle. The remaining 40% of the gait cycle makes up the swing phase of gait and it includes sub divisions of initial swing, mid swing, and terminal swing. During each phase of gait, contributions from all three planes of movement result in a normal gait pattern.4

Sagittal Plane Kinematics in Gait

The greatest amount of angular motion at the knee occurs in the sagittal plane during normal gait. The knee typically begins in a near fully extended position at initial contact and then progresses through a biphasic pattern of sagittal plane motion. (Figure 1) As the knee progresses from initial contact to loading response, it flexes to approximately 20 degrees of flexion. (Figure 2) This represents the peak knee flexion angle during the stance phase of gait. The knee then begins to extend during mid stance to a near fully extended position. Following this period of extension, the knee begins to flex during the pre-swing phase in preparation for swing phase, at which time adequate knee flexion is needed to allow toe clearance. Most authors agree that between 60 degrees and 70 degrees of knee flexion is needed to successfully accomplish the swing phase of gait.4-7

Figure 1.
Sagittal Plane Knee Kinematics During Gait
Figure 2.
Loading response with vertical ground reaction force posterior to knee joint

Sagittal Plane Kinetics in Gait

Muscular contributions to a normal gait pattern in a sagittal plane are determined by the external knee flexion-extension moment at the knee.6 The external moment is the rotational force (or torque) that is imposed on a joint by the environment during closed-chain activity. The magnitude and direction of this force is determined by the location of the vertical ground reaction force in relation to the axis of rotation of the joint in question.1 In response to this externally imposed force, the body responds with an equal and opposite internally generated moment to counteract this external moment and allow maintenance of an upright position and progression through the normal gait cycle. This internal moment is typically generated through the coordinated recruitment of the musculature surrounding the joint.

In the sagittal plane, a biphasic pattern of kinematic activity is also observed. As an individual initiates a gait cycle and begins the initial contact phase, the vertical ground reaction force is typically anterior to the knee, creating an external extension moment at the joint. This torque is counterbalanced by a brief, initial activation of the hamstrings and gastrocnemius musculature. As the knee begins to flex and proceed into loading response, the vertical ground reaction force moves posterior to the knee joint axis, which generates an external knee flexion moment. (Figure 2) In order to develop this equal balance of moments, the body generates an internal extension moment through an eccentric activation of the quadriceps musculature to control knee flexion and limit the flexion excursion to 20 degrees.4,6

As the body progresses to midstance and the knee begins to extend again, the vertical ground reaction force begins to approach the knee joint center. During this phase, knee extension motion is achieved through the contribution of several muscles. The quadriceps continue to assist with knee extension initially, however, as midstance progresses the contribution of the quadriceps musculature decreases.8 At this time, extension is accomplished through femoral advancement over a stabilized tibia, which is driven by the momentum of the body generated by the swing limb. The tibia is stabilized through muscle activation of the soleus muscle at the same time.4 As a result of this knee extension mechanism driven by momentum generated from the body, the quadriceps muscle activity in the stance limb ceases at the end portion of midstance. From this point forward, the lower extremity progresses through terminal stance and pre-swing. At this time, the lower extremity is primarily preparing for swing phase, and few gait deviations related to multi-ligament knee injuries are expected to be observed.

Frontal Plane Kinematics and Kinetics in Gait

The normal knee experiences only between 8 degrees and 12 degrees of motion in the coronal plane during a gait cycle. This motion is primarily utilized to maintain balance over the stance limb during gait. The knee's peak abduction (valgus) angle occurs during the progression of initial contact to loading response. Conversely, peak knee adduction (varus) motion is achieved during the swing phase of gait.9 Muscular stability is provided in the coronal plane by muscles oriented in both the frontal and sagittal plane. A contribution to frontal plane stability is generated directly by the iliotibial band (ITB), in addition to contributions from the long head of the biceps femoris and upper gluteus maximus muscles, which serve to increase tension in the ITB.4 Despite their alignment in the sagittal plane, frontal plane joint stability can be generated through co-contraction of the quadriceps and hamstrings musculature. Lloyd et al10,11 noted that 80% of medial lateral stability in the knee is generated through this co-contraction of the quadriceps and hamstrings musculature during dynamic tasks.

Transverse Plane Kinematics in Gait

Similar to the frontal plane, the quantity of rotational motion during gait is smaller than that observed in the sagittal plane. Typically, the knee experiences between 8 degrees and 13 degrees of motion during a typical gait cycle.4,9 At initial contact, the femur is externally rotated on an internally rotated tibia. As the knee progresses from initial contact to loading response, the tibia continues to progress to its position of maximum internal rotation at the end of loading response. The dynamic control of this motion is minimal.6 The majority of transverse stability at the knee is provided by static structures surrounding the knee. This lack of dynamic stability makes injury to the static stabilizers more debilitating during gait as there is a lack of dynamic support to compensate for a lack of static stability. The body's limited dynamic stability to resist the internal tibial rotation occurring at loading response is provided by the tensor fascia lata and the biceps femoris muscle.4

PATHOLOGIC GAIT AS A RESULT OF A MLKI: SAGITTAL PLANE

Abnormal gait patterns can occur in all three planes as a result of injury to the static stabilizers in the knee. Injury to one or more of the surrounding knee ligaments can result in excessive demands on the dynamic knee stabilizers. If the dynamic stabilizers are insufficient to compensate for the lack of static stability, abnormal gait motion and moments can result. The most common gait abnormalities discussed in the literature are in the sagittal plane in a patient with an ACL deficient knee.

Berchuck et al12 first discussed a typical ACL deficient knee gait pattern in 1990, which they termed a “quadriceps avoidance pattern.” In their study of 16 ACL deficient subjects, these authors noted that 75% of the participants presented with a reduction in internal knee extensor moment. This was interpreted by the authors as an absence of quadriceps femoris activation. Essentially, the authors noted a failure of the subjects' knees to progress through the normal biphasic pattern of sagittal plane flexion and extension moments and rather, remained in a stable position, without quadriceps muscle activation through stance phase until pre-swing, when the subjects began to flex their knee in preparation for swing (Figure 3 and and44). The theorized mechanism behind this gait pattern was that insufficient quadriceps muscle strength resulted in the subjects' inability to control the eccentric quadriceps muscle contraction necessary during loading response of gait with a compensatory increase in hamstring muscle activation to control anterior shear during functional movements. Hence, in the absence of the dynamic stability of quadriceps muscle, the knee would “rest on the ligaments” and rely on the static capsular and ligamentous structures of the knee to provide passive, rather than dynamic, support.

Figure 3.
Sagittal Plane Knee Kinetics During Gait
Figure 4.
Frontal Plane gait abnormalities: Varus Thrust

Other reports have noted quadriceps reduction, or a decrease of the external flexion (quadriceps muscle balanced) moment, rather than full quadriceps muscle avoidance or total absence of the external flexion moment. For example, using a similar experimental design to the study by Berchuk et al,12 Roberts et al13 attempted to determine if the quadriceps muscle avoidance pattern was as prevalent as first described in a population that was ACL deficient. A video based motion analysis with electromyography (EMG) on a cohort of 18 ACL deficient patients found that quadriceps muscle activity was present during most of stance phase. This finding was counter to the finding of the absence of the external flexion moment by Berchuk et al,12 inferring no quadriceps muscle activity during this phase of gait. In addition, Roberts et al13 noted that all of the subjects that they studied exhibited the presence of an internal knee extension moment, though this moment was reduced, compared to normal subjects. Hence, the quadriceps muscle avoidance gait pattern was reported to be less common in patients with ACL deficiency than previously described. Roberts et al13 were not alone in their findings. More recently, Torry et al14 and Ferber et al15 also analyzed the gait of those with ACL deficiency and noted a significantly less frequent prevalence of quadriceps avoidance gait than was first proposed by Berchuck et al.12

Rudolph et al16 proposed an alternate mechanism for the reduction in internal knee extensor moment that Berchuck et al12 reported during the stance phase of gait following ACL injury. These authors compared the gait of a cohort of patients with ACL deficiencies who were able to participate in cutting and pivoting activities (labeled copers) to a cohort of patients with ACL deficiencies who were unable to participate in activities of daily living without instability (labeled non-copers). Similar to Roberts et al,13 Torry et al,14 and Ferber et al,15 these authors noted that both copers and non-copers demonstrated significant levels of quadriceps femoris muscle activity, further substantiating the theory that quadriceps muscle avoidance gait in patients with ACL deficient knees was less prevalent, and quadriceps muscle reduction more likely, than initially described. Rudolph et al16 went on to suggest that the less functional cohort of patients (non-copers) were more likely to demonstrate quadriceps femoris and hamstrings muscles co-contraction during loading response and stance as a means to stabilize the knee joint. These patients presented with a decreased internal knee extensor moment. Contrary to the interpretation by Berchuck et al12 that the reduced knee extensor moment was an indication of little or no quadriceps femoris muscle activation, Rudolph et al16 demonstrated that this moment reduction was more likely a sign of relatively less quadriceps muscle activity compared to hamstrings muscle activity. The relative hamstring muscle activity may be increased as a means to stabilize the ACL deficient knee, rather than the suggestion by Berchuck et al12 of the absence of quadriceps femoris muscle activity. Therefore, in the presence of ACL deficiency, patients appear to present with one of several abnormal gait patterns, ranging from a potential complete absence of quadriceps muscle moment, to a reduction in quadriceps muscle activity, to a relative reduction in quadriceps muscle activity in relation to increased hamstring muscle activation as a co-contraction knee stabilization mechanism in these patients.14

In the absence of the ACL in the knee joint during gait, the patient may become dependent on the dynamic stabilizers as well as the secondary static stabilizers. Several authors have noted that the MCL becomes the primary restraint to anterior tibial translation during gait and functional tasks in the absence of the ACL.17-19 Hence, following an ACL/MCL injury, the static stability of the knee is significantly decreased, the knee joint may become primarily reliant on the dynamic stability provided by the surrounding musculature.

PATHOLOGIC GAIT AS A RESULT OF A MLKI: FRONTAL PLANE

Gait abnormalities in the frontal plane also often occur following MLKI. The most common abnormalities are a varus thrust with varus bony alignment in the frontal plane, which can be termed a “double varus” pattern, or a combination of varus thrusting into the frontal plane with hyperextension, termed a “triple varus” gait pattern.20 The varus thrust gait pattern (Figure 4) is typically seen in an individual with anatomic varus aligned knees, in the presence of lateral joint laxity or lateral collateral ligament injury. During the stance phase of gait, the patient thrusts laterally, creating tensile forces on the lateral knee and compressive forces on the medial knee structures. The double varus knee thrusts laterally during stance phase of gait, as it simultaneously thrusts into hyperextension creating stress on the lateral and posterior lateral knee structures, specifically the posterior lateral corner of the knee. In the presence of a lateral collateral ligament injury, the cruciate ligaments now serve as the primary stabilizers to varus and valgus movements.3,21 In a patient with MLKI involving the lateral collateral ligaments, posterior lateral corner, and the cruciate ligaments, the knee becomes dependant on the dynamic stabilizers to resist this abnormal frontal plane movement. If the quadricep and hamstring muscles are unable to provide the required dynamic stability during loading response and stance phase, continued stress is placed on the lateral structures of the knee. In addition, if patients adopt this gait pattern in a post operative situation following reconstructive procedures on the cruciate ligaments or the lateral/posterior lateral knee joint, continued high tensile loads on these healing tissues can result in tissue failure.

PATHOLOGIC GAIT AS A RESULT OF A MLKI: TRANSVERSE PLANE

Pathologic thrusts and gait abnormalities may also be observed in the transverse plane during the stance phase of gait as the result of knee laxity following a MLKI. Again, an initial position of knee hyperextension and a varus alignment of the knee facilitate such a gait pattern. The “triple varus gait pattern” was described by Noyes et al20,22 as a syndrome combining a varus osseous alignment of the knee joint, lateral tibofemoral compartment separation due to LCL insufficiency, and knee hyperextension with involvement of the PCL. Together, this combination of abnormalities can result in a thrusting gait pattern with pathologically increased tibial rotation. The thrust can occur during the stance phase of gait, as the knee thrusts into a varus-hyperextended position, with subsequent traction force at the lateral compartment. In addition, a rotational force can occur at the tibiofemoral joint. When the tibia is internally rotated, this force is accentuated and it is decreased with external tibial rotation.23 As has been observed in gait abnormalities that involved a near extended or hyperextended knee position in stance phase, a relative reduction in the quadriceps muscle ability to eccentrically control the movement of the knee from near full extension at initial contact to 20 degrees of flexion during loading response is often demonstrated. If the patient has an underlying quadriceps muscle weakness, either due to injury or recent surgery, the patient may avoid this position due to lack of dynamic stability, an abnormal gait pattern, or a motor pattern may be adopted to successfully compensate for the task.

The potential adverse outcomes as a result of these abnormal gait patterns are substantial. Following a MLKI that is being managed conservatively, a need exists to protect healing tissues during gait and rehabilitation. Abnormal gait patterns that place excessive tensile forces on healing tissue may prolong or deter ultimate healing of the injured ligaments. Similarly, in a post operative scenario, reconstructed or repaired tissue must also be considered to allow for adequate healing time. Therefore, abnormally high repetitive tensile loads during gait must be controlled. In addition to the short term consequences of altered gait, such as altered healing of ligaments, a long term sequelae may exist as well. Stergiou et al24 and others25 theorized that the excessively high tibial rotations occur during gait in patients with an ACL deficient and ACL reconstructed knee and it may be an underlying mechanism for the development of osteoarthritis. These authors suggest that the abnormally high shearing that occurs following ACL injury, or in patients with a MLKI, places abnormally high forces on the articular cartilage, which may ultimately result in early cartilage tissue breakdown. Therefore, current evidence indicates that gait re-training may be a critical component to successful short term and long term outcomes for patients following MLKI and reconstruction.

GAIT RE-TRAINING

Gait re-training has been described previously by several authors as a key component to successfully resuming activity following a MLKI or surgery.22,23,26 If a patient demonstrates an abnormal gait pattern either post injury or post-operatively, an abnormally high tensile or torsional stress will be placed on healing tissues, which could potentially deter or interrupt the healing and maturational process of the ligament.26 Essentially, two components are required for the successful implementation of a gait re-training program. First, the patient must possess or develop sufficient underlying quadriceps muscle strength to safely ambulate. Many of the abnormal gait patterns observed following a MLKI are in part or entirely related to the knee in a hyperextended position, which results in decreased demand on the quadriceps femoris musculature, as a potential means of compensation for insufficient strength. Typically following injury and surgery, a marked deficit in quadriceps muscle strength occurs. Therefore, the physical therapist must first address any underlying quadriceps muscle strength impairments prior to implementing, or in conjunction with, the gait re-training component of the plan of care. Only after adequate strength development and motor activation is achieved can the patient be expected to feel sufficiently comfortable and confident to develop a gait pattern that is dependent on quadriceps muscle strength and the ability to fluidly activate and control concentric and eccentric activation of the quadriceps muscle.

Following the development of the required level of quadriceps muscle strength, the next phase of gait re-training should focus on the development of the normal biphasic pattern of sagittal plane motion during stance. Typically, the development of the progression of knee flexion from 0 degrees at initial contact to 20 degrees during loading response should be the focus. Neuromuscular facilitation exercises and activities during gait or with supplemental interventions such as a heel lift can be utilized.23,26 Neuromuscular re-education during gait training should focus on early knee flexion following initial contact, and controlled progression of knee flexion during loading response, in addition to maintenance of an upright trunk posture to facilitate hip extensor activation. Heel lifts can force the knee into a flexed position following initial contact, also allowing for increased facilitation of quadriceps muscle contraction during this phase of gait.

The efficacy of a pre-surgery gait re-training program was investigated by Noyes et al.23 The authors categorized gait abnormalities in this population into two distinct patterns, with the efficacy of a gait re-training program reported for each pattern. These authors23 described a Type II gait pattern, which was defined as a hyperextension, whereby the patient maintained a hyperextended knee throughout stance. They also described a Type I gait pattern in which the patient demonstrated a quick “back and forth” motion into flexion and hyperextension while progressing through stance. Noyes et al23 implemented a gait re-training program in both cohorts and reported greater success with gait re-training, especially in the ability to normalize sagittal plane kinematics during a normal gait cycle, in the Type II (hyperextend knee) pattern patient when compared to those with rapid and oscillatory sagittal plane knee movement during stance.

SUMMARY AND CONCLUSION

A MLKI can potentially be a devastating and limb threatening injury for patients. Understanding the underlying biomechanics of the static and dynamic stabilizers of the knee provides a framework to develop an efficacious and safe treatment plan to address underlying impairments with the goal of maximizing dynamic stability of the knee, while protecting the static stabilizing structures. Gait re-training is an important component of any treatment plan to ensure high tensile loads are not being placed on healing tissue, which could ultimately result in ligament failure. If the patient is able to successfully address the impaired function, quadriceps muscle weakness, and gait abnormalities successfully, the patient may be progressed through the early and end stages of rehabilitation without underlying tensile stresses that often coincide with these gait abnormalities and long term failure.

REFERENCES

1. Neuman DA. Knee. In: Neuman DA, editor. (ed). Kinesiology of the Musculoskeletal System. St. Louis, MO: Mosby, Inc; 2002:434–76
2. Grood ES, Noyes FR. Diagnosis of knee ligament injuries: Biomechanical precepts. In: Feagin JA, editor. , (Ed). The Crucial Ligaments.Churchill Livingston;1994:245–60
3. Grood ES, Suntay WJ. A joint coordinate system for the clinical description of three-dimensional motions: application to the knee. J Biomech Eng. 1983;105:136–44 [PubMed]
4. Perry J. Gait Analysis: Normal and Pathological Function. Thorofare, NJ: Slack Inc; 1992
5. Gyory AN, Chao EY, Stauffer RN. Functional evaluation of normal and pathologic knees during gait. Arch Phys Med Rehabil. 1976. 57:571–7 [PubMed]
6. Hewett TE, Paterno MV, Noyes FR. Neuromuscular contributions to knee kinematics and kinetics: Normal versus pathological state. In: Lephart SM, Fu FH, editors. (Eds).
7. Proprioception and Neuromuscular Control in Joint Stability. Champaign, IL: Human Kinetics; 2000
8. Nissan M. Review of some basic assumptions in knee biomechanics. J Biomech. 1980;13:375–81 [PubMed]
9. Inman V, Ralston H, Todd F. Human Walking. Baltimore: Williams and Wilkins; 1981
10. Kettelkamp DB, Johnson RJ, Smidt GL, et al. An electrogoniometric study of knee motion in normal gait. J Bone Joint Surg Am. 1970; 52: 775– 90 [PubMed]
11. Lloyd DG. Rationale for training programs to reduce anterior cruciate ligament injuries in Australian football. J Orthop Sports Phys Ther. 2001;31:645–54 [PubMed]
12. Lloyd DG, Buchanan TS. Strategies of muscular support of varus and valgus isometric loads at the human knee. J Biomech. 2001;34:1257–67 [PubMed]
13. Berchuck M, Andriacchi TP, Bach BR, Reider B. Gait adaptations by patients who have a deficient anterior cruciate ligament. J Bone Joint Surg Am. 1990;72:871–7 [PubMed]
14. Roberts CS, Rash GS, Honaker JT, et al. A deficient anterior cruciate ligament does not lead to quadriceps avoidance gait. Gait Posture. 1999;10:189–99 [PubMed]
15. Torry MR, Decker MJ, Ellis HB, et al. Mechanisms of compensating for anterior cruciate ligament deficiency during gait. Med Sci Sports Exerc. 2004;36:1403–12 [PubMed]
16. Ferber R, Osternig LR, Woollacott MH, et al. Gait mechanics in chronic ACL deficiency and subsequent repair. Clin Biomech (Bristol, Avon). 2002;17:274–85 [PubMed]
17. Rudolph KS, Axe MJ, Buchanan TS, et al. Dynamic stability in the anterior cruciate ligament deficient knee. Knee Surg Sports Traumatol Arthrosc. 2001;9:62–71 [PubMed]
18. Haimes JL, Wroble RR, Grood ES, Noyes FR. Role of the medial structures in the intact and anterior cruciate ligament-deficient knee. Limits of motion in the human knee. Am J Sports Med. 1994;22:402–9 [PubMed]
19. Shelburne KB, Torry MR, Pandy MG. Muscle, ligament, and joint-contact forces at the knee during walking. Med Sci Sports Exerc. 2005;37:1948–56 [PubMed]
20. Sullivan D, Levy IM, Sheskier S, et al. Medical restraints to anterior-posterior motion of the knee. J Bone Joint Surg Am. 1984;66:930–6 [PubMed]
21. Noyes FR, Schipplein OD, Andriacchi TP, et al. The anterior cruciate ligament-deficient knee with varus alignment. An analysis of gait adaptations and dynamic joint loadings. Am J Sports Med. 1992;20:707–16 [PubMed]
22. Schipplein OD, Andriacchi TP. Interaction between active and passive knee stabilizers during level walking. J Orthop Res. 1991;9:113–9 [PubMed]
23. Noyes FR, Barber SD, Simon R. High tibial osteotomy and ligament reconstruction in varus angulated, anterior cruciate ligament-deficient knees. A two- to seven-year follow-up study. Am J Sports Med. 1993;21:2–12 [PubMed]
24. Noyes FR, Dunworth LA, Andriacchi TP, et al. Knee hyperextension gait abnormalities in unstable knees. Recognition and preoperative gait retraining. Am J Sports Med. 1996;24:35–45 [PubMed]
25. Stergiou N, Ristanis S, Moraiti C, Georgoulis AD. Tibial rotation in anterior cruciate ligament (ACL)-deficient and ACL-reconstructed knees: A theoretical proposition for the development of osteoarthritis. Sports Med. 2007;37:601–13 [PubMed]
26. Ristanis S, Giakas G, Papageorgiou CD, et al. The effects of anterior cruciate ligament reconstruction on tibial rotation during pivoting after descending stairs. Knee Surg Sports Traumatol Arthrosc. 2003;11:360–5 [PubMed]
27. Medvecky MJ, Zazulak BT, Hewett TE. A multidisciplinary approach to the evaluation, reconstruction and rehabilitation of the multi-ligament injured athlete. Sports Med. 2007;37:169–87 [PubMed]

Articles from North American Journal of Sports Physical Therapy : NAJSPT are provided here courtesy of The Sports Physical Therapy Section of the American Physical Therapy Association