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Letters and Responses |
Associate Professor Department of Physical Therapy North Georgia College and State University Dahlonega, GA 30597
To the Editor:
"Quadriceps Femoris and Hamstring Muscle Function in a Person With an Unstable Knee" by Maitland and colleagues (January 1999) detailed the examination of knee instability using gait analysis and tests of muscle inhibition in a patient with an anterior cruciate ligament (ACL) repair. The authors described their evaluation, intervention program, and outcomes for a single subject who demonstrated knee instability during gait 8 months after ACL reconstruction. I sincerely believe that this form of communication (case report) is a useful reporting mechanism for our profession, and I applaud their effort.
While reading this article, I was confronted with several confounding questions, which require some clarification. Because I did not actually have an opportunity to see the patient, my questions and comments are directed at the statements made in the article and, therefore, may not be accurate.
In the first paragraph of the article, the authors make the statement, "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 tests and isolated quadriceps femoris muscle contraction." Within the context of this part of the authors' presentation, this statement is valid. However, it does not, as the authors imply, then become an automatic extrapolation to the function of this tissue during the mid-stance and terminal stance phases of gait. During the phases of gait referred to in this article (ie, mid-stance to terminal stance), the ACL may not be the primary connective tissue constraint to anterior translation of the tibia on the femur. Perry would suggest that the primary connective tissue constraint is the soleus muscle or the gastrocnemius-soleus-popliteus muscle complex.1 In fact, when the knee of Maitland and colleagues' patient was in 14 to 38 degrees of flexion during mid-stance, as illustrated in Figure 5, most authors would agree that the ACL would be relatively lax.2 This would suggest, especially in this patient, whose injury was several years old, that the resultant gait pattern was a learned adaptation to the loss of the ACL function or perhaps a weakness in the gastrocnemius-soleus muscle complex, or both.1,3 The dysfunction of the ACL appears to create this pattern of abnormal quadriceps femoris and hamstring muscle activity during mid-stance and terminal stance.3 Although this patient did develop the abnormality, it would have been useful to know whether there was any inhibition or weakness in the gastrocnemius-soleus muscle complex, because these are the muscles that are primarily responsible for control of the tibia during mid-stance and terminal stance. Theoretically, this suggests that there is a synergistic activity, as yet undiscovered, between the action (restraining activity) of the gastrocnemius-soleus muscle complex and the function of the ACL during mid-stance and terminal stance.
The previous thought process then led me to my next question: Why was the focus of the intervention program directed at strengthening the quadriceps femoris and hamstring muscles at 20 degrees of knee flexion? Their rationale was that 20 degrees of knee flexion is the knee angle in people without knee instability during the mid-stance phase of gait.2,3 Perry would disagree.1 In fact, except during initial loading, the knee does not approach 20 degrees of knee flexion until weight bearing has begun to shift to the opposite lower extremity (pre-swing). If their rationale had been that their patient's peak quadriceps femoris and hamstring muscle torques were achieved during the 20-degree range, as it appears that they were (Figs. 4 and 5), their argument would have been improved.
This then led to my next question: Why did they test the patient at 90 degrees of knee flexion using an isometric test and train the patient using concentric contractions or isometric contractions at 20 degrees? As the authors so clearly presented, this patient's movement impairment occurred during a dynamic, probably eccentric, activity, and yet he was trained with a 2.2-kg weight attached to his ankles using, I assume, concentric contractions. This amount of weight would not approach the dynamic torque force required during mid-stance and terminal stance, nor does it begin to approach the initial torque forces that the patient could develop prior to training (Fig. 7). In addition, the necessary weight required to achieve a training effect to attain the desired outcome would need to approach 60% of the peak torque requirements. The principle of the specificity of training would indicate that this patient's training may have been enhanced with a greater amount of torque demand applied in the same range and angles required to effect the desired outcome. Perhaps more important, however, is that testing and training should be complete using the same methods. If we are going to train a patient for dynamic activities, then we should test the patient using a dynamic test. In this case, the testing (ie, isometric contractions at 90o of knee flexion) was not specific to the angle or type of muscle activity required during training or gait.
Finally, I want to comment on the amount of treatment this patient received. Knowing the current health care milieu, I would question the ability of any clinical practice being allowed to treat a patient for 2 hours per visit for 24 visits. Few, if any, third parties would authorize or support that amount of treatment, and no administrator would authorize the costs required to provide this amount of care. Thus, in effect, this patient's intervention program could not have taken place without supporting funds from alternative sources. Granted, the patient deserves the highest quality of treatment, regardless of his or her ability to pay, but I find that this case outcome does not justify the time and cost required.
This article has provided us with a greater amount of examination and evaluation information about a patient than the average clinician would ever have available in the clinic. It clearly demonstrates how far our profession may need to go in the clinical examination and evaluation of our patients. I would caution, though, that we should be careful not to extrapolate from isolated static findings to dynamic situations and that our treatment programs should be directed at the specific impairment identified and be strenuous enough to produce the desired outcomes.
References
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
Customer Service Engineer Motion Analysis Corp Santa Rosa, Calif
Adjunct Assistant Professor Human Performance Laboratory University of Calgary
Dr Irwin's letter raises several points for discussion. In part, the letter illustrates the difficulty in determining in vivo structural-functional relationships during activities of daily living. He presents a key issue: Does the anterior cruciate ligament (ACL) restrict anterior motion of the tibia relative to the femur during the stance phase of gait? Dr Irwin cites Henning et al1 as suggesting that the ACL may be "lax" during stance.
Several research methods have been used in an attempt to determine the effect of ACL injury on tibiofemoral joint motion during weight bearing: mathematical modeling, cadaver studies, radiological imaging, and in vivo instrumentation.
In a recent mathematical modeling study (Liu and Maitland, unpublished research) of ACL-intact and ACL-deficient knees, we found that, at 16 degrees of knee flexion, during single-leg stance, there was a resultant shear force in the tibiofemoral joint that was stabilized by the ACL. Abnormal anterior displacement of the tibia relative to the femur resulted from simulated ACL injury, and relatively high levels of hamstring muscle activation were required to reposition the tibia on the femur. In another mathematical evaluation of the knee, Shelburne and Pandy2 found that, between 0 to 10 degrees of knee flexion, there was a resultant shear force that hamstring muscle co-contraction could not overcome. They also found that beyond 10 degrees, there would be no resultant force on the ACL.
Devita et al3 obtained force-plate data for individuals with ACL-deficient knees. From the force-plate data, the authors calculated a resultant knee extensor torque past mid-stance for this subject group, implying that there would be a shear force at the knee. Devita et al remarked that these patients were at risk of further injury to the knee.
Torzilli et al4 applied various external loads to cadaveric knees. The authors reported that an applied compressive load to the ACL-intact knee caused a substantial anterior translation of the tibia on the femur. The translation was increased significantly by sectioning of the ACL.
Excessive anterior displacement of the tibia on the femur during weight bearing has also been measured more directly by radiographic studies. DeJour et al5 reported abnormal congruity of the tibiofemoral joint in individuals with ACL-deficient knees during weight bearing correlated to anatomical variation in tibial slope. Egund et al6 confirmed these findings and remarked that the displacement induced by weight bearing indicates an abnormal joint position due to ACL injury, probably occurring frequently during activities of daily living.
Direct measurement of ACL strain has been reported by Henning et al.1 The authors (whom Dr Irwin cites) stated that (in order of increasing strain) cycling, half-squats, and walking produced elongation of the ACL. Henning et al stated that "normal walking produced 36% as much elongation [of the ACL] as an 80-lb Lachman test."1
Beynnon et al7 also used in vivo strain gauge measurement of ACL elongation to measure ACL strain in the human knee. The authors showed that the maximum ACL strain values produced by active flexion-extension of the knee in a non-weight-bearing position and the squat exercise are similar, with positive strain values between 10 and 20 degrees of knee flexion.
Another method of in vivo measurement of tibial displacement relative to the femur was published by Yack et al.8 The authors used an electrogoniometer to measure relative displacement in ACL-injured and contralateral knees. They found that the parallel squat exercise produced a mean of 7 mm of anterior tibial translation in individuals with an ACL-deficient knee, a significant increase compared with the uninjured knee.
The individual case presented in our article is unusual because of the extremely abnormal position of the tibiofemoral joint during weight bearing. We measured radiologically a change of position of the tibia relative to the femur of about 2 cm. We are not entirely sure what interplay of factors led to this extreme situation, but the lack of a functional ACL is believed to be an important component.
Dr Irwin's letter describing the interaction between muscular control and ligamentous stability also illustrates our current limitations in understanding the knee as a complex structure during functional activities. Most studies have focused on quadriceps femoris muscle-hamstring muscle-ACL-posterior cruciate ligament interaction, but Dr Irwin points out that there is a potential effect of the medial and lateral gastrocnemius muscles on tibiofemoral stability. Tibone et al9 reported considerable variability in gastrocnemius muscle electromyographic activity for individuals with ACL-deficient knees. Three of his subjects with ACL-deficient knees had minimal gastrocnemius muscle electromyographic activity during stance. The effect of gastrocnemius muscle tension on shear force at the knee has been evaluated with mathematical models (Liu, unpublished data). Increased gastrocnemius muscle force was found to produce a slight increase in posterior displacement of the femur on the tibia. Perry,10 whom Dr Irwin cites, stated that the gastrocnemius and soleus muscles are primarily ankle plantar flexors. The plantar flexors of the ankle control the tilt of the tibial plateau and, therefore, indirectly affect the anterior-posterior shear forces at the knee. Perry stated that increased gastrocnemius muscle activity would increase the burden on the quadriceps femoris muscle as a consequence of increased forces that tend to flex the knee. In the sagittal plane, there is interplay between flexion and extension forces and anterior and posterior shear forces caused by muscles crossing the knee joint.
Dr Irwin states that the knee angle during gait does not reach 20 degrees of flexion until pre-swing (terminal stance). Thus, he questions the choice of variables used for the retraining process. The knee angle during gait has been measured by many individuals and has been found to have some variability. Noyes et al11 reported a range of knee joint angles during mid-stance (ie, 5°–15°) for uninjured subjects. Individuals with ACL-deficient knees, however, may tend to maintain more knee flexion. Devita et al3 reported a mean knee flexion angle of 20 degrees at mid-stance for people with ACL-deficient knees. The precise knee angle to be used in training remains somewhat arbitrary. In fact, the efficacy of training regimens suggested in our article warrants much more systematic evaluation than the descriptive study we have presented.
References
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