Letters to the Editor.

Knee Instability

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 tact, 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? 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 90 [degrees] 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.

Scot Irwin, DPT, CCS
Associate Professor
Department of Physical Therapy
North Georgia College and State University
Dahlonega, GA 30597

References

[1] Perry J. Gait Analysis: Normal and Pathological Function. New York, NY: McGraw-Hill Inc; 1992.

[2] Henning CE, Lynch MA, Glick KR Jr. An in vivo strain gauge study of elongation of the anterior cruciate ligament, Am J Sports Med. 1985;13:22-26.

[3] Devita P, Hortobagyi J, Barrier J, et al. Gait adaptations before and after anterior cruciate ligament reconstruction surgery. Med Sci Sports Exerc. 1997;29:853-859.

Author Response:

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 al[1] 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 Pandy[2] 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 al[3] 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 al[4] 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 oil 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 al[5] 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 al[6] 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, halt: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 al[7] 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 lemur 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 al[9] reported considerable variability in gastrocnemius muscle electromyographic activity for individuals with ACL-deficient knees. Three of Iris 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 torte 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 threes 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 threes 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 al[11] reported a range of knee joint angles during midstance (ie, 5 [degrees]-15 [degrees]) for uninjured subjects. Individuals with ACL-deficient knees, however, may tend to maintain more knee flexion. Devita et al[3] 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 tact, the efficacy of training regimens suggested in our article warrants much more systematic evaluation than the descriptive study we have presented.

Murray E Maitland, PhD, PT
Associate Professor and Physical Therapist
Sport Medicine Centre
University of Calgary
2500 University Dr NW
Calgary, Alberta, Canada T2N 1N4
[e-mail]

Stanley V Ajemian
Customer Service Engineer
Motion Analysis Corp
Santa Rosa, Calif

Esther Suter, PhD
Adjunct Assistant Professor
Human Performance Laboratory
University of Calgary

References

[1] Henning CE, Lynch MA, Glick KR Jr. An in vivo strain gauge study of elongation of the anterior cruciate ligament. Am J Sports Med. 1985;13:22-26.

[2] Shelburne KB, Pandy MG. Determinants of cruciate-ligament loading during rehabilitation exercise. Clinical Biomechanics. 1998;13:403-413.

[3] Devita P, Hortobagyi J, Barrier J, et al. Gait adaptations before and after anterior cruciate ligament reconstruction surgery. Med Sci Sports Exerc. 1997;29:853-859.

[4] Torzilli PA, Deng X, Warren RF. The effect of joint-compressive load and quadriceps muscle force on knee motion in the intact and anterior cruciate ligament-sectioned knee. Am J Sports Med. 1994;22:105-112.

[5] DeJour H, Neyret P, Bonnin M. Monopodal weight-bearing rediography of the chronically unstable knee. In: Jackob RP, Staubli H-U, eds. The Knee and Cruciate Ligaments. Berlin, Germany: Springer-Verlag GmbH & Co KG; 1992:568-576.

[6] Egund N, Friden T, Hjarbaek J, et al. Radiographic assessment of sagittal knee instability in weight bearing: a study on anterior cruciate-deficient knees. Skeletal Radiol. 1993;22:177-181.

[7] Beynnon BD, Johnson RJ, Fleming BC, et al. The strain behavior of the anterior cruciate ligament during squatting and active flexion-extension: a comparison of an open and a closed kinetic chain exercise. Am J sports Med. 1997;25:823-829.

[8] Yack HJ, Collins CE, Whieldon TJ. Comparison of closed and open kinetic chain exercise in the anterior cruciate ligament-deficient knee. Am J Sports Med. 1993;21:49-54.

[9] Tibone JE, Antich TJ, Fanton GS, et al. Functional analysis of anterior cruciate ligament instability. Am J Sports Med. 1986;14:276-284.

[10] Perry J. Gait Analysis: Normal and Pathological Function. New York, NY: McGraw-Hill Inc; 1992:95.

[11] 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.

Bell Palsy

To the Editor:

Kudos to Ms Brach and Dr VanSwearingen for their fine case study on the use of facial neuromuscular retraining in treating a patient with Bell's palsy (April 1999). I am concerned as to the unfortunate decision to use the term "Bell palsy" rather than "Bell's palsy" throughout the article. To quote Larry Lundy, MD, of the Mayo Clinic, Jacksonville, who presented a lecture, "Clinical Evaluation of Acute Facial Palsies" at the American Academy of Otolaryngology-Head and Neck Surgery Foundation's Conference on Facial Nerve Disorders in Washington, DC, in March 1999: "The most common type of acute facial palsy is Bell's palsy, aka, idiopathic facial palsy or herpes simplex facial palsy." Bell's palsy was extensively discussed at this meeting, in which I was an invited panelist, but no one called it "Bell palsy." Also, you will not easily find the use of the term "Bell palsy" in a literature review. (However, to weaken my argument, I have included one in my references. The irony does not escape me.)

The authors state that Bell's palsy is of unknown etiology. That is certainly what "idiopathic" infers. In the last few years, however, there has been much research published concluding that the cause is viral. Bauer and Coker stated, "aided by developments in molecular biology techniques, an increasing number of investigators have reported evidence for a viral etiology in many cases of `idiopathic' facial paralysis."[1] Adour and associates concluded that "sufficient clinical, laboratory, magnetic resonance imaging, and pathology data have accumulated to add veracity to the hypothesis that herpes simplex causes Bell's palsy."[2] I conclude with 3 studies done by Naoaki Yanagihara, MD, and associates in Japan, who have published strong research evidence for herpes simplex virus as the causative agent of Bell's palsy.[3-5]

Bell's palsy is a diagnosis of exclusion.[6] Some 80 to 100 other known causes of facial paralysis (mostly rare) have been identified, although Bell's palsy is the most common. For example, herpes zoster oticus (also known as Ramsay Hunt syndrome) is often mistaken for it. Herpes zoster oticus has a similar presentation, but is characterized by significant pain, particularly periauricular, and the presence of vesicles in the ear canal or externally. Usually, the recovery process is longer and less complete.

To conclude, Bell's palsy is no longer considered idiopathic, and physicians who are setting the standards of care today therefore recommend treatment with an antiviral medicine during the acute stage. To call this condition "Bell palsy" is akin to an ostrich putting its head in the sand ... you can do it due to an editorial policy, but you will not be with the great majority of the rest of the medical community.

Todd Henkelmann, PT
Clinical Director, Facial Rehabilitation Services
Eagle Physical Therapy
Mars Professional Building
Pittsburgh St, Suite 101
PO Box 1095
Mars, PA 16046-1095

References

[1] Bauer CA, Coker NJ. Update on facial nerve disorders. Otolaryngol Clin North Am. 1996;29:445-454.

[2] Adour KK, Ruboyianes JM, Von Doersten PG, et al. Bell's palsy treatment with acyclovir and prednisone compared with prednisone alone: a double-blind, randomized, controlled trial. Ann Otol Rhinol Laryngol. 1996;105:371-378.

[3] Nakamura K, Yanagihara N. Neutralization antibody to herpes simplex virus type 1 in Bell's palsy. Ann Otol Rhinol Laryngol Suppl. 1988;137:18-21.

[4] Murakami S, Mizobuchi M, Nakashiro Y, et al. Bell palsy and herpes simplex virus: identification of viral DNA in endoneurial fluid and muscle. Ann Intern Med. 1996;124(1 pt 1):27-30.

[5] Sugita T, Murakami S, Yanagihara N, et al. Facial nerve paralysis induced by herpes simplex virus in mice: an animal model of acute and transient facial paralysis. Ann Otol Rhinol Laryngol. 1995;104:574-581.

[6] Petruzzelli GJ, Hirsch BE. Bell's palsy: a diagnosis of exclusion. Postgrad Med. 1991;90:115-118, 121-122, 125-127.

Author Response:

We thank Mr Henkelmann for his interest in the case reported and our understanding of the disorder. An explanation for the terminology ("Bell palsy") is in order, and a brief review of the reported evidence indicates wily the argument for viral causation of Bell palsy is incomplete and unacceptable.

The use of the term "Bell palsy" instead of "Bell's palsy" was the recommendation of tire Editor, in accordance with the current American Medical Association (AMA) guidelines for eponyms.[1] Based on the AMA guidelines, the possessive ending should be dropped from eponyms. According to the AMA guidelines, "there is continuing debate over the use of the possessive form; however, a transition toward the nonpossessive form may be gradually taking place.[1(p470)] Our response as authors to the edit of "Bell's palsy" to "Bell palsy" was to cite the current usage in Dorland's Illustrated Medical Dictionary, 28th edition, which indicates "Bell's palsy" as the acceptable terminology.[2] We requested an exception to the guidelines for eponyms to allow the use of "Bell's palsy." In not accepting our request, the Editor acted as an editor, conforming to the AMA guidelines and assuring that Physical Therapy is consistent with the format of other reputable biomedical journals. We respect the decision.

The assertion that the cause of Bell palsy has been demonstrated in recent research reports to be viral, particularly herpes simplex virus (HSV), cannot be supported. Neither the references cited by Mr Henkelmann[3-8] nor others provide evidence that HSV causes Bell palsy. Bauer and Coker,[3] reviewing the evidence for an HSV etiology for Bell palsy, stated that the serologic evidence is variable. In human studies, seroconversion to HSV ranged from 0 to 15.6% of the cases of Bell palsy. The 15.6% seroconversion rate was reported for a sample of 45 patients with Bell palsy.[4] Among a larger sample of patients with Bell palsy, seroconversion to HSV was documented in only 165 of 1,830 patients (8.9%).[9] In 2 animal studies,[7,10] seroconversion to HSV followed perineural injection of HSV, consistent with a causal hypothesis. Ill one of the studies, however, none of the animals developed facial paralysis.[10]

Evidence for a virally induced origin tot Bell palsy has also been based on isolation of HSV from specimens of the facial nerve retrieved during decompression surgery to relieve the symptoms.[6] The evidence tot HSV is limited, as only 14 of 170 individuals with Bell palsy underwent the decompression surgery, and HSV was isolated in a subset of the surgical cases.[6] The evidence tot causation tails because HSV has also been isolated from over 70% of geniculate and trigeminal ganglia of 8 random autopsy specimens recovered from cadavers of adults who did trot have Bell palsy.[11]

Although Adour et al[4] concluded that HSV is the cause of Bell palsy, the evidence lot the specific viral origin remains variable. In 1996, Adour et al[4] reported better recovery among patients with Bell palsy given antiviral treatment compared with anti-inflammatory treatment in a randomized controlled clinical trial. More recently, De Diego et al[12] reported the opposite finding, that is, a better outcome tot patients with Bell palsy who are treated with an anti-inflammatory drug compared with those treated with the antiviral medication in a prospective randomized controlled clinical trial.

Epidemiologists apply several concepts to determine causal relations: strength, consistency and specificity of association, temporal sequence of events and dose response, and experimental evidence.[13] The argument tot HSV as causal tot Bell palsy is weak. Herpes simplex virus is (1) present in 15.6% or fewer of cases, (2) present in individuals who do not have the facial paralysis of Bell palsy, (3) present in equal titers among individuals with and without Bell palsy, (4) associated with facial paralysis in only some of tire cases in which HSV has been experimentally induced within the animal, and (5) variably associated with better outcomes in randomized controlled clinical trials of medical interventions.

We appreciate the interest in assuring the accuracy of the information shared and the review of literature provided by Mr Henkelmann. Discussions with peers and even among noted panelists on a topic are valuable; however, we are reminded that the discussions are not a substitute for careful review of the peer-reviewed literature when searching for evidence-based practice.

Jessie M VanSwearingen, PhD, PT
Jennifer S Brach, PT, GCS
Department of Physical Therapy
University of Pittsburgh
6035 Forbes Tower
Pittsburgh, PA 15260
([e-mail])

References

[1] Iverson C. Flanagin A. Fontanarosa PB. ct al. America, Medical Association Manual of Style: A Guide for Authors and Editors, 9th ed. Baltimore, Md: Williams & Wilkins; 1998.

[2] Dorland's Illustrated Medical Dictionary. 28th ed. Philadelphia, Pa: WB Saunders Co; 1994.

[3] Bauer CA, Coker Ny. Update on facial nerve disorders. Otolaryngol Clin, North Am. 1996;29:445-434.

[4] Adour KK, Ruboyianes JM, Von Doersten PG, et al. Bell's palsy treatment with acyclovir and prednisone compared with prednisone alone: a double-blind, randomized, controlled trial. Ann Otol Rhinol Laryngol. 1996;105:371-378.

[5] Nakamura K, Yanagihara N. Neutralization antibody to herpes simplex virus type 1 in Bell's palsy. An, Old Rhinol Laryngol Suppl. 1988;137:18-21.

[6] Murakami S, Mizobuchi M, Nakashiro Y, et al. Bell palsy and herpes simplex virus: identification of viral DNA in endoneurial fluid and muscle. Ann Intern, Med. 1996;124(1 pt 1):27-30.

[7] Sugita T, Murakami M, Yanagihara N, et al. Facial nerve paralysis induced by herpes simplex virus in mice: an animal model of acute and transient facial paralysis. Ann Otol Rhinol Laryngol. 1995;104:574-581.

[8] Petruzzelli GJ, Hirsch BE. Bell's palsy: a diagnosis of exclusion. Postgrad Med. 1991;90:115-118, 121-122, 125-127.

[9] Morgan M, Nathwani D. Facial palsy and inflection: the unfolding story. Clin Infect Dis. 1992;14:263-271.

[10] Mulkens PS, Bleeker JD, Schroder FP. Acute facial paralysis: a virological study. Clin Otolaryngol. 1980;5:303-310.

[11] Furuta Y; Takasu T, Sato KC, et al. Latent herpes simplex virus type 1 in human geniculate ganglia. Acta Neuropathol (Berl). 1992;84:39-44.

[12] De Diego JI, Prim MR De Sarria MJ, et al. Idiopathic facial paralysis: a randomized, prospective, and controlled study using single-dose prednisone versus acyclovir three times daily. Laryngoscope. 1998;108:373-375.

[13] Lilienfeld DE, Stolley PD. Foundations of Epidemiology. 3rd ed. New York, NY: Oxford University Press; 1994:261-267.

Letters to the Editor

Letters to the Editor provide a forum for discussion of all matters that are important to the physical therapy profession. Letters responding to articles should be received on a timely basis to ensure meaningful dialogue. Due to space constraints, we ask that letters be less than 600 words. All letters should be signed.

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