The Effect of Excessive Subtalar Joint Pronation on Patellofemoral Mechanics:

Transcription

1 /87/ $02.00)0 THE JOURNAL OF ORTHOPAEDIC AND SPORTS PHYSICAL THERAPY Copyright Q 1987 by The Orthopaedic and Sports Physical Therapy Sections of the American Physical Therapy Association The Effect of Excessive Subtalar Joint Pronation on Patellofemoral Mechanics: A Theoretical Model DAVID TIBERIO, MS, PT* Excessive compression of the lateral articular surfaces is frequently a major component of patellofemoral dysfunction. Many subjects exhibiting symptoms of this disorder have structural deviations throughout the lower extremity which combine to produce malalignment of the patellofemoral joint. Included in these malalignment factors is excessive pronation of the subtalar joint. Excessive rotation of the lower leg which accompanies subtalar joint pronation has been cited as a major contributor to patellofemoral dysfunction. Although the excessive rotation of the lower leg will disrupt the normal mechanics of the tibiofemoral joint, the specific link between tibial rotation and patellofemoral symptoms has not been established. This paper presents a theoretical model which describes the compensation that can occur at the tibiofemoral joint to deal with the excessive tibial rotation. The link between the tibiofemoral compensation and increased patellofemoral compression is delineated. Factors which determine whether this increased compression becomes symptomatic are discussed. Disorders of the patellofemoral joint constitute a large segment of the cases requiring therapeutic intervention at the knee. In recent years the fitness boom, increased athletic participation by females, and the popularity of endurance activities have combined to increase the prevalence of patellofemoral dysfunction. A heightened interest in the cause and treatment of these disorders has developed in surgical and nonsurgical practitioners. Research data on the symptoms, etiological factors, and treatment are now available. Many of these reports indicate that abnormal pronation of the subtalar joint (STJ) may be an important component of patellofemoral dysfunction,'2* '* l2 especially in cases of "excessive lateral pressure syndrme." symptoms through pronation of the STJ, has been 'implicated most freqently.'.." James" may have stated this hy- pothesis most succinctly when he wrote "... when internal tibial rotation is increased or prolonged with excessive pronation, more transverse rotation must be absorbed in the knee joint with subsequent disturbance of the normal tibio-femoral rotational relationship and an alteration in normal patellofemoral mechanics." However, the nature of the "disturbance" and the specific "alteration" that he alludes to have not been adequately described. PURPOSE The purpose of this article is to present a theoretical mechanism, "compensatory internal rotation of the femur" (CIRF), by which excessive STJ of l pronation l becomes the precipitating factor in the l the use Of foot OrthOses has been re- pathomechanics of excessive lateral compression ofl led-"^"'"^ The specific role of abnormal pro- syndrome. The model will address the effect that nation in excessive lateral pressure, and the bio- this internal rotation has on patellofemoral trackmechanical basis for successful treatment have ing, and the circumstances under which this not been made clear. Excessive internal rotation compression is likely to become symptomatic. of the lower leg, which accompanies excessive REVIEW OF THE LITERATURE 'Program in Physical Therapy, school of Allied Health Professions, University of Connecticut, stows, CT The term patellofemoral dysfunction has been used to describe many different pathological tis- 160

2 JOSPT October 1987 EXCESSIVE SUBTAL -AR JOINT PRONATION 161 sue states. Some are distinct entities, while others are related by symptoms or etiological factors and differ only in degree of severity. Reider et a1.16 divided their cases into three categories: 1) those showing evidence of frank dislocation, 2) those whose symptoms indicate partial dislocation or subluxation, and 3) those with the primary symptom of pain, which they called chondromalacia. Unfortunately, even the term chondromalacia has been used to describe a variety of conditions affecting the patellofemoral joint. Ficat and Hungerfords and others394 have investigated patients with "chondromalacia" in order to identify these different conditions based on their symptoms. A significant number of these patients exhibited clinical signs of excessive compression of the articular surfaces. Pain, attributed to increased patellofemoral compression, is found in different aspects of the joint. Newell and Bramwell14 found that 30% of the patients with "patellar compression syndrome" had pain on the lateral aspect of the joint. It is this specific condition, increased lateral compression, that the model will address. The common denominator in these studies was that patients presented with abnormal structural alignment of fhe lower extremity. Symptoms may include pain, effusion, clicking or grating, "collapsing" of the joint, and even medial joint line pain.3v8s16 Structural abnormalities include: an increased Q angle, genu valgum, patella alta, and internal rotation of the femoral condyles caused by excessive femoral anteversin., '18. DY - namic abnormalities contributing to excessive lateral pressure include dysplasia of the vastus medialis obliqs.', and tightness of the lateral retinaclum. Recently attention to etiology and treatment has focused on these dynamic factors, while an increased Q angle remains a primary concern of most practitioners. In addition, malalignment due to structural deviations in the foot and lower leg has been ob- erved.'-' These "indirect" factors include tibial varum, external tibial torsion, and varus deformities of the forefoot and rearfoot. All of these deviations are likely to cause the STJ to pronate more than normal. This excessive pronation which increases the biomechanical demands on the knee joint, has been identified as a major component of "miserable malalignment syndrome."" It is interesting to note that excessive STJ pronation, which results in increased internal rotation of the lower leg, is incongruous with the concept of an increased Q angle during dynamic function. Although an individual may statically exhibit an excessive Q angle, the increased internal rotation will serve to decrease this angle during locomotion. A few authors have attempted to establish a biomechanical basis for the observed connection between excessive STJ pronation and excessive lateral patellofemoral compression as well as the successful treatment of the condition by reducing the STJ pronation. James1' listed factors producing "excessive compensatory rotation" of the tibia. He stated that the obligatory internal rotation of the tibia would disrupt the "normal tibial-femoral rotational relationship" and change the "patellofemoral mechanics." He did not speculate as to what specific change would occur or how this would affect the compressive forces on the articular cartilage. Larson12 and Paulos et a1.15 similarly wrote that "femoral anteversion and internal femoral rotation" position the patella medially and result in a "more lateral insertion to the patellar tendon." Regarding foot mechanics during running, both stated that "there is pronation of the foot with external rotation of the tibia as the knee extends." A discrepancy in this statement arises because, during closed chain kinematics, if the STJ pronates the tibia must internally rotate. Buchbinder et al2 may have presented the most biomechanically "congruent" hypothesis. They noted an increased femoral rotation that occurs when excessive internal rotation of the lower leg is present. In attempting to support their theory, they stated that with "prolonged pronation both the origin and the insertion of the quadriceps are located lateral to the patella" and that the "internal rotation of the limb" created "an abnormal pull on the patella." These statements seem antagonistic to the increased internal rotation of the lower leg, which straightens the quadriceps alignment. The reasons for the apparent inconsistencies in these hypotheses may be an overemphasis placed on the role of the Q angle. It seems that a biomechanical rationale for an increased Q angle and lateral pull of the patella was necessary in order to justify increased lateral compression. These hypotheses may have taken the wrong direction while searching for the specific link between excessive STJ pronation and lateral patellofemoral pain. KINEMATICS OF NORMAL LOCOMOTION The human body completes a repetitive pattern of motion in order to move from place to place.

3 162 TlBERlO JOSPT Vol. 9, No. 4 This pattern, called a gait cycle, has a specific sequence which requires synchronous interaction between the joints of the lower extremity. A gait cycle has two primary phases: a stance phase when the foot is in contact with the supporting surface, and a swing phase when the lower extremity is advancing forward to renew ground contact. The stance phase can be subdivided into three functional divisions: contact, midstance, and propulsion (Fig. l).17 The contact phase begins when the heel strikes the ground and continues until the entire foot is on the ground (foot flat). The midstance phase extends from foot flat until the heel lifts off the ground. The propulsive phase begins with heel rise and ends with toe off. The STJ (Fig. 2) is slightly supinated at heel strike. During the contact phase, the STJ pronates. Once the foot is in full ground contact, the STJ reverses its function and begins to supinate. It supinates throughout the midstance'and propulsive phases, passing the neutral position just before heel rise. When the STJ pronates during ground contact (closed chain pronation), the calcaneus everts and the head of the talus slides medially and plantarflees.' The medial movement of the head of the talus results in a medial rotation of the body of the talus. Because of the tight fit of the talus into the ankle joint mortise, the lower extremity must internally rotate with the transverse plane motion of the talus during STJ pronationg (Fig. 3). During supination, the movement of the talus is reversed, and the lower leg must externally rotate. Figure 4 depicts the movement of the knee joint during ambulation. The knee is essentially in full extension when stance begins, and flexes 15- KNEE aexas LEG Closed Chain PRONA77ON of the Subtalar Joint t I STANCE GAlT CYCLE I Fig. 1. Functional divisions of stance phase. (HS, heel strike; FF, foot flat; HR, heel rise; TO, toe off). GAlT ST1 CYCLE MOTION - - Fig. 3. Internal rotation of the lower leg with closed chain pronation. (Adapted with permission of American Physical Rehabilitation Network, 1984.) GAlT CYCLE KNEE Fig. 2. Motion of the subtalar joint during the gait cycle. (HS, heelstrike; FF, foot flat; HR, heel rise; TO, toe off). (Reproduced with permission of American Physical Rehabilitation Network, 1984.) Fig. 4. Motion of the knee joint during the gait cycle. (HS, heel strike; FF, foot flat; HR, heel rise; TO, toe off). (Reproduced with permission of American Physical Rehabilitation Network, 1984.)

4 JOSPT October 1987 EXCESSIVE SUBTAL AR JOINT PRONATION during contact phase. Knee extension is then initiated and continues during the midstance phase. The requirement for external rotation of the tibia during the last is well chronicled.13v19 Less appreciated is the fact that the tibia must internally rotate during the first 15-20' of the knee flexion. Therefore, as the knee flexes during contact phase the tibia internally rotates, and as the knee extends during midstance phase the tibia externally rotates. This obligatory action is often called automatic rotation, and is different from the tibia1 rotation that can occur independent of flexion or extension when the knee is flexed more than It, therefore, is no chance occurrence that during the first two phases of stance, the knee flexes when the STJ pronates and the STJ supinates when the knee extends. The synchronous actions of the knee and STJ, during the contact and midstance phases, are interdependent motions, and the rotation of the lower leg is an obligatory action that is necessary for normal kinematics of both joints. EXCESSIVE PRONATION AND COMPENSATORY INTERNAL ROTATION OF THE FEMUR+ (CIRF) Since the gait cycle is not only sequential, but necessitates synchronicity between joints, abnormal STJ motion will affect knee biomechanics. Excessive pronation will delay the external rotation of the lower leg which accompanies STJ supination. This delay results in a cornpensatory reaction at the tibiofemoral joint and may produce patellofemoral symptoms. The theoretical compensation and the resultant pathomechanics will now be described. At the beginning of midstance phase, the flexion at the knee and the pronation at the STJ should have ended and started to reverse. If, for some reason, the STJ remains pronated or continues to pronate the tibia cannot externally rotate. Figure 5 shows the theoretical motion of the STJ during stance when it compensates for a forefoot varus deformity. The increased pronation during midstance phase creates a biomechanical "dilemma" for the tibiofemoral joint. Normal mechanics dictate that the tibiofemoral joint extend during midstance phase as the body traverses over the fixed foot; but it cannot acquire the external rotation of the tibia needed for extension. The locomotor system faced with this problem must compensate in some manner or the sup- NEUTRAL P R 10..-, STANCE PHASE STJ MOTION FOREFOOT VARUS H S F F HR T 0 Fig. 5. Excessive pronation of the subtalar joint as a compensation for a forefoot varus deformity. Solid line represents the normal motion of the subtalar joint. (Reproduced with permission of American Physical Rehabilitation Network, 1984.) porting structures of the tibiofemoral joint will be traumatized. One relatively efficient compensatory mechanism is for the femur to internally rotate on the tibia (CIRF), providing the necessary rotation for extension. Since the foot is fixed on the ground, the femur and the body above can accommodate the tibiofemoral joint in this manner. Unfortunately, what is good for the tibiofemoral joint is not beneficial for the patellofemoral joint. The CIRF disrupts the normal biomechanics of the lower extremity while altering patellofemoral tracking. At the time of this compensation, the patella is gliding in the femoral trochlear and the quadriceps is still contracting. When the femur internally rotates, the cmpression between the lateral articular surface of the patella and the lateral femoral condyle is increased. This results in "relative" lateral tracking of the patella when the tibiofemoral joint is near full extension, caused by the. CIRF. Whether this cornpensatory action of the femur becomes symptomatic will depend on many factors. Certainly the degree of abnormal pronation is one such factor. A few degrees of extra pronation, causing a minor compensation at the knee is unlikely to increase patellofemoral compression enough to produce symptoms. On the other hand, large structural deviations can easily precipitate pain. The timing of abnormal pronation is an important factor. Five extra degrees of pronation that occur during midstance hold more potential for producing pain than five degrees that occur during contact phase. Since the STJ should be supinating during midstance, the extra pronation at this time is actually a much greater functional deviation and will require greater compensation on the part of the femur.

5 164 TlBERlO JOSPT Vol. 9, No. 4 An additional factor is the structural alignment of the entire lower extremity. The presence of any of the malalignment factors will make an individual experiencing CIRF more susceptible to patellofemoral problems. Anterversion of the femur, which results in an internally rotated position of the femoral condyles, is very likely to be present in a patient with lateral compression pain. The summative effect of starting with the condyles facing inward and the compensatory rotation of the femur may increase the lateral compression beyond the symptomatic threshold. Likewise, CIRF will accentuate the effect of vastus medialis weakness or tightness of the lateral retinaculum. DISCUSSION This model of compensatory internal rotation of the femur is not intended to promote excessive STJ pronation as the most important factor in increased lateral pressure syndrome. The Q angle and other more accepted factors remain important considerations. It is hoped that this biomechanical model will elevate excessive STJ pronation to "equal status" when the causes of abnormal patellofemoral mechanics are sought. Practitioners, hopefully, will be stimulated to develop and utilize skills in the evaluation and treatment of foot and lower leg dysfunction. If there is merit in this model, then there is a warning to surgical practitioners who attempt to improve patellofemoral mechanics. Even the best surgical procedures may be found lacking if the cause of the pathomechanical condition is excessive STJ pronation. There is an even greater challenge to nonsurgical practitioners. Since it would be rare for surgery to be performed without an attempt at conservative treatment, physical therapists must evaluate the structure and function of the STJ in all their patients with patellofemoral dysfunction. Otherwise, an unnecessary surgical procedure may be performed because the "whole" patient was not evaluated. Although the model focused on patellofemoral problems, excessive STJ pronation also increases the stresses on the medial supporting structures of the knee, occasionally to the symptomatic level. Also, if CIRF does not occur, the internal structures of the knee may be damaged when the knee tries to extend. In addition, the model did not address the important relationship between pelvic rotation and transverse plane motions of the lower extremity, and the compensatory mechanisms that could occur proximal to the femur. The model did not attempt to describe the specific mechanisms by which foot and leg abnormalities produce excessive STJ pronation. Readers should also be aware that external compensatory rotation of the femur (CERF) can also occur. Conditions preventing normal STJ pronation or causing abnormal STJ supination may produce abnormal external rotation as the knee flexes during contact phase. This compensation may increase medial patellofemoral compression or traumatize the iliotibial band as it crosses the lateral femoral condyle. Much research needs to be performed regarding the biomechanical link between both types of compensatory rotation (CIRF and CERF) and specific knee injuries. SUMMARY This theoretical model of compensatory femoral rotation is not presented as a solution to all patellofemoral problems. It proposes a biomechanical rationale for persistent patellofemoral symptoms which are refractory to treatment directed at the knee. It describes the effect of excessive STJ pronation on the tibiofemoral joint, the possible compensatory action of the femur to deal with the excessive pronation, and the resulting pathomechanics at the patellofemoral joint. It presents some of the factors which determine whether the compensatory femoral rotation will become symptomatic. The model is presented to assist practitioners in treating a complex musculoskeletal condition. Although the model is based on biomechanical facts, its validity needs to be established through research and the scrutiny of clinicians who will match the patient's symptoms with the results of the biomechanical examination, and who must analyze the efficacy of their therapeutic interventions. Acknowledgments. The author expresses his appreciation to Michael Zito, MS, PT for his editorial assistance in writing this article; and to Michael Witmer, PT, ATC, and Gary Gray, PT, ATC for their collegial dialogue which fostered the concepts of the biomechanical model. REFERENCES 1. Bogdan RJ, Jenkins D, Hyland T: The runner's knee syndrome. Sports Med 78: , Buchbinder MR. Napora NJ, Biggs EW: The relationship of abnormal pronation to chondromalacia of the patella in distance runners. J Am Podiatry Assoc 69: Cox JS: Chondromalacia of the patella: a review and update--part 1. Contemp Orthop 6:17-30, DeHaven KE, Doland WA, Mayer PJ: Chondromalacia patellae in athletes. Am J Sports Med , 1979

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