Caught Between a Talar Rock and a Hip Place

Context is king. Our context is the patellofemoral articulation without regard to congenital, structural pathogenesis. Patellofemoral pain syndrome (PFPS) describes an umbrella diagnosis that covers an approximated twenty-five per cent of all knee injuries. PFPS presents clinically as diffuse anterior or retropatellar knee pain which is most typically exacerbated by functional activities that involve knee flexion while under weight bearing context, such as stair negotiation, prolonged sitting, squatting or kneeling.4,9 Despite a rather comprehensive incidence, the precise pathomechanics of PFPS remain unclear in their entirety. Notwithstanding, two biomechanical theories dominate the literature. These theories may be divided broadly into two models: the local impairment model and the remote impairment model. The former implicates a neuromuscular imbalance among the distal vasti and the latter neuromuscular deficits across the proximal hip musculature. Each perspective will be discussed with regard to several fundamental articles, which represent current thinking built on research over time.

The Local Impairment Model

The local impairment model, to be more specific, examines the relative influence of the vastus medialis obliquus (VMO) and the vastus lateralis (VL) on the patella. As the distal contractile tissue of the vasti gradually interdigitate with and transition to tendon, the patella is invested. In this way, the VMO and the VL can directly impose tensile forces on the patella and draw it posteromedially or posterolaterally, respectively. PFP has been postulated to result from an imbalance between these forces, with the VL exerting a more dominant pull than the VMO, which tends to aberrate the patella laterally relative to the femoral trochlea.2,9,11 This deviation creates compressive and shearing stresses that degrade the patellar articular cartilage over time.

Controlled studies that have sought to elucidate the role of the VMO in PFPS have typically asked morphological or neuromuscular questions. A recent study published by Jan et al. in The American Journal of Sports Medicine examined the insertion level, fiber angle and volume of the VMO in PFPS knees compared to healthy controls. While variation did exist, the study could not determine whether the observed differences were the result of atrophy in response to pain or pain in response to morphology.2 Wilson et al. report a decreased in vivo VMO tendon strain in PFPS compared to healthy controls and with reference to the VL. Strain defines change in length per initial length and is purported to reflect VMO weakness in this study.11 Among a cohort of male cadets of the Belgian Royal Military Academy, Van Tiggelen et al. found that delayed VMO to VL onset timing predicts PFP in previously healthy knees. The study was constructed prospectively and correlates delayed VMO neuromuscular activity with the development of PFP after six weeks of basic military training.9 Having collected electromyographic VMO, VL and tibialis anterior data only, one may only speculate whether or not additional predisposing variables subsisted prior to basic military training and, further, if these were primary and vasti timing ancillary to the development of PFPS.

These suspended questions aside, resistance training has been shown to enhance vasti neuromuscular control in general and independent of mode. Wong and Ng report enhanced EMG characteristics of the VMO relative to the VL after eight weeks of either strength or hypertrophy specific resistance training. These data lend direct relevance to clinical practice as both prospective and cross-sectional studies have linked global knee extension force deficits with PFPS.12 In this way, irrespective of the neuromuscular timing onset between the VMO and the VL, resistance training offers general and beneficial gains in knee extension force regardless of mode.

The Remote Impairment Model

The remote impairment model argues that PFPS is driven not directly from local deficits, but rather indirectly from proximal and distal pathomechanics. Internal femoral rotation, which may occur in isolation from or in accord with the tibia, tends to posture the knee in a valgus attitude. As the tibia interacts with the talocrural and talocalcaneal articulations, additional movement variables are introduced. For simplicity and scope, solely contributions from the femur will be considered at this time.

When excessive internal rotation occurs unchecked during weight bearing conditions the patella displaces laterally. Therefore, PFPS may result from the femur rotating underneath the patella rather than the patella tilting on a fixed femur.3,4,5,7 In following, the contractile tissues of the hip, specifically the iliopsoas, the gluteus medius and the gluteus maximus, work directly to accelerate and decelerate the femur through varied planes. Traditionally assigned pure sagittal plane movement, it is forgotten that the iliopsoas actually serves as a secondary external rotator and thus may influence transverse plane kinematics.8 Furthermore, an inflexible iliopsoas maintains the pelvis in an anterior pelvic tilt, an organization coupled with femoral internal rotation. Tyler et al. evaluated the importance of hip strengthening and flexibility in the treatment of PFPS and found a sixty-six per cent successful outcome after a six-week therapeutic exercise protocol. Having uniquely incorporated trial of the iliopsoas, Tyler et al. demonstrated a more significant correlation between hip flexion strength gain and a positive PFPS outcome as compared with hip abduction or adduction strength gain.8

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Using dynamic magnetic resonance imaging, Powers et al. reported that lateral patellar tilt and lateral patellar displacement during a weight-bearing squat was the result of internal rotation of the femur, as opposed to movement of the patella.3,4,5,7

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Powers and colleagues argue that the gluteus maximus and gluteus medius offer the greatest capacity for controlling internal femoral rotation. The gluteus maximus is a strong hip extensor and external rotator and claims the largest anatomical cross sectional area in the lower extremity.10 The gluteus medius functions primarily as a hip abductor, but secondarily generates an external rotation moment. Mascal, Landel and Powers established significant reductions in PFP, improved lower extremity kinematics and return to function after a fourteen-week therapeutic exercise regimen. The interventions focused on recruitment and endurance training of the hip, pelvis and trunk musculature and yielded significant improvements in gluteus medius and gluteus maximus force production as measured by hand-held dynamometry testing.3 Consequent to case study design and small study number, these results should naturally be generalized only with measured prudence.

Souza and Powers evidenced increased peak hip internal rotation motion in females with PFP compared to age-matched healthy controls when averaged across a drop jump, a step down and a running task. Hip extensor torque production was revealed to be deficient by sixteen per cent and hip abductor torque fifteen per cent. Moreover, gluteus maximus muscle activity showed ninety-one per cent greater muscle activity during running and sixty-four per cent greater activity during the step down maneuver. The authors conjecture that these data reflect cumulative attempts to recruit weak and indolent musculature.7

In a recent study published in the British Journal of Sports Medicine, Cowan et al. investigated the neuromuscular control of the anterior and posterior fibers of the gluteus medius in healthy controls and in the presence of PFP. Employing EMG, a step up task revealed both portions of the muscle to be delayed in the PFP group when referenced against the controls. Intriguingly, individuals with PFP were also found to have decreased trunk side flexion strength compared to asymptomatic individuals.1 These data are consistent with the work of Zazulak and colleagues who established that lateral angular trunk displacement deficits and low back pain predict knee injury in female and male athletes, respectively.13

Remarks

While the preceding review considered recent and fundamental primary literature under basic scrutiny, a complete examination of methodological and statistical power is beyond its scope. Despite a rather comprehensive incidence, the precise pathomechanics of PFPS remain unclear in their entirety. And although excellent thinking and competent studies support each model, it seems that no singular model holds absolute predictive strength in isolation. These and other data function most robustly in concert. From these studies we learn patterns and assemble trajectories to better anticipate and resolve pathology.

REFERENCES

1. Cowan SM, Crossley KM, Bennell KL. Altered hip and trunk muscle function in individuals with patellofemoral pain. Br J Sports Med. 2009;43:584-588.
2. Jan M, Lin D, Lin J, Lin CJ, Cheng C, Lin Y. Differences in sonographic characteristics of the vastus medialis obliquus between patients with patellofemoral pain syndrome and healthy adults. Am J Sports Med. 2009;37:1743-1749.
3. Mascal CL, Landel R, Powers CM. Management of patellofemoral pain targeting hip, pelvis, and trunk muscle function: 2 case reports. J Orthop Sports Phys Ther. 2003;33:647-660.
4. Powers CM. Rehabilitation of patellofemoral joint disorders: a critical review. J Orthop Sports Phys Ther. 1998;28:345-354.
5. Powers CM. The influence of altered lower-extremity kinematics on patellofemoral joint dysfunction: a theoretical perspective. J Orthop Sports Phys Ther. 2003;33:639-646.
6. Smith TO, Nichols R, Harle D, Donel ST. Do the vastus medialis obliquus and vastus medialis longus really exist? A systematic review. Clin Anat. 2009;22:183-199.
7. Souza RB, Powers CM. Differences in hip kinematics, muscle strength, and muscle activation between subjects with and without patellofemoral pain. J Orthop Sports Phys Ther. 2009;39:12-19.
8. Tyler TF, Nicholas SJ, Mullaney MJ, McHugh MP. The role of hip muscle function in the treatment of patellofemoral pain syndrome. Am J Sports Med. 2006;34:630-636.
9. Van Tiggelen D, Cowan S, Coorevits P, Duvigneaud N, Witvrouw E. Delayed vastus medialis obliquus to vastus lateralis onset timing contributes to the development of patellofemoral pain in previously healthy men. Am J Sports Med. 2009;37:1099-1105.
10. Voronov AV. Anatomical cross-sectional areas and volumes of the muscles of the lower extremities. Human Physiology. 2003;29:201-211.
11. Wilson NA, Press JM, Zhang L. In vivo strain of the medial vs. lateral quadriceps tendon in patellofemoral pain syndrome. J Appl Physiol. 2009;107:422-428.
12. Wong YM, Ng G. Resistance training alters the sensorimotor control of vasti muscles. J Electromyogr Kinesiol. 2009;doi:10.1016/j.jelekin.2009.02.006
13. Zazulak BT, Hewett TE, Reeves NP, Goldberg B, Cholewicki J. Deficits in neuromuscular control of the trunk predict knee injury risk. Am J Sports Med. 2007;35:1123-1130.