What Are Effective Therapies for Anterior Knee Pain?

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Chapter 95 What Are Effective Therapies for Anterior Knee Pain?

JENNY. MCCONNELL, B App Sci (Phty), Grad Dip, Man Ther, M Biomed Eng

Anterior knee pain or patellofemoral (PF) pain is one of the commonest conditions presenting to clinicians involved in the management of sports injuries.^1,² Prospective cohort studies report incidence rates of 7% to 15% in sporting and general populations.³^–⁶

Currently, the cause of patellofemoral pain (PFP) is not known, but patients present with stereotypical symptoms, namely, anterior knee pain aggravated by flexed knee activities, both loaded, such as climbing stairs and squatting, and unloaded, such as sitting with the knee flexed (“moviegoer’s” knee).

SOURCES OF PAIN

Much speculation had been made about the source of PFP, but evidence is mounting that the richly innervated infrapatellar fat pad could be a significant player.^7,⁸ A recent study by Bennell and colleagues,⁹ in which the fat pad of asymptomatic individuals was injected with hypotonic saline, confirmed the finding that the fat pad can be a potent source of knee pain symptoms that are not just confined to the infrapatellar region but can refer to the proximal thigh as far as the groin. In addition, the lateral retinaculum seems to be responsible for some PF symptoms because numerous studies demonstrate nerve damage in the lateral retinaculum of patients with PFP, including nerve fibrosis, neuroma formation, and increased number of myelinated and unmyelinated nerve fibers with a predominant nociceptive component.¹⁰^–¹²

Factors Predisposing to Patellofemoral Pain

Several factors predisposing an individual to PFP have been identified, ranging from overuse and training errors to faulty biomechanics. Structural causes of PFP are divided into intrinsic and extrinsic causes. Intrinsic structural factors are uncommon and relate to dysplasia of the patella or femoral trochlea and the position of the patella relative to the trochlea. Extrinsic structural faults are reported to cause a lateral tracking of the patella.^1,^{13, 14} The extrinsic factors include increased Q angle, hamstrings and gastrocnemius muscle tightness, abnormal foot pronation, and quadriceps muscle dysplasia.

The Q angle, representing the line of pull of the rectus femoris muscle, has long been the benchmark of orthopedic surgeons to indicate PF function. Its value is widely debated in the literature, with many authors questioning the diagnostic relevance of the static Q angle, suggesting the dynamic Q angle has greater relevance.^1,^{15, 16} The dynamic Q angle is affected by the position of the hip from above and the foot below during weight-bearing activities. The alignment of the hip and the foot is particularly critical at 30 degrees of knee flexion when the patella should be engaging in the trochlea. Many individuals with PFP have “squinting” patellae and an associated internal rotation of the femur, which has been hypothesized to cause tightness in the tensor fascia latae muscle and weakness of the gluteus medius muscle. Evidence in the literature of poor hip and pelvic control is limited, although there is some support that the hip abductor and rotator strength is decreased in individuals with PFP sufferers.¹⁷^–¹⁹ However, others claim that hip abductor and external rotator strength is no different in PFP subjects and healthy control subjects.²⁰ In addition, soft-tissue flexibility of various structures in the lower limb such as iliotibial band, hamstrings, gastrocnemius, and anterior hip structures has been suggested as being a factor in PFP syndrome, but the findings are quite disparate.

Abnormal foot biomechanics such as excessive, prolonged, or late pronation, which alters tibial and even entire lower limb rotation at varying times through range, has been proposed to adversely affect PF joint mechanics.^15,^{21, 22} Intrinsic and extrinsic causes of abnormal foot position exist. The intrinsic causes relate to static foot postures such as forefoot and rearfoot varus and valgus. The extrinsic causes relate to the foot being lateral to the weight-bearing line, such as genu valgus and internal rotation of the femur, or the weight being borne on the lateral aspect of the foot, such as tibial varum. However, one research group has conflicting conclusions about the influence of foot pronation in subjects with PFP, suggesting that statically increased rearfoot varus may be a contributing factor in PFP,²³ whereas dynamically, individuals with PFP do not demonstrate excessive foot pronation or tibial internal rotation compared with asymptomatic individuals.²⁴

The most common cause of PFP cited in the literature is quadriceps muscle weakness particularly of the vastus medialis oblique (VMO). Ideally, the synergistic relation between the VMO and vastus lateralis (VL) should maintain the alignment of the patella in the femoral trochlea, especially in the first 30 degrees of knee flexion, before the patella is fully engaged in the trochlea. It has been proposed that this balanced activation of the VMO and VL is disrupted in patients with PFPS. The issue of whether the disruption is in part a motor control dysfunction has been investigated by Mellor and Hodges,²⁵ who found that synchronization of motor unit action potentials is reduced in subjects with PFP (38%) compared with control subjects (90%). However, the evidence to support an imbalance in the activation of the vasti (either decreased activation of VMO or enhanced activation of VL) is contentious.²⁶^–²⁹ Differences in methodology (particularly with respect to the use of electromyography [EMG]) and the inherent heterogeneity in the PFPS population may account for some of the inconsistencies in study results.

Although there is inconclusive evidence to support or refute an imbalance in the magnitude of vasti activation in patients with PFPS, disrupted activation of the vasti may take the form of delayed activation of the VMO relative to the VL. It has been hypothesized that the VMO, which has a smaller cross-sectional area than the VL, must receive a feed-forward enhancement of its excitation level to track the patellar optimally.^30,³¹ Many studies that have examined individuals with PFPS have supported this hypothesis, by demonstrating that the EMG activity and reflex onset time of the VMO relative to the VL is delayed, when compared with asymptomatic individuals.³²^–³⁴ However, the issue remains controversial in the literature, with some studies demonstrating no differences in EMG onsets,^27,^{28, 35, 36} but a more recent study by Cowan and colleagues³⁴ found that although the majority of subject with PFP have a delayed onset of VMO relative to VL on a stair-stepping task (67% concentrically, 79% eccentrically), there were still some subjects whose VMO preceded VL activation. In addition, these investigators found that some of the control subjects (no history of PFP) exhibited a delayed onset of the VMO relative to the VL (46% concentrically and 52% eccentrically) on the stair-stepping task. Cowan and colleagues’³⁴ study may clarify some of the discrepancies found in the literature with regards to timing. The stratification of the groups occurs only when there are sufficient subject numbers to tease out the difference. Some of the earlier studies may not have a statistical significance because the power calculations had not been done and there were too few subjects.

Individuals with PFP not only demonstrate a delay in the onset of VMO relative to the VL but also relative to the prime mover (tibialis anterior and soleus, respectively) after postural perturbation where subjects were required to rock back on their heels or go up on their toes in response to a light stimulus.³⁷ In control subjects, the VMO preceded the prime mover and was activated with the VL.³⁷ This feed-forward strategy used by the central nervous system to control the patella can be restored by physical therapy rehabilitation strategies directed at altering muscle recruitment in functional movements.³⁸

TREATMENT

PFP is not a self-limiting condition, so it is important to identify strategies that will alleviate the symptoms of this often chronic condition. The majority of patients with PFP respond to nonoperative (physical therapy) management, which aims to not only improve patellar tracking through active (quadriceps or VMO retraining) and passive (realignment procedures such as tape, brace, stretching) interventions but also improve lower-limb mechanics both proximally by pelvic muscle training and distally by enhancing foot function with orthotics or muscle training. Initially, the clinician needs to be able to significantly reduce the patient’s symptoms. This is often achieved by taping or bracing the patella. One group of investigators suggests that bracing may even prevent the development of PFP in athletic individuals.³⁹

Patellar taping should unload painful structures to enable the patient to be pain-free while doing activities. Theoretically, using tape could also provide a sustained stretch of the tight lateral structures, making use of the creep phenomenon, which occurs when a constant low load is applied to viscoelastic material such as the lateral retinacular tissues. Length of soft tissues can be increased with sustained stretching, and the magnitude of increased displacement is dependent on the duration of the applied stretch,⁴⁰ although there have been no studies to show changes in retinacular tissue length after taping.

Short-term pain reduction does occur with patellar taping and bracing ⁴¹^–⁴⁵ (Level of Evidence I), and research continues to focus on mechanisms to explain this pain relief. Two randomized, clinical trials did not find any benefits of using a medial glide tape while doing physical therapy in addition to physical therapy intervention.^46,⁴⁷ The problem with both these studies is that the beneficial effect of tape was not established, and the tape was applied only for the physical therapy session, not while the individuals were doing other potentially painful weight-bearing activities.

A few studies have evaluated the effects of patellar taping and bracing on radiographic patellar alignment in patients with PFPS with conflicting results. Although improvements have been noted in some studies,⁴⁸ other studies failed to find radiologic evidence of changed patellar position.⁴³ A number of factors including different measurement procedures (weight bearing vs. non–weight bearing), taping techniques, and subject attributes may contribute to the disparate results.

Although no evidence has been reported that patellar tape can change the activation magnitude of the VMO or VL,⁴⁹ there is evidence that taping the patella can alter the onset timing of the VMO relative to the VL during stair ambulation.^50,⁵¹ Cowan and colleagues⁵⁰

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