Foot Hyperpronation

Get to the Foundation of Your Patient’s Problem
Healthcare is changing- and regardless of who is ultimately paying for your care, they want results. Now, more than ever, you must recognize the “functional” diagnoses that contribute to your patient’s “structural” problems. This article will discuss the identification and successful management of Foot Hyperpronation- a commonly overlooked “functional” problem that delays recovery.

The foot and ankle combination is a complex tool that is called upon to perform two seemingly contrary roles; a flexible shock absorber that contours to irregular surfaces, and a rigid propulsive lever. “Pronation” plays a vital role in the foot’s ability to multitask. (1,2,3)

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Foot pronation is the combined movement of eversion, abduction, and dorsiflexion that results in flattening of the longitudinal arch. (4) In a normal gait cycle, the process of pronation begins at heel strike, progresses through mid-stance and then reverts back toward supination to prepare a rigid lever for forward propulsion. (4-7) In a healthy foot, pronation is limited to approximately 8 degrees. (5-7) Movement beyond 8 degrees is termed “hyperpronation.”

Since the longitudinal axis of the tibia is medial to the body of the calcaneus, loading this joint forces the heel laterally in relation to the tibia (calcaneal eversion). As the center of gravity moves medially, the foot may compensate by rotating laterally, making it a poor lever. The repetitive stress of hyperpronation causes significant strain on the soft tissues of the foot. The relatively inelastic medial band of the plantar fascia is often stressed beyond its capacity to elongate, causing irritation in those who hyperpronate. (10) Traction from hyperpronation contributes to posterior tibial tendinopathy and posterior tibial nerve irritation (tarsal tunnel syndrome). (11)

The effects of hyperpronation are not localized to the foot. Due to the unique shape and tight fit of the ankle mortise, hyperpronation causes internal rotation of the tibia. (12) This torque continues up the kinetic chain and results in internal rotation of the femur, which moves the femoral head and acetabulum backward, causing anterior tilt of the pelvis, and hyperextension of the lumbar spine (see figure 1). (7,8,14,15)

Hyperpronation stresses the knee through a number of mechanisms. In particular, a lowered arch combined with internal tibial rotation places significant valgus stress on the knee. (8) This challenges the medial collateral ligament and anterior cruciate ligament and is a well-recognized contributor to injuries of these structures. (16,17) Additionally, internal rotation of the tibia and femur cause a relative lateral displacement of the patella, driving the lateral patellar facet into the lateral femoral condyle. (18) Not surprisingly, low arches and hyperpronation are commonly associated with patellofemoral pain. (19-22) Longstanding misalignment of the patellofemoral joint is associated with degeneration. (19,22,23)

Not all of the torsional energy of tibial internal rotation is dissipated by the knee. In fact, much of it travels through the knee into the thigh and is absorbed by the hip. (18) Internal rotation of the femur has a detrimental effect on several muscle groups, including the quadriceps, hip adductors, and hip abductors (gluteus medius). (8) Foot hyperpronation and hip abductor weakness are known biomechanical coconspirators- hyperpronation causes stretch weakness of the gluteus medius, and gluteus medius weakness allows excessive hip adduction which causes increased foot arch loading during ambulation. So in a self-perpetuating cycle, the compensatory changes that occur upstream in response to hyperpronation serve to exacerbate problems at the foundation.

Internal rotation of the femur causes the pelvis to shift anteriorly. (8) This further contributes to “stretch weakening” of the gluteal and abdominal muscles and adaptive tightening of the hip flexors (lower crossed syndrome). This process limits hip extension, which in turn increases extension forces on the lumbar spine facets. (8) What’s more, the functional leg length inequality of a unilateral flat foot may cause lateral bending of the lumbar spine toward the affected side, further increasing facet compression. (8) As expected, hyperpronation contributes to lower back pain. (14,25-32)

Foot hyperpronation and pes planus and are distinctly separate problems, with the former being “dynamic” and the latter “static.” However, the two are related and the negative effects of hyperpronation may be compounded in low-arched patients.

The body employs various compensatory mechanisms to offset foot hyperpronation – although these corrections do not come without a cost. (8) Foot hyperpronation ultimately causes joints higher in the kinetic chain to absorb more shock. (8,20,21,30) The increased load on the knees, hip, and spine is compounded during athletic activity, particularly running and jumping. While the “functional” diagnosis of foot hyperpronation can present asymptomatically, it is a well-known contributor to a multitude of painful “structural” diagnoses throughout the lower body.

There is no “typical” presentation for foot hyperpronation, but the condition should be considered in any patient with lower chain symptomatology, particularly those with plantar fasciitis, Achilles tendinopathy, metatarsalgia, medial tibial stress syndrome (shin splints), patellofemoral pain syndrome, greater trochanteric pain syndrome, and low back pain. Longstanding hyperpronation may lead to ligamentous laxity and degeneration of affected joints. (19-23,39,40)

Clinical evaluation for foot hyperpronation begins with visual inspection of a barefoot patient. (41) Ideally, a sagittal plane projecting forward from the axis of the tibia should also pass through the second ray of the foot. Patients with hyperpronation commonly demonstrate excessive forefoot abduction. This may be assessed by observing the degree of foot abduction from behind- aka “too many toes sign.” Visual inspection of the posterior ankle will often demonstrate calcaneal eversion, as evidenced by inward “bowing” of the Achilles tendon. Sliding a finger beneath a standing patient’s medial longitudinal arch may provide a simple assessment of static arch height.

As noted earlier, hyperpronation is a functional problem (not simply “flat feet”), so it must be assessed functionally. The navicular drop test is a useful functional measurement. The test begins with marking the position of the seated patient’s navicular by placing a dot over their navicular tuberosity, while their foot is in a non-weight bearing and neutral position. The clinician then places an index card on the floor next to the patient’s foot and marks the index card at the position of the dot. The patient then stands (on both feet), and the clinician marks the new position on the card. If the navicular drops more than 10 mm, the test is positive for hyperpronation. (42,43) Normal navicular drop is 6 to 8 mm. (42)

Posterior tibialis weakness is another possible contributor to foot hyperpronation. Weakness of this muscle is suggested by excessive calcaneal eversion when performing a heel raise. Muscular assessment should include evaluation of hip abductor strength via the Trendelenberg sign or knee valgosity on single leg squat or single leg step up. Since the Achilles tendon inserts slightly lateral to midline, a hypertonic gastroc/soleus will result in some degree of calcaneal eversion and increased pronation. Clinicians should assess flexibility of the gastroc and soleus in passive ankle dorsiflexion.

The management of foot hyperpronation includes prescribing arch supports as well as exercises to control motion at the hip and ankle. (35) Factors, including the degree of hyperpronation and the functional demands of the patient, will dictate whether custom or prefabricated orthotics are most appropriate. Clinicians should be cautious to avoid excessive arch buttressing, as this could produce a paradoxical result. (47) Likewise, bulky orthotics or shoes with excessive cushioning may have an adverse effect on proprioception and balance. (47)

Inadequate ankle dorsiflexion may force excessive pronation through the mid foot. Stretching exercises and myofascial release may be appropriate for restrictions in the gastroc and soleus muscles.

Strengthening exercises should be directed at the foot and hip, specifically the posterior tibialis and hip abductor muscles. Traditional strength training does not necessarily change faulty movement patterns. (54) Exercise programs should incorporate proprioception, beginning with simple balance training like a single leg stance or Vele’s, then progressing to lunges on an unstable surface, like a Bosu or Dynadisc. (55-57) Strengthening exercises for the hip abductors could include a posterior lunge, clam with band, or sidebridge.

Obesity exacerbates hyperpronation; therefore, diet and exercise recommendations may be appropriate for overweight patients. (64,65) Hyperpronators should avoid shoes with narrow toe boxes or high heels. (11) Of note- hyperpronation is common in children, as the development of the longitudinal arch is usually not complete until the age of 8. (41) Some studies suggest that shoe wear in children is detrimental to the development of a healthy longitudinal arch. (62,63)

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