Chiropractors now have access to myriad advanced testing options.
MRIs, diagnostic ultrasounds, and CT scans help confirm diagnoses like disc lesions, stenosis, and tears of a labrum or meniscus. These structural pathologies, however, are often signs rather than causes of the patient’s underlying problem.
Structural diagnoses are frequently the result of longstanding functional deficits that generate pathoanatomic changes and, eventually, symptoms. Diagnosing underlying functional deficiencies does not require any specialized equipment other than a keen sense of observation. This is one way to identify and manage hip abductor weakness, a commonly overlooked contributor to many lower body complaints.
Etiology of dysfunction
The muscles of the hip provide not only local stability but also play an important role in spinal and lower extremity functional alignment.1-4 While weakness in some hip muscles (hip extensors and knee extensors) is well tolerated, weakness or imbalance in others can have a profound effect on gait and biomechanical function throughout the lower half of the body.5 Weakness of the hip abductors, particularly those that assist with external rotation, has the most significant impact on hip and lower extremity stability.5,6
The gluteus medius (GM) is the principal hip abductor. It originates on the ilium just inferior to the iliac crest and inserts on the lateral and superior aspects of the greater trochanter. While the principal action of the GM is hip abduction, clinicians will appreciate its more valuable contribution as a dynamic stabilizer of the hip and pelvis—particularly during single-legstance activities like walking, running and squatting.
The GM contributes approximately 70 percent of the abduction force required to maintain pelvic leveling during single-leg stance. The remainder comes predominantly from two muscles that insert onto the ilio tibial band: the tensor fascia lata and upper gluteus maximus.7
Incompetent hip abductors and external rotators allow for excessive adduction and internal rotation of the thigh, leading to a cascade of biomechanical problems. These include pelvic drop, excessive hip adduction, excessive femoral internal rotation, valgus knee stress and internal tibial rotation.1,8-13
The first functional manifestation of hip abductor weakness occurs when the contralateral pelvis is allowed to drop during single-leg-stance activities (positive uncompensated Trendelenburg). This causes relatively excessive thigh adduction and internal rotation of the weak leg, creating significant biomechanical disadvantages at the knee and hip. Excessive adduction of the thigh leads to increased tension on the iliotibial band predisposing the tissues beneath to compressive irritation.14-16
Runners with iliotibial band problems frequently demonstrate hip abductor weakness on the affected side.17
Chronic gluteal dysfunction may lead to myofascial trigger points, tendinopathy, and musculotendinous strains.18 Prolonged thigh adduction can lead to a self-perpetuating cycle of “stretch weakness.”19
Downstream, hip abductor and external rotator weakness allow for dynamic knee valgus (knockknee) during single-leg stance.20-23 Uncontrolled thigh adduction is biomechanically coupled with femoral internal rotation, a combination recognized as contributing to medial collateral and anterior cruciate ligament sprains and tears.24,25
Excessive thigh adduction and femoral internal rotation also cause a relative lateral displacement of the patella, driving the lateral patellar facet into the lateral femoral condyle, often symptomatically.26-29 Research confirms that patients with patellofemoral pain demonstrate hip abductor weakness when compared to an asymptomatic population.30,31
Not all of the torsional energy from excessive femoral internal rotation is dissipated by the knee. Some of it travels into the tibia and can contribute to medial tibial traction periostitis (shin splints), and foot hyperpronation. Foot hyperpronation and hip abductor weakness are known biomechanical co-conspirators.
GM weakness allows excessive hip adduction, which causes increased foot arch loading during ambulation. In turn, hyperpronation causes stretch weakness of the GM, generating a self-perpetuating cycle where downstream biomechanical problems exacerbate trouble at the hip.
It is thus clear that GM weakness allows excessive femoral adduction and internal rotation. Internal rotation of the femur forces the femoral head backward, causing the pelvis to shift into anterior nutation.32 This triggers stretch weakening of the gluteal and abdominal muscles and adaptive shortening of the hip flexors (i.e., lower crossed syndrome).33
Anterior nutation of the pelvis limits hip extension, which increases extension forces on the lumbar facets and contributes to low-back pain.32
Corrections at a cost
The body requires balance and strength in all planes for optimal performance. Hip abductor weakness forces the lower kinetic chain to employ various compensatory mechanisms, and these corrections come with a cost.5,34 While the functional diagnosis of hip abductor weakness can present asymptomatically, it is also a well-known contributor to several painful structural diagnoses throughout the lower body and can be a useful predictor of lower extremity injury.35 This weakness may present particularly in females.
There is no “typical” presentation for hip abductor weakness, but clinicians should consider the problem in any patient with lower chain symptomatology, particularly those with hip tendinopathy, greater trochanteric pain syndrome, iliotibial band syndrome, patellofemoral pain syndrome, ACL injury, medial knee pain, and lower back pain.
Clinical evaluation for hip abductor weakness begins with a visual inspection to ensure that the thigh and leg are in relative sagittal plane alignment. A basic functional assessment is the Trendelenburg test, which entails having the patient cross their arms over their chest and lift one leg at a time, while you look for pelvic drop or knee valgus. The presence of an uncompensated pelvic drop when performing the Trendelenburg maneuver suggests GM weakness.
Longstanding weakness can result in compensatory lateral trunk flexion over the stance leg or moving the ipsilateral arm out to the side.7 Functional testing should progress from a simple single leg stand into a single leg squat and finally, a single leg 6-inch step down.
The primary goal of management is to strengthen the hip abductors, thereby improving function during weightbearing activities.36 In symptomatic patients, hip abductor strength correlates with improvement.17,37 Moreover, athletes with stronger hip abductors are less likely to sustain lower extremity injuries.38</sup<
An electromyographic analysis by Kristen Boren demonstrated that the most effective exercises for strengthening the GM are (in order of effectiveness): side plank abduction with the affected leg on bottom, side plank abduction with the affected leg on top, single leg squat, clamshell progression No. 4 (side-lying clamshell with knees and ankles separated approximately 8 inches), and a front plank with hip extension.39
Patients with hip abductor weakness commonly demonstrate hypertonicity or myofascial irritation in the lumbar erectors, hip flexors, and thigh adductors. Stretching and myofascial release may be necessary.
Postural stressors that create prolonged static loading or lengthening of the GM should be avoided. These include hanging on one hip while standing, sitting cross-legged, and sleeping in a side position with hip flexion and adduction.7
Patients with fallen arches and those who hyperpronate may benefit from using orthotics or arch supports in their footwear. These types of orthotics have been shown to increase the activation of the gluteus muscle during single-leg-stance activities.40
Achieving exceptional outcomes often requires identifying and removing the functional stressors that predispose patients to structural changes and symptoms. Patients who understand why their hip abductor weakness is contributing to their pain will be more likely to take action, thereby improving your clinical outcomes.
Tim Bertelsman, DC, CCSP, FACO, has been practicing in Belleville, Ill., since 1992. He is a Diplomate of the Academy of Chiropractic Orthopedists, and has lectured nationally on various clinical and business topics and has been published extensively. He is co-founder of ChiroUp.com, through which he can be contacted.
Brandon Steele, DC, DACO, FACO, is currently in private practice at Premier Rehab in the greater St. Louis area. He began his career with a residency at the Central Institute for Human Performance. He currently lectures on clinical excellence and evidence-based treatment of musculoskeletal disorders. He can be contacted through ChiroUp.com.
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13 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(1):12-9.
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