IP syndrome is likely the most underdiagnosed ailment in runners. The likely reason for such underdiagnosis is that both patients and clinicians tend to focus in on the effect (pain) than the cause. The syndrome, as it occurs in distance runners, starts as a loss of function with little to no pain. Then it shows up as secondary problems in other areas of the body. A common early complaint with this malady is that it seems more difficult than usual to get going in the early part of a race or workout.
The hip is a ball and socket joint which allows for 3 planes of freedom. Range of motion (ROM) of the hip includes approximately 120° of flexion, 20° of extension, 40° of abduction, 25° of adduction, and 45° each of internal rotation and external rotation. The resting position of the hip is considered to be 30° of flexion and 30° of abduction.
The ilio-psoas is actually two muscles. The psoas and iliacus muscles originate from the lumbar spine and pelvis, respectively, and are innervated by the first three lumbar nerve roots. These muscles converge to form the iliopsoas muscle. The IP inserts onto the lesser trochanter of the proximal femur. The psoas major tendon exhibits a characteristic rotation through its course, transforming its ventral surface into a medial surface. The iliac portion of this tendon has a more lateral position, and the most lateral muscle fibers of the iliacus muscle insert onto the lesser trochanter without joining the main tendon.
The iliopsoas muscle passes anterior to the pelvic brim and hip capsule in a groove between the anterior inferior iliac spine laterally and iliopectineal eminence medially. The musculotendinous junction is consistently found at the level of this groove. The iliopsoas muscle main function is as the prime mover of hip flexion. This is of utmost importance because hip flexion is the drive behind a distance stride. (Also, it is an external rotator of the femur). So when this muscle starts to lose strength, power or flexibility, the muscles that assist in these actions often feel the brunt manifesting in injury. Loss of hip flexion leads to hamstring injuries. Loss of external rotation leads to sciatica and associated hip injuries.
With all this anatomy, physiology, and kinesiology available, one would think that hip function would be utterly predictable and relegated to boring academic trivia. In fact, this is far from the truth. With each and every change in hip position, muscles change the force they apply on a joint. Sometimes even a small change in position can cause a hip muscle to have a completely opposite function. Put another way, a muscle can be an internal rotator of the hip. Change the position of the hip a few centimeters and it is now an external rotator of the hip. For this reason, it is not unheard of for seeming contradictory injuries including the knee, calf or even back problems to result from this syndrome.
Diagnosis is best done with a clinical “hands-on” exam. X-rays are always negative for findings of IP syndrome. Sonograms may assist with diagnosis but are rarely diagnostic by themselves. MRIs are most helpful of any imaging tests. Hence, much of the needed information to determine treatment course is supplied through the clinical exam.
Treatment starts with the basics: Rehab the deficient muscle functions. If the muscle is weak, strengthen it. A type of crunch is a good tool. A common mistake is to do a traditional crunch which emphasizes concentric strengthening at the expense of eccentric strengthening. There are variations that can customize these exercises for distance runners and individual needs. If the muscle is tight, stretching is paramount. The lunge is an effect maneuver, so long as it done properly (many people stretch the psoas fibers at the expense of the iliacus fibers). Also, long standing cases need to have stretching and the scar tissue freed up before strengthening become effective.