Femoral Acetabular Impingement

By Deborah Pate, DC, DACBR

Femoral acetabular impingement (FAI) is a major cause of early osteoarthritis or degenerative joint disease of the hip, especially in young, active patients. It is characterized by abnormal contact of the acetabulum and the femur during the limits of physiologic hip range of motion, particularly during flexion and internal rotation. Clinical manifestations of the syndrome include groin and/or posterior hip pain.¹

FAI is classified as either "pincer" or "cam" impingement. The cam form comes from the Dutch word for cog; the femoral head has lost its spherical shape, which allows abnormal contact between the head of the femur and the acetabulum. The pincer form comes from the French word meaning to pinch; the acetabulum covers too much of the femoral head. This overcoverage results in the labral cartilage being pinched between the rim of the acetabulum and the anterior femoral head-neck junction.

Commonly, a combination of both forms exists, described as mixed. It is postulated that FAI may very well be a contributing pathway to the development of premature degenerative joint disease.² The suspected etiology of this disorder is abnormal development of the physis, but it can also occur in slipped capital femoral epiphysis (SCFE), Legg-Calve-Perthes disease, and malunited femoral neck fractures.

Lesions identified by imaging include characteristic tears of the anterior and posterior labrum, paralabral cyst formations and synovial herniation pits at the site of mechanical impact of the femoral neck, and osteochondral injuries of the acetabular roof and femoral head. However, the hip studies are often read as normal, particularly plain films. Many of the early findings are very subtle and frequently are considered normal.

The first step in the assessment of this disorder is getting a good history, of course. Hip impingement pain is typically experienced anteriorly in the groin, but patients might also complain of associated lateral and posterior discomfort. Pain is often described as dull or aching in nature, worsening after prolonged periods of sitting. Occasionally, an exacerbation of sharp pain with activity is reported. Duration of symptoms is variable. Patients often report an inciting incident as the initial cause of the pain, but onset can also be insidious.

AP pelvis demonstrates pistol-grip deformity (arrow).The physical examination is very important in these cases. Frequently, the patient has an antalgic gait. Range of motion is decreased and should be compared to the unaffected side. Typically, internal rotation with the hip at 90 degrees of flexion is markedly limited relative to the other side. Flexion and abduction can also be restricted compared to the opposite side.

The most important finding indicating hip impingement is a positive impingement test, which has been shown to be present in more than 90 percent of patients with confirmed FAI.¹ The test is performed by having the patient supine on the examination table. The affected hip and knee are flexed to 90 degrees. The hip is then adducted and internally rotated in this flexed position. A positive test involves a sudden, often sharp pain in the hip. This maneuver often recreates the patient's symptoms. To complicate matters, there is a posterior impingement, which can be tested by forced external rotation of the hip while in full extension.

Once the diagnosis of FAI is suspected, plain films should help to confirm the diagnosis, if one knows what to look for. There are a number of specialized imaging modalities that can be used to help determine the extent of the problem, as well as treatment options, but initially, a simple anteroposterior view of the pelvis and a lateral view of the affected hip should be adequate. The radiographic features of this disorder will vary depending on which type of impingement predominates (cam or pincer), but let's summarize the general findings.

Cam impingement demonstrates an aspherical femoral head with a predominate "bump," often referred to as a pistol-grip deformity. The cam impingement is more common in young males. These osseous bumps lead to a decreased femoral head-neck offset, which is defined by the distance between the widest diameter of the femoral head and the most prominent part of the femoral neck. It is thought that the main cause of cam impingement is growth abnormalities of the capital femoral epiphysis.

Pincer-type impingement demonstrates overcoverage of the acetabulum in relationship to the femoral head and a linear indentation at the head-neck junction of the femur. There are many ways of measuring the depth of the acetabulum. A software program has even been developed to determine the depth of the acetabulum.

Lateral hip pincer-type impingement with linear erosion.My suggestion would be to compare the symptomatic hip to the asymptomatic hip. Compare the medial aspect of the acetabulum with the ilioishial line. There should be some visible gap between the two, and the ilioishial line should lie medial to the margin of the acetabulum. Then evaluate the amount of coverage of the femoral head. You can use the extrusion index, which is A + E divided by E. Normal should be about 25 percent. Again, compare the coverage of the femoral head with the asymptomatic side. The femoral head should never be completely covered by the acetabulum. About one-fourth of the head should lie outside the superior margin of the acetabulum.

A pitfall to be aware of is that a pseudo-deep acetabulum can be produced on an anteroposterior radiograph that is centered over the hip.¹ Do not use the AP spot view of the hip to determine the depth of the acetabulum. Only use the AP view of the pelvis due to differences in the central ray. The pincer-type impingement is more common in women. One can think of the pincer impingement as associated with acetabular pathomorphologies, but once the stage is set, most patients demonstrate a combination of both types of impingements, with one perhaps being more predominant.

Left: Pitt�s pit (arrow) now indicative of impingement.Right: Os acetabuli (arrow) line of sclerosis (arrows), indicative of impingement.Secondary signs on radiographic findings are: herniation pits, ossification of the labrum and os acetabuli.² In fact, I'm certain some of you will remember when "Pitt's pit" was once considered a normal finding, as was the os acetabuli. Now we must consider those findings indicative of impingement.

It is important to be aware that hip impingement syndrome frequently is present in spite of a reported normal radiographic study of the hip, either due to an inability to recognize the subtle changes or even the possibility of finding the problem before radiographic findings are present. The history and clinical findings are of utmost importance, including a positive impingement test. If the patient had previous films that were negative, I recommend requesting the films before relying on a radiology report. If films are not available, at least take the AP pelvis to determine if there are any radiographic findings that would indicate impingement. Early diagnosis is crucial for the patient to avoid the progression of impingement syndrome to osteoarthritis.

References

1. Leunig M, Ganz R. Femoroacetabular impingement: a common cause of hip complaints leading to arthrosis [in German]. Unfallchirurg 2005;108:9-17.
2. Beck M, Kalhor M, Leunig M, Ganz R. Hip morphology influences the pattern of damage to the acetabular cartilage: femoroacetabular impingement as a cause of early osteoarthritis of the hip. J Bone Joint Surg Br 2005;87:1012-8.
3. Ito K, Leunig M, Ganz R. Histopathologic features of the acetabular labrum in femoroacetabular impingement. Clin Orthop Rel Res 2004;429:262-71.
4. Tannast M, Siebenrock K, Anerson S, Femoroacetabular impingement: radiographic diagnosis - what the radiologist should know. AJR 2007;188:1540-52.
5. Leunig M, Beck M, Kalhor M, et al. Juxta-articular cysts at the anterosuperior femoral neck: high prevalence in hips with femoro-acetabular impingement. Radiology2005;244:237-46.

Functional Evaluation of the Hips, Part 1

By Jeffrey Tucker, DC, DACRB

This article explains the importance and purpose of measuring medial and lateral rotation of the hips with the patient in the prone position. Insufficient hip rotation control can cause local hip pain, a pain-producing compensation in the lumbopelvic region or the knees. The ideal range of medial hip rotation motion is approximately 35 degrees (without pelvic rotation). The ideal range of lateral hip rotation is approximately 35 degrees from neutral without pelvic motion.¹

I am not as interested in the exact number of degrees of rotation as I am interested in testing for excessive or decreased degrees of the range of rotation. In Shirley Sahrmann's bookDiagnosis and Treatment of Movement Impairment Syndromes, she notes less than 30 degrees of lateral or medial rotation is movement impairment. I am also looking for symmetry or asymmetry of these movements. Evaluating excessive motion and/or decreased range of movement will provide information about the quality of movement at the hips. This is sometimes referred to as neuromotor control or movement coordination.

This evaluation will add another piece of the puzzle to understanding the biomechanics of the lower extremities during physical activities such as gait. It has been my experience that altered movement patterns in the hips may result in alterations of the load distribution across the patellofemoral joint^2,3,4 and lumbosacral region,⁵ causing pain and dysfunction in these areas.

Gathering information about movements is part of a functional examination. Poor quality or altered movement patterns are usually more easily detected when we break down a component of the overall movement (e.g., gait). Recognizing poor hip rotation in the prone position may be easier than recognizing a faulty gait pattern during physical activities. Measuring the hips in a supine position with the hips flexed 90 degrees does not seem as functional as measuring the hips in a prone position with the knees together.

Procedure

The patient should be in the prone position on a flat table. Stand to the contralateral side of the table, to the side of the hip being examined (stand on the left side of the patient while testing the right hip). Grasp the patient's foot and passively bend (flex) the knee to 90 degrees. Make sure the knees are together and the thigh is in the neutral position. Slowly move the foot away from you, causing medial rotation of the hip. Evaluate how far the hip moves without moving the pelvis. Is it more than 35 degrees? Is it less than 30-35 degrees? Slowly move the foot toward your body, producing lateral rotation of the hip. Is it more than 35 degrees? Is it less than 30-35 degrees?

Interpretation

Excessive medial rotation of the hip (common): This indicates poor stability (ability to maintain a stabile core and move the extremities) function or excessive length of the hip joint capsule and the lateral rotator stability muscles, posterior gluteus medius and intrinsic hip lateral rotators (piriformis, gemellus superior, obturator internus, gemellus inferior, obturator externus, quadratus femoris).

The gluteus medius arise from the outer surface of the ilium, anterior to the TFL. The muscle converges to form a tendon that attaches to the lateral surface of the greater trochanter. The gluteus medius has fibers that attach forward and posterior of the greater trochanter. The posterior border of the gluteus medius may blend with the piriformis. Together with the glute minimus, the glute medius abducts and medially rotates the hip joint.

Therefore, if the G med is not firing properly, there will be excessive medial rotation at the hip. The glute minimus and medius are fundamental in keeping the trunk in an upright position when the contralateral foot is raised during walking. The hip joint capsule surrounds the acetabulum and neck of the femur. A number of ligament bands help keep the femur and acetabulum in check. The capsule can get tight or become loose.

Excessive lateral rotation of the hip: This indicates either poor stability function or excessive length of the medial rotator stability muscles (anterior gluteus medius and minimus).

Decreased lateral rotation of the hip (common): This includes shortening of capsule and shortening of myofascial structures (TFL/ITB). To differentiate between capsule or TFL, examine the end feel. Take the leg into abduction by 1 inch and if decreased restriction occurs, the TFL/ITB is limiting the movement. If there is no change, the capsule is causing the decreased lateral rotation.

The tensor fascia lata arises from the anterior part of the outer lip of the iliac crest, the lateral aspect of the anterior superior iliac spine and the upper part of the anterior border of the iliac wing. You should keep in mind that in addition to arising from the iliac crest, the iliotibial band (ITB) attaches into the posterior gluteus maximus muscle in the back. The gluteus maximus through the ITB also attaches on the tibia distally.

This is an important point to remember because the TFL/ITB muscle is producing movement of both the proximal and distal aspects of the thigh, which reinforces the maintenance of a relatively constant position of the femoral head in the acetabulum during hip extension. The TFL assists in the flexion, abduction and medial rotation of the hip joint and extension of the knee joint. Use specific muscle length tests to confirm myofascial shortening.

Decreased medial rotation of the hip: This includes shortening of the capsule and myofascial structures (piriformis or superficial fibers of gluteus maximus). The superficial fibers of the gluteus maximus attach proximally to four structures: the thoracolumbar fascia, the iliac crest, the sacrum and the coccyx. They travel distally to the deep part of the muscle and end in a tendinous sheet, which passes lateral to the greater trochanter and is attached to the iliotibial tract of the fascia lata. The iliotibial tract runs down the anterior lateral side of the thigh. It blends with the capsule of the knee joint to attach to Gerdy's tubercle, the lateral condyle of the tibia and the head of the fibula. Again, poor control at the hip does cause knee dysfunction.

The piriformis arises from the anterior aspect of the second to fourth segment of the sacrum between and lateral to the sacral foramina. Its tendon is attached to the upper border and medial aspect of the greater trochanter. The piriformis laterally rotates the extended hip joint and abducts the flexed hip joint. Differentiate by end feel. Assess specific muscle-length tests to confirm myofascial shortening.

When the glute maximus and piriformis are the dominant muscles producing hip extension, their proximal attachments provide more optimal control of the femur in the acetabulum than do the hamstring muscles. If the attachments of the piriformis and glute maximus muscles are overactive at the femur, they will not provide proper control of the proximal femur during hip extension.

References

1. Van Dillen LR, Sahrmann SA, Norton BJ et al. Reliability of physical examination items used for classification of patients with low back pain. Phys Ther 19998;78:979.
2. Brody LT, Thein JM. Nonoperative treatment for patellofemoral pain. J Orthop Sports Phys Ther 1998;28:336-44.
3. Witvrouw E, Lysens R, Bellemans J, Cambier D, Vanderstraeten G. Intrinsic risk factors for the development of anterior knee pain in an athletic population. A two-year prospective study. Am J Sports Med 2000;28:480-9.
4. Cesarelli M, Bifulco P, Bracale M. Study of the control strategy of the quadriceps muscles in anterior knee pain. IEEE Trans Rehabil Eng 2000;8:330-41.
5. Fredericson M, Cookingham CL, Chaudhari AM, Dowdell BC, Oestreicher N, Sahrmann SA. Hip abductor weakness in distance runners with iliotibial band syndrome. Clin J Sport Med2000;10:169-75.

Sacroiliac Pain and the Long Posterior Sacroiliac Ligament

By Warren Hammer, MS, DC, DABCO

Sacroiliac pain has multifactorial causes, and the long posterior sacroiliac ligament (LPSL) may be a significant factor. The LPSL is the most superficially located sacroiliac joint (SIJ) ligament, is easily palpated and has been associated with sacroiliac/back pain. This ligament is directly caudal to the posterior superior iliac spine (PSIS) and connects the PSIS (and a small part of the iliac crest) with the lateral crest of the third and fourth segment of the sacrum.¹ Tenderness of the ligament is often found just below the PSIS. Both men and women are often found to be tender in these areas, particularly women experiencing peripartum pelvic pain.

In a study on peripartum pelvic pain, involvement of this ligament was useful in differentiating between mainly lumbar and pelvic complaints.² A histological study of the relations of this ligament showed the middle of the ligament as a confluence of three layers: the erector spinae aponeurosis, the deep fascial layer and the gluteal aponeurosis. It was noted that in the deep fascial layer lateral branches of the dorsal sacral rami were identified.³ The authors state that sacroiliac joint pain may be due to an entrapment neuropathy of the lateral branches of the dorsal sacral rami at the long posterior sacroiliac ligament. The fascia of the gluteus maximus muscle also covers the ligament.

A study was conducted utilizing sensory stimulation-guided sacroiliac joint radiofrequency neurotomy on these sacral lateral branches in a group of 14 patients with pain in the sacroiliac area. Sixty-four percent of the patients experienced relief, with 36 percent experiencing complete relief. Fourteen percent experienced no improvement, but none of the patients was made worse.⁴

To understand just how increased tension in the LPSL may be related to pain, it is necessary to understand the function of the long ligament and its association with the sacrotuberous ligament. The sacrotuberous ligament (STL) restricts sacral nutation while the LPSL restricts sacral counternutation. Sacral nutation increases in load-bearing situations such as standing and sitting. Nutation also occurs when lying prone compared to lying supine.^5,6 Although the above ligaments have opposite functions, there is some increased tension in the LPSL when the sacrotuberous ligament is loaded. This may be explained by some connections between the two ligaments.

It gets somewhat complicated when you include all the connections associated with the STL and the LPSL. Both ligaments are affected by muscular connections. Traction to the biceps femoris greatly increases tension to the STL, with hardly any influence on the LPSL. Shortening of the biceps femoris has been shown to limit sacral nutation by way of the STL relating short hamstrings to lower back pain.⁷ Traction on the thoracolumbar fascia in the direction of the latissimus dorsi muscle causes sacral nutation and slackens the LPSL. Therefore, it appears that increased tension in the thoracolumbar fascia or fascia latae (overlying the biceps femoris) will have the effect of exerting tension on these ligaments.

The gluteus maximus muscle can cause slacking of the LPSL when contracting.¹ Manipulation of the iliac bones most probably creates nutation and counternutation of the sacrum, and may affect the tension of the above ligaments. The multifidus and the erector spinae contribute to nutation, and these muscles should help slacken the LPSL. Counternutation usually occurs in unloaded supine positions. Counternutation in the supine position can change to nutation by maximally flexing the hips and using the legs as levers to posteriorly rotate the iliac bones relative to the sacrum. This occurs in the labor position, creating space for the head of the baby during delivery.⁸

To conclude, the LPSL is tensed when the SI joints are counternutated and slacked when nutated. Both the erector spinae and STL can counterbalance the slackening of the LPSL. Pain localized to the LPSL area could therefore indicate sustained counternutation of the SIJ. It is thought that a positive active straight-leg-raise test might indicate a counternutated SIJ.⁹

Counternutation occurs when the lumbar spine is normally flattened, which occurs late in pregnancy as women counterbalance the weight of the fetus.⁷ If this posture is creating pain, there may be excessive tenderness just inferior to the PSIS. It seems like a good idea to palpate just below the PSIS for localized tenderness on patients with localized sacroiliac pain.

Years ago, I attended a seminar conducted by John McMennell, MD, who was renowned for his expertise in manipulative diagnosis and treatment. He said that a normal ligament should not palpate painful. Exerting mechanical load on this area by way of friction massage, Graston Technique, or any deep-pressure method might be advised.

References

1. Vleeming A, Pool-Goudzswaard AL, Hammudoghlu D, et al. The function of the long dorsal sacroiliac ligament: its implication for understanding low back pain. Spine1996;21(5):556-62.
2. Vleeming A, de Vries JHJ, Mens JM, van Wingerden JP. Possible role of the long dorsal sacroiliac ligament in women with peripartum pelvic pain. Acta Obstet Gynecol Scand2002;81(5):430-6.
3. McGrath C, Nicholson H, Hurst P. The long posterior sacroiliac ligament: a histological study of morphological relations in the posterior sacroiliac region. Joint Bone Spine, Sept. 24, 2008 [E-pub ahead of print].
4. Yin W, Willared F, Carreiro J, Dreyfuss P. Sensory stimulation-guided sacroiliac joint radio frequency neurotomy: technique based on neuroanatomy of the dorsal sacral plexus.Spine 2003;28(20):2419-25.
5. Sturesson B, Uden A, Vleeming A. A radio-stereometric analysis of movements of the sacroiliac joints during the standing hip flexion test. Spine 2000a;25(3)L364-8.
6. Sturesson B, Uden A, Vleeming A. A radio-stereometric analysis of the movements of the sacroiliac joints in the reciprocal straddle position. Spine 2000b;25(2):214-7.
7. Vleeming A, Van Wingerden JP, Snijders CJ et al. Load application to the sacrotuberous ligament; influences on sacroiliac joint mechanics. Clinical Biomechanics 1989;4(4):204-9.
8. Vleeming A, Stoeckart R. The role of the pelvic girdle in coupling the spine and the legs: a clinical-anatomical perspective on pelvic stability. In: Vleeming, et al. Movement, Stab-ility & Lumbopelvic Pain. New York: Churchill Livingstone/Elsevier, 2007.
9. Mens JMA, Vleeming A, Snijders CJ, et al. The active straight leg raising test and mobility of the pelvic joints. Eur Spine 1999;8:468-73.

Anterior Femoral Glide Syndrome

By Marc Heller, DC

I am not a chiropractic philosophy writer, but once a year my editor cuts me a little slack. If I am a good chiropractor, it's because of my failures. I learn the most from the patients who I couldn't help initially: the tough cases, the ones in which I wrack my brain to figure out what I am missing.

These tough cases, the ones that require you to think out of the box, are the ones that push you, if you are willing. It's easy to just keep adjusting them, work out the same trigger points, and convince yourself that one more or 10 more treatments will solve the problem, but that doesn't usually work. A recent study tells us that we can predict by the second visit which patients will respond best, at least in cases of lower back pain.¹ The study implies to me that when the patient is not improving quickly, you have to look with new eyes. What I would suggest is that you go back, re-examine them and think of the whole kinetic chain, maybe even the patient's biochemistry and underlying emotional pieces.

At the bare minimum, I believe we need to be experts not only at manipulation, but also at addressing soft tissue and rehabilitation. If the goal is to restore more normal motion, thus improving function and reducing pain, all three of these pieces are necessary.

An accurate musculoskeletal diagnosis includes not only what joint is not moving, but also what joint is moving too much, what specific tissues are the pain generators, and what movement or lack of movement is stressing the pain generator. Shirley Sahrmann states, "A joint develops a directional susceptibility to movement, which then becomes the 'weak link' and most often the cause of pain."²

We have to become more evidence-based. At the same time, we shouldn't become handcuffed to what is absolutely certain. Musculoskeletal research is difficult to do, and its particularly difficult to look at the big picture: the integration of the multiple factors that can contribute to ongoing or recurrent pain syndromes. As Craig Liebenson states, "Lack of evidence of effectiveness is not the same as evidence of ineffectiveness. According to Lewit, we work at the level of acceptable uncertainty."³

Many of you have followed my interest in the hip joint. I am grateful for the contribution of Lucy Whyte Ferguson, DC.⁴ Even using trigger-point work and manipulation of the hip with the wishbone maneuver, as outlined by Dr. Whyte Ferguson, I found too many patients' hip problems recurring, and too many for whom I could not consistently restore normal motion.

I was introduced to a model from Sahrmann that made sense of the two patterns I have seen in the hip. She calls it the anterior femoral glide syndrome, and mentions an internally rotated version and an externally rotated version. Sahrmann's model talks about what accessory movements are dysfunctional. In anterior femoral glide syndrome, the proximal femur moves improperly during hip flexion. Instead of gliding posterior to provide room for the flexion, it glides anterior, jamming into the anterior hip capsule and causing pain and limitation of flexion. What causes this? Sahrmann talks about familiar muscular imbalances. The hamstrings are too tight and are not balanced by the gluteus maximus. During hip extension, the hamstrings create a bowstring effect, pushing the femoral head forward. The posterior structures around the hip are too tight, contributing to the anterior motion. The psoas is weak and long, allowing the forward motion and not stabilizing the hip up into its socket. This view of the psoas is consistent with Sean Gibbon's point of view. He sees the psoas as a local and global stabilizer, likely to be inhibited.

Sahrmann looks at two versions of this hip joint problem. In the first, which she describes as more common, the femur tends to be medially rotated. This tends to occur more in females and goes with genu valgum, pronation, and anteversion of the hip. In this pattern, there is a clear dominance of the tensor fascia latae (TFL) over the gluteus medius, thus pulling the hip into medial rotation. The hip external rotators are likely to be weak. The medial hamstrings are dominant over the lateral hamstrings. Whenever the patient stands on the affected leg, the hip is internally rotated; the hip rotates more easily into internal rotation than external rotation. If you have the patient step up onto a step, you'll see a sudden medial rotation motion at the knee on the involved side.

The second version is the one I am more familiar with, perhaps because it is my own pattern. It involves an externally rotated femur which lacks medial rotation. It's more of a male problem, and is consistent with a more rigid overall structure, one that may include a supinated foot. Sahrmann states that the groin pain is more medially located in these patients. These are the patients for whom the wishbone maneuver, a mobilization with eccentric muscular activity, seems to be most effective.⁵

In both of these anterior femur problems, the pain is likely to start in the groin and then spread to the whole hip. These patterns can be the missing link in lumbar and sacroiliac conditions, as well as with lower extremity problems.

Psoas, Psoas, Psoas

Weakness of the psoas is an important factor in these anterior hip patterns. Sahrmann talks about this, but her book is seven years old now, and there is new research and new methods to rehab the psoas. I recommend you read Sean Gibbons' long article on the psoas.⁶ I used to think of the psoas as an overactive hip flexor. I now think of the psoas as an inhibited lumbar spine and hip stabilizer. If the psoas is not able to contract in a timely manner, the femoral head will drop anterior and lateral, jamming into the hip capsule. Psoas weakness also plays into lumbar instability patterns. Gibbons' model for testing the psoas involves testing lumbar stability and seeing if psoas contraction can change the palpatory feel of lumbar hypermobility. I suspect that we can test the psoas in a different way, testing the effects of psoas weakness on the insertion rather than the origin.

Here is my hypothesis about another way to test the psoas. If the patient has a hard time flexing the involved hip, teach them to contract the psoas, ideally both supine and side-lying. Have them fire the psoas for a few repetitions, correcting for substitution and not overfiring. Local stability exercises often feel so mild that the patient wants to work too hard. To understand this model of how to rehab the psoas, see my description below, Gibbons' article, and/or print the handout from my Web site.⁷

First, the patient has to understand the exercise and be able to do it at least close to correctly. Then have them hold this mild psoas contraction supine, and simultaneously flex the hip, either passively or actively. If this makes the hip easier to flex, with less of a groin pinch, it shows that the psoas is dysfunctional, and needs rehab. I love to show my patients exercises that make an immediate difference in their symptoms or signs. It's the best rehab motivator I know.

The basic exercises to retrain or recruit the psoas are deceptively simple. Suck the hip gently up into the socket, primarily using the psoas. The doctor should initially provide a gentle traction down the long axis of the hip to increase proprioception. Here's the tricky part: You have to suck the femur up into its socket without hiking the hip (which indicates overactivity of the iliocostalis lumborum and/or the quadratus lumborum). You have to activate the psoas without overactivating the TFL and/or the rectus femoris.

While lying supine, raising the upper body up onto the elbows may help take out the hip hikers. Externally rotating the thigh may help take out the TFL and/or rectus femoris. It's OK initially to fire the rest of the inner core while activating this, using the pelvic floor (Kegel), the lower abs and the multifidi. The local stabilizers are all going to inherently co-contract.

The goal, ideally, is to isolate the psoas as much as possible. Another good position for psoas rehab is side-lying, drawing the hip into the socket. In this position, the key is to control pelvic rotation. Personally, I found these exercises somewhat difficult to learn but rewarding. Once you have the basic motion down, you can integrate it into more global hip flexion.

Another Hip Mobilization Method

One aspect of this problem is that as the distal part of the femur flexes, the proximal convex femur head in the concave acetabulum has to rotate and glide in an inferior direction. If this doesn't happen, you get that feeling of jamming in the groin. One way to correct this is via the Mulligan concept.⁸ Mulligan's model basically says to find a direction of passive pressure (applied by either the doctor or the patient) that allows more joint motion. Repeat that assisted motion over and over to reset the neuromuscular system.

In this case, a superior-to-inferior pressure on the proximal hip usually allows for easier hip flexion. You can provide this with manual pressure; use a wide belt to pull the proximal hip inferior. You can follow this up with home self-mobilization procedures. The patient can use the heel of their own hands, pressing inferior while they lift the leg. The patient also can use a belt, strapped from the involved groin down to the opposite foot, to provide the same superior-to-inferior pressure while flexing the hip.

These simple techniques often have dramatic benefit. Try them out. Have fun integrating them into your practice; your patients will thank you for it.

References

1. Malmqvist S, Leboeuf-Yde C, Ahola T. The Nordic back pain subpopulation program: predicting outcome among chiropractic patients in Finland. Chiropractic & OsteopathyNovember 2008;16:13.
2. Sahrmann SA. Diagnosis and Treatment of Movement Impairment Syndromes. St. Louis: Mosby, 2002.
3. Liebenson C. Comments on Spinedoc Web discussion group, Oct. 30, 2008.
4. Whyte Ferguson L. Knee pain: addressing the interrelationship between muscle and joint dysfunction in the hip and pelvis and the lower extremity. Journal of Bodywork and Movement Therapies 2006;10:287-96.
5. Heller M. The hip joint: myofascial and joint patterns. Dynamic Chiropractic, May 7, 2007.www.dynamicchiropractic.com.
6. Gibbons S, Comerford M, Emerson P, et al. Rehabilitation of the stability function of psoas major.
7. www.marchellerdc.com/pro_resources/Articles/#Ex.
8. www.bmulligan.com/about/concept.html.