Ilio-Psoas Syndrome

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.

More about me

https://www.lifetimerunning.net/2018/11/profile-robert-chasen-has-been-running.html?fbclid=IwAR35zTq-PVNvfUHHgPyFKSylHzmad3X_CezUJBKRcIq5QQFdoBLqdRITjfs 

10 Years After

It has been a while since I have posted.  Here is a post Amby Burfoot did on me.

https://www.100klifetimemiles.com/2014/02/robert-chasen-has-run-138000-lifetime.html?fbclid=IwAR2_-nJljI0n3LjEM_FdJE0bafx9YhBpSX_wqTc6bKxPQTvwcHUaJeLouUk

Leather and Lace- Part 1

Hate those pesky shoelaces that become undone even when double or triple knotted? Try this link to a first part of my pearls series. Who says that an old dog cannot pass on new tricks.

view here

Stress Fractures

The young, intelligent and fast Camille Herron wrote this interesting piece on her blogsite about stress fractures. It is a thorough look at the causes of this malady and what she had to do to overcome her recurrent stress fractures.

Do Foot orthotic Devices Work?

This post is in response to Jon Waldron , the author of the excellent Newton North blogsite. He asked me to comment on the January 17 article in the New York Times, so here are my thoughts.

In summary, the article doubts the effectiveness of foot orthotic devices (FODs) with the author backing up her points with quotes from the co-director of a human performance lab in Canada. FODs are usually discussed in terms of how they modify pronation and supination. These terms are one of the most simplified and abused terminologies in journalism today. With this article, add sensationalism to that list. It gets "eyeballs" to the Times website and sparks commentary but is not much good for more than that. This is because those eyeballs would glaze over if any attempt at what we really know about these foot motions were ever presented. These said motions describe tri-plane motions around a single joint and not a whole foot. For example pronation at the subtalar joints generally causes most of the foot to be a loose bag of bones while supination makes the bones to be a "rigid lever." However, at the neighboring mid-tarsal joints, pronation locks the foot rigid while supination causes the loose bag of bones" situation. That is the effect of only 2 of the 33 joints on basic foot motion. Dare we add in the others? How about force changes from the 100 or so muscles and tendons or the peak forces on the 26 foot bones. Don't forget the angular velocities transmitted from the rest of the body. We live in a world that is not black and white but somewhere along the spectrum of gray. The answer far less pessimistic than that of Gina Kolata article in the New York Times and far less optimistic than a foot orthotic device (FODs) chain that claims 98 percent sucess with its clients. IMHO, I see this as that classic academic/theoretical voice clashing with the clinical/practical stirred by the journalistic tempest in a teapot. For those of you that see a tipping point towards academia (Dr Benno Nigg) and away from the fee for service clinicians, think again. The article does not disclose that the good doctor has a financial interest with MBT shoes (Masai Barefoot Technology). These shoes are supposed to create instability and inefficiency in the short term to strengthen feet for the long term. Their thinking and selling point for their shoe line is that if you strengthen the muscles involved, you don't have to correct for any deformity. Hence, you can now better understand his obtuse comment that FODs are only a short term solution.

Of course foot orthotics devices work when given to someone who actually needs them and the results are long term. There is too much evidence based medicine to refute this. The kicker is that less than 10% of the injured runners that seek my care show clinical evidence that they would even benefit from FOD therapy. So we are talking about a small percentage of the general running population. Let me digress. Every runner that enters my office is screened for deviations at the subtalar and midtarsal joints as well as a host of other clinical and historical information. Dr Richard Schuster measured over 10,000 runners and found statistical correlations between these numbers and certain injuries. For example, he found a high correlation between abnormally high forefoot varus and patello-femoral syndrome. Then I take into account any structural and material "defects" in the foot or even specific things in the past medical history to honestly and profesionally decide whether a custom FOD is a viable treatment for this person or whether other avenues need to be persued. There are people "prescribed" FODs by unscupulous practioners and clinics that don't have much clinical evidence that they actually need them. People who get devices they do not need won't be helped and are sometimes hurt by such teatment. This is further fed by patients that think they need them, or maybe just want them. Then there is the group of people that show some evidence of needing correction but are given the wrong prescription. One area sports clinic had their FODs made by a 7 dollar per hour nurse's aide with no formal training. The outcome of wrong presciptions lead to truly random outcomes. one of the more common errors I see is how the foot impression is captured. Clouding the issue is that how a FOD fits into a shoe can affect how well or how badly the foot functions in that shoe.

For the record, I do think that some form of strengthening of specific foot stuctures within a reasonable margin of error can be injury reducing. However, I doubt that these new "toning shoes" are that answer. In that small percentage of people that have foot deformities that cause stress and forces that exceed safety limits of what that body part can handle, something must be done to reduce it. In those special cases, custom made proper prescription FODs perform quite well.

Take two and you WILL be calling me in the morning

Use aspirin analogs (or other NSAIDs like motrin and Aleve) have been touted as half of the gold standard of the first aid of sports injuries. However such drugs might not be the gold standard it is cracked up to be.

Aspirin or acetylsalicylic acidwas dicovered in 1827 when a crude product was extracted from willow bark. In 1844, another related chemical was extracted from the oil of Gaultheria (oil of wintergreen). This related compound is still used today an an ingredient of liniments, such as Ben-Gay. Aspirin in the form we know today was introduced in 1899. This inexpensive "wonder drug became a staple of medicine chests worldwide.

An oral dose is absorbed rapidly through the stomach and small intestines and is bound to blood proteins. Apreciable amounts can be detected in the blood within 30 minutes with peak amounts in about 2 hours. It is removed from our bodies by the kidneys and, to a lesser extent, the liver.

In even low doses, asprin analogs makes platelets (a component of blood) less sticky. This is good for ailments where stickiness causes clots like heart attacks and strokes. However it is negative when talking about a fresh musculo-skeletal injury. Excessive bleeding into the injury site causes hematoma formation which can delay healing or even cause incomplete healing.

At higher doses of these drugs you mask mild to moderate pain. It takes even higher doses to reduce imflammation. However, even if you dose yourself correctly to adress the imflammation, this might not be a good thing. Researchers at the Cleveland Clinic recently published a study that adds to growing evidence that swelling actually plays a key role in healing soft-tissue injuries. The result is a classic tradeoff between short-term and long-term benefits: reducing swelling with ice or drugs may ease your pain now, but slow down your ultimate return to full strength.

When you sustain an injury, your body’s first response is to send cells called macrophages to clear away the damaged cells by literally digesting them. This initiates a complex process of repair and regeneration that triggers swelling, in part because macrophage-induced damage pokes holes in the muscle membrane, allowing fluid to rush in.

What the Cleveland study showed is that these macrophages, in addition to causing swelling, are also the primary source of “insulin-like growth factor-1,” which crucial to the growth hormone process which rebuilds our body tissues. If you take away the swelling, you also lose the growth factor.

This finding offers an explanation for clinical evidence about the double-edged effects of otherr anti-inflammatory drugs that has been mounting for several years. A review published last month in The Lancet found that injections of cortisone, a powerful anti-inflammatory steroid, brought initial relief for tendon injuries such as tennis elbow, but produced significantly worse outcomes six and 12 months later compared with patients who did nothing or performed physiotherapy exercises.

There is a use for anti-imflamatory drugs in certain situations. However, there are many more cases of abuse where the short term clouds the long term. So take two and you WILL be calling me in the morning.