Archive for July 2009

Many runners have had this and those that have dread it. Typically, runners complain of a sharp or aching pain on the outside/lateral part of the knee just above the joint line of the knee and sometimes just below the knee.  Most runners complain of pain initiation around the same point in or at the end of a run that will not get better unless you rest.   Sometime it is associated with downhill running or with the heel strike phase of gait.

What is Iliotibial band syndrome (ITB), how do we treat it and more importantly how to we prevent it?

First the anatomy.  The iliotibial band is a thick band of connective tissue on the outside of the thigh, which stretches from the outside of the pelvis (iliac crest), over the hip and knee and inserts just below the knee. The ITB is contiguous with a muscle group called the tensor fascia lata near the pelvis whose job it is to  abduct or extend the hip and leg outwards.

The ITB functions to stabilize the knee from internally rotating during the heel strike and knee bending phase.   If you have abnormal gait mechanics, the ITB can rubs back and forth against the lateral femoral condyle and become inflamed.  There are some athletes where the pain gets so bad, they have to drop out of competition until it is adequately treated. Unfortunately rest, ice, compression and elevation alone will not help this problem in the long run.

Typically weak hip abductors are the culprit. They fatigue with time, thus allowing the femur to internally rotate, which explains why it happens in the middle or end of the run. Sometime the multifidi muscle groups in your low back aren’t firing properly.

Having sacroiliac joint dysfunction can be the underlying problem. This causes an anatomic asymmetry in the pelvis and sacrum which can subtly cause a gait discrepancy, which forces the hip abductors to work harder, fatiguing them prematurely causing ITB pain. Other anatomical asymmetries can contribute like high or low arches, over-pronation, leg length discrepancies, or if you are bow legged or have a tight ITB.

How do we treat this problem? In the acute phase of inflammation, if you’re an athlete training for a competition, you might have to decrease the amount of hill running or do more slight (1-2% grade) uphill or treadmill running only. Others should avoid running, deep squats, excessive stairs, bowling, tennis or wrestling that will stress the hip abductors and put more friction on the ITB.

After every run or exacerbating activity, the athlete should ice and elevate the outside of the knee to help with pain and inflammation.  A foam roller to help massage and stretch the ITB can help as well and can be picked up at your local sports store. A 7 day course of an anti-inflammatory medication can help as well but as usual, talk to your doctor or health care provider before starting this.

In order to truly treat and prevent recurrences however, you have to strengthen your hip abductor muscles and correct any underlying asymmetry or SI joint dysfunction. Picture those 1980’s exercise videos of Jane Fonda on her side, doing side leg lifts (4 x 15 reps) and that’s the mainstay of strengthening. Another exercise is to drop your leg down off a step slowly while firing your butt muscles (4 x 15 reps). A more advanced exercise is to do one legged squats.

A well trained musculo-skeletal sports medicine physician, physical therapist or chiropractor can help correct SI joint dysfunction. Talk to your sports medicine physician about how to correcting arch, knee, or leg length asymmetries.

If a solid regimen at home doesn’t work, see your doctor about maybe trying a round of formal physical therapy. Occasionally for athletes that fail this, I have done a cortisone injection or other type of injection. If all else fails, surgery to release the back 2cm of the ITB where it is rubbing against the femoral condyle can help but this should be the last option.

Here is a nice instructional video of an easy to do hip abductor strengthening regimen on Youtube. Thanks to Kristie La Tray, the fitness trainer in the video!

References:
1. Panni AS, Biedert RM, Maffulli N, Tartarone M, Romanini E. Overuse injuries of the extensor mechanism in athletes. Clin Sports Med 2002;21:483-98.
2. Ekman EF, Pope T, Martin DF, Curl WW. Magnetic resonance imaging of iliotibial band syndrome. Am J Sports Med 1994;22:851-4.
3. Taunton JE, Ryan MB, Clement DB, McKenzie DC, Lloyd-Smith DR, Zumbo BD. A retrospective case-control analysis of 2002 running injuries. Br J Sports Med 2002;36:95-101.
4. Messier SP, Edwards DG, Martin DF, Lowery RB, Cannon DW, James MK, et al. Etiology of iliotibial band friction syndrome in distance runners. Med Sci Sports Exerc 1995;27:951-60.

Is a meniscal tear in either knee the start of that dreaded spiral of aging that eventually results in osteoarthritis of the knee?  The answer is a qualified yes. Some of the factors relate directly to your age at the time of injury, the treatment, where the tear is and the fact that after about 35 years of age the blood supply to the meniscus and its ability to heal itself goes down tremendously. There are at least 3 known studies that point to this being the case, each telling a slightly different story.

We know from a study in France that if you tear your meniscus at an age less than 35 and have that torn section removed at that time, you may need some sort of surgery for resultant osteoarthritis in the same knee on average 26 years later. If you are older than 35 however, that number of years to surgery dramatically changes to only about 10 years.1

Another study done on people who underwent menisectomy (removal of torn section) showed that the knee that had the torn meniscus was much more likely to develop osteoarthritis compared to the uninjured side.2

Yet another study looked at the associations between meniscus tears and osteoarthritis, symptoms of knee pain and radiographic signs of arthritis. The study showed that meniscal tears were indeed associated with osteoarthritis on Xrays as well as knee pain. Further, they saw increased osteoarthritis in the medial and lateral (middle and side) compartments of the knee after injury. They concluded that meniscal tears were likely an early event in the process towards developing osteoarthritis.3

So if you’re young and spry and get a meniscal tear, you may get arthritis in your knees down the road but it will likely take decades. If you are older, and a little more creaky however, and get a meniscectomy,  you may be at higher risk for developing arthritis. There are still other factors like obesity, amount of high impact activity level, genetics, and stability of the knee ligaments that may also contribute to this process.

The bottom line is that If you get a knee injury that causes the knee to swell, lock, catch or buckle, this may be a sign of meniscal tear and I encourage you to get your knee checked out by a sports medicine physician or health care provider that is comfortable dealing with this kind of problem.

References:
1)    Neyret, P, Donell, ST, Dejour. Osteoarthritis of the knee following meniscectomy. Br J Rheumatol 1994; 33:267.
2)    Boszotta, H, Helperstorfer, W, Kolndorfer, G, et al. Long-term results of arthroscopic meniscectomy. Aktuelle Traumatol 1994; 24:30
3)    Ding C, Martel-Pelletier, J etal. Meniscal tear as an osteoarthritis risk factor in a largely non-osteoarthritic cohort: a cross-sectional study. J Rheumatol 2007; 34(4):776-84

I have many patients of all BMI’s, and many with osteoarthritis. I have noticed a connection between obesity and osteoarthritis, especially in the knees. Normally osteoarthritis is slowly progressive with time, age and activity but a small percentage of people exhibit particularly rapid deterioration of cartilage. Many clinicians and researchers suspect that obesity may increase the RATE of cartilage loss that leads to osteoarthritis. Now a new study confirms these suspicions.

Frank Roemer, M.D. and his team from Boston University’s department of radiology have identified several MRI and demographic based risk factors for rapidly progressive cartilage loss. The study looked at 347 knees in 336 patient’s. Their average BMI was 29.5 which is considered overweight. Cartilage loss was identified and defined by MRI findings. They followed the subjects over 30 months.

The top risk factors for rapidly deteriorating cartilage included obesity, the only demographic factor.  Age, gender, ethnicity were not found to be risk factors.  All the other risk factors were MRI findings so I won’t go into too much detail but they can be found here.

Even a one point drop in BMI is significant. The study found that a gain of one unit of BMI was associated with an 11% increased risk for rapidly deteriorating cartilage and thus arthritis. So logic says that a drop of one unit will significantly decrease that risk. So the goal is weight loss of any kind, not necessarily a huge drop.

So why do we care? It’s yet another confirmation that obesity leads to health problems. More importantly however is that since obesity is a BASELINE risk factor, everyone who is obese should take steps early, BEFORE the onset of cartilage loss and eventually osteoarthritis. Most important is to see your physician or health care provider to discuss getting on a sustainable weight loss regimen.

As a sports medicine and family medicine physician, I urge parents to go one step further. Parents should take preventive steps to ward off obesity in their kids, even if they are only ages 2 or older. Again, talk with your health care provider to find out how and/or look at this very helpful tip sheet, courtesy of the state department of New York.

See the original study here via Medical News Today

Another brain focused blog for you!

A fascinating study by Dr. Matthew During, M.D., Ph.D. from Ohio State University shows that an injection of the activated gene BDNF (brain-derived neutrotrophic factor) into the brains of mice caused a dramatic reduction in fat content and thus obesity, an effect that is apparently permanent!

BDNF is a normally found gene that is widely involved in a variety of feeding habits, development of new brain and heart blood vessels, and other neuromodulatory effects that include an important role in the development and survival of dopaminergic and serotonergic neurons.

Dr. During has simply injected the gene into the brain with “instructions” to turn BDNF on.  When expressed, it controls not only how much we eat but how efficiently we burn calories. Within an hour of the single injection, insulin levels in the mice dropped by a third. Within weeks of injection, the mice shed half their weight.

While it’s too early to say if this will work in humans, this could form the basis for treatment of morbidly obese patients who have failed other, less invasive approaches. Sadly however, many experimental treatments that are designed to manipulate appetite suppressant hormones work well in mice, but don’t pan out when tried in humans.

Where this technique is different is that it works on the genetic level rather than hormonal levels that are how former experimental appetite suppressant drugs work.  Hormonally based drugs are subject to positive and negative feedback that makes it difficult to sustain long term weight loss. Hopefully a genetic approach will work better long term, though I worry about the potential side-effects on other organ systems as well as psychiatric effects given how widespread the use of BDNF in the body and brain is.

Source: Ohio State University

References:

1)    Molecular therapy of obesity and diabetes by a physiological autoregulatory approach, Nature Medicine, Volume 15, Number 4, April 2009.
2)    http://www.nature.com/mp/journal/v8/n2/full/4001221a.html

As a sports medicine and family medicine doctor, and indeed in this blog, I tend to focus on exercise, musculoskeletal and metabolic rather than neurologic conditions. In part, this is because, most of the research surrounding exercise are in these three areas.  However, while blood flow to the brain is the most important task for the circulatory system, yet there is little research into the effects of exercise on perfusion to the brain.  I recently read an article in this month’s Exercise and Sport Sciences Reviews that starts to address this deficiency.  Hirofumi Tanaka from the University of Texas at Austin concludes that exercise actually helps brain blood flow both during and after exercise.

The traditional thought was that during exercise, blood supply is constant to the brain but  is shunted away from the rest of the body and pushed to the muscles. After all, you can’t have a functioning stomach if you have just been killed by that lion because you could not run away. Brains are thought to have an intrinsic auto-regulatory function that allows this constant blood supply to keep us conscious even while exercising. According to experts Shigehiko Ogoh, Ph.D. and Philip Ainsle, Ph.D., from Toyo University in Japan and the University of North Texas, blood flow actually increase during and after exercise.

Cerebral blood supply is a complicated maze with its own set of rules since it is such a critical organ. Autoregulation as well as external cues like the level of carbon dioxide in the blood, blood pressure and how much blood the heart pumps out are all implicated in determining the amount of blood that is reserved for the brain during exercise.

What is interesting to me is the implication for diseases caused in part by a lack of blood flow to the brain like strokes, vascular dementia, as well as Alzheimer’s disease.  Ainslie PN, et. al in the Journal of Physiology showed that aerobic activity increases blood supply to the brain both during and after exercise. Preliminary research suggests that aerobic exercise may indeed prevent the decline of brain function that has been associated with these diseases and age related decline. Decreased brain blood flow has also been implicated in “brain fatigue,” that feeling of sluggishness that comes for instance after a poor nights sleep.  Perhaps, this may explain why exercise improves mood, overall energy and sense of well-being, as well as decreases the severity of depression in sufferers.

So what’s the take home message? While this area of research is in its infancy, suffice to say, the research certainly suggests that we should all exercise aerobically regularly, as long as it is safe to do so as determined by your physician or health care provider.

References:
1)    Tanaka, Hirofumi. Cerebral Blood Flow: Sleeping Beauty Awakened by Exercise. Exercise and Sport Sciences Reviews. 2009:37: 111
2)    Ogoh S, Ainslie PN. Regulatory mechanisms of cerebral blood flow during exercise: new concepts. Exerc. Sports Sci. Rev. 2009; 37: 123-9
3)    Ainslie PN, Cotter JD, George KP, et al. Elevation in cerebral blood flow velocity with aerobic fitness throughout healthy human ageing. J. Physiology. 2008; 586:4005-10