Taking a Deeper Look at Hip Strength and Knee Pain (Part I)

Today I’m revisiting the relationship between knee pain and hip strength. That’s because after this post, in which I mentioned a study that showed that strengthening muscles in the hip didn’t improve the biomechanics of runners, I got this comment from “Knee Pain”:

You've cited studies saying that these types of structuralist exercises don't help knees. I'm wondering if there are some other studies that show that these exercises to help knees? Otherwise, gosh, where are our physical therapists getting the guidance to tell us all to do all these hip/glut exercises? (I've been given that advice by three professionals helping me with my knee problem.)

This is a very good point.

It’s not as if a couple of physical therapists were lying in a meadow, gazing at cloud formations on a lazy summer day, and one said to the other, “What about the hips? Try strengthening the hips?” And the other replied, “Sure. Why not?” So they began treating chronic knee pain by focusing on stronger hips, other physical therapists blindly followed their lead, and this treatment gradually became accepted protocol.

On the contrary: Therapists giving you such advice might cite various studies of their own if pressed for evidence. For example, here’s a recent one that looked at 28 female subjects with patellofemoral pain (14 underwent hip strengthening, 14 constituted the control group).

It reaches what looks like a slam-dunk conclusion:

A program of isolated hip abductor and external rotator strengthening was effective in improving pain and health status in females with [patellofemoral pain] compared to a no-exercise control group. The incorporation of hip-strengthening exercises should be considered when designing a rehabilitation program for females with PFP.

Here’s another one -- actually it’s a couple of case studies, so only two subjects were involved. For both individuals, treatment “occurred over a 14-week period and focused on recruitment and endurance training of the hip, pelvis, and trunk musculature.” The result, in part:

Both patients experienced a significant reduction in patellofemoral pain.

Well, that does seem convincing! But let’s take a step back and ask, more deeply: What do such studies really show?

MINDING THOSE P’S and Q’S

First, let’s look at a slightly different kind of study, though it’s very much related. The researchers wrote up its results in the January 2008 edition of the Journal of Orthopaedic & Sports Journal Therapy. It goes by this rather dull name:

Hip Strength and Hip and Knee Kinematics During Stair Descent in Females With and Without Patellefemoral Pain Syndrome.

A prominent star on the online copy of the report signifies that it won an “excellence in research” award by a sports physical therapy group.

The researchers begin the journal article with a sort of embarrassing sidenote, if you’re a believer in the pre-eminent role of structure in causing injuries. For a while, there was a fascination with the relationship between the “Q angle” (the quadriceps angle, which shows the propensity for the patella to track improperly) and patellofemoral pain syndrome. The hypothesis: The size of the Q angle correlates with the incidence of knee pain (the larger the angle, the more problems). Women in particular, with their wider hips, are likely to have a larger Q angle.

However, “many studies have not supported the relationship between an increased Q angle and PFPS [patellofemoral pain syndrome],” we are told.

Oh well.

Moving along.

REACHING FOR A HOLISTIC THEORY 

The “Kinematics During Stair Descent” study delves into why hip strengthening makes sense as a treatment. Now this is actually a very important thing if you want a solid, holistic theory of the relationship between weak hips and bad knees. It’s one thing to show that strengthening the hips helps reduce pain (which we’ll return to later), but why?

Okay, remember the simple “x leads to y” explanation in my earlier post. I’m going to use that, except with some big words thrown in:

Hip abductor and hip rotator weakness --> too much hip adduction and internal rotation --> stress on the patellofemoral joint causing pain.

Again, the short form:

Muscle weakness in hip --> bad form --> knee injury

So, based on this analysis, what would you expect to find in people with PFPS? A couple of things: (1) weak hip muscles (2) bad form.

HOW THE STUDY WAS SET UP 

The study’s methodology appears pretty solid (to my relatively untrained eye).

The experimental group consisted of 18 females with PFPS who reported to the University of Kentucky Biodynamics Laboratory for testing. Each was matched with a healthy female (the control group), in terms of age, weight and height.

Subjects with PFPS were asked to rate their pain. Also, all participants had their leg strength tested, by a handheld dynamometer that was 99 percent accurate. For the researchers to be able to make careful observations about form, everyone in the study was videotaped with a seven-camera system as they descended a short set of stairs while wearing reflective markers at key locations on their bodies.

The results: Weakness in hip muscles was indeed found. The subjects with knee pain “generated 24 percent less hip external rotator torque and 26 percent less hip abductor torque compared to controls.”

So far, so good for the structuralist model. Then the problems start.

FIXING A PROBLEM THAT DOESN’T EXIST

The study’s other major finding, beyond that of weak muscles, undoubtedly made its researchers more than a tad uncomfortable:

Subjects with hip weakness did not demonstrate excessive hip internal rotation, hip adduction and knee valgus compared to controls.

Oops.

Remember our causal chain again:

Muscle weakness in hip --> bad form --> knee injury

In the structural analysis, strengthening the hips should work because it corrects the bad form that caused the injury.

But if there isn’t any evidence of “bad form,” what does that mean? Why are you trying to fix “bad form” if there’s no “bad form” to fix?

That’s a head scratcher, but there’s an even bigger revelation -- a real bomb -- that the authors of the report drop at the end.

THE STUDY’S BOMBSHELL

Before we get to that, imagine that I tell you that 90 percent of everyone with patellofemoral pain syndrome in a study is found to also have something I refer to as “x”. You might think, “Well, let’s find a way to get rid of ‘x’! That should correct their PFPS!”

Then if I told you “x” was “depression,” you might retort, “Of course they’re depressed! They have knee pain. Take care of the PFPS, and you’ll get rid of the depression!”

Cause and effect. It’s absolutely critical to get those in the right order.

Now, for the University of Kentucky study, check out this admission about the weaker hip muscles (my bold):

It remains elusive if such weakness was the cause or the result of PFPS.

CAUSE AND EFFECT: WHAT MAKES THE MOST SENSE?

That’s a hole big enough to drive two trucks through. Think about it. The patellofemoral pain syndrome subjects had weaker hip muscles. But what are the chances they had weaker quad muscles too -- and weaker other leg muscles as well? After all, we’re told that the average duration of their problems was 14.4 months, “indicating a chronic condition.”

What happens when you have a chronic condition that discourages you from using your legs and knees normally, so you use them less? The associated muscles weaken. That’s a powerful argument for PFPS helping to create weak hips, not the other way around.

And, if the structuralist model was correct, you’d at least expect to find evidence of bad form during the stair-descending exercise -- which wasn’t the case.

So the structuralist explanation for weak hips causing knee pain appears to be a long way from proven.

But let’s return to the original studies. They show that strengthening hips did reduce knee pain. So maybe your attitude is this:

Who cares why it works? Maybe it works for a different structuralist reason. Maybe it works for a non-structuralist reason. All that matters to me is it works! Why don’t I do it for that reason?

Next week: Why not, indeed? A look at the Big Picture when it comes to treatments for patellofemoral pain syndrome.

Update: Since writing this, I've found this good essay by Paul Ingraham, "Does Hip Strengthening Work for IT Band Syndrome?", in which he asserts "'weak hips' is a weak theory." Have a look!

More Evidence on the Limits of Surgery

What would you do, if you were a surgeon, and a knee you happened to be operating on for an ACL tear was found to have deep cartilage lesions?

This seems like a no brainer, right? You’re already inside the joint. You see damaged cartilage. Why not fix it, to the best of your ability?

Well, what if your intervention makes absolutely no difference.

Check out the findings of this study.

Between 1991 and 1995, 43 patients were treated during surgery for tears of the anterior cruciate ligament but not for associated cartilage lesions. The defects were significant too: Outerbridge grades 3 and 4, signifying that at least half the cartilage, and sometimes all of it, had worn away at a given location.

The study’s researchers followed up with the subjects 10 and 15 years after the surgery. Outcomes were compared with those of a matched group who had the same operation performed, and who went through the same rehab program, but who didn’t have any cartilage lesions.

The difference?

None.

There was absolutely no disadvantage to leaving those severe lesions untreated.

In fact, there may have been an advantage. Because consider this: The best possible outcome should be that of the group with ACL tears but no lesions. But the group with ACL tears and lesions that were left untreated fared as well as this “gold standard” group.

That leaves one group that wasn’t included in the study: patients with ACL tears and treated lesions.

How would such subjects have done? It’s impossible to know, but they couldn’t have done any better than the other two groups, be definition. There’s no way that a surgeon can “fix” cartilage defects in a way that makes them better than what they were before the tissue was damaged. But it’s possible that these people might have done worse. Yikes!

One of the authors of the study, Wojciech Widuchowski, said in a presentation (my bold):

Our conclusions are these cartilage lesions found during ACL reconstruction left with no treatment do not appear to affect the clinical outcome at 10 and 15 year follow-up. Our study seems to reinforce the question whether treatment of a symptomatic lesion provides improvement over that of the natural history.

So the study has good and bad news:

(1) It’s pessimistic about the ability to improve areas of bad cartilage in the knee joint by using surgery to “clean up” or otherwise fix them.

(2) It’s optimistic about the ability of knees with damaged tissue to do acceptably well on their own (Note: that’s what the results seem to suggest anyway).

Strengthening Your Quads: Another Reason It’s a Failed Approach

A number of times, I’ve expressed my frustration with physical therapy’s obsession with quad strengthening to treat weak, painful knees.

On this blog, I once compared strengthening your quads before strengthening your joints as being similar to putting your shoes on before your socks.

And in Saving My Knees, I related how following this advice almost ruined my knees.

To me, this approach just doesn’t make much sense.

Now here’s some clinical evidence:

In September 2010, the Journal of Pain reported the results of an interesting study. The question that researchers set out to investigate: Does knee pain reduce muscle strength?

A test was performed on 18 healthy subjects. To create knee pain, “hypertonic saline” was injected into the fat pad near their patellas. After that, subjects had their maximum muscle strength measured while flexing and extending their legs. On a separate day, a placebo that caused no pain was injected into the fat pad, then the strength measurements were made again.

The findings: muscle strength was 5 to 15 percent lower under conditions of induced knee pain. The amount of reduction was proportionate to the severity of the pain. The conclusion (my bold):

This study showed that knee joint pain has a significant impact on muscle function. The findings provide evidence of a direct inhibition of muscle function by joint pain, implying that rehabilitative strengthening exercises may be antagonized by joint pain.

In other words, your joint pain is working at cross purposes with your attempts to strengthen muscles in your leg. You’re trying to make muscle fibers stronger when they’re able to effectively function at only 85 to 95 percent (or maybe even less, if your knee pain is quite severe) of capacity.

Now be careful to grasp the full import here -- the 85 to 95 percent doesn't refer to the percentage of your maximum strength if you were fit and toned. It’s 85 to 95 percent of your existing strength.

You may be thinking: Well, 85 to 95 percent doesn’t sound too bad. But remember the optimal way to strengthen muscles. You push them to their limit, then they respond by going through a repair/rebuild cycle.

But if you can recruit only 85 percent of their strength, how can you push them hard enough? (Note that I’m not even addressing the elephant in the room -- should you try to push this hard anyway and risk further damage to your joints?)

By the way, an interesting corollary to these findings should be that the worse your knee pain is, the less successful the strengthening approach should be. And, at least based on anecdotes I’ve heard, that sounds just about right.

Try To Be Optimistic Because How You Feel Affects What You Feel

Here’s a knee pain finding with a message well-worth heeding.

A South Korean study of 660 men and women, all older than 65, found that being depressed can make symptoms of knee osteoarthritis feel worse.

Researchers used X-rays to measure how severe each subject’s osteoarthritis was. Naturally, those with the most damage reported the most pain. However, some of the subjects with mild to moderate arthritis also reported severe pain.

Now, setting aside limitations of X-ray measurements (and there are many, for conditions that involve soft tissues), what can we learn here?

An Arthritis Today article about this study quotes Jon T. Giles, an assistant professor of medicine at Columbia University:

“Painful sensations are relayed through the brain in a very complex way, and can be modulated up or down,” he says. With stress, poor sleep, anxiety and depression, which are known to influence pain levels, “stimuli feel more painful than they would in someone without the adverse psychosocial factors.”

Now here are a few of my thoughts.

And if you have knee pain, you’ll be relieved to know that none equates to “Don’t worry, be happy.”

Because chronic knee pain stinks.

Of course there’s a good chance you’re depressed. If you’re anything like I was, you’re depressed because you have discomfort and pain most of the time. You’re depressed because merely climbing a set of stairs or carrying your toddler across the room causes a flare-up in your joints. You’re depressed because you know that almost everything you want to do in your life will involve your knees, and you’re doubtful that they’ll ever be normal again.

In short, you have a lot of very good reasons for feeling depressed.

Still.

Negativity levies a real tax on your body. That’s an inescapable truth. So even though you may be perfectly justified in your anger/bitterness/sadness, you have to realize you’re paying a price for it.

What to do? Here are a couple of ideas.

First, consider a de-stressing activity, such as meditation. I did it for a while, during my knee pain recovery (this was a period, by the way, when it wasn’t just my knees giving me problems). I found it useful.

Second, get into a long-term program that has one objective: healing your knees. This will restore something that is essential to getting better: hope.

This brings me to a closing rant.

In the Arthritis Today article, reactions to the study above included this suggestion: that care providers such as doctors screen patients for conditions such as depression and refer them for treatment (drugs, etc.) when needed.

I can imagine, upon hearing this, a gathering of doctors murmuring in approving tones, “Yes, yes, that sounds like an excellent idea.”

Arrrgh.

Here’s what irks me about that seemingly sensible suggestion. One major reason that knee pain patients suffer depression is because no one shows them a path to escaping knee pain. In this regard, doctors are the worst, from my experience.

In many cases, I suspect (again drawing from my experience), patients bounce around among doctors who just kind of shrug and say “You have knee pain, but I wouldn’t advise surgery just yet.” Further, patients are diagnosed with unhelpful, baffling terms such as “patellofemoral pain syndrome” that don’t tell them, in clear, specific terms, what’s wrong with their knees.

And then they’re found to be depressed. Well, no kidding.

Before doctors go about blithely prescribing pills for depression related to knee pain, they might want to ask themselves if they’ve done everything possible for their patients in terms of finding a good, long-term plan for eventually escaping that pain.

Bad Knees, Weak Hips, and the Other Problem With Structuralism

If you’re a runner, perhaps you’ve heard this theory before:

Runners with weak hip stabilizers appear to have tendencies to rotate the thigh inward and to excessively adduct the hip (i.e. run knock-kneed) to create stability to compensate for the weakness of the hip stabilizers. These maladaptive movement patterns put strain on the knee, and over time an injury emerges.

I took that from this article in “Competitor: Your Online Source for Running.” The author of the piece further simplifies the hip-knee relationship to:

Muscle weakness in hip --> bad form --> knee injury

Assuming you believe all that, you should also see a common sense solution:

Strengthen the weak hip muscles.

Easy enough, huh? Apparently not.

20 women (who weren’t injured yet who showed signs of abnormal adduction while running) participated in a study where half went through a six-week program of hip strengthening and instruction in single-leg squats. The other half (the control group) did their normal training.

And the results?

Nothing. Nada. Zilch.

The knock-kneed runners who strengthened their hips continued to run the same way as before.

So was lack of hip strength really causing them to run knock-kneed? Or was it something else?

And, more to the point if you’re a structuralist type (someone intent on tracing problems back to crookedness and muscle imbalances): How fixable anyway is what you think is wrong? (I’ll set aside the question of whether running knock-kneed predisposes you to injury -- let’s assume for now that it does).

This seems to be “the other problem” with structuralism. The number one problem, I think, is that the search for structural deficits is overused as a diagnostic tool. The “other problem” (the depressing one, really): It’s very hard/impossible to correct many structural “faults.”

A great example is leg length discrepancy. Having legs of different lengths, in the structuralist world view, sets you up for all sorts of problems. But what’s the remedy? Unfortunately, you can’t mail order an evenly matched set of limbs.

Have no fear though. In a long, fascinating essay on structuralism (subtitled “The Story of the Obsession With Crookedness in the Physical Therapies”), Paul Ingraham notes a 1984 study showing that leg length discrepancy doesn’t make any difference for back pain (within reason of course -- if a doctor saws six inches off your right leg after a car crash, yeah, that’s going to affect your walking and a whole bunch of other things).

And so it is with other bits of structuralist orthodoxy, Ingraham goes on to explain. Another study looked at imbalances of major muscles in elite players in the Australian Football League. Any structuralist worth his salt can tell you what that should lead to: higher rates of injuries. But researchers found that “asymmetry in muscle size was not related to number of injuries.”

Ingraham’s essay is a terrific read for its bountiful evidence and good insights. For instance, he says structuralists are masterful dot connectors. He gives this as an example of how they think:

A podiatrist might tell you that your fallen arches (dot!) cause greater strain in your knees (dot), which in turn force you to use your hips differently (dot!), which leads to hip weakness (dot), then muscle imbalance in the core (dot!), which finally results in back pain (dot!).

What’s the first thing you notice there? I’ll tell you what I see: the potential for incredible, bewildering complexity. After all, almost everything in our lower extremities can be connected, somehow, to almost everything else. Treating chronic knee pain under such a belief system then becomes like solving some higher order math equation. This suggests your treatment will probably be long and frustrating, as your structuralist, dot-connecting physical therapist explores various hypotheses about what might be “truly” causing your knee pain.

My approach was much simpler. I operated on the assumption that my joints were just injured, or weak, and needed to be slowly strengthened and coaxed back to health.

This approach worked very well for me. I suspect it would work very well for many other people suffering from chronic knee pain too.

What Are You Waiting For? Get Moving!

As I’ve noted in the past, I get regular e-mail alerts from Google about the latest Internet content that relates to knee and cartilage problems. Sometimes a theme will emerge, repeated across a number of alerts. One theme I’ve written about several times before: Lose weight! Another I’m writing about today: Get moving!

If you have chronic knee pain, don’t take it lying (or sitting) down. You need to move that bad joint to have any hope of saving it. All the evidence firmly points in that direction.

Let’s start with the University of Minnesota School of Public Health. Researchers there reviewed 193 studies conducted between 1970 and 2012 that looked at treatments for osteoarthritis-related knee pain that didn’t involve drugs or surgery.

This meta-analysis showed:

Exercise fared the best at improving pain and mobility, as long as subjects followed through with a program, while the researchers found that few physical therapy interventions were as effective.

The favored activities: low-impact aerobic exercise and water exercise (yes!) as well as strength training (eh -- be careful!).

A Wall Street Journal reporter noted the shift in thinking that has occurred, writing “Doctors increasingly are recommending physical activity to help osteoarthritis patients, overturning the more traditional medical advice for people to take it easy to protect their joints.” Exercise reduces pain and improves mobility of the hurt joint.

“The most dangerous exercise you can do when you have arthritis is none,” Kate Lorig, director of the Patient Education Research Center at Stanford University, says in the Journal article.

In fact, the reason you have problems in the first place may be because you’re not moving enough. According to Indian orthopedic surgeon Madan Hardikar, there are two key causes of knee pain: (1) for the old, it’s natural wear and tear of the joints (2) for the young, it’s a sedentary lifestyle (he cites the country’s IT workers, who put in 12- to 15-hour workdays at a computer and who often don’t get any exercise outside work either).

To conclude, here’s a cool arthritis story (even though it doesn’t involve knees, but hands):

Margaret Crowell was an elite tennis player who had osteoarthritis in her thumbs and hands. An orthopedic specialist said nothing could be done to prevent the disease from worsening.

Luckily, Crowell refused to believe him and give up. She discovered the benefits of gentle exercise and movement and managed to reverse her symptoms. Now she gives classes for older adults that emphasize slow stretching and agility movements.

So there you go.

As with the need to lose weight, there’s no debate here.

Move, move, move!

With Knee Pain, What We Believe Influences How We Interpret What We See

This is a famous drawing:

What do you see?

Do you see the dainty, pert-nosed young beauty, her head turned away? Or the large-featured old hag?

If you see the young woman, and your friend sees the hag instead, your first reaction may be to scoff and say, “No way! Look again!”

Now, suppose you are studying cartilage defects in human knees and learn the following set of facts:

* Between 34 and 62 percent of people having knee surgery are found to have cartilage defects.

* Some 50 percent of athletes (from recreational to professional) who have cartilage defects don’t have knee pain.

* The vast majority of people with moderate knee osteoarthritis don’t have functional limitations.

What would you conclude?

Colin Hoobler, a physical therapist, connects the dots thusly in this Q&A:

“... it’s entirely possible that your knee pain isn’t caused by your cartilage defects, but something else (muscle weakness, inflexibility and/or lack of coordination).”

(A quick aside: the “lack of coordination” explanation for knee pain I find a bit odd; I’ve never encountered it before and it seems to make sense mainly if this lack of coordination causes you to fall on your knees a lot. :))

Now, if you remember back to last week, you’ll realize that on the matrix for knee pain treatment and beliefs, Mr. Hoobler probably belongs in the upper right corner (among those recommending treatment that is “Not Joint Focused”). He will work on addressing your muscle weakness, tightness and general klutziness.

That’s because, when presented with the group of facts above, he sees one picture. But might there be another picture here, if we look again?

Certainly.

It might be described like this:

“It’s entirely possible that your knee pain is caused by your cartilage defects, but you don’t have to get rid of them to become pain-free, as they’re actually quite common and don’t always cause problems.”

This is great news! This belief (that I didn’t have to restore my cartilage to a pristine state) sustained me during a long recovery from knee pain.

In fact, this was my thought process as I embarked on the journey:

“An MRI shows I have “mild” chondromalacia, but my knees are really crunchy and always inflamed. Any MRI is imperfect*, so maybe it hasn’t detected what’s really wrong with the cartilage (after all, chondromalacia starts with damage deep within the tissue). I’m betting the problem is with my cartilage. I can either despair -- oh no, it’s damaged and will never be perfect again -- or I can take solace in the fact that lots of people are walking around with defects and feel fine. I just have to strengthen the tissue slowly (and hopefully it will heal along the way, as it’s done in various studies). Yeah! I can do this!”

But why would some defects be painful while others aren’t? Recall that cartilage has no nerves. Hugely significant. So the tissue itself isn’t sending out pain signals, but rather nearby structures are. Pain may result when the cartilage becomes too thin or too soft or too ragged -- but it won’t be a problem with all lesions.

So when you look at your bad knees, what picture do you see?

* Serendipity! As I was writing this, along came this brief article saying that MRI exams underestimated the size of cartilage defects by 70 percent (compared with what surgeons actually found during an arthroscopy), according to one study. So that MRI that suggests you have a small problem, or no problem at all, may not be trustworthy.