Trendelenburg Test (one-legged standing / balance)

Note how glut medius is more about supporting the upright posture when lifting the other leg, and glut max is more about power and propelling the body forward and upward.

Note how glut medius is more about supporting the upright posture when lifting the other leg, and glut max is more about power and propelling the body forward and upward.

Orthopedic and osteopathic use of this test is usually about hip and gluteus medius function. It is possible, though, to make great use of the test to observe how various parts of the lumbar spine and pelvic joints are working. 

It is good to use this test after the standing 'looking' part of the exam, either before or just after we have asked the patient to actively move in various directions. We can start by saying that when it comes to gleaning information about the functioning of a patient's lumbar spine from this test, we are not so much interested in how 'wobbly' the patient is. In fact, it is perfectly possible for a patient to be quite wobbly on either leg and yet - from a spinal point of view - balance well (as long as it is the same type of 'wobbliness' on each leg).

So many factors (neurological, learning patterns, problems with other areas in the lower extremities, etc.) affect wobbliness.

Note in the left picture how the LEFT glut medius is not able to stop the trunk dipping to the right as the person lifts his right leg.

Note in the left picture how the LEFT glut medius is not able to stop the trunk dipping to the right as the person lifts his right leg.

But what we are looking in this article is predictions about asymmetrical functioning in the lumbar spine. So a key concept to focus on when observing this test is to realize that when a patient lifts his knee (say to waist height) it is required - in perfect balance - that the lumbar spine side-bends towards to the lifted leg.

ANY failure of the lumbar spine to side-bend in a particular direction (and, of course, lateral flexion is the key movement - along with extension - of this area of the spine) will therefore affect the way the patient balances.

You can observe this. With the patient's right knee (for example) at waist height, how well does the lumbar spine bend to the right, with a nice apex of the concavity (convex on the standing leg) at L3-4? In fact, you are just as much interested in the way the patient's lumbar spine laterally flexes during this balance test as you are in the way they balance on the grounded leg.

Observe the grounded leg and the position of the trunk above it. Clearly, in advanced hip disease, or in paralysis of the gluteus medius (e.g. polio, or L4-5 motor affected radiculopathy) we observe the trunk dropping towards the lifted leg. But in the vast majority of cases, we are interested in more subtle clues than this. A failure to bend to the right in the lumbar spine will thus variably produce the following signs;

  • A hitch or adjustment in stance as the patient commences the right leg lift
  • A lean to the left of the trunk, so as to reduce the effort required by the left hip abductors
  • A straight, not right sidebent, lumbar spine
  • In more subtle cases, and where the patient is quite fit and coordinated, they might 'hide' these signs - you will need to look very carefully in these cases)

And, of course, comparison of both leg balances will provide a lot of information that you can use to predict the problems you are likely to find in the rest of the active and passive exams.

Thinking further afield, it is possible to also make predictions from this test as to how the lower extremities will be affected by an asymmetrical pattern of balance (caused by a side-bending failure in the lumbar area).

For example, if balance on the left leg is poor, and a patient takes up running (having previously been sedentary) then we can infer that 'collateral' strains will go through the left knee (the grounded leg) during the whole stance phase of running, whereas it is at heel strike on the right leg when an abnormal 'jolt' will go through the system. Whether symptoms will emerge to trouble the patient will, of course, depend on many other factors.

Interpreting risks

An article on caught my eye the other day, which discussed the nature of medical test results and the interpretation of risk. Take a look, as it claims that doctors are not as good as they should be at interpreting (on behalf of patients) the significance of test results.

In this article they gave the example of a patient (a 50 year old women, about whom no medical information is known) who has just had a test for breast cancer.

Note - the reliability of a particular test is assessed over time by medical researchers comparing tests results on patients and then seeing (using other follow up tests and procedures) how many of the patients actually had the disease that the test was saying they did or did not have. This way, they get a fairly decent estimate of how good the test is.

In this BBC article example, the breast cancer test had a sensitivity rate of 90%. What sensitivity means is, if we had perfect knowledge that a group of people DID have the disease, what percentage of times would the test come out as positive (positive in medical parlance means the test indicates you HAVE the disease or condition)? In our example, on average 90% of outcomes, or 9 times out of 10, the test would give a positive (correct) result. Of course, the perfect test would be 100% sensitive. 

Some terminology here. 90% of the test results would thus result in a TRUE POSITIVE. But 10% of the results would be a FALSE NEGATIVE (i.e. you are told you don't have the disease but you actually do). 

But if you just walked in off the street, and had the test (with no-one knowing if you had the disease or not) and got a positive result then, knowing that the test is 90% sensitive, one error of thinking, commonly made, is that you might think that this means there is a 90% chance that you have the disease. Not at all - read on.

We need to understand something else here - what is known as the specificity of the test. Some more terminology. In the example given in the article, they had a specificity rate of 91%. And what this means is, if we had perfect knowledge that a group of people did NOT have the disease, how often would the test produce a (correct) negative result? In the example given, it is 91%. Meaning, if the test was performed 100 times, 91 of those times would produce a negative result i.e. what we might call a TRUE NEGATIVE. But 9 of those times would produce a positive result when you don't actually have the disease - in other words, 9 FALSE POSITIVES. Again, if a test had perfect specificity (100%) all would be great.

This is a key concept - a test needs to be assessed for how reliable it is when it is performed on groups that DO have the disease, but also for how reliable it is when it is performed on groups that don't. It may not be intuitive, but these two things are completely separate. Even if a test is performed on the same person repetitively, these types of errors will produce some false negatives or some false positives (depending on whether the person does or does not have the condition). Where tests have similar levels of sensitivity and specificity, that's just a coincidence - they can be quite different because it all depends on the underlying logic, science and fallibility of the measuring process.

The ideal combination would be a test that had 100% sensitivity, and 100% specificity. To my knowledge, and you will not be surprised to hear this, there are few if any tests that are so accurate. If a test was 100% accurate in both these ways, the test would have perfect predictive power, and you could completely rely on it. But this never happens in the real world. Again, a test might be quite sensitive, but have worse specificity, or vice versa.

Well, so far we have more of an idea of the issues involved. But, about half of the gynecologists in the BBC article apparently concluded from the above data that the chances of the women having cancer from the positive test alone, was in fact 90%. Oops - this is completely wrong, as we shall see.

The problem is that, in the real world of imperfect tests that do not have 100% sensitivity and 100% specificity, we can't assess the significance of test results without knowing what proportion of the overall population actually have the disease (this proportion is known as the prevalence rate).

To take a silly example, if we knew that 100% of the population always had the disease we can see that we don't need the tests. We know the answer already! And, if we knew that the prevalence rate was zero, we also know the answer already and don't need the tests. But anything in between we need to have a handle on. Why?

Well, because the test does not have perfect sensitivity or specificity (the test has a tendency to throw up false positives and false negatives) we have to weight or balance the size of these outcomes by the prevalence of the disease. Specifically;

  • Imagine you got a positive result - you would be interested to know how likely - adjusted for prevalence - is a true positive compared to a false positive.
  • And if you got a a negative result? You would be interested, instead, in how likely - adjusted for prevalence - is a true negative compared to a false negative.

An example. If the same number of people in the population have the disease as those who don't (a prevalence rate of 50%) then the 'weights' applied to the false positive effect are the same as the weights applied to the false negative effect. And in this case, with both sensitivity and specificity in the BBC example being 90% (actually the latter was 91% but that is near enough) then it is true to say the the lady with the positive result would have a probability of 90% of having the disease. But only in this example of a prevalence of 50%. And even then, the specificity has to be the same as the sensitivity. What if the proportion of the disease in the population was actually only 1%?

Well, we can see 'intuitively' that this causes a problem. If someone walks off the street and has the test, there is only 1 chance in a 100 that they have the disease. If the test is performed on them, the likelihood of a true positive (where they do have have the condition and the test produces a correct result) is very much less than the likelihood of a false positive (where they don't have the condition and the test produces an incorrect result).

Why? The test - if you have the disease - returns true positives 90% of the time. But the test, if you don't have the disease, still returns false positives 9% of the time (100 minus the specificity of 91). But - we still have to adjust for the prevalence of the disease. After we have multiplied true positive returns of 90% by 1% (the prevalence rate) to produce 0.9% and false positive returns of 9% by 99% (100 minus the prevalence rate) to still get very nearly 9.0%, we find that any positive result is thus approximately 10 times more likely to be a false alarm that a true positive.

Hence the true likelihood of having the disease, following a positive test result, is (in this example) 10%.

And we can see, all other things being equal, that if;

  • we increase the prevalence of the disease, any positive result from a test mean we are more likely to have the disease
  • we decrease the specificity, OR decrease the sensitivity, any positive result from a test means we are less likely to have the disease
  • if we decrease the specificity, any negative result from a test is slightly less likely to be correct
  • and so on...

To give you some idea, if we drop the sensitivity and specificity of the test we used in the above example to 75%, then we have to raise the prevalence of the disease from 1% to 3% to produce the same likelihood of having the disease if we get a positive result from the test.

So, if you have to explain this to patients, or have your own chat with your doctor, I hope this all helps you be a little better prepared!

(Footnote: this BBC podcast of July 2014 gives an excellent overview of the issues - highly recommended - you won't be able to listen after July 2015!)














So, what's my problem?

We always bump into this. There we stand, trying to figure out what is causing the patient's pain, and the patient says "So - what is causing my problem?". And we suddenly realise that what we want to say (for example, the way we might explain the problem to a fellow practitioner) is completely at odds with the way that the patient can understand it. Of course, experienced practitioners know that the simplest thing to do is to answer in ways that the patient can 'see' (or hear, or even feel - whatever their modality of thinking).

Really fed up...

Really fed up...

But we also need to structure our own thoughts about what seems to be happening, and why. For this we need to bear two concepts in mind. First, what appears to be the sequence of cause and effect? This linear way of thinking about spinal function and dysfunction has merit, but may also be sneakily deceptive. Second, thinking about the problem as a system - where multiple interacting factors generate spinal dysfunction as a failure of adaptation - and where we are more interested in the integrity of coping mechanisms.

So the following is a few ideas about all this...

Looking at it from the patient's point of view, the vast majority just seem to want to know what is actually hurting - not even what is causing the hurt. So if they have the dull ache of fatiguing, tired erector spinae, they want to hear that their muscles are aching (lumbago is a good word for this). If one tells them that their muscles are damaged and aching, then even better - because they can make a connection between damage and pain. But they do seem to be far less interested in the actual causes of their pain.

There are many reasons for this, of course, including;

  • their fears and apprehensions
  • whether the patient is active or passive about the health and functioning of their body
  • whether the patients sees their body as an 'it' or as part of their own responsibility
  • and so on ...

When it comes to communicating the nature of the problem to the patient, it is useful to have formed a quick assessment of where they are coming from as - irrespective of your diagnostic or technical expertise - a patient's impression of how good you are seems to depend heavily on whether you 'made sense' or not!

Having said all this, what then matters to us is making some decisions. To start with, we could use the following approach. Decide whether;

  • damaged tissues are generating pain through inflammatory mechanisms or
  • non-damaged tissues are generating pain through non-inflammatory mechanisms (muscle fatigue, even some type of ligamentous nociceptors)

In the first case we need to decide if the structure was damaged through an extrinsic injury (e.g. "I was kicked in the back playing soccer") or by an intrinsic fault of spinal functioning (e.g. a sitting patient suddenly looks to the right, and because of excessive muscle tension below the cervical area, abnormally rotates and tears some of the capsular fibres of a facet joint in the neck).

But in both cases of damaged tissues, we are primarily interested in the healing rate of the patient, and how we can - either through treating the patient, or through advising the patient, speed up this healing rate.

In the second case of non damaged tissues causing pain, we are not interested in tissue healing rates, but rather in how we can alter spinal functioning in such a way that the abnormal excessive load on the structures generating the pain is reduced enough to 'give them a break'.

If we do this accurately, some patients can respond immediately with a sense of ease and symptom reduction, whereas for others it can take a while for the spinal system to re-adapt. As we all know, age, length of time having had the problem, general health and vitality, and the presence of pre-existing patterns all play in a part in this re-adaptation rate.

Then we can consider the multi-factorial nature of most problems. For example, take a migraine pattern where a number of factors (e.g. spinal posture, foods, alcohol, psychological stress) all combine as a pattern generator for the migraine itself. Very probably, there is a certain trigger 'threshold' which, if reached by the addition of these combining factors, will spill over into a migraine. Say that in a certain patient, the sum of the combining factors is just below the symptom trigger threshold, but then an increase in the intensity of one of these factors, or even the addition of a smallish new factor, trips the pattern into symptom mode.

In this example, what is the problem? The pre-existing factors, or the new factor? Clearly, this is a 'straw and camel's back' type of question - but any proper answer to the question is more than just semantics or of difficulty in communicating these concepts to a puzzled patient, because thinking about these things allows us to decide where we can help, and we can help the most.

So when a patient asks us "so, what's my problem?" - is it any wonder we - most of the time - have to simplify?

Thoracic spine - some ideas

  1. The thoracic spine has a major influence on the way the neck works, even in not very active people, and has a massive influence on upper extremity function.
  2. The thoracic spine does not have such a big influence on lumbo-pelvic function, except in very active people or in people whose lumbar spine is only just coping.
  3. The thoracic spine has a particular set of ways in which it is influenced by, and influences, the health and vitality of the person.
  4. The key mechanical focus of the thoracic spine is a) how well does it rotate? and b) how well does it extend?
  5. Failure to rotate and extend will affect a particular direction of neck rotation and (less so) side-bending (i.e. if some thoracic segments will not rotate well to the right, they will affect - mainly through myofascial effects - the ability of the neck to move to the right), and will affect the ability of the shoulder joint to rise to true 180 flexion.
  6. Failure to rotate in a particular direction of one, or more, segments generally indicates stiffness of the opposite side of the segment - for example, if analysis shows that T3-5 does not rotate well to the right, then it is T3-5 on the left that are likely to be stiff and dysfunctional.
  7. One-sided restrictions as in the example above are more common than 'neutral' bilateral stiffness at a particular level, particular in young and middle aged people.
  8. Abnormal muscle tone and pain generally develops on the opposite side to the stiffness (in other words, they develop on the same side as the difficulty turning.
  9. Stringy, thinner (less muscle mass) and less tender segment musculature generally develop on the same side as the stiffness.
  10. The role of manipulation is to release the stiffness identified in point (6), to restore the failed rotation and extension at the segment in a particular direction - in other words, manipulation must be directional in its purpose.
  11. In terms of the actual manipulative technique, this is achieved by manipulative techniques that aim to challenge the inability of the segment to rotate in the desired direction - minimal amplitude techniques can do this in ways that do not discomfort the patient.
  12. Finally, manipulation is thus generally performed on the non-tender side of the thoracic spine - in the case of a patient who has thoracic pain, a higher level of thinking should be done if one is tempted to manipulate the same side as the pain.

Complex or complicated?

Is the problem posed by trying to understand the way the spine works a complex problem, or a complicated problem - or both?

What does it matter, you might ask? Well, let's just see if we can shed some light on the difference between the two.

I think that a complicated problem is one where there are lots of parameters. For example, if we have two members of a set (a, b) there can only be one relationship between the two. For three members, it is three. For 4, it is 6. We can see that as the number of members of a set rises, there is a step change in the number of interactions between the two (a triangular number sequence).

So far so good. Because all that means is that a complicated problem is one where it becomes more difficult to 'see' what is going on as the number of parameters rises - but, there are in principle no computational impediments to understanding the system, if we have sufficient time and a powerful enough number cruncher.

Now, I wonder if the spine is like this? To understand this, look at weather forecasting. People used to think that forecasting the weather was an example of a complicated problem. "If only we could measure all the starting parameters of a weather state, we could forecast the weather etc.". But, experience since the mid 60's and the work of people like Lorenz has shown how calculating changes in the weather state is incredibly difficult. This seems to be for two reasons. First, there are non-linear relationships between many of the different weather 'factors'; this makes it even more difficult to predict a change in the state of the system for any given number of, and relationship between, and change in variables. Secondly, the state of the system at any point therefore becomes extraordinarily sensitive to the starting position of the variables (the so-called 'measurement problem', where small changes in starting conditions have dramatic effects on the predicted system state). Thus we find weather forecasts are fairly reliable up to 4-5 days, but still then tail off dramatically, despite impressive models and incredibly fast super-computers compared to 20 years ago.

And the spine? Well, there are clearly a huge number of variables that affect spinal function and healing responses (two of the key things we are interested in). We know that physiology of function and of structure is all about non-linearity (for example, the way that collagen can suddenly fatigue, or how homeostatic negative feedback loops can fail). And we know it is impossible to measure accurately any of the variables in the system!

So the spine is more complex than it is complicated. Why does it matter if the spine is an example of a complex or a complicated problem?

Well, the reason is that despite the apparently awesome challenge posed by complexity, it is possible to see beyond the complex and to simplify in a way that adds value and does not just produce apparent insights. This is something you cannot do with a very complicated system (you can't extract insights from a complicated problem, you can only crunch it).

So because the spine is a complex problem we can legitimately try to generate reliable heuristics about reactions to treatment and testing (see the TED talk below for a neat explanation of this). Simplification might actually extract value. Ecologist Eric Berlow doesn't feel overwhelmed when faced with complex systems. He knows that more information can lead to a better, simpler solution. Illustrating the tips and tricks for breaking down big issues, he distills an overwhelming infographic on U.S. strategy in Afghanistan to a few elementary points.

Cause & Effect

I've thought a lot about the notion of cause and effect, and how it is such a difficult thing to get get a firm grip on. Indeed, from a systems point of view, our traditional ideas about cause and effect may be largely misleading.

When it comes to musculo-skeletal dysfunction and pain, the concept of X causing Y (where Y can be pain, tenderness, altered function and so on) is probably only 'correct' in trauma histories. You know, the patient who says "I was absolutely fine until I hammered my big toe..." etc.

For anything else ("it just seems to have built up for no reason over the last few weeks...") pinning down cause and effect is a lot harder. 

Actually, we always spend a bit of time asking the patient "What's changed or different then, compared to...?". And often the patient will finally confess to something (more work, taken up jogging, different car seat and so on) that allows us to say "Well, there you are then!". 

At this point the patient will often feel a bit better. There is a powerful human need to have some explanation for worrying things, and any answer - however thin and shaky - will often work for the patient. Indeed, there is some evidence that the patient's left hemisphere demands an explanation - as long as it kind of makes sense, whereas the right hemisphere is a lot happier with uncertainty (see McGilchrist). I digress, though suffice to say, woe betide the practitioner who fails to address the basic human need for a simple explanation. "Your facet joint has slipped..." may make a lot of us squirm - but it works.

So cause and effect is tricky. 

Actually, patients often seem to have some grasp of the concept of compensation. When we say that their mid back is hurting because the lumbar spine won't extend well, they often say "Ah, because it's compensating?".

As an aside, at this point I often explain to patients that a spine that is not working well does not just generate pain and stiffness, but uses more energy than a spine which is working as well as it can. In absolute terms, because the spinal system has to be a big consumer of  the total energy available to the human body, that has to be quite a lot. 

This always get me musing on what is the difference between adaptation and compensation and coping, or are they the same thing? 

The Oxford defines adaptation as "the process of change by which an organism or species becomes better suited to its environment".

And compensation as "something that counterbalances or makes up for an undesirable or unwelcome state of affairs". defines coping as "to face and deal with responsibilities, problems or difficulties, especially successfully, or in a calm and adequate manner".

Actually, all three words have other dictionary meanings as well, but the above seemed closest to what we have in mind and use in everyday practice life. 

So it seems that the word compensation may be closest to what we want.

Let's take an example. Say the left lumbo-sacral joint gets stiff in such a way that the segment can't bend to the left at all well. We can easily see that during locomotion, the spine will spend more time bending to the right than to the left - i.e. at that level of the lumbar spine, there will be a mass shift right, with a) an altered loading going through the right hip abductors during stance phase (compared to the left) and b) greater erector spinae output on the left side above the lesion (to counterbalance things). And so on.

If the compensation 'chosen' works optimally (meaning there is no better solution available) for this person at that moment in time, then all we can say is that there is the least increase in energy usage across the spine and the least probability of pain.

As professionals, we often use the term 'failure' or 'breakdown' of compensation - the idea being that if structures begin to hurt, as a secondary response to some original change in function, it is because the system has 'failed to cope'. 

I'm not sure this is always the correct way to think about things.

In one sense it is; for example, if a small car engine is badly tuned, it won't get up a steep hill, whereas a huge car engine, badly tuned, easily will. Similarly, if an athlete has enormous amounts of muscle and energy, he/she might easily 'cope' with a problem that would overwhelm someone a lot weaker.

But in another sense, it may not be. The fact that pain does not develop in the case of the athlete does not mean that the compensation chosen is optimal. Presumably, the best compensation would be one that produced the least increase in total energy usage in any time period, while minimising the risk of structures failing to cope at some point in the next or subsequent time periods. This has got to be a complex function of a number of factors - I wonder if it has been modelled properly?

One thing we can be sure about - human's will have similar ways in which they compensate for significant dysfunction, but will vary in the details. And successful compensation may fluctuate as it shifts the 'solution' around from period to period.

How about adaptation? Perhaps we ought to reserve this term for when the body has altered its structure, over time, as a response to the compensational functional changes that started the whole process? For example, a muscle forced to work 'harder' by altered function elsewhere might be able to adapt by become stronger. Presumably this can happen where the muscle is still able to work in the way it wants to (alternating power and relaxation cycles). This process of adaptation might not be possible if the muscle is instead asked to switch on in a more tonic way, something it was not designed to do. In this situation, there may be a more rapid path to coping failure and symptoms. 

We get clues from patient reactions to treatment as to whether we have helped 'causes' or 'effects'. For example, if a patient says "I felt great for a few days but then it all came back", then - clearly - all we did was successfully treat the compensation mechanism and allow it to cope a bit better for a while, but we have not treated further back in the chain. Whereas, if they say "I didn't feel any different for a few days, but then it started to get better", we know we have done something right.

Finally, when patients say "the sore bit was better following treatment, but the other - normally good - side was achy for a few days", we can probably surmise that structures that have been 'under-working' as a result of the original problem and subsequent compensation mechanism have had to do some real work, and groaned as they adapted to it.

Placebo - quirks

I was reading an interesting book the other day (Cracked: Why Psychiatry is Doing More Harm Than Good, by James Davies) about modern 'medical' (or drug) psychiatry. In it he mentioned an interesting quirk about side-effects and the placebo response that I hadn't been aware of.

He was writing about how - in the case of anti-depressants - there is only a small additional benefit over and above placebo conferred by taking the drug. In fact, this small additional benefit is typically only a few points on the 51 point Hamilton Scale (a standard before and after test often used in trials in this area). So the larger proportion of the total benefit is indeed the placebo effect.

But then he went on to mention how some of that additional benefit that the drugs have relative to placebo might be a quirk of the side-effects of the drugs.

It goes like this. All enrolled in the trial are told they might be on the active drug, or might be on a placebo. They have to be told of likely side-effects from taking the drug. In other words, they might get side-effects, IF they are allocated to the active drug.

Now, if someone is allocated to the drug (but does not know) then IF they get a side-effect, they then might well think "Hang on! That must mean I'm on the active drug?". Knowing this might well generate an incremental placebo benefit compared to not knowing.

Now, of course, some people NOT on the active drug might develop side-effects similar to the drug side-effects (either for independent reasons such as getting a dry mouth if they have a cold, or as an active placebo - actually nocebo - type response itself).

But it is reasonable to assume that this latter effect will be smaller than the former, and the difference between the two will presumably be greater the stronger and more diverse the side-effects of the active drug!

So some of the headline additional benefit (already rather small) marketed by big pharma may be somewhat illusory.

Neat, eh?

I wonder whether we bump into this with patients? "You might develop a reaction to treatment if we have done the right thing today and got those stiff segments moving...". Or some such.

But like I said, the placebo sure is slippery.