7 absolutely crucial facts you didn’t know about tendons

In this blog post we are going to discuss 7 absolutely crucial facts about tendons that you probably didn’t know, but that are very important to improve your tendinopathy rehab.

Let’s jump right into it:

1. The nociceptive driver of pain in tendons is unknown. Pathology seen on imaging is not the driver of pain. Vascularity is not the source of pain, merely a marker of tendon degeneration. On top of that, there are no sensory nerves deep in the tendon, but in the periphery around the tendon. Nerves that grow into a pathological tendon, are sympathetic nerves, not sensory. At last, central sensitization is probably less a problem in lower limb pathology compared to upper limb pathology (Plinsinga et al. 2015, Plinsinga et al. 2018).


2. We are not able to repair/heal degenerative tendon pathology. In other words, no surgery, no shockwave therapy, no injections whatsoever and not even exercise is able to repair or heal a degenerated tendon. Docking et al.(2019) reason that with little ability to sense tensile load, the cells in the degenerative part of the tendon may be under-stimulated and not receive the necessary mechanical stimuli to remodel, explaining the limited capacity of the pathological tendon to remodel and normalize. While you think that this might be bad news, the good news is: it’s also not necessary. A study by Tsehaie et al.(2017) showed that 24 weeks of eccentric exercises for the Achilles tendon did not produce changes outside the limits of detectable change in the tendon, but yet patients improved. They also found that o MRI parameter at baseline predicted the change in symptoms, so even if your MRI looks terrible, it doesn’t matter.

Figure from https://www.ultrasoundcases.info/partial-ruptures-7335/#gallery-2


3. The tendon loading rate probably explains why tendinopathy is associated with repetitive stretch-shorten cycle (SSC) rather than heavy loads. The SSC occurs during any activity that requires the tendon to store and release energy like a spring. Everything else is easy for a tendon e.g. eccentric movements, high weight. The loading rate is calculated in BW/sec. Here are two examples for the patellar and the Achilles tendon in different activities. So the highest loading rate for the patellar tendon is to land in a stop jump sequence, like in a basketball or volleyball, while leg pressing 3x bodyweight has a very low loading rate. This is the same for the Achilles tendon where calf raises have a very low loading rate for the tendon while running and hopping have a very high strain rate. Interestingly, the very best athletes who can run fast or jump high are the ones who are also at risk to develop tendon pathology the most, probably because they can load their tendons faster than anyone else. This phenomenon is also called the “Jumper’s knee paradox”, described in an article by Visnes et al. (2013)

Patellar tendon tensile load and loading rate in typical activities:

Figure from a presentation of Jill Cook

Achilles tendon tensile load and loading rate in typical activities:

Figure from a presentation of Jill Cook

4. The Combination of compressive loads and tensile loads are more damaging to any of the two alone. A study by Soslowsky et al. (2002) compared 3 groups of mice to each other: In 1 group they manipulated the acromial arch to simulate external compression, one group had higher tensile loads as they had to run on a treadmill more than other groups and a combined group. They found that extrinsic compression did not cause injury until overuse activity was introduced. While compressive properties may be important, tensile properties are more relevant properties in a tissue such as a tendon. The results show that the combination of external compression plus tensile loads led to the greatest injury.

Figure from Soslowksy et al. (2002): Injury created by overuse plus extrinsic compression is greater than the injuries created by overuse or extrinsic compression alone. Significant differences relative to control are indicated by a ‘‘*’’ inside each bar (average +- standard deviation). Significant differences between single factors (E=Extrinsic, OV=Overload and multiple factors (OV/E) are indicated by a ‘‘*’’ above each pair of bars.

5. Intense loading of tendons results in net collagen degradation for up to 36h. A study by Magnussen et al.(2010) showed this effect in three groups of very intense exercise, which were 36km of running, 1 hour of repetitive kicking and 10 sets of 10 repetitions of knee extension at 70% maximal voluntary contraction. This means that we need sufficient recovery time to prevent tendinopathy and it’s advisable to space out training sessions for the tendon to every other day or less.

Figure from Magnussen et al. (2010)

6. A pathological tendon has more good structure than a normal tendon (Docking et al. 2015). This means we can load these tendons because we have loads of good tissue. Any therapies for tendon pathology are not necessary, because we cannot change the structure of the pathological part anyways. For this reason, Docking and colleagues came up with the quote “Treat the donut, not the hole” – in other words, focus on the healthy structure and not the pathological part.

Figure from Docking & Cook et al. (2015)


7. 66% of Achilles tendon ruptures are asymptomatic ruptures (Kannus et al. 1991). This means these people never had Achilles tenderness, stiffness, pain or dysfunction. However, there had to be some kind of pathology present in the tendon as the authors showed that 98% of ruptured tendons had degenerative pathology, while 2% had other pathology. Jill Cook explained this in a Twitter post stating that it’s impossible to rupture a normal tendon in vivo without pathology.

Interestingly, a study by Yasui et al. (2017) showed that only 4% with Achilles tendinopathy go on to rupture the tendon. So pain in tendinopathy might actually be protective of a rupture and this is a very good and re-assuring message for patients who are in tendon pain and afraid to rupture their tendons.

Alright, how many of those 7 were completely new to you?
As always, thanks a lot for reading!

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We have probably click-baited you into reading this blog post, because you might be looking for THE magic exercise or FIX to make low back pain magically disappear. The truth is: There is no and can never be one single exercise that is the best for low back pain or any other hurtful body part or muscle or whatsoever. In fact, this way of thinking is very simplistic and focusing on a body part or pathology rather than the person. If there was 1 best exercise our profession would basically become redundant and patients could follow cookie cutter approaches.

But let’s first look at the effectiveness of different forms of exercise for patients with low back pain:

First of all, a meta-analysis by Searle et al. (2015) has shown that strength and resistance exercises as well as coordination/stabilization exercises are effective in reducing pain in patients with chronic low back pain although effect sizes are usually rather small. So that’s pretty good news, now let’s look a bit closer at different exercise programs and their effectiveness:

A study by Marshall et al. (2013) compared Pilates exercises with stationary biking and while Pilates was superior at 8 weeks, the results were equal in the long-term at 6 months.

Then there is this pretty well-known study by Shnaydermann et al. (2013) who have found that walking is as effective as specific exercises for the low back at 6 weeks. It has to be mentioned though that the people in the study were all sedentary, so we cannot assume that the outcome would be the same in a more active population.

Furthermore, there is tons of research that compared core stabilization exercises with general strengthening exercises for the low back. Some of these studies by Smith et al. (2014), Saragiotto et al. (2016), Luomajoki et al. (2018), Wang (2012), Coulombe (2017) amongst others show that low-load stabilization exercises might be a tiny bit better at reducing pain at short-term but all of them show that general strengthening is equally effective at long-term.

At last, a study by Aasa et al. (2015) compared low-load motor control exercises with deadlifts. In the study, the low-load motor control group outperformed the high-load group on short-term, but again- long-term results were equally effective. So the good news from all of these studies is that doing something is better than nothing. So one might argue that the best exercise is the one that gets done.
But why choose for one form of exercise only?

Ben Cormack from Cor-Kinetic compares different exercise modes as different vitamins that our body needs just like in a balanced diet. So you might want to incorporate strength, high-load and low load, coordination, power, endurance and graded exposure exercises as well as movement games etc. into a well-balanced exercise program.
Glasgow et al. (2015) thus also mention that an optimal loading program consists of different key variables and mechanisms.

One thing we know from research is that patients with low back pain often display with decreased movement variety. So using different exercise modalities might be one way to increase movement variability.

What is very interesting is that we are always thinking that getting stronger, more flexibe , better at activating certain muscles, or improving movement “faults”  etcetera is what explains the effects of our exercise program. However, a systematic review by Steiger et al. (2012) has shown that treatment effects are NOT attributable to changes in the musculoskeletal system. There might be other changes that are responsible for the effects such as: Diffuse noxious inhibitory control, the release of pain reducing chemicals in your brain, maybe just more movement in itself, or psychosocial factors such as decreased movement-related fear, increased confidence etc., but in fact: We just don’t know really!

So how specific should we be? Aspecific problems such as aspecific low back pain probably do not have to be body-part or structure specific, but also benefit from a more general approach. On the other hand, a specific problem such as Achilles tendinopathy, in which we know the nociceptive structe, will benefit more from a structure-specific approach such as load on the Achilles tendon by calf raises for example.
But even if we we have a structure-specific problem, we should not only be specific to a certain joint, tendon or muscle, but specific to the person in front of us!

Research always looks at the average effect of a group with two or more very standardized interventions. However, the person in front of you could deviate from this standardized mean. For example: Isometric exercises generally work well to decrease pain. At the same time, research has shown that exercise-induced analgesia might not occur in patients with central sensitization, but actually increase pain levels. This means that we will always have to be flexible and adapt our treatment if it does not seem to be effective in our patients after 2 or 3 sessions, even if research might suggest otherwise.

Another big reason that there can never be THE single best exercise for every person is because different people need different amounts of vitamin. So what you’ll have to ask yourself with every exercise you’re giving to patients is what do you want them to get from this exercise?

It could be that you are trying to increase tissue capacity or exercise adherence. Another target could be to challenge their belief structure or to alter their movement strategies or it could be pain relief. On top of that, the ideal exercise is tailored to a patients level of skill and irritability.
All of these different areas should influence exercise selection to make it person-specific!

For example, a young weightlifter who has to return to high-level performance after a first episode of low back pain might need maximum strength, power and work on his technique. On the other hand a 70 year old sedentary pensioner with chronic low back pain and apprehension to bend forward due to maladaptive illness-beliefs will probably need a graded exposure program with lots of re-assurance and education.

For the very same reasons, we cannot expect that generic exercises will lead to optimal outcomes. The challenge for us as therapists is to listen to our patient’s story and to ask ourselves which vitamins he or she needs and to then select the appropriate exercises to give them these different vitamins.

Alright, this was our blog on “the best exercise for low back pain”. Shout-out at this point to Ben Cormack from Cor-Kinetic who inspired useto discuss various concepts in this blog. If you want to know how we apply these concepts in different exercise programs check out our online course "Orthopedic Physiotherapy of the Spine"
Thanks a lot for reading, bye!


How to Massively Improve Your Knowledge about Low Back Pain in the Next 5 Days for FREE

5 absolutely crucial lessons you won't learn at university that will improve your care for patients with low back pain immediately without paying a single cent



I’m sure a lot of students and therapists out there have learned that radicular pain and radiculopathy follow a dermatomal distribution. But is that really true and exactly like we have learned it from textbooks?
First of all, let’s distinguish between radicular pain and radiculopathy. Even though "radicular pain" and "radiculopathy" are synonymously used in the literature, they are not the same. Radicular pain is defined as "pain evoked by ectopic discharges originating from a dorsal root or its ganglion". It’s the neuropathic, electric pain that patients feel shooting down the leg.

Radiculopathy is yet another, distinct entity. It is a neurological state in which conduction is blocked along a spinal nerve or its roots (Bogduk et al. 2009). This leads to objective signs of loss of neurologic function such as sensory loss called hypoesthesia or anesthesia in the sever form, motor loss called paresis or atrophy in the severe form, or impaired reflexes called hyporeflexia or areflexia if they are completely absent.If radicular pain or radiculopathy or both are present, we are talking about radicular syndrome, which is an umbrella term.


Does radicular pain follow a dermatomal pattern?

Okay, so now let’s see if radicular pain follows a dermatomal pattern. A study by Murphy et al.(2009) observed pain patterns in patients with radicular pain and found the following:

Radicular pain in the cervical spine followed a dermatomal distribution in only 30% of cases, while in the lumbar spine it was slightly better with 36%. Now let’s look at specific dermatomes separately.

For the cervical levels only C4 seems to be more or less reliable with 60% - although we have to be careful with the interpretation here as there were only 2 patients with an affected nerve root at C4. All other levels do not seem to be reliable.

It doesn’t get much better for the lumbar spine:

It seems that only level S1 might be more or less reliable with 65% of patients with an S1 nerve root compression reporting pain in the dermatomal distribution of S1. All other levels did not follow a dermatomal distribution regularly. It has to said though that Murphy and colleagues included patients with multi-level disease, which probably decreased the reliability a bit. Another, more recent study by McAnany et al. (2019) observed pain patterns in cervical radiculopathy. They found that only 54% fit the regular dermatome pattern like described in the Netter anatomy book. In the non-standard distribution dermatomal levels differed by 1.68 levels either cranially or caudally from the standard.


How reliable are dermatomes, myotomes and reflexes?

Okay, so if radicular pain is not reliable and mostly reported as shooting, electric pain along the whole distribution of the arm or the leg – how reliable are our dermatomes, myotomes and reflexes?

A study by Rainville et al. (2017) compared sensory changes and weakness in patients with C6 and C7 radiculopathy. They concluded that these symptoms have limited value to differentiate between the two levels. Al Nezari et al. (2013) performed a meta-analysis to see if a peripheral neurological examination is able to diagnose the level of lumbar disc herniation.They state that sensory, motor and reflex testing all had a low sensitivity, moderate specificity and limited diagnostic accuracy to determine the level of disc herniation. So while a neurological examination may help to confirm the presence of radicular syndrome and to assess hypofunction to establish a baseline and to monitor treatment progress, it cannot determine the affect level of nerve root compression.

Now what is the reason that our dermatome maps are so unreliable? The literature mentions several possibilities. First, there is huge variability in the brachial and lumbosacral plexus. If we look at cadaver studies for the brachial plexus, a typical textbook anatomy of the brachial plexus was only found in 37-77% of cases. Two major variations are described in the brachial plexus:

We are talking of “prefixation” when nerve root C4 contributes considerably to the plexus and T1 does not or only minimally. This variation has a prevalence of between 26-48%. The second variation is called “postfixation”. This is the case if there is only little or no contribution from C5 and considerable innervation from T2. This variation is present in 4% of the population. A prefixation or postfixation can shift the observed pattern of cervical radiculopathy cranial or caudal depending on the anatomic variant present.

A second reason is that intradural connections of rootlets in more than 50% of cadavers are found by C5 and C6 and C6 and C7. Such a connection between rootlets of different nerve roots is called anastomosis.

Third, textbooks commonly used in medical health programs contain multiple, conflicting dermatome maps. On top of that, the seminal basis that formed dermatomal maps are flawed in various ways. For example, the map created by Garrett and Keegan in 1948 have never been confirmed by follow-up studies up to this day, yet this map is mostly used in textbooks. Lee et al.(2008) have evaluated the literature and created a composite dermatome map based on published data from 5 papers they considered to be the most experimentally reliable. Their map looks like this, which might be a bit different to what you and we have learned at school:

Okay, let’s summarize: So neither radicular pain, nor radiculopathy seem to follow a strict dermatomal pattern of maps we have learned in school. So with our clinical examination, we’re probably not able to determine which nerve root is affected. At the same time, this information is probably way more important for surgeons than for us as physiotherapists. If someone is suffering from radicular symptoms coming from L5 or S1 won’t probably change our management strategy in any important way. You may want to continue doing your neurological assessment to confirm radiculopathy and to evaluate the degree of hypofunction . At the same time keep in mind the high degree of anatomical variation and that predicting the affected level is impossible.

Alright, we hope this answered the question thoroughly. Comment down below if you were surprised about actual evidence and if you have any further questions. A lot of this information and much more can be found on our online course on the spine.


How to Massively Improve Your Knowledge about Low Back Pain in the Next 5 Days for FREE

5 absolutely crucial lessons you won't learn at university that will improve your care for patients with low back pain immediately without paying a single cent


Fact & Fiction around lumbar disc herniations

Hardly any musculoskeletal topic has received as much media coverage as herniated discs and probably every person knows some family member or neighbor who has had one. At the same time, a lot of misconceptions have been spread about the topic and a lot of patients suffering from low back pain fear that they herniated a disk. We’ve decided to aggregate the research surrounding lumbar disc herniations to separate facts from fiction:

Anatomy of an intervertebral disk










An intervertebral disc consists of strong fibrocartilage designed for shock-absorption and is firmly anchored into the vertebral bones above and below by the vertebral end plates. Furthemore, it is surrounded by strong ligaments, so there is absolutely no way a disc can slip.


Disk Herniations

Herniations are broadly defined as a localized or focal displacement of disc material beyond the limits of the intervertebral disc space. The disc material may be the nucleus, cartilage, fragmented apophyseal bone, annular tissue, or any combination thereof. First of all, the presence of disc tissue extending beyond the edges
of the ring apophyses, throughout the circumference of the disc, is called ‘‘bulging’’ and it’s not considered a form of herniation. 

There are 3 categories of disc herniations: We are talking about a disc protrusion if the greatest distance between the edges of the disc material presenting outside the disc space – so the D-line- is less than the distance between the edges of the base of that disc material extending outside the disc space, which is presented by the B-line.

In an extrusion, the D-line is bigger than the B-line:

And in a sequestration - which is a subclass of a disc extrusion -the extruded disc material has no continuity with the disc of origin:


Prevalence of disk herniations in healthy subjects

Table fromBrinjikji et al. (2015)

It’s important to realize that disc protrusions are very common, also in healthy people. A famous study by Brinjikij et al. (2015) showed that almost one third of 20 healthy year olds have a disk protrusion. The numbers increase with age up to 43% at the age of 80, so almost every second person without low back pain has a herniated disk. Disk bulges are even more common by the way with 84% at the age of 80. So even if your MRI scan does show a bulging or protruding disc you should realized that these findings are completely normal and much like “gray hair from the inside”. Pain is complex and cannot be explained by an MRI scan alone.


What are risk factors to suffer from a lumbar disk herniation?

Let’s see what the evidence says about risk factors to be hospitalized due to a lumbar disk herniation irritating a nerve root:
In a chinese study Zhang et al. (2009) report that family history so genetic predisposition was by far the biggest risk factor. This was followed by lumbar load at work and strenuous work, while regular physical exercise and sleeping on a hard bed were both protective. Furthermore, a study in Swedish construction workers (Wahlström et al. 2012) and two systematic reviews with meta-analysis revealed that smoking (Huang et al. 2016), obesity and overweight (Shiri et al. 2014) as well as being taller than 1 meter 90 or 6 foot 3 are further risk factors.
An interesting literature review by Belavy et al. (2016) showed an increased risk for lumbar disc herniations in astronauts after return to earth. They concluded that the most likely cause thereof was a swelling of the intervertebral disc in the unloaded condition. Conclusion: Intervertebral disks need load to stay healthy. Not surprisingly, studies from Bowden et al. (2018) and Belavy et al. (2017) also show that physical activity, particularly vigorous activity, and running are beneficial to maintain intervertebral disc health.


What is the course of a symptomatic disk herniation?

Okay, so let’s say you or your patient are one of the unlucky ones who experience sciatica from a herniated disc pressing on a lumbar nerve root. How long does this take to heal? In a Dutch study by Vroomen et al. (2002), 73% of patients showed major improvement at 12 weeks without surgery. On long-term Konstantinou et al. (2018) found a less positive course with 55% of patients reporting improvement of sciatica after 12 months.
For some reasons, a lot of patients assume that having a disc herniation is something they will have to live with for the rest of their lives. However, a study by Elkholy et al. (2019) followed 9 patients with lumbar disc herniations and sciatica. Spontaneous resorption of the herniated disc was found in ALL patients in a mean time of around 9 months, while they recovered way earlier with a mean of roughly 6 weeks. This shows again that you can recover although you still have a hernia, so structure is just one component of many influencing someone’s pain experience. By the way, larger and/or sequestrated discs were associated with an even faster resorption. A meta analysis from Zhong et al.(2017) confirms these findings showing that spontaneous resorption was reported in 66% of patients across eleven different studies.


Management options

So a herniated disc and sciatica do not necessarily mean that you need to get surgery. In the Netherlands about 5-15% of patients with lumbosacral radicular syndrome end up getting surgery (NHS Standaard Radiculair Syndroom). But how effective is surgery? A systematic review by Jacobs et al. (2011) showed that conservative treatment and surgery are equally effective after 1 and 2 years. The only advantage that surgery might offer is a faster pain relief for patients with 6-12 weeks of radicular pain. However, other options for pain relief should be considered first such as NSAIDs, weak opioids or epidural injections, like the NICE guidelines from the UK suggest.
While surgery or just time usually improves a patient’s leg pain, a lot of patients we see do not improve their back pain. Probably the main role for us as clinicians in these cases is education and re-assurance (possible by showing them our video) and by helping patients to regain confidence in their backs. This can be done be achieved with a graded activity or graded exposure programs to challenge specific movement-related fears such as bending over. If you need some inspiration for that, check out our video in the top right corner.

Alright, this was our posts on facts and fiction around lumbar disc herniations. Comment down below if you still have any questions or if you were surprised about actual evidence around a couple of persistent myths. A lot of this information and much more can be found on our online course on the spine.


How to Massively Improve Your Knowledge about Low Back Pain in the Next 5 Days for FREE

5 absolutely crucial lessons you won't learn at university that will improve your care for patients with low back pain immediately without paying a single cent

How knowledge about statistics will make you a better evidence-based physio

Statistics is one of the most confusing topics for physios and physio students. Most probably this is due to the fact that we care more about people and health than we care about math, right?


Well, I get that you are more interested in assessing your patient properly, good handling and the latest treatment methods, but I gotta tell you that you need to know the statistical values of a special test and even numbers about prevalence, pre-test and post-test probablilities of questions you ask your patients during your whole anamnestic process!
I would even dare to say that without the knowledge of the above-mentioned numbers, you will have no clue how much value you can put on certain questions you ask your patient (and the answers thereof) and you will perform special tests without really knowing what a positive or negative outcome will tell you.
When I see or hear that a physio performs a special test like the Thessaly test for meniscus lesions, it is positive, and they are 100% sure afterwards, that their patient has a meniscus lesion, it makes me cringe!

That´s why I urge you to to continue reading my post in which I will try to give you an insight into how you can and should use statistics to become a better physio and how that knowledge increases your awareness of your clinical reasoning process!

In general, you will start with your screening, then your anamnesis, followed by basic assessment. On the basis of the information you got during the aforementioned parts, you are forming your hypotheses that you would either like to confirm or reject.  This is where sensitivity and specificity come into play. So let´s first have a look at what sensitivity and specificity are! The easiest way is to watch the short video we have made a while ago:

So to sum it um again: A negative outcome in a 100% sensitive test can rule out the disease (SnNOut) and a positive outcome in a 100% specific test can rule in the disease (SpPIn).
With the two mnemonics SnNOut and SpPIn it´s relatively easy to put these two concepts into practice.
Most of the time, you will get a better grasp on their definition and what they actually are if you are able to calculate these values using a 2×2 table. Watch our next video, which will show you how to do the calculation part:

Unfortunately, in real life there are hardly any 100% accurate tests, which is why you will have a lot of false positive and false negative results . On top of that, sensitivity and specificity tell us how often a test is positive in patients who we already know have the disease or not. In practice, we however do not know wether our patients have a certain condition or not. What we rather do in practice is to interpret the results of a positive or negative test.
You usually want know what the probability is that the patient actually has the disease with a positive outcome and how high the probability is that a patient does not have the disease with a negative outcome.
These values are called positive predictive value (PPV) and negative predictive value (NPV), also called post-test probabilities. You guessed it – we have another video that explains these values with the help of the 2×2 table and shows you how to calculate these values:

Now, like mentioned in the video PPV and NPV are a great tool if you have a good idea about the prevalence of your patient group and if this prevalence is identical with the the prevalence of the RCT, where you have gotten your statistical values from for a specific test in the first place. If this is not the case, PPV and NPV become pretty much useless.
Imagine how the pre-test probability of an anterior cruciate ligament (ACL) rupture changes in different settings: For example, the prevalence of patients with an ACL tear in a general practice will be much lower than in a sports clinic that is specialized in knee injuries. The higher the prevalence, the higher your PPV and the lower your NPV will be.
Maybe well make a video on that as well in the future, but it´s important to remember that we need a better value than the PPV and NPV, which is where the likelihood ratios come into play.

The likelihood ratio combines both sensitivity and specificity and tells us how likely a given test result is in people with the condition, compared with how likely it is in people without the condition. Watch the following video about likelihood ratios and how you can calculate them:

In the example we used the Lachman test, which one of the most accurate tests that is out there in clinical practice, but let´s look at our beloved Thessaly test and how our example plays out there:
According to Goossens et al. (2015) the Thessaly test has a sensitivity of 64% and a specificity of 53%, which results in a LR+ of 1,36 and a LR- of 0,68. As you can already see, these values are pretty close to LR = 1, which tells us that they will change the probability that a person has a meniscus lesion very little. To apply these values to our example of our ACL tear case, we know that ACL tears are often accompanied by meniscal tears. Although our patient does not report about any locking or catching sensations, we estimate our pre-test probability at about 30%.
Our nomogram will look like this:


Based on the (more accurate) calculations we end up with the following post-test probabilities:
– Pre-test odds: Prevalence/(1-prevalence) = 0,3/(1-0,3) = 0,43
– Post-test odds (LR+): 0,43 x 1,36 = 0,58
Post-test probability (LR+): post-test odds / (post-test odds+1) = 0,58/(0,58+1) = 0,37 (so 37%)
– Post-test odds (LR-): 0,43 x 0,68 = 0,29
Post-test probability (LR-): post-test odds / (post-test odds+1) = 0,29/ (0,29+1) = 0,22 (22%)

So with a positive Thessaly test, you have increased your chances of a mensical lesion from assumed 30% to 37% and with a negative Thessaly test you have decreased your chances to 22%.
See why I am freaking out if people perform a test and then they assume that their patient definitely does or does not have a certain condition?! And this is all based on an assumption of the pre-test odds, which most people even forget to take into consideration!

If you want to perform multiple tests, say you want to add the Anterior Drawer test in our ACL example, you will base your pre-test probability on the post-test probability of the Lachman test. So in case of a positive Lachman, you will start with a pre-test probability of 95% and with a negative Lachman you will start with a pre-test probability of 19%.
While most tests either have a positive or negative outcome, there are also test clusters with multiple outcomes. So if you take the cluster of Laslett for example, for 2 out of 5 positive tests you will end up at an LR+ of 2.7, for 3/5 at an LR+ of 4.3 etc.


Be aware though, that with a very high pre-test probability, another test has little value and it is better to start your treatment. The same is true for a very low pre-test probability in which case you don´t test and also do not treat the condition.
As an example, if a patient presents to you with sudden onset of low back pain, neurological symptoms in both legs, problems with micturition and saddle anesthesia, you would be pretty sure that this patient has cauda equina syndrome, which is a red flag and requires urgent surgery. So if you are say 99% sure of your diagnosis, a straight leg test (SLR) with a LR- of 0.2 will decrease the post-test probability to 95%, which is still very high and you would still want to send this patient for surgery.
In turn, if the test was positive, you would probably go from 99% to 100% certainty, so why bother testing in the first place, especially if this is an urgent referral for surgery?

The same is true for a very low pre-test probability. If a patient presents to you without radiating pain below the knee, the chance of this patient for radicular syndrome due a disc herniation is very low, say we assume 5%. So what would happen in this case if you performed the SLR with a LR+ of 0.2? You would end up at a post-test probability of 10% and if the test is negative the post-test probability would have decreased to maybe 4%. So if you are almost certain, that a patient does not have a certain disease, why test it in the first place?
Of course, in practice the decision to do a certain test always depends on various factors such as costs, severity of a disease, risks of the test etc.

Now let´s get back to what I claimed in the beginning, that statistical values help you to evaluate the outcome of your questioning during your patient-history taking.
In fact, every question can be seen as a special test, in which the answer (yes or no) will either increase or decrease the probability that a patient has a certain condition.This is also the reason why a thorough anamnesis is most of the times more important than special testing, because you are basically performing a series of special tests in a row,
if you are a good clinician who knows how to form a hypothesis based on your patient’s answers.

So let´s take another example: How does a positive answer to the question about prolonged use of corticosteroids influence the chance of a spinal fracture?
According to Henschke et al. (2009), prolonged use of corticosteroids has a positive LR+ of 48.5. The prevalence (pre-test probability) of a spinal fracture presenting to primary care can be estimated between 1%-4% according to Williams et al. (2013) in patients who present with low back pain.
So with prolonged corticosteroid use, we will end up with a post-test probability of 33% although we assumed only 1% of prevalence in this example calculation.
I think it´s fair to say that this question about corticosteroids should always be asked in the screening procedure for spinal fractures!
Now let´s take a look at another red flag that is commonly used in the screening for malignancy in patients with low back pain: Insidious onset of low back pain.
According to Deyo et al. (1988, I admit this is a pretty old study) the LR+ for this question is 1.1. According to Henschke et al. (2009) the prevalence of malignancy in patients with low back pain is even lower than 1%, but we will calculate with this 1% just for simplicity.
So the red flag insidious onset increases the post-test probability of malignancy as the cause of low back pain from 1% to exactly 1,1%. I think we can agree that this red flag should be kicked out of any guideline in which it is listed.

I know this was a long post and congratulations and respect if you made it till here! My goals were to give you an explanation about how to work with statistical values like sensitivity, specificity, PPV, NPV and especially the likelihood ratios and to make you aware about their importance in your whole physiotherapeutic process.
It would be fantastic if you could take the prevalence of a certain hypothesis into account with your future patients, have an idea about the impact of your anamnestic questions on the pre-test probability and if you could properly evaluate the power of your special testing.


Feel free to ask questions in the comment and to share this blog post if you found it helpful!

Thank you for reading!


Goossens P, Keijsers E, van Geenen RJ, Zijta A, van den Broek M, Verhagen AP, et al. Validity of the Thessaly test in evaluating meniscal tears compared with arthroscopy: a diagnostic accuracy study. J.Orthop.Sports Phys.Ther. 2015;45(1):18-24, B1

Henschke N, Maher CG, Ostelo RW, de Vet HC, Macaskill P, Irwig L. Red flags to screen for malignancy in patients with low-back pain. Cochrane Database Syst.Rev. 2013;(2):CD008686. doi(2):CD008686.

Williams CM, Henschke N, Maher CG, van Tulder MW, Koes BW, Macaskill P, et al. Red flags to screen for vertebral fracture in patients presenting with low-back pain. Cochrane
Database Syst Rev 2013;1:CD008643.