Heel Pain in Runners

Heel Pain in Runners – More than Just Plantar Fasciitis!

Heel Pain in Runners - More than Just Plantar Fasciitis!

Heel Pain is a common overuse injury in recreational runners. There are multiple causes of heel pain in runners and the most common cause is plantar fasciitis or plantar fasciopathy. Plantar fasciopathy is an appropriate description since this condition is not inflammatory. Risk factors include limited ankle dorsiflexion, increased body mass index, standing for prolonged periods of time, and a recent increase in training volume or speed in runners. Plantar fasciitis is common in both the athletic population and sedentary people. With appropriate treatment, 80% of patients with plantar fasciitis will improve within 12 months. The peak incidence is between the ages of 40 to 60.



The classic signs and symptoms of plantar fasciitis are pain to the medial tubercle at the insertion of the plantar aponeurosis, pain worse upon standing in the morning, and standing after long periods of inactivity. The incidence of Plantar Fasciitis in runners ranges from 4.5 to 10% and represents the third most frequently experience running-related musculoskeletal injury in this systematic review by Lopes et al. (2012)

The high incidence of PF in runners is not surprising, if one considers the role of the plantar fascia and the longitudinal arch, in the force absorption, associated with long-distance running.


Physical Examination:

On palpation, the patient will be tender to palpation on the proximal plantar fascial insertion at the anteromedial calcaneus. The windlass test is a useful test for this condition and is described  in the following video:

A positive result is heel pain reproduced by forced dorsiflexion of the toes at the metatarsophalangeal joints with the ankle stabilized. The windlass test has a specificity of 100% and a sensitivity of 32% as shown by De Garceau et al. (2003).


Differential Diagnosis:

There are multiple causes of chronic heel pain in runners and it is important to be aware of other pathologies in this area, as outlined in the picture below:Heel Pain in Runners

Key Differential diagnoses in the running population, include fat pad contusion in the heel, calcaneal fracture, and retrocalcaneal bursitis. Calcaneal fractures may present with localized tenderness and usually occurs after trauma or a spike in training volume or speed. Retrocalcaneal bursitis presents with insertional Achilles tendon discomfort and is located in a more posterior position. In the following 5-minute video, I will go more in-depth about the differential diagnosis:



In the case of uncertain diagnosis or when a patient presents with persistent heel pain, for more than 3 months or if symptoms are worsening, diagnostic imaging is recommended to confirm the diagnosis and to rule out other differentials.  As a therapist dealing with runners, it is important to be aware of the multiple causes of heel pain and key differential diagnosis, other than plantar fasciitis.

This blog article is taken from our Running Rehab - From Pain to Performance Online Course. To learn more about the management of running-related foot and ankle injuries, including plantar fasciitis, check our comprehensive online Running Rehab Course with access to all information on initial assessment to management of all running injuries.
If you would like to watch another free webinar about hip pain in runners, feel free to sign up below!

Thanks a lot for reading!

Benoy Mathew,

Lower Limb Specialist Physio

Creator (Running Rehab Course)



De Garceau D, Dean D, Requejo SM, Thordarson DB. The association between diagnosis of plantar fasciitis and Windlass test results. Foot & ankle international. 2003 Mar;24(3):251-5.

Lopes AD, Hespanhol LC, Yeung SS, Costa LO. What are the main running-related musculoskeletal injuries?. Sports medicine. 2012 Oct;42(10):891-905.



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10 Mistakes Why ACL Rehab Regularly Fails

10 Mistakes Why ACL Rehab Regularly Fails – Are You Making These Mistakes?

10 Mistakes Why ACL Rehab Regularly Fails - Are You Making These Mistakes?!

The aim of this blog is to summarize the key aspects why we may fail to achieve optimal results after ACL injury and/ or ACL reconstruction. Note that this summary is not meant to blame anyone. But just to make sure we can do better in the future.

10 Mistakes Why ACL Rehab Regularly Fails

1) Lack of clinically applicable guidelines

The first limitation we are currently dealing with is that there are  only a limited amount or there is a lack of clinically applicable guidelines for rehabilitation after ACL injury and ACL reconstruction. Some guidelines have been published but these guidelines remain very general and non-specific.

2) Gap between research and practice

Secondly, there is clearly a gap between what we know from research and what is typically done in clinical practice. This can be due to many reasons. For example for many of us physical therapists, it can be very challenging to keep up to date. Given the fact that a lot of research remains behind a paywall and that we often have minimal time to dig into the individual studies while working all day in the clinic. Our ACL Rehab online course might offer of course a good opportunity to get up to date again. Furthermore, as mentioned in my first points the research findings are often too non-specific to apply directly in clinical practice.

3) Most patients are not ready when RTS

A third important barrier to achieve optimal results of ACL injury is that a lot of patients are not ready when they return to sport. A lot of patients just return because they think they can return based on no test, no criteria or just based on time after injury or reconstruction. They often lack the physical, psychological and physiological capacities to return successfully to sport and performance. Hereby increasing the chance for a second ACL injury or other lower extremity injuries or reduced performance and lower quality of life.

4) No criteria-based progression

Number four is related to the previous point actually. A lot of therapists progress the athletes during the rehab continuum based on no criteria or criteria that might not be sufficient to deal with the demands of the following phase or return to sport. A rehab based on criteria based progressions can be very helpful to set clear goals and guide your exercise prescription according to the functional level of your patient.


5) Low quality rehab
Point 5 is also really essential and is focused on the quality of the rehabilitation. Without optimal rehab, you will not go for results you are achieving or you wish to achieve. However, we see that the rehab quality is often relatively poor in general (Dingenen et al. 2021), not for everyone, but in general. And even though it might be very difficult to define high-quality rehab, there are some key points to pay attention to. First, I think we often fail to achieve the full potential of an athlete. This can be due to the fact that there is in general not enough knowledge on all aspects that need to be trained. Or a lack of knowledge and skills to be able to target all the aspects that need to be addressed in your rehab program to return to sport and to return to performance. In addition, we are often not specific enough in our exercise prescription. A detailed exercise prescription is important to achieve desired training goals. One of the points here that we also addressed in this online course is the fact that often rehab is underloaded. We need to train hard and smart to get the results that we want to achieve, especially if you really want to return to sports performance.

6) Rehab is often rushed
In point six, I want to remind you that there is no need to rush during rehab.There should be no such things as skipping a few steps or phases to speed up recovery. However, in reality we often progress too quick during rehab. We know that both from a functional but also from a biological perspective, you need time to achieve the maximum potential after this kind of serious injuries. In my online course we use a combination of criteria focusing on the functional status of the patients in combination with time after injury and potentially the reconstruction as well.

The take-home message here from this sixth point is then: don't hurry. Be patient. Take your time to improve and to achieve your goals. From a patient perspective rehab after ACL injury can be very tough journey.

7) Poor compliance & motivation
Studies have shown that patient compliance with the rehab program and motivation to do rehab are key points in the prognosis of the outcome. You can have the best rehab program in the world but an exercise therapy program can only be effective when it's effectively done. Patients who have a lower compliance and patients who don't follow the program as it should be and patients who have a lower motivation to do the rehab typically have less optimal outcomes after ACL injury and reconstruction. We as physical therapists play a key role in motivating the patients and keeping the compliance as high as possible. For example, by setting realistic expectations, having an open communication with your patients, setting goals both on the short and on the long-term. Provide feedback and engage the patient in the rehab program. Remember to progress your program, make it challenging and don’t forget to have some fun.

8) Rehab is not targeted to the individual
A scooping review of Linda Truong et al in 2020 reported that a lot of psychological, social and contextual factors are present and influence all stages of recovery following a traumatic sports-related injury. A better understanding of these factors and both at the time of injury, but also throughout the whole rehab, could assist in optimizing injury management. Or to achieve the desired results of the patient for example promoting return to sports but also promotes long-term quality of life and long-term joint health. What we often do wrong is that we don't target the intervention enough to the individual person in front of us. No two rehabs will be exactly the same. Not only because of the physical impairments associated with ACL injury or reconstruction but also because of the psychological, social and contextual factors having a strong influence on the recovery process.

Take home messages here: treat the person not only the knee.

9) Poor communication
Across the whole rehab process, a clear and open communication between all stakeholders involved is crucial. Depending on the level and age of the athletes different persons can be involved. As first of course, we think about the person himself. We use a patient-centered approach. It's not you as a physical therapist who should be important. It's all about the patient. You're working over long period of time with this patient so take care that you build a strong patient therapist relationship. In addition, communication with the orthopedic surgeon in case of an operation with the physician, athletic trainer, parents, maybe strength and conditioning coaches in some cases; all other people potentially involved are important. Everyone involved in the process should be on the same line. All of them should know what the specific goals and phases are What the patient can do or not to do. Personally, I think we as a physical therapist can have a leading role in this whole process. However this might also change over time in some circumstances where for example strength and conditioning coaches might take over when heading the patient back to performance training and on-field retraining. Especially on a higher level, getting a player back to performance It's really teamwork. On a lower level, it can be that the physical therapist takes the lead across the whole rehab process.
Take home messages: Work together. Share decisions and use an open communication with a patient in the center.

10) Regulations & Limitations of the healthcare system
The regulations and limitations of the healthcare system also play a role. Depending on the county where you working in, the insurance company of the patient, or the financial situation of your patient. The number of physical therapy visits might vary substantially. Some patients might only have a few sessions to complete this whole rehab program, which can hamper the quality also of the program, of course. And this can also lead to more difficult progressions across all the levels that are needed to return to performance. In this case, patient education very clear exercise prescription formulation, and trying to achieve very high patient compliance with the program and motivation with the rehab program will be even more important.


If you click on this link you can also find a summary of these 10 points in the infographic I made for you. I hope you enjoy reading and can learn some lessons from these points to improve the quality of your rehab program. 


Thanks for reading!


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Core Stability

The Myth Of Core Stability

The Myth of Core Stability & Its Role in Chronic Low Back Pain

“Yeah, you have a weak core, you gotta do core stability exercises man”. If we had received one cent per time that a weak or unstable core had been blamed for a patient's low back pain in the health or fitness industry, we would surely be millionaires by now. In this blog, we will have a look back in time to see where the idea of an unstable core came from and discuss why the concept is BS.

Hodges et al. (1996) Interestingly, the onset of the Multifi (MF) do not seem to differ in this study

Almost 25 years ago, Hodges et al. conducted a study in which they found a delayed onset of contraction of the transverse abdominis of 50 milliseconds when patients with chronic low back pain raised their contralateral arm compared to a healthy group.
This paper has triggered the core stabilization craze that we are still seeing in the health industry today. In short, the concept was born that the deep stabilizers, namely the transverse abdominis and the multifidi would act as a corset to stabilize the lumbar segments around mid-range, which was termed „neutral zone“. In 2008, however, a study by Alisson et al. measured the transverse abdominis bilaterally and found that both sides act independently. So the left side contracts when you raise your right arm and the other way round. They concluded that the TrA does not act as a corset and that the idea of the muscle as a bilateral stabilizer needs to be revised.



Anyways, let’s assume that the function of the TrA is still that of a stabilizer of the lumbar spine. While this delayed muscle onset was measured in a laboratory setting, we will have to ask ourselves if we can detect this „dysfunction“ in the clinic. In practice, the pressure biofeedback unit was invented to determine the function of the TrA and multifidi. But how accurate is this measure really? Lima et al. In the year 2012 compared the validity of the pressure biofeedback unit to electromyography and found a very poor diagnostic accuracy with both sensitivity and specificity of 60% - and then we are not talking about the delayed onset of contraction, but just A contraction of the muscles.
What about movement control tests? Luomajoki et al. (2008) Showed that a test battery of 6 different had a substantial intra- and inter-rater reliability. If you’re curious about the battery, check out the video in the top right corner. While these tests are reliable, we don’t know if they are also valid: In other words, how do patients with low back pain perform these tests compared to subjects without pain? And even if there was a marked difference between groups, how do we know if those movement “flaws” are relevant to the persistence of back pain?
We know that people move differently in pain and it could very well be that this altered movement strategy is an effect rather than the cause of pain.



But let’s continue and assume that the TrA has an important stabilizing function and that we can accurately detect patients with a delayed onset of contraction in the TrA and multifidi. What then happened in practice is that we started to perform training for those muscles in either supine or four-point kneeling position. But how is strength training gonna fix the timing issue? Lederman in 2008 compares that to trying to play to piano faster by exercising with finger weights and performing push-ups. On top of that how is being able to perform a draw-in maneuver in a supine position going to carry over to activities of daily living? The idea to train those muscles in a supine or kneeling position with slow speed contradicts the principle of specificity and similarity or transfer. The only thing that would make sense is to train the speed of movement and to hope that the system will somehow reset itself.

To overcome this issue, proponents of core stability came up with the solution to teach everyone to continuously brace their cores in order not to have to worry about onset timing. This proposal is completely abnormal and not how our nervous system works. Show me one patient who is consciously co-contracting voluntarily all the time – it’s not possible because our nervous system wants to perform a task and then organizes muscle activity to achieve that task and not the other way round. This is like driving in reverse all the time. That’s the same reason why most patients have such difficulty performing a proper draw in maneuver. Not sure if you are like me, but I always hated to give this exercise to patients because I knew it would be super weird and over-complicated to explain this exercise to patients and they would often not be able to do it even if I tried with different cues or the pressure biofeedback unit.

At last, we’d like to add that increased co-contraction of the trunk muscles happens involuntarily in a lot of patients with low back pain. The low back pain researcher Kjartan Vibe Fersum said the following (and we stole this from Jarod Hall’s lecture on the topic by the way) „If people in pain walk like a plank, maybe don’t put them in a plank“.

To make the story short, research has then also shown that training does not improve feed-forward activation of deep abdominal muscles (Vasseljen et al. 2012, Allison et al. 2012)

Okay, so now let’s say that unless all that we’ve stated earlier, we would be able to change the onset timing of the TrA and multifidi – does it even matter?
Credits to Jarod Hall again for assembling the following list of studies who have shown that:

  • No association between change in onset an LBP (Vasseljen et al. 2012)
  • Spine stabilization exercises in the treatment of chronic low back pain: a good clinical outcome is not associated with improved abdominal muscle function (Mannion et al. 2012)
  • Wong et al. (2014) – systematic review: changes in morphometry or activation of transversus abdominis following conservative treatments tend not to be associated with the corresponding changes in clinical outcome

If we look a bit broader than just the TrA or multifidi Steiger et al. (2012)  performed a systematic review looking at different target aspects of performance and their influence on treatment outcomes for low back pain. They found that the treatment effects could NOT be attributed to any change in the musculoskeletal system such as mobility, strength, or endurance.
This was to expect because there are no simple solutions to complex problems. Back pain is multi-factorial and research has shown that psychosocial factors like depression, anxiety, movement-related fear, coping, workplace satisfaction, etc. All influence the prognosis.
So to sum it up: 1) The TrA does probably not have a corset function to stabilize the spine. 2) We are not able to accurately assess TrA or multifidi function in practice. 3) Slow strength training for the TrA or multifidi does not transfer to onset timing of contraction of those muscles and research also shows that it’s not possible to alter onset timing. 4) Neither onset timing, nor strength or endurance of the TrA and multifidi are relevant for a positive outcome. If you are a regular follower this sounds a hell lot like the myth-busting we did for scapular dyskinesis, right? For all of those reasons, the very same researchers who have come up with the concept like Hodges or who have build research on this concept like Peter O’Sullivan or Chad Cook have all moved on. If they have abandoned the concept of core stability – and remember for some it was a huge part of their professional career – so can you!

But we’re not completely done yet and we ask you to keep reading a little bit longer. Despite all of the reasons we have mentioned, low-load motor control exercises do seem to be effective to improve low back pain. 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.

Saragiotto et al. (2016)

So while core stability is not the holy grail, it still is an option for rehab. However, this is not because the deep lumbar muscles are trained to fix an unstable spine. We think they work because they are useful especially at the beginning of a progressive loading program of the spine. Similar to other exercise programs, the positive outcome is likely to be explained by aspecific 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 leaving out the awkward draw in maneuvers, it’s okay to train your pelvic tilts, dead bugs, bird dogs, Waiter’s bow, and so on. But do them with the idea of a gradual loading program and not with the idea to selectively activate deep muscles to stabilize the spine. If the concept of an unstable spine is explained to a patient it can do a lot of harm and create unnecessary worry and fear-related movement.

Okay, this was a bit of a longer blog on the myth of core stability. As always, we’ve put all the references of this video into the description down below. More content like this on the spine can be found on our online course "Physiotherapy of the Spine". Thanks a lot for reading!



Allison GT. Abdominal muscle feedforward activation in patients with chronic low back pain is largely unaffected by 8 weeks of core stability training. Journal of physiotherapy. 2012;58(3):200.

Coulombe BJ, Games KE, Neil ER, Eberman LE. Core stability exercise versus general exercise for chronic low back pain. Journal of athletic training. 2017 Jan 1;52(1):71-2.

Hodges PW, Richardson CA. Inefficient muscular stabilization of the lumbar spine associated with low back pain: a motor control evaluation of transversus abdominis. Spine. 1996 Nov 15;21(22):2640-50.

Jarod Hall's Video on Back Pain and Core Stability: https://www.youtube.com/watch?v=LdukopYcBtk

Lederman E. The myth of core stability. Journal of bodywork and movement therapies. 2010 Jan 1;14(1):84-98.

Lima PO, Oliveira RR, Moura Filho AG, Raposo MC, Costa LO, Laurentino GE. Concurrent validity of the pressure biofeedback unit and surface electromyography in measuring transversus abdominis muscle activity in patients with chronic nonspecific low back pain. Brazilian Journal of Physical Therapy. 2012 Oct;16(5):389-95.

Luomajoki H, Kool J, De Bruin ED, Airaksinen O. Reliability of movement control tests in the lumbar spine. BMC musculoskeletal disorders. 2007 Dec 1;8(1):90.

Luomajoki HA, Beltran MB, Careddu S, Bauer CM. Effectiveness of movement control exercise on patients with non-specific low back pain and movement control impairment: a systematic review and meta-analysis. Musculoskeletal Science and Practice. 2018 Aug 1;36:1-1.

Mannion AF, Caporaso F, Pulkovski N, Sprott H. Spine stabilisation exercises in the treatment of chronic low back pain: a good clinical outcome is not associated with improved abdominal muscle function. European Spine Journal. 2012 Jul 1;21(7):1301-10.

Saragiotto BT, Maher CG, Yamato TP, Costa LO, Costa LC, Ostelo RW, Macedo LG. Motor control exercise for nonspecific low back pain: a Cochrane review. Spine. 2016 Aug 15;41(16):1284-95.

Smith BE, Littlewood C, May S. An update of stabilisation exercises for low back pain: a systematic review with meta-analysis. BMC musculoskeletal disorders. 2014 Dec 1;15(1):416.

Steiger F, Wirth B, de Bruin ED, Mannion AF. Is a positive clinical outcome after exercise therapy for chronic non-specific low back pain contingent upon a corresponding improvement in the targeted aspect (s) of performance? A systematic review. European Spine Journal. 2012 Apr 1;21(4):575-98.

Vasseljen O, Unsgaard-Tøndel M, Westad C, Mork PJ. Effect of core stability exercises on feed-forward activation of deep abdominal muscles in chronic low back pain: a randomized controlled trial. Spine. 2012 Jun 1;37(13):1101-8.

Wang XQ, Zheng JJ, Yu ZW, Bi X, Lou SJ, Liu J, Cai B, Hua YH, Wu M, Wei ML, Shen HM. A meta-analysis of core stability exercise versus general exercise for chronic low back pain. PloS one. 2012 Dec 17;7(12):e52082.

Wong AY, Parent EC, Funabashi M, Kawchuk GN. Do changes in transversus abdominis and lumbar multifidus during conservative treatment explain changes in clinical outcomes related to nonspecific low back pain? A systematic review. The Journal of Pain. 2014 Apr 1;15(4):377-e1.

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Kaltenborn’s Concave-Convex Rule – Flawed or Just Misinterpreted?

Kaltenborn's Concave-Convex Rule - Flawed or Just Misinterpreted?


The concave-convex rule by Freddy Kalternborn is taught in many physio school throughout the world and chances are high your have learned it too. But does its concept stand the test of time and evidence or is it flawed like many other concepts?

The rule in a nutshell

Schomacher (2009)

The concave-convex rule by Kaltenborn tells us which part of the joint capsule is stressed when we move an adjacent joint partner:

When a convex joint surface is moving, the roll and glide occur in the opposite direction.

When a concave joint surface is moving, the roll and the glide occur in the same direction.
You can watch a video in the top right corner in which we cover the concept in more detail

Kaltenborn used this knowledge of arthrokinematics to determine the appropriate direction of translational glide in order to determine which part of the joint capsule should be mobilized. But is it really that simple?



Does roll and glide happen in a joint according the rule?

Bayens et al. (2000) examined joint kinematics of the glenohumeral joint in the late preparatory phase of throwing and they found that glenohumeral joint does not act as a ball-and-socket joint. In their study, the humeral head actually translated posteriorly in the late cocking phase – contrary to what we would expect. There is more evidence showing that roll and glide in a joint does not seem to follow the Kaltenborn rule: Scarvell et al. (2019)  found that knee flexion was actually coupled with a posterior translation of the femoral condyles – contrary to what we would expect based on the Kaltenborn rule. The same is true for another study of Bayens et al. (2006) where they found a posterior translation of the radial head during supination in the proximal radio-ulnar joint, while the convex–concave rule predicts anterior gliding of the radial head. How can those findings be explained?

Schomacher (2009) argues that we should not forget that the humeral head is rolling posteriorly in the late throwing phase which will of course move the humeral head posteriorly. The net translation of the humeral head in this study is only a few millimetres. To put this into perspective, consider an adult-size humeral head with a circumference of 16 cm. A motion of 90° of GH joint abduction occurring purely due to a rolling motion (with no concurrent anterior glide at the articular surface) would theoretically cause the humeral head to just roll of the glenoid about 4 cm. Clearly, a significant, concurrent anterior glide of the humeral head must occur and the fact that the humeral head moves only a couple of millimetres is proof of a significant glide. So despite the results of Bayens, there is no contractiction to the Kaltenborn rule. In order to really say something about rolling and gliding, we have to differentiate between movement of the center of the head of the humerus and the movement of the joint surfaces, for example with dynamic radiographs.


Does the rule tell us which in which direction we have to mobilize?

Let’s look at a study by Johnson et al. in (2007) who used the concave-convex rule to increase external range of motion in patients with frozen shoulder:
Based on the the concave-convex rule of Kaltenborn the authors argued that in external rotation of the glenohumeral joint, the convex part (head of the humerus) will glide anteriorly, while it will roll posteriorly on the concave part (in this case, the glenoid) – similar to the reasoning we have for the apprehension test.

So what Johnson and colleagues reasoned that – following the Kaltenborn rule – they would have to perform posterior to anterior glides in order to increase external rotation. So one group performed PA glides, while the control group performed joint glides from anterior to posterior, so AP glides. The results were surprising as the PA intervention group improved external rotation by just 3 degrees, while the AP control group improved external rotation ROM by 31.3°

Although the PA group was mobilizing according to the Kaltenborn rule, the posteriorly directed joint mobilization technique was more effective than an anteriorly directed mobilization technique for improving external rotation ROM in subjects with adhesive capsulitis. Both groups had a significant decrease in pain.

Our takes on this study is first of all that we're wondering if external rotation is rather a spin movement in the joint than an actual roll and glide movement. We would rather expect a pure roll and glide in horizontal abduction. Second of all, Neuman (2012) points out that the convex-concave rule was never intended to establish the direction of a manual glide, applied at a joint, that would best increase a targeted movement. The rule merely describes the arthrokinematic pattern that minimizes the inherent migration of the center of the convex member in the direction of the roll.
Physiotherapist should not mobilize a pathological joint according to a rule, but treat pathological clinical findings, which are in correlation with the patient’s complaints. Neuman argues that perhaps the capsular tightness associated with the patients’ pathology caused the humeral head to migrate to a more anterior resting position than normal relative to the glenoid. The use of a posterior glide might have preferentially stretched parts of the capsule, allowing the humeral head to be more centralized relative to the glenoid. This new position might, in turn, have partially unloaded the anterior capsule, thereby allowing greater external rotation. Without objective data on which part of the capsule was most restricted and the position of the humeral head at the start and end range of motion, this scenario is purely a speculation, and others are possible.

The questions is: Can we even influence a joint capsule given that join mobilization only happens in the toe phase when we have a look at the stress-strain curve of collagen?
We might be able to create a little bit of creep if we hold the mobilizations at end-range, but as often with manual therapy, the effects are probably neurophysiological. That could also explain why it is probably less relevant which part of a certain capsule is stressed.

Bogduk (2005)


Is the Kaltenborn rule just misinterpreted?

Okay, let’s sum it up: Is the Kaltenborn concave-convex rule flawed or just misinterpreted? No, it still describes arthrokinematic movement in terms of role and glide in a joint. Can it be used to determine into which direction we have to mobilize in order to improve a specific osteokinematic movement? Probably less so. The rule might be a starting point, but for each patient we will have to assess limitations in range of motion and roll and glide individually, thereby keeping the low reliability in mind. Given the evidence on the working mechanisms of manual therapy it might be irrelevant which part of a joint capsule we are stressing as stretching a capsule is probably not possible and the effects on pain and increased range of motion are likely be achieved through this neurophysiological mechanism.



Baeyens JP, Van Roy P, Clarys JP. Intra-articular kinematics of the normal glenohumeral joint in the late preparatory phase of throwing: Kaltenborn's rule revisited. Ergonomics. 2000 Oct 1;43(10):1726-37.

Baeyens JP, Van Glabbeek F, Goossens M, Gielen J, Van Roy P, Clarys JP. In vivo 3D arthrokinematics of the proximal and distal radioulnar joints during active pronation and supination. Clinical Biomechanics. 2006 Jan 1;21:S9-12.

Neumann DA. The convex-concave rules of arthrokinematics: flawed or perhaps just misinterpreted?.

Schomacher J. The convex-concave rule and the lever law. Manual therapy. 2009 Oct;14(5):579.

Johnson AJ, Godges JJ, Zimmerman GJ, Ounanian LL. The effect of anterior versus posterior glide joint mobilization on external rotation range of motion in patients with shoulder adhesive capsulitis. journal of orthopaedic & sports physical therapy. 2007 Mar;37(3):88-99.

Scarvell JM, Hribar N, Galvin CR, Pickering MR, Perriman DM, Lynch JT, Smith PN. Analysis of kneeling by medical imaging shows the femur moves back to the posterior rim of the tibial plateau, prompting review of the concave-convex rule. Physical therapy. 2019 Mar 1;99(3):311-8.


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5 Reasons why you should be careful using clinical prediction rules in practice

5 Reasons why you should be careful using clinical prediction rules in practice

The Ottawa ankle are the classic example how great a simple clinical prediction rule can improve clinical practice. However, there are many challenges and barriers why you should be careful using clinical prediction rules in practice. In this blog article, we’ll discuss which problems CPRs are facing:

Clinical prediction rules (CPRs) are mathematical tools that are intended to guide clinicians in their everyday decision making. CPRs are created using multivariate statistical methods, are designed to examine the predictive ability of selected groupings of clinical variables. Clinical prediction rules may best be classified into three distinct groups: diagnostic, prognostic and prescriptive. Studies that focus on predictive factors related to a specific diagnosis are known as diagnostic CPRs. Clinical prediction rules that are designed to predict an outcome such as success or failure are considered prognostic. Clinical prediction rules designed to target the most effective interventions are identified as prescriptive. Their advantage is that they can help clinicians to make quick decisions that may normally be subject to underlying biases.

An example of a predictive CPR, which we will refer to in this video is the CPR of Flynn et al. (2002)  for the success of lumbar manipulation: If 3 or more of the following 5 items are present, the likelihood for success with manipulation is increased by a factor of 2.6, with 4+ or more with a factor of 24. These factors are no symptoms distal to the knee, onset of symptoms shorter than 30 days, a FABQ score <19, hypomobility of the lumbar spine and hip internal rotation of more than 35 degrees in at least one hip.


CPRs have to undergo 3 stages prior to full implementation in a clinical setting:

  1. Derivation: In this phase CPRs are derived using multivariate statistical methods to examine the predictive ability of selected groupings of clinical variables.
  2. Validation: The CPR is tested in a similar clinical setting (which is called internal validation), then the CPR is tested then different clinical setting (which is called external validation)
  3. Impact: Measurement of the usefulness of the rule in the clinical setting in terms of cost-benefit, patient satisfaction, time/resource allocation, etc. usually tested in randomized controlled trials

The last step would be the Implementation phase in which widespread acceptance and adoption of the rule in clinical practice is achieved.

Keogh et al. (2014) have found 434 individual rules up until the year 2014. Only 54,8% of them had been validated and merely 2.8% had undergone impact analysis. Most of the studies were conducted in the domain of cardiovascular and respiratory diseases followed by the musculoskeletal domain.

So the first caveat here is that although there are a lot of CPRs, many of them have not been validated, let alone have undergone impact studies and we can thus not say if using them will improve clinical practice. The CPR of Flynn is one of the few predictive CPRs we know that have been successfully validated two years later by Childs et al. (2004) in a randomized controlled trial. They found that the odds of a successful outcome of patients who were positive on the CPR with 4 out of 5 items compared to to patients who were negative on the rule and received exercise was 60.8.

Like the CPR of Flynn and colleagues, most clinical prediction rules used in musculoskeltal practice are predictive CPRS. Those CPRs use baseline criteria, called treatment effect modifiers which are gathered from a physical examination to inform the type of treatment that a patient should preferentially receive. Unfortunately, there are other potential pitfalls of clinical predictions rules, which Haskins and Cook (2016) pointed out in an editorial for the BJSM:

  1. A lot of simple, derivative modeling methods used by in many studies capture prognostic factors, rather than prescriptive factors. In other words, the rules identified patients who were going to improve anyway, regardless of the treatment they received. If we take the CPR of Flynn again, a duration of symptoms less than 30 days or no symptoms distal to the knee and a low level of fear avoidance are general positive prognostic factors who favor recovery independent of the treatment. In reality, the natural history associated with those signs and symptoms is very favorable, meaning that the improvement will not be associated with the care received, but with time.
  2. Many prescriptive CPRs contain non-modifiable factors such as age, gender or duration of symptoms that cannot be changed by treatment. To maximize the potential of the model the predictors should be mediating factors that can be influenced by treatment such as fear, catastrophizing, strength loss or flexibility
  3. Another important point is that factors included in the model should have high reliability. In case of the Flynn CPR, one factor in the model is “hypomobility of the lumbar spine”. A systematic review of van Trijffel et al. (2005) however, has shown that inter-rater reliability in the lumbar spine is only poor to fair. This will make it difficult for different raters using the CPR to use the same conclusion on this item.
  4. Most CPRs are underpowered due to insufficient sample sizes which lead to extremely wide confidence intervals indicating a lack of precision of a CPR’s predictive accuracy. In Flynn’s study we have a 95% confidence interval running from 4.63 to 139.41 in case of 4 or more positive items. So the effect of the manipulation in patients who score positive on the CPR can be moderate, but in can also be huge with and odds ratio of 139 in 95 out of 100 cases.

Alright, let’s summarize the reasons why we should be not blindly rely on CPRs for clinical practice: Most of the CPRs have only been derived, but never (successfully) validated, let alone have reached clinical impact phase. The outcomes in one study and a particular setting cannot be simply transferred to your clinical setting. A lot of factors in a CPR are positive prognostic factors who are associated with a favorable natural course. So those patients were going to improve anyways. At last, it’s important that reliable and modifiable factors are included into a model to maximize it’s potential, while studies should increase their sample sizes in order to describe the effect of the CPR with a higher precision.

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Adams ST, Leveson SH. Clinical prediction rules. Bmj. 2012 Jan 16;344:d8312.

Childs JD, Fritz JM, Flynn TW, Irrgang JJ, Johnson KK, Majkowski GR, Delitto A. A clinical prediction rule to identify patients with low back pain most likely to benefit from spinal manipulation: a validation study. Annals of internal medicine. 2004 Dec 21;141(12):920-8.

Cook C. Potential pitfalls of clinical prediction rules.

Chad Cook's Blog Article: https://relief.news/2016/09/05/rip-prescriptive-clinical-prediction-rules/

Flynn T, Fritz J, Whitman J, Wainner R, Magel J, Rendeiro D, Butler B, Garber M, Allison S. A clinical prediction rule for classifying patients with low back pain who demonstrate short-term improvement with spinal manipulation. Spine. 2002 Dec 15;27(24):2835-43.

Haskins R, Cook C. Enthusiasm for prescriptive clinical prediction rules (eg, back pain and more): a quick word of caution.

Keogh C, Wallace E, O’Brien KK, Galvin R, Smith SM, Lewis C, Cummins A, Cousins G, Dimitrov BD, Fahey T. Developing an international register of clinical prediction rules for use in primary care: a descriptive analysis. The Annals of Family Medicine. 2014 Jul 1;12(4):359-66.

van Trijffel E, Anderegg Q, Bossuyt PM, Lucas C. Inter-examiner reliability of passive assessment of intervertebral motion in the cervical and lumbar spine: a systematic review. Manual therapy. 2005 Nov 1;10(4):256-69.

Wallace E, Johansen ME. Clinical prediction rules: challenges, barriers, and promise.

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