The Myth Of Core Stability

The Myth of Core Stability & It's 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 patients low back pain in the health or fitness industry, we would surely be millionaires by now. In this video 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 came to the conclusion that the TrA does not act as a corset and that the idea of the muscle as a bilateral stabilizer needs to be revised.

 

Assessment:

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 are able to 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 a 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.

 

Treatment:

But let’s continue and assume that the TrA has an important stabilizing function and that we ARE able to 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 compare 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 supine position going to carry over to activities of daily living? The idea to train those muscles in 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 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 exactly the same reasons why most patients have such difficulty to perform 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 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 expected 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 have an influence on 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 programmes, 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 programme and not with the idea to selectively activate deep muscles in order 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!

 

References:

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.

 

References

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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References:

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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6 RISK FACTORS FOR TENDINOPATHY THAT YOU NEED TO KNOW (#5 MIGHT SURPRISE YOU!)

6 RISK FACTORS FOR TENDINOPATHY THAT YOU NEED TO NOW (#5 MIGHT SURPRISE YOU)

Tendinopathy has a multifactorial etiology that is not well understood. Risk factors are often separated into extrinsic factors, so those acting on the body from the outside and intrinsic factors, so all factors acting from within the body. In their narrative review, Peter Malliaras & Seth O'Neill (2017) discuss 3 different classes of risk factors. They are looking at:

1) Load-related (extrinsic) factors

2) Biomechanical (intrinsic) factors

3) Other individual and systemic factors (which can be classified as intrinsic) as well.

 

Load-related extrinsic factors

Figure from Komi et al. (2000)

1) Load: Stretch-shorten cycle loads        

Repetitive stretch-shortening cycles of the muscle tendon unit such as walking and running for Achilles tendinopathy or jumping for patellar tendinopathy are associated with tendinopathy. The tendon load may only be able to explain part of the story.  In running and submaximal hopping the Achilles tendon load is reported to be 6-8 times and 8-10 times bodyweight respectively, while the load during maximal isometric plantar flexion contraction is only 3.5 times bodyweight.
On the other hand, the load on the patellar tendon during squatting is similar to a spike jump take off with 4.8 times bodyweight and 5.2 times bodyweight respectively. The crucial difference between fast+high load activities and slow +high load activities like in rehab is the tendon strain rate. While in squatting it is about 1-2 times bodyweight per second, it is as high as 40 times bodyweight per second in a spike jump take off. This probably explains why tendinopathy is associated with repetitive stretch-shortening cycles while slow and heavy loading is not.

 

2) Compression:

A classic study by Soslowky et al. (2002) manipulated mice so that one group had an enlarged acromial roof (group E), another group was overloaded by downhill running (group OV) and a third group had both external compression and overload combined (Group OVE/E). The results of that trial showed that compression alone did not lead to pathology, but a combination of compressive and tensile loads was more damaging than tensile loads alone.

 

3) Change in load

The most common cause for tendinopathy are training errors involving sudden changes in load. This encompasses any fluctuations in intensity, frequency, or duration of exercise or a combination of all three. For this reason, tendinopathy is often seen in athletes in pre-season after a holiday break. Like mentioned before, important is a change in energy storage type of loads as they stress the tendon the most. When taking patient history in patients in who you suspect tendinopathy ask for hill or speed sessions, marathon or similar events, if they have bought a sports watch or Fitbit which motivated them to push harder, preseason breaks or a change in shoes or training surface

 

4) Load parameters

Higher Load duration, intensity and frequency are associated with  with patellar pain and Achilles tendinopathy. This fits the evidence of Magnussen et al. (2010) who have found that repeated intense loading without sufficient recovery may be a risk factor for tendon pathology. Be aware, that this association is not consistent however and that a change in load may be a confounder in this relationship.

 

5) Biomechanical and neuromuscular factors (intrinsic factors):

Individual biomechanics, including movement kinetics and kinematics, foot posture, flexibility, neuromuscular capacity and structural anatomy may influence tendinopathy risk. However, the relationship between biomechanics and the development of tendinopathy is a mess. If you want to have a look at individual articles, we are highly recommending to you to start with this narrative review of Malliaras & O'Neill (2017).
In general, it seems that extremes in biomechanics might be risk factors worth paying attention to during rehab. For example, both increased and decreased dorsiflexion are described as risk factors in the development of Achilles tendinopathy. The same is true for increased as well as decreased hamstring flexibility for patellar tendinopathy.

The link between neuromuscular changes and pain is even less clear. Comparable to other body regions and pathologies cross-sectional students don’t allow us to say if neuromuscular impairments such as decreased strength are a consequence of pain or if they are a risk factor leading to tendon pain.
For our rehab, this means the following: while a good loading program is necessary for all patients, interventions to target biomechanical factors and neuromuscular changes might be necessary for some patients who are at the extreme ends of the spectrum. Similar to other body regions and with all the individual variation in posture and movement between individuals it’s difficult to really say which posture or movement is “faulty”.
At last, if we do assume to have found a biomechanical or neuromuscular factor the question is if we are able to change those factors by therapy.

 

6) Individual and systemic factors (intrinsic factors):
Multiple systemic factors have been linked with tendinopathy including age, high cholesterol, adiposity and genetics. These systemic risk factors are thought to reduce the capacity of the tissue to tolerate load, gradually altering tendon capacity so that an extra walk, a quick dash across the road, or a day spent gardening may be sufficient to overload the tendon triggering symptoms. Systemic factors might also play a greater role in case of bilateral involvement or in tendinopathy where load seems to play a smaller role such as in pes anserinus tendinopathy.  Furthermore, these systemic factors combined with biomechanics might be able to explain why under similar loading conditions some athletes develop tendinopathy and others don’t. Finally, cognitive and emotional factors such as anxiety, illness beliefs and fear-avoidance behavior can influence a person’s pain experience and should not be disregarded.
The envelope of function by Scott Dye beautifully summarizes the risk factors involved in the etiology of tendon pain:

So the envelope of function is the load/frequency distribution defines the safe or homeostatic range of load acceptance. So if the combination of load and frequency exceed your envelop of function it will lead to pathology. It’s also interesting to see that suboptimal loading may lead to disuse effects, which we know is especially a problem in tendons. Peter Malliaras adds that biomechanics can directly influence the load in this graph.

On the side systemic and individual factors will all have an influence on an individual propensity to develop pain.

Alright, this was our blog on risk factors for tendinopathy. We hope you enjoyed reading it! If you love tendons and would like to learn more about the topic, check out our video on 7 absolutely crucial facts about tendon you didn’t know. As always, thanks for reading! Physiotutors

 

References

Magnusson SP, Langberg H, Kjaer M. The pathogenesis of tendinopathy: balancing the response to loading. Nature Reviews Rheumatology. 2010 May;6(5):262.

Malliaras P, O’Neill S. Potential risk factors leading to tendinopathy. Apunts. Medicina de l'Esport. 2017 Apr 1;52(194):71-7.

Soslowsky LJ, Thomopoulos S, Esmail A, Flanagan CL, Iannotti JP, Williamson JD, Carpenter JE. Rotator cuff tendinosis in an animal model: role of extrinsic and overuse factors. Annals of biomedical engineering. 2002 Sep 1;30(8):1057-63.

Isometrics in tendinopathy – a wonder weapon to decrease pain?

Isometrics in tendinopathy – a wonder weapon to decrease pain?

Are isometrics the wonder weapon to decrease pain in tendinopathy? In this blog we will discuss where the isometrics “trend” came from and what the evidence says about it!

In 2015 Dr. Ebonie Rio and colleagues started a bit of trend when they conducted a cross-over trial in 6 volleyball players with patellar tendinopathy. Their results were astonishing with all players experiencing an immediate decrease in pain from an average of 7/10 on the NRS to 0 with only one of the 6 reporting a remaining pain of 1– for at least 45 minutes after the isometric contractions.The protocol they used were 5 sets with 45 seconds contraction in a leg extension machine and an effort of 70% of the maximal voluntary effort. They also found that isometrcis were able to decrease cortical inhibition and an increase in strength of 19%.They compared the isometric intervention with an isotonic intervention and the effects seen in the isometric group could not be achieved in the isotonic group:

Figure from Rio et al. (2015)

The same authors did a follow up in-season study with jumping athlets two years later in which they compared an isometric programme and an isotonic programme to each other. In this study the results were a bit more heterogenous with both groups with a greater immediate pain decrease in the isometric group:

Figure from Rio et al. (2017)

A recent study by Holden et al. (2019) looked at the effect of isometrics in patellar tendinopathy as well and did not find any analgesic effect:

Holden et al. (2019)

However, a high percentage of women and a relative high average age is untypical for patellar tendinopathy, which is usually a disease of young jumping men. So it could be that the diagnosis of patellar tendinopathy was no correct in some cases.
Now while those two studies were conducted for patellar tendinopathy, let’s look if we can transfer these results to other tendons.
Looking at the Achilles tendon, Seth O’Neill and colleagues did a study in 2018 in which they had a group of patients with Achilles tendinopathy performing isometric contractions of the plantar flexors. They found no immediate pain relief nor improved motor output in patients with Achilles tendinopathy:

Figure from O'Neill et al. (2018)

A study of Riel et al. In the year 2018 examined the effects of isometrics, isotonics and walking on pain for plantar fasciitis. They found that there was no change in pain for any of the groups before to after the exercises:

Riel et al. (2019)

At last, Coombes et al. In the year 2016 looked at isometrics on lateral epicondylalgia. In their study, isometric contractions above the patients’ pain threshold actually increased their pain levels after the exercise, while isometric contractions below the patients’ pain threshold had no effect compared to a control group:

Figure from Coombes et al. (2016)

Another study from Stasinopoulos et al. In the year 2017 compared three exercise groups in the treatment of lateral epicondylalgia: One group performed eccentric training, another eccentric-concentric training and the third group combined eccentric-concentric training with isometrics. The authors argued that most grip activities require isometric contraction of the wrist flexors and extensors, so adding isometric exercises for LE makes absolute sense. They found that adding concentric led to superior results at pain, function and grip strength at 4 and 8 weeks:

Table from Stasinopoulos et al. (2017)

However, the follow up time of the study was rather short and should at least have been 12 weeks. On top of that the combined isometrics group performed a higher exercise volume with more time under tension which could explain the superior results.

So while isometrics are certainly no magic bullet, what role do they play in tendinopathy rehab? First of all,  isometrics are a great option to start exercising if everything else is too painful – and this is not only limited to tendinopathy but other conditions as well. Be aware that they must progress to isotonic exercises, because you want to recover muscle function over the full range of motion instead of just 1 angle. So move on as soon as a patient is able to tolerate isotonic loads.
What can be derived from all of those studies is that isometrics do seem to work really well in some subjects and can actually make things worse in other subjects. To keep it simple, give them a try with the patient in front of you and if they respond favourably, keep doing them, if they don’t move on.
While 45 minutes of pain relief might not be a goal that is important in the average patient, this might be useful for athletes as a warm-up to decrease pain during the ensuing exercise session or competition. Isometrics are also less tiring for athletes in-season as they are less tiring than isotonic exercises. One can surely argue if it is desirable to achieve short-term pain reduction in order to load a painful tendon during sporting activities and if this might actually lead to detrimental effects.

Alright, this was our blog on isometrics for tendinopathy. If you were surprised by the results, you will love our blog on 7 facts about tendinopathy you didn’t know! Thanks so much for reading. 

 

References:

Coombes BK, Wiebusch M, Heales L, Stephenson A, Vicenzino B. Isometric exercise above but not below an individual’s pain threshold influences pain perception in people with lateral Epicondylalgia. The Clinical journal of pain. 2016 Dec 1;32(12):1069-75.

Holden S, Lyng K, Graven-Nielsen T, Riel H, Olesen JL, Larsen LH, Rathleff MS. Isometric exercise and pain in patellar tendinopathy: A randomized crossover trial. Journal of Science and Medicine in Sport. 2020 Mar 1;23(3):208-14.

O’Neill S, Radia J, Bird K, Rathleff MS, Bandholm T, Jorgensen M, Thorborg K. Acute sensory and motor response to 45-S heavy isometric holds for the plantar flexors in patients with Achilles tendinopathy. Knee Surgery, Sports Traumatology, Arthroscopy. 2019 Sep 1;27(9):2765-73.

Rio E, Kidgell D, Purdam C, Gaida J, Moseley GL, Pearce AJ, Cook J. Isometric exercise induces analgesia and reduces inhibition in patellar tendinopathy. British journal of sports medicine. 2015 Oct 1;49(19):1277-83.

Rio E, Van Ark M, Docking S, Moseley GL, Kidgell D, Gaida JE, Van Den Akker-Scheek I, Zwerver J, Cook J. Isometric contractions are more analgesic than isotonic contractions for patellar tendon pain: an in-season randomized clinical trial. Clinical Journal of Sport Medicine. 2017 May 1;27(3):253-9.

Silbernagel KG, Vicenzino BT, Rathleff MS, Thorborg K. Isometric exercise for acute pain relief: is it relevant in tendinopathy management?.

Riel H, Vicenzino B, Jensen MB, Olesen JL, Holden S, Rathleff MS. The effect of isometric exercise on pain in individuals with plantar fasciopathy: a randomized crossover trial. Scandinavian journal of medicine & science in sports. 2018 Dec;28(12):2643-50.

Stasinopoulos D, Stasinopoulos I. Comparison of effects of eccentric training, eccentric-concentric training, and eccentric-concentric training combined with isometric contraction in the treatment of lateral elbow tendinopathy. Journal of Hand Therapy. 2017 Jan 1;30(1):13-9.

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