7 crucial facts about lower limb tendons


7 crucial facts you didn’t know about tendons

7 crucial facts about lower limb 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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Pathomechanics of lower limb muscle and tendon injuries



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.


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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