Bookmark and Share

Call us now at: 02 9922 6806

appointment times

Achilles Tendonosis

by Martin Krause


The Achilles tendon is a thick strong mass of avascular collagen fibres who attains it's nutrition through the process of diffusion of nutrients down a pressure gradient. Achilles injuries are usually classified into acute tears and paratendonosis. The latter occurs frequently in males over the age of 40, whose high testosterone and reduced chondroitin-6-sulphur levels mean that their collagen matrix has become drier and more brittle. Ironically, these people can present with swelling in the mid substance of the tendon due to neovascularization of the tendon. In contrast, acute ruptures of the tendon can occur at any age, and hence these people may present clinically with complete rupture of the Achilles substance from the bone, mid tendon or musculotendonous junction ruptures. It commonly occurs in sprinting and jumping sports where fast changes in muscular lengthening and shortening occur. People with large tight calves and those with a pes cavus (high arched) foot are at greater risk of getting such a tear. On the other side of the coin, are the people with long flattened arches which make them slow and/or weak in their supination component of push-off. These people frequently develop a mid medial calf tear. Over-active lateral gastrocnemius and underactive soleus have also been implicated as has excessive eversion of the ankle during the stance phase of gait. Finally, some people have a very low insertion of their deep calf muscle (the soleus) on the Achilles making the tendon inherently shorter. Complete and partial tears are treated with camwalker boots, complete immobilsation or surgery with or without autologous grafts such as using the plantaris tendon. 

MRI ruptured achilles

Chronic swelling inside the tendon sheath can lead to severe pain. Depending upon pathology a necrotic area of degeneration within the tendon may occur with concommittant blood vessel infiltration leading to further pain and swelling. Other factors leading to a potential Achilles problem also include myofascial-immune pathology, metabolic-immune-bursa pathology, and low back pathology (L5/S1 intervertebral disc), the latter resulting in neurologically generated tightness and weakness in the muscles of the calf and ankle. Additionally, people with chronic lateral ankle instability also seem to be at risk of Achilles tendonopathy. In fact, the inverse dynamics of energy transfer, where muscles crossing 2 joints are seen as energy straps, implicate the entire lower limb in Achilles pathology.

Creaby et al (Medicine & Science in Sports & Exercise . 49(3):549-554, March 2017.) found the impulse of the hip adduction and external rotation moments as well as the peak hip external rotation moment to be significantly increased in runners with AT compared with their healthy counterparts. However, the two groups displayed similar hip and ankle joint angles as well as ankle joint moments during running. The identified differences in hip joint biomechanics found in the present study compliments previous research that provided evidence of altered hip neuromuscular control in runners with AT (Azevedo et al, Br J Sports Med. 2009;43(4):288–92; Franettovich Smith et al, Med Sci Sports Exerc. 2014;46(3):594–9 ). Taken together, these findings reinforce the need to consider proximal lower-limb function in the assessment and rehabilitation of runners with AT.

Achilles Tendonopathy


Achilles tendonosis ultrasound CrossSectionalAchillesTendonosisUS

The kinetic chain

The Achilles tendon forms part of a kinetic chain of accelerating levers (bones) around which energy is transfered and dissipated through lengthening (eccentric) and shortening (concentric) contractions between the foot and thorax.

Inverse dynamics in an accelerating lower limb include the capture and release of kinetic energy through the conservation of angular momentum. 

Clinical implications of inverse dynamics

Tendons act as buffers, delay energy absorption by muscles and therefore act as attenuators and shock absorbers and hence have implications for neural control (Roberts & Konow 2013, Ex Sp Sc Rev, 41, 4, 186-193). If tendons are injured, or if a pain state exists the ability to engage the elastic components of movement is diminished. In fact, people with chronic ankle instability (CAI) have been shown to have decreased energy dissipation at the knee during jumping (Terada et al 2013, Med Sc Ex Sc, 44, 11, 2120-2128). CAI makes those people more likely to have injuries to the knee, hip and spine. Mind maps can be generated which illustrate the multifactorial nature of calf tightness and achilles pathology. It should be noted that this 'mind map' was generated 7 years before researchers vindicated the use of such an approach. This is a 'classic' example whereby clinical reasoning can define the treatment rationale even in the abscence of evidence based physiotherapy (EBP). In this case, the amelioration of clinical signs and symptoms provides the face and construct validity to drive the EBP, where the 'mind map' is a construct from a combination of energy transfer biomechanics and clinical reasoning.

Cognitve filtering

The mind map highlights the need to develop a structured approach to treating an Achilles tendon problem. Multiple hypotheses testing requires a mechanism of filtering multiple information so that the clinical signs and symptoms can be integrated with knowledge from pathophysiology, which subsequently generates decision making and treatment strategies based on testable clinical pattern generation.

Refinement of the working hypothesis

All clinical findings (impairments measures) need to be assessed in relationship to the subjective examination (disability measures, past and current history w.r.t mechanism of injury/onset and/or aggravating/easing factors) in order to determine a diagnosis and prognosis based on the stage, stability, irritability and severity of the disorder. This process should also identify whether we are dealing with misuse, overuse, abuse or disuse as a precipitating factor in it's onset and/or chronicity. By defining the disorder into these categories the clinician is consciuosly 'filtering' the multitude of information to form a 'clinical picture'.

Multimodal approach to multifactorial dimensions of a problem

The clinical reasoning process is used to confirm and negate correlations between the multiple variables. These findings must then be integrated into the neuro-matrix to determine a management plan which encompasses the goals and asperations of the client.

Predictive reasoning

The ultimate goal for the musculoskeletal physiotherapist is to integrate the neuro-matrix into a clinically useful management strategy where predictive reasoning enhances the clients confidence in their therapist and in their own decision making processes

Treatment options

Treatment could consist of

  • Camm walker boot
  • Dry needling, myofascial release & soft tissue massage
  • Kinetic or dynamic taping
  • Foot - ankle taping, orthotics/heel raise
  • Muscle energy techniques for lumbar spine - SIJ dysfunction
  • Metabolic consideration - Mg-Ca, Na-K balance
  • Nutritional Considerations - protein-carbohydrate, creatine supplementation
  • Joint mobilisation to the foot, inferior and superior fibula, hip, sacrum & lumbar spine
  • Functional closed chain oscillatory eccentric - concentric exercises for lumbar spine, hip, knee and ankle
Whilst working at The Rennbahn Klinik, Basel, Switzerland, (1992-1993) we found that there was a tendency for an increased incidence of Achilles tendinosis in athletes with a history of chronic lateral ankle instability. We demonstrated that as the subjects go into plantar flexion, during heel raising, there is a tendency for increased shortening on the medial side of the tendon due to excessive inversion accompaning plantarflexion.
Furthermore, some instances of chronic lateral ankle instability are accompanied by a subluxating navicular (due to torn talonavicular ligament) which causes prolonged pronation during mid stance, with reduced supination and hence power during 'push off'. Additionally, vibrotactile deficits, of the plantar surface of the foot, have been identified adults with chronic ankle instability (Hoch et al 2012, Med Sc Sp Ex, 44, 4, 666-672). These changes may reflect alterations in spinal and cortical neuronal processing in the central nervous system which may affect peripheral afferent receptor activity. These may be powerful arguments for 'feedforward training', virtual reality balance training and the use of soft tactile orthotics and barefoot running on variable surfaces such as soft sand, 'FinnenBahnen' and pine forest.

Lateral ankle instability contributing to a Achilles tendonopathy

If lateral ankle instability is accompanied by calcaneal valgus during mid stance (foot flat phase), then the medial aspect of the achilles is lengthened greater than the lateral aspect, creating torsion within the tendon. Subsequently, such torsion results in weakened push off and paradoxically excessive calcaneal varus on heel raising, reversing the medial-lateral lengthening and tension relationship within the achilles. Therefore, ankle instability needs to be addressed in the management of Achilles Tendinosis.

Motor control of countermovement jumps

Countermovement jumps have been demonstrated to improve with eccentric Achilles tendon loading. Neural modulation of the muscle -tendon control strategy was shown to change after 1 bout of practice. These changes included a decrease in the magnitude of fascicle lengthening and shortening, which was accompanied by an increase in tendon shortening without a change in ankle ROM (Hirayama et al 2012, Med Sc Sp Ex, 44, 8, 1512-1518). Motor control suggests that the 'degrees of freedom' are controlled using a mass spring analogy of oscillations around a point of CNS stability. This stability is based on the balance of muscle tone as well as predicted feedforward movement oscillations.

Plyometrics and eccentric muscle adaptation (Martin Krause 2003)

The eccentric component to this exercise cause more profound changes to the connective tissue of the muscle (broadening and streaming of Z bands). Investigations into eccentric exercise revealed pain 8 hours after initial exercise which was maximal 48 hours later (Newham, Mills, Quigley, Edwards 1983). These investigators found low frequency fatigue 10 minutes after a 20 minute period of stepping (Newham et al 1983). Additionally, they demonstrated progressive increases in IEMG during the exercise in the rectus femoris (160% increase) and vastus medialis (140% increase) in the eccentric contracting leg (Newham et al 1983). Mechanical damage to the sarcoplasmic reticulum resulting in less calcium release for each excitatory action potential was suggested as the cause of the low frequency fatigue (Newham et al 1983).

Muscles undergo fatigue and weakening after several bouts of concentric and eccentric exercise. Moreover, this fatigue and weakness is usually more extreme after eccentric exercise in the untrained individual. A number of sites in the myo-fibrillar complex such as reduce binding sensitivity and capacity of Troponin C for calcium, altered troponin-tropomysosin interaction to impaired binding and force generation by actin and myosin have been implicated in impaired force generation (Green 1990). Indeed, in the absence of any association between relaxation rates and Calcium kinetics raises support for the notion of a rate-limiting process controlling the relaxation of fatigued muscles being located in the contractile proteins (Hill et al 2001). During fatigue the relaxation times can be prolonged as much as 50% (Bigland-Ritchie et al 1986) thus resulting in increased force generation during sub-maximal stimulation due to tetanic fusion despite a substantial fall in the maximum tetanic force (Bigland-Ritchie et al 1986).

The initial overall loss of force production seen may be due to Desmin and Titan damage (Lieber & Friden 2002). Desmin acts as an extra-sarcomeric mechanical stabilizer between adjacent Z discs and the attachment to the costomere at the sarcolemma (Lieber, Shah & Fridén 2002). The costomere complex contains Talin, Vinculin & Dystrophin which attach to the trans-sarcolemmal proteins Integrin and Dystrophin associated proteins. These proteins allow the lateral transmission of force from actin to the basal lamina containing type IV collagen which is contiguous with the endomysium (Kovanen 2002). Desmin loss after eccentric exercise can occur within 5 minutes, possible as a result of increased intracellular Calcium leading to Calpain activation and selective hydrolysis of intermediate filament network (Lieber & Fridén 2002).  This may result in the ‘popping of sarcomeres’ of different length may loose their myofilament overlap of actin and myosin (Lieber & Fridén 2002). Hence, reduced force production would be expected. Additionally, the release of matrix metalloproteinase (MMP) which may degrade the extramyocellular type IV collagen (Korskinen, Kovanen, Komulainen et al 1996). However, this effect occurs many days after exercise (Korskinen et al 1996) and could even effect torque production 28 days after exercise (Lieber & Fridén 2002). This has significant implications in exercise training prescription.

Tendon properties under loading

A meta-analysis of increased loading on in-vivo tendon propeerties (Wiesinger et al 2016, Med Sc Sp Ex,47, 9, 1885-1895) confirmed a nearly systematic change in tendon properties with training. The patella tendon appears more amenable to change than the achilles tendon in terms of tendon stiffness. A rapid increase in Young's modulus is often paired with tendon stiffening and remains elevated within the first months of trainng in a rather monotonic fashion, whereas long term, years of training was associated with a larger tendon cross sectional area, without any evidence of differences in material properties. Mechanisms of change include extracellular matrix (ECM) enzymes involved in collagen turn-over, such a matrix metalloproteinases. Furthermore, an up-regulation of the stress response cytokines and growth factors (insulin like growth factor or transforming factor-beta-one) have been observed in Acchiles tendons in vivo and patella tendons in vitro.

Is muscle injury the result of an imbalance between intra-muscular transverse and longitudinal forces?

Is muscle tightness due to an imbalance between force and velocity and hence the development of power? This highlights the need for specificity with training and rehabilitation.

Force damping and recoil leads to efficient transfer energy which in the case of walking has been related to sinusoidal movement. Longer lower limb tendons, especially the Achilles Tendon, and stiffer lower limb joints have been shown to lead to improved running efficiency (Hunter et al 2011, Med Sc Ex Sp, 43, 8, 1492-1499). Clinically, however, we need to differentiate between the 'floppies' and the 'stiffies' as tendon-muscle complexes can be long and stiff as well as short and stiff in individuals with strong collagen complexes versus those with weaker more pliable ones. Other investigators also found that six weeks of plyometrics training improved running performance and the ECR (energy cost of running) despite no measurable changes in MHC (myosin heavy chains) and titin isoforms. This plyometric intervention improved 3000m time trial performance and oxygen consumption. Plyometric training consisted of 15 sessions. The sessions included total contact time of between 60 to 228, and the intensity of vertical jumps increased progressively using a slightly modified Spurrs protocol to avoid injury. Vastus lateralis was used as a biopsy site. (Pellegrino et al 2015, Med Sc Sp Ex, 48, 1, 49-56). In my clinical experience, regardless of the site of lower limb tendonopathy, similar to principals of myofacial trains (eg deep myofascial train of the calf is continuous with underside of the patella), the entire kinetic chain needs to be treated and the plyometric exercise protocol should resemble sporting specificity. For example, soccer players should be able to do at least 3 sets of 30 heal drop/raises, 3 sets of 90 one leg bridging, 3 sets of 90 hip drop/hitches and 6 sets of 60 quads 'hover' eccentric/concentric activity.  

The concepts of Young's modulus of elesticity and the Hills Model of viscoelasticity should not be confused with the Mass-Spring Concept of motor control and Inverse Dynamics.

Conclusion : the Swedish method of treatment using eccentric calf loading for optimal collagen alignment

The Swedish method of rehabilitation for Achilles Tendinosis has used the concepts of eccentric loading to propogate nutrition to the muscles, encourage lengthening of the actin-myosin resting position as well as improve viscoelasticity through enhanced collagen turnover. Thereby, a mechanical input is transduced to a cellular response. However, Achilles tendinopathy has an aberrant strain response to eccentric exercise. Researchers concluded that Achilles Tendinosis is a bilateral systemic process where they found that both the symptomatic and asymptomatic tendons were thicker and hypoechoic when compared with control tendons. Furthermore, they showed altered fluid movement within the tendon matrix which was characterized by lower acute anteroposterior response to eccentric exercise (Grigg et al 2012, Med Sc Sp Ex, 44, 1, 12-17). Moreover, human muscle proteome modification after acute or repeated eccentric exercises is towards a switch to an oxidative metabolism Hody et al 2011, Med Sc Sp Ex, 43, 12, 2281-2296), which suggestive of protection against DOMS as well as a progenetor for recovery and repair.

The science behind a 12 week eccentric training for Achilles Tendonosis are an increase in collagen synthesis (Langberg et al 207) and reduced neovascularization (Ohberg et al 2004) leading to reduced capillary engorgement and improved venous return (Knobloch et al 2007). These latter authors demonstrated a 45% improvement in capillary blood flow and reduced pain on a VAS after a 12 week eccentric training progam. Furthermore, Webborn (2008) suggested that clinical improvements were also related to nerve blood flow issues coined "neoneurovascularization". Achilles tendon stiffness has been shown to increase with plantar flexion training by between 16% and 29% (Kubo & Ikebukuro 2012 Med Sc Sp Ex, 44, 11, 2111-2117). However, these values are lower than increases of between 58% and 83% in patella tendon stiffness after knee extensor training. These results suggest a difference in the plasticity of the two tendon types. Furthermore, sprinters appear to have a more elastic patella tendons, whereas endurance runners had stiffer patella tendons when compared to lesser trained individuals. These differences appear to be the result of higher blood flow in the patella tendon when compared with the achilles tendon (Kubo & Ikebukuro 2012). Improvements in blood flow to the Achilles tendon was only shown after repeated contractions of 70% MVC whereas 50% MVC showed no change in perfusion. Furthermore, these investigators demonstrated improvements (7.7%) in achilles tendon perfusion (total haemoglobin and oxygen saturation) from 20 minutes of heating using a hot pack. The generalised reduction in Achilles perfusion when compared to the patella tendon may partially explain the greater propensity to rupture achilles tendons.

Achilles tendon stiffness has been shown to increase with plantar flexion training by between 16% and 29% (Kubo & Ikebukuro 2012 Med Sc Sp Ex, 44, 11, 2111-2117). However, these values are lower than increases of between 58% and 83% in patella tendon stiffness after knee extensor training. These results, in line with previous comments, suggest a difference in the plasticity of the two tendon types. Furthermore, sprinters appear to have a more elastic patella tendons, whereas endurance runners had stiffer patella tendons when compared to lesser trained individuals. These differences appear to be the result of higher blood flow in the patella tendon when compared with the achilles tendon (Kubo & Ikebukuro 2012). Improvements in blood flow to the Achilles tendon was only shown after repeated contractions of 70% MVC whereas 50% MVC showed no change in perfusion. Furthermore, these investigators demonstrated improvements (7.7%) in achilles tendon perfusion (total haemoglobin and oxygen saturation) from 20 minutes of heating using a hot pack. The generalised reduction in Achilles perfusion when compared to the patella tendon may partially explain the greater propensity to rupture achilles tendons.


Knobloch K et al (2007) Eccentric training decreases paratendon capillary blood flow and preserves paratendon oxygen saturation in chronic Achilles tendinopathy. Journal Orthopeadic Sports Physical Therapy, 37, 5, 269-276

Kubo K, Ikebukuro T (2012) Blood circulation of Patella and Achilles tendons during contractions and heating. Med Sc Sp Ex, 44, 11, 2111-2117

Langberg H et al (2007) Eccentric rehabilitation exercises increases peritendinous type I collagen synthesis in humans with Achilles tendinosis. Scandinavian Journal Medicine Science Sports, 17, 3, 298-299.

Webborn ADJ (2008) Novel approaches to tendonopathy. Disability Rehabilitation, 1-6.

Requires an eccentric muscle contracting and elongating progam

See links to

Achilles Tendonosis (Pdf)

Foot Biomechanics and the effects of orthotics

Metabolic - Nutritional considerations

Muscle energy techniques

Last update : 20 February 2017


Trending @ Back in B Physio

  • Thu 14 Sep 2017

    Cervical Spine implications in concussion

    Neck aetiology in Post Concussion Syndrome (PCS) symptoms A 14 year old son of a friend of mine presented to A&E, in August 1016, after receiving an impact to the head during AFL (Australian Rules Football). Althogh his SCAT3 scores were relatively mild, he went on to suffer severe lethergy, resulting in a lengthy abscence from school, culminating in a return to school for exams in the first week of December 2016. By December, even a 30 minute walk was extremely fatiguing. To place this into perspective, he had been playing academy grade AFL for several seasons and was an extremely fit outdoor adventurer. Confounding Variables : end of season injury and hence no follow up from the academy suffers from Hypermobile Joint Syndrome (HJS) and possibly Ehlers Danlos Syndrome (EDS), however Beighton score 4/9. suffers from food intolerances, particularly to Glutin and diary, but also some other foods. Potential IBS. had just gone through a growth spurt (190cm) Imaging : Brain MRI normal Medical Examination : Balance remained impaired to tandem walking and single leg stance. The vestibular occular motor scale showed significant accomodation deficit of 15cm and there was a mild exacerbation of symptoms. ImPACT testing revealed adequate scores and reaction time of 0.65 which is within acceptable range. History : School holidays December - January. Return to school and was placed in the lower classes. Prior to his concussion he was a top 10 student at an academically selective high school. Took up basketball and rowing as summer sports. Academic results tanked. Several Basketball injuries (Feb - April 17') as a result of what apppeared to be muscular imbalances from the relatively recent growth spurt, as well as taking on a new sport. Showed little interest in returning to AFL as no-one had followed him up during the previous year.  Current History : September 2017 showed a continued decline in academic levels. School teachers noted an inability to concentrate. Academic results still well below pre-concussion levels. Fatigue continuing to be problematic.  Literature Review : Post Concussion Syndrom (PCS) is defined as "cognitive deficits in attention or memory and at least three or more of the following symptoms: fatigue, sleep disturbances, headache, dizziness, irritability, affective disturbance, apathy, or personality change" Predictors of PCS are uncertain. However, the following clinical variables are considered factors at increasing risk. These include prior history of concussion, sex (females more prominant), younger age, history of cognitive dysfunction, and affective disorders such as anxiety and depression (Leddy et al 2012, Sports Health, 4, 2, 147-154). Unlike the 'old days' which recommended a dark room and rest for several weeks post concussion, the consensus appears to be a graded return to exercise in order to restore metabolic homeostasis. Incredibly, highly trained young individuals can find even exercises in bed extremely demanding. Kozlowski et al (2013, J Ath Train, 48, 5, 627-635) used 34 people 226 days post injury to conclude significant physiological annomalies in response to exercise which may be the result of 'diffuse cerebral swelling'. Researchers have noted lower systolic and higher diastolic blood pressure in PCS (Leddy et al 2010, Clin J Sports Med, 20, 1, 21-27). Due to autonomic dysfunction manifested in altered cardiovascular and pulmonary responses (Mossberg et 2007, Arch Phys Med Rehab, 88, 3, 15-320) some clinicians have recommended the use of the exercise program for POTS (Postural Orthostatic Tachycardia Syndrome). This is a 5 month program which recommends only exercise in the horizontal position for 1-4 months, including recumbent bike, rowing ergometer and swimming laps or kicking laps with a kick board. Month 4 upright bike and Month 5 upright training such as a elliptical trainer or treadmill. Progressive exercise therapies have also included 20 minutes per day, 6 days per week, for 12 weeks of either treadmill or home gym exercises at 80% of the heart rate at which their concussion symtoms are exacerbated. Their programs were individually modified as the heart rate provoking symptoms increased. When compared to the 'control group', this intervention was shown to improve cerebral perfusion on fMRI, increase exercise tolerance at a higher heart rate, less fatigue and were showing activation patterns in areas of the brain on performing math processing test which were now normalised (Leddy et al 2010, Clin J Sports Med, 20, 1, 21-27). Graded exercises could also have included 'motor imagery' as espouse by the NOI group and the work of Lorrimer Moseley (University South Australia) when dealing with chronic pain. Ongoing Symptoms : The literature review by Leddy et al (2012) found that ongoing symptoms are either a prolonged version of concussion pathophysiology or a manifestation of other processes, such as cervical injury, migraine headaches, depression, chronic pain, vestibular dysfunction, visual disturbance, or some combination of conditions. Physiotherapy Assessment : One year PCS, fatigue continued to persist. Cognitive deficits with school work were becoming more apparent. Assessment using various one leg standing tests employing oscillatory movement aroud the hips and knees for kinetic limb stability and lumbopelvic stability, which had been employed 6 months previously for Basketball injuries were exhibiting deficits, despite these being 'somewhat good' previously. Due to the Joint Hypermobility Syndrome (JHS) it was difficult to ascertain neck dysfunction based on range of movement testing. Palpation using Australian and New Zealand manual therapy techniques revealed marked muscle spasm throughout the cervical spine. Thoracic ring relocation testing also revealed several annomalies, which may have also accounted for some autonomic dysfunction. Eye - Neck proprioceptive assessment using blind folds and laser pointer also demonstrated marked variance from the normal. Occulomotor assessment and training Headache : Commonly referred to as cervicogenic headaches, one in five headaches in the general population are thought to be due to the cervical spine. The Upper Cervical Spine is particularly vulnerable to trauma because it is the most mobile part of the vertebral column, with a complex proprioceptive system connecting the vestibular apparatus and visual systems. It also coincides with the lower region of the brainstem and fourth ventricle. The brainstem houses many neurones associated with autonomic responses to pain and balance. Imaging of the fourth ventricle for swelling of the 'tonsils' and Arnold Chiari malformations are recommended when symptoms persist. In particular, children and adolescents are more vulnerable to neck contusions due to the proportionately larger head and less developed musculature. Cervical vertigo and dizziness after whiplash can mimic symptoms of PCS.. Mechanoreceptor dysfunction and vertebrobasilar artery insufficiency should be part of the differential diagnosis. Mechanical instability of the Upper Cervical Spine should also not be missed. Cervicogenic Headaches Further Interventions : Neurocognitive rehabilitation of attention processes. Psychological intervention using cognitive behavioural therapy (CBT). Neuro-opthalmologist to assess and treat smooth pursuit eye tracking. Naturopath for food intolerances. Conclusion  Investigations into people with persisting PCS applied more force over time to control balance. Helmich et al (2016, Med Sc Ex Sp, 48,  12, 2362-2368) proposed that in regard to cognitive processes, the increase of cerebral activation indicates an increase of attention demanding processes during postural control in altered environments. This is relevant in so far as individuals with post concussive symptomatology have a variety of symptoms including headache, dizziness, and cognitive difficulties that usually resolve over a few days to weeks. However, a subgroup of patients can have persistent which last months and even years. Complications in differential diagnosis, can arise clinically, when neck dysfunction and altered motor control occur concurrently due to both neck and cerebral pathology. For example, Whiplash and other traumatic head and neck injuries can result in pathology to both regions, whereas, more discreet altered cognitive processing from concussion can result in altered neck motor control. Uploaded : 16 September 2017 Read More
  • Thu 24 Aug 2017

    Pain in the Brain - neural plasticity

    Pain in the Brain and Neural Plasticity There are several mechanisms that can create a sensation of pain, which has been described as 'an unpleasent sensory and emotional experience in response to perceived or potential tissue damage'. Pain can be the result of peripheral sensitisation from peripheral inflammation, vascular compromise, necrosis, swelling, etc. Importantly, higher centres of the central nervous system not only perceive such sensitization of the peripheral nerve receptors, they can also modulate and control the intensity and tolerability of the perceived sensation through descending modulation at the peripheral receptor and in the spinal cord and through transcortical mechanisms depending on the 'meaning' and 'context given to the pain. Moreoever, the higher centres can create a 'state' of perceived 'threat' to the body through emotions such as fear and anxiety. Rather than the brain acting as a filter of unwanted sensation, in the higher centre induced pain state, rumination and magnification of sensations occur to create a pathological state.  Paradoxically, representation of body parts such as limbs and individual muscles can reduce in perceived size. In such instances the pain doesn't represent the sensation of pathology but rather pain has become the pathology. Hence, the brain generates pain in the brain, where the pain is perceived to be some sort of non-existant inflammatory or pathological sensation in the periphery. Evidence for this neural plasticity comes from imaging studies, where brain white matter structural properties have been shown to predict transition to chronic pain (Mansour et al 2013, Pain, 154, 10, 2160-2168). Specifically, differential structural connectivity to medial vs lateral prefrontal cortex and connectivity between medial prefrontal cortex and nucleus accumbens has been shown in people with persistent low back pain. In this case the back pain becomes the inciting event and given the persons' structural propensity, establishes specific functional coonectivity strength.  further reading Peripheral input is a powerful driver to neuroplasticity. Information gathered by touch, movement and vision, in the context of pain can lead to mal-adaptive plasticity, including the reorganisation of the somatosensory, and motor cortices, altered cortical excitability and central sensitisation. Examples of somatosensory reorganisation come from the work of Abrahao Baptista when investigating chronic anterior knee pain, who not only demonstrated reduced volume of Vastus Medialis but also is cortical translocation to another part of the cortex.   The same researcher has shown that maximal tolerable electrical stimulation (eg TENS) of muscles can induce normalisation of the cortical changes through a process called 'smudging'. Transcortical stumilation has also been applied as a cortical 'primer' prior to the application of more traditional therapy such as motor re-training, exercise, and manipulation. Body illusions are another novel way to promote the normalisation of cortical function through adaptive neuroplasticity. Examples come from people with hand athritis, whose perception of their hand size is underestimated (Gilpin et al 2015 Rheumatology, 54, 4, 678-682). Using a curved mirror, similar to that in theme parks, the visual input can be increased to perceive the body part as larger (Preston et al 2011 DOI: 10.1093/rheumatology/ker104 · Source:PubMed ) . Irrespective of size, watching a reflection of the hand while performing synchronised movements enhances the embodiment of the reflection of the hand (Whitkopf et al 2017, Exp Brain res, 23, 5, 1933-1944). These visual inouts are thought to affect the altered functional connectivity between areas of the brain thereby affecting the 'pain matrix'. Another, novel way of looking at movement and pain perception is the concept of the motor engram. This has been defined as motor skill acquisition through the modification and organisation of muscle synergies into effective movement sequences. The learning process is thought to be acquired as a child through experientially based play activity. The specific neural mechanisms involved are unknown, however they are thought to include motor map topography reflecting the capacity for skilled movement reorganisation of motor maps in a manner that reflects the kinematics of aquired skilled movement map plasticity is supported by a reorganisation of cortical microcircuitry involving changes in synaptic efficacy motor map integrity and topography are influenced by various neurochemical signals that coordinate changes in cortical circuitry to encode motor experience (Monfils 2005 Neuroscientist, 11, 5, 471-483). Interestingly, it is an intriguing notion that accessing motor engrams from patterns aquired prior to the pain experience might lead a normalisation of brain activity. My personal experience of severe sciatica with leg pain, sleepness nights and a SLR of less than 30 degrees, happened to coincide with training my 9 year old sons soccer training. I was noticing that the nights after i trained the children, I slept much better and my range of movement improved. I commenced a daily program of soccer ball tricks which i had been showing the kids, including 'juggling', 'rainbows' and 'around the worlds'. Eventually, I even took up playing soccer again after a 30 year abscence from the sport. Other than new activity related pain issues (DOMS), four years on, the sciatica hasn't returned. I can only conclude that this activity activated dormant childhood motor engram, worked on global balance, mobilised my nerve, encouraged cross cortical activity and turned my focus into finctional improvement. Alternatively, the altered pain state can result in a hostage like situation, whereby the pain takes control. Similar to the 'Stockholm Syndrome' where the hostage begins to sympathise with their captors, so do some peoples brain states, where it begin to sympathise with the pain, creating an intractable bondage and dysfunctional state.  Uploaded : 28 August 2017 Read More
  • Thu 03 Aug 2017

    Sickle Cell Trait and Acute Low Back Pain

    Researchers believe that lumbar paraspinal myonecrosis (LPSMN) may contribute to the uncommon paraspinal compartment syndrome and that sickle cell trait (SCT) may play a role. Sustained, intense exertion of these lumbar paraspinal muscles can acutely increase muscle size and compartment pressure and so decrease arterial perfusion pressure. This same exertion can evoke diverse metabolic forces that in concert can lead to sickling in SCT that can compromise perfusion in the microvasculature of working muscles. In this manner, they believe that SCT may represent an additional risk factor for LPSMN. Accordingly, they presented six cases of LPSMN in elite African American football players with SCT. See link below Read More
  • Thu 03 Aug 2017

    Ibuprofen, Resistance Training, Bone Density

    Taking Ibuprofen immediately after resistance training has a deleterious effect on bone mineral content at the distal radius, whereas taking Ibuprofen or undertaking resistance training individually prevented bone mineral loss. Read More
  • Tue 11 Jul 2017

    Mitochondrial Health and Sarcopenia

    The aging process (AKA 30 years of age onwards), in the presence of high ROS (reactive oxygen species) and/or damaged mitochondrial DNA, can induce widespred mitochondrial dysfunction. In the healthy cell, mitophagy results in the removal of dysfunctional mitochondria and related material. In the abscence of functional removal of unwanted mitochondrial material, a retrograde and anterograde signalling process is potentially instigated, which results in both motor neuronal and muscle fibre apoptosis (death) (Alway, Mohamed, Myers 2017, Ex Sp Sc Rev, 45, 2, 58-69). This process is irreversible. Investigations in healthy populations, have shown that regular exercise improves the ability to cope with regular oxidative stress by the buffering and 'mopping up' of ROS agents which are induced as a result of exercise. It is plausible and highly probable that regular exercise throughout life can mitigate against muscle fibre death (Sarcopenia). Importantly, this process of muscle fibre death can commence in the 4th decade of life. and be as much as 1% per year. Reduction of muscle mass can result in immune and metabolic compromise, including subclinical inflammation, type II diabetes as well as the obvious reduction in functional capacity for activities of daily living. Published 11 July 2017 Read More
  • Thu 22 Dec 2016

    Ehlers Danlos Syndrome

    Is your child suffering Ehlers Danlos Syndrome? Hypermobile joints, frequent bruising, recurrent sprains and pains? Although a difficult manifestation to treat, physiotherapy can help. Joint Hypermobility Syndrome (JHS) When joint hypermobility coexists with arthralgias in >4 joints or other signs of connective tissue disorder (CTD), it is termed Joint Hypermobility Syndrome (JHS). This includes conditions such as Marfan's Syndrome and Ehlers-Danlos Syndrome and Osteogenesis imperfecta. These people are thought to have a higher proportion of type III to type I collagen, where type I collagen exhibits highly organised fibres resulting in high tensile strength, whereas type III collagen fibres are much more extensible, disorganised and occurring primarily in organs such as the gut, skin and blood vessels. The predominant presenting complaint is widespread pain lasting from a day to decades. Additional symptoms associated with joints, such as stiffness, 'feeling like a 90 year old', clicking, clunking, popping, subluxations, dislocations, instability, feeling that the joints are vulnerable, as well as symptoms affecting other tissue such as paraesthesia, tiredness, faintness, feeling unwell and suffering flu-like symptoms. Autonomic nervous system dysfunction in the form of 'dysautonomia' frequently occur. Broad paper like scars appear in the skin where wounds have healed. Other extra-articular manifestations include ocular ptosis, varicose veins, Raynauds phenomenon, neuropathies, tarsal and carpal tunnel syndrome, alterations in neuromuscular reflex action, development motor co-ordination delay (DCD), fibromyalgia, low bone density, anxiety and panic states and depression. Age, sex and gender play a role in presentaton as it appears more common in African and Asian females with a prevalence rate of between 5% and 25% . Despite this relatively high prevalence, JHS continues to be under-recognised, poorly understood and inadequately managed (Simmonds & Kerr, Manual Therapy, 2007, 12, 298-309). In my clinical experience, these people tend to move fast, rely on inertia for stability, have long muscles creating large degrees of freedom and potential kinetic energy, resembling ballistic 'floppies', and are either highly co-ordinated or clumsy. Stabilisation strategies consist of fast movements using large muscle groups. They tend to activities such as swimming, yoga, gymnastics, sprinting, strikers at soccer. Treatment has consisted of soft tissue techniques similar to those used in fibromyalgia, including but not limited to, dry needling, myofascial release and trigger point massage, kinesiotape, strapping for stability in sporting endeavours, pressure garment use such as SKINS, BSc, 2XU, venous stockings. Effectiveness of massage has been shown to be usefull in people suffering from chronic fatigue syndrome (Njjs et al 2006, Man Ther, 11, 187-91), a condition displaying several clinical similarities to people suffering from EDS-HT. Specific exercise regimes more attuned to co-ordination and stability (proprioception) than to excessive non-stabilising stretching. A multi-modal approach including muscle energy techniques, dry needling, mobilisations with movement (Mulligans), thoracic ring relocations (especially good with autonomic symptoms), hydrotherapy, herbal supplementaion such as Devils Claw, Cats Claw, Curcumin and Green Tee can all be useful in the management of this condition. Additionally, Arnica cream can also be used for bruising. Encouragment of non-weight bearing endurance activities such as swimming, and cycling to stimulate the endurance red muscle fibres over the ballistic white muscles fibres, since the latter are preferably used in this movement population. End of range movements are either avoided or done with care where stability is emphasized over mobility. People frequently complain of subluxation and dislocating knee caps and shoulders whilst undertaking a spectrum of activities from sleeping to sporting endeavours. A good friend of mine, Brazilian Physiotherapist and Researcher, Dr Abrahao Baptista, has used muscle electrical stimulation on knees and shoulders to retrain the brain to enhance muscular cortical representation which reduce the incidence of subluxations and dislocations. Abrahao wrote : "my daughter has a mild EDS III and used to dislocate her shoulder many times during sleeping.  I tried many alternatives with her, including strenghtening exercises and education to prevent bad postures before sleeping (e.g. positioning her arm over her head).  What we found to really help her was electrostimulation of the supraspinatus and posterior deltoid.  I followed the ideas of some works from Michael Ridding and others (Clinical Neurophysiology, 112, 1461-1469, 2001; Exp Brain Research, 143, 342-349 ,2002), which show that 30Hz electrostim, provoking mild muscle contractions for 45' leads to increased excitability of the muscle representation in the brain (at the primary motor cortex).  Stimulation of the supraspinatus and deltoid is an old technique to hemiplegic painful shoulder, but used with a little different parameters.  Previous studies showed that this type of stimulation increases brain excitability for 3 days, and so we used two times a week, for two weeks.  After that, her discolcations improved a lot.  It is important to note that, during stimulation, you have to clearly see the humerus head going up to the glenoid fossa" Surgery : The effect of surgical intervention has been shown to be favourable in only a limited percentage of patients (33.9% Rombaut et al 2011, Arch Phys Med Rehab, 92, 1106-1112). Three basic problems arise. First, tissues are less robust; Second, blood vessel fragility can cause technical problems in wound closure; Third, healing is often delayed and may remain incomplete.  Voluntary Posterior Shoulder Subluxation : Clinical Presentation A 27 year old male presented with a history of posterior shoulder weakness, characterised by severe fatigue and heaviness when 'working out' at the gym. His usual routine was one which involved sets of 15 repetitions, hence endurance oriented rather than power oriented. He described major problems when trying to execute bench presses and Japanese style push ups. In a comprehensive review of 300 articles on shoulder instability, Heller et al. (Heller, K. D., J. Forst, R. Forst, and B. Cohen. Posterior dislocation of the shoulder: recommendations for a classification. Arch. Orthop. Trauma Surg. 113:228-231, 1994) concluded that posterior dislocation constitutes only 2.1% of all shoulder dislocations. The differential diagnosis in patients with posterior instability of the shoulder includes traumatic posterior instability, atraumatic posterior instability, voluntary posterior instability, and posterior instability associated with multidirectional instability. Laxity testing was performed with a posterior draw sign. The laxity was graded with a modified Hawkins scale : grade I, humeral head displacement that locks out beyond the glenoid rim; grade II, humeral displacement that is over the glenoid rim but is easily reducable; and grade III, humeral head displacement that locks out beyond the glenoid rim. This client had grade III laxity in both shoulders. A sulcus sign test was performed on both shoulders and graded to commonly accepted grading scales: grade I, a depression <1cm: grade 2, between 1.5 and 2cm; and grade 3, a depression > 2cm. The client had a grade 3 sulcus sign bilaterally regardless if the arm was in neutral or external rotation. The client met the criteria of Carter and Wilkinson for generalized liagmentous laxity by exhibiting hyperextension of both elbows > 10o, genu recurvatum of both knees > 19o, and the ability to touch his thumbto his forearm Headaches Jacome (1999, Cephalagia, 19, 791-796) reported that migraine headaches occured in 11/18 patients with EDS. Hakim et al (2004, Rheumatology, 43, 1194-1195) found 40% of 170 patients with EDS-HT/JHS had previously been diagnosed with migraine compared with 20% of the control population. in addition, the frequency of migraine attacks was 1.7 times increased and the headache related disability was 3.0 times greater in migraineurs with EDS-HT/JHS as compared to controls with migraine (Bendick et al 2011, Cephalgia, 31, 603-613). People suffering from soft tissue hypermobility, connective tissue disorder, Marfans Syndrome, and Ehler Danlos syndrome may be predisposed to upper cervical spine instability. Dural laxity, vascular irregularities and ligamentous laxity with or without Arnold Chiari Malformations may be accompanied by symptoms of intracranial hypotension, POTS (postural orthostatic tachycardia syndrome), dysautonomia, suboccipital "Coat Hanger" headaches (Martin & Neilson 2014 Headaches, September, 1403-1411). Scoliosis and spondylolisthesis occurs in 63% and 6-15% of patients with Marfans syndrome repsectively (Sponseller et al 1995, JBJS Am, 77, 867-876). These manifestations need to be borne in mind as not all upper cervical spine instabilities are the result of trauma. Clinically, serious neurological complications can arise in the presence of upper cervical spine instability, including a stroke or even death. Additionally, vertebral artery and even carotid artery dissections have been reported during and after chiropractic manipulation. Added caution may be needed after Whiplash type injuries. The clinician needs to be aware of this possibility in the presence of these symptoms, assess upper cervical joint hypermobility with manual therapy techniques and treat appropriately, including exercises to improve the control of musculature around the cervical and thoracic spine. Atlantoaxial instability can be diagnosed by flexion/extension X-rays or MRI's, but is best evaluated by using rotational 3D CT scanning. Surgical intervention is sometimes necessary. Temperomandibular Joint (TMJ) Disorders The prevelence of TMJ disorders have been reported to be as high as 80% in people with JHD (Kavucu et al 2006, Rheum Int., 26, 257-260). Joint clicking of the TMJ was 1.7 times more likely in JHD than in controls (Hirsch et al 2008, Eur J Oral Sci, 116, 525-539). Headaches associated with TMJ disorders tend to be in the temporal/masseter (side of head) region. TMJ issues increase in prevelence in the presence of both migraine and chronic daily headache (Goncalves et al 2011, Clin J Pain, 27, 611-615). I've treated a colleague who spontaneously dislocated her jaw whilst yawning at work one morning. stressful for me and her! Generally, people with JHD have increased jaw opening (>40mm from upper to lower incisors). Updated 18 May 2017  Read More
  • Fri 09 Dec 2016

    Physiotherapy with Sharna Hinchliff

    Physiotherapy with Sharna Hinchliff    Martin is pleased to welcome the very experienced physiotherapist Sharna Hinchliff to Back in Business Physiotherapy for one on one physiotherapy sessions with clients in 2017.  Sharna is a passionate triathelete and mother and has had several years experience working locally and internationally (New York and London) in the field of physiotherapy. Originally from Western Australia, Sharna graduated from the world renowned Masters of Manipulative Physiotherapy at Curtin University. read more Read More
  • Mon 07 Nov 2016

    Pilates – with Brunna Cardoso

    Pilates – with Brunna Cardoso Martin is pleased to welcome the bubbly Brunna Cardoso to Back in Business Physiotherapy for Pilates Classes in February 2017.  Brunno is an experienced pilates instructor and has had several years experience training with pilates instructors in Brazil. Read more Read More

Funding, Advertising and Linking Policy

This site is set up as a free of charge service to the community. Back in Business Physiotherapy pays for all aspects of this website and does not endorse any paid advertising on this site. Back in Business Physiotherapy does have an affiliate program with Lunar pages who host this website. Additionally, the links to Human Kinetics and Amazon may result in Back in Business Physiotherapy receiving a small commission for precisely those books if purchased on those sites. Links to other sites are based on the relevance of that sites information to the principles of this websites desire to enhance the standards of Physiotherapy. Unless I am the author of the content of a linked site, these links are not based on reciprocal agreements. No banner adds or pop-ups should appear on your browser as a result of browsing this website. However, if you leave this website to a related one, Back in Business Physiotherapy cannot accept responsibility for neither changes in their contents nor their advertising or privacy policies.

image removed

Updated : 10 May 2014

No responsibility is assumed by Back in Business Physiotherapy for any injury and/or damage to persons or property as a matter of product liability, negligence, or from any use of any methods, products, instruction, or ideas contained in the material in this and it's related websites. Because of rapid advances in the medical sciences, the author recommends that there should be independent verification of diagnoses and exercise prescription. The information provided on Back in Business Physiotherapy is designed to support, not replace, the relationship that exists between a patient/site visitor and their treating health professional.

Copyright Martin Krause 1999 - material is presented as a free educational resource however all intellectual property rights should be acknowledged and respected