An Evidence Based Approach to Treating Tendon Problems A new model for clinical reasoning..

An evidence based approach to treating tendon problems.
Introducing a new clinical model for diagnosis and management of muscolskeletal problems.
By David Poulter PT


A Simple proposition: Pain does not equal inflammation.

There is a lot of evidence to suggest that 90% of what we thought was tendonitis is in fact tendonosis. The troubling aspect of this evidence is that 90% of patients presenting with tendon problems are receiving the wrong treatment. (12,16) Tendonosis is being treated as though it is an acute inflammatory condition. Current evidence suggests that most tendon problems lack an inflammatory mediator (prostaglandin E2). There is some discussion as to whether tendonitis is a precursor to tendonosis, but the current evidence leans towards the hypothesis that it is not.(2,16,17)

The literature also suggests that we have been treating everything as though it was inflamed. Recent studies have demonstrated that NSAIDS used in the early treatment of tendon problems are ineffective and may retard the healing process. There is evidence that used later in the condition they may be of some benefit.(9,10)

Simply put tendosis is a painful condition brought on by overloading connective tissue, which cannot keep pace with remodeling. There is no evidence of inflammatory cells in tissue samples; hence the condition does not follow a normal healing cycle. There is strong evidence of organized cell death “apoptosis” and increased tenocite activity, with disorganized collagen alignment. There is also strong evidence of neovascularization around the affected tendon.(2,3,7)

The literature suggests that neovascularization (new immature blood vessels) may be the cause of some of the pain, there has been work done by Alfredson and his group on sclerosing the vessels, which leads to athletes becoming pain free. These neovessels are also enriched with new nerves, which may also contribute to the pain.(4)

There is also strong evidence that the neurotransmitters Glutamate and Substance P have been found in high concentrations, in people with tendonosis, and a lack of prostaglandin E2. The relationship to pain production is still not clearly understood.(2,3,8,9)

Alfredson’s group in Sweden has done a lot of work on using eccentric loading to treat tendonosis, with good outcomes.(1,14,18) Purdham has also done work at the Australian Institute of Sport using incline eccentric squats for knee tendonosis with good results.(26) There is also strong evidence that eccentric programs have good effect on treating hip adductor problems, lateral elbow problems and shoulder tendonopahy.(14,19,12,26,27,28,29)

Current research also demonstrates good outcome from using Nitric oxide (glycerin trinitrate patches) in the treatment of tendonosis of the elbow, shoulder and Achilles.(20,23,24,25)

The Active/ Inactive model

I have propsoed a simple model known as the Active / Incative model for clinical reasoning. The model is based on the symptomatic and mechanical responses of patients to loading.

Definitions:

Mechanical Loading Strategy = Repeated movements, static
positions, functional tasks, manual techniques.

Active Condition = During the application of certain mechanical loading strategies there will be a change in the symptomatic presentation and / or the mechanical presentation, this change will remain on cessation of the loading strategy.

Inactive Condition = During the application of certain
mechanical loading strategies there may be a change in the symptomatic presentation and / or the mechanical presentation, but the change will never remain on cessation of the loading strategy.

The active/Inactive model is represented below in figure 1.

Figure 1. Poulter (c) 2008

The Active/Inactive model can be used to classify common musculoskeletal problems. This allows for simple treatment strategies to be carried out.

It can be seen that in the Active/Inactive model "Tendonosis" is classified as an Inactive pathalogical condition, which comes about as a result of Wolff's law. Wolff's law simply put states "Form follows Function". Tendonosis put in simple terms is the tissues failure to remodel succesfully to an external load being applied. The collagen disaray, cell apoptosis and glutimate presence are all refelctions of Wolff's law and the tissues failed adaptation to loading. (11, 12, 15)

We often give the beneficial effects of Wolff's law the label "Remodelled", the adverse effects are often given the label "Degenerated".

Good news: Even though Tendonosis is labelled as a degenerative condition it can be remodelled using the correct eccentric loading strategies. (1,2,3,4,5,,6,12,13)

The active/inactive model can be used to classify all common muskuloskeletal conditions, based on their symptomatic and mechanical responses to loading.

On the left side of the model I propose three ways that tissue can be damaged to lead to an active condition.

1. Over stressing tissue. Tissues have a stress strain curve which represents their response to external loading. Most tissues go through and elastic, to palstic, then failure phase. Over stressing tissue can lead to permenant deformation of the tissue, without necessarily breaking the tissue. If the tissue has an innervation this may case pain and micro fracturing of the tissue.

If the tissue doesn't have an innervation then it may displace (nucleus palposus), tear (labrum of hip or shoulder), or over stretch (inner annulus of disc) and lead to pain by placing stress on an innervated structure.

2. Inflammation. Inflammation can be casued by systemic auto immune disease such as Rheumatoid arthritis, Ankylosing Spondylitis, Psoriatic arthristis, Lupus, Reiters Disease, Stills Disease and other common arthitidese. It is well documented that these conditions go through active cycles and remissions.

3. Trauma. Simply put "tissue fracture". This leads to bleeding, clot formation and then the normal healing cycle. The first phase of trauma invovles inflammation caused by the tissue damage.

On the right hand side of the model there are three ways of returning to inactive.

1. Healing. There are recognised phase to the healing process. It is important to remember that each pahse is a predomination and that the other phses are taking place at a lower level all through the healing process.

Phases of Wound Healing
The entire wound healing process is a complex series of events that begins at the moment of injury and can continue for months to years. This overview will help in identifying the various stages of wound healing.

I. Inflammatory Phase
A) Immediate to 2-5 days
B) Hemostasis
Vasoconstriction
Platelet aggregation
Thromboplastin makes clot
C) Inflammation
Vasodilation
Phagocytosis

II. Proliferative Phase or Fibroplastic Phase.
A) 2 days to 3 weeks
B) Granulation
Fibroblasts lay bed of collagen
Fills defect and produces new capillaries
C) Contraction
Wound edges pull together to reduce defect
D) Epithelialization
Crosses moist surface
Cell travel about 3 cm from point of origin in all directions

III. Remodeling Phase
A) 3 weeks to 2 years
B) New collagen forms which increases tensile strength to wounds
C) Scar tissue is only 80 percent as strong as original tissue

2.Natural resolution: Natural resolution is different from healing becasue it does not go through a formal process of stages and does not take 6-12 weeks to show results functionally. Mytosis is a form of repair which can not be discribed in terms of healing, molecular reconstitution due to water reabsorption, hysteresis after tissue creep, realignment of tissue after stress are all examples of natrual resolution.

Non vascularized, non innervated tissues can not heal but they can under go remodeling and change their structure molecularly. They can also be affected by creep and hysteresis.

Resolution of pain and stiffness after a manipulation can not be described in terms of healing, but is a form of natural resolution.

3. Treatment: "Removal of the nasty things to provide an optimal environment for recovery."

Follows the D.Re.Ma.R concept of treatment. (Poulter 2008)

Diagnose, Reduce, Maintain, Restore Function

Classification using the active / inactive classification system



1. I.D.I.O.T.

Victims of creep also known as I.D.I.O.T. syndrome. Sustained loading with g
(gravity) over Time of normal tissue leads to
CREEP and the nociceptive system kicks in to warn of impending
damage to the tissue.

“I Do It Over Time”

This is superimposed on other problems.

This class is inactive non pathological


2. Mal-adaptation

This occurs as connective tissues (including scar) obey Wolff’s law. Generally this can be called other names such as degeneration, adaptive shortening, adhesions, “dysfunction”, instability from degenerative changes can also be included in this class.

The recent literature has also suggested that common tendon pathologies, and even muscular, capsular and ligamentous problems, are caused by an abortive remodeling process which cannot keep pace with the stress applied to them.
The pathology produces is Tendonosis.

Tendonosis is an inactive tendon pathology. ( Khan 2000, Cook 2000 )

Two ends of the spectrum of mal -adaptation are shortened scar or adhesion , restricting motion, or degenerative changes leading to abnormal excessive motion, often classed as instability, with tendonois changes in the middle.

Stable ………………Mal-adaptation………………unstable
(inactive pathological) (inactive pathological )
(Mechanical)


3. Re-arrangement


This class is defined by its active symptomatic and mechanical presentation. Hypothetically this is over stretching of the contents or supporting structures of a joint, leading to temporary or even permanent incongruity of the joint. It is often labeled as, subluxation, dislocation, instability, “derangement”, internal derangement.

Active pathological (mechanical primary, with possible secondary chemical)

4. Trauma

Simply put this involves tissue fracture, leading to a cascade of chemically mediated events, cardinal signs being, heat, redness, swelling and pain. (Calor, rubor, tumor, dalor). Trauma can range on a spectrum from mild to major, depending on the degree of damage and extent of the tissue damaged.

Active pathology (Mechanical leading to primary chemical, secondary mechanical from tissue swelling)

Mechanical Treatment Approach

I.D.I.O.T. (victim of creep): Avoidance of provocative postures and positions. Postural alteration, slouch overcorrect, regular interruption of sustained postures.

Mal-adaptation (with restrictive loss of function): “REMODEL.” Controlled return of stress / function using HURT not HARM principle. Understanding the patient is essential, it takes time to produce a restriction of function due to soft tissue changes and the patient is generally fearful and avoiding pain.

Note you cannot stretch mal-adapted tissue; it has to be remodeled over time. Patient generated forces are adequate to bring about remodeling over time if the appropriate functional stress is applied often enough.

Mal-adaptation (with instability): The treatment of mal-adaptation with excessive motion or instability is postural control and stability exercises (strengthening of postural control muscles). Neuromuscular re-education is often required to allow stability during function.

Mal-adaptation Tendonosis, ligosis, myosis, fasciosis.: The treatment of the “Osis”
is similar to remodeling the short contracted tissue form of mal-adapted tissue. The affected tissue needs loading in a gradual and repetitive fashion. “Eccentric loading”
allows us to apply load to the tenonosis to begin remodeling. In the case of myosis eccentric muscle work and often isometric muscle work allows remodeling to be achieved.
It is important to keep in mind the HURT not HARM system of applying load to the tissue.
Remodeling of and “osis” is a painful procedure and can take many months. Patient education and expectations should be addressed as part of the overall treatment strategy.

Rearrangement: The treatment of rearrangement follows the simple orthopedic principle of D.R.eM.aR.:
Diagnose, Reduce, Maintain & Restore Function. Patient self generated repeated movement to end range; static positions; patient forces and therapist forces are all used in the reductive stage. The P.O.O.M.M. Patient Centered Force Progression Model is followed.
(Over pressure can also be synergistic)Patient generated
Over pressure (Patient)
Over pressure (Therapist)
Mobilization
Manipulation.

Postures and positions are used in the maintenance stage.

Patient self generated repeated movements are used in the restoration of function stage.

Trauma (Tissue fracture): The treatment of trauma follows the D.R.eM.aR principle.
During the reduction phase the R.I.C.E. principle can be followed. (Rest, Ice, Compression, Elevation), in the first few days. Movement testing should begin as soon as possible, using the Hurt not Harm principle. A sign that movement is indicated is that the patients pain becomes intermittent.

Movement in the presence of healing is indicated as long as the symptomatic response to loading is monitored closely. Early controlled movement will give the message to the healing tissue to lay down in a functional orientation and prevent the development of mal-adaptation.


References:

1.Alfredson H et al: Heavy-Load Eccentric Calf Muscle Training For the Treatment of Chronic Achilles Tendinosis. THE AMERICAN JOURNAL OF SPORTS MEDICINE, Vol. 26, No. 3 1998

2.Alfredson H. In situ microdialysis in tendon tissue: high levels of glutamate,but not prostaglandin E2 in chronic achilles tendon pain. Knee Surg Sports Traumatol Arthrosc;7:378–81;1999.

3.Alfredson et al In vivo investigation of ECRB tendons with microdialysis technique—no signs of inflammation but high amounts of glutamate in tennis elbow. Acta Orthop Scand; 71 (5): 475–479;2000

4.Alfredson H, Ohberg L: Neovascularisation in chronic painful patellar tendinosis--promising results after sclerosing neovessels outside the tendon challenge the need for surgery. Knee Surg Sports Traumatol Arthrosc. 2005

5.Alfredson H, Ohberg L: Sclerosing injections to areas of neo-vascularisation reduce pain in chronic Achilles tendinopathy: a double-blind randomised controlled trial. Knee Surg Sports Traumatol Arthrosc. 2005

6.Alfredson H, Ljung BO, Thorsen K, Lorentzon R: In vivo investigation of ECRB tendons with microdialysis technique--no signs of inflammation but high amounts of glutamate in tennis elbow. Acta Orthop Scand. 2000

7.Alfredson H: Chronic tendon pain--implications for treatment: an update. Curr Drug Targets. 2004

8.Alfredson H, Lorentzon R: Chronic tendon pain: no signs of chemical inflammation but high concentrations of the neurotransmitter glutamate. Implications for treatment? Curr Drug Targets. 2002

9.Almekinders LC et al. An In Vitro Investigation Into the Effects of Repetitive Motion and Nonsteroidal Antiinflammatory Medication on Human Tendon Fibroblasts. The American Journal of Sports Medicine 23:119-123 (1995)

10. Almekinders LC et al. Etiology, diagnosis, and treatment of tendonitis: an analysis of the literature. Med Sci Sports Exerc. ,Aug;30(8):1183-90,1998

11.Cook JL et al: Overuse Tendinosis, Not Tendinitis Part 2: Applying the New Approach to Patellar Tendinopathy. THE PHYSICIAN AND SPORTSMEDICINE - VOL 28 - NO. 6 - JUNE 2000

12.Cook JL, Khan KM, Purdam CR. Conservative treatment of patellar tendinopathy. Physical Therapy in Sport;2:54–65; 2001

13. Gotoh M, Hamada K, Yamakawa H, et al. Increased substance P in subacromial bursa and shoulder pain in rotator cuff diseases. J Orthop Res,16:618–21.1998

14. Holmich P et al. Effectiveness of active physical training as treatment for longstanding adductor-related groin pain in athletes: randomised trial. THE LANCET • Vol 353 • February 6, 1999

15. Khan KM, Cook JL, Bonar F, Harcourt P, Astrom M: Histopathology of common tendinopathies. Update and implications for clinical management. Sports Med. 1999

16.Kahn et al .Where is the pain coming from in tendinopathy? It may be biochemical, not only structural, in origin. Br. J. Sports Med.34;81-83;2000

17. Khan KM et al: Overuse Tendinosis, Not Tendinitis Part 1: A New Paradigm for a Difficult Clinical Problem. THE PHYSICIAN AND SPORTSMEDICINE - VOL 28 - NO. 5 - MAY 2000

18. Knobloch et al Eccentric Training Decreases Paratendon Capillary Blood Flow and Preserves Paratendon Oxygen Saturation in Chronic Achilles Tendinopathy. JOSPT. May 2007

19. Macintyre IG. Heavy Eccentric Loading for a Recalcitrant Case of Lateral Epicondylosis in a Hockey Player: A Case Report . Graduate Education and Research, Canadian Memorial Chiropractic College,2007

20. Murrell GA. Using nitric oxide to treat tendinopathy. Br. J. Sports Med.;41;227-231;2007

21. Ohberg L, Alfredson H. Effects on neovascularisation behind the good results with eccentric training in chronic mid-portion Achilles tendinosis? Knee Surg Sports Traumatol Arthrosc. 2004 Sep;12(5):465-70. Epub 2004

22. Ohberg L, Lorentzon R, Alfredson H. Eccentric training in patients with chronic Achilles tendinosis: normalised tendon structure and decreased thickness at follow up. Br J Sports Med;38(1):8-11, Feb 2004

23. Paoloni JA, Appleyard RC, Nelson J, et al. Topical nitric oxide application in the treatment of chronic extensor tendinosis at the elbow: a randomized, doubleblinded, placebo-controlled clinical trial. Am J Sports Med;31:915–20,2003

24. Paoloni J, Appleyard R, Murrell GAC. A randomized double-blind placebo
controlled clinical trial investigating the use of topical nitric oxide
application in the treatment of Achilles tendonitis. J Bone and Joint Surg
(Am);86-A:916–22,2004

25. Paoloni JA, Appleyard RC, Nelson J, et al. Topical glyceryl trinitrate application in the treatment of chronic supraspinatus tendinopathy: a randomized, doubleblinded, placebo-controlled clinical trial. Am J Sports Med ;33:806–13, 2005

25. Purdam CR et al: A pilot study of the eccentric decline squat in the management of painful chronic patellar tendinopathy. Br J Sports Med ;38:395–397; 2004

26. Scott A, Khan KM, Roberts CR, Cook JL, Duronio V. What do we mean by the term "inflammation"? A contemporary basic science update for sports medicine. Br J Sports Med. 2004

27. Tyler T et al The Effectiveness of a Preseason Exercise Program to Prevent Adductor Muscle Strains in Professional Ice Hockey Players. The American Journal of Sports Medicine 30:680-683 (2002)

28.Young et al Eccentric decline squat protocol offers superior results at 12 months compared with traditional eccentric protocol for patellar tendinopathy in volleyball players. Br J Sports Med;39(2):102-5; Feb 2005

29. Yuan et al. Apoptosis in rotator cuff tendonopathy. Journal of Orthopedic Research. Vol26, no 6 1372-1379; 2006

Retlouping a new clinical technique for regaining knee extension in post surgical patients

Retlouping is a new simple to perform clinical technique for regaining knee extension in post surgical patients. It can be used on ACL reconstruction , PCL reconstruction, through to total knee arthroplasties.

A second feature of Retlouping is that it will increase apparent hamstring flexibility.

This can be a safe and effective way of regaining flexibility, without stretching. In numerous studies traditional stretching has been shown to be ineffective in increaseing flexibility, preventing delayed muscle onset pain, providing protection from injury, and stretching will actually decrease strength if performed before balsitic activities. (1,2,3,,4)

In a recent small sample randomized trail (5) Retlouping was shown to be superior to traditional hamstring stretching on improving flexibility in a group of professional Gaelic Football players.

What is Retlouping?

Excerpt from a recent paper on Retlouping (5)

"Retlouping has evolved from a series of chance observations by American Physical Therapist David Poulter.

In personal communication in 2007, Poulter explained the origin of Retlouping and its possible mechanism of action.

As a therapist, Poulter used the long sitting position to differentiate between neural tension and muscle tightness causing restriction of forward bend. He reports that while his patients were in the long sitting position with their feet dorsiflexed against the wall, he would instruct them to flex and extend their neck whilst assessing if this had any effect on the tension in their legs. He reports that he experimented with allowing the clients to relax back and support themselves on their hands to release the tension in their legs before moving their head, to see if this would produce neural tension. By chance on reassessment, he observed that those who performed this second manoeuvre, now known as retlouping, had an increased ability to forward bend after the procedure. After further observation it became apparent that if the feet remain dorsiflexed and supported against the wall, the eyes kept open and all tension removed from the legs by leaning back and supporting the upper body on the hands, the procedure was even more effective. Neck rotation was then introduced as a component to the procedure, with better results.

So what is the possible cause and effect of Retlouping?

Poulter hypothesizes that the procedure is not simply one of altering neural tension, as the patients often reported no adverse feeling of tension in their legs. Nor has the effect anything to do with stretching tight muscles, as the patients did not feel any stretch or tension in their legs during the procedure. He therefore hypothesizes that the logical explanation for the effect seems to be one of neural inhibition, “Simply put the theory according to Poulter is as follows: it appears to reboot your neurological computer and lessen the tone to the hamstrings”.

The key to the neural involvement is the open eyes and the rapid movements of the neck. The eyes, the ears and the neck are all intimately involved in sending neural input to the cerebellum to tell our body about positions in space and control balance.

The hamstrings are strong postural-gravity muscles, which prevent us from falling forward when we bend at the hips to touch our toes. The balance mechanisms inform the cerebellum that we are going to fall and hence the tone in the hamstring increases to prevent us.

Poulter continues by saying that some people may have lost the ability to lessen the tone or switch it off; they have essentially patterned themselves in to this restriction of the forward bend position. Retlouping recreates the forward bend position but in a stable supported position. There is increased neural input informing the cerebellum that even though the neck, ears and eyes are moving rapidly, everything is stable and hence the tone of the hamstrings is reduced. Poulter also hypothesizes that this is a primitive pattern that is recognized by the brain and when you stand up the effect lasts. Poulter proposes that Retlouping is an alternative to hamstring stretching, allowing athletes to increase the flexibility of the hamstrings without stretching. Until now, there was no experimental evidence to support this clinical observation.

The results of this study show that Retlouping is statistically significantly better than stretching when using the forward bend or toe touch test only. This test according to Devlin (6) is inaccurate in the measurement of the hamstring muscle length as there is no stabilization at the hip and the lumbar spine. However retrospectively the inclusion of this test adds support to Poulter’s theory about the mechanism of Retlouping.

The toe touch test or forward bend as it is referred to in this study assesses general lumbar spine and hamstring muscle flexibility by allowing movement at the spine, pelvis and the hip (Bennell 2000) as the subject bends forward. Therefore it may be safe to say that many structures are involved during the procedure. The Active Knee Extension Test is thought by many authors (Devlin (6)and Rolls and George (7)) to be more selective than other tests at measuring hamstring muscle length alone, because the hip and pelvis are stabilized in set positions. With regards to the SLR both Rolls and George (7) and Devlin (6) support each others work by saying that movement occurs in many structures during the performance of a SLR, namely neural mobility. The results of this study show that retlouping had a direct and significant effect on the general lumbar spine and hamstring muscle flexibility test, i.e. the forward bend or toe touch test.

This result adds support to Poulter’s theory that Retlouping works by decreasing the tone in the hamstrings as the subject bends forward, allowing further flexibility gains to be achieved. Retlouping had no significant effect on hamstring muscle length alone i.e. the active knee extension test and on the SLR which predominantly involves neural mobility. It is clear that the retlouping process is very different from stretching and an important area for future research would involve the ability to understand fully and prove what its mechanism might be. "

Retlouping case studies:

Case study 1

64 year old female.

3 weeks s/p Right total knee replacement.

Having daily CPM at home prior to attending first appointment.

Walking with one cane and noticeable limp.

Scar well healed. Moderate swelling of the knee.

Day one range of motion Flexion 93 degree
Extension 24 degree lag.

Daughter reported that it was difficult to get knee straight with the CPM. Patient reported having increased pain with attempts to extend knee.

RETLOUPING procedure initiated on bed using board at end of bed.
During procedure patient reported decrease in knee pain, and a feeling like the knee was relaxing.
The Retloup procedure was carried out through 3 cycles.

After knee flexion was still 93 degrees, extension was now a 3 degree lag.

The patient was excited by the result and said she would continue to perform the procedure at home.


Second visit ( two days later)

The patient reported that she could now walk without a limp and that the knee felt more stable and less painful. She had performed the Retloup procedure sitting on a long coffee table with her feet against the wall, due to the fact she couldn’t get down to the floor.

Her knee was able to fully extend on the second visit.
Knee flexion was now 97 degrees.

Her extension remained full over the next two visits.


Case study 2

37 year old male

11 days s/p right arthroscopic ACL reconstruction with allo graft. Staples still in situ.

Reporting constant dull ache in knee , pain weight bearing. Walking full weight bearing with limp. (No brace, removed due to discomfort at MD orders)

Patient reported a fear of moving the knee, he had not bee doing any exercises prior to attending the clinic as he thought it was too early to move his knee.

On examination: Good scar healing staples in situ. Minimal swelling.

Range of motion: Flexion 80 degrees
Extension 20 degree lag with guarding when attempting
further motion, due to pain.

RETLOUPING procedure initiated on floor. Procedure carried out three time through.

Range of motion after Retlouping: Flexion 80 degrees
Extension full and patient able to contract
quads and perform SLR.

Patient reported decreased knee pain. Able to attain slight hyper extension with heel on towel roll.

Patient said he would perform the Retloup procedure for the next to days as part of his rehab program.

Second visit (two days later)

Patient walking with less visible limp. Reporting decreased knee pain, with increased feeling of stability.

Range of motion: Flexion 90 degrees
Extension 5 degree lag

Patient demonstrated Retloup procedure and attained full knee extension again. The patient reported he hadn’t had time to do the procedure this morning prior to his appointment time at 8am.

Case study 3

19 year old female college basket ball player.

Injured left knee in training. Tore ACL and medial meniscus.

12 weeks s/p ACL repair patella tendon graft with meniscal repair.

Received traditional ACL post op rehab. Unable to attain full knee extension over the 12 week rehab period.

Father attended a course I was teaching and saw a demonstration of Retloup procedure.

On returning home demonstrated the procedure to his daughter and her therapist. The daughter carried out the procedure and attained full extension in 4 minutes.
Prior to Retlouping , extension mobilization and passive stretching of knee and hamstrings had been performed daily for the whole rehab period.

She continued the procedure as a home exercise and stopped all other extension stretches, (which had been causing pain). She is now 18 weeks post op and has full extension and slight hyper extension with full quads control.


We have used the RETLOUP procedure on over 30 post op knees in our clinic with similar results.

Common patient reports.

· Feeling of knee relaxing and sagging in to extension.
· Decease in knee pain whilst performing the Retloup procedure.
· Strange tingle/ twitching in the quads.
· A feeling on standing that the knee will hyperextend.
· Temporary feeling on not knowing where the knee is in space.

References:

1. Herbert RD, Gabriel M. Effects of stretching before and after exercising on muscle soreness and risk of injury: systematic review. BMJ. Aug 31;325(7362):468.,2002

2. Ingraham SJ. The role of flexibility in injury prevention and athletic performance: have we stretched the truth? Minn Med. 2003 May;86(5):58-61.

3.Shrier I; Gossal K. Myths and Truths of Stretching Individualized Recommendations for Healthy Muscles. THE PHYSICIAN AND SPORTSMEDICINE - VOL 28 - NO. 8 - AUGUST 2000

4. Shreir I . Stretching before exercises: An evidence based approach. Br J sports Med 34: 324-25, 2000

5. Durack K. Retlouping : Is it an alternative to hamstring stretching? Masters Thesis, University of Galway , Ireland, 2007

6. Devlin L. Recurrent posterior thigh symptoms detrimental to performance in rugby union. Predisposing factors. Sports Medicine 29(4) pp. 273-287, 2000.

7. Rolls A, George K. The relationship between hamstring muscle injuries and hamstring muscle length in young elite footballers. Physical Therapy in Sport 5 , pp. 179-187, 2004.

To receive a patient handout on Retlouping please e-mail DCPOULT@aol.com