Category Archives for "Conditions and Treatments"

Shoulder Impingement Syndrome

What is it?
  • Injury to the rotator cuff tendon(s) when there is narrowing between the head of the humerus and the coraco-acromial arch (the arcomion & the coracoacromial ligament attaching to the coracoid process) thus causing subacromial crowding. [1,2,3,4]
  • Resulting in micro trauma, ischemia, swelling / inflammation further impingement
  • Primarily affects the supraspinatus tendon but can also affect the infraspinatus[1,2,3]

Causes of Subacromial Crowding[1,2,3,4]
Congenital Variations
  • Size or shape of the coracoid or acromion processes (boney areas)
  • Coracoacromial ligament / subacromial bursal thickness
  • Degree of mid-back ‘thoracic’ kyphosis; excessive curve further facilitates rounding of the shoulder blade ‘scapula’ thus decreasing subacromial space
Developmental or degenerative Factors
  • Post traumatic / post surgical rotator cuff scarring
  • Post trauma ‘sprain’ of acromialclavicular joint separation, laxity in ligaments
  • Osteophyte formation
  • Calcium deposit in rotator cuff tendon
Traumatic factors
  • Disruption of ligament, cartilage and rotator cuff or biceps tendons in shoulder
  • Shoulder subluxation / dislocation
Biomechanical factors
  • Weakness of depressors of glenohumeral head (rotator cuff muscles) due to nerve injury or disuse
  • Capsular restriction due to tightness / adhesions
  • Weakness of shoulder blade muscle stabilizers altering alignment / movement
  • Rotator cuff muscle imbalance
  • Adhesive capsulitis ‘frozen shoulder’
Classification of impingement in 3 stages[1,8]
Stage 1
  • Any age: (usually under 30 years) repetitive shoulder use “overhead athletes”
  • Reversible rotator cuff injury
  • Local tenderness to palpation
  • Restricted range of motion and weakness
  • Tendinosis / tendinopathy of rotator cuff tendon which can become fibrotic
Stage 2
  • Usually 30 to 40 years of age
  • Pathology not reversible by time or / and modifying activity alone
  • Local tenderness to palpation and with movement, crepitus with movement
  • Loss of active & passive range of motion
Stage 3
  • Usually greater than 40 years
  • Some degree of irreversible pathology
  • Continued increase pain on palpation and with movement
  • Loss of active range of motion greater than passive motion
  • Atrophy ‘loss in size’ of rotator cuff and shoulder musculature
Signs & Symptoms to look out for[1,2,3,4,8]
  • Pain in lateral upper arm, deltoid insertion, subacromial area (below boney process)
  • Can be from repetitive arm, shoulder use (athletics: tennis, swimming, throwing overhead, computer use, overhead motion)
  • Inability to lower arm from 90 degrees slowly or smoothly with or without pain
  • Painful arc: catching of swollen rotator cuff tendon(s) or bursa
Other Possible Diagnosis[1,2,3.4]
  • Torn labrum (cartilage)
  • Instability (due to torn ligament)
  • Rotator cuff / Long head Biceps tendonitis, Bursitis
  • Cervical (neck) pathology: disc / nerve root
  • Adhesive Capsulitis (Frozen Shoulder)
Treatment & Management

Research studies, using randomized control trials, reveal that treatments consisting of manual therapy, using joint mobilizations, and specific prescribed Physiotherapy exercises are most effective for recovery versus strengthening exercises alone.[3,5,6]Treatments are aimed towards restoring joint alignment and mobility by breaking up joint capsule restrictions (scar tissue) and correcting muscle imbalances and kinesthetic & proprioceptive awareness.[5,6] Activity modification can also aid in the management of or / and further prevention of the pathology from occurring.

The use of non-corticosteroid medication & corticosteroid injections has a role in the treatment of inflammation and pain control.[7]

When conservative treatment fails and the shoulder impingement is causing considerable pain & dysfunction, arthroscopic surgery followed by manual therapy and exercise has shown to be effective.[8]

For more information about shoulder impingement or shoulder injuries please contact InSync Physio.

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References
  1. ^ Pyne. Diagnosis and Current Treatment Options of Shoulder Impingement. Current Sports Medicine Reports. 251 – 255, 2004 March.
  2. ^ Fu et al. Shoulder Impingement: A critical review. Clinical Orthopaedics and Related Research. 269: 162 – 173, 1991 August.
  3. ^ Kamkar et al. Nonoperative Management of Secondary Impingement Syndrome. Journal of Orthopaedics and Sports Physical Therapy. 17(5): 212 – 224, 1993 May.
  4. ^ Payne et al. The Combined Dynamic & Static Contributions to Subacromial Impingement: A Biomechanical Analysis. The American Journal of Sports Medicine. 25 (6): 801 – 808. 1997.
  5. ^ Senbursa et al. Comparison of Conservative Treatment with & without Physical Therapy for patients with Impingement Syndrome: A prospective, randomized clinical trial. Knee Surgery, Sports Traumatology, Arthroscopy. 15(7): 915 – 921. 2007.
  6. ^ Bang et al. Comparison of Supervised Exercise with & without Manual Physical Therapy for patients with Shoulder Impingement Syndrome. The Journal of Orthopaedic and Sports Physical Therapy. 30(3): 126 – 137. 2000.
  7. ^ Akgun et al. Is Local Subacromial Corticosteroid Injection Beneficial in Subacromial Impingement Syndrome? Clinical Rheumatology. 23(6): 496 – 500. 2004.
  8. ^ Brox et al. Arthroscopic Surgery versus Supervised Exercises in patients with rotator cuff disease (stage 2 impingement syndrome): A Prospective, randomized, controlled study in 125 patients with a 2-½ year follow-up. Journal of Shoulder and Elbow Surgery. 8(2): 102 – 111. 1999.

Wry Neck (Non Traumatic Neck Injury)

What is it?

Have you ever woken up with a sore or stiff neck because you slept on it funny? Have you ever done a prolonged activity such as driving, being on the computer or playing sports where you felt stiff or soreness in your neck afterwards? These kinds of injuries are usually non-traumatic in nature. It is commonly known as wry-neck or also referred to as “torticollis”, and is a condition in which muscle spasms occur from soreness and stiffness in the neck causing it to be out of alignment.[1]

What causes it?

Wry neck can occur due to the prolonged or sudden stretch of the neck for a few possible reasons. The shock absorbing cushion called the meniscoid structures within the zygoapophyseal joint of the neck vertebra can become blocked and jammed in its rest position, swelling and thickening of ligaments / capsules and the surround soft tissue around the joint(s), or a slow shift of the disc in the neck vertebra can all cause muscle spasms. Moreover, old injuries causing unstable joints, constant “self adjustments”, and hyperflexibility can all be contributing factors to developing wry neck.[1]

As well, it can also occur following an upper respiratory tract infection (mainly affecting children), which causes the lymph gland under the neck muscle to swell; this is known as “Grisel’s Syndrome”. Non-activity related causes of torticollis include neurological disorders or tumors.[1]

What to look for? (Signs and Symptoms)

There is usually a limitation of movement toward one side and the posture is slightly flexed away from the painful side. You can wake up with pain on one side initially which can then occur on both sides. Initially the pain can be localized but may later radiate to other areas in the neck, shoulders, arms, hands or fingers.[1] As well, you may experience a headache.

Treatment

Using ice and resting your neck for the first 48 to 72 hours is the recommended first step. Swelling, pain and having the neck vertebra out of alignment can cause the joints to lose its normal range of motion. More over, the altered function of the neck causes imbalances such as muscle weakness and tightness to develop. Physiotherapy, through the use of manual therapy and specific exercises, has been shown to help in the restoration of the movement of the neck joints and the optimal functioning of the muscle imbalances that can occur.[2,3,4] The use of Intramuscular Stimulation (IMS) has also been shown to be beneficial in these types of neck injuries5. Overall, successful management of wry neck includes regaining joint mobility, muscle strength and flexibility, as well as retraining the coordinated movements.[2,3,4]

For more information about neck injuries please contact InSync Physio.

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References
  1. ^ Orthopaedic Division: Diploma of Advanced Orthopaedic Manual and Manipulative Physiotherapy. 2002; 45.
  2. ^ Gross AR, Hoving JL, Haines T, Goldsmith C, Kay T, Aker P et al. Manipulation and Mobilisation for Mechanical Neck Disorders. The Cochrane Library 2004; 4.
  3. ^ Magee DJ, Oborn-Barret E, Turner S, et al. A systematic overview of the effectiveness of physical therapy intervention on soft tissue neck injury following trauma. Physiotherapy Canada; (Spring): 111-130.
  4. ^ Kennedy C. Cervical Spine: Exercise interventions for the Cervical Spine. Ortho Div Review Nov 1998; 13-29.
  5. ^ Gunn C. The treatment of Chronic Pain: Intramuscular Stimulation for Myofascial Pain of Radicular Origin. 2nd Ed; 1996: 51-60.

Whiplash (Traumatic Neck Injury)

What is it?

Whiplash “Whiplash Associated Disorder (WAD)” occurs when a certain force is transmitted to the neck or “cervical spine”. Motor vehicle accidents, any sudden forceful movements of the neck, a fall causing impact on the head, or sports involving impact to the head can result in injury. Any acceleration and deceleration forces absorbed can cause damage to structures of the neck.[1]

A small amount of force can sometimes cause more significant injury than large amounts of sudden force. Reasons for this is largely due to the fact that the degree of damage depends on the amount of force involved as well as the direction of the force.[1]

Signs and Symptoms

Signs and Symptoms can occur immediately after impact or may take a day or two to develop.

Here is a scale to help you understand how whiplash signs and symptoms can be classified and how to grade its severity:[1]

Grade Signs and Symptoms
0 No complaints about the neck
1 Stiffness, pain or tenderness only
2 Stiffness, pain, increased soreness, loss in mobility
3 Stiffness, pain soreness, loss in mobility, Neurological Signs of weakness in shoulder, arm or hand(s), pain or loss in sensation in shoulder, arm, hand(s)
4 Stiffness, pain soreness, loss in mobility, Neurological Signs of weakness in shoulder, arm or hand(s), pain or loss in sensation in shoulder, arm, hand(s), AND Fracture or dislocation
Note Symptoms and disorders that can occur in all grades, but are not limited to: deafness, dizziness, ringing in ears, memory loss, difficulty with swallowing, and jaw pain (TMJ)
Treatment and Management For Whiplash

*** If you are experiencing symptoms that are similar to either grade 3 or grade 4 whiplash it is highly recommended that you see a doctor immediately. Radiology must confirm grade 4 classifications WAD.[3]

For grades 1-3 whiplash, immediately following your injury apply ice for 10 to 15 minutes every hour for the first 3 days. Early physiotherapy intervention using manual therapy to guide soft tissue and joint movements, therapeutic ultrasound, electrical stimulation, and specific home exercises are very effective.[2,4,5] Dry Needling intramuscular stimulation (IMS) is also effective in controlling pain and reducing muscle spasms and promoting therapeutic increase in mobility.[6] After the first few days and beyond if your function in activities and perhaps even sport participation increases it is important to continue to achieve functional mobility and strength of injured segments.[2,3,4,5] Progressive techniques using manual therapy, massage and specific home exercises and postural education is very effective to achieve this.[2,4] Dry needling (IMS) can also help to progress with your recovery.[6]

Full functional recovery from Whiplash can take anywhere from 6 weeks up to 12 weeks or longer depending on the severity and nature of the injury. As you begin to recover and resume certain activities, and even participation in sports within the first 2- 3 weeks, your joints, ligaments, and muscles are still healing.[1,4] By regaining joint mobility, strengthening muscles and retraining the coordinated movements of injured areas you will get back “InSync” to your active lifestyle.

For more information about neck injuries please contact InSync Physio.

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References
  1. ^ Spitzer WO, Skovron ML, Salmi LR, Cassidy JD, Duranceau J, Suissa S et al. Scientific monograph of the Quebec Task Force on Whiplash-Associated Disorders: redefining “whiplash” and its management. Spine 1995; 20(8 Suppl): 1S-73S.
  2. ^ Gross AR, Hoving JL, Haines T, Goldsmith C, Kay T, Aker P et al. Manipulation and Mobilisation for Mechanical Neck Disorders. The Cochrane Library 2004; 4.
  3. ^ Magee DJ, Oborn-Barret E, Turner S, et al. A systematic overview of the effectiveness of physical therapy intervention on soft tissue neck injury following trauma. Physiotherapy Canada; (Spring): 111-130.
  4. ^ Rosenfeld M, Seferiadis A, Carlsson J, Gunnarsson R. Active intervention in patients with whiplash-associated disorders improves long-term prognosis: a randomized controlled clinical trial. Spine 2003; 28(22): 2491-2498.
  5. ^ Verhagen AP, Scholten-Peeters GGM, de Bie RA, Bierma-Zeinstra SMA. Conservative treatments for whiplash. The Cochrane Library 2004; 4.
  6. ^ Gunn C. The treatment of Chronic Pain: Intramuscular Stimulation for Myofascial Pain of Radicular Origin. 2nd Ed; 1996: 51-60.

Knee ‘ACL’ Anterior Cruciate Ligament Injuries

Function of the ACL

The primary function of the ACL is to provide stability in the knee and restrain anterior displacement of the tibia relative to the femur. It also acts to restrain internal-external rotation and varus-valgus angulations and combinations of. Therefore an injury to the ACL causes a loss in stability in the knee joint.

Causes
  • Non-contact sudden deceleration force
  • Quick unopposed force of quadriceps
  • Contact force to posterior aspect of knee, but also to the sides is possible
What to Look For – Signs and Symptoms
  • 72% with apparent hemarthrosis (blood accumulated in joint)
  • “Pop” sound an time of injury
  • Feeling of instability (giving way)
  • High percent of ACL tears present with meniscal tears and collateral ligament injuries (Common is the Triad = ACL + MCL + Meniscus)
Classifications
  • Grade 1 = small partial tear / sprain
  • Grade 2 = moderate partial tear
  • Grade 3 = complete rupture
Treatment and management

Proper treatment can only be applied when a correct diagnosis can be made. A clinical examination will help to assist this.

Initial Stage of Rehabilitation Phase 1 (0- 6 weeks)
  • Swelling control: (PRICE) protect, rest, ice, compress, elevate
  • Counter-act protective muscle spasms
  • Restore pain free passive mobility (regaining full extension priority)
  • Restore pain free active mobility
Intermediate Stage of Rehabilitation Phase 2 (6 weeks to 4 months)
  • Continued increase in active and passive mobility of joint (regaining full range of mobility)
  • Begin strengthening / muscle balance of knee and core stability
  • Balance / proprioception
  • Begin cardiovascular strengthening
Progressive Stage of Rehabilitation Phase 3 (4 to 8 months)
  • Continued increase in active and passive mobility of joint
  • Progressive strengthening / muscle balance of knee, lower extremities and core stability
  • Progressive Balance / proprioception, exercise program
  • Dynamic functional strengthening program return to high level activity

Research studies reveals that ALC tears are problematic because of functional instability, which results in meniscal injuries, secondary instabilities, and early onset osteoarthritis. Incidence of meniscal tear in ACL deficient knee is 40% at year one, 60% at year five, 80% at year ten. Osteoarthritis occurs in 60%-90% by year 10-15. Surgical intervention may be an option depending on the your current situation.

For more information about knee ACL injuries please contact InSync Physio.

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References
  1. Eitzen I, Moksnes H, Snyder-Mackler L, Risberg M. A progressive 5-week exercise therapy program leads to significant improvement in knee function early after anterior cruciate ligament injury. JOPST. 2010; (40) 11, 705-721.
  2. Fitzgerald GK, Axe MJ, Snyder-Mackler L. A decision-making scheme for returning patients to high-level activity with nonoperative treatment after anterior cruciate rupture. Knee Surg Sports Traumatolog Arthros. 2000; 8:76-82.
  3. Hurd WJ, Axe MJ, Snyder-Mackler L. A 10 – year prospective trial of a patient management algorithm and screening examination for highly active individuals with anterior cruciate ligament injury, Part 1 Outcomes. Am J Sports Med. 2008; 36:40-47.
  4. Ibid, 48-56.
  5. Silvers H, Mandelbaum B. Prevention of anterior cruciate ligament injury in the female athlete. Br J Sports Med. 2007; 41: 152-159.

Achilles Tendon Pain

Anatomy

The strongest tendon in the body conjoins the gastrocnemius and soleus muscles to the heel bone (calcaneous). The average length is about 15 cm and does not have a true synovial sheath covering and protecting it but rather a single cell layer of fatty areolar tissue called a paratenon. Blood supply is evident in three locations, being most vascular proximally where it attached to the muscles and least in the mid section of the tendon.

Common Causes

  1. Achilles Tendinitis / Bursitis
    This is an inflammatory condition of the attachment of the achilles tendon / bursa to the heel bone called the calcaneous.
  2. Achilles Tendinopathy
    This is a non-inflammatory condition of the mid-section of the Achilles tendon. This area has increased tenderness on palpation versus the non-affected side. It is characterized by degenerative changes of the tendon (tendinosis). This is the more prevalent of the two types of Achilles tendon pain.

Prevalence

Achilles tendon disorders are reported in a wide variety of sports. Seen amongst a variety of athletics it is more symptomatic during training as opposed to during competition. It accounts for up to 9% in recreational & competitive runners. People who are less active are not immune to this either. Although there is an increased prevalence of Achilles injuries as age increases, the mean age for Achilles disorders is reported to be between 30-50 years of age.

Risk Factors for Achilles Tendinopathy

  1. Abnormal dorsiflexion range of motion (Specifically decreased dorsiflexion with the knee extended)
  2. Tendon structure as identified with diagnostic ultrasound imaging
  3. Abnormal range of motion in the hind-foot (subtalar joint)
  4. Decreased plantar flexion strength
  5. Increased foot pronation (flat feet)
  6. Possible Medical conditions: obesity, hypertension, hyperlipidemia, diabetes
  7. Extrinsic factors: (training errors, environmental factors, faulty equipment)

Diagnosis / Classification

  1. Localized pain / stiffness in Achilles tendon
  2. Intermittent pain related to activity or exercise
  3. Stiffness upon weight bearing after prolonged immobilization (such as sleeping)
  4. Stiffness & pain at the commencement of exercise training session that lessens as exercise continues. – As condition worsens a progression of pain may be felt at the end of the exercise session ro pain throughout the duration of activity occurs
  5. Decrease plantar flexion endurance
  6. Arc sign: area of palpated swelling moves with dorsiflexion & plantar flexion
  7. “Royal London Hospital Test”: positive when tenderness at 3 cm proximal to calcaneous with ankle in slight plantar flexion, that decreases as ankle is dorsiflexed

Other Possible Diagnoses

  1. Acute Achilles tendon rupture
  2. Partial tear of Achilles tendon
  3. Retrocalcaneal bursitis
  4. Posterior ankle impingment
  5. Irritation or neuroma of sural nerve
  6. Os trigonum syndrome
  7. Accessory soleus muscle
  8. Achilles tendon ossification
  9. Systemic Inflammatory disease
  10. Insertional Achilles tendinopathy

Is Additional Imaging Useful?

Likely that both ultrasound and MRI imaging will play an important role in verifying tendon structure to augment clinical decision-making.

Prognosis / Outcome

  • Long-term prognosis for patients with acute-to-subchronic Achilles tendinopathy favourable with non-operative treatment. (Follow-up studies show 71% to 100% are able to return to prior level of activity
  • Significant decreases in pain and improvement in function reported following 6 to 12 weeks of intervention
  • If conservative therapy is unsuccessful, surgery recommended to remove fibrotic adhesions / degenerative nodules to restore vascularity – (Paavola et al found 29% of those with acute to subacute Achilles tendinopathy required surgical intervention with favourable outcome)

Treatment / Intervention

  • Eccentric Loading – specifically designed strengthening program
  • Stretching
  • Foot Orthoses
  • Hands-on Manual Therapy to restore ankle joint mobility and soft tissue release techniques
  • Addressing other joint imbalances higher up: hip / SI joint & spine
  • Taping
  • Electric modalities
  • Heel lifts

For more information about achilles tendon pain please contact InSync Physio.

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References
  1. Ackermann PW, Salo PT, Hart DA. Neuronal pathways in tendon healing. Front Biosci. 2009;14:5165-5187.
  2. Alfredson H, Cook J. A treatment algorithm for managing Achilles tendinopathy: new treatment options. Br J Sports Med. 2007;41:211-216. http://dx.doi.org/10.1136/bjsm.2007.035543
  3. Alfredson H, Lorentzon R. Chronic Achilles tendinosis: recommendations for treatment and prevention. Sports Med. 2000;29:135-146.
  4. 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;13:338-344. http://dx.doi.org/10.1007/s00167-004-0585-6
  5. Alfredson H, Pietila T, Jonsson P, Lorentzon R. Heavy-load eccentric calf muscle training for the treatment of chronic Achilles tendinosis. Am J Sports Med. 1998;26:360-366.
  6. Alfredson H, Thorsen K, Lorentzon R. In situ microdialysis in tendon tissue: high levels of glutamate, but not prostaglandin E2 in chronic Achilles tendon pain. Knee Surg Sports Traumatol Arthrosc. 1999;7:378-381.
  7. Ames PR, Longo UG, Denaro V, Maffulli N. Achilles tendon problems: not just an orthopaedic issue. Disabil Rehabil. 2008;30:1646-1650. http:// dx.doi.org/10.1080/09638280701785882
  8. Amiel D, Kuiper SD, Wallace CD, Harwood FL, VandeBerg JS. Age-related properties of medial collateral ligament and anterior cruciate ligament: a morphologic and collagen maturation study in the rabbit. J Gerontol.1991;46:B159-165.
  9. Andersson G, Danielson P, Alfredson H, Forsgren S. Nerve-related characteristics of ventral paratendinous tissue in chronic Achilles tendinosis. Knee Surg Sports Traumatol Arthrosc. 2007;15:1272-1279. http://dx.doi.org/10.1007/s00167-007-0364-2
  10. Astrom M, Rausing A. Chronic Achilles tendinopathy. A survey of surgical and histopathologic findings. Clin Orthop Relat Res. 1995;151-164.
  11. Barge-Caballero E, Crespo-Leiro MG, Paniagua-Martin MJ, et al. Quinolone-related Achilles tendinopathy in heart transplant patients: incidence and risk factors. J Heart Lung Transplant. 2008;27:46-51. http://dx.doi.org/10.1016/j.healun.2007.09.021
  12. Bjordal JM, Lopes-Martins RA, Iversen VV. A randomised, placebo controlled trial of low level laser therapy for activated Achilles tendinitis with microdialysis measurement of peritendinous prostaglandin E2 concentrations. Br J Sports Med. 2006;40:76-80; discussion 76-80. http://dx.doi.org/10.1136/bjsm.2005.020842
  13. Bjur D, Alfredson H, Forsgren S. The innervation pattern of the human Achilles tendon: studies of the normal and tendinosis tendon with markers for general and sensory innervation. Cell Tissue Res. 2005;320:201-206. http://dx.doi.org/10.1007/s00441-004-1014-3
  14. Bleakney RR, White LM. Imaging of the Achilles tendon. Foot Ankle Clin. 2005;10:239-254. http://dx.doi.org/10.1016/j.fcl.2005.01.006
  15. Brown R, Orchard J, Kinchington M, Hooper A, Nalder G. Aprotinin in the management of Achilles tendinopathy: a randomised controlled trial. Br J Sports Med. 2006;40:275-279. http://dx.doi.org/10.1136/bjsm.2005.021931
  16. Buckwalter JA, Woo SL, Goldberg VM, et al. Soft-tissue aging and musculoskeletal function. J Bone Joint Surg Am. 1993;75:1533-1548.
  17. Carr AJ, Norris SH. The blood supply of the calcaneal tendon. J Bone Joint Surg Br. 1989;71:100-101.
  18. Christenson RE. Effectiveness of specific soft tissue mobilizations for the management of Achilles tendinosis: single case study—experiexperimental design. Man Ther. 2007;12:63-71. http://dx.doi.org/10.1016/j.math.2006.02.012
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  21. Cummins EJ, Anson BJ, Carr BW, Wright RR. The structure of the calcaneal tendon (of Achilles) in relation to orthopedic surgery: with additional observations on the plantaris muscle. Surg Gynecol Obstet.1946;83:107-116.
  22. Curwin S, Stanish W. Tendinitis: Its Etiology and Treatment. Lexington, MA: Collamore Press; 1984.
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  24. Damholt V, Termansen NB. Asymmetry of plantar flexion strength in the foot. Acta Orthop Scand. 1978;49:215-219.
  25. Donoghue OA, Harrison AJ, Laxton P, Jones RK. Orthotic control of rear foot and lower limb motion during running in participants with chronic Achilles tendon injury. Sports Biomech. 2008;7:194-205.
  26. Elveru RA, Rothstein JM, Lamb RL. Goniometric reliability in a clinical setting. Subtalar and ankle joint measurements. Phys Ther. 1988;68:672-677.
  27. Fahlstrom M, Jonsson P, Lorentzon R, Alfredson H. Chronic Achilles tendon pain treated with eccentric calf-muscle training. Knee Surg Sports Traumatol Arthrosc. 2003;11:327-333. http://dx.doi.org/10.1007/s00167-003-0418-z
  28. Fahlstrom M, Lorentzon R, Alfredson H. Painful conditions in the Achilles tendon region in elite badminton players. Am J Sports Med. 2002;30:51-54.
  29. Fordham S, Garbutt G, Lopes P. Epidemiology of injuries in adventure racing athletes. Br J Sports Med. 2004;38:300-303.
  30. Fredberg U, Bolvig L. Significance of ultrasonographically detected asymptomatic tendinosis in the patellar and achilles tendons of elite soccer players: a longitudinal study. Am J Sports Med. 2002;30:488-491.
  31. Gardin A, Bruno J, Movin T, Kristoffersen-Wiberg M, Shalabi A. Magnetic resonance signal, rather than tendon volume, correlates to pain and functional impairment in chronic Achilles tendinopathy. Acta Radiol. 2006;47:718-724. http://dx.doi.org/10.1080/02841850600774035
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  35. Knobloch K, Kraemer R, Jagodzinski M, Zeichen J, Meller R, Vogt PM. Eccentric training decreases paratendon capillary blood flow and preserves paratendon oxygen saturation in chronic achilles tendinopathy. J Orthop Sports Phys Ther. 2007;37:269-276.
  36. Kujala UM, Sarna S, Kaprio J. Cumulative incidence of achilles tendon rupture and tendinopathy in male former elite athletes. Clin J Sport Med. 2005;15:133-135.
  37. Lee KH, Matteliano A, Medige J, Smiehorowski T. Electromyographic changes of leg muscles with heel lift: therapeutic implications. Arch Phys Med Rehabil. 1987;68:298-301.
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  40. Paavola M, Kannus P, Paakkala T, Pasanen M, Jarvinen M. Long-term prognosis of patients with achilles tendinopathy. An observational 8-year follow-up study. Am J Sports Med. 2000;28:634-642.
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  43. Roos EM, Engstrom M, Lagerquist A, Soderberg B. Clinical improvement after 6 weeks of eccentric exercise in patients with mid-portion Achilles tendinopathy — a randomized trial with 1-year follow-up. Scand J Med Sci Sports. 2004;14:286-295. http://dx.doi.org/10.1111/j.1600-0838.2004.378.x
  44. Saltzman CL, Tearse DS. Achilles tendon injuries. J Am Acad Orthop Surg. 1998;6:316-325.
  45. Sanders TG, Rathur SK. Impingement syndromes of the ankle. Magn Reson Imaging Clin N Am. 2008;16:29-38, v. http://dx.doi.org/10.1016/j.mric.2008.02.005
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