Stability of the Acromioclavicular Joint


The acromioclavicular joint (AC joint) is situated between the acromion and the clavicle and promotes motion within 3 planes: AP gliding of the acromion during protraction and retraction of the scapula, tilting of the acromion arm adduction and abduction, and rotation of the clavicle during shoulder abduction and adduction. The AC joint is a gliding synovial joint supplied by the suprascapular and lateral pectoral nerves.


Passive Stabilizers

      1. Articular Capsule: The articular capsule completely surrounds the articular margins, and is strengthened above and below by the superior and inferior acromioclavicular ligaments.
      2. Superior Acromioclavicular Ligament: This ligament covers the superior articulation and extends between the upper part of the acromial end of the clavicle and the adjoining part of the upper surface of the acromion. It is composed of parallel fibers, which interlace with the aponeuroses of the trapezius and deltoid. Below it is in contact with the articular disk when this is present.
      3. Inferior Acromioclavicular Ligament: This thinner ligament covers the under part of the articulation and is attached to the adjoining surfaces of the two bones. It is located below with the tendon of the supraspinatus.
      4. Coracoclavicular Ligament: This ligament serves to connect the clavicle with the coracoid process of the scapula. It does not properly belong to this articulation, but is usually described with it, since it forms an efficient means of retaining the clavicle in contact with the acromion. It consists of the trapezoid and conoid ligaments.
      5. Trapezoid Ligament: This ligament is broad, thin, and placed between the coracoid process and the clavicle. It is attached below to the upper surface of the coracoid process and above to the under surface of the clavicle. Its posterior border is joined with the conoid ligament.
      6. Conoid Ligament: This ligament is a dense band of fibers with its base directed upward. It is attached by its apex to the base of the coracoid process, medial to the trapezoid ligament, and above to the coracoid tuberosity on the under surface of the clavicle.
      7. Coracoacromial Ligament: This ligament runs from the coracoid process to the acromion. It is attached to the acromion just in front of the articular surface for the clavicle and by its broad base to the whole length of the lateral border of the coracoid process. This ligament, together with the coracoid process and the acromion, forms a vault for the protection of the head of the humerus.

The table above outlines the contributions and actions of the primary stabilizers of the AC joint.

Overall, the AC joint capsule, conoid ligament and the AC ligaments resist movement of the distal clavicle primarily in the horizontal plane (anterior to posterior direction) with respect to the scapula. Resistance to posterior translation is important because instability of the distal clavicle in the posterior direction can lead to abutment with the spine of the scapula. The coracoclavicular ligament complex is the primary restraint to vertical translation at the AC joint, but it has significant influence in the horizontal plane as well. In addition to stabilizing the AC joint in the vertical plane, the coracoclavicular ligaments also strengthen the AC articulation and mediate scapulohumeral motion by attaching the clavicle to the scapula.

Dynamic Stabilizers

The dynamic stabilizers of the acromioclavicular joint are the trapezius and the deltoid musculature. The fibers from these muscles blend with the superior acromioclavicular ligament and contribute to its strength with contraction of the muscular fibers. The deltoid and trapezius provide dynamic suspensory support and their importance increases in the presence of torn ligaments. In grade V AC joint injuries, in addition to disruption of all of the stabilizing ligaments (as in a grade III or IV injury), the deltoid and trapezius muscles and fascia are more extensively detached from the clavicle. Therefore, the role of these muscles in AC joint stability must be appreciated during any AC joint surgical reconstruction. Also, a structured active rehabilitation program that focuses on gaining strength of shoulder girdle muscles, including the deltoid, trapezius, sternocleidomastoid, and subclavius, as well as the rotator cuff and periscapular stabilizers, is indicated for patients who are treated non-surgically for AC joint injuries.


Bontempo, N, Mazzocca, A. Biomechanics and treatment of acromioclavicular and sterno-clavicular joint injuries. British Journal of Sports Medicine. 2010. Vol 44(5) p 361-369. Fukuda K, Craig EV, An KN, et al. Biomechanical study of the ligamentous system of the acromioclavicular joint. Journal of Bone Joint Surgery America. 1986. Vol 68 p 434-440. Gray, Henry. Acromioclavicular Articulation. Anatomy of the Human Body 20th Edition. Philadelphia: Lea & Febiger, 1918; Online edition at Inc. 2000. Lizaur, A, Marco, L, Cebrian, R. Acute dislocation of the acromioclavicular joint: Traumatic anatomy and the importance of deltoid and trapezius. Journal of Bone and Joint Surgery. 1994. Vol 76(4) p 602-606. Simovitch, R, Sanders, B, Ozbaydar, M et al. Acromioclavicular Joint Injuries: Diagnosis and Management. Journal of the American Academy of Orthopedic Surgeons. 2009. Vol 17(4) p 207-219 Wheeless, Clifford. Acromioclavicular Joint. Wheeless’ Textbook of Orthopaedics. 2011. Online text:

Non-Musculoskeletal Causes of Shoulder Pain

Below are charts listed of various conditions, which could cause shoulder pain along with a brief description and signs and symptoms of each condition. These are some conditions to keep in the back of your mind when a patient presents with shoulder pain that you feel may not fit well into a specific MSK category.

Infectious Disorders
  • This is a respiratory condition where there is an infection of the lung.
  • Can be caused by bacteria or viruses
  • S/S: cough, fever, shaking chills, shortness of breath, mucus production, sweating, headache, loss of appetite
  • Diagnosis: chest x-ray
Herpes Zoster
  • Shingles (herpes zoster) is a painful, blistering skin rash due to the varicella-zoster virus, the virus that causes chickenpox.
  • S/S: one-sided pain, tingling or burning, red patches on the skin, followed by small blisters, pain, muscle weakness
  • Diagnosis: history, presence of blisters, skin sample
Tuberculous Arthritis
  • This is an infection of the joints caused by tuberculosis
  • S/S: decreased joint movement, night sweats, joint swelling, low grade fever, muscle atrophy and spasms, weight loss
  • This condition usually starts slowly and involves only one joint
  • Diagnosis: x-rays, skin test, chest x-ray, biopsy
Acute Cholecystitis & Gallstones
  • Cholecystitis is sudden inflammation of the gallbladder
  • Gallstones are hard, pebble-like deposits that form inside the gallbladder
  • S/S: abdominal pain that is located on the upper right side or upper middle of the abdomen. It can spread to the right shoulder blade. Patient may also have clay coloured stool, fever, nausea, vomiting, and jaundice signs.
  • Diagnosis: liver function tests, blood tests, ultrasound, x-ray
Splenic Rupture
  • Usually occurs after trauma to the chest wall
  • Presentation varies but most patients with minor focal injury to the spleen complain of left upper quadrant abdominal tenderness. Left shoulder tenderness may also be present as a result of subdiaphragmatic nerve root irritation with referred pain.
  • S/S: tachycardia, tachypnea, restlessness, anxiety, pallor, rebound tenderness
  • This is a surgical emergency, send to hospital
  • A collapsed lung, or pneumothorax, is the collection of air in the space around the lungs. This buildup of air puts pressure on the lung, so it cannot expand as much as it normally does when you take a breath.
  • May result from chest trauma, such as gunshot or knife wounds, rib fracture, or after certain medical procedures
  • S/S: Sharp chest pain, made worse by a deep breath or a cough, shortness of breath, chest tightness, easy fatigue, rapid heart rate, bluish colour
  • Diagnosis: send to hospital for chest x-ray or arterial blood gasses
  • Chest pain or discomfort that occurs if an area of the heart muscle doesn’t get enough oxygen-rich blood.
  • Angina may feel like pressure or squeezing in the chest. The pain also can occur in your shoulders, arms, neck, jaw, or back.
  • S/S: chest discomfort, nausea, vomiting, pallor
Acute Myocardial Infarction
  • A heart attack occurs when blood flow to a part of your heart is blocked for a long enough time that part of the heart muscle is damaged or dies.
  • S/S: chest pain, anxiety, cough, fainting, light-headedness, nausea, vomiting, palpitations, sweating, shortness of breath, rapid pulse, abnormal blood pressure
Subclavian Steal Syndrome
  • This is when there is retrograde blood flow in the vertebral artery associated with proximal ipsilateral subclavian artery stenosis or occlusion
  • S/S: Patients are usually asymptomatic however muscle cramping can occur in the upper extremity, dizziness, vertigo, visual disturbances
Aortic Aneurysm
  • Swelling/dilation of the aorta
  • Most do not produce symptoms however abdominal, back and shoulder pain can occur
  • Diagnosis: ultrasound, x-ray, abdominal exam
AVN of Humeral Head
  • Cellular death of bone components due to an interruption in the blood supply. Primarily affects the shoulder, knee and hip
  • Keep this in mind if you are unable to reproduce the patients pain or if they do not respond to conservative therapy
  • MRI is the diagnostic tool of choice
Auto-Immune, Metabolic and Other
Ankylosing Spondylitis
  • Inflammatory disease which can affect both the peripheral and axial joints causing pain
  • S/S: low back pain that comes and goes, worst at night, pain typically gets better with activity or exercise, long standing joint pain unresponsive to conservative care
  • Back pain may begin in the sacroiliac joints
  • Other inflammatory conditions can also cause shoulder pain (RA, RS, PS etc.) so look for any family history of these conditions and send for further testing is suspicion is high
Polymyalgia Rheumatica
  • Polymyalgia rheumatica (PMR) is an inflammatory disorder involving pain and stiffness in the shoulder and usually also the hip
  • Almost always in people > 50 years old
  • PMR may occur alone, or with or before giant cell arteritis
  • The most typical symptom is pain and stiffness in both shoulders and the neck
  • S/S: fatigue, anemia, weight loss, depression, fever
  • person has long-term, body-wide pain and tenderness in the joints, muscles, tendons, and other soft tissues. Cause is unknown
  • Signs and symptoms are highly variable and non-specific. Some signs and symptoms may include: IBS, memory problems, numbness or tingling in hands/feet, palpitations, reduced ability to exercise, tension or migraine headaches
  • Diagnosis: 3 months of widespread pain with tenderness at 11/18 areas
Lung Cancer, Pancoast Tumour & Metastasis
  • Shoulder pain from lung cancer can be from referred pain along the phrenic nerve within the lungs or from spread of the lung cancer into the bones of the shoulder
  • Pancoast tumours are a form of lung cancer that grow near the upper part of the lungs and can invade tissues near the shoulder. They often cause pain in the shoulder that radiates down the arm.
  • S/S: cough, coughing up blood, shortness of breath, night pain, night sweats, unexpected rapid weight loss. Also look for a history of smoking or exposure to second hand smoke


Bach PB, Silvestri GA, Hanger M, Jett JR. Screening for lung cancer: ACCP evidence-based clinical practice guidelines (2nd edition). Chest. 2007;132:69S-77S. PubMed: 17873161 Bjerke, S, Giebel, J. Splenic Rupture. Medscape Reference. 2011. Cited at: Chen, M, Zieve, D. Myocardial Infarction, Angina. Subclavian Steal, Aortic Aneurysm, AVN. PubMed Health. A.D.A.M. Medical Encyclopedia. 2011. Cited at: Dugdale, D, Vyas, J, Zieve, D. Tuberculous arthritis. PubMed Health. A.D.A.M. Medical Encyclopedia. 2011. Cited at: Gonter, N. Ankylosing Spondylitis. PubMed Health. A.D.A.M. Medical Encyclopedia. 2011. Cited at: Hadjiliadis, D, Zieve, D. Pneumonia. PubMed Health. A.D.A.M. Medical Encyclopedia. 2011. Cited at: Kaufman, D, Zieve, D. Collapsed Lung. PubMed Health. A.D.A.M. Medical Encyclopedia. 2011. Cited at: Longstreth, G, Zieve, D. Acute Cholecystitis and Gallstones. PubMed Health. A.D.A.M. Medical Encyclopedia. 2011. Cited at: Makover, M, Zieve, D. Fibromyalgia. PubMed Health. A.D.A.M. Medical Encyclopedia. 2011. Cited at: Vorvick, L, Vyas, J, Zieve, D. Shingles: Herpes Zoster. PubMed Health. A.D.A.M. Medical Encyclopedia. 2011. Cited at:

Nerve Flossing

Neural mobilization is a treatment modality used to treat pathologies of the nervous system. Neurodynamics is a term referring to the integrated biomechanical, physiological, and morphological functions of the nervous system. It is essential that the nervous system is able to adapt to mechanical loads and it must undergo distinct mechanical events such as sliding, elongation, cross-sectional change, angulation and compression. If those dynamic mechanisms fail, the nervous system is vulnerable to neural edema, ischaemia, fibrosis, and hypoxia which can cause altered neurodynamics.

Neural mobilization can be used for treatment of adverse neurodynamics. The primary objective is to restore the balance between the relative movement of neural tissues and surrounding mechanical interfaces which allow reduced intrinsic pressures on the neural tissue and promotes optimum physiologic function. The hypothesized benefits of neural mobilization techniques include facilitation of nerve gliding, reduction of nerve adherence, dispersion of noxious fluids, and increased neural vascularity. The theory is that neural mobilizations are effective in breaking up adhesions and bringing about mobility.

Efficacy of Neural Mobilisation in Sciatica

Sciatica is a symptom and not a diagnosis. It is a non-specific term commonly used to describe symptoms of pain radiating downward from the buttock over the posterior or lateral side of the lower limb. It is often caused by compression of the nerve. Neural mobilizations for the sciatic nerve involves a supine straight leg raise to induce longitudinal tension. The sciatic nerve runs posteriorly from the hip to the knee joint. To induce dural motion through the sciatic nerve, the leg was raised, fully extended past 35 degrees in order to take up slack in the nerve. Since the sciatic nerve is completely stretched at 70 degrees, pain beyond that point is usually of hip, sacroiliac, or lumbar spine origin. The unilateral straight leg raise causes traction on the sciatic nerve, the lumbosacral nerve roots, and the dura mater. Adverse neural tension produces symptoms from the low back area extending into the sciatic nerve distribution of the affected lower limb. To add additional traction into the proximal aspect of the sciatic nerve, hip adduction was added to the straight leg raise.

A study done by Sarkari et al. compared groups of patients who either were treated with neural mobilization along with conventional treatment or who were treated with only conventional treatment for the sciatica type symptoms. It was found that the neural mobilization technique is effective in increasing range of motion at the hip and decreasing pain thus reducing the symptoms of sciatica.

Upper Limb Nerve Mobilization

The radial, ulnar and median nerve all supply the hand with motor and sensory aspects. The nerves have elasticity like a rubber-band and shorten and lengthen as one moves their arm. With repetitive trauma, microscopic adhesions can bind the nerve. When the nerve overstretches, we experience sensations such as pain, numbness, tingling, or coldness in the fingers. Nerve gliding is an effective treatment that can help decrease nerve symptoms. It is very important not to overstretch the nerve when exercising otherwise you can create symptoms. Feeling some tension is good when performing the exercises but do not stretch to the point that you feel pain or numbness. A sustained hold can be used for 10 seconds or a gentle nerve pump to clear any adhesions.

Median Nerve at the Elbow



Begin with the elbow, fingers and wrist bent. Bend the neck to the other side, while lifting the elbow backwards, keeping it and the wrist and fingers bent.



Bend the neck towards the arm, and ilft the shoulder. Bend the elbow, wrist and fingers. While keeping the neck away and shoulder lifted, straighten the elbow, wrist and fingers.

Median Nerve at the Wrist



Bend the elbow, wrist and fingers. Then, bend the neck away, while moving the shoulder backwards and straightening the elbow, keeping the wrist and fingers flexed.



Bend the neck towards the shoulder, and flex the elbow, wrist and fingers. Next, keep the head and elbow in the same place, while straightening the wrist and fingers.

Ulnar Nerve at Elbow



Keep a straight elbow, and bend the fingers and wrist. Turn the shoulder inwards while moving it backwards, keeping the elbow straight, and bend the neck to the opposite shoulder.



Bend the neck towards the shoulder, lift the shoulder up, and turn it outwards. Straighten the elbow, and bend the wrist and fingers backwards. Bend the elbow, keeping the wrist and fingers bent backwards.

Ulnar Nerve at Back of Wrist



Straighten the elbow, and bend the wrist and fingers backwards. Bend the shoulder backwards, and bend the elbow, without moving the wrist or fingers.



Straighten the elbow, and bend the wrist and fingers backwards. Keep the elbow straight, and flex the wrist and fingers.

Ulnar Nerve at the Front of Wrist



Flex the fingers and wrist. Bend the shoulder backwards, and bend the elbow, keeping the wrist and fingers flexed.



Start with the elbow straight and wrist flexed. Keeping the elbow straight, bend the wrist and fingers backwards.

Radial Nerve at Spiral Groove



Bend the elbow, and bend the wrist and fingers backwards. Bend the neck away from the shoulder, and lift the arm forward, while lifting the elbow up, keeping it bent.



Bend the neck towards the shoulder, bend the elbow, and bend the wrist and fingers backwards. Turn the arm backwards. Without moving the neck or shoulder, straighten the elbow, and flex the fingers and wrist.

Radial Nerve at Elbow



Bend the elbow, and bend the wrist and fingers backwards. Bend the neck away from the shoulder. Raise the arm to the level of the shoulder, and straighten the elbow.



Bend the elbow, and move the hand beside the shoulder. Bend the wrist and fingers backwards. Turn the hand outwards, and flex the wrist and fingers.

Ulnar Nerve at the Front of Wrist



Bend the elbow; bend the wrist and fingers backwards. Keep the hand beside the shoulder. Move the hand in front of the shoulder, and straighten the elbow without moving the wrist or fingers.



Bend the elbow and keep the hand beside the shoulder. Bend the wrist and fingers backwards. Flex the wrist and fingers only.


Ellis, R.F., Phty, B. & Hing, W.A. (2008). Neural mobilization: A systematic review o Rrandomized controlled trials with an analysis of therapeutic efficacy. The Journal of Manual & Manipulative Therapy, 16(1): 8-22. Kostopoulos, D. (2004). Treatment of carpal tunnel syndrome: a review of the non-surgical approaches with emphasis in neural mobilization. Journal of Bodywork and Movement Therapies, 8: 2-8. Sarkari, E. & Nultani, N.K. (2007). Efficacy of Neural Mobilisation in Sciatica. Journal of Exercise Science and Physiotherapy, 3(2): 136-141.

Neck Pain Task Force and the Neck Disability Index

The Neck Pain Task Force (NPTF) was established in 2000 with the purpose to inform and empower the public (people with neck pain) or who are at risk of developing neck pain. The outcome was to hopefully change the attitudes and beliefs about neck pain and its prevention, diagnosis, treatment and management. A total of 31,878 citations were screened, 1203 relevant articles were accepted for review and 552 scientific papers were deemed appropriate for the best evidence synthesis. There was also multiple original research projects conducted within the Task Force mandate

Epidemiology of Neck Pain

      • Most people can expect to experience neck pain at some point in their lives although most will not have a serious disruption in their activities of daily living.
      • The 12 month prevalence of neck pain was a wide range depending on what study you looked at. The range was from 12.1% to 71.5% in the general population and from 27.1% to 47.8% in workers.
      • Each year, the number of workers who are limited in their activities due to pain is 11.0% to 14.1%.
      • Individuals seeking care in the emergency room for traffic-related whiplash associated disorders (WAD) has increased over the last three decades.

Risk Factors for Neck Pain

      • Neck pain has a multifactoral etiology with non-modifiable and modifiable risk factors.
      • Non-modifiable risk factors include age, gender, and genetics. Modifiable risk factors include smoking, physical activity participation, sedentary work position, repetitive work, and precision work.
      • There is no evidence that degenerative changes in the cervical spine are a risk factor for neck pain.
      • There is a lack of evidence that workplace interventions were effective in reducing the incidence of pain in workers.
      • Devices that prevented head extension during collisions were found to be preventative.

Course and Prognosis

      • Between 50 and 80% of those who experience neck pain at some point will report pain again 1 to 5 years later.
      • Prognosis is multifactorial. A good prognosis was associated with younger age. A poor prognosis was associated with pool health, prior episodes of neck pain, poor psychological health, worrying and becoming angry in response to neck pain.
      • Workers who did physical activity were more likely to show improvements in their pain.
      • Compensation and legal matters is prognostic of poor recovery from a WAD.

Assessment of Neck Pain

      • There is not much evidence that shows that diagnostic procedures for neck pain without severe trauma or radicular symptoms have validity and utility.
      • CT scans have better validity and utility in cervical trauma for high-risk or multi-injured patients.
      • The clinical physical exam is more predictive at excluding a structural lesion or neurological compression than at diagnosing any specific etiologic condition.
      • Reliable and valid self-assessment questionnaires given to neck pain patients can provide useful information for management and prognosis.

Treatments for Neck Pain (Non-invasive and Invasive)

      • Educational videos, mobilization, manual therapy, exercises, low-level laser therapy, and acupuncture have appeared to have some benefit.
      • Interventions that focus on returning to work as soon as possible were more effective.
      • Evidence is present for short term symptomatic improvement of radicular symptoms with epidural or selective root injections with corticosteroids.
      • No evidence to support the use of cervical disc arthroplasty in patients with neck pain who do not have primary radicular pain.

Vertebrobasilar Stroke Study Findings

There was an association between chiropractic services and subsequent vertebrobasilar artery stroke in individuals less than 45 years of age. However, there was as similar association observed in patients receiving services from their general practitioner. This is probably due to the fact that patients who are seeking medical care whether from their GPs or chiropractors for headaches or extreme neck pain may be suffering already from vertebrobasilar artery dissection-related pain.

A New Classification System for Neck Pain

A 4-grade classification system of neck pain severity has been developed to assist clinicians in their clinical decision making for patient care.

Grade 1 Neck Pain

      • No signs of symptoms suggestive of major structural pathology
      • Little or no interference with ADLs
      • Likely to respond to minimal intervention that includes pain control and reassurance

Grade 2 Neck Pain

      • No signs of symptoms suggestive of major structural pathology
      • Major interference with ADLs
      • Requires pain relief and early intervention aimed at prevention long-term disability

Grade 3 Neck Pain

      • No signs of symptoms suggestive of major structural pathology
      • Presence of neurological signs (ie: decreased DTRs, weakness, and/or sensory deficits)
      • May required further investigation and more invasive treatments

Grade 4 Neck Pain

      • Signs and symptoms of major structural pathology (ie: fractures, myelopathy, neoplasm, or systemic disease)
      • Requires prompt investigation and treatment

When choosing treatments to relieve grades 1 and 2 neck pain, patients and their clinicians should consider the potential side effects and personal preferences regarding treatment options.

The Neck Disability Index

Outcome assessment is important in modern health care to assure quality and contain costs. It usually starts on the first visit where a baseline is established and goals are then set. Outcome assessment tools should be easy to administer and inexpensive as well as reliable, and valid. By using them, health care providers can document patient status and progress or decline over time.

The Neck Disability Index (NDI) was developed in the late 1980’s by Dr. Howard Vernon and first published in the Journal of Manipulative and Physiological Therapeutics in 1991. The NDI was modelled as a similar instrument for assessing self-rated disability in low back pain patients, the Oswestry Low Back Pain Disability Questionnaire. Dr. Vernon received permission from the developer of the “Oswestry Index” to modify it for use in neck pain patients. There have been many other questionnaires for neck pain patients that have been developed, but the NDI is the most widely used of them all.

The NDI has been shown to be highly reliable on the test-retest reliability. The NDI has also been shown to be valid by comparing NDI scores to other measures of pain and disability. The NDI consists of 10 items, each with a score up to 5, for a total score of 50. The lower the score, the less the self-rated disability. If at the time of reassessment the patient has a score that is 5 points lower than on intake, this is regarded as a clinically important change.

0 – 4 = No disability

5 – 14 = Mild disability

15 – 24 = Moderate disability

25 – 34 = Severe disability

35 or over = Complete disability

Halderman, S., Carroll, L., Cassidy, JD., Schubert, J. & Nygren A. (2008). The bone and joint decade 2000-2010 task force on neck pain and its associated disorders. Spine, 33 (4S), S5-S7. Liebenson, C. (2007). Rehabilitation of the spine (2nd ed). Chapter 8: Outcome Assessment. Lippincott Williams & Wilkins Vernon HT. & Mior SA. (1991). The Neck Disability Index: a study of reliability and validity. Journal of Manipulative & Physiological Therapeutics, 14:409-415.


SMT and Mobilization of the Cervical Spine

Grant, R. (2002) Physical Therapy of the Cervical and Thoracic Spine: 3rd edition. St. Louis, Missouri: Churchill Livingstone

Although there may be several definitions for spinal manipulation and mobilization, they are defined as the following by Grant (2002):

Spinal Manipulation: a passive maneuver in which specifically directed manual forces are applied to vertebral articulations of the body – a high velocity thrust directed specifically at an isolated joint.

Spinal Mobilization: a non-thrust form of manipulation directed at joint dysfunction.

Potential working mechanisms for rationalizing SMT / Mobilization in the use of neck pain:

      • Mechanical alteration of tissues: as a consequence of the restoration of joint mobility, the detrimental effects of immobilization of joints will be minimized.
      • Neurophysiological effects: mechanoreceptors are stimulated as a consequence of the spinal manipulation, thereby having an effect through the large diameter fibers in modulating pain. Several other neuromuscular mechanisms have been also suggested.
      • Psychological influences: the laying on of hands has strong psychological effects for a patient

Grant et. al. performed a systematic review on 10 RCTs on the treatment of neck pain with SMT and mobilization. Three trials included patients with acute neck pain and seven trials included patients with sub-acute and chronic neck pain. For our purposes, we will only look at the results regarding acute neck pain patients:

      • Nordemar/Thorner: report of a remarkably quick symptom reduction in some patients treated with cervical mobilization.
      • McKinney and Mealy studies: both found positive effects of mobilization in combination with other conservative interventions (exercise, heat, ice, analgesics, therapeutic modalities, etc

Interestingly enough, all three of these studies looked only at mobilization rather than manipulation. Regardless, results were all positive!

Haneline, M., Cooperstein, R. (2009) Chiropractic care for patients with acute neck pain: results of a pragmatic practice-based feasibility study. Journal of Chiropractic Medicine. 8(3): 143-155

Some studies have shown that acute neck pain can affect up to 40% of the population. Unfortunately to date, there has been no form of treatment proven to be highly effective in treating this condition and thus, there is also little research done on the topic of acute neck pain. This is mainly due to the fact that by the time a neck pain patient actually enters an RCT, they are no longer in the acute stage.

The overall purpose of this study was to determine the feasibility of using chiropractic treatment/SMT on patients with acute neck pain. A report of treatment outcomes (pain, disability) and patient satisfaction will be made.


      • Patients with acute neck pain were recruited and were included in the study if they fulfilled the following criteria: recent onset neck pain, generally healthy, between 18-71 years of age, signed informed consent). The chiropractors continued to use their regular protocols in managing patient care.
      • Outcomes: NDI, percentage of time in pain, post-treatment patient satisfaction


      • 99 patients with acute neck pain at a mean age of 42 were involved in this study.
      • 10 chiropractors contributed data to this study – practice-based methodology
      • Patients were overall very satisfied with their chiropractic care with 96% of them indicating that they were either “very satisfied” or “satisfied” and would return for chiropractic care upon future pain.
      • 7.8% of patients had transient minor adverse effects to chiropractic care which consisted of increased neck pain and dizziness.
      • Several patients also received therapeutic modalities along with chiropractic care (SMT and mobs).
      • NDI scores and percentages of time in pain also decreased by clinically significant amounts.
      • A total of 1235 cervical SMT was performed with 74% of them being below the level of C4.

This study also showed positive results in favor of both SMT and mobilization

Leaver, AM., Maher CG., Herbert RD. (2010) A randomized controlled trial comparing manipulation with mobilization for recent onset neck pain. Archives of Physical Medicine & Rehabilitation. 91:1313-1318

The purpose of this study was to determine whether HVLA cervical SMT is more effective than cervical mobilization using low velocity variable amplitude techniques in patients with recent onset neck pain. The idea is that since the risk of stroke is associated with SMT and not mobilizations, they wanted to know if the risk could be justified.


      • 182 subjects randomized into two equal groups and each group received 4 treatments over a 2-week period.
      • Outcome measures:
        • # Of days required to recover from neck pain
        • Time taken for recovery of normal activity
        • Pain (using NRS)
        • Disability (NDI
        • Function (patient specific functional scale)
        • Global perceived effort and health-related QOL (SF-12)


      • The use of HVLA C/S SMT did not yield a more rapid recovery from the acute neck pain than did mobilization – nor did it yield any greater benefit for any outcome measure
      • The median time for recovery from neck pain for the SMT group was 47 days compared to 43 days for the mobilization group.
      • There were no statistically/clinically significant differences in any measures between the groups.
      • No serious adverse events were reported in either group.
      • Both groups had significant reductions in pain scores at 2 weeks


      • If safety is a concern, mobilization yields equal benefit for recent onset neck pain in comparison to HVLA SMT. Both forms of therapy clearly offer patient benefits, but the risks are simply lower with mobilization.

Gross, AR., Hoving, JL., Haines, TA, et. al. (2004) A Cochrane Review of Manipulation and Mobilization for Mechanical Neck Disorders. SPINE. 29(14): 1541-1548

This systematic review assessed the effect of manipulation and mobilization either alone or in combination with other treatments on pain, function/disability, patient satisfaction and global perceived effects in adults with mechanical neck disorders.


      • – Manipulation Alone:
        • 4 RCTs from 5 publications assessed the effect of a single session of neck SMT. Single sessions did not result in short-term pain relief for acute, sub-acute, and chronic neck pain when compared to control groups (other treatments deemed to be ineffective).
        • 5 RCTs assessed the effect of 6-20 sessions of SMT conducted over 3-11 weeks against various comparisons (soft tissue therapy, exercise, acupuncture, physiotherapy, etc). No group showed more success than another for all outcomes.
        • 3 RCTs found no difference in short and intermediate-term pain relief when SMT was compared to mobilization for acute, sub-acute, and chronic neck pain.
      • Mobilization Alone
        • 4 trials compared mobilization against cold pack, collar, nerve stimulation, and acupuncture. No difference in pain and function outcomes for all types of mechanical neck pain.
      • Multimodal Care:
        • 6 trials compared manipulation and/or mobilization in combination with various physical medicine agents. No differences were found in benefit for pain relief, improvement in function, and global perceived effect for various neck pain subtypes.
        • 15 trials looked at mobilization/manipulation with exercise intervention. When compared to a wait list control, there was strong evidence of maintained long-term benefit favoring multimodal care for pain relief, improved function, and global perceived effect.


      • Mobilization and manipulation when used with exercise is beneficial for acute, sub-acute, and chronic mechanical neck pain. When done alone, manipulation and mobilization was not beneficial in comparison to the control/comparison groups, and when compared to one another, neither mobilization nor manipulation was superior.
      • More studies are required.

With all of this being said, it has been concluded by a few studies that manipulation does not yield any greater patient benefits in reducing pain/increasing function than does simple spinal mobilizations. Either form of treatment, is however, most effective when combined with some form of physical activity and strengthening exercise.


Medial Tibial Stress Syndrome – AKA – Shin Splints

Medial Tibial Stress Syndrome (MTSS) is a condition that plagues many runners each year. Also known as shin splints, MTSS is pain felt on the posteriomedial border of the tibia occurring during exercise usually due to repetitive running on hard surfaces or forcible excessive use of foot flexors. Approximately 10-20% of all runners will experience a bout of MTSS during their career. Although runners are the most typically affected athletes, those who participate in ballistic sports such as basketball, dance and tennis are also at risk.

Causes of Medial Tibial Stress Syndrome

Causes for this condition can be broken down into intrinsic and extrinsic mechanisms. Intrinsic mechanisms include altered biomechanics and anatomical alignment, decreased muscle strength, decreased flexibility, low bone mineral density, and hormonal imbalances. The extrinsic factors that can lead to the development of MTSS include the type of surface the activity occurs on, the quality of the footwear and making changes in training techniques and running mechanics. Running on an asphalt surfaces, uphill or stairs can elicit pain. A shoe with a lot of shock absorption in the soles as well as the use of insoles or orthotics is beneficial. Changes in frequency, duration or training intensity should be done gradually to minimize potential onset of pain. With overtraining, the pain can represent a continuum ranging from periosteal irritation to a tibial stress fracture.

Diagnostic Criteria

A diagnosis of MTSS occurs when the following are present:

      1. Pain must be a result of exercise, lasting for hours after exercise.
      2. The athlete should not be experiencing any signs of numbness or compression in the lower leg.
      3. The pain must be in a general area, spanning an area larger than 5cm on the posteriomedial border of the tibia.
      4. The athlete should experience some diffuse discomfort upon digital palpation of the distal third of the tibia.
      5. The posteriomedial surface of the tibia may be uneven during palpation.

A Prospective Study

A prospective study by Hubbard et al. (2009) determined some contributing factors to MTSS by investigating healthy collegiate athletes from NCAA Division I and II cross-country, tennis, soccer, volleyball, cheerleading and track and field teams. Subjects with MTSS had significantly increased plantarflexion range of motion and less years of running under their belts. Also, athletes who had a previous history of MTSS and stress fracture are significantly more likely to develop MTSS again.

Previous History of MTSS and Stress Fracture

With MTSS, the tibia is chronically inflamed due to injury and the repetitive force of running further prevents the affected site from healing properly. Because of this, MTSS is a reoccurring injury and the incidence of stress fractures is significantly higher in these athletes. Magnusson et al. (2003) determined that the regional bone density in the tibia is lower in athletes who experience MTSS. Once the MTSS resolves the regional bone mineral density increases by approximately 19%. It is postulated that the inflammation that occurs with MTSS impedes osteoblastic activity which leaves the bone in a weakened state. Since athletes generally push through the pain, they are putting greater stress on the tibia which develops “microcracks” that could potentially manifest themselves into full fractures.

Running History

An individual who has had more athletic experience over the course of their lives and begin playing sports as children are less likely to develop MTSS later on in their running career. Wolf’s Law applies in that the tibia may adapt and adjust to the forces placed on it from running over extended periods of time and become stronger.

Orthotic Use

Hubbard et al. found that the subjects who wore orthotics were 53% more likely to develop MTSS than those who did not. The orthotics were being used to help correct any lower extremity misalignments such as excessive pronation which is a risk factor for developing MTSS. It was hypothesized that the orthotics did not cause the MTSS but were not properly casted to relieve the symptoms the patient was receiving. A properly casted orthotic has been shown to have positive symptom relief.


MTSS can be difficult to treat and keeping athletes away from activities that will slow healing or aggravate the condition can be challenging. The acute phase treatment options include resting and applying ice. Therapy option includes physical therapy modalities such as ultrasound, whirlpool baths, phonophoresis, soft tissue therapy to symptomatic musculature, electrical stimulation, and unweighted ambulation such as deep-water running and cycling to maintain the athlete’s level of fitness and conditioning. The subacute phase consists of modifying the training routine. The goal of the treatment should focus on modifying training regimens and addressing biomechanical abnormalities. Following the subacute phase, stretching and strengthening exercises should be prescribed. Exercises should focus on strengthening the tibialis anterior and other muscles controlling both inversion and eversion of the foot. Strengthening of the core hip muscles may also be beneficial. A return to running can occur when there is absence of clinical findings and radiographic evidence of healing.

Barnes, A., Wheat, J. & Milner, C. (2007). Association between foot type and tibial stress injuries: a systematic review. British Journal of Sports Medicine,42, 93-98. Hubbard, TJ., Carpenter, EM. & Cordova, ML. (2009). Contributing factors to medial tibial stress syndrome: A prospective investigation. Medicine & Science in Sports & Exericse, 41(3), 490-496. Krenner, BJ. (2002). Case report: Comprehensive management of medial tibial stress syndrome. Journal of Chiropractic Medicine, 1(3), 122-124. Magnusson, HI., Ahlborg, HG., Karlsson, C., Nyquist, F. & Karlsson, MK. (2003). Low regional tibial bone density in athletes with medial tibial stress syndrome normalized after recovery from symptoms. American Journal of Sports Medicine, 31(4), 596-600. O’Connor, FG. & Wilder, RP. (2001). Textbook of Running Medicine, McGraw-Hill: New York, New York. Shamus, E. & Shamus, J. (2001). Sports Injury Prevention & Rehabiliation: McGraw-Hill: New York, New York.


McKenzie Spinal Rehabilitation Methods

The McKenzie Method management of common lower cervical and lower lumbar spinal symptoms uses patient generated movements for acute and chronic symptoms. It promotes independence in self-care while educating the patient on movement and positioning strategies. The McKenzie Method recognizes three clinical patterns or syndromes of mechanical and symptomatic responses to loading for which therapeutic movement and positioning strategies may be used.

      1. The Postural Syndrome
      2. The Dysfunction Syndrome
      3. The Derangement Syndrome

The phenomenological patterns (the what) and the pathoanatomical models (the why) of the syndromes are both considered.


Phenomenological Pattern

In this syndrome, the patient has full and pain-free range of motion. The symptoms are intermittent because they only occur with sustained end range loading which is a position that is usually only assumed intermittently. It takes time for the end rage loading to be provocative therefore symptoms are in response to an abnormal amount or duration of load at the end range. Symptoms cease once the end range loading ceases. To fix this problem, avoidance of loading at the end range of motion is suggested which will result in the resolution of symptoms. Although the postural syndrome can occur in any movement plane direction, the movement plane direction most responsible for lower cervical and lower lumbar postural syndrome symptoms is sustained flexion.

Pathoanatomical Explanation

When a tissue is normal but the load is too much, symptoms can result. An example would be a bent finger. If a healthy finger is hyperextended far enough, an abnormal amount of force is placed on normal structures which causes discomfort.

Clinical Intervention

Flexion is the most frequent posture that individuals find themselves in throughout the day. Sitting is reported by most patients to be causing or aggravating lower cervical and lower lumbar symptoms. The maintenance of lordosis in the cervical and lumbar spine is key to remaining symptom free. The McKenzie Method uses the slouch-overcorrect-relax strategy to help patients find the appropriate lordotic sitting posture. The patient begins in a slouched, provocative sitting position and then overcorrects by hyper-extending the lumbar spine and hyper-retracting the head and neck at the same time. The patient then releases 10% of the extension and they will find themselves in a neutral sitting position.

For the postural syndrome, the moto “if it hurts, don’t do it” applies. The solution is to avoid loading at the symptomatic mechanically unimpeded end range.


Phenomenological Pattern

In this syndrome, there is a loss of range of motion with a new, premature, and symptomatic end range established. Repetitive loading at the end range during a physical exam results in no significant changes during the examination other than a temporary increase in discomfort every time loading at the impeded end range occurs. Symptoms are only present when loading at the impeded end range occurs and cease when the loading stops. Movement in other planes has no effects. Correction is achieved by loading at the mechanically impeded end range on a frequent basis.

Pathoanatomical Explanation

The problem here is short tissue. There are normal load being applied to abnormal tissue. The solution is to increase flexibility by doing frequent end range loading to encourage tissue remodelling.

Clinical Intervention

Stretching is the technique that is used to increase flexibility. Many terms such as spasm, hypertonicity, hyperactivity, contracture, etc are used to explain the shortened musculature. With spasm, motion restriction is huge so the spine is held in the direction of the muscle action (pull) and neutral positioning cannot be achieved. With muscle shortening less severe than a spasm, movement may occur beyond neutral into the movement plane opposite the shortened muscle’s pull but a painful restriction is still present in that opposite direction.

For the dysfunction syndrome, the moto “no pain no gain” applies. The solution is to pursue loading at the symptomatic mechanically impeded end range.


Phenomenological Pattern

Repetitive loading in one movement plane compresses and displaces intradiscal nuclear material in another (usually opposite) movement plane direction. The end range of the detrimental direction is mechanically unimpeded as intervertebral disc material is displaced or pushed out of the way. There is less resistance to compression of the disc. The accumulation of displaced intradiscal nuclear material causes a painful obstruction to end range loading. The solution to fix this problem is to compress the accumulated nuclear material to send it back where it came from (centrally in the disc).

Pathoanatomical Explanation

Repetitive loading in one movement plane compresses and displaces intradiscal nuclear material in another (usually opposite) movement plane direction. The end range of the detrimental direction is mechanically unimpeded as intervertebral disc material is displaced or pushed out of the way. There is less resistance to compression of the disc. The accumulation of displaced intradiscal nuclear material causes a painful obstruction to end range loading. The solution to fix this problem is to compress the accumulated nuclear material to send it back where it came from (centrally in the disc).

Acute Spinal Antalgia Paradigms of McKenzie Method Derangement Management

Patients presenting with acute spinal deformities (antalgia) are unable to achieve neutral spinal positioning in the movement plane direction opposite the antalgia. The McKenzie Method management strategy is to first achieve neutral spine and then to recover the lost movement range while being guided by centralization and peripheralization symptoms. In order to determine which loading strategy is preferred, there are a few criteria that must be considered: the centralization phenomenon and which adverse mechanical responses resolve.

Lumbar Kyphotic Antalgic Management- Extension Principle-Posterior Derangement

A patient presenting with a lumbar kyphotic antalgia typically has symptoms that are central or symmetrical and do not radiate below the knee. There are many progressive steps that are taken to reverse the antalgia.

        1. Patient is prone on the table with a pillow under the abdomen so that they relax in a position accommodating the antalgia.
        2. The pillow is removed and the patient lies flat and prone (neutral positioning).
        3. Recovery of extension begins by having the patient rise up on their elbows and to rest in that position for a few moments.
        4. Prone extension (push-up position). Buttocks must be relaxed because if the gluteus maximus is flexed, the buttocks will flex the lumbar spine. This position should be repeated up to 10 times.

Symptoms of centralization or peripheralization are monitored throughout each step. It is a positive prognosticator if symptoms become more central or diminish at each extension end range loading. If radiation to the extremities occurs every time loading at end range occurs, this is a sign that end range loading is not the most effective strategy.

      1. Once extension in the prone position is tolerated, within 1-2 days, the patient should be able to tolerate extension in a standing position.

Cervical Acute Kyphotic Antalgia Management -Extension Principle – Posterior Derangement

      1. Patient lays supine and the head rest on a pillow to support the flexed antalgic position.
      2. Manual traction is applied in the direction of the flexion antalgia. Cervical retraction can be performed in a slow, gentle, repetitive manner to achieve lower cervical extension and neutral head and neck positioning.
      3. Extension is introduced from the retracted position.
      4. At extension end range, very small rotations of the head are performed to facilitate further extension.

Centralization and peripheralization are monitored throughout. At home treatment exercises can be prescribed. These include seated retraction and seated retraction with extension.

Acute Coronal Antalgia Management

With antalgia in the coronal plane, unilateral and extremity symptoms are more common than with sagittal antalgia. The treatment progression for coronal antalgia involves the two-step progression of recovering motion in the coronal plane that is opposite to the antalgia followed by the recovery of motion in the extension (Sagittal) plane. This progression is called the lateral-then-extension principle. If extension end range loading is performed before recovery of the coronal movement in the direction opposite the antalgia, the patient may worsen.

Lumbar Acute Scoliosis Antalgia Management

Lateral shift is equivalent to antalgia and is either right or left depending on the direction of the coronal deviation of the trunk over the pelvis. Side gliding is the movement of the trunk relative to the pelvis in the coronal plane with the shoulder kept level. In a patient with a lateral shift, the progressions are:

      1. Side gliding against the wall. If this is not tolerated, slight flexion (10 degrees) with the manoeuvre may be beneficial.
      2. Extension may be performed at the end range of the coronal movement opposite the antalgia when improvement is noted.

Lumbar Acute Scoliosis Antalgia Management

      1. Patient is supine with head placed on a pillow so that the antalgia is maintained.
      2. Axial traction is applied in the direction of the antalgia.
      3. While maintaining traction, a lateral flexion mobilization is conducted in the direction opposite the antalgia until the painful obstruction is met at which point the position is held.
      4. Treatment progresses with slight extension.
      5. With progression, seated lateral flexion mobilizations with head and neck in a retracted position.

Acute Lordotic Antalgic Management-Flexion Principle – Anterior Derangement

This occurs usually due to short posterior muscular structures that need to be stretched. The McKenzie Method uses flexion strategies to compress intradiscal nuclear material that has accumulated within the anterior intervertebral disc space to return that material to a more central location. The patient would be educated to avoid any extension end range loading.

Liebenson, C. (2007) Rehabilitation of the Spine (2nd Ed) Chapter 15: McKenzie Spinal Rehabilation Methods. Lippincott Williams & Wilkins: Philadelphia.


Anatomy of the Infrapatellar Fat Pad

The infrapatellar fat pad is also known as Hoffa’s fat pad and is a fibrous scaffold stuffed with adipose tissue. It acts as a deformable space filler and helps with the distribution of synovial fluid within the joint. The pad is intra-articular but also extra-synovial as it lies between the antero-inferior synovial membrane and more anterior structures of the knee joint.

Anterior to the fat pad is the lower surface of the patella, patellar ligament, and adjoining fibrous capsule. Posterior to the fat pad lays the trochlear surface of the femur, medial and lateral condyles of the femur and the deep infrapatellar bursa and tibia. The fat pad is attached superiorly to the lower inner border of the patella. Posteriorly it is attached to the infrapatellar plica via the ligamentum mucosum which runs postero-superiorly to attach to the intercondylar notch of the femur. Its distal attachment is to the periosteum of the tibia and to the anterior horns of the menisci.

The synovial lining covering the fat pad is of an adipose type and the periphery has a rich vascular supply which allows it to assist in the production of synovial fluid and removal of debris. On the other hand, the central part of the fat pad (closer to the patellar ligament) has less vascularisation. There are also innervations of the fat pad which are divided into anteromedial and anterolateral portions. The anteriomedial portion is supplied by branches from the saphenous, tibial and obturator nerves as well as nerve to vastus medials. The anterolateral portion is supplied by articular branches from the nerve to vastus lateralis, tibial and recurrent peroneal and common peroneal nerves. These innervations are important when considering possible referral patterns.

The infrapatellar fat pad has recently been a topic of interest due to its suspected involvement in anterior knee pain. Mechanisms for symptomatic knee pain include direct injury to the fat pad and impingement syndromes from repetitive microtraumas resulting in hypertrophy of the fat pad. The fat pad may become impinged between the femur and the tibia. Direct injury may occur with injury to the anterior cruciate ligament, patellar tendon, patellar dislocation and through surgical procedures.


      • Tenderness and swelling at the bottom and under the patella which could cause the bottom of the patella to be tilted outwards
      • Medial knee pain
      • Pain with extreme flexion or extension
      • Positive Hoffa’s Test – patient is lying with their knee bent with the examiner’s thumbs are pushing on both sides along the patellar tendon. Patient is asked to straighten their leg. Apprehension or pain is considered positive.

Conservative Treatment

      • Rest and avoidance of aggravating factors
      • Cryotherapy
      • Soft tissue therapy to surrounding tight and symptomatic musculature strengthening of the surrounding musculature
      • Taping of the Patella – one method is to tape the upper surface of the patella to allow more space for the structures beneath the lower surface of the patella.
      • If conservative treatment does not work, surgery can be tried

In 1904, Hoffa described an impingement syndrome in the knee which was caused by edema and swelling of the infrapetallar fat pad. Hoffa described the symptoms as swelling on both sides of the patella and pain on the median side of the knee. Also, the knee either can’t be straightened or bent. After awhile, there is typically atrophy of the quadriceps. One option for treatment is complete resection of the infrapatellar fat pad from the knee. A study done by Bohnsack et al in 2005 took ten fresh frozen human cadaver knee specimens and measured infrapatellar tissue pressures throughout ranges of motion in the anterior knee.

The following were results of the study:

      • There was significant increase of infrapatellar tissue pressure at knee flexion 1000 in all extension moments with highest pressures at almost full extension
      • Average volume of the anterior knee compartment was inversely proportional to the pressure inside the infrapatellar fat pad. Thus swelling of the fat pad increases pressure to even higher levels in knee flexion and extension
      • The infrapatellar fat pad has a biomechanical dampening function in knee flexion 1000
      • Hypertrophy of the fat pad results in impingement which leads to chronic compression and ischemia. Ischemia causes increase distribution of Substance-P which causes chronic neurogenic tissue inflammation with edema, extravasation of plasmaproteins and leukocyte adherence. A lipomatous tissue necrosis may be the consequence at the endpoint of chronic Hoffa’s syndrome.

Another study showed that as a knee is moved from extension towards flexion there is an increase in the patellofemoral force due to the deterioration of the patellar tendon lever with flexion. In order to maintain the same moments with flexion of the knee, the quadriceps muscle must produce higher forces. Increased force production of the quadriceps results in increased patellofemoral force. After infrapatellar fat pad resection, there was a decrease of patellofemoral force between 1200 and 200 of knee flexion. The authors suggested that there was an increase in biomechanical efficiency of the quadriceps tendon seen with infrapatellar fat pad resection. They also concluded that with improved position of the patella in the trochlea groove as well as improved patellofemoral gliding resistance, there was a decrease in patellofemoral force after resection.

Bohnsack, M., Wilharm A., Hurschler, C., Ruhmann, O., Stukenborg-Colsman, C. &Wirth, C.J. (2004). Biomechanical and kinematice influences of a total infrapatellar fat pad resection on the knee. The American Journal of Sports Medicine¸ 32, 1873-1880. Bohnsack, M., Hurschler, C., Demirtas, T., Ruhmann, O., Stukenborg-Colsman, C. & Wirth, C.J. (2005). Infrapatellar fat pad pressure and volume changes of the anterior compartment during knee motion: Possible clinical consequences to the anterior knee pain syndrome. Knee Surgery and Sports Traumatology Arthroscopy, 13, 135-141. Eivazi, M.G.& Selfe, J. (2008). Infrapatellar fat pad lesions: Theoretical considerations and practical implications. Physical Therapy Reviews,(12)1: 11-16. Swan, A. & Mercer, S. (2005). Anatomy of the infrapatellar fat pad. Journal of Physiotherapy, 33: 19-21.


Running and Shoe Assessment

Running is becoming an increasingly popular activity. However, it is becoming apparent that although it is good for your body, the constant pounding of your feet on a hard surface can exacerbate many biomechanical problems or predispose you to injuries. An injured runner presenting to a chiropractic/physiotherapy clinic can be a complex case and it is important to collect pertinent information from the patient. Specific questions about previous injuries, potential risk factors, training patterns, and goals should be asked. They should also be asked about a history of musculoskeletal injuries such as stress fractures, tendonitis, strains, and surgeries.

Training errors are the most common source of running injuries because runners often attempt to train too much, too soon, too fast. The athlete’s training habits should be investigated in detail. A sudden and rapid increase of running mileage is a frequent training error. Athlete’s who also participate in “speed work” also are at risk for developing overuse injuries. These shorter duration, increased intensity to workouts require physical demands on the musculoskeletal system that many endurance athletes are not yet ready to perform. Also athletes who train on a treadmill during colder months and then transition suddenly to land-based running in the spring frequently encounter injuries. The treadmill cushions shock and assists the contact foot to propel backward.

Shoe Assessment
Ill-fitting or worn-out running shoes can contribute to overuse injuries. It is important for a clinician to instruct their patient to bring in their last two pairs of shoes to the initial evaluation because valuable information can be garnered from examining the shoes. Running shoes can be divided into three general types:

      1. Motion Control (anti-pronation)
      2. Stability (neutral)
      3. Shock absorbing (cushioning)

Generally, shoes tend to wear down after 300-500 miles. Shock absorbing shoes tend to wear down more quickly than motion control shoes. When assessing a shoe:

      • Determine age and mileage of shoe
      • Determine if shoe is too tight or too loose for the size of the foot
      • Look at last: straight (hyperpronators) vs curved (high arched feet)
      • Look at shoe torsion: stiffness
      • Look for anti-pronation materials: foot bridge or medial arch materials
      • Look at heel counter and height
      • Look for shock-absorbing material
      • Determine type of shoe
      • Determine wear patterns: asymmetry
      • Determine if type of shoe matches foot type

The wear pattern of an older shoe also can offer clues in determining if the shoe fits the foot type. If excessive wear is seen on the lateral aspect of the forefoot, a pes cavus foot with instability to pronate should be suspected.

Running Analysis

Compared with walking, running requires a greater joint range of motion and has greater eccentric muscle demand. A video of a runner viewed in multiple planes provides the best picture of the running form. A systematic running analysis that evaluates each joint in all three planes is suggested.

Macera, CA. (1992). Lower extremity injuries in runners. Advances in prediction. Sports Medicine, 13(1): 50-57.

Powers, CM. (2003). The influence of altered lower-extremity kinematics on patellofemoral joint dysfunction: a theoretical perspective. Journal of Orthopedic Sports Physical Therapy, 33(11):639-646.

Plastaras, CT., Rittenberg, JD., Rittenberg, KE., Press, J. & Akuthota, V. (2005). Comprehensive functional evaluation of the injured runner. Physical Medicine and Rehabilitation Clinics of North America, 16: 623-649.

Foot Orthotics

The functional foot orthosis can be divided into four parts.

      1. The Shell
        Made of thermoplastic material and is moulded to the cast of the foot. It supports the means of correction.
      2. The Post (Correcting Platform)
        The material that holds the shell in the functional position desired.
      3. The fore-foot extension
        An accommodative extension spanning the width of the forefoot. It is used to cushion, improve function and redistribute pressure in the plantar surface of the foot.
      4. The Cover
        Interface placed between the shell of the orthosis and the foot.

There are three types of orthotics used when considering the basic structure.

      1. Rigid
        Constructed from a hard material such as plastic and is used for people who are walking and/or standing for long periods of time. They are designed to help control movement and function.
      2. Soft
        Constructed out of a soft, pliable material and is used to help with balance, absorb shock, and help relieve pain. Often used for those who have diabetes or have some foot malformation.
      3. Semi-rigid
        Made for athletes and is made of soft material with hard plastic placed in appropriate places. They are designed to allow for dynamic movement with guidance through proper movement.

Orthotic Add On’s

      1. Heel Lifts
        • is an extrinsic post
        • used to correct leg length inequalities or Achilles tendonosis
      2. Extrinsic Rear Foot Posts
        • is extra-firm posting material added to the plantar surface of the orthotic to help stabilize
        • Purpose -> used for over pronators, unstable feet and people who weigh >240lbs
        • Options -> Neutral-add stability for patients w/ rigid/cavus feet
          Varus for moderate-severe over pronators
        • Contraindications -> tight shoes, supinators, varus or valgus rearfoot
        • adds bulk to the orthotic and should only be incorporate into shoes which can accommodate a slightly bulkier orthotic.

      3. Metatarsal pads
        • 6mm dome shaped pad which is used to lift and spread the metatarsals helping recreate the transverse arch
        • Purpose -> used to treat dropped metatarsals, metatarsalgia, hallux valgus, interdigital neuroma, interdigital bursitsis, excessive callusing and reduced transverse arch
        • recommended to be placed bilaterally
        • Contraindications -> rigid/immobile foot, tarsal coalition

      4. Full Heel Cushion
        • Foam pad covering the entire heel area
        • Purpose -> for patients with plantar fasciitis, non-centrally located heel spur, loss of fat pad, or for additional rear-foot shock absorption
        • used bilaterally to avoid causing leg length differences
        • Contraindication -> a shallow heel counter in shoe (will cause heel to stick out of shoe)

      5. Heel Spur pads
        • Horseshoe shape 3mm pad which is around the outside of the heel area.
        • Purpose -> to lift the calcaneus off the orthotic relieving pressure at the site of a spur
        • Contraindications -> non-centrally located heel spur, shallow heel counter in shoe

      6. Hole in Heel (with foam)
        • 1” hole in the orthotic shell under the calcaneus, with or without the hole filled with foam
        • Purpose -> used when there is a heel spur but the shoes will not accommodate the heel spur pad

      7. Reverse Morton’s Extension
        • 3mm foam pad under 2-5 MTP joints. Used to take pressure off the 1st metatarsal phalangeal joint and slightly dorsiflex the 1st tarsal.
        • Purpose -> patients w/ plantar-flexed 1st ray, hallux limitis, sesamoiditis, severe forefoot valgus deformity.
        • only available with a full length orthotic and should be used with a metatarsal pad

      8. Morton’s Extension
        • 3mm foam pad under the 1st MTP joint from the distal end of the orthotic to the distal end of the joint. Used to raise and immobilize the first toe.
        • Purpose -> patients with dorsiflexed first ray, turf toe, hallux rigidus or patients with a short 1st metatarsal.
        • only available for a full length orthotic and only used with a metatarsal pad

      9. 1st Metatarsal Cut Out
        • 450 cut to the orthotic under the 1st metatarsal phalangeal joint at the distal-medial aspect. Slightly plantar flexes the 1st ray by dropping the head of the 1st metatarsal and pronate the forefoot.
        • Purpose -> functional hallux limitis, supinators. Because it causes the forefoot to pronate, it allows better toe-off and a better heel strike.
        • should not be used in a patient who has a pathological 1st toe
        • Contraindication -> Osteoarthritis in the 1st MT, forefoot varus

Michaud, TC. (1997). Foot orthoses and other forms of conservative foot care. Newton: Massachusetts.
Philps, JW. (1995). The functional foot orthosis (2nd ed). Churchill Livingstone, New York: New York.
Reiley, MA. (1995). Guidelines for prescribing foot orthotics. Berkeley: California.
Valmassy, RL. (1996). Clinical biomechanics of the lower extremities. Mosby, St.Louis, MN.
Wu, KK. (1990). Foot orthoses: Principles and clinical applications. Williams & Wilkins, Baltimore: Maryland.

Etiology of Adhesive Capsulitis

Adhesive Capsulitis, or frozen shoulder (FS), is a shoulder condition characterized by pain with stiffness and limitation in range of motion. This limitation of motion is felt as a mechanical block at the end range during passive testing. Souza describes a critical test for differentiating FS in the acute stage is to have the patient actively position the shoulder to degree of maximal movement. At this point, the practitioner will not be able to induce further movement within the joint. Active and passive restrictions are the same, unlike other conditions where greater passive movement is obtained. This occurs in the fibrotic stage of FS. The condition generally affects 0.5% of the general population. For the most part, presenting patients will be over 40 years of age, and more commonly female. Also, of those diagnosed, 10% will suffer FS bilaterally. Reoccurrence rates are very rare.

FS has a natural history ranging from 10-32 months until recovery. This greatly varies. As a general rule, the greater range limitations and longer duration of the frozen stage, the longer the thawing stage until range of motion is recovered. Mild losses in range of motion and symptoms can prevail for years following the majority of functional recovery.


        1. Pre-adhesive: proposed to be caused by synovitis, and inflammation causing primarily pain
        2. Adhesive: thickened synovitis due to migration of inflammatory mediators and fibroblasts
          *** the above 2 stages can be easily confused with a rotator cuff impingement or a bursitis at presentation, lasting 1-2 months in duration
        3. Fibrotic: adhesions, decreasing ROM but with improvement in pain symptoms
          ***most variable, lasting many months and may predict the length of the thawing stage
        4. Thawing: severe painless restrictions that begin to improve as the capsule slowly remodels collagen

*** average 9-12 months, dependent on length of fibrotic stage

The exact mechanism of action is unknown. Zuckerman proposed a useful classification system:

      1. Primary – idiopathic; no history, examination, or imaging to explain pain and loss of ROM
      2. Secondary
        • Intrinsic
          • AC joint arthritis, RC tears or tendinitis, age (over 40 years)
        • Extrinsic
          • Neurologic disease, pulmonary disease, cardiac disease or surgery, shoulder trauma or humerus, fracture, surgery
        • Systemic
          • Diabetes (especially insulin dependent or type I)
          • Thyroid disease (most commonly those with hyperthyroidism)

Proposed Theories

      1. Microtrauma, which initiates a repetitive inflammatory response within the capsule leading to accumulation of fibroblasts and collagen production. This excess collagen formation overrides the required degeneration and remodeling of collagen. Therefore, fibrosis results leading to stiffening within the ligaments and capsule. Structures commonly involved when assessed with arthroscopy include the rotator interval, between the subscapularis border and supraspinatus intra-capsular tendon, and along the anterior superior and anterior inferior glenohumeral ligaments. This initial inflammatory stage causes pain with a gradually worsening decrease in range of motion.
      2. Sympathetic nervous system malfunction causing decreased blood supply and fibrosis. This may be similar to the vascular deficiencies resulting from cardiac or pulmonary disease and diabetes, which all demonstrate a higher incidence of FS. This may explain the osteopenic humeral head witnessed during FS, which resolves once the course of FS has finished.
      3. Although initially suspected, previous trauma or immobilization is likely not the cause of FS. What is more likely is that immobilization during the initial trauma may impede the prognosis and recovery as increased cross linkages of collagen cause further restrictions and loss of range of motion within the capsule.

The Diabetic Patient
Diabetics are at an increased risk of developing FS, with an incidence of approximately 4.3%. Type I diabetics are at an increased risk. Some research sites as high as 20% incidence of FS in diabetics. This is similar to injuries such as Dupuytren’s contracture, carpal tunnel syndrome, and flexor tenosynovitis. Endocrine disorders such as diabetes will increase the amount of scarring and adhesions with any acute injury, as well as a general delay in healing process and capabilities. Also, hyperglycemia may lead to increased cross-linkages in the collagen matrix, exemplifying the lack of remodeling occurring in the capsule. This results in a longer prognosis, and frequent sustained loss of range of motion following the course of FS. Dr. Souza reports improved diabetic response with proprioceptive neuromuscular facilitation (PNF) stretching. Rhythmic stabilization (alternating between external and internal rotation) may be effective for inducing movement within the capsule. If this is ineffective, recent research by Ogilvie-Harris supports the usage of arthroscopic surgery for diabetics with FS. Following treatment, the majority of patients in a small sample study regained significant range of motion and were relatively pain free following surgery. No major complications were documented. This may be considered following 6 months of failed conservative therapy.

The etiology of FS is unknown. It causes an accumulation of inflammatory mediators and increased collagen production without adequate tissue remodeling. This results in later fibrosis and adhesions within the capsule, primarily at the rotator interval. The initiating event, if existing, has not been identified. Also, diabetics are at an increased risk, especially if insulin dependent. This is important to consider both in diagnosis and prognosis of diabetic patients who present with acute shoulder pain and stiffness. It is also very important to recognize the stage of FS in order to manage efficiently and appropriately.

Kazemi, M. (2000). Adhesive capsulitis: A case report. JCCA, 44(3), 169-176.
Ogilvie-Harris, D. (2003). The diabetic frozen shoulder: Arthroscopic release. Journal of Arthoscopic and Related Surgery, 13(1), 1-8.
Sandor, R. (2000). Adhesive capsulitis: Optimal treatment of ‘frozen shoulder’. Sports Medicine, 28(9)
Sousa, T. (2009). Differential Diagnosis and Management for the Chiropractor: Protocols and Algorithms.
Zuckerman, J. (1994). Definition and classification of frozen shoulder. Journal of Shoulder and Elbow Surgery, 3.



Deep vein thrombosis is the formation of a blood clot in a vein within the body. A common site of concern is in the lower limb. If the clot breaks off and travels in the blood stream it is referred to as an embolus and can cause serious insult or death if it travels towards the lungs, heart, or brain. The purpose of this learning objective was to determine the risk factors for DVT formation and recognition of flags within a history and examination that may warrant further medical investigation.

Blood clots will form when blood flow is altered within the venous system. Some risk factors include:

      • Immobilization or bedrest
      • Smoking
      • genetics (family history)
      • oral contraceptives
      • lower extremity or pelvis injury and fractures
      • heart failure
      • obesity
      • recent surgical procedures (up to 29% will develop a DVT)
      • prolonged travel (when other risk factors are present)

It is also possible for the condition polycythemia to exist, which causes excess blood cell production within the bone marrow. DVTs most commonly occur in adults 60+ years of age, but not always. DVTs in the upper leg are more likely to form a thrombosis and travel towards the lungs than those in the lower leg.

There are a majority of symptoms that we can assess through history and physical examination to identify the need for medical referral. To consider DVT as a differential, these will be unilateral. These include:

      • Changes in skin colour
      • Increased warmth
      • Leg pain or tenderness
      • Edema

You can also measure the differences between the thickest part of calf with the narrowest bilaterally to determine the extent of edema present.

Prior to a referral, ABI can be completed to distinguish the differences in blood pressure between the legs and arms. Normal values fall between 0.9-1.3 and are calculated by dividing lower limb BP over upper limb BP. Values below 0.9 can indicate peripheral arterial disease. This is indicated when the pressure in the arms is greater than that in the legs. Also, a difference greater than 20mmHg between sides can be indicative of vascular changes such as DVT blockage. When further referral is required, a Doppler ultrasound examination is ordered. This can be indicated in a referral letter to the medical professional. High frequency sound waves are directed towards the arteries and veins being studied and can detect changes in frequency of blood flow, which may indicate a clot or DVT. There are no specific risks associated with this assessment and the procedure in non-invasive. Further, anti-thrombin or D-dimer tests can be used to determine the coagulability of the blood.

When diagnosed with a DVT, patients will be prescribed anti-coagulant medication in order to thin the blood and prevent clot formation. These will not dissolve existing clots present. Heparin is most often prescribed and taken simultaneously with Warfarin orally. Once dosages are corrected, Warfarin will be the only drug taken and may be taken long-term for high-risk individuals. Further, compression stockings may be worn to increase the pressure and circulation in the legs. This decreases the risk of clots by promoting increased blood flow. When this conservative treatment fails, operative surgery may involve inserting a filter to prevent thrombosis from travelling towards the lung. Large clots can also be removed surgically.

Many DVTs will dissolve naturally. However, some patients may have long-term pain and swelling, which is referred to as post-phlebitis syndrome. Compression stockings have shown to greatly reduce the likelihood of this condition. Compression stockings at a pressure of 8-15mmHg are used for the treatment of DVTs. However, interestingly, insurance coverage must be over 20mmHg. The stockings are knee high and custom stockings may be used post-surgery or during times of sustained immobility.

When a pulmonary embolus occurs, this is life threatening. Rapid treatment is required to prevent this from occurring. It is our responsibility as health care practitioners to recognize the risk for DVT and embolus formation. Patient education is also important. They should be aware of the signs including:

          • Chest pain
          • Difficulty breathing
          • Coughing blood (hemoptysis)
          • Fainting (syncope)
          • Loss of consciousness

Pressure stockings prescribed by a medical practitioner will improve blood flow and reduce the risk for clots. Obviously, removal of modifiable risk factors will also lessen the likelihood of blood clot formation. Eat well and exercise daily! Quit smoking, especially if taking oral contraceptives! Those at high risk may receive heparin injections prior to long flights.

Suzie, M. The Orthotics Group: Compression stocking seminar. March 2009.
Geerts, W. et al. (2008). Prevention of venous thromboembolism: American college of chest physicians evidence-based clinical practice guidelines (8th edition). Chest, 133(6), 381-453.
Gerhard-Herman, M., et al. (2006). Guidelines for non-invasive vascular laboratory testing: A report from the American society of echocardiography and the society of vascular medicine and biology. J Am Soc Echocardiogr, 19(8), 955-972.
Snow, V. et al. (2007). Management of venous thromboembolism: A clinical practice guideline from the American college of physicians and the American academy of family physicians. Ann Intern Med, 146(3), 204-210.


Differential Diagnoses for Intra-articular Wrist Pain

I selected this topic because wrist pain is a fairly common entity amongst the general population. However, the exact cause of the wrist pain is rarely known. There are so many sensitive, pain producing structures in the wrist that it becomes difficult to determine where the pain is coming from. I wanted to create a list of differentials for intra-articular wrist pain of mechanical origin. Even if this list does not help me rule in or rule out the cause of the pain, it will still provide me with guidance regarding proper management of the patient.

      1. Kienbock’s (AVN Lunate)

        • Usually post-traumatic but can be insidious. The exact cause is unknown.
        • Arterial supply to the lunate is scarce, sometimes only have one main artery. Therefore, if this artery is disrupted, even with the slightest sprain, necrosis can occur.
        • Usually unilateral
        • Negative ulnar variance could be risk factor


        • Pain over palpation of the lunate
        • Decreased grip strength
        • Limited range of motion of the wrist, usually extension


        • Radiographs can help in later stages
        • Scintigraphy is very sensitive
      2. AVN Scaphoid

        • Usually post-traumatic but can be insidious
        • Blood supply to the Scaphoid is limited so trauma to the area can easily disturb blood flow


        • Pain over the anatomical snuff box
        • Pain with radial deviation and axial loading


        • Radiographs can help in later stages
        • Scintigraphy is very sensitive
      3. Chronic Wrist Sprain

        • Often caused by repetitive trauma, such as sports, FOSH or direct trauma
        • Not an issue if it is a low grade chronic wrist sprain that causes stretching to the ligaments


        • Pain with loading of the wrist, especially at end ranges
        • Notable pain with palpation over the carpal bones involved


        • Most sprains do not cause enough damage to have any observable findings on imaging
        • Imaging is mostly used as a tool to rule out other pathologies
        • It is primarily a clinic diagnosis
      4. Scapholunate Instability (D.I.S.I.)

        • The most common form of carpal instability
        • Disruption of both the ligamentum radioscapholunatum and the interosseous scapholunate ligament leading to carpal diastasis
        • History of trauma and repetitive strain to the wrist


        • Weakness
        • Pain over the scapholunate junction
        • Positive Watson’s scaphoid shift test


        • Radiographs show the gap on >3mm (Terry Thomas sign) on PA and also >600 scapholunate angle on lateral view
      5. Lunotriquetrial Instability (VI.S.I.)History
          • Mechanism of injury is usually extension and radial deviation
          • Feeling of instability is common
          • Painful end range wrist motions


          • Tenderness to direct pressure over the lunotriquerial joint or shearing of the joint
          • Painful crepitus or clunking
          • Positive Ballottment or shuck test


          • Often does not shown up on radiographs and needs an arthrogram to properly diagnose
        • Osteoarthritis

          • Primary osteoarthritis commonly affects the trapeziometacarpal joint and sometimes the trapezioscaphoid joint
          • Secondary osteoarthritis can commonly occur anywhere in the wrist after infection or old trauma.


          • Marked tenderness over the joints noted above
          • Pain while starting an activity, followed by increase pain and stiffness after the activity
          • May see swelling within the wrist joints, hear crepitus or have palpable osteophytes


          • Radiographs to assess damage to the cartilage and underlying sub-chondral bone
        • Triangular Fibrocartilage Tear – Ulnar Impaction Syndrome

          • Painful clicking with wrist motions
          • History of repetitive trauma caused by ulnar deviation
          • Repetitive trauma over stresses the TFCC leading to tearing and damage


          • Tenderness over the dorsal anatomical depression just distal to the ulnar head
          • Pain on ulnar deviation and loading (with or without rotation), usually accompanied with crepitus or roughness
          • Pain with lift up test (supinated hands underneath the desk attempt to lift desk upwards)


          • Radiographs are usually negative are commonly not indicated. May see an ulnar variance which is the cause of the excessive pinching
          • To accurately diagnose, usually need MRA or Arthroscopy

It is also important to know that neoplasms, metastasis and benign tumours very rarely occur in the wrist!


Bozentka D. Scapholunate Instability. University of Pennsylvania Orthopaedic Journal. 1999. 12; 27-32
Magee DJ. 2008. Orthopedic Physical Assessment Fifth Edition. Canada. Elsevier Saunders.
Vizniak NA. 2011. Quick Reference Evidence Based Physical Conditions Manual. Canada. Professional Health Systems Inc.
Vugt R, Bijlsma J, Vugt A. Chronic Wrist Pain: Diagnosis and Management. Development and Use of a New Algorithm. Annals of Rheumatic Disease. 1999. 58; 665-674.
Yochum T, Rowe L. 2005. Essentials of Skeletal Radiology 3rd Edition. USA. Lippincott Williams & Wilkins.

Conservative Management of Hip OA

Aqua Therapy

          • From a clinical perspective, aqua therapy seems to have its benefits with OA patients. This can be attributed to the fact that it involves ROM exercises in a simulated low gravity environment.
          • A Cochrane review in 2007 looked at the effectiveness of aqua therapy for hip OA and concluded that there is lack of high quality evidence in this field. However, aquatic exercise does appear to have so some short term effects such as slightly decreasing pain and slightly increasing function over the first 3 months. Long term conclusions cannot be drawn.
          • When aqua therapy ceases it appears that so do the therapeutic benefits, insisting that it is a supportive measures of exercise and not something that can be done transiently
          • It is unknown what the proper frequency and duration of aqua therapy yet. It is also unknown if aqua therapy have an effect on joint degradation as x-ray measures have never been taken.
          • In conclusion, aqua therapy is not essential for treatment of hip OA. However, due to its low cost and low risk it seems like a reasonable trial of therapy if the patient is interested in it.


          • No studies have been performed that address the benefits of ultrasound for OA of the hip.
          • Ultrasound has been proven beneficial for OA of the knee, therefore you may b able to extrapolate its effectiveness for OA of the hip.
          • In conclusion, ultrasound should not be used as sole intervention for hip OA. If used at all it should be combined with other modalities. Unfortunately, this will mask the effectiveness of ultrasound.


          • Out of all the randomized control trials, only 3 have been performed solely on OA of the hip. The rest have been performed on the knee or mix of both knee and hip.
          • When looking specifically at the hip OA studies it was found that none of the studies were of high enough validity to drawn any conclusions. There was either bias, high drop out rates, no long term follow up etc.
          • When all acupuncture studies were grouped together for peripheral osteoarthritis, it was shown that acupuncture is statistically significantly better than sham acupuncture in terms of pain and function. However, this difference was consistently very small and did not meet clinical relevance standards.
          • Most studies were looking at traditional Chinese medicine acupuncture and therefore the sham points were points away from the meridians. This could explain why the sham acupuncture group was proven to be effective for OA of the hip. It could be possible that it does not matter where the needle goes as long as it is inserted around the hip musculature.
          • In conclusion, similar to ultrasound, acupuncture does not have enough evidence to be used as a sole intervention for hip OA. However, its use should be used on a clinical trial basis.


          • Glucosamine is a popular therapeutic intervention for osteoarthritis. It has been a popular choice due to its subjective decreases in pain and increased function and range of motion.
          • When pooling all studies, glucosamine showed no beneficial effects in terms of decreased pain and increased WOMAC function. However, when studies that just included the Rotta Preparation of glucosamine, the results indicated that glucosamine was superior to placebo with respect to pain and function.
          • The Rotta Preparation is just a pharmaceutical company that prepares glucosamine a specific way. Their studies show the best results for glucosamine.
          • Glucosamine is a low risk supplement with no known adverse events.
          • In conclusion, the research is still uncertain surrounding glucosamine for OA. However, due to its safety and effectiveness in Rotta prep studies, trials of glucosamine can be performed for patients with hip OA. Attempt a 3-6 month therapeutic trial to see if it is effective.


          • In terms of exercise for OA of the hip, it makes sense that this should be included in rehab programs for all OA patients. It is important to keep the joint and muscles around it very healthy.
          • However, the research supporting exercise for hip OA is only silver evidence. Only 5 RCT’s could be included in this study and they only show a minimal effect on pain and no benefits in terms of self reported physical function.
          • Exercise is such a broad term, which can be problematic in these types of research studies. This is because proper exercise prescription is important for recovery. Some exercises can be beneficial where as others can be somewhat detrimental.
          • For such a common condition the level of research is quite scarce.
          • The RCT that showed the best results for OA of the hip was a study that had patients engage in a Tai Chi program. This exercise program is low impact and primarily closed chain which may implicate why it was so successful. Most other programs were targeted at knee and hip OA with non specific exercises.
          • In conclusion, despite the low quality research, it is important to include exercise for your hip OA patients. The question is what type of exercises, how often do you do them etc? From a pathophysiological perspective, it would make sense to work on exercises that focus on hip stability in a low impact method. As well as hip mobility exercises.

Manual Therapy

          • There has only been one reliable study on the effectiveness of manual therapy on hip OA. It compared the effectiveness of exercises vs. manual therapy for patients with hip OA.
          • From this limited available evidence, there is sliver level evidence that manual therapy has a beneficial effect compared with exercise therapy in those with hip OA both in short and long term in pain and physical functioning.
          • The manual therapy that was applied was stretching of hip muscles and traction, mobilizations and manipulations of the hips for 5 weeks (9 total treatments).
          • The exercise program was the same frequency and duration but just included general stretch and strengthening program.
          • Manual therapy was significantly better in terms of VAS at rest, VAS with walking and Harris Hip Score.
          • In conclusion, manual therapy of the hip should not be used in isolation but should be used in combination with other modalities such as exercise.

Bartels EM, Lund H, Hagen KB, Dagfinrud H, Christensen R, Danneskiold-Samsøe B. Aquatic exercise for the treatment of knee and hip osteoarthritis. Cochrane Database of Systematic Reviews 2007, Issue 4.

Fransen M, McConnell S, Hernandez-Molina G, Reichenbach S. Exercise for osteoarthritis of the hip. Cochrane Database of Systematic Reviews 2009, Issue 3.

French HP, Brennan A, White B, Cusack T. Manual Therapy for Osteoarthritis of the Hip and Knee – A Systematic Review. Manual Therapy 2011. 16; 109-117.

Manheimer E, Cheng K, Linde K, Lao L, Yoo J, Wieland S, van der Windt DAWM, Berman BM, Bouter LM. Acupuncture for peripheral joint osteoarthritis. Cochrane Database of Systematic Reviews 2010, Issue 1..

Rutjes AWS, Nüesch E, Sterchi R, Jüni P. Therapeutic ultrasound for osteoarthritis of the knee or hip. Cochrane Database of Systematic Reviews 2010, Issue 1.

Towheed T, Maxwell L, Anastassiades TP, Shea B, Houpt JB, Welch V, Hochberg MC, Wells GA. Glucosamine therapy for treating osteoarthritis. Cochrane Database of Systematic Reviews 2005, Issue 2.

Common Hand Deformities

For this learning objective I wanted to look at common hand deformities and the pathology that they are linked with. Hand deformities are common, especially in the aging population. Hence it is important to be able to understand the various hand deformities so that they can be easily recognized. Below are some examples of common hand deformities:

heberdens and bouchards nodes1. Heberden’s and Bouchard’s Nodes
Osteophytosis of the DIPs usually associated with osteoarthritis. These nodes do not have a correlation with Rheumatoid Arthritis. Similar to Heberden’s nodes, Bouchard’s nodes are osteophytosis of the PIPs. They can be commonly found in both OA and RA. Like any arthritic condition these nodes can sometimes be debilitating while at other times be asymptomatic.

boutonniere deformity2. Boutonniere Deformity
This can also be called the button hole deformity, it is when there is a rupture of the central band of the extensor digitorum tendon at the middle phalanx leading to hyperextension of the MCP & DIP & hyper-flexion of the PIP joint. This condition is commonly seen in hand trauma events or slowly over time with RA.

mallet finger3. Mallet Finger
As the picture depicts, similar to the Boutonniere Deformity this also occurs due to rupture of the extensor digitorum tendon. This time it ruptures at the distal phalanx. Therefore, the patient is unable to extend the distal phalanx actively leaving the distal phalanx permanently flexed. This injury often occurs in baseball players when an outstretched finger is jammed into a hard surface putting the distal phalanx into hyper flexion.

swan neck deformity4. Swan Neck Deformity
This is another finger deformity that has a hyperextended PIP and hyperflexed DIP. This is most often found in RA patients after the disease has progressed significantly. The volar ligaments and soft tissues of the PIP begin to erode leading to volar instability of the PIP. It can also occur in Ehlers-Danlos Syndrome.

trigger finger5. Trigger Finger
A swollen nodule forms in the flexor digitorum superficialis tendon (or flexor pollicus longus) just proximal to the first annular pulley. It begins with snapping during flexion and extension of the finger as the nodule passes through the sheath. One the tendon becomes too big the finger becomes locked in a flexed position. The cause of this condition remains unknown. Treatment options are usually injections or surgery.

dupuytrens contracture6. Dupuytren’s Contracture
This condition consists of hypertrophic nodular fibroplasias of the palmar aponeurosis resulting in flexion contraction deformity of the fingers (most often ring finger and pinky finger). This usually occurs in males over the age of 40. There is a familiar trend and this is also seen in heavy labourers that use their hands frequently.

seal fin deformity7. Seal Fin Deformity (Zig Zag Sign)
This occurs when there is ulnar deviation of the fingers and wrist. Degenerative and erosive changes take place at the MCP which cause the shift to take place. This is part of the degenerative cascade of Rhuematoid Arthritis. It is usually present with other RA degenerative changes.

Alexander C. Heberden’s and Bouchdard’s Nodes. Annals Of Rheumatic Disease 1999, 58; 675-678

Anderson D. Mallet Finger – Management and Patient Compliance. Australian Family Physician. 2011, 40; 47-48

Johnsson PM, Eberhardt K. Hand Deformities are Important Signs of Disease Severity in Patients with Early Rheumatoid Arthritis. Rheumatology. 2009, 48(11); 1398-1403

Lundin AC, Eliasson P, Aspenberg P. Trigger Finger and Tendinosis. Journal of Hand Surgery. 2011, 9; 406-411

Rehman S, Goodacre R, Day PJ, Bayat A, Westerhoff HV. Dupuytren’s: A Systems Biology Disease. Arthritis Research and Therapy. 2011, 13(5); 238

Scott DL, Smith C, Kingsley G. Joint Damage and Disability in Rheumatoid Arthritis: An Updated Systematic Review. Clinical and Experimental Rheumatology. 2003, 25(5); 20-27

Vizniak, N.A. Quick Reference Clinical Consultant Muscle Manual. Professional Health Systems Inc, 2008.

de Quervain’s Tenosynovitis

Before you can begin to decide how to treat de Quervain’s (dQ), you must first be able to understand what causes it and what is going on at the tissue level. If you understand these two processes, you can formulate a treatment plan that makes sense.

What is dQ?finklesteins test

          • Tendinosis of the sheath that encapsulates abductor pollicis brevis (APL) and extensor pollicis brevis (EPB)
          • The irritation usually occurs at the radial styloid
          • Pain with thumb movements such as abduction, flexion and resisted extension
          • No gold standard for diagnostic purposes

hand anatomyAnatomy

          • The two tendons (APL and EPB) are encapsulated in a sheath that is covered by the extensor retinaculum around the level of the radial styloid
          • Once travelling from the underneath the retinaculum the two tendons insert on the forearm
          • The APL and EPB run underneath extensor digitorum and run medially to extensor carpi radialis brevis and longus

What causes dQ?

          • dQ is a typical overuse injury or traumatic injury
          • It occurs when the stress on the APL and EPB are beyond physiological tolerance. This can be a notable traumatic incident, or it can be repetitive strain of the tendons
          • From a mechanism of injury standpoint, it usually occurs with combination of gripping or pinching postures along with wrist deviations. A common example being gripping an object while ulnar deviating the wrist.

What is the pathophysiology?

          • There are no reports on natural history of de Quervain’s
          • Impaired sliding of the APL and EPB. This impaired gliding is thought to be caused by thickening of the extensor retinaculum of the wrist.
          • Does not seem to involve inflammation. The predominant features on histological examination are degenerative changes (myxoid degeneration, fibrocartilaginous metaplasia, and deposition of mucopolysaccharide).
          • Pain then is most likely elicited by mechanical impingement between the tendon and its narrowed fibro-osseous canal resulting in stimulation of nociceptors. Therefore, de Quervain’s is an intrinsic, degenerative disease as opposed to an extrinsic, inflammatory cause.
          • Therefore, it should be considered a tendinosis or tenosynovosis as opposed to a tendinitis
          • On histological analysis the tendons appear thickened and enlarged with peritendinous edema.
          • Area of the radial styloid is the most logical place for there to be an increase in friction
          • Entrapment of EPB and APL in the dorsal compartment of the wrist
          • Power Doppler US shows neovascularisation of the extensor retinaculum of patients with de Quervain’s compared to patients without de Quervain’s.
          • Patients with de quervains never show enlarged tendons, neovascularisation or pertendinous fluid.

2) WHAT ARE THE TREATMENT OPTIONS FOR de Quervain’s Tenosynovitis?

What are conservative measures?


            • Only one controlled trial ever done. Looked at corticosteroid injections of methylprednisolone and bupivacaine in 9 pregnant women vs. splinting.
            • Corticosteroid injection patients showed significant decreases in pain compared to the splint population at 1-6 days. The corticosteroid group had complete relief of pan.
            • There is only one small clinical trial and it is hard to draw conclusions from this
            • There was no follow up with these patients, so the long term effects are unknown

wrist braceOther Treatments

      • Avoid aggravating activities
      • Splinting
      • STT – remove tension between outcropping musculature and forearm extensors
      • Hand and wrist rehab – eccentric loading (limited evidence)
      • Ice and heat
      • Laser to facilitate tissue healing
      • Sclerosing therapy – has been proven in small clinical trials to remove neovascularisation. A small trial of 3 patients with sclerosing and eccentric loading showed almost complete resolution at 6 weeks with respect to pain and function

wrist surgeryWhat are surgical measures?
Operative includes

      • Slitting or removing a piece of the tendon to improve gliding
      • Usually avoided
      • Case series with 43 patients suggested surgery was successful in 90% of patients after 3 years

Peters-Veluthamaningal C, van der Windt DAWM, Winters JC, Meyboom-de Jong B. Corticosteroid Injections for de Quervain’s Tenosynovitis. Cochrane Collaboration. 2009. July 8. Knobloch K, Gohritz A, Spies M, Vogt P. Neovascularization in de Quervain’s disease of the wrist: novel combined therapy using sclerosing therapy with polidocanol and eccentric training of the forearms and wrists – a pilot report. Knee Surg Sports Tramuatol Arthroscop. 2008. 16; 803-805. Huisstede B, Middlekoop M, Randsdorp M, Glerum S, Koes B. Effectiveness of Interventions of Specific Complaints of the Arm, Neck and/or Shoulder: 3 Musculoskeletal Disorders of the Hand. An Update. Archives of Physical and Medical Rehabilitation. 2010. 91; 298;314 Sharma R, Thukral A, Kumar S, Bhargava. Effect of Low Level Lasers in de Quervain’s Tenosynovitis: Prospective Study with Ultrasonographic Assessment. Physiotherapy. 2002. 88(12): 730-734.

Low Back Pain and Obesity

According Bener et al (2003), obesity was proven to be a risk factor for LBP. The prevalence of obesity is higher in females with LBP than in males with LBP according to their study. To conclude whether there is a causal association between obesity and back pain, it is necessary to consider the weight evidence, both for and against. Overall, there is some evidence in favor of a causal explanation. In general, obesity might be positively associated with LBP either because excessive body weight could have mechanical ill effects on the back caused by excessive weight-bearing or that there could be a biochemical explanation for such a link. In addition, obesity in itself might have some influence on LBP due to poor lifestyle habit and loss of muscle mass. Bener and company came to a conclusion that obesity is moderately positively associated with LBP.

According to Shiri et al (2008), obesity is associated with LBP in women but not in men. In their study, a number or weight-related factors were considered and waist circumference was the strongest determinant of LBP in women. Important to note, waist circumference and BMI measure different aspects of obesity. Waist circumference is a strong predictor of both visceral and subcutaneous adipose tissues (abdominal obesity). They concluded that abdominal obesity was the primary weight-related risk factor for LBP and that obesity may exert its effects on LBP via mechanical stress, metabolic/inflammatory pathways, or interplay of both.

Mirtz et al (2005) performed a literature review using Medline to determine whether obesity is associated with low back pain. They concluded that the available data is still controversial with no clear-cut evidence connecting low back pain with obesity. Although it is true that people with increased BMIs demand more from their musculoskeletal systems, there is still no fine evidence to draw a cause and effect relationship. Furthermore, obesity is more common in women, whereas overweight is more common in men (may help explain the Shiri results). What they feel to be the main concern in linking obesity as a causal factor for LBP is the numerous variables encountered in these people. These include negative self images, sedentary lifestyles, muscular weakness, etc. Being overweight, however, also has a tendency to cause a greater likelihood of developing spondylosis, osteoarthritis, and disc herniation (according to some studies). They end by saying that individuals with a BMI under 30 are at minimal risk of developing LBP while those whose BMI increases to over 30 are at moderates risk of developing LBP (>40 = high risk). Lastly, an important question to think about is does someone become overweight/obese due to back pain, or does obesity cause back pain?

Webb et al (2003) also concluded that obesity (>30 BMI) is a strong predictor of back pain with disability.

Manchikanti (2000), like many of the above articles already presented, agrees that there are several hypotheses relating to a linkage between obesity and LBP: Increased mechanical demands resulting from obesity have been suspected of causing LBP through excessive wear and tear, and it has also been suggested that metabolic factors associated with obesity may be detrimental. Obesity, defined as being 30% over ideal weight, influences normal body mechanics by making it more difficult to sit, stand, and walk and increases the time required to recover from an injury. Fatty tissue is a stress on the body even when a person is not injured, as it decreases blood flow carrying nutrients for healing to the injured area. Since it is well known that too much fat is associated with loss of endurance, it is presumed that obesity also makes rehabilitation more difficult for the low back injury patient since poor endurance and cardiovascular fitness may hinder full participation in therapy.

Some consider obesity a strong contributor to back pain while others consider it only a possible or minor contributor (if any at all). In a systematic review highlighted in this article by Leboeuf-Yde, 32% of all studies reported a statistically significant positive weak association between body weight and low back pain. Due to a lack of overall evidence, however, body weight should be considered as a possible weak risk indicator of back pain.

Several studies do show that lumbar disc herniation symptoms were more common in people who were overweight or who had a larger waist circumference. Lastly, other studies showed that increased BMI scores were associated with more frequent osteophytes at the lumbar spine (recurring themes).

In conclusion, it is quite clear that any positive cause and effect relationship between obesity and LBP is still somewhat controversial. There is some evidence to suggest that obesity does indeed cause LBP, but no scientific evidence exists to hang your hat on.

Bener, A., Alwash, R., Gaber, T. (2003) Obesity and Low Back Pain. Collegium Antropologicum. 1: 95-104

Manchikanti, L. (2000) Epidemiology of Low Back Pain. Pain Physician. 3(2): 167-192
Mirtz, T.A., Greene, L. (2005) Is obesity a risk factor for low back pain? An example of using the evidence to answer a clinical question. Chiropractic and Osteopathy. 23(2)

Shiri, R., Solovieva, S., Husgafvel-Pursianen, K. (2008). The association between obesity and the prevalence of low back pain in young adults. American Journal of Epidemiology. 167(9): 1110-119

Webb, R., Brammah, T., Lunt, M. (2003) Prevalence and predictors of intense, chronic, and disabling neck and back pain in the UK General Population. SPINE. 28(11) 1195-1202

Pathomechanics of Sub-Acromial Impingement

A basic definition of sub-acromial impingement is when the sub-acromial space becomes narrowed in some fashion causing the pain sensitive structures within that space to become compressed and painful. The first step, is to determine how does the narrowing of the sub-acromial space occur, because by reversing this process, there will be improved shoulder girdle mechanics and function with decreased pain.

Defining the Sub-Acromial Space


Superior Border – Acromioclavicular joint and the Coracoacromial arch consisting of the coracoid, acromion and coracoacromial ligament. The posterior portion of the coracoacromial arch is where impingement usually occurs.

Inferior Border – Head of the Humerus

Contents – Sub-acromial bursa, supraspinatus tendon, infraspinatus tendon, teres minor tendon, long head of biceps

Normal Sub-Acromial Biomechanics

In order to achieve forward elevation above 90 degrees, the rotator cuff must pass under the coracoacromial arc. There will always be contact between the arch and rotator cuff because the sub-acromial space is a relative space. Some studies have even shown rotator cuff contact with the arch at 0 degrees. The contact is at the anterolateral component of the coracoacromial arch. As the arm elevates the contact moves medially. The humerus contacts the undersurface of the supraspinatus in a proximal to distal fashion with forward elevation. During arm movements the primary bursal contact is with the supraspinatus insertion. Sub-acromial bursa lies superior to the rotator cuff muscles and extends from the proximal 1/3 of the humerus (underneath deltoid) to medially beyond the AC joint. Bursa is heavily innervated. The rotator cuff muscles function as a unit to compress the humeral head into the glenoid fossa during movements. This limits the translation of the humeral head on the glenoid and allows for proper rotational movement. Thus the rotator cuff is very important for stability of the GH joint.


Problems usually arise during 70-120 degrees of arm elevation. As mentioned before, the subacromial space is not big and the contents within the space can easily become compressed against the coracoacromial arch. Therefore, any excess superior translation of the humeral head means more compression will occur. Extra wear and tear can exist as well with overhead athletes that put their arm through high loads and velocities in an abducted position. When your arm is abducted and taking from ER to IR with high loads and velocities, this can cause wear and tear on the sub-acromial structures. Repetitive unprotected overhead motion leads to insult of tissues in the subacromial space, which causes inflammation and tissue damage which starts the vicious cycle.

Causes of Sub-Acromial Impingment

There are inherent variations with respect to the acromion. Shape of acromion is important. There are three different shape types.2

Type 1 – Flat – 18%

Type 2 – Curved – 41%

Type 3 – Hooked – 41%

It was found that flat acromions were only associated with 3% of full thickness tears whereas hooked acromions were associated with 70% of full thickness tears.

These are different from natural acromion variations. These are adaptive in nature. Anterior acromial spurs are not that common at 14% of cadaveric specimens, but they were associated with 70% of rotator cuff tears. There are several theories as to why there is anterior spur formation. One is that the humerus superiorly migrates and abuts the underside of the acromion causing a reactive bone spur formation. Another theory is that the humerus continually abuts against the coracoacromial ligament leading to slight bowing of this ligament leading to a traction osteophytes being formed at the insertion. In patients with rotator cuff tears it has been found that some of them have thickened, hypertrophied and shortened coracoacromial ligaments.

Also a common cause of sub-acromial impingement is humerus migration superiorly. The bursa and tendons abut against the coracoacromial arch leading to pain. When the deltoid fires it causes superior translation of the humerus. If the rotator cuff is not strong enough to provide the stability required during movement then the deltoid forces are not counter balanced, leading to impingement. Also with patients that have GIRD (Glenohumeral internal rotation deficit), sometimes they can get impingement because the posterior capsule tightness will limit IR of GH joint leading to subsequent anterior and superior translation of the humeral head.

Poor scapular mechanics can lead to impingement. Weakness of dorsal scapular stabilizers and tightness of pectoralis minor, short head of biceps and coracobrachialis lead to scapular protraction and anterior tilting. When the scapula is in this position it places the acromion in a more horizontal position, thus there is a relative lowering of the roof of the coracoacromial arch and decrease in the subacromial space.


Wilk K, Reinold M, Andrews J. The Athlete’s Shoulder. 2md ed. Philidelphia: Churchill Livingstone Elsevier; 2009.

Clinical Effectiveness of Foot Orthotics

Orthotic usage is extremely prevalent in the running population. Orthotics can range from custom-made, custom-fit implements, to off-the-shelf generic insoles. Their desired purpose allows for wide variety in material, shape, and formation. Depending on the type of injury, different types of orthotics are thought to provide different functions. Orthotic intervention can be intended to alleviate symptoms, prevent deformity, and enhance performance.

A review done by Stefanyshyn et al. in 2006, analyzed the effects of foot orthotics on both general and specific running injuries. Results are summarized in the table below:


In summary, the above “general” studies found high success rates of orthotic intervention in relieving running injury and pain. In the studies that directly assessed the effects of orthotics on specific running injuries, relief rates were observed to be generally quite high. All pain relief rates were above 64% and the average rate was approximately 80%.

Richter et al., performed a systematic review and meta-analysis asking two very important clinical questions regarding foot orthotics: In patients with or at risk for musculoskeletal overuse conditions, do foot orthotics provide clinically meaningful improvements, and are they cost effective? A total of 23 RCTs were included in the systematic review. Overall, the evidence supported the use of foot orthotics to prevent first-time occurrence of lower limb overuse conditions and show no difference between custom and prefabricated foot orthoses. The evidence was insufficient to recommend foot orthoses for the treatment of lower limb overuse conditions.

A third review by Landorf et al. in 2000, used the following outcome measures to evaluate foot orthotic intervention success: patient satisfaction, pain and deformity, position and motion, muscle activity, oxygen consumption.

Patient Satisfaction

– 4 patient satisfaction surveys conducted on foot orthotics

  • In a retrospective study of 180 people with athletic injuries:
    • 70% indicated their orthotics had “definitely helped”
    • 78% felt their “posture had improved”
  • In a retrospective study of 81 people:
    • 91% of patients were satisfied with their orthotics
    • 94% of patients were still wearing their orthotics
  • Gross et al. surveyed 500 long distance runners:
    • 76% reported complete resolution or great improvement of their symptoms
  • It can be concluded that patients are generally very satisfied with their prescribed foot orthotics

Pain and Deformity

– Overall, Mixed results. Here is a highlight of the positive studies:

  • Custom fitted foot orthotics with metatarsal padding was shown to relieve sesamoid pain in 8/10 patients.
  • 34/40 patients with plantar fasciitis improved with foot orthotics – also more effective than NSAIDS, and viscoelastic heel cup.
  • Patients with pedal OA wearing prescription orthotics experienced a significantly longer period of pain relief than NSAIDS drug users.
  • Semiflexible functional foot orthotics were significant in reducing symptoms associated with patellofemoral pain syndrome in 102 patients.
  • Foot orthotics significantly decreased plantar callus in people with diabetes and deformity in RA.
  • Functional foot orthotics can prevent and slow the progression of hallux valgus deformity in RA.
  • Military orthotics significantly reduced the incidence of metatarsal stress fractures in low-arched feet and femoral stress fractures in high-arched feet.
  • For patients with OA of the medial knee joint, a wedged insole significantly reduces pain and discomfort.
  • Great results were also yielded with simple inexpensive orthotics: this raises the question of the effectiveness of expensive orthotics versus less expensive methods in reducing symptoms.

Position and Motion

– Greatest area of attention in past studies:

  • Functional foot orthotics have been shown to significantly reduce the amount and rate of pronation in walking and running.
  • Other studies have been shown to decrease internal tibial rotation
  • A recent study found that semirigid rearfoot posting significantly changed patella alignment (with the patella moving medially) in participants with excessive rearfoot pronation.
  • Lateral forefoot wedges decreases strain in the plantar fascia.

Muscle Activity

– Only one study to date on the effects of orthotics on EMG activity of muscles in the leg. There was a statistically significant increase in the duration of tibialis anterior activity following heel strike in the orthotic condition, and no change in peroneus longus and gastrocnemius.

  • Further research is required.

Oxygen Consumption

– A number of studies have been performed on the effect of orthotics and oxygen consumption.

  • Although the results are mixed, most studies show a negative effect when walking or running in association to oxygen consumption. This confers with research on limb mass and footwear, which shows an overall increase in the weight of a limb causes an increase in oxygen consumption. The improvement in biomechanical efficiency with the foot orthotics in these studies was outweighed by the negative effect of the weight of the orthotics themselves.

Although several of these studies summarized assessed orthotic usage in conjunction with other treatment modalities, results still look promising. Although orthotics do, however, appear to have a positive effect on running injuries, a conclusive statement directly linking orthotics to decreasing running injuries is not possible to make based on the current research. It is more accurate to state that the use of orthotics is associated with a relief from running injuries!

Now for a look at the proposed biomechanical mechanisms at how foot orthotics exert their therapeutic effects upon the body (a few were highlighted in aforementioned studies):

Skeletal Alignment

– Extreme positions of foot varus or valgus are thought to lead to excessive loading conditions during running and subsequent injuries. Excessive eversion during running combined with increased tibial rotation has been proposed to result in overuse injuries. To only name a few, a wide variety of running injuries including patellofemoral pain, plantar fasciitis, shin splints (medial tibial stress syndrome), achilles tendonitis and stress fractures have been linked to these aforementioned biomechanical risk factors. With that being said, a primary focus of orthotic intervention is to address foot alignment. Several studies in the past have shown mixed results regarding whether or not orthotic intervention in runners actually alters foot alignment and indirectly, also skeletal alignment. Further research is required in this field.

Cushioning of Impact Forces

– Increasing cushioning with the use of orthotics attempts to decrease the magnitude and rate of loading of the external impact forces during heel strike. Large impact forces have been traditionally proposed to be associated with running injuries, but like the idea of decreasing pronation, results from studies have been mixed. Several studies showed that custom-molded foot orthotics significantly reduce the vertical impact loading rate, while others studies have yielded contrasting results.

Decreasing Muscle Activity

– Several authors have proposed that orthotics should functionally support the preferred movement path of the lower extremities during running. As an example, rather than aligning the skeleton, orthotics may help guide and support the skeleton to most efficiently follow its own preferred path. If achieved, muscle activity would be reduced since the orthotics would partially replace the function of the muscles in supporting this preferred path. This, evidently, would yield reduced fatigue and a potential reduction in running injuries.

Reduced Joint Loading

– Another proposed mechanism of orthotics is to attempt to reduce the loading of the ankle and knee joint during running. Internal ankle inversion moments and resultant knee joint moments have been associated with lower extremity running injuries. Several studies have shown that medial posting has been found to systematically decrease ankle inversion moments. Like many of these proposed mechanisms, further studies are required in fully understanding these associations.

Other Proposed Orthotic Functions

– It is proposed that orthotics change the lever arm of the ground reaction force about the subtalar joint, influencing the joint power and ultimately work at the joint. An increased sensory feedback under the plantar surface of the foot has also been proposed during running.

Although there are several proposed mechanisms for which orthotics exert their positive effects upon the body, a great deal of them still require further study. For the time being, it is important that orthotics, do indeed decrease patient pain and increase functionality – the exact mechanism remains to be fully understood.


Landorf, K.B., Keenan, A.M. (2000). Efficacy of foot orthoses – what does the literature tell us? Journal of the American Podiatric Medical Association. 90(3): 149-158

Richter, R.R., Austin, T.M., Reinking, M.F. (2011) Foot orthoses in lower imb overuse conditions: a systematic review and meta-analysis. Journal of Ahtletic Training. 46(1) 103-106

Stefanyshyn, D.J., Hettinga, B.A. (2006) Running injuries and orthotics. International SportsMed Journal. 7(2): 109-119

Risk Factors of Neck Pain for the Office Worker

Computer use and neck pain in the office are two continuously growing trends, I thought I would investigate the possible risk factors and predictors towards this seemingly causal relationship. Posture plays a large role in workplace ergonomics and decreased prevalence of musculoskeletal complaints and there are a large number of other contributing variables that largely impact neck pain occurrence in the office.

Cagnie, B., Danneels, L., Van Tiggelen, D. (2007) Individual and work related risk factors for neck pain among office workers: a cross sectional study. European Spine Journal. 16: 679-686

The purpose of this study was to estimate the one-year prevalence of neck pain among office workers and to determine which physical, psychological and individual factors are associated with neck pain. 512 office workers filled out an approved in-depth online questionnaire. Dependent variables tracked in the questionnaire involved the presence of neck pain during the preceding 12 months. Independent variables were broken down into the following categories: individual (gender, age, height/weight, marital status, education, smoking, sleeping hours, leisure time), work-related physical factors (duration of employment, physical tiredness at end of day, physical workload, computer use, breaks during work, climatological conditions), and work-related psychological factors (mental tiredness at end of day, work variation, job satisfaction, and social support).

What they found was that the etiology of work-related neck disorders are multi-dimensional and are associated and influenced by a complex array of individual, physical, and psychological factors.

Key Points:

  • 12-month prevalence of neck pain was 45.5% (18.1% of workers still had continuous pain).
  • 3% of workers reported that there was a relation between their current job and neck complaints
  • 2% reported that their neck complaints started during their current job.
  • 2% went on sick leave due to their neck complaints.
  • Highest prevalence of neck pain in the age group between 40-49 years old.
  • Interestingly enough, hours of sleep at night were not linked to the likelihood of subsequent neck pain.


Risk Factor Odds Ratios: Individual Factors


Risk Factor Odds Ratio: Work-Related Physical Factors


Risk Factor Odds Ratio: Work-Related Psychosocial Factors


Some possible explanations towards the strongest risk factors

  • Sex difference: Smaller female stature and lower strength of shoulder musculature (In this study, 18% of females, and 11% of males reported neck pain).
  • Age: Increased neck pain prevalence with increased age may be explained by the increasing degeneration of the cervical spine.
  • Leisure: Stimulation of physical activity may constitute one of the methods of reducing musculoskeletal morbidity in the working sedentary population
  • Positive relation between neck flexion and neck pain – proven to be an increased risk of neck pain in workers who spend a high percentage of their working time with neck flexion.
  • Stationary positions: When performing work with hands/fingers muscles of the neck and shoulders must act as stabilizers (ie: static contraction of the shoulder musculature to keep arms at right angles during computer use, etc). Sitting for long periods of time is normally also accompanied by curvature of the spine and increased pressure on the discs, ligaments and muscles.

Stress: consistent evidence that stress is highly associated with chronic neck pain.

Breaks permit a reduction in exposure but more importantly, also permit muscle relaxation.

Hush, JM., Michaleff, Z., Maher, CG., et al. (2009). Individual, physical, and psychological risk factors for neck pain in australian office workers: a 1-year longitudinal study. European Spine Journal. 18: 1532-1540

The goal of this study was to prospectively evaluate a range of risk factors for neck pain in office workers as well as to attain an estimate of its 1-year incidence. 53 office workers without neck pain at baseline were studied and followed for one year. Individual, physical, workplace and psychological factors were measured at baseline.

The following predictors were used in this study:

  • Individual factors (age, gender, exercise)
  • Physical factors (C-spine ROM, cervical spine posture, endurance of cervical extensor muscles)
  • Workplace factors (total duration of sitting, sitting time between breaks, psychosocial workplace factors assessed using the job content questionnaire and job dissatisfaction subscale).
  • Psychological distress (anxiety, depression, etc).

What they found after one year was the following:

  • 26 of the 53 office workers (49%) reported an episode of neck pain during the 1-year follow up. (35% received chiropractic / physiotherapy during that time)
  • Major risk factors for neck pain include the female gender, decreased cervical flexion-extension motion, a sedentary lifestyle, depression, anxiety, and psychological stress
    • 3x more likely to develop neck pain in the office if female
    • Exercising more than 3x/week = 1.5x less likelihood of developing neck pain
    • Increased range of C-spine flexion and extension was protective indicating that office workers with a total range >120 degrees were 2.3x less likely to develop neck pain.
    • Office workers with high psychological stress had, on average, 1.6x greater probability of developing neck pain

Conclusive remarks: The female gender and high psychological stress may increase the risk of developing neck pain, whereas a greater mobility of the cervical spine and frequent exercise may be protective mechanisms for the office worker.

Risk Factors for Neck Pain in the Office


Eltayeb, S., Staal, JB., Hassan, A., et al. (2009). Work related risk factors for neck, shoulder and arm complaints: a cohort study among Dutch computer office workers. Journal of Occupational Rehabilitation. 19: 315-322

The purpose of this study was to investigate the relationship between work-related physical and psychological characteristics and complaints of the neck, shoulders, and forearms. Data was used from a prospective cohort study among 264 computer office workers with a follow-up period of 2 years. Similar to the 2 studies above, questionnaires were completed and potential risk factors were divided into work-related physical and work-related psychological factors. Potential confounders taken into consideration were age, sex, and previous histories of neck complaints.

After two years of following these office workers, it was concluded that neck complaints had the highest prevalence at 31%. The four main predictors of neck pain in office workers are the following:

  • Irregular head and body postures
  • Task Difficulty / Job Demands
  • Number of working hours per day at a computer
  • Previous history of neck complaints (Odds Ratio of 7.2)


The lifetime prevalence of neck pain is over 70%, and point prevalence is between 12% and 34%. Needless to say, these numbers are even higher for the office worker. From a physiological point of view, the first study by Cagnie et. al. came up with a great explanation for this: “Selective and sustained activation of Type 1 motor units can be seen as the most influential hypothesis for the development of muscle damage due to sustained low-intensity tasks (ie: a desk job). This may lead to calcium accumulation in the active motor units and other homeostasis disturbances due to limitations in local blood supply and metabolite removal in muscle compartment with larger number of active motor units”. A desk job often places continual stress and demands as well as constant contraction on neck/shoulder musculature, and if not kept to a minimum through ergonomic intervention, frequent breaks, and psychosocial health practices, neck pain generally ensues.

From these studies, it is fairly obvious to see that neck pain is a common issue in office workers (especially those with extensive computer use). It is also important to understand that these overlying musculoskeletal neck complaints are often multi-factorial in nature and can occur due to individual, psychosocial, physical, and work-related predictors. In patients presenting with a neck complaint, it is therefore, important to obtain a comprehensive history regarding their day-to-day duties at work. Identifying these factors that predispose individuals to persistent neck problems may contribute to primary and secondary prevention. With that being said, chiropractors can play an imperative role in understanding these above workplace risk factors and educate their patients by gaining awareness and assisting them in minimizing/eliminating these contributing factors at their desks on a daily basis.