Cervical spine Clinical anatomy & Motor control Part 1

Certainly, in the literature, there is mounting evidence of an association between chronic mechanical neck pain and altered neuromuscular control” (O’Leary, Falla & Jull., 2011, p.452).

There was a lot of research regarding deficits in the deep cervical neck flexor muscles(DCNF) – longus colli and longus capitus. Further research has investigated in the presence of motor control dysfunction throughout range of motion of cervical spine dysfunction and aimed to determine the best treatment approaches for such deficits.

Some of this changes in motor control that we hear about are:
•       Increased activity in the superficial neck flexor muscles,
•       Reduced coordination of the deep neck flexor muscles.
•       Reduced endurance in the deep neck extensors.


What are the muscles  referring to?

Global movers are involved in the generation of torque and produce a range of movement. They function in a phasic manner.When find dysfunctional there is a spasm, pain and restricted range of movement joint .Local stabilizers are the deeper muscles that control segmental control and neutral positioning of a joint. Dysfunction in the local muscles results in inhibition of function, delayed timing or recruitment deficiencies and loss of segmental control and neutral joint positioning.

There are three main groups of cervical muscles which  enable control of posture and segmental movements:

1.      The deep cervical flexors – longus colli and longus capitus.
2.      The deep neck extensors – semispinalis cervicis and multifidus.
3.      The suboccipital muscles – rectus capitus posterior major & minor, and obliquus capitus superior and inferior.


We are  familiar with deep neck flexors (DNF). The literature often refers to the superficial muscles which become relative stiffness in the presence of neck pain and the deep neck flexors which become dysfunction.

The  superficial flexor muscles of the cervical spine include  sternocleidomastoid(SCM) and anterior scalenes (AS):•        Sternocleidomastoid functions bilaterally to create neck flexion and  to create ipsilateral lateral flexion and contralateral rotation. The SCM is innervated by a spinal root of the accessory nerve.

Anterior scalene : it  functions to elevate the first rib, and similar to SCM it creates ipsilateral lateral flexion and contralateral rotation. The anterior scalene is innervated by C4, C5, and C6 nerve roots (Cleland, 2005).

When referring to the deep flexor muscles , we are talking about longus colli and longus capitus. The function of longus colli and longus capitus is to maintain cervical lordosis and provide segmental control (Fall, Bilenkij & Jull., 2004).

When these muscles activate they create cranio-cervical flexion (CCF) and support cervical lordosis anteriorly (Jull, Sterling, Treleavan, Falla & O’Leary., 2008).

Longus capitus is innervated by C1-3 spinal segments and longus colli from C2-6 (Cleland., 2005).


Sternocleidomastoid                        Anterior scalene




The flexor group consists of SCM, AS and DNF but the extensor group is consists of a lot more muscles. There are 4 layers of cervical extensors From most superficial to deep (Schomacher & Falla., 2013, p.360-361).

Here are 4 layers of extensors muscles group

•       Layer 1: Levator scapulae and upper trapezius not only primarily considered to be muscles of the shoulder girdle but also  form a superficial layer over the cervical extensor group. Upper trapezius is innervated by a spinal root of the accessory nerve and levator scapulae from the dorsal scapula nerve (Cleland., 2005).

•       Layer 2: Splenius capitus and cervicis which acts bilaterally as an extensor and ipsilaterally to produce rotation. Splenius capitus and cervicis are innervated by dorsal rami of the middle cervical spinal nerves (Cleland., 2005).

•       Layer 3: Semispinalis capitus is primarily a cervical extensor and unilaterally to create lateral flexion. Both innervated by dorsal rami of spinal nerves (Cleland., 2005).

•       Layer 4: Semispinalis cervicis and multifidus. These are  known as the  deep cervical extensors (DNE or DCNE). Semispinalis cervicis acts a cervical extensors and multifidus as a segmental stabiliser.

They provide posterior support of cervical lordosis in relation with the deep neck flexors and prevent a forward head position (Jull, Sterling, Treleavan, Falla & O’Leary., 2008). These muscles are also innervated by dorsal rami of cervical spinal nerves (Cleland., 2005).
Upper trapezius                   Semispinalis capitus


Splenius capitus and cervicis



These four muscles form the suboccipital muscle group and which should be  rehabilitated separately to the deep cervical extensors.

•       Rectus capitus posterior major & minor – head extension and ipsilateralbrotation
•       Obliquus capitus superior – head extension and side bending.
•       Obliquus capitus inferior – ipsilateral head-on-neck rotation.

The suboccipital muscle group is important to provide proprioception and contribute to the visual and vestibular systems. They control cranio-cervical lordosis and small head-on-neck movements. Dysfunction results into sensorimotor impairment, altered kinaesthetic sense and , oculomotor control . It can lead to cervicogenic dizziness. All of these muscles are innervated by the suboccipital nerve C1 (Cleland., 2005).

Why we are beginning with the clinical anatomy?

I think, it is clinically very important to understand which muscles lie in our hands on palpation.Their fiber direction and their innervation. Dysfunction or nerve injury can lead to changes in cervical motor control.
So that we can assess motor control with a deeper understanding of what we might expect to find, what normal and abnormal results are and what the clinical relevance of these findings are.




The author states that patients with neck pain will often display reduced muscle activation in the DCNF during the  craniocervical flexion (CCF) as well as delayed activation during postural perturbations (Schomacher & Faller., 2013). Not only do we notice that patients with neck pain have different levels of control over muscle activation patterns but they also lack endurance (Jull, O’Leary, Falla., 2008, p.529).

In regards to WAD, Jull, O’Leary & Falla (2008) found that patients display higher levels of EMG activity in SCM and AS when compared to asymptomatic controls. Other studies have shown a similar pattern, of increased activity in upper trapezius, SCM and AS in patients with chronic neck pain from both insidious and traumatic origin (Falla, Bilenkij & Jull., 2004).

There are three major questions that researchers are trying to solve in regards to flexor muscle dysfunction. One is whether these deficiencies in deep cervical neck flexor (DCNF) control and increased activation in superficial neck muscles are associated with each other. Is there a cause and effect relationship between the two?

One thing that is not clear, if the motor control impairments spontaneously resolved with the recovery of neck pain. Many studies suggest that  specific training is required to improve posture, strength and endurance (Jull, O’Leary, Falla., 2008; Jull., 2008; O’Leary, Falla, Ellior & Jull., 2009; Falla., 2004). What this research suggests that maybe the motor control deficits don’t improve at the same rate as pain. If we don’t make it a priority to assess motor control during the initial treatment sessions, we have no objective measure of whether or not exercises are required. Once pain and movement has resolved, most patients might wrongly assume they have fully recovered and convincing them to perform a home exercise program which might be difficult. HOwever, if we document changes in strength, coordination and endurance early in our treatment. This help us  to monitor changes in these aspects of recovery, then we can promote more compliance in our patients to complete their rehabilitation.




Schomacher & Falla (2013) published a paper in recent times highlighting the importance of the cervical extensor muscles.

“Patients with neck pain often display increased activation of the superficial neck extensors and delayed activity in semispinalis cervicis and multifidus” (Schomacher & Faller., 2013, p. 362). Which you could say is similar to the changes observed in the cervical flexor muscle group, where anterior scalene and sternocleidomastoid are observed to have increased activation while there is reduced activation in the deep cervical flexors.

“When changes in activation patterns occur in semispinalis cervicis it is generalised across all fascicles of the muscle, not just localised to the painful segment” (Schomacher & Faller., 2013, p. 362). Therefore if semispinalis cervicis is a cervical extender, changes may occur across the entire muscle belly that effects it’s ability to control and perform cervical extension across multiple levels. Why these changes occur, in both muscle groups remains unclear and possibly related to a variated of mechanisms (Schomacher & Faller., 2013).  These “studies have shown that patients with mechanical neck pain have deficiencies in maximal strength, endurance, precision during dynamic movement, and sustained isometric contraction, efficiency of contraction, and repositioning acuity” (O’Leary, Falla, Elliot & Jull., 2009., p. 327).

Take home message from the research :

My hope is that this provides sufficient evidence to support and justify why we need to be paying closer attention to the muscular control of the cervical spine.

•       We now know that they develop in most cases of neck pain and aren’t specific to one type of injury or pathology.

•       We don’t know how long it takes for the changes to develop but we do know that they don’t spontaneously resolve.

•       This means we need to be responsible for assessing our client’s cervical motor control, monitoring it during their recovery and ensuring that optimal motor control is restored.

New mindset when palpating or assessing a patient with neck pain. Before we learn how to perform the tests, first think about what muscles lie in the region you are palpating, which nerves involved them, and which movements these muscles contribute to.

“Sufficient evidence already exists to indicate that assessment of cervical muscle function should be routine in the clinical examination of patients with mechanical neck pain” (O’Leary, Falla, Elliot & Jull., 2009., p. 327).


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  2. O’Leary, S., Falla, D., Elliott, J. M., & Jull, G. (2009). Muscle dysfunction in cervical spine pain: implications for assessment and management. journal of orthopaedic & sports physical therapy, 39(5), 324-333.
  3. Falla, D. (2004). Unravelling the complexity of muscle impairment in chronic neck pain. Manual therapy, 9(3), 125-133.
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  5. Falla, D., Bilenkij, G., & Jull, G. (2004). Patients with chronic neck pain demonstrate altered patterns of muscle activation during performance of a functional upper limb task. Spine, 29(13), 1436-1440.
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  7. Edmondston, S., Björnsdóttir, G., Pálsson, T., Solgård, H., Ussing, K., & Allison, G. (2011). Endurance and fatigue characteristics of the neck flexor and extensor muscles during isometric tests in patients with postural neck pain. Manual Therapy, 16(4), 332-338.
  8. Jull, G. A., O’Leary, S. P., & Falla, D. L. (2008). Clinical assessment of the deep cervical flexor muscles: the craniocervical flexion test. Journal of manipulative and physiological therapeutics, 31(7), 525-533.
  9. Schomacher, J., & Falla, D. (2013). Function and structure of the deep cervical extensor muscles in patients with neck pain. Manual therapy, 18(5), 360-366.
    SELVARATNAM, Peter, et al. Headache, orofacial pain and bruxism. 2009.
  10. O’Leary, S., Falla, D., & Jull, G. (2011). The relationship between superficial muscle activity during the cranio-cervical flexion test and clinical features in patients with chronic neck pain. Manual therapy, 16(5), 452-455.
  11. Falla, D., Jull, G., O’leary, S., & Dall’Alba, P. (2006). Further evaluation of an EMG technique for assessment of the deep cervical flexor muscles. Journal of Electromyography and Kinesiology, 16(6), 621-628.
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    VAN ETTEKOVEN, H.; LUCAS, C. Efficacy of physiotherapy including a craniocervical training programme for tension‐type headache; a randomized clinical trial. Cephalalgia, 2006, vol. 26, no 8,
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Flexor Hallucis Longus (FHL):

Origin: Posterior surface of the distal 2/3rds of the fibula, interosseous membrane, and adjacent intermuscular septa and fascia.

Insertion: Base of the distal phalanx of the great toe, plantar surface .

Nerve: Tibial nerve arising from the sciatic nerve via the sacral plexus, originating from nerve roots L5, S1, and S2.


Phalanges: flexion of the interphalangeal joint of the great toe and assists in flexion of the metatarsophalangeal joint

Ankle: Plantar flexion of the foot, as well as, aaccesory  invertor of the foot and ankle.

Relative Location:

The flexor hallucis longus (FHL) is located lateral to the tibialis posterior. The anterolateral border combined with the periosteum of the fibula and posterior intermuscular septum.

Integrated Function:


Stabilizes the tibiotalor & subtalor joints,transverse tarsal, tarsometatasal, metatarsophalangeal, interphalengeal joints.

Eccentric action :

The FHL eccentrically decelerate extension of the metatarsophalangeal and interphalangeal joints, as well as dorsiflexion and eversion of the ankle.


The FHL work synergistically with the tibialis posterior to eccentrically decelerate eversion during the mid-stance of gait cycle. In addition, it also helps medial gastronemus and plantaris . It also assist in push off and landing mechanics during gait cycle.

A functional relationship may exist between the FHL, the tibialis posterior and tibialis anterior in control of the talus. Some evidence state that the FHL may control talar inversion via the groove in the talus and the sustentaculum tali of the calcaneus.


The FHL cross several joints, but likely have their largest impact on the interphalangeal joints – capable of producing plantar glide. In claw toe deformity the extensor hallucis longus and extensor digitorum longus may also contribute to dysfunction by producing excessive dorsal glide of the metatarsophalangeal joints.

Course of FHL:

The FHL has an interesting course, running through a groove on the posterior medial talus and continuing through a groove inferior to the sustentaculum tali.

During contraction of the FHL this creates an anterior and superior force on the medial side of the talus. This may have functional implications on talar and calcaneal mechanics, specifically an ability to contribute to inversion and a varus tilt of the talus and calcaneus . It potentially anterior glide of the talus on the tibia.

Fascial Integration of the FHL

The most obvious relationship exists between the posterior tibial fascia and the combined FHL and FDL. Which links the deep posterior compartment muscles by function and fascia.

Additionally, the  tendinous slips of the FHL may distribute the load in the forefoot, especially during toe-off phase of gait cycle. This increases the weight-bearing on the forefoot and eventually helps the FHL support the medial longitudinal arch of the foot .

Lower Leg Dysfunction (LLD):

These muscles are long due to excessive eversion at the subtalar joint and tilt of the talus, but rather than resulting in a decrease in tone, the inhibition of prime movers results in over-use and hyper-facilitation of these synergistic muscles.

When tibialis posterior is inhibited , the FHL become synergistically dominant. That is to state that the overactive fibularis muscles result in altered reciprocal inhibition of the tibialis posterior and a relative increase in FHL activity to compensate for a lack of force production in inversion. Furthermore , there is evidence suggest that the FHL and FDL may play a similar role at the metatarsalphalangeal joints, compensating for inhibited short toe flexors.

Excessive pronation:

The change in arthrokinematics and activity may limit extension of the toes  a compensation pattern that generally leads to excessive pronation (eversion) from heel-off to toe-off during the stance phase of gait cycle.

To sum up, the FHL is long and over-active, acting as overactive synergists. This clearly indicate that this muscles should be released, but do not stretched or activated. This trigger points in these muscles are often mistaken for gastrocnemius and soleus trigger points during self-administered release technique.


image coutsey : wikipedia.com

FHL Trigger Points :

Palpation results in tenderness (trigger points or tender points) and may result in radiating symptoms along the muscle and its tendons. Based on the theoretical model of trigger point development it would seem likely that “trigger points” are dysfunction at the “motor point” of a muscle, and release will decrease tonicity via reflexive inhibition or ischemic pressure .



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Proactivephysiotherapy, hamstring, assesment, lower limb

Hamstring muscles strain : Assessment & Risk factors

Hamstring muscle strain injuries  are common in sports  which required acceleration, deceleration, rapid change in direction.

According to Schache et al 2009 & Heiderscheit et al 2005 Hamstring injuries are proposed to occur during the terminal swing phase of running as a consequence of an eccentric contraction. Sometimes hamstring late firing also contribute to strain.

There are two mechanisms of hamstring injuries. .

  1. Type 1: high intensity running with the injury occurring during late swing phase involving the proximal musculotendinous junction of the long head of biceps femoris.
  2. Type 2: stretching of the hamstring complex due to an extreme joint position involving mostly semimembranosus and the proximal tendon.

The majority of hamstring injuries occur at the biceps femoris (BF) long head.

What are the RISK FACTORS?

Many research papers have considered a potential risk factor for hamstring muscles strain injury however other authors inconsistently identified as contributing to the injury.

In addition to that, A systematic review and meta-analysis research said   risk factors for hamstring injury

  • Older age
  • Increase quadriceps peak torque
  • Past history of hamstring injury

There are Other strength measures such as hamstring: quadriceps ratio, which is the best commonly perceived to be predictive of injury, were not associated with a hamstring injury (Freckleton & Pizzari, 2013).



Here you can predict the differential diagnosis for hamstring strain injury

  1. lumbar spine (disc/ facet joint),
  2. SIJ dysfunction, gluteal/piriformis/Gemelli trigger points,
  3. Hamstring tendinopathy, avulsion injuries,
  4. vascular claudication and compartment syndrome (Brukner & Khan, 2006).

The subjective assessment is a key point to correctly diagnose an injury. Players with a hamstring injury will report sudden onset of pain localized to the hamstring region with a clear mechanism or incident.  (Pizzari, et al., 2010).  A particularly previous hamstring injury is also important of the major risk factors for future hamstring injuries (Freckleton, et al., 2012).

There are some  positive clinical signs, and symptoms for hamstring injury (Bennell, et al., 1999):

  • Immediate onset of posterior thigh pain,
  • Tenderness on palpation,
  • Reproduction of pain on a stretch of hamstring,
  • Reduced straight leg raise ROM,
  • Reduced strength on a resisted active contraction of hamstrings


What should you include in your  physical examination ?

  1.  lumbar spine AROM,
  2. Slump test
  3. SLR, active knee extension test (AKE),
  4. passive hamstring muscle stretch and palpation of pelvic musculature for trigger points and reproduction of posterior thigh pain.
  5. Resisted contraction of the hamstrings should be tested in multiple positions of knee flexion (Brukner & Khan, 2006).

Palpation is the most important aspect of the physical examination to help identify location and severity of the injury (Pizzari, et al., 2010).


A  study investigated the use of the single leg hamstring bridge(SLHB) as a clinical test in predicting hamstring injuries in football players. The hamstring muscles in a functional position similar to terminal swing and assesses endurance parameters rather than peak torque.

SLHB test could be used to screen and identify athletes who are potentially at risk of sustaining a hamstring injury. It may be used to evaluate an athlete to return to sport.




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  3. Askling, C., Saartok, T., & Thorstensson, A. (2006). Type of acute hamstring strain affects flexibility, strength, and time to return to pre-injury level. British Journal of Sports Medicine40(1), 40-44.
  4. Croisier, J. L. (2004). Factors associated with recurrent hamstring injuries. Sports Medicine34(10), 681-695.
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  6. Freckleton, G., Cook, J., & Pizzari, T. (2013). The predictive validity of a single leg bridge test for hamstring injuries in Australian Rules Football Players. British journal of sports medicine.
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  14. Schache AG, Wrigley TV, Baker R, et al. Biomechanical response to hamstring muscle strain injury. Gait Posture 2009;29:332–8.12
  15. Schneider-Kolsky M, Hoving J, Warren P, et al. A comparison between clinical assessment and magnetic resonance imaging of acute hamstring injuries. Am J Sports Med 2006;34:1008
  16. The predictive validity of a single leg bridge test for hamstring injuries in Australian Rules Football Players   2014 Apr;48(8):713-7. doi: 10.1136/bjsports-2013-092356. Epub 2013 Aug 5.

Clinical reasoning & treatment for lateral epicondylitis

Tendons are the tissue that attaches the muscles to the bones. Overuse in the upper extremities can result in the diagnosis of the tendonitis or the tendonitis of the wrist, elbow or shoulder. The most common wrist or forearm problems include tendinopathy of the muscles that extend the wrist, otherwise known as tennis elbow.

The major muscles that move the wrist have their origin at the elbow. If the wrist is improperly used, pain may arise in the forearm and/or outside of the elbow. Tennis players and athletes who use backhand and does repetitive motions that extend and fled the wrist is, particularly at risk. Lateral elbow pain may not affect only such players or athletes but also affect who use a screwdriver or hammer on the daily bases or those who great amount of time in gardening taking, painting. The patient who works with a pronated forearm and flexed wrist like computer workers also feel lateral elbow pain and burning sensation which is called as (supinator syndrome).

Clinical reasoning in determining the nature of elbow pain:

Tennis elbow is the common nomenclature for lateral elbow pain.

It is caused due to one or more following consequence,

maligned bones in the elbow and/or carpals, tendonopathy, capsular pain, radial nerve pain, neck and thorax dysfunction.


Clinical reasoning of tennis elbow, proactive physiotherapy 


Treatment strategies :

Frequently tennis elbow is treated with local ultrasound, stretching and wrist strengthening, however, there are several reasons need to be addressed and treatment should be planned accordingly.

Depending on the examination findings, treatment could include

  • joint mobilizations to the elbow, cervical and thoracic spines
  • soft tissue massage of the scalenes, levator scapula, upper trapezius, latissimus dorsi, wrist flexors
  • dry needling of supinator, pronator teres, common extensors, posterior rotator cuff, upper trapezius, thoracic erector spinae
  • Exercises for scapulothoracic-cervical mobility & stability (rhythm)
  • exercises for thoracic (vertebrae & ribs) mobility and cervical mobility & stability
  • mobilization with movement (MWM’s – Mulligan’s technique) for upper ribs, wrist, and elbow
  • Mulligan’s and/or McConnell’s taping
  • Kinesiotaping
  • prescription of elbow or wrist brace
  • strengthening exercises for the shoulder, elbow and wrist muscles.
Shoulder joint

Shoulder impingement syndrome : Contribution of scapula



The shoulder is a ball and socket synovial joint . The shoulder is such a fascinating joint with 180 degrees of freedom, which relies on excellent dynamic movement.

How should we use it in the diagnosis of shoulder pain?

In early 1980, Neer et all describes Shoulder impingement and researched for many years and some of the original work . As our understanding of impingement has expanded we have come to realise that there are types of shoulder impingement i.e internal and external, and primary and secondary (Ludewig & Braman, 2011).

What is Internal versus external impingement?

It depends on the site of the impingement. If it is located in the subacromial space it is known as external impingement. If it is located within the glenohumeral joint it is known as internal impingement (Cools, Cambier & Witvrouw, 2008).


External impingement : According to Neer et all, when there is compression between the rotator cuff tendons or long head of bicep tendons, between the humeral head and the undersurface of the acromion, coracoacromial ligament .

Internal impingement : compression of the supraspinatus tendon and/or infraspinatus tendon between the humeral head and posterosuperior glenoid rim. This usually occurs at 90 degrees abduction and external rotation.

Remember , when you simply saying “shoulder impingement” as a diagnosis. This label does not indicate you:
• Which structures are involved.
• Where is the exact site of impingement


What is Primary and secondary impingement?

When there is injury to shoulder joint, it gradually leads to structural narrowing of the subacromial space due to acromioclavicular athropathy, or pathology within the tissues in the subacromial space .

According to Lewis (2011) et all, many people directly jump to the assumption that if structures are impinged, surgery is required to ‘make more room’, but it’s not the case. The pathology lies within tendon itself.

Secondary impingement :

• Glenohumeral joint instability, which can lead to excessive humeral head translation and/or poor position of the humerus in relation to the scapula. In addition to that subscapularis inefficiency to maintaining huneral head in central position.

• Scapula dyskinesis

• GIRD (glenohumeral internal rotation deficit) There is a loss of glenohumeral internal rotation and increase in external rotation, often the posterior cuff & capsule become tight and there is excessive anterior translation of the humeral head resulting in secondary impingement also we can say it’s shoulder medial rotation uncontrol movement. ( Lewis2011 et all)

Many authors said that secondary impingement can affect the rotator cuff tendons or long head of biceps, and it can be both internal and external (Burkhart, Morgan & Kibler 2003; Cools, Cambier & Witvrouw, 2008; Ludewig & Braman, 2011).


The knee movement occurs in sagittal plane only which we consider 1) flexion and 2) extension. Shoulder is complex joint and it has many range of motion which are even more complex.

When we see shoulder patient walk into our clinic , First question comes in our mind where to start assesment. The key to improving your assessment of shoulders is to have a routine checklist in your assessment technique. For instance you should always assess the injured then the non-injured side. According to chief complaint make order of your test because if you prove ke pain initially then all test will be false positive . You should always assess movements in the same order.

Cools et al (2008) published a fantastic paper outlining an assessment algorithm to assist clinicians in their screening of shoulder patients with suspected impingement and clinical diagnosis. This algorithm is a great place to start when you’re developing skills in shoulder assessment.

The images below represent the Hawkin’s Kennedy, Neer, and Jobe test for shoulder impingement described in the algorithm above (Cleland, 2005).




after reading this algorithm the scapula assistance test & scapula retraction test will become your routine clinical test

(Cools, Cambier & Witvrouw 2008)


Scapula assistance test : assesses the impact of correcting scapula position on shoulder pain and impingement symptoms during active shoulder elevation. the clinician assists the scapula into upward rotation while the patient elevates their arm and observes if there is a change in pain.


Scapula retraction test assesses the impact of maintaining scapula position during loading and assessing the impact on pain. For the scapula resistance test the therapist resists the scapula into retraction while assessment pain in the resisted elevation in an abducted and internally rotated position.

Let’s gather all points :

When assessing a shoulder you should always try to focus on the following:

• Carefully observing the functional aggravating position.
• Reproducing shoulder symptoms and then trying to change them with scapula positioning, muscle activation exercises or manual therapy.

• If there is a reduction in pain it indicates a ‘green light’ to go ahead and treat with same rehabilitation.

• If there is Red light during your assessment – you will need to reconsider your diagnosis, consider a referral for medical imaging and/or referral to a specialist.




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6) Kibler, W. B., Sciascia, A. D., Bak, K., Ebaugh, D., Ludewig, P., Kuhn, J., … & Cote, M. (2013). Introduction to the second international conference on scapular dyskinesis in shoulder injury—the ‘Scapular summit’report of 2013.British journal of sports medicine, bjsports-2013.

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