November 2010 Andrews University
The CERVICAL SPINE
During rotation of the head in a weight-dependent position the entire body tends to rotate in the same direction. This produces a force that threatens to penetrate whatever ground surface supports the body. This is resisted by ‘ground reaction’. This vertical thrust through the body is responsible for the formation of the typical scoliotic curve seen in the spine during rotation.
All vertebrae must obviously rotate in the same direction but the vertical loading creates a distinct change in the side-bending that occurs within the spine and this occurs at the thoraco-lumbar junction.
The entire spine above this junction forms one half of a ‘C’ curve i.e., every joint rotates and side bends ipsilaterally.
In an average individual whose head rotates 90 degrees, up to 70% of this occurs at the craniovertebral joints. The remaining 30 degrees occurs in the segments C2/3 to T11/12. No research has been done to see exactly how much the thorax contributes to this rotation but a simple experiment suggests it is significant.
If the cooperative thoracic motion is lost e.g., through articular dysfunction or FHP, rotation of the head is significantly impacted.
Compensation for such a functional loss will invariably occur in the cervical spines ‘weakest links’ i.e., the lower three segments. In the ‘average’ person with a habitual FHP these segments prematurely deteriorate.
The abnormal biomechanical demands created by a loss of thoracic motion will tend to compromise these segments further making them ‘structurally unsound’. This in turn can precipitate foraminal compression (especially at C5/6) and cervical segmental fixation (e.g, a ‘wry neck’).
Not surprisingly, mobilization or manipulation of the thorax can significantly alleviate cervical symptoms and restore function. This has led to the erroneous suggestion that therapists do not need to manipulate the cervical spine as long as the thorax is corrected.
The LUMBAR SPINE
In Gracovetsky’s concept of the ‘Spinal Engine’ we see how the psoas muscle produces potential kinetic energy within lumbo-pelvic spring by torsioning the entire lumbar spine and pelvis during the terminal ‘stride’ phase of gait.
Storing potential kinetic energy within inert tissues (e.g., capsules; ligaments) and reusing it with each successive step has made human gait (striding) the most biomechanically efficient form of locomotion of any other mammal on earth.
However, if all of this energy were stored within the annulus of discs, neural arches of the lumbar spine and the pelvic joints and ligaments, structural fatigue and failure would occur fairly rapidly. To avoid this, the body has developed two secondary ‘storehouses’ of potential kinetic energy.
As the hip moves from mid-stance to close-pack (extension and internal rotation) it transfers a large amount of torsional energy to the joints of the lower limb, especially the feet (see article ‘The hip bones connected to the foot bone’), where kinetic energy is stored in distortion of the joint capsules and ligaments of the lateral foot.
Superiorly one doesn’t have to look far an obvious spring mechanism, the thorax. The multiplicity of joints and the flexibility of the rib cage provide an obvious store of potential kinetic energy. This is enhanced by the pendular swing of the upper limbs and shoulder girdles.
If either of these secondary kinetic energy stores (i.e, the hip or thorax) is unavailable due to motion dysfunction, then the energy must be stored and contained within the lumbar spine and pelvic joints themselves.
As mentioned previously this would lead to inert tissue failure.
The most obvious sites of such ‘fatigue’ or failure would be the annulus fibrosis of the lumbar segments and/or its osseous neural arches presenting clinically, most usually, as lumbar segmental instability.
Having either rotational hypomobility of the thorax or loss of close-packing in the hip would predispose to lumbar segmental deterioration. Having both thoracic and hip joint hypomobility virtually guarantees it.
Since a habitual FHP is one cause of thoracic hypomobility, if this (posture) is not attended to during treatment of a lumbar instability, future thoracic problems can sabotage an otherwise successful program. When faced with temporary success, of a lumbar stabilization program, assessment of hip and thorax motion is therefore essential.
A habitual FHP also compromises lumbar spine function because of the displaced line of gravity. It is estimated (ref. J Oldham) that for every inch the body’s line of gravity is displaced forwards, loading of the lumbo-sacral junction increases by a factor of two. As an example, a 200lb man with a 3 inch displacement would have, not 100lbs of loading at the L/S junction, but 800lbs!! Trying to rehabilitate a lumbar disc protrusion or segmental instability under such circumstances would be impossible.
The SHOULDER GIRDLE
During elevation through flexion/abduction the range of motion between 0 and 150 degrees occurs predominantly at the glenohumeral and acromio-clavicular joints.
At 150 degs lower serratus anterior contracts isometrically, changing the axis of motion of the shoulder girdle to an oblique line drawn from the sterno-claviclar joint to the inferior angle of the scapular.
This means that further displacement of the arm through a sagittal plane is facilitated by the girdle moving into depression and retraction.
This movement occurs exclusively at the sterno-clavicular joint and the prime mover is the lower trapezius, controlled eccentrically by pectoralis minor and the upper fasciculus of serratus anterior.
During this motion (150-200 degs) the upper thoracic spine is seen to move into extension and ipsilateral side bending and rotation.
If the thorax cannot perform this motion, end-range elevation (150-200 degs) is limited, not mechanically, but by inhibition of inner range contraction of lower trapezius. On assessment this is picked up as a trapezius’ lag’.
The purpose of this thoracic involvement is described in detail in the paper ‘The Functional Shoulder Girdle’, but here is a brief review.
The movements of glenohumeral flexion and abduction, along with shoulder girdle retraction and depression all produce a posterior rotation of the clavicle when produced in isolation. However, when moved collectively during functional elevation through flexion the clavicle hardly rotates at all.
Simultaneous thoracic movement of extension and ipsilateral rotation and side bending produces a motion in the manubrium that exactly counteracts the potential posterior rotation of the clavicle. The best analogy to this phenomena is to walk up a down escalator. If your speed exactly matches the escalator you actually don’t move at all, in space.
But why is it necessary to minimise rotation of the clavicle?
During embryological development the pre-vertebral (deep cervical) fascia invests ALL structures residing in, or passing through, the cervical region. This includes the mandible, clavicle, cervical muscles and nerves of the cervical and brachial plexus.
Clinical observation suggests that the fascial investment of the clavicle acts is as if it were wrapped around in an ‘ALPHA orientation’. (See paper ‘Cervico-clavicular Syndrome’).
In other words, any rotation of the clavicle (anterior or posterior) would act like a ‘winch’, tightening the deep cervical fascia and compromising neurological and vascular structures to the upper limb.
During elevation through flexion the motion of the manubrium, produced by motion of the thoracic spine, ensures that the clavicle cannot rotate in relation to the deep cervical fascia. This provides neutral fascial tension and optimal neuro-vascular mobility, which leads us, conveniently, to our final scenario.
A SYNOPSIS of the JOINT MOTION, MUSCLE ACTIONS and THORACIC INVOLVEMENT during ELEVATION OF THE ARM through FLEXION/ABDUCTION
BETWEEN 0-150 DEGS OF ELEVATION
At the glenohumeral joint:
As the arm is moved through a sagittal plane the glenohumeral joint moves through flexion (90-100 degs), abduction (90-100 degs) and external rotation (60-80degs).
The prime movers are the deltoid and rotator cuff muscles (with the notable exception of subscapularis) contracting concentrically.
The antagonists (controllers) are the subscapularis, the ‘bicipittal groove muscles’ (pectoralis major; latissimus dorsi; teres major) and the ‘coracoid muscles’ (short head of biceps; coraco-brachialis), all contracting eccentrically.
NOTE: C5 palsy or C6 facilitation can cause significant resistance to this phase of motion.
At the acromioclavicular joint on a fixed clavicle:
The inferior angle of the scapula is displaced lateral and anterior (50-60 degs), causing an ‘upward rotation’ of the glenoid surface.
The prime movers are all parts of the trapezius and the middle and lower portions of serratus anterior (C6). Both muscles are contracting concentrically.
The antagonists are levator scapulae (C2/3 and C3/4) and the rhomboids (C4/5/6), working eccentrically.
NOTE: At this point, the nerve roots and cords of the brachial plexus are under optimal tension.
Further elevation of the arm would tend to posteriorly rotate the clavicle around its longitudinal (coronal) axis. This would place an untenable tension on the deep cervical fascia seriously threatening the neuro-vascular tissue entering the arm.
BETWEEN 150-200 DEGS of ELEVATION
At the sternoclavicular joint:
At about 150 degs of arm elevation the inferior angle of the scapula is seen to stop moving. This is presumably the effect of lower serratus now contracting isometrically.
This changes the axis of motion of the shoulder girdle to an oblique axis between the inferior angle of the scapula and the sternoclavicular joint.
The entire girdle is seen to go into depression and retraction. The prime mover is the lower trapezius working concentrically in its inner range.
The antagonists are the pectoralis minor (C8) and the upper fasciculus of serratus anterior (?C7) working eccentrically.
At the thoracic joints:
The upper half of the thoracic spine is seen to extend, rotate and side bend ipsilaterally towards the elevating arm.
Because of the rigidity of the 1st thoracic ‘ring’ the manubrium follows the T1 vertebra producing a posterior and inferior displacement of the right sternoclavicular surface.
At the ‘menisco-manubrial’ articulation this displacement causes a relative anterior rotation of the clavicle. This relative anterior rotation of the clavicle counteracts the potential posterior rotation being created by the scapula thus minimizing increased tension in the deep cervical fascia.
Proposed neuro-musculo-skeletal co-ordination
It would appear (M Cummerford) that as the glenohumeral and acromioclavicular joints reach their limit of movement articular receptors trigger off a reflex contraction of lower trapezius (inner range) and the ipsilateral thoracic extensors.
Together these muscle groups create depression and retraction of the shoulder girdle with associated extension, ride side bending and rotation of the upper thoracic spine.
So, it would appear that from an articular point of view there are two requirements for full elevation through flexion/abduction between 150-200 degs:
1) Full motion at the G/H and A/C joints. Restriction of motion is most commonly caused by muscular hypertonus due to facilitation from cervical compensatory hypermobility or postural deterioration.
2) Full motion of the thoracic segments into extension, side bending and ipsilateral rotation. This combination of movements may be impeded in a number of ways:
a) a chronic, habitual forward head posture (bilateral loss of extension)
b) an anterior fixation (flexion subluxation) of a thoracic segment (bilateral loss of extension)
c) a unilateral loss of upper thoracic Z-joint motion into extension and side bending (detectable by the ‘manubrial test’)
Any of the above dysfunctions will tend to inhibit the inner range concentric contraction of lower trapezius. This loss of functional movement will lead to compensatory hypermobility of the A/C and or G/H joints, a classic case of peripheral dysfunction from central hypomobility.
Another, very uncommon, ‘culprit’ is superior subluxation of the 1st costo-transverse joint. This lesion effectively lessens the rigidity of the 1st thoracic ‘ring’. This means that thoracic spine motion cannot be effectively translated into appropriate manubrial motion.
Also, this lesion will mechanically deform the 1st costal cartilage which makes up a significant amount of the inferior sternoclavicular joint surface. This may impede normal sterno-clavicular joint motion.
NEURAL MOBILITY through the CERVICO-BRACHIAL FASCIA
In 1984, at the same IFOMT conference that ‘The Functional Shoulder Girdle’ was presented a young(ish) Bob Elvy was presenting his Doctoral thesis on the ‘Upper Limb Neural Tension Test’.
Of note was that his wonderfully videoed anatomical demonstrations of neural motion with upper limb motion had left all tissues intact except for the deep cervical fascia. Anatomical and clinical reasoning can quickly see the connection between abnormal fascial tension and abnormal neural mobility.
The paper ‘Cervico-clavicular Syndrome’ (1982) postulated that abnormal fascial tension could compromise the mobility and resting tension of cervical nerve roots.
For example, a habitual FHP will encourage the shoulder girdles to adopt an elevated and protracted position. This fixates the clavicle into an anteriorly rotated position which will produce excessive tension in the lower cervical fascia, compromising the nerve roots C8 and T1.
In conclusion, excessive clavicular rotation may result statically from abnormal postural changes of the shoulder girdles (from e.g, a FHP), or dynamically through thoracic motion dysfunction.
The abnormal resting position, or dynamic motion, of the clavicle is mediated through the sternoclavicular joint.
Forward head posture; paraesthesia and/or numbness in the ulnar region of the arm or hand. Sound familiar? Did someone say ‘Thoracic Outlet Syndrome’?