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Clinical and diagnostic picture of the shoulder

The shoulder is not a single joint but its movement is connected to several perfectly synchronized joints stabilized by capsular ligament complexes and activated by different muscle groups.

The shoulder joint
Shoulder stability and mobility must necessarily find a compromise.

Several shoulder disorders are in fact located in structures involved in stability (capsular-labral complex) and motility (cuff tendons) and are triggered by degenerative (arthrosis) and traumatic processes (fractures).



Most frequently disorders

Disorders

SHOULDER TREATMENT: REHABILITATION VS SURGERY

In shoulder treatment, as in medicine in general, accurate diagnosis is essential to increasing the chances of an effective clinical outcome.

It is important to think of the shoulder as a joint whose function depends on a complex kinetic chain, composed of other joints which must be coordinated by a neuro-muscular system in all its components. So it is clear that dysfunction of a "proximal (or distal) ring" can have a negative impact on the workings of the shoulder as a whole, resulting in symptoms of a clinical (pain or restricted movement) or anatomical/pathological nature (subacromial bursitis, cuff tears, disinsertion of the labrum, osteochondral defects, and so on). A careful review of the most reliable specialist literature shows that new etiopathogenetic explanations of frequent lesions of the rotator cuff have evolved in recent years. Pioneering work by Bigliani and Morrison named reduction of the subacromial space due to a hooked acromion as the most frequent cause of inflammation/degeneration of the subacromial bursa and tendinous tissue. Other authors have pointed to the tendinous structures of the rotator cuff of the locus minoris resistentie, represented by hypovascularized areas subject to particular strain, in particular on the articular side.

Our clinical and surgical experience, once again backed up by the growing body of orthopedic, physiatric, neurophysiological and biomechanical literature, suggests more dynamic etiopathogenetic theories highly suited to what might be considered the most mobile joint in the human body.

We have noticed how many authors place great emphasis on diagnostic tests or diagnostic investigations (Jobe, Yocum, Impingement test/sign, etc) which when properly executed can reveal latent clinical conditions caused by tears or inflammation which permit diagnosis.

A functional examination of the joint must include an accurate and systematic assessment of active, but especially passive, joint motion. Passive function must be assessed on various levels, in particular in abduction and adduction with internal and external shoulder rotation. Any reduction of R.O.M. due to capsular contraction must be given serious consideration since this can significantly alter the specificity and sensitivity and therefore the result of the above tests.

An elegant study by Uhthoff and Boileau describes cases of global capsular contraction (easy to diagnose) and cases localized to just some areas of the "glenohumeral capsule". These are very tricky to identify in that the symptoms and positive clinical tests perfectly match the better known "subacromial impingement syndrome". However, rehabilitative and surgical treatment of impingement is based on quite different assumptions than that of capsulitis. The physician must therefore be instructed and trained to identify and discriminate between these two pathologies which have the same symptoms but require different treatment.

An example may make this clearer. In a "localized" capsular contraction of the postero-inferior region, elevation of the arm produces a "yo-yo effect", i.e. antero-superior motion of the humeral head which establishes a dynamic contact with the coracoacromial joint, causing inflammation of the bursa and the tendons (long head of the biceps, rotator cuff, etc). Thus bursitis and tendinitis are the end of a chain of effects triggered by the posterior capsular contraction, requiring targeted rehabilitative treatment designed to stretch the posterior capsule. In patients suffering from capsulitis, the ideal surgical treatment for subacromial impingement— acromionplasty—is at best useless, and at worst counterproductive.

We must stress that in cases of frozen shoulder specific and well executed tests are essential, such as a true antero-posterior x-ray view, able to discriminate between the onset of capsular damage and symptoms of arthrosis/degeneration which require a quite different response.

An interesting theme to develop, now and in the future, will be to try to understand the intrinsic (or apparently intrinsic) causes of primary capsular contractions which are today generically attributed to genetic, immunological and metabolic factors or to mechanical adaptation.

Lesions may occur not only as a result of capsular inflammation or contracture, but also due to disturbances in the kinetic chain. This is a highly complex mechanism in which force is generated and transmitted in a proximal-distal direction and is extremely important in professional athletes, for example those taking part in throwing events. It is less important, but not negligible, in everyday patients, in whom articulation of the shoulder must be seen as formed not only by the humerus and the scapula, but also by the sliding of the scapula on the chest. Thus good shoulder function depends not only on the rotator cuff but also on scapular-thoracic stability, whose effectiveness in turn depends on lumbar-pelvic stability. Fluid and functional shoulder movement therefore depends on the synchrony of the kinetic chain.

Happee and Van der Helm have clearly shown how the thoracoscapular muscles deliver around 40% of the energy required for acceleration of the arm during anteflexion and how, if the scapula is used incorrectly, the metabolic cost of the cuff is increased by 13%.

In a dyskinetic shoulder if the sporting task (e.g. throwing) or functional scope remain the same, the organism tends, for a limited period to compensate (catch-up) through arthro-kinematic (humerus out of the safe zone), or biofunctional mechanisms (cuff overload). In time, unless a proper balance is restored, this overload may produce symptoms caused by anatomical changes which develop slowly depending on the type of activity, the 'quality' of movement and the genetic profile which influences both the characteristics of the tissues and the morphotype of the patient.

The kinetic chain is coordinated by the sensorimotor system, which is defined as all of the sensory, motor and central integration and processing components involved in maintaining joint stability and coordination. It consists of the visual system, the vestibular system and the somatosensory (in particular proprioceptive) system.

The proprioceptive mechanism is defined as the afferent information arising from peripheral areas of the body (including receptors in the static and dynamic restraints), and contributes to joint stability, posture control and motor control.

There are cutaneous, capsuloligamentous and myotendinous receptors. The capsuloligamentous and myotendinous receptors gather information arriving via the afferent pathways and are modulated by the central nervous system. Various muscle groups are activated and coordinated via the efferent pathways. The interplay between capsuloligamentous restraints and muscles is key. It is not fully appreciated in the maintenance of scapular-thoracic coordination and stability at the glenohumeral joint, but is under the influence of mechanical and sensorimotor factors. This interplay is very clear from the different anatomical connections including those between the infraspinatus and the capsular tissue.

The existence of a "reflex arc" from mechanoreceptors within the glenohumeral capsule to muscles crossing the joint confirms and extends the concept of synergism between the passive and active restraints of the glenohumeral joint. Receptors, which have the task of transforming physical energy into an electrical stimulus, are numerous in myotendinous and capsular tissue; they are divided into rapidly and slowly adapting types which work in an integrated fashion and with different excitement thresholds.

What happens if these peripheral receptors fail to function correctly?

Deafferentation refers to damage to mechanoreceptors, cutting off neural supply and reducing or eliminating the afferent supply arising from the damaged structure. One of the most interesting causes of deafferentation is muscle fatigue, trauma and hyperlaxity, which can alter receptor function in such a way that the central nervous system receives incorrect information. This modulates the efferent pathways, thus creating a problem.

An external impingement may often be related to deafferentation. Let us look at how fatigue of the scapulo thoracic muscles can lead to a lesion.

It is important to remember that fatigue may often be a manifestation of a genetic predisposition or of postural defects, and might be viewed as any reduction in the maximal capacity to generate force or power. This leads to the production of bradykinins, lactic acid, prostaglandins, potassium and serotonin. The effect of these substances on free nerve endings is to create a stimulus which is transmitted to the posterior horns. These afferent fibers which conduct the stimulus induced by muscle fatigue activate a gamma circuit. The neuromuscular spindle lengthens as a result of the excitability of the gamma motor neuron induced by fatigue; when the alpha stimulus arrives the neuromuscular spindle does not have the expected length, leading in turn to abnormal afferent output from the muscle spindle. The end result may be affected by joint position and direction of movement and this may lead to an anatomical lesion over time.

The failure of interplay in the kinetic chain, for instance due to fatigability of the latissimus dorsi and serratus anterior, can lead to scapulo-thoracic diskinesia. If the kinematics of the scapula on the chest is altered, the scapula retracts less, subacromial compliance is reduced, abnormal forces and stresses are placed upon the tissues associated with the shoulder girdle, so the tendons and the bursa become inflamed. With time, after repetitive overhead lifting or under conditions requiring a static shoulder posture, lesions can progress and lead to the clinical picture we know as subacromial impingement, this time due to insufficient scapular-thoracic diskinesia. This is a classic example of how deafferentation due to receptorial fatigue can lead to lesions over time.

The anatomical lesion may also influence deafferentation, thus generating a vicious circle in which deafferentation worsens the lesion and the lesion worsens the deafferentation. Damage to the soft tissues or cartilage takes a period of time during which the first signs are of inflammation, then fibrillation, then a partial tear and finally a full thickness tear.

This brings us to the concept of the "evolving lesion": these are lesions which evolve with time so that the pain threshold is slowly exceeded and the lesion becomes clinically evident. A correct balance of functional requirement, rest, adaptation of movement, use of painkillers and anti-inflammatory drugs, compensation mechanisms or constitutional/rehabilitative adaptation will determine the evolution of the anatomical changes and the clinical evidence of the lesion. The treatment of such gradual lesions depends on how early the patient is examined, and whether the tissue is at a stage of inflammation or reversible degeneration (assessed by clinical investigation). Generally we would opt for rehabilitative treatment, bearing in mind certain variables which in our experience may affect the case or the type of treatment: the condition of the damaged tissue, the patient's sex, age, work / sport, goals, etc.

Where the anatomical lesion is more pronounced, it is preferable in the majority of cases (not possible for all lesions) to repair the lesion and then proceed to rehabilitation with a view to treating the eventual causes of the mechanism which led to the lesion. Rehabilitation which ignores these aspects can result in surgical failures, for example, of rotator cuff repair.

Indeed recent studies have found a high incidence of relapse of surgically repaired cuff lesions. Identified using ultrasound and MR, such re-tears are often asymptomatic, the main noticeable effect being a loss of strength.

The difficulty of eliminating the postural defect and mechanical weakness by rehabilitation may justify the failure of the anatomical repair and therefore the loss of strength. Pain remission might be due to deafferentation of the pain receptors which inevitably follows bursectomy, release, debride and repair of unstable redundant margins. Rehabilitative post-surgical treatment nevertheless improves subacromial compliance and the kinetic chain.

Leaving aside high impact trauma, shoulder pathologies are generally the result of anatomical lesions of varying degree and location which appear as a slow and progressive result of dysfunctions of the kinetic chain often brought on by reduced neuromuscular efficiency.

Thus we can introduce a new concept, the "emerging lesion". To demonstrate how these criteria can be applied to different shoulder pathologies, let us take a patient suffering from microinstability, where disturbances of the cuff or more frequently small lesions of the capsulo-labral complex have been created. Because the athlete has had good posture and good neuromuscular control over the years, such anatomical lesions created by repeated overuse will remain asymptomatic thanks to a variety of adaptive mechanisms; if overhead activity demands made on the athlete increase, i.e. muscle fatigue, which we discussed earlier, or if the athlete ceases his or her activity for a long period and then begins again, he loses the good posture, the neuromuscular control and the chances of compensation are reduced. Should this situation persist without correct rehabilitative treatment, the clinical picture worsens and the anatomical lesions which were previously asymptomatic become symptomatic (emerging lesion).

Finally, when is surgery indicated and when rehabilitation?

A well-designed, global diagnosis and good patient selection can provide for the best treatment. Other factors such as work environment, age, sex, goals, quality of rehabilitation and genetic profile may also influence the decision. It is also important to remember the concepts and implications we have discussed: the "evolving lesion" which evolves slowly over time, and the "emerging lesion" which requires an external event to emerge clinically. "Evolving lesions", through deafferentation which might be the manifestation of different factors (muscle fatigue, trauma, laxity, etc.) may gradually turn into "emerging lesions" and therefore become symptomatic.

It is quite possible, therefore, to be faced with tissue damage which has only recently become symptomatic, but with longstanding morpho-functional causes which can seriously affect the outcome of rehabilitation and/or surgery.


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