Anterior shoulder subluxation- internal rot/external rot?

8o
Hi,
Recently i came across with this article stating maintaininig external rotation of glenohumearl joint improves the healing process than maintain in internal rotation. traditionally we are maintain the subluxed shoulder(anterior) in internal rotation. anyone hasa tried this approach?

http://www.mja.com.au/public/issues/...r10335_fm.html[/link]

anatomically you need external rotation in order for the huneral head to avoid impingement as you either abduct or flex into elevation. Without the external rotation you should never move the arm into elevation. I can't see how you can have a functional shoulder unless you maintain external rotation.
Half or full trays and positioning in abd and at least nuetral rotation in lying are helpfull in maintaining range
A sling will not prevent subluxation for you.
highmode

This was covered in a previous message that perhaps was deleted during the hacker attack. Anyway the anatomical length of the superior glenohumeral ligament is short (supportive) in external rotation and is lengthened (slack) in internal rotation.

Given that a patient does not exhibit any muscle activity about the glenohumeral joint post stroke (flaccid paralysis) then it would stand to reason that position would affect subluxation. I believe the laxity in the GH joint capsule alone permits about 2.5-3cm subluxation without any muscle activity. So if you add it all up - flaccid shoulder, internal rotation (i.e. lengthening of the superior glenohumeral ligament) = subluxation. Therefore maintaining an amount of external rotation (even a neutral GH joint) should assist minimise the rate and likelyhood of subluxation.

I have seen a few studies looking at muscle stimulation for the external rotators during flaccid paralysis to prevent subluxation but none have proven any direct benefit as yet. That said I believe that was more the fault of the study and that one should perhaps combine this approach with Upper Limb exercises focusing on lateral and behind reaching activities to facilitate practise and stimulate restoration of function.

The physical therapist can provide splints and braces to support joints and limbs, to treat and prevent complications (eg, shoulder-hand syndrome, spasticity), and to assist the patient in walking.

Early after stroke, patients often have flaccid paralysis that can potentiate further complications such as contractures, joint subluxation, and nerve pressure palsies. For instance, common upper extremity examples are shoulder subluxation, ulnar neuropathy, and elbow flexion contractures. Physical therapy should focus on appropriate positioning and avoidance of traction, which can harm joints previously stabilized by muscular tone. Range of motion (ROM) should be preserved during this phase. Later efforts can be pursed to reeducate weak musculature through modalities that provide sensory feedback.

Good shoulder function is a prerequisite for effective hand function, as well as for performing multiple tasks involving mobility, ambulation, and activities of daily living (ADL). A common sequela of stroke is hemiplegic shoulder pain that can hamper functional recovery and subsequently lead to disability. Hemiplegic shoulder pain can begin as early as 2 weeks poststroke but typically occurs within 2-3 months poststroke. Good shoulder function is a prerequisite for effective hand function, as well as for performing multiple tasks involving mobility, ambulation, and activities of daily living (ADL). A common sequela of stroke is hemiplegic shoulder pain that can hamper functional recovery and subsequently lead to disability. Hemiplegic shoulder pain can begin as early as 2 weeks poststroke but typically occurs within 2-3 months poststroke.

Once the inciting injury to the brain occurs, the flaccid stage evolves with a state of areflexia. This stage of areflexia includes loss of muscle tone and volitional motor activity, variable sensory loss, and loss of muscle stretch reflexes.

Muscular support of the humeral head in the glenoid fossa by the supraspinatus and deltoid muscles is lost. This leads to downward and outward subluxation of the humeral head, with the only support coming from the joint capsule. The shoulder capsule is thin and is composed of 2 tissue layers. The inner synovial layer, the stratum synovium, is highly vascular but poorly innervated, making it insensitive to pain but highly reactive to heat and cold. The outer layer, the stratum fibrosum, is poorly vascularized but richly innervated, predisposing it to pain from stretch. For this reason, added capsular stretch in a flaccid shoulder may predispose the capsule to irreversible damage and the shoulder to pain.

Flaccidity of the trapezius, rhomboids, and serratus anterior muscles leads to depression, protraction, and downward rotation of the scapula, which leads to significant angular changes of the glenoid fossa, subsequently contributing to subluxation. Also, the spine begins to flex laterally toward the hemiparetic side because of the elimination of the righting reflex, further altering the scapulothoracic relationship.

However, it was compared that the affected and unaffected shoulders by using a 3-dimensional radiographic technique that determines the true position of the humeral head in relation to the scapula. This technique revealed less downward rotation of the glenoid fossa than originally expected, and no significant relationship was found between the extent of scapular orientation and the severity of subluxation. Subsequently, it was concluded that scapular position does not contribute as much to inferior subluxation as was originally thought. Teasell points out that this now appears to be the most widely accepted viewpoint.

Glenohumeral subluxation basically is defined as a partial or incomplete dislocation that usually stems from changes in the mechanical integrity of the joint. Subluxation is a common problem in patients with hemiplegia, especially during the flaccid stage, and often occurs within 3 weeks poststroke.


Subluxation appears to be caused by the weight of the flaccid arm applying direct mechanical stretch to the joint capsule as well as traction to unsupportive muscles of the shoulder. It suggests that other factors contributing to subluxation include improper positioning, lack of support in the upright position, and pulling on the hemiplegic arm when transferring the patient.


Controversy exists as to an association between shoulder subluxation and pain. Subluxation has been a commonly sited cause of shoulder pain and disability, longitudinal data suggests a correlation between early subluxation and shoulder pain. However, it has been found no significant correlation between the presence of subluxation and the occurrence of pain, no association between the severity of subluxation and the degree of pain. Numerous cases of subluxation without pain have been documented, as well as cases of a painful shoulder without subluxation.


A correlation between subluxation and RSD also has been studied. It has been found that subluxation was present in 74.3% of patients with RSD and 40% of patients without RSD; of these same patients, 78.6% with subluxation and 38.1% without subluxation reported shoulder pain. It was concluded that shoulder subluxation might be a causative factor of RSD as well as shoulder pain.


Therapists usually can diagnose subluxation by palpating and measuring anatomical landmarks (fingerbreadths and calipers, respectively) during physical examination.


Others believe that there are no precise clinical means to measure the degree of subluxation, and if one could be devised, then the benefit of treatment would be validated.


Several radiographic methods that give a reliable measure of subluxation have been proposed, but some require specialized equipment that is not widely available.

Treatment of subluxation by reduction remains a controversial means of controlling shoulder pain. Slings, arm boards, troughs, and lap trays have not proven to be effective and may result in overcorrection in some cases. Sling use also may cause lateral subluxation, impair proprioception, interfere with functional activities, or promote undesirable synergy patterns; furthermore, sling use may not prove beneficial in preventing shoulder subluxation. Strapping also has been attempted with variable results. Even though sling use and other supportive devices remain controversial, Yu et al report that treatment of shoulder subluxation continues to be the standard of care for several reasons, including the following:


Painful shoulder subluxation most commonly is present when the UE is in a dependent position. Painful shoulder subluxation improves with joint reduction.


Subluxation may have a role in the pathogenesis of other painful conditions by stretching local neurovascular and musculoskeletal tissues.


Early prevention is warranted since chronic shoulder pain often is refractory to treatment.


Subluxation may inhibit functional recovery by limiting shoulder ROM.

Because of the unproven effectiveness of support devices, a newer form of treatment, neuromuscular electrical stimulation (NMES), has provided some moderate success in the prevention and treatment of subluxation. It was demonstrated substantial reduction in subluxation, and possibly enhancement of motor recovery and reduction of shoulder pain. However, it is debated whether NMES should be used prophylactically or whether its use should be held until subluxation develops.

See Upper Extremity Motor Relearning

Neuromuscular electrical stimulation

Since no sling design definitively prevents or treats shoulder subluxation, an effective alternative available is NMES. It was reported that the aim of NMES is to reduce subluxation of the hemiplegic shoulder without the use of restrictive splints. NMES may even elicit strong sedative effects on pain by acting on sensory nerves. It is believed that it also could be used prophylactically as a temporary means of splinting the shoulder until recovery of motor function is sufficient enough to support the glenohumeral joint. Numerous other studies have suggested that it also improves spasticity and enhances muscle strength of the hemiparetic limb.
A study found that patients with hemiplegia and subluxation who received 5 weeks of NMES had significantly more improvement in pain relief, reduced subluxation, quicker motor recovery, and possibly facilitated recovery of shoulder function. These results were maintained for up to 2 years. However, it was recommended that patients continue exercising to maintain control of their pain. In chronic hemiplegic stroke and TBI patients, there was used percutaneous NMES (perc-NMES) in the posterior deltoid and supraspinatus muscles 6 hours per day for 6 weeks. This resulted in reduced subluxation and improvements in pain and disability. These results were maintained during 3 months of follow-up. It was subsequently followed this up with a study comparing transcutaneous-NMES with perc-NMES. It was found that perc-NMES is less painful, has a much easier application, and has potential for long-term use.
This study also found a reduction of shoulder subluxation, with possible enhancement of recovery and improvement in shoulder pain. At this point, the optimal muscles and number to stimulate has not been established. Using muscles with strong superior and medially directed forces, as well as those stabilizing the scapula, may significantly enhance the efficacy of this intervention.

Even after 6 months poststroke, forced active repetitive movements of the paretic limb through the use of NMES appears to enhance motor and functional recovery. This has been clinically proven to occur as a result of neuroplasticity, in which active repetitive training of the hemiparetic limb causes functional reorganization in the adjacent intact cortex, subsequently allowing for maximum motor recovery. There was treatment of the extensor digitorum communis (EDC) and extensor carpi radialis (ECR) by combining neuromuscular stimulation with active repetitive wrist and finger extension exercises for one hour per day for a total of 15 sessions, subsequently producing significantly enhanced motor recovery that was maintained for up to 12 weeks. However, no significant functional effect was proven.

See Biofeedback and electrical Stimulation for Motor recovery in Stroke

Active repetition

The use of active repetition has been shown to maximize motor relearning when used in the appropriate candidate. It is found that stroke patients who were less severely impaired (ie, possessed some early volitional arm movement) prior to treatment benefited from the use of early additional therapies that involved repetitive movements and functional tasks. However, patients with severe arm impairment showed very little improvement in function irrespective of receiving additional therapies. This data supports previous clinical trials that suggest there is no current physical therapy approach that results in sustained improvements of upper limb function in patients who are severely impaired. In patients who are severely impaired, the use of adaptive techniques and equipment may be an appropriate rehabilitation strategy.
Following basic concepts be used during muscle reeducation:

Patient should visualize (ie, mirror) specific movements.
Verbally reinforce intended movements and encourage the feel of specific motions.
Copy similar motions performed simultaneously by the contralateral arm.
Position the UE to decrease scapular depression and retraction.
Apply sensory stimulation simultaneously to movements.
Use prone exercises to stimulate righting reflexes that tend to imitate primitive motor function.
Start seated and standing stimulation exercises to help decrease subluxation and modify synergy patterns.
Attempt to increase passive range of motion (PROM) with gentle slow motion, rhythmic stabilization, or voluntary contraction followed by relaxation or gentle stretching.
Avoid vigorous traction on the arm when stretching connective tissue around the spastic joint.
Use of electric stimulation can enhance muscle relaxation.
Use the functional arm to simultaneously train the paretic arm to improve ROM and proprioceptive stimulation.
Use modalities (eg, ice, transcutaneous electrical nerve stimulation [TENS], vibration) to diminish spasticity.
Surgical Intervention: In the past, surgical release of tendons and muscle was commonly performed on patients experiencing prolonged spasticity and synergy. For patients experiencing a painful spastic shoulder, surgical transection of the subscapularis and pectoralis tendons was performed to eliminate internal rotation and adduction forces. Hecht et al reported that following treatment, up to 88% of these patients had improved pain and increased ROM, with some developing active abduction. Today, this form of treatment rarely is used.

Stroke syndromes present with various alterations in motor, sensory, and cognitive function, each unique in clinical presentation and prognosis. Although there are general principles of stroke recovery, no two patients share the same experience. Understanding the correlated physiologic and anatomic changes in the brain helps identify which syndrome is present and how best to institute comprehensive rehabilitation to meet the individual needs of the patient.

Share your own views and thoughts about that.

Sdkashif,
You refer to many articles that have interesting conclusions:
- about the association between shoulder subluxation, RSD and pain;
- that no sling design definitively prevents or treats shoulder subluxation;
- studies about neuromuscular electrical stimulation, including the one that shows reduction of shoulder subluxation, with possible enhancement of recovery and improvement in shoulder pain.

Could you give me the refrences to these studies?

Thanks
catia

The valuable references are as follows:

Brandstater ME: Stroke rehabilitation. In: DeLisa JA, et al, eds. Rehabilitation Medicine: Principles and Practice. 3rd ed. Philadelphia: Lippincott-Raven; 1998

Cailliet R: The shoulder in the hemiplegic patient. In: Shoulder Pain. 3rd ed. Philadelphia: FA Davis Co

Carr JH, Shephard RB: A Motor Relearning Programme for Stroke. 2nd ed. Oxford: Butterworth-Heinemann; 1992

Kingery WS: Complex regional pain syndrome. In: Grabois M, et al, eds. Physical Medicine & Rehabilitation: The Complete Approach. Maldin, Mass: Blackwell Science;

Kirshblum SC: Spinal and upper extremity orthotics. In: DeLisa JA, et al, eds. Rehabilitation Medicine: Principles and Practice. 3rd ed. Philadelphia: Lippincott-Raven

Morris DM: Constraint-Induced Movement Therapy for Motor Recovery After Stroke. NeuroRehabil 1997

Snider R: Reflex sympathetic dystrophy. In: Essentials of Musculoskeletal Care. Rosemont, Ill: American Academy of Orthopedic Surgeons; 1997

Teasell RW: "The Painful Hemiplegic Shoulder". Physical Medicine and Rehabilitation: State of the Art Reviews 1998

Van Buskirk C, Webster D: Prognostic Value of Sensory Deficit in Rehabilitation of Hemiplegics. Neurology 1955

Physical Therapy of the Shoulder. Second Edition By Robert A. Donatelli

Cash's Textbook of neurology for Physiotherapists. 4th Edition by Patricia A. Downie

Tidy's Physiotherapy. 13th Edition by Stuart Porter

Physical Rehabilitation. Assessment and Treatment. Third Edition. By Susan B. O'Sullivan & Thomas J. Schmitz

Clayton"s Electrotherapy. 10th Edition By Sheila Kitchen & Sarah Bazin

Clinical Electrotherapy. Second Edition by Nelson & Curriera

Therapeutic Expercises. Foundation and techniques. Third Edition by Carolyn Kisner & Lynn Allen Colby