Painful hemiplegic shoulderMaria João Leite, SpR Rehabilitation Medicine, Centro Hospitalar do Porto, Hospital de Santo António

GH subluxation:Occurs in the flaccid stage as a consequence of

the weakened supraspinatus and scapular

stabilization muscles (trapezius and serratus

anterior) . No consensus in its relation to shoulder

pain. Might be a causative factor of RSD.

Dg: Palpation of anterior and posterior GH joint,

Sulcus sign, Feagin test, Rowe test for inferior

instability, X-rays (medial rotation; Axillary view;

3D-research)

Treatment: Carefull with seating, positioning,

support in the upright position and transfers. Early

passive movements and progressive muscle

strengthening. Debated wether sNMES should be

prophylactic or therapeutic. suture capsular

plication, thermal capsulorrhaphy (Shrinkage)

Adhesive capsulitis :

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. Later stage in the recovery process,

when chronic irritation or injury, inflammation, or

lack of movement eventually results in adhesions

Diffuse pain and limited ROM in passive

movements, especially ER and abduction..

Dg: MRI; Arthro-MRI and arthrography

(decreased in joint capacity and obliteration of

axillary fold)

Treatment: Heat, manual mobilization

exercises (Codman and pendulum), capsule

stretching exercise, analgesics and oral

corticosteroids and/or intra-articular injections

distension arthrography, manipulation under

anesthesia, stellate ganglion block, arthroscopic or

open surgery release

Spasticity/GH-scapular Instability

Impingement:

Spasticity and sinergy patterns of movement interfere

with mechanisms preventing impingement (humerus

impinges earlier in acromion and coracohumeral ligament

in abduction and forward flexion). Shoulder impingement

shoulder was found to be related to rotator cuff

insufficiency, posterior capsulartightness, GH instability,

scapular motion disorder and kiphotic deformity.

Treatment: PNF and other facilitative approaches,

Hydrotherapy, Heat, US, massages, sNMES, Biofeedback,

antispasticity medication, NSAIDs casting and orthotics,

progressive muscle strengthening, scapular taping, motor

points blocks (upper and lower subscapular,

musculocutaneous nerves), nerve blocks

(suprascapularis), subacromial lidocaine and

corticosteroids injection shoulder stabilization surgery

(instrumentation- fixation devices, capsulorrhaphy)

Rotator cuff inflammation/rupture:

In flaccid stage glenoid fossa tilts inferiously because of

scapular stabilization muscles and weakned rotators cuff.

After gaining some abduction strength, the uncoordinated

agonist and antagonist action of the scapular stabilization

muscles increases the scapular rotation angle and slide

motion and the glenoid fossa face superiourly.

Continuous pain radiating to the deltoid tuberosity with

abduction above 90 degrees.

Dg: Appley test, Painful Arc, Provocative Resisted

isometric tests for rotator cuff muscles, Impegement

(Neer, Hawkins, Yocum), X-rays, US, MRI, Arthroscopy

Tx: Progressive muscle strenghtning, NSAIDs, US,

TENS, HVGS, Iontophoresis, Corticosteroid subacromial

injections artroscopy (suture anchors,

reconstrution, superior capsule and CH ligament release )

Subacromial bursitis :

Lateral shoulder pain that radiates down

the arm when moved

Dg: US, MRI, lidocaine injection

Tx: NSAIDs, ROM exercises, Ice,

Corticosteroids injection, Iontophoresis

Biceps tendinitis and subluxation:

“Overwork” as a secondary shoulder

depressor. Anterior shoulder pain, at groove

biccipital, radiating to elbow cotovelo and

exacerbated by movement (Shoulder and

elbow flexion, forearm supination).

Dg: O`Brien compression, Speed,

Lippman, Yergason tests, tenderness in the

biccipital groove, idocaine injection test,

local anesthetic block at the bicipital

groove. Image: X-ray, US, MRI,

Tx: NSAIDs, Ice, Corticosteroid

injection , circundation and pendulum

exercises, US, progressive muscle

strenghthening, sNMES

tenotomy,tenodesis.

Brachial plexus traction neuropathies:

Traction neuropathy (positioning,

transfers, hypoesthesia, neglect)

Segmentar muscular atrophy, claw hand,

abnormality at the beginning of spasticity

of the involved muscles, atypical return of

distal function.

Dg: MRI and Electrodiagnosis

Supportive care (passive exercises,

sensory and sNMES) until return of

function

Complex regional pain

syndrome: The International Association for the

Study of Pain (IASP) categorization

states that RSD develops secondary to

noxious stimuli that are not limited to

the distribution of a single peripheral

nerve , while causalgia starts after a

nerve injury. There is still no consensus

on the pathophysiology (incidence 10-

23%)

According to IASP the diagnostic

criteria for CRPS are: 1. Spontaneous

severe, burning pain, allodynia,

hyperalgesia 2. Evidence of edema, skin

blood flow abnormality and abnormal

sweating in the region of the pain since

the inciting even 3. Exclusion Diagnosis.

Upper extremity is commonly affected.

MCP joint tenderness to be the best

diagnostic indicator

Dg: Three phases bone scintigraphy,

electrodiagnostic testing, thermography

Tx: Positioning, avoidance of painful

stimuli, ROM exercises, NSAIDs, short

course oral steroids, tricyclic

antidepressants, gabapentin, US,

sNMES, ganglion block

Thalamic syndrome: Pain evolve spontaneously or

be evoked by touch, and it is often

severe, diffuse, and disabling;

hyperpathia.

Tx: analgesics, antidepressants

(ie, tricyclic antidepressants), and

anticonvulsants, sympathetic blockade

and a guanethidine block,

Conclusion: O desenvolvimento de omalgia no hemiplégico está relacionado com AVC severo e pobre outcome funcional. Shoulder pain is a common and debilitating symptom for a large

number of people following a stroke and currently there is poor evidence regarding effective treatments. Contudo a identificação do mecanismo exacto pode ser dificil, com muitos regimes de

tratamento actuais variando de acordo com as assumções feitas sobre a causa. A subluxação ocorre precocemente. O músculo subescapular e em menor extensão o peitoral maior, desenvolvem

uma grande actividade tónica, com consequente desequilíbrio muscular. Existe evidência forte que a EEF melhora a função muscular, dor, subluxação e ADM. Existe evidência moderada que a

mobilização precoce resulta em diminuição da dor, o uso de cintas não melhorem a ADM e função do Msup, bem como o posicionamento prolongado não prejudique a ADM e/ou a dor, bem

como qto ao uso de injecção de CCT para melhoria dasa ADM e dor e administração oral de CCT na melhoria do SDRC por pelo menos as 4 1ª semanas. Existe evidência limitada que os

slings previnam a subluxação GH e que o bloqueio motor do supraescapular e peitoral melhorem o desiquilibrio muscular, ADM e dor.

Stroke:

A stroke is a brain parenchymal destruction by alteration or interruption of arterial blood

supply or venous drainage. The change in the structure causes a loss of function.

After a brain injury, brain and body progress through a series of stages (7 Brunnstrom

Stages of Motor Recovery): flaccidity and areflexia (no voluntary muscle movements),

spasticity without synergy patterns (some spastic tone, no voluntary movement, synergies

elicited through facilitation), increase in spasticity and synergic patterns emerge (synergistic

movements may be elicited voluntarily), decreased spasticity and regain of motor control

(stronger synergy patterns), complex movement combinations (spasticity continues to

declines, synergy patterns become more coordinated, and voluntary movements begin to

become more complex- cingulate gyrus, premotor areas), spasticity wanes (coordination and

movement patterns near normal, trouble with more rapid complex movements), normal.

The mesencephalon (rubrospinal tract- flexor synergy), pons and medulla (vestibulospinal

tract- extensor synergy) contains the nuclei whose afferent and efferent systems facilitate

these synergies. Usually the premotor cortex, cerebellum and vestibular system exert

control over these patterns and modulate its coordination role. In patients with

cerebrovascular syndrome, upper connections are affected in severe way and the basic

patterns are released to work in reflex-mediated paths. These patterns are in the upper

limb: flexion (shoulder retraction, adduction and internal rotation; depression, protaction

and downward rotation of scapula,;forearm pronation, elbow, wrist and finger flexion) and

extension synergy (shoulder protaction, abduction, forearm supination, elbow, wrist

extension and finger flexion).

At this stage the goal of treatment is to release the pattern of disinhibition of synergies and

retrain the paralyzed agonists.

Shoulder:

Shoulder girdle is composed by 3 true anatomical main joints (sternoclavicular, acromioclavicular e

glenohumeral) e 2 functional/physiological (false) main joints (scapulothoracic and subacromial). The

joints work together in a harmonious rhythm, allowing the overall movement of the shoulder (3

degrees of freedom and the long axis of the humerus can coincide with the 3 main axis thereby

permitting internal and external rotation) . The shoulder is the most mobile joint, with large humeral

head articulating with a shallow small glenoid socket (with the fibrocartilaginous labrum enlarging and

deepening the socket, thus enhancing osseous stability and conformity of the articulating surfaces),

being the majority of the stability determined by muscles (dynamic stabilizers-increased

capsuloligamentous stiffness, helping to appropiately direct the forces crossing the GH joint),

ligaments and capsule (static stabilizers- limit translation and rotation of the humeral head on the

glenoid)). This anatomical configuration provides greater joint mobility in exchange for lower

stability (necessity of balancing the force couples muscle strenght and endurance).

Cailliet has proposed that normal anatomic position involves a well-approximated glenohumeral

joint, proper glenoid fossa angle (forward, upward and outward), and proper scapular alignment with

the vertebral column (4).

The GH ligament is the most important static stabilizer, while the rotator cuff (ie, supraspinatus,

infraspinatus, subscapularis and teres minor) acts as the prime dynamic stabilizer (periarticular

transverse muscles). Deltoid (clavicular and scapular fibers), long head of biceps and triceps, coraco-

brachialis and clavicular head of pectoralis major, also contribute to maintain humeral head in glenoid

cavity, as well as capsule (long muscles). Trapezius, rhomboids and levator scapulae provide a correct

scapular alignment. Vertebral column is maintained in a upright alignment through erector spinae

muscle tone and righting medular reflexs.

During flaccid and areflexic phase (“Swinging arm”), the muscle tone is lost, such as the voluntary motor activity, sensitivity and muscle stretch reflexes. The loss of support for the humeral head

by the supraspinatus and deltoid; for scapular orientation and glenoid fossa by the trapezius, rhomboids and serratus anterior, contribute to inferolateral subluxation of the humeral head and

subsequent capsular stretch and trauma induced rotators cuff injury. Also, the spine begins to flex laterally toward the hemiparetic side because of the elimination of the righting reflex, further

altering the scapulothoracic relationship.

The first evidence of upper limb spasticity/synergic pattern (cortical/subcortical stroke) is the internal rotation (subscapularis, pectoralis major (clavicular head), serratus anterior, teres major) and

adduction (teres major, rhomboids, latissimus dorsi, peitoral major) of the humerus, scapular downward and outward rotation (rhomboids overwhelme trapezius and serratus anterior), progressing to

pronation of the forearm (pronator quadratus, pronator teres, flexor carpi radialis), elbow flexion and depression of the humeral head (biceps brachii) (rotator cuff and scapular instability- muscle

imbalance). It is believed that this pattern of synergy is due to an inability of antagonistic muscles to relax when the agonist muscles contract [Ia (static and dynamic) and II (static) afferents and

interneurons released from upper connections to higher centres to efferents γd and γs, with this efferent under control of extrapyramidal pathways- reticulospinal, rubrospinal, vestibulospinal,

tectospinal tracts) , with decreased stretch reflex threshold], thereby creating a co-contraction . In synergy phase the goal of treatment is to retrain the oppressed agonists, releasing the uninhibited

synergy patterns, starting opponents movements (PNF and other facilitative approaches).