Shoulder pain is one of the important complications in patients with hemiplegia after stroke, with an incidence of about 21%-72%, usually occurring within 2-3 months after stroke. Shoulder pain is not only present in the resting position, but also during passive activities, mostly during external rotation and abduction of the shoulder joint. Shoulder pain can seriously affect the prognosis of stroke. It can cause severe depression affecting sleep at night, hinder daily life care, reduce daily functional activities such as bursting to eat, dressing, washing, and moving around, and lead to difficulties in mobility and transfer. Prevention, early diagnosis and early treatment of shoulder pain are very important and can significantly improve the quality of life of hemiplegic patients.
1.The etiology and mechanism of shoulder pain
The etiology of shoulder pain after hemiplegia is still debated, and there are several possible causes.
(1) Subluxation of the shoulder joint
The commonly described shoulder subluxation refers to glenohumeral dislocation, which is a common post-stroke comorbidity and the main cause of post-stroke shoulder pain, with an incidence of 60% to 80%. Bender concluded that subluxation of the shoulder joint resulted in a significant angular change in the shoulder socket. In the flaccid phase, due to reduced tone and muscle paralysis of the muscles surrounding the shoulder joint (mainly the deltoid and supraspinatus) and proprioceptive impairment, there is a loss of pulling mechanism on the shoulder joint, lack of muscle support in the shoulder, and the presence of gravity on the affected upper extremity in the patient’s sitting or standing position, which overstretches the shoulder capsule, rostro-humeral ligament and surrounding soft tissues, causing the The head of the humerus is semi-dislocated from the glenoid of the shoulder joint. The shoulder joint capsule is rich in nerve receptors and is stimulated to cause shoulder pain. Zorowitz found a significant correlation between shoulder subluxation and shoulder pain and demonstrated that adhesions between the biceps tendons cause shoulder pain, and that shoulder subluxation can also cause distraction injuries and brachial plexus injuries.
(2) Abnormal muscle tone
Abnormal muscle tone (spasticity or tardive dyskinesia) has been suggested as a factor in the development of post-stroke shoulder pain, with 85% of hemiplegic patients experiencing shoulder pain during the spastic phase and 18% during the bradykinesia phase. The supraspinatus and deltoid muscles, which play a supporting role for the humeral head in the shoulder joint, lose muscle tone during the flaccid phase, resulting in a downward and lateral subluxation of the humeral head, which is supported only by the joint capsule, which is very weak and contains only 2 layers of fibers, and the internal synovial layer is richly vascularized but not innervated. The internal synovial layer is rich in blood vessels but has few innervations and is insensitive to pain, but sensitive to heat and cold. The outer fibrous layer is rich in nerves but little innervation and is sensitive to pulling pain. Paralysis of the trapezius, rhomboid, and anterior serratus muscles leads to scapular depression, anterior protrusion, and downward rotation, subsequently producing shoulder pain from subluxation of the shoulder joint.??? Chae et al. suggested that the increased pull on the joint capsule during the flaccid phase tends to cause irreversible damage to the joint capsule producing shoulder pain? During the spastic phase, a flexor co-movement pattern occurs with flexor spasm, which is manifested by posterior retraction of the scapula and inferior rotation of the shoulder joint with internal rotation and internal retraction. The increased tone of the subscapularis and pectoralis major muscles further promotes the spasm of the anterior rotator muscle group (anterior rotator muscle anterior rotator circularis radialis carpi radialis). The spasm of the rhomboid muscle leads to depression and downward rotation of the scapula, and the spasm of the latissimus dorsi muscle leads to internal retraction, extension and internal rotation of the humerus. Biceps spasm further promotes humeral head depression and elbow flexion, thus interfering with the normal scapular and humeral coordinated activities necessary for glenohumeral abduction. The periosteal area where the spastic muscles attach is subjected to continuous pulling, and at this time there is a lack of reflex muscle activity, causing shoulder pain.
(3) Inappropriate position maintenance and treatment of the affected limb
Early movement of the patient after stroke depends on nurses, therapists, physicians, ancillary staff and family members. Trauma caused by improper handling of the patient’s affected limb is a major cause of shoulder pain. Improper traction of the affected upper extremity and training of the patient’s upper extremity with passive movements, position changes and transfers that do not follow the shoulder-humeral rhythm of the upper extremity predispose the patient to shoulder joint injury. Multiple repeated injuries can lead to bleeding, exudation and aseptic inflammatory reactions in the shoulder. The prevalence and factors associated with shoulder pain in post-stroke patients were studied by Lindgren et al. 63% of patients developed post-hemiplegic shoulder pain in the first 6 months after stroke, and patients who required transfer assistance were more likely to develop shoulder pain. kumar et al. analyzed the prevalence of shoulder pain in patients who received three different rehabilitation training methods, with exercise training by a therapist, using an elliptical shape equipped with pulleys Dromerick et al. found that when the passive range of motion was reduced, shoulder pain was reduced in 43% of patients. et al. reported an increased incidence of shoulder pain in patients who did not undergo proper rehabilitation in the first week after stroke.
(4) Shoulder-hand syndrome
It is also known as reflex sympathetic dystrophy syndrome, with an incidence of about 20%, often occurring within 3 months after stroke. It is thought to be the main cause of hemiplegic shoulder pain. Its occurrence is related to incorrect movement patterns in the early stages of stroke patients, resulting in obstruction of fluid return to the upper extremity of the shoulder and wrist injuries, and vasomotor dysfunction after central nervous system injury. The main mechanism of vasomotor dysfunction after central nerve injury is that damage to the vasomotor center caused by damage to the cerebral cortex and subcortical or conduction tract causes increased sympathetic excitability and vasospastic response in the affected limb, resulting in local tissue dystrophy and edema and pain around the scapula and in the hand and wrist, and painful stimulation is further transmitted to the spinal cord via peripheral sensory nerves, causing abnormal excitation of spinal cord interneurons. The painful stimulus is further transmitted to the spinal cord via peripheral sensory nerves, causing abnormal excitation of spinal cord interneurons, resulting in a vicious circle. In addition, excessive stretching of the affected hand joints can also cause inflammatory reactions, edema and pain, and fluid leakage during infusion may also be an important cause of shoulder-hand syndrome.
(5) Brachial plexus nerve and peripheral nerve injury
is a possible cause of hemiplegic shoulder pain. Many studies have suggested that flaccid paralysis and strain injuries are possible mechanisms of brachial plexus nerve injury, and strain injuries are usually caused by lack of muscle support in the shoulder joint due to flaccid paralysis or by pulling on the affected limb when moving the patient. Comatose patients are at high risk for strain injuries. The axillary nerve bypasses the surgical neck of the humerus and a subluxation of the shoulder joint may produce a strain on the axillary nerve. The suprascapular nerve passes through the suprascapular notch and branches out into sensory branches that innervate the acromioclavicular and glenohumeral joints, thus creating the potential for compression at the suprascapular notch and shoulder pain due to strain from abnormal scapular position. Brachial plexus strains can severely prolong recovery time and impede active motor recovery, while upper motor neuron injuries superimposed on lower motor neuron injuries can exacerbate shoulder pain, lead to muscle contractures, and prolong recovery of shoulder motor function. chino reported neurogenic injuries to the deltoid and supraspinatus muscles in 75% of patients with shoulder subluxation. kaplan found that 5 patients with hemiplegia Atzmon et al. reported electromyographic evidence of axillary nerve injury after shoulder subluxation, suggesting that the axillary nerve could be compressed and peripheral nerve damage could be associated with the following factors: reduced muscle tone in the upper limb of the patient’s side in the early stages of stroke, when inappropriate position placement and nerve damage were observed. (i) the peripheral nerve strain is easily caused by proper position placement and shoulder joint movement. (2) The presence of severe muscle spasm on the affected side and the shoulder-hand syndrome may also damage the peripheral nerve due to impaired nutrition of the peripheral nerve tissue.
(6) Rotator cuff tear
The rotator cuff, also known as the tendon cuff, is composed of the supraspinatus, infraspinatus, teres minor and subscapularis muscles. When the subscapularis, infraspinatus, teres minor and teres minor muscles pass in front, above and behind the shoulder joint, they are close to the joint capsule and there are still many tendon fibers woven into the wall of the joint capsule, so the contraction of the rotator cuff muscle group plays an important role in stabilizing the shoulder joint. Studies have shown that rotator cuff tears account for a high percentage of patients with shoulder pain, and improper rotation of the scapula and humeral head can damage the rotator cuff. The normal mechanism for rotator cuff protection of the affected limb is lost after hemiplegia, and the pulling caused by lifting and handling the affected limb may damage the rotator cuff and cause shoulder pain. Some studies have suggested that passive external exhibition of the affected limb may lead to rotator cuff injury, which in turn may lead to shoulder pain.
(7) Adhesive arthrogryposis
After stroke, the loss of dynamic stability and muscle imbalance in the affected shoulder joint causes repeated abrasion and impingement of the tissues between the rostral shoulder dome and the humeral head, such as the subacromial bursa, rotator cuff, and biceps tendon, resulting in tissue inflammation and the formation of adhesive capsulitis, which may be a potential causative factor for shoulder pain. Pathological changes sequentially appear as hemorrhagic edema, fibrous degeneration, tendon synovitis, and bony changes. On MRI images of the patient, signal disturbance at the supraspinatus attachment and fluid accumulation in the shoulder joint were seen.Lo et al. performed arthrography and clinical examination of patients with hemiplegic shoulder pain and found adhesive capsulitis in 50% of the patients, which was considered to be the main cause of shoulder pain.Ikai et al. found joint capsule reduction in 74% of 23 patients by arthrography (this change could be explained by adhesive capsulitis). This change can be explained by adhesive capsulitis), and the shoulder pain was associated with external rotation dysfunction.
(8) Thalamic pain
Some hemiplegic shoulder pain is associated with damage to the thalamus. In hemiplegic patients with thalamic pain, there is loss of sensation on the hemiplegic side, including the shoulder, nociceptive hyperalgesia or spontaneous burning-like pain, in addition to the usual loss of proprioception, unilateral neglect, pain can be constant but often aggravated by emotional changes, visual or auditory stimuli, temperature, skin irritation. posterior limb of the internal capsule or parietal lobe injury is thought to be associated with it.
(9) Other factors
Pre-existing lesions of the shoulder joint may induce shoulder pain after hemiplegia, such as osteoarthritis, chronic injury, degeneration of the cartilage and surrounding soft tissues on the joint surface, and braking or inappropriate treatment of the hemiplegic limb may aggravate the pre-existing lesions and cause shoulder pain.
2.Prevention and treatment of shoulder pain
(1) Correct body position and early shoulder joint movement
After the onset of stroke, patients have low muscle tone. Correct positioning of the affected limb is clinically important to prevent shoulder joint subluxation, scapular retraction and swelling of the wrist and hand, and to prevent shoulder pain. One study that provided instructions to treatment group members, including patients and family members, on how to avoid injury to the affected limb found that the incidence of shoulder pain decreased from 27% to 8% when respondents were aware of the potential for shoulder joint injury.
Early activity can prevent adhesive joint lesions caused by braking, but inappropriate activity can cause periarticular soft tissue damage and shoulder pain. In the flaccid phase, passive activity should be the main activity, together with active assisted activity. In the spastic phase, the affected upper limb usually shows scapular retraction, shoulder joint internal retraction and internal rotation, and upper limb flexion spasm. Continuous, slow pulling of the affected upper limb flexors and lengthening of the affected trunk muscles, active activity of the upper limb extensors and the application of scapular and shoulder joint release can reduce the flexor tone of the affected upper limb, so that the patient can The patient can fully extend the scapula forward to coordinate the functional activities of the shoulder joint and upper limb during the activity, and also play a role in preventing shoulder pain.
(2) Shoulder sling
A shoulder sling can protect the upper extremity of delayed hemiplegia when the patient stands or transfers, and is commonly used in the early post-stroke period. However, prolonged and inappropriate use can enhance abnormal muscle tone, promote synergistic flexor patterns, inhibit upper extremity sway, cause soft tissue contractures, and have some negative effects on limb symmetry, balance, and proprioception. The sling can be discontinued when the muscle tone of the muscles around the shoulder joint is restored to a level that can prevent subluxation, and its use should be accompanied by manual training. However, there is no conclusive evidence to date that the shoulder belt can prevent or reduce subluxation of the shoulder joint and its potential secondary symptoms.
(3) Physiotherapy and exercise therapy
Physical therapy has long been used to treat shoulder pain, including cold and heat therapy, and electrotherapy. Short-wave electrotherapy applies high-frequency electromagnetic fields to the scapular muscles to reduce nerve excitability and muscle tone, while medium-frequency electrotherapy has obvious analgesic and local blood circulation improvement effects, so it is suitable for the treatment of hemiplegic shoulder pain. Studies have concluded that ice water immersion, alternating hot and cold water immersion and compression centripetal winding are effective for shoulder-hand syndrome because they improve vasodilation and contraction, promote venous reflux, reduce swelling and relieve pain.
Exercise therapy mainly includes Bobath,Brunnstrom and proprioceptive neuromuscular easing. In the early post-stroke period, hemiplegic patients often lose joint mobility in the shoulder joint. Snels recommends that preventive therapy should be started as early as possible, usually 1-2 days after stroke, to maintain upper extremity support and joint range of motion through early passive joint movement, without damaging the shoulder joint and its surrounding Painless total joint mobility of the shoulder is maintained without damage to the shoulder joint and its surrounding tissues. During the flaccid phase, passive shoulder joint activities promote functional recovery of the affected upper extremity, prevent joint adhesive lesions caused by braking, and promote muscle strength recovery. During the spastic phase, passive and active assistance exercises against spasm can gradually increase joint mobility, adjust abnormal muscle tone, relieve muscle spasm, and maintain the stability of the glenohumeral joint.
(4) Drug therapy
Analgesics, anti-inflammatory drugs, antispasmodics, and botulinum toxin have been used to treat post-hemiplegic shoulder pain. After 10 days of oral low-dose corticosteroids (methylprednisolone 32 mg/day), shoulder pain disappeared in almost all 32 patients. Two weeks of treatment, followed by two weeks of gradual drug taper, produced no side effects. These drugs are helpful in post-hemiplegic hypertonia, but the cognitive side effects may limit their use.
The main mechanism of botulinum toxin is to act at the neuromuscular junction and inhibit the release of acetylcholine from the presynaptic membrane, causing muscle denervation, thus reducing muscle tone and relieving muscle spasm. yelnik et al. injected botulinum toxin type A into the subscapularis muscle in patients with post-stroke shoulder pain, and the shoulder pain was reduced and the range of motion of shoulder abduction and external rotation was increased.
(5) Functional electrical stimulation
Functional electrical stimulation can improve the motor control of the upper limbs in stroke patients. By stimulating the supraspinatus and the middle and posterior deltoid muscles, it can activate the nerve fibers of these two groups of muscles and effectively improve the tone of the stimulated muscles. Sheffler suggested that it could be used as a temporary splinting therapy to prevent shoulder pain until muscle relaxation around the shoulder joint is restored, and other authors suggested that it could improve spasticity and improve muscle strength in the hemiplegic limb. Ekim et al. studied the effect of functional electrical stimulation on the prevention of subluxation and shoulder pain in patients with shoulder joint distraction after stroke and found that functional electrical stimulation was effective in preventing subluxation, relieving pain and improving joint range of motion and upper limb function.
(6) Surgery
If conservative treatment is ineffective, shoulder pain is very severe, and the muscles around the shoulder are very stiff, surgery may be considered, including release of tendon contracture, repair of rotator cuff tears, stellate ganglion block, etc. Indications for surgery are: severe restriction of joint range of motion severe pain interfering with skin cleaning or preventing rehabilitation intervention, surgery is usually intervened after 6 months of block to promote spontaneous functional recovery as much as possible. One study reported that surgical severance of the subscapularis and pectoralis major tendons to eliminate the forces of internal rotation and internal retraction resulted in improved shoulder pain, increased joint range of motion, and improved active abduction in 88% of patients. The need for surgical intervention has now been reduced with improved rehabilitation techniques.