Poststroke shoulder pain

Opening Vignette

Michael usually comes alone to see you in the clinic for management of his diabetes mellitus and hypertension. Today, you were surprised to see him in a wheelchair, accompanied by his daughter. Michael had recently been discharged from the hospital after a left pure motor stroke that happened 2 months ago. He asked you for painkillers, as there was increasing pain in his left shoulder over the past 1 week. He described it as a persistent ache, which worsens on movement of his left arm. He denied any falls or trauma to his left shoulder.

WHAT IS POSTSTROKE SHOULDER PAIN?

Poststroke shoulder pain (PSSP), also known as hemiplegic shoulder pain, is a common debilitating condition that occurs after stroke. The onset of PSSP can occur as early as 2 weeks poststroke, but it typically occurs within 2–3 months.[1] Patients generally report a gradual onset of shoulder pain at rest or in certain posture, on the side ipsilateral to the neurological impairment. On clinical examination, there are often signs of shoulder subluxation and rotator cuff impingement. The predisposing factors include inappropriate positioning during upright position and traction force on shoulder joint during transfers, flaccid paresis, spasticity, poor motor function and reduced range of motion.[2]

HOW RELEVANT IS THIS TO MY PRACTICE?

Poststroke shoulder pain interferes with motor retraining and recovery after a stroke. It often causes physical distress to patients and affects the performance of activities of daily living, resulting in poorer functional recovery, depression and reduced quality of life.[3] It has also been associated with withdrawal from rehabilitation programmes, prolonged hospital stay and poor recovery of arm function in the first 12 weeks after a stroke.[3]

HOW COMMON IS THIS IN MY PRACTICE?

Studies have shown that the annual incidence of shoulder pain can be as high as 2.5%, with a lifetime prevalence of up to 67% in the population.[4] Annually, about 1% of adults consult their primary care doctor for new shoulder pain.[5] The most common aetiologies include pathologies in rotator cuff (e.g. rotator cuff tendinopathy from heavy lifting or repetitive movements) and glenohumeral joint (e.g. capsulitis or frozen shoulder).[5] For primary care doctors who see stroke patients, the prevalence of PSSP is 22%–47%.[6] Among the stroke patient population, the most significant predictors of PSSP are age, female gender, increased tone, sensory impairment, left-sided hemiparesis, haemorrhagic stroke, hemispatial neglect and stroke severity.[6] Given the high prevalence of PSSP, family doctors should be aware of the possible aetiologies and consider the range of potential interventions. In this way, the treatment approach may be tailored to each patient with PSSP.

The causes of PSSP can be divided into three main categories: (a) impaired motor control and tone changes, (b) soft tissue lesions, and (c) altered peripheral and central nervous activity [Box 1].[7] Often, the cause of PSSP is multifactorial.

Box 1.

Pathologies underlying poststroke shoulder pain.[7]

(1) Impaired motor control and tone changes

• Flaccidity

• Spasticity

• Loss of motor function

• Glenohumeral subluxation, scapular dyskinesis, spasticity of shoulder muscles

(2) Soft tissue lesion

• Impingement syndrome

• Rotator cuff tendinopathy

• Bicipital tendinopathy

• Adhesive capsulitis

• Myofascial pain

(3) Altered peripheral and central nervous activity

• Peripheral nerve entrapment

• Complex regional pain syndrome

• Central poststroke pain

• Central hypersensitivity

Glenohumeral subluxation results from the weakness of the muscles surrounding the glenohumeral joint. It may occur immediately after a stroke, when the affected arm has a flaccid muscle tone and is most vulnerable to instability. The onset of subluxation does not always result in PSSP immediately. The pain usually becomes more apparent when spasticity develops.[8] In clinical practice, subluxation is commonly measured by the number of fingerbreadths between the acromion and the humeral head, by having the patient seated and his/her arm in a dependent position, which allows the weight of the limb to distract the humeral head from the glenoid fossa[7] [Figure 1].

Figure 1.

Clinical assessment of shoulder subluxation.

Spasticity is most commonly defined as “a motor disorder characterised by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome”.[9] Flexor tone predominates in the hemiplegic upper extremity and results in scapular retraction and depression as well as internal rotation and adduction of the shoulder. The two main muscles that contribute to this abnormal position of the shoulder are the subscapularis and the pectoralis major.[1] The local mechanical destabilising effects due to subluxation and spasticity of the shoulder often lead to soft tissue lesions, such as rotator cuff tendinopathy, impingement and tears, adhesive capsulitis, subacromial/subdeltoid bursitis and biceps tendinopathy.

Central poststroke pain (CPSP), formerly known as thalamic pain syndrome of Déjerine and Roussy, is a form of central neuropathic pain occurring in patients affected by a stroke involving the spinothalamocortical pathway.[10] It occurs in 8%–14% of patients poststroke and in most cases, develops within 6 months of stroke onset and its incidence decreases thereafter.[10] It is characterised by constant or intermittent pain and is associated with sensory abnormalities, particularly of thermal sensation.[10]

Complex regional pain syndrome (CRPS) is characterised by severe continuous pain in a nondermatomal distribution, affecting the extremity associated with sensory, motor, vasomotor sudomotor and trophic abnormalities. Diagnosis can be challenging, as there is no confirmatory test. It is a clinical diagnosis made using the new International Association for the Study of Pain (IASP) clinical diagnostic criteria [Box 2].[11]

Box 2.

International Association for the Study of Pain clinical diagnostic criteria.[11]

(1) Continuing pain, which is disproportionate to the inciting event

(2) Must report at least one symptom in three of the four categories below:

• Sensory: reports of hyperaesthesia and/or allodynia

• Vasomotor: reports of temperature asymmetry and/or skin colour changes and/or skin colour asymmetry

• Sudomotor/oedema: reports of oedema and/or sweating asymmetry

• Motor/trophic changes: reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or tropic changes (hair, nail, skin)

(3) Must display at least one sign at the time of evaluation in two or more of the categories below:

• Sensory: evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or deep somatic movement)

• Vasomotor: evidence of temperature asymmetry and/or skin colour changes and/or skin colour asymmetry

• Sudomotor/oedema: evidence of oedema and/or sweating asymmetry

• Motor/trophic changes: evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or tropic changes (hair, nail, skin)

(4) There is no other diagnosis that better explains the signs and symptoms

WHAT CAN I DO IN MY PRACTICE?

While PSSP is likely multifactorial in nature, careful assessment should be made to delineate major aetiology of pain. This includes a complete history taking and thorough physical examination, before a comprehensive treatment plan customised to each patient is recommended. A multifaceted approach is often useful, especially counselling the patient and his/her caregiver on the appropriate use of analgesia and other medications, positioning and range of motion exercises. Important outcomes include pain reduction or relief, improved passive and active range of motion, motor recovery and return of functional use of upper limb. Management strategies listed below are based on evidence-based review of stroke rehabilitation[1] and systematic reviews.[12,13]

Preventive strategies of PSSP include the following: (a) joint protection methods such as positioning and supporting the affected arm at rest, in upright position and during functional mobility — regular arm sling with thumb loop [Figure 2] and taping can be used to prevent injury and shoulder subluxation during the flaccid stage of affected arm muscles; (b) educate the patient, his/her caregiver and healthcare professionals to correctly handle and position the affected arm — for instance, never pull the affected arm during transfers and bed mobility or put the affected arm first into the sleeve before the other arm during upper body dressing; (c) avoid overhead exercises of the affected arm, unless adequate support of the scapula and instructions to the patient are provided; and (d) daily passive stretching and range of motion exercises of the affected shoulder, such as abduction–adduction, flexion–extension and external–internal rotation, help to reduce spasticity [Figures 3 & 4].

Figure 2.

Arm sling with thumb loop.

Figure 3.

Passive range of motion of shoulder (abduction).

Figure 4.

Passive range of motion of shoulder (flexion).

Physical modalities used to address shoulder pain due to impaired motor control and soft tissue lesions include shoulder range of motion exercises, massage, acupuncture, electrical stimulation, strapping, slings and other supports to minimise glenohumeral subluxation. In an analysis of seven systematic reviews, Dyer et al. reported significant benefits in terms of pain reduction for interventions, including acupuncture, orthoses, botulinum toxin injection and electrical stimulation.[13] However, the authors advised practitioners to consider the range of potential interventions and tailor their approach to individual presentation, guided by local circumstances, expert opinion and growing literature base.[12,13]

Passive range of motion, stretching and therapeutic exercises (within limits of pain) — as described in the abovementioned preventive strategies — are still the first-line treatment to reduce shoulder pain. Oral analgesia, especially nonsteroidal anti-inflammatory drugs (NSAIDs), is often necessary to reduce physical discomfort at rest and during exercises. Besides the well-known increased risk of serious upper gastrointestinal complications related to NSAIDs, ischaemic stroke risk associated with NSAID use appears to be higher in patients with previous ischaemic stroke and transient ischaemic attack, and in younger or male patients.[14] Concomitant use of aspirin, anticoagulants and platelet aggregation inhibitors appears to mitigate this risk.[14] Nonetheless, NSAIDs should be prescribed judiciously.

For treatment of pain due to soft tissue lesions such as impingement syndrome, rotator cuff tendinopathy or adhesive capsulitis, intra-articular injection, subacromial corticosteroid injection and suprascapular nerve block may be considered.[1]

Pharmacological options for spasticity management are oral medications (such as baclofen, tizanidine, benzodiazepines), intramuscular injections (botulinum toxin), nerve blocks (using alcohol) and intrathecal baclofen.[1,12,13] Baclofen, a γ-aminobutyric acid agonist, is widely used for treatment of spasticity. The usual starting dose of baclofen ranges from 5 mg every evening to 5 mg three times a day. The dose can be increased by 5 mg per dose every 3 days based on response and tolerability. Maximum dose is 80 mg per day in divided doses.[15] Dosage adjustment is needed for patients with renal impairment, depending on estimated creatinine clearance using the Cockcroft–Gault formula.[15] Common side effects are sedation, constipation, nausea and hypotonia. Baclofen should be used with caution in patients with existing seizure disorder due to possible loss of seizure control when treated with baclofen.[15]

Antidepressants such as amitriptyline and nortriptyline, and antiepileptics such as lamotrigine and gabapentinoids (gabapentin, pregabalin) can be used as first-line treatments of CPSP,[10,16] while oral corticosteroids are considered to be the only anti-inflammatory drugs that have proven effectiveness in treatment of early/acute phase of CRPS.[16] Studies have reported a range of starting dose (30–60 mg) of oral prednisolone with variable tapering regimen and duration of treatment (2–12 weeks).[17]

WHEN SHOULD I REFER TO A SPECIALIST?

Indications for referral to a specialist include severe pain or marked spasticity despite a trial of pharmacological agents for pain and spasticity, limited range of motion that leads to functional impairment and interferes with hygiene or posturing, as well as complex psychosocial factors perpetuating the pain.

Referral to rehabilitation medicine physician can be made for specialised management of spasticity such as intramuscular injection of botulinum toxin, nerve block and serial casting. In addition, a rehabilitation medicine physician in collaboration with a multidisciplinary team, consisting of physiotherapists and occupational therapists, can prescribe additional therapeutic exercises, splints (resting hand splint, ankle–foot orthoses) and physical modalities such as transcutaneous electrical stimulation. In refractory cases where contracture or complete tears of tendons has resulted in severe pain and interferes with hygiene, referral to an orthopaedic surgeon is an option for consideration of tendon release, surgical repair of rotation cuff tears and scapular mobilisation.

In conclusion, an optimal combination of physical rehabilitation strategies with cost-effective pharmacological management is essential to provide favourable treatment outcomes of PSSP.

TAKE HOME MESSAGES

1. Poststroke shoulder pain is a common debilitating problem where patients present with shoulder pain at rest or in certain posture, on the side ipsilateral to the neurological impairment.

2. Increasing severity of the neurological impairment or inappropriate handling of the hemiplegic arm may predispose to the development of shoulder pain.

3. Apart from local mechanical causes such as subluxation, rotator cuff impingement and spasticity, PSSP may also be caused by neurogenic causes, e.g. poststroke central pain.

4. While PSSP is likely multifactorial in nature, careful assessment should be made to delineate major aetiologies of pain.

5. Treatment of PSSP should be targeted, and a multidisciplinary approach is often useful.

6. Referral to a rehabilitation medicine physician should be considered if the pain is severe or non-responsive to treatment, or if complex psychosocial factors perpetuate the pain.

7. Patients may expect further investigations and specialised management, such as botulinum toxin injection for spasticity, if indicated.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

Closing Vignette

You assessed Michael and noted that he had left shoulder subluxation and mild spasticity of his left shoulder abductors, elbow and wrist flexors. You explained that the shoulder pain was due to spasticity and gave Michael and his daughter advice on proper positioning of his left upper limb. You taught them passive stretching and range of motion exercises to do daily. You also prescribed a 1-week course of ketoprofen 50 mg TDS and Anarex two tablets TDS. Before leaving the consult room, Michael agreed to return for a review in 2–3 weeks.

SMC CATEGORY 3B CME PROGRAMME

Online Quiz: https://www.sma.org.sg/cme-programme

Deadline for submission: 6 pm, 05 September 2024

Question: Answer True or False
1. Poststroke shoulder pain (PSSP) can occur as early as 2 weeks poststroke.
2. Poststroke shoulder pain is not associated with poor recovery of arm function and withdrawal from rehabilitation programme.
3. The most significant predictors of PSSP are age, female gender, left-sided hemiparesis, sensory impairment, hemispatial neglect and stroke severity.
4. Inappropriate positioning of the hemiplegic arm may predispose to the development of PSSP.
5. The cause of PSSP is often multifactorial, including impaired motor control, soft tissue lesions and altered peripheral and central nervous activity.
6. Glenohumeral subluxation always results in PSSP.
7. Shoulder subluxation can be measured by the number of fingerbreadths between the acromion and the humeral read in the clinical setting.
8. Spasticity is commonly defined as “a motor disorder characterised by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the lower motor neuron syndrome”.
9. Soft tissue lesions of the shoulder joint often occur as a result of local mechanical destabilising effects due to glenohumeral subluxation and spasticity of the subscapularis and pectoralis major muscles.
10. Central poststroke pain (CPSP) is formerly known as thalamic pain syndrome of Déjerine and Roussy.
11. Central poststroke pain is a form of central neuropathic pain that may occur after a stroke involving the spinothalamocortical pathway.
12. Complex regional pain syndrome (CRPS) is characterised by constant or intermittent pain in a nondermatomal distribution.
13. The diagnosis of CRPS is based on the new International Association for the Study of Pain clinical diagnostic criteria.
14. Range of motion, stretching and therapeutic exercises are the first-line treatment for PSSP.
15. Nonsteroidal anti-inflammatory drugs (NSAIDs) should be used judiciously, as ischaemic stroke risk associated with NSAID use appears to be higher in patients with previous ischaemic stroke.
16. The pharmacological agents for spasticity management include baclofen, tizanidine, botulinum toxin injection and nerve block.
17. The first-line treatments of CPSP are antidepressants (amitriptyline and nortriptyline) and antiepileptics (lamotrigine, gabapentin, pregabalin).
18. The rehabilitation medicine physician provides specialised management of poststroke spasticity such as intramuscular injection of botulinum toxin, nerve block and serial casting.
19. In refractory cases of PSSP due to complete tendon tears or contractures, referral to orthopaedic surgeon should be made for consideration of surgical repair of rotator cuff tears and tendon release.
20. The choice of cost-effective pharmacological agents alone is sufficient to provide favourable treatment outcomes of PSSP.