Pathophysiology: Hemiplegic glenohumeral subluxation

 Multifactorial cause
 Shoulder pain prevalent in 16-72% of stroke patients
 Pain starts w/in 3 wks of stroke
 Risk factors of shoulder pain: UE weakness and stroke severity
 Link btwn painful hemiplegic shoulder and glenohumeral subluxation + spasticity
Shoulder joint
 Very mobile, relies on muscles and ligaments for stability;
o Vulnerable to secondary complications after stroke or neurological in
 Weakness from strokehumeral head to shift out of socket (glenoid cavity)
inferior direction; gravity also involved, and weak muscle shoulder strength
 Subscapularis and pectoralis major mm may play important role bc they have
high tonic activity)->muscle imbalance in shoulder
 Sub can occur right after stroke when UE has flaccid toinevulnerable to
instability
 Pain becomes apparent at onset of spasticity
o M.C. physical signs of post-stroke shoulder pain are bicipital tendo
tenderness, supraspinatus tenderness, and positive Neer sign.
o Palpate space btwn acromion and top of humerus.
 Potential complications of subluxation include Complex regional pain syndrome
and secondary brachial plexus injury
1. Slings/positioning
a. Reduce gravity effect on glenohumeral joint (hypothesis)
b. Controversial for holding arm in flexed position, inhibiting shoulder
mvmt, ^ contractures, etc, cause lateral sublux, interfere w/ ADLs
c. Unclear which sling type is best, not proven to be effective
d. Moderate evidence says that prolonged positioning/ slings prevents
subluxation
i. Positioning: avoid supine-lying positions. Protract shoulder and
bring arm forward to counteract scapular tendency for retraction
2. Strapping
a. Conflicting evidence that it reduced pain and prevents subluxation
b. Adjunct to other techniques
c. AEs skin irritations and constant reapplication by professional
3. Physical therapy: minimize/reduce instability as goal
a. Focused on strengthening muscles surrounding shoulder joint i.e.
deltoids
b. Function of deltoids: arm elevation, maintains humerus in glenoid socket
c. Active arm exercise to improve ROM and lessen pain
4. Electrical neuromuscular stimulation (ENS)
 a. Superficial application of currentmuscle contraction and ^ muscle
recruitment; slows muscle atrophy and improves strength
b. Gate control theory of pain: activates myleinated sensory fibers and
disrupts pain signals of unmyelinated C fibers
c. Deltoids and supraspinatus are most commonly treated
d. Treatment guidelines say 6h per day, 5 days per wk for duration 6 wks, at
frequencies 35-50Hz.
e. Two methods:
i. Functional electrical stimulation (FES)
ii. Transcutaneous electrical nerve stimulation (TENS): lower
intensity and higher freq vs FES.
f. Inconclusive evidence
i. Several studies suggest improvement in reduction of pain and
upper limb function and others say ENS a/w deterioration of arm
function (esp in severe paralysis).
5. Injections: Intra-articular, intramuscular B toxin, or steroids
a. Used to tx muscle spasticity and alleviate PHS
b. Randomized controlled trials w/ B toxin tx reduced pain; subscapularis
mc injection site
c. Trial w/ triamcinolone acetonide+ B toxin were hard to interpret
d. Moderate evidence says corticosteroid injections doesn’t improve pain/
ROM
6. Surgery
a. Targets muscle spasticity to relieve pain
b. Braun et al: Resected tendons of subscapularis and pectoralis mm
c. Pts had intensive PT during post opless pain and ^ ROM
d. Pts re-experienced pain 6 months later
7. Aromatherapy
a. Decrease in PNS response thru smell and touch that promotes relaxation
to modify pain perception
References:
1.“Post Stroke Pain: Identification, Assessment, and Therapy”. Cerebrovasc Dis 2015;39:190-
201 https://doi.org/10.1159/000375397
2. Painful hemiplegic shoulder in storke patients: Causes and management.
https://pmj.bmj.com/content/postgradmedj/77/912/645.full.pdf