Post Stroke Pain PMR Refresher Course

1. Post stroke pain
Venugopal Kochiyil
Rehabilitation and Pain Medicine Physican
Modbury Hospital and Flinders Medical Centre
Adelaide, South Australia, Australia

2. Introduction
• Pain issues are common in stroke
• Chronic pain is seen in approx. 50% of patients
• Underreported, under identified and under treated
Vasc Health Risk Manag 2012;8:407-413

3. Why is it important?
• Experience greater cognitive and functional decline
• Fatigue
• Depression
• Suicidality
• Lower quality of life
• Poor rehab outcomes
Cerebrovasc Dis 2015;39:190-201

4. Risk factors
• Age of stroke onset
• Female
• Premorbid – alcohol, statin, PVD, Depression
• Clinical – spasticity, reduced upper extremity
movement, sensory deficit
• Stroke related – ischemic stroke, thalamic location,
brain stem location
Cerebrovasc Dis 2015;39:190-201
Pain 2011;152:818-824

5. Identifying post stroke pain
• Stroke deficits – language, neglect
• Assessment of pain
• Which scale to use

6. Chronic pain after stroke
H Klit et al Lancet Neurology 2009;8:857-68

7. Central post stroke pain
• First described by Dejerine and Roussy
• Called thalamic syndrome
• Can arise from lesions involving any sensory tracts

8. Epidemiology of CPSP
• Seen in approx 9% of strokes
• Can occur with infarcts or hrrages
• Usually within 3-6 months of stroke (earlier onset
within a month possible)
• Young age, previous depression, current smoking,
baseline stroke severity are considered to be risk
factors

9. Pain types
• Constant pain / intermittent pain usually within a
smaller area than sensory impairment
• Described as burning, aching, pricking, lacerating or
throbbing
• Evoked pain
• Allodynia and hyperalgesia, aftersensations
• Increased by emotional stress and physical activity,
cold, heat and fatigue
• Improves with relaxation

10. Localization and pathophysiology
• Thalamic lesions – 33 % (VPM/VPL involvement)
• Spinothalamic tract but trigeminothalamic and
lemniscal pathways are also important
• Brain stem – lateral medullary syndrome (25 – 44%)
• More in right hemispheric strokes (?)
• Primary sensory cortex is rarely associated but insular
cortex
• Small vessel disease
Cerebrovasc Dis 2015;39:190-201
PMR 2017; 9: 63-75

11. Treatment
• Difficult to completely abolish
• Medications are frequently unsatisfactory
• Make sure that this is CPSP
• Patient education
• Treat concomitant depression, anxiety or sleep
disturbances

12. Pharmacological management
• Not much scientific evidence on how to treat
• RCTs are rare and involved only limited number of
patients
• Antidepressant medications – Tricyclics, SSRI,
SNRIs
• Anticonvulsants – CBZ, Lamotrigine
• Gabapentin, Pregabalin
• IV lignocaine and ketamine for acute symptoms

13. Current standards
• Amitriptyline – first line (IASP, EFNS, CPS)
• Gabapentin/Pregabalin- first line (EFNS, CPS)

14. Pharmacological management
• Methyl prednisolone

15. Non pharmacological options
• TENS
• rTMS
• Motor cortex stimulation – around 50% success rate
• Deep brain stimulation (PAG, PVG, sensory thalamus
and medial leminiscus) with a success rate of 20-50%
• Cognitive behavioral therapy
• Caloric Vestibular stimulation
• Poor outcomes with destructive lesioning like medial
thalamotomy

16. Regional pain
• Mostly involve shoulder (11 to 40%)
• Predictors are motor loss, sensory loss, low mood and prior
shoulder pain, spasticity
• Can occur as early as 2 weeks post-stroke
• Onset time of 2-3 months post stroke is more typical
• Negatively affect rehabilitation outcomes

17. Pathophysiology
• Multifactorial – Glenohumeral subluxation,
impingement, rotator cuff tears, biccipital tendinitis,
adhesive capsulitis
• Spasticity is a contributor especially subscapularis
and pectoralis major (but poor correlation in many
studies)

18. Spasticity
• Flexor tone/flexor synergy predominates
• Scapular retraction & depression
• Internal rotation & adduction of shoulder
• Internal rotators predominate
• External rotation is the last shoulder function to
recover

19. Shoulder subluxation
• Characterised by presence of a palpable gap between
acromion and humeral head
• Multifactorial
• Poor correlation with shoulder pain
• No evidence that it can be reduced once occurred
• Subluxation needs to be prevented

20. Prevention
• Joint protection strategies – during rest, during
functional mobility, during wheelchair mobility
• Shoulder slings are controversial beyond flaccid stage
• Arm board, supportive pillows may be useful
• Avoid overhead pullies
• Avoid moving shoulder beyond 90 degrees flexion or
abduction
• Educate patient, family and staff in correctly handling
the involved arm
• Early therapy (electrical stimulation)
Harrison RA, Field T. Cerebrovas Dis 2015;39:190-201

21. Treatment
• Mechanical stablisation
• NSAIDs
• Spasticity medications
• TENS
• FES – supraspinatus and posterior deltoid
• Botulinum toxin – subscapularis, pectoralis major
• Treatment of contractures.

22. Spasticity related pain
• Is there a correlation between spasticity and pain?
• What is the mechanism – neuropathic/nociceptive
• Overlaping networks of spasticity and pain

23. Treatment
• Therapy
• Pharmacology
• Injections

24. CRPS
• 2 to 49% of patients with stroke develop CRPS
• Impaired biomechanics of GH joint could be a reason
• Corticosteroids as treatment
• Mirror therapy

25. Post stroke headache
• Poorly characterised
• Approx. 10% of patients
• Those with history of tension or vascular type
headache tend to develp
• Mostly a tension type of headache not aggravated by
movement
• Trigeminovascular system could be the cause
• Medications