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Post Stroke Pain - Dr Venugopal Kochiyil

Post Stroke Pain
PMR Refresher Course

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Post Stroke Pain - Dr Venugopal Kochiyil

  1. 1. Post stroke pain Venugopal Kochiyil Rehabilitation and Pain Medicine Physican Modbury Hospital and Flinders Medical Centre Adelaide, South Australia, Australia
  2. 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. 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. 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. 5. Identifying post stroke pain • Stroke deficits – language, neglect • Assessment of pain • Which scale to use
  6. 6. Chronic pain after stroke H Klit et al Lancet Neurology 2009;8:857-68
  7. 7. Central post stroke pain • First described by Dejerine and Roussy • Called thalamic syndrome • Can arise from lesions involving any sensory tracts
  8. 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. 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. 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. 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. 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. 13. Current standards • Amitriptyline – first line (IASP, EFNS, CPS) • Gabapentin/Pregabalin- first line (EFNS, CPS)
  14. 14. Pharmacological management • Methyl prednisolone
  15. 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. 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. 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. 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. 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. 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. 21. Treatment • Mechanical stablisation • NSAIDs • Spasticity medications • TENS • FES – supraspinatus and posterior deltoid • Botulinum toxin – subscapularis, pectoralis major • Treatment of contractures.
  22. 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. 23. Treatment • Therapy • Pharmacology • Injections
  24. 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. 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

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