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Post Stroke Pain Syndromes

Post Stroke Pain Syndromes. Susan Stickevers, MD Residency Program Director, PM&R SUNY Stony Brook. Epidemiology. Annually, 500, 000 people in the US have a first stroke 200, 000 have a recurrent stroke 80% of strokes are ischemic, either thrombotic or embolic in origin

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Post Stroke Pain Syndromes

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  1. Post Stroke Pain Syndromes Susan Stickevers, MD Residency Program Director, PM&R SUNY Stony Brook

  2. Epidemiology • Annually, 500, 000 people in the US have a first stroke • 200, 000 have a recurrent stroke • 80% of strokes are ischemic, either thrombotic or embolic in origin • 5 million people in the US have had a stroke & are living in the community setting • Of these, 1.1 million have limitations in their daily functioning or ability to perform activities of daily living • 100, 000 people have stroke as their primary diagnosis & are receiving in home health care

  3. Risk Factors for Stroke • Increasing age • Hypertension • Obesity • Diabetes • Physical Inactivity • Heart Disease • Tobacco Use

  4. Epidemiology of Post Stroke Pain • Prevalence of Post Stroke Pain estimated in studies to be as low as 19% of stroke survivors to as high as 70% • Langhorne et al followed more than 300 consecutive patients after stroke • 43% of the stroke patients had pain after their stroke • Increasing levels of dependency correlated with increasing levels of pain

  5. Risk Factors for Post Stroke Pain • Risk factors for the development of post stroke pain have not been fully delineated • Most post stroke pain manifests itself within several weeks to months after the stroke • Pain in the immediate post stroke period is not uncommon

  6. Distribution of Post Stroke Pain in 1,100 Stroke Survivors from 7 Rehab Facilities

  7. Distribution of Post Stroke Pain in 1,100 Stroke Survivors (con’t)

  8. Post Stroke Shoulder Pain • The shoulder may develop pain in the post stroke patient • Pain may be generated by : • Adhesive capsulitis / bursitis • Traction or compressive neuropathy • Soft Tissue Trauma • Glenohumeral Subluxation • Spasticity • Central Post Stroke Pain (CPSP)

  9. Hemiplegic Shoulder Pain • It was formerly believed that upper extremity pain following stroke was due to flaccidity of the upper extremity, and resultant shoulder subluxation • Study : 219 subjects with post stroke shoulder pain • 85% of patients with spasticity had pain • 18% of patients with flaccidity and shoulder subluxation had pain

  10. Pain Related to Spasticity in the Hemiplegic Patient • Post stroke spasticity pain is focal • Most commonly affected sites with post stroke spasticity related pain are : • Shoulder • Wrist • Fingers • Legs • Feet

  11. Treatments – Pain Related to Spasticity • Use of oral anti - spasticity agents • **Dantrolene is preferred due to lack of CNS side effects** • Botulinum Toxin A & chemodenervation with phenol have been demonstrated to be effective in reducing pain in most studies for spasticity related pain in the shoulder, forearm & foot

  12. Chemodenervation for Muscle Imbalance in Hemiplegic Shoulder • Subscapularis spasticity limits external rotation following stroke, and pectoralis muscle spasticity brings about limitation of shoulder abduction • Chemodenervation offers the ability to alleviate the imbalance & relieve shoulder pain

  13. Chemodenervation for Hemiplegic Shoulder • Hecht, 1992 – Retrospective study of 13 patients with spastic hemiplegia with limited & painful ROM of the shoulder who received phenol nerve blocks to subscapularis muscle innervation • Results : Immediate & significant improvement in ROM observed in abduction, flexion, & external rotation • Relief of pain with previously painful movements noted

  14. Botulinum Toxin A for Hemiplegic Shoulder Pain Related to Spasticity • Hecht, 1995 – Prospective study of 20 patients receiving botulinum toxin injections to the subscapularis & pectoralis muscles • Results : • 85% benefited from subscapularis block • 55% benefited from pectoralis major block • 45% exhibited improved AROM

  15. Botulinum Toxin Injection for Hemiplegic Shoulder Pain Related to Spasticity • Bhakta et al, 1996 : • 17 patients received a single course of intramuscular botulinum toxin to biceps, FDP, FDS, and FCU • Shoulder pain improved in 6/9 subjects who had shoulder pain prior to injection

  16. Botulinum Toxin A for Hemiplegic Shoulder Pain – AJPMR Marciniak Study, 2012 • Randomized Double Blind Placebo Controlled trial of botulinum toxin A vs. saline placebo in 37 hemiplegic subjects • Modified Ashworth score of 3 - 4 • 21 patients received the study drug • Patients injected solely in the shoulder adductors and internal rotators, specifically the pectoralis major and some patients were also injected in teres major • Dose administered was limited to 140-200 units

  17. 2012 Marciniak Botulinum Toxin A Hemiplegic Shoulder Pain Study • Pain reduction experienced by patients on placebo and treatment group was equivalent – there was no significant reduction in shoulder pain in those receiving botulinum toxin • The patients receiving the botulinum neurotoxins had improved hygiene and disability assessment scores • Marciniak et al, American J. of PM&R December 2012

  18. Shoulder Pain Following Stroke • Development of shoulder pain following stroke is associated with loss of external rotation, NOT subluxation • Zorowitz, 1996 • Use of hemisling should be discouraged if at all possible as the sling holds the upper extremity in an adducted & internally rotated position which can lead to a loss of external rotation

  19. Optimal Positioning of the Hemiplegic Shoulder • Randomized Controlled Trial in 36 Australian Hemiplegic Stroke Patients • Positioning of the shoulder in maximal external rotation for two 30 minute treatment sessions per day significantly reduced the development of contractures compared to controls. Ada et al, 2005

  20. Effect of Slings on the Hemiplegic Shoulder • It is generally believed that hemislings should be used in the initial stages following stroke to support the affected arm. • Their use is controversial because hemislings can encourage flexor synergies, inhibit reciprocal arm swing during ambulation, contribute to flexion contractures of the upper extremity, and discourage use of the affected arm & hand • A hemisling holds the affected shoulder in a position which accentuates adduction & internal rotation, which may lead to shortening of tonically active muscles • A sling is the best method however to support a flaccid arm while a patient is standing or transferring • Lapboards & arm troughs may be used to support the arm while seated • As tone returns to shoulder muscles, the risk of shoulder subluxation decreases, and then sling use may be discontinued

  21. Evidence Based Medicine : Slings for Hemiplegic Subjects • Cochrane Review, 2005 • The review, conducted by Ada et al, included only 4 randomized controlled trials regarding use of slings & shoulder supports for hemiplegic patients • Conclusion : There was limited evidence that shoulder slings prevented subluxation associated with hemiplegic shoulder pain • There was limited evidence that shoulder slings influence clinical outcomes • The best method to support the hemiplegic shoulder has yet to be determined

  22. Strapping the Hemiplegic Shoulder – Common Practice in Australia / New Zealand • Use of adhesive tape, (Fixomull Stretch), or Elastoplast adhesive bandage to prevent or reduce severity of shoulder subluxation • Three studies : Griffin & Bernhardt, Ancliffe et al, Hanger et al. • A review of these three studies in Australia & New Zealand revealed that : • Strapping the hemiplegic shoulder does not improve upper limb function or range of motion • There was conflicting data in the three studies regarding whether or not strapping could reduce shoulder pain.

  23. Use of Active Therapies to Reduce Pain in the Hemiplegic Shoulder • There was evidence that aggressive range of motion of the shoulder with overhead pulleys resulted in increased rates of shoulder pain • Kumar, 1990 • There was evidence that Bobath (NDT) for the hemiplegic shoulder was associated with greater pain reduction than cryotherapy • Partridge et al, 1990 • There was evidence that gentle range of motion exercises were the preferred method of treatment for the hemiplegic shoulder • Addition of ultrasound application to the shoulder to the ROM exercises did not change outcomes • Inaba et al, 1972 • There was limited evidence that providing oral NSAIDS to a stroke patient with shoulder pain improved ROM & functional recovery • Poduri et al,1993 • No statistically significant benefit from CPM for the shoulder compared with therapist supervised self ROM • Lynch et al, 2005

  24. Intraarticular Injections • Subacromial Bursa Injections • Glenohumeral Joint Injections • Often used clinically for adhesive capsulitis or bursitis which develops following CVA • What evidence supports this practice?

  25. Injections for Relief of Hemiplegic Shoulder Pain • There is only one randomized controlled trial in 35 Dutch hemiplegic subjects with shoulder pain injected X 3 with triamcinolone 40 mg vs saline placebo in the affected glenohumeral joint • Snels et al, 2000 • No significant improvement was observed in pain or function of the affected shoulder with triamcinolone injection

  26. Electrical Stimulation for Preventing & Treating Post Stroke Shoulder Pain • Application of functional electrical stimulation (FES) to the hemiplegic shoulder is believed to improve muscle tone & strength, as well as reduce pain • The **supraspinatus & posterior deltoid** muscles are usually treated as they maintain correct alignment of the glenohumeral joint & reduce shoulder subluxation • Ideal intensity of treatment is 6 hours / day, five days per week, for a total of 6 weeks, at frequencies between 35 – 50 Hz • Paci et al, 2005

  27. Cochrane Review, 2001 – FES for Hemiplegic Shoulder • Price & Pandyan conducted this systematic review of 4 studies on electrical stimulation (both TENS & FES) used for prevention and treatment of post stroke shoulder pain • They concluded that there was insufficient evidence from which to draw conclusions. • There was evidence that FES, in addition to conventional therapy, improved function but was not superior than conventional therapy for preventing shoulder pain • **FES did improve passive external rotation of the shoulder & improved glenohumeral subluxation compared to baseline **

  28. Meta – Analysis on Effect of FES on Shoulder Subluxation Following Stroke • Ada & Foongchomcheay (2002) • Review of 6 randomized controlled trials • Results suggested that early treatment with electrical stimulation prevented the development of shoulder subluxation in the hemiplegic subject while later treatment helped to reduce pain when used in conjunction with conventional therapy

  29. Effect of FES on Hemiplegic Shoulder Pain • 11 studies conducted • All 11 of the studies reported a benefit associated with FES treatment including improved muscle function, tone, EMG activity, pain, subluxation and range of motion • The improvement was maintained for up to 24 months of follow up • Studies : Chae et al, 2005, Yu et al, 2004, Wang et al, 2000, Linn et al, 1999, Renzenbrink & Ijerman, 2004, Baker & Parker, 1986, Faghri et al, 1994, 1997, Chantraine et al, 1999, Kobayshi, 1999.

  30. Surgical Treatment for Hemiplegic Shoulder Pain • Involves resection of subscapularis & pectoralis muscle tendons to relieve internal rotation & adduction of shoulder • Surgery was followed up by post op passive range of motion & positioning of the shoulder, as well as pulley exercises • 10/13 patients operated on regained 90 degrees of passive abduction & 20 degrees of external rotation within 2 months of surgery, but six months later, all 13 patients reported pain & discomfort • Braun et al, 1971

  31. Complex Regional Pain Syndrome Type 1 • Typically appears within 9 weeks of following stroke • Studies have shown the incidence of post stroke CRPS to range between 12.5% - 70% • Symptoms include : • Pain • Hyperalgesia or allodynia • Joint Stiffness • Swelling • Autonomic Abnormalities

  32. Complex Regional Pain Syndrome • The following are predictive of the development & severity of CRPS following stroke : • Motor deficits • Sensory deficits • Spasticity • Coma following stroke

  33. Keys to Avoiding Development of CRPS • Early rehabilitation interventions! • Avoidance of trauma to the limb

  34. Shoulder Hand Syndrome • Is a type of CRPS that is limited to the upper extremity after stroke • Pathophysiology of this disorder is not known, however, this disorder appears to be related to the severity & the etiology of the stroke, neural reorganization following the stroke, spasticity, motor and sensory deficits following the stroke • Severe motor deficits which are slow to resolve post stroke increase the likelihood of developing shoulder – hand syndrome

  35. Early ROM exercises Avoid shoulder subluxation Prevention & treatment of upper extremity contractures Active exercise if possible Frequent passive range of motion Heat / Cold Modalities including contrast bathes Hand desensitization program, including vibration, massage, brushing, stroking TENS Analgesics High Dose Steroids Stellate Ganglion Block Guanethidine Bier Block Sympathectomy Management of Shoulder Hand Syndrome

  36. Pharmacological Management of Shoulder Hand Syndrome • Braus et al, 1994 : Randomized controlled cross – over trial involving 36 hemiplegic patients with SHS resulting from MCA stroke • Randomized to receive either 8 mg methylprednisolone or placebo over 4 weeks • All patients received daily physical therapy • No significant improvement was noted in SHS in the placebo group after 4 wks. – switched to study drug • Patients on steroid treatment demonstrated significant improvement in shoulder hand syndrome that was maintained at 6 months • 31/36 patients became almost symptom free within 10 days of treatment with low dose corticosteroids

  37. Use of Calcitonin for SHS • Hamamci et al, 1996 : • Controlled trial of 41 hemiplegic subjects with SHS • All patients received conventional physical therapy as part of inpatient rehabilitation • 25 patients received 100 IU salmon calcitonin daily for 4 wks • 16 patients received saline placebo injections • Pain was measured on a numerical rating scale • By the end of the 4th week, patients receiving calcitonin had significantly lower median pain scores compared to controls (Pain Level 1 vs. Level 5) • Patients receiving calcitonin reported less tenderness & improved ROM • No difference in hand edema between groups

  38. Post Stroke Central Pain Syndrome • Central Pain Syndrome is defined as neuropathic pain that results from damage to or dysfunction of the central nervous system, including the brain, brainstem, and spinal cord • Formerly called the post thalamic syndrome, however, lesions in the brainstem, pons, thalamus, and areas lateral & superior to the thalamus can also cause central post stroke pain • Leijon et al, Pain, 1989 • Estimated as occurring in 8 - 12% of all stroke patients • May occur at any time following a stroke, in the immediate post stroke period, or years later • Develops immediately after the stroke in 20% of patients • Occurs within one month after the stroke in 50% of all patients affected • 30% of patients who develop this syndrome claim onset of pain between one month and three years following the stroke.

  39. Central Post Stroke Pain • Can be caused by both ischemic and hemorrhagic strokes • Pain is mild in 1/3 of affected subjects, and moderate to severe in 2/3 of subjects • CPSP usually results from a lesion of vascular origin, however some cases of CPSP are neoplastic in origin

  40. Post Stroke Central Pain Syndrome • Common Symptoms : • Muscle Pain or Cramping / Squeezing • Dysesthesias – Burning most commonly described (seen in 60% of CPSP pts.) • Hyperpathia • Allodynia - seen in 50% of CPSP pts. • Intermittent shooting or lancinating pain • Circulatory Pain • Visceral Pain • Pruritis

  41. Hypoesthesia & Autonomic Instability in CPSP • Hypoesthesia, which is a weaker than normal sensory reaction to stimuli, is common in CPSP • 95% of CPSP pts. have impaired pain & temperature sensation • 50% also have hypoesthesia to touch, vibration, and kinesthesia • Autonomic instability is also seen in these pts, but it is not clear if it is secondary to a superimposed CRPS

  42. CPSP : The Pain Generators • Large lesions of the ventral posteromedial thalamic nucleus, (VPM), or ventral posterolateral thalamic nucleus, (VPL), or posterior limb of the internal capsule frequently cause hemi – body pain • CPSP may occur following lesions at any level in the spinothalamocortical pathway • Damage to the spinothalamic – cortical sensory pathways (mainly lateral medulla, thalamus, posterior limb of the internal capsule, cortical and subcortical zones of the post central gyrus and insular region) is believed to play a significant role in the pathogenesis of post stroke central pain

  43. Theories on the Pathogenesis of CPSP • Dejerine & Roussy : • an irritable focus in the lesioned tracts produces this pain syndrome • Boivie : • CPSP originates from hyperirritability in surviving cells in a lesion along the pain pathway (spinothalamic or thalamocortical pathway)

  44. CSPS Secondary to Brainstem Involvement • In CSPS secondary to brainstem involvement, impairments in facial sensation are generally ipsilateral to the lesion, whereas extremity involvement is contralateral, and the distribution of pain may follow the same pattern

  45. Treatments for Central Post Stroke Pain • Antidepressants • Anticonvulsants • Antiarrhythmics • Opioids • Steroids • Intrathecal Baclofen • Rehab Techniques • Regional Anesthesia • Electrical Stimulation • Deep Brain Stimulation • Neuroablative Procedures • Transcranial Magnetic Stimulation

  46. Amitriptyline for Central Post Stroke Pain • Double blind, three phase, crossover placebo controlled trial in 15 patients, mean age 66, started with 25 mg elavil titrating up to 75 mg • Treatment given in randomized order for 4 weeks, separated by 1 week washout period in which patients were administered amitriptyline, carbamazepine, or placebo • Amitriptyline produced a significantly greater reduction of pain when compared to placebo at week 4 • Pain reduction was positively correlated with plasma concentration of Elavil > 300 nmol/l • Carbamazepine did not produce a statistically significant reduction in pain at doses up to 800 mg / day • Leijon & Boivie, Central Post Stroke Pain, A Controlled Trial of Amitriptyline & Carbamazepine. Pain, 1989, 36: 27 - 36

  47. Mexilitene for Central Post Stroke Pain • Awerbuch, 1990 : • 9 patients with central pain following stroke were administered 150 mg / day of mexilitene for 3 days followed by 300 mg / day for 3 days, followed by 10 mg / kg / day for one month • Mexilitene produced a significant improvement in pain in 8/9 patients • Need to monitor for QT interval prolongation while on mexilitene • Follow Up Study : up to 800 mg oral mexilitene / day for up to 12 weeks in 12 subjects : No effect Nicholson, Neurology, 2004

  48. Morphine • Generally ineffective for CPSP • Attal, Neurology, 2002 : Double blind placebo controlled study in 15 subjects with central pain, only 5/15 had CPSP : • IV morphine (average dose 16 mg) decreased pain for up to 120 minutes, but did not decrease evoked pain to stimulus. • In a subsequent follow up year long study with oral morphine 60 – 140 mg / day, only 3/15 patients remained on the oral morphine after one year due to side effects or limited efficacy of the drug • Arner & Meyerson, Pain, 1991 : Minimal clinical response to opiates prescribed for central post stroke pain

  49. Levorphanol for CPSP • Rowbotham et al, 2003 : • 5 CPSP patients placed on 0.75 mg Levorphanol • 5 CPSP patients placed on 0.15 mg Levorphanol for 8 weeks • 0.75 mg dose of levorphanol reduced pain by 36 % as compared with a 21% pain reduction in the low strength group • Only 3/10 patients with CPSP remained in the study due to side effects or limited efficacy of the study drug

  50. Tramadol • One case report describes a treatment resistant case of CPSP which responded to one infusion of IV tramadol 50 mg followed by daily oral administration of codeine 20 mg and milnacipran 25 mg • The patient had complete relief for 6 days • Symptom recurrence developed after cessation of the codeine and milnacipran • Further research is needed

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