Multimodal Chronic Pain      Treatment     New Directions               N. Lee Smith MD         Center for MindBody Health...
Focus• Acute vs Chronic Pain• Nociceptive vs Neuropathic vs Central• The common role of central sensitization  – Prototype...
Acute pain = a symptomChronic pain = a diseaseIf acute pain goes under-treated,          more chronic pain
Chronic post-surgical pain•   Thoracotomy       50-60%•   Amputation        50%•   Breast surgery    33%•   Inguinal herni...
Pain Treatment:      How are we doing?   “Pain can be relieved effectively     in 90% of patients, but is not     relieved...
Acute pain is often       inadequately treated:               Why?• Fear of opiods: MD  – 1/2 of fractures receive them  –...
What percent of chronic pain patients say,“Opiates give me little or no        pain relief”?                53%   American...
Distinguishing different types of pain     Nociceptive                                Neuropathic                         ...
Pain Distribution    • Use a body pain      diagram    • Have a patient color      all areas of the body in      which the...
Pain DistributionNeuropathic              Back   Front
Pain DistributionArthritis             Back   Front
Pain DistributionFibromyalgia               Back   Front
The Diagnosis of Fibromyalgia Officially:• Chronic widespread pain                       (> 3 months)• Tender points      ...
Comorbidities of FM50% of FMS patients also havethe most common disorder seen inGI Clinics           (@ half of GI pts)
Comparison of pain                              thresholds                                            IBS                 ...
Comparison of pain thresholds                     of IBS patients and controls                          Pain produced by r...
Central Hypersensitization-      Amplification Syndromes• Irritable bowel syndrome  (& functional Upper Gastrointestinal p...
How doeshypersensitization occur?  In whom is this more likely?
Fibromyalgia:        Contributing Factors• Genetic predisposition• Neurotransmission and sleep abnormalities• Triggering e...
Neurotransmission     Issues             Inhibitory tracts               (NE, DA, 5HT)                                    ...
CSF Substance P in FMS4540353025                                          Normals20                                       ...
Fibromyalgia: Pain Processing Disorder    fMRI Evidence: Augmentation         fMRI = functional magnetic resonance imaging...
FMS: Neurotransmission        Abnormalities (in CSF)• Low central serotonin function                                      ...
Pharmacological     Targets for      Treatment                                   Deep sleepAntidepressants    (NRIs)   Tra...
Grading Pain Severity                           For example   • Nuisance:             after exercise aches   • Distracting...
Neuropathic Pain:             >50% Reduction        7        6        5                                             Na ACs...
Anticonvulsants:              Neural stabilizers• Sodium channel block     (e.g., divalproex, lamotrigene)• Calcium channe...
Positive Pharmacological Trials          for Fibromyalgia• Anticonvulsants: Pregabalin (30% get 50% improvement)• Dual act...
SNRIs for Pain• Duloxetine  – FDA indicated in four types of pain• Minacipran  – For fibromyalgia  – More NE than serotonin
Tricyclics for Pain• Second generation: more NE; fewer side effects  – nortriptylene  – desipramine  – cyclobenzaprine: be...
Opiates in Neuropathic Pain     Meta-analysis of 22 studies (n=521)  • Intermediate term (1+ months):      – VAS reduction...
How to tell if opiate responsive?            (Note well: Function)• Good initial response: use long acting opiod  – Should...
Two Anti-hyperalgesic Opiates:• Buprenorphine  – Unique receptor profile  – Patch = different dosing than SL• Tapentadol  ...
Chronic Pain Treatment:                       Opiates and NSAIDs         6         5         4Pain                        ...
Myofascial Pain Syndrome  is a common cause of chronic or resistant pain      →Trigger points
Myofascial Pain  Syndrome: Treatment• Principles  – 1. Inactivation of trigger points  – 2. Muscle Rehabilitation  – 3. Re...
Myofascial Pain   Syndrome: Treatment1. Inactivation of trigger points• Injection of local anesthetic (lidocaine + bipuvic...
Myofascial PainSyndrome: Treatment2. Muscle Rehabilitation• Stretching, strengthening• Postural exercises• Movement:   – m...
Myofascial Pain Syndrome:      Treatment- Prevention3. Control of contributing factors:• Mechanical: Correct repetitive, t...
Who is likely to get chronic pain ifacute pain treatment is suboptimal ?• Personal or family history of     CNS hypersensi...
Pain treatment:The earlier, the better
Which Medication to Start?• Depends on dominant patterns of problems:  – Sleep + pain + tingling + anxiety: Anticonvulsant...
Treating Chronic Pain Disorders Five important parts (interdisciplinary):• Treat early and aggressively• Treat CNS neuroch...
Self Care Websites                     OFFER      Organization for Fatigue and Fibromyalgia              Education and Res...
Neural stabilizing Nutrients• Vitamins B6 (25-50 mg), B12 (550-1000 mcg),  methylfolate (2.5-7.5 mg)• Omega3 fatty acids (...
Sleep Stages    Non REM              REM      Benzos,    Some SSR Is,     Venlafaxine   4       Blocks           3    21  ...
Deep Sleep Effects         of CNS Medications• Antidepressants  – Suppress:      most SSRIs (exceptions: sertraline, cital...
Why More Pain    with Anxiety and Depression?• Up-regulated pain sensory response   – Increased Substance P   – Low CNS se...
Pain correc conf
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Pain correc conf
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  • Most double-blind or single-blind studies investigating multimodal analgesia with a combination of nonsteroidal anti-inflammatory drug (NSAID) and opioid, with or without local anesthetic, show lower pain scores, a need for fewer analgesics, and prolongation of the time needed for postoperative analgesia compared with control groups. 1 Reference: 1. Jin F, Chung F. Multimodal analgesia for postoperative pain control. J Clin Anesth. 2001;13:524–539.
  • Chronic pain can be of mixed etiology with both nociceptive and neuropathic characteristics, as in some back pain conditions
  • Studies have demonstrated that patients with IBS have a heightened state of visceral sensitivity. 1 In 1980, Whitehead et al evaluated pain thresholds of a total of 25 IBS patients and 20 healthy controls. By distending a rectosigmoid balloon in a stepwise fashion, the investigators found that pain thresholds in IBS patients were significantly lower than in controls ( P <0.05). 2 Studies evaluating the pain thresholds of other GI disorders involving the esophagus 3 and stomach 4 have shown similar findings. References: 1. Ritchie J. Pain from distension of the pelvic colon by inflating a balloon in the irritable colon syndrome. Gut . 1973;14:125-132. 2. Whitehead WE, Engel BT, Schuster MM. Irritable bowel syndrome: physiological and psychological differences between diarrhea-predominant and constipation-predominant patients. Dig Dis Sci . 1980;25:6:404-413. 3. Richter JE, Barish CF, Castell DO. Abnormal sensory perception in patients with esophageal chest pain. Gastroenterology . October 1986;91:845-852. 4. Mearin F, Cucala M, Azpiroz F, Malagelada J-R. The origin of symptoms on the brain- gut axis in functional dyspepsia. Gastroenterology. October 1991;101:999-1006.
  • Functional magnetic resonance imaging (fMRI) data provide supporting evidence that FM is a central pain disorder and demonstrate the presence of cortical/subcortical pain processing in FM. 1 fMRI was used to evaluate cerebral activation patterns during the application of painful pressure in FM patients (n=16) and controls (n=16) 1 Each patient underwent fMRI while pressure was applied to the thumbnail bed; 13 regions of increased brain activation were revealed in the FM group, compared with 1 in the control group 1 The graph depicts pain intensity against stimulus intensity. In FM patients, a low stimulus pressure produced a high pain level; however, in stimulus pressure controls, a similar pressure resulted in low levels of pain 1 Enhanced responses were noted in multiple areas of the brain, including somatosensory primary and secondary cortex, insula, putamen, and cerebellum; this provides supporting evidence that CNS alterations may underlie FM pathophysiology 1 Reference: 1. Gracely RH, Petzke F, Wolf JM, Clauw DJ. Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia. Arthritis Rheum . 2002;46:1333-1343.
  • Pain correc conf

    1. 1. Multimodal Chronic Pain Treatment New Directions N. Lee Smith MD Center for MindBody Health Director, Stress Medicine Omega Pain Clinic and Lifetree Clinical Research Salt Lake City, Utah
    2. 2. Focus• Acute vs Chronic Pain• Nociceptive vs Neuropathic vs Central• The common role of central sensitization – Prototype: Fibromyalgia• Multimodality treatment: – How to reduce opiates with good relief?• Myofascial Trigger Points
    3. 3. Acute pain = a symptomChronic pain = a diseaseIf acute pain goes under-treated, more chronic pain
    4. 4. Chronic post-surgical pain• Thoracotomy 50-60%• Amputation 50%• Breast surgery 33%• Inguinal hernia 30%• C-section 12% Why? And who is more likely? How to prevent this?
    5. 5. Pain Treatment: How are we doing? “Pain can be relieved effectively in 90% of patients, but is not relieved effectively in 80% of patients” Walco, New Engl J Med 1994;331:8Chronic pain is often misunderstood
    6. 6. Acute pain is often inadequately treated: Why?• Fear of opiods: MD – 1/2 of fractures receive them – 42% come to ER for pain: • 3/4 leave in moderate to severe pain• Patient fears: 3/4 prefer non-opiate
    7. 7. What percent of chronic pain patients say,“Opiates give me little or no pain relief”? 53% American Pain Foundation Survey 2007
    8. 8. Distinguishing different types of pain Nociceptive Neuropathic Central Caused by nerve Caused by tissue damage Snsitization lesion or dysfunction • Arthritis • Fibromyalgia • Painful Diabetes • Injuries • Low back pain • Shingles, PHN • Postoperative pain • Neck pain • Sciatica • Trigeminal neuralgia
    9. 9. Pain Distribution • Use a body pain diagram • Have a patient color all areas of the body in which they feel painAdapted from pain drawing provided courtesy of L Bateman. Back Front
    10. 10. Pain DistributionNeuropathic Back Front
    11. 11. Pain DistributionArthritis Back Front
    12. 12. Pain DistributionFibromyalgia Back Front
    13. 13. The Diagnosis of Fibromyalgia Officially:• Chronic widespread pain (> 3 months)• Tender points (11/18 officially)• Also – Fatigue – Unrefreshed sleep – Cognitive problems – ComorbiditiesAm. College Rheumatology, Criteria for Fibromyalgia, Arthritis Rheum 33:160-172, 1990
    14. 14. Comorbidities of FM50% of FMS patients also havethe most common disorder seen inGI Clinics (@ half of GI pts)
    15. 15. Comparison of pain thresholds IBS Normal ColonicReference: Whitehead et al. Gastroenterology. May 1990;98:1187-1192. Distension
    16. 16. Comparison of pain thresholds of IBS patients and controls Pain produced by rectosigmoid balloon distension 60 IBS % Reporting Pain 40 20 Normal 0 20 60 100 140 180 Rectosigmoid balloon volume (mL)cf. Irritable Bladder Reference: From Whitehead et al. Dig Dis Sci. June 1980;25:404-413..
    17. 17. Central Hypersensitization- Amplification Syndromes• Irritable bowel syndrome (& functional Upper Gastrointestinal pain)• Irritable bladder More• Migraine, tension and TM Jt. Headaches Chronic• Fibromyalgia (or multiple pain) Syndromes Pain• Non-cardiac chest pain• Restless legs syndrome• Anxiety and some depression disorders
    18. 18. How doeshypersensitization occur? In whom is this more likely?
    19. 19. Fibromyalgia: Contributing Factors• Genetic predisposition• Neurotransmission and sleep abnormalities• Triggering events• Disordered sensory processing
    20. 20. Neurotransmission Issues Inhibitory tracts (NE, DA, 5HT) When inhibition is lacking, the nervous system hypersensitizes SP
    21. 21. CSF Substance P in FMS4540353025 Normals20 FMS1510 5 0 Vaeroy Russell Welin Bradley
    22. 22. Fibromyalgia: Pain Processing Disorder fMRI Evidence: Augmentation fMRI = functional magnetic resonance imaging. Gracely et al. Arthritis Rheum. 2002;46:1333-1343.
    23. 23. FMS: Neurotransmission Abnormalities (in CSF)• Low central serotonin function } ⇒ deep sleep loss, anxiety)• Low central norepinephrine function ⇒ fatigue, pain, cognition ADs• Low dopamine function ⇒ ↓attention, ↓pleasure, ↓ sex, RLS }• High Substance P ⇒ pain amplification ACs• High Glutamate Russell J Arth Rheum 1994;37:1543-1560
    24. 24. Pharmacological Targets for Treatment Deep sleepAntidepressants (NRIs) Tramadol Inhibitory tracts Tapentadol (NE, DA & 5HT) Dopamine agonists NSAIDsIf present: Anticonvulsants, trigger SP neural stabilizers points?
    25. 25. Grading Pain Severity For example • Nuisance: after exercise aches • Distracting: menstrual cramps, OA, finger burn residual • Disabling: migraine, toothache • Worst Possible: labor, severe burns, kidney stone 50% 30%0___1____2____3____4_____5____6____7____8_____9___10 nuisancedistracting disabling worst
    26. 26. Neuropathic Pain: >50% Reduction 7 6 5 Na ACs(CBP,OXC)Number 4 TCAsneeded Tramadolto treat 3 Ca ACs(PGB,GBP) SNRIs(dulox,venla) 2 SSRIs 1 0 Na+ TCAs Tram Ca++ SNRIs SSRIs ACs ACs Gilron et al. CMAJ 2006;175(3) Cochrane Database SR 2006;3:CD003726
    27. 27. Anticonvulsants: Neural stabilizers• Sodium channel block (e.g., divalproex, lamotrigene)• Calcium channel modulation (e.g.,pregabalin, gabapentin)• GABA enhancers (e.g., tiagabine, baclofen)These ↓ Glutamate release Using meds with complementary mechanisms in lower dose may be better than high doses of one mechanism
    28. 28. Positive Pharmacological Trials for Fibromyalgia• Anticonvulsants: Pregabalin (30% get 50% improvement)• Dual action “antidepressants”: (30-40% get 50% improved) – Milnacipran, Duloxetine, Venlafaxine – Tricyclics (about 1/3 improve with low dose) – Cyclobenzaprine (10-30 mg) – Tramadol (28% reduction)• Dopamine agonists: (75% improve; about 40% get 50% improv.)• Gamma hydroxybuyrate (GHB) (30% get 50% improvement) Usually, these are used in combination
    29. 29. SNRIs for Pain• Duloxetine – FDA indicated in four types of pain• Minacipran – For fibromyalgia – More NE than serotonin
    30. 30. Tricyclics for Pain• Second generation: more NE; fewer side effects – nortriptylene – desipramine – cyclobenzaprine: better deep sleep (in low dose)
    31. 31. Opiates in Neuropathic Pain Meta-analysis of 22 studies (n=521) • Intermediate term (1+ months): – VAS reduction from placebo = 1.4 / 10 – No reduction in disability or mental health scores • In all but one study • Short term: Sometimes helpful (contradictory results ) Eisenberg E. JAMA 2005;293:3043-3052One opiate is FDA-approved for neuropathic pain: tapentadol
    32. 32. How to tell if opiate responsive? (Note well: Function)• Good initial response: use long acting opiod – Should be dose responsive• If poorly responsive after 2-3 titrations: Initiate an escape strategy• If initially partially responsive (“Taking the edge off”: change opiate, and other factors need addressing – Strongly consider an antihyperalgesic opiate
    33. 33. Two Anti-hyperalgesic Opiates:• Buprenorphine – Unique receptor profile – Patch = different dosing than SL• Tapentadol – Weak opiate + NRI – Indicated for both chronic pain and neuropathic pain These two appear to have less abuse potential
    34. 34. Chronic Pain Treatment: Opiates and NSAIDs 6 5 4Pain Meth 5.0+Ibu 600mg Meth 2.5+Ibu 600mg 3Rating Methadone 5.0mg Methadone 2.5mg 2Change 1 0 0 0.5 hr 1 hr 2 hr 3 hr 4 hr Ferrer-Brechner Am J Med 1984;77:78-83
    35. 35. Myofascial Pain Syndrome is a common cause of chronic or resistant pain →Trigger points
    36. 36. Myofascial Pain Syndrome: Treatment• Principles – 1. Inactivation of trigger points – 2. Muscle Rehabilitation – 3. Reduce all contributing factors
    37. 37. Myofascial Pain Syndrome: Treatment1. Inactivation of trigger points• Injection of local anesthetic (lidocaine + bipuvicaine) – Precision in placement of the needle a the point of maximal tenderness is essential – A local “twitch response” is usually obtained⇒Followed by vigorous massage and stretching
    38. 38. Myofascial PainSyndrome: Treatment2. Muscle Rehabilitation• Stretching, strengthening• Postural exercises• Movement: – massage, acupressure (strain/counterstrain) These maintain the gains
    39. 39. Myofascial Pain Syndrome: Treatment- Prevention3. Control of contributing factors:• Mechanical: Correct repetitive, tensing movements – Posture and lifting improvement• Aerobic exercise• Stress resilience: – Treat anxiety and depression – Experiential cognitive behavioral resilience training
    40. 40. Who is likely to get chronic pain ifacute pain treatment is suboptimal ?• Personal or family history of CNS hypersensitivity disorders – and sleep problems• History of abuse, trauma or childhood neglect  high CRF and sympathetic tone For surgery in these, consider pre-emptive analgesia
    41. 41. Pain treatment:The earlier, the better
    42. 42. Which Medication to Start?• Depends on dominant patterns of problems: – Sleep + pain + tingling + anxiety: Anticonvulsant – Pain + depression/anxiety + fatigue + cognitive: NSRI • R/O bipolar (Add sleep agent) – Pain alone: tramadol or cyclobenzaprine? – Fluctuating pain + mood/anxiety or anger: Anticonvulsant (± Atypical neuroleptic)Often, thoughtful combinations are best
    43. 43. Treating Chronic Pain Disorders Five important parts (interdisciplinary):• Treat early and aggressively• Treat CNS neurochemical hypersensitizing issues – Anticonvulsants (3 types), dual antidepressants, DA and alpha-2 agonists• Treat sleep well (particularly deep stages)• Carefully paced exercise• Treat “stress”: Experiential cognitive-behavioral methods• Consider trigger points• This reduces opiate requirements and improves function
    44. 44. Self Care Websites OFFER Organization for Fatigue and Fibromyalgia Education and Research http://www.offerutah.org/ University of Michigan Fibromyalgia Center Dr. D. A. Williams and Dr. M. Careyhttp://www.med.umich.edu/painresearch/patients/self.htm
    45. 45. Neural stabilizing Nutrients• Vitamins B6 (25-50 mg), B12 (550-1000 mcg), methylfolate (2.5-7.5 mg)• Omega3 fatty acids (2000 mg bid)• Magnesium• D-L phenylalanine (500 mg bid)
    46. 46. Sleep Stages Non REM REM Benzos, Some SSR Is, Venlafaxine 4 Blocks 3 21 Body repair
    47. 47. Deep Sleep Effects of CNS Medications• Antidepressants – Suppress: most SSRIs (exceptions: sertraline, citalopram) —Trend to suppress: venlafaxine and bupropion – Improve: amitriptylene, nortriptylene, doxepin cyclobenzaprine, trazodone, mirtazepine atypical neuroleptics (TCAs and 5HT2 blockers) tiagabine sodium oxybate (GHB) pregabalin and gabapentin Citera G. Clin Rheumatol 2000;19(1):9-13
    48. 48. Why More Pain with Anxiety and Depression?• Up-regulated pain sensory response – Increased Substance P – Low CNS serotonin and norepinephrine function – Low endorphins• Up-regulated inflammation – Increased prostaglandins – Excess immune stimulation (  IL-1, IL-6 & TNF & auto- Ab)• Excess sympathetic tone• Loss of deep stage sleep

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