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Ähnlich wie Pain and Modern Medicine, Stephanie Davies, Head of Service, Pain Medicine Unit, Fremantle Hospital, Perth, WA
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Pain and Modern Medicine, Stephanie Davies, Head of Service, Pain Medicine Unit, Fremantle Hospital, Perth, WA
- 1. Pain and Modern Medicine Dr Stephanie Davies MBBS, FANZCA, FFPMANZCA Head of Service, Fremantle Hospital Pain Medicine Unit Adj. A/Prof Curtin University, School of Physiotherapy Senior Lecturer UWA, School of Medicine
- 2. Pain “ Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” IASP (1979) “ Chronic pain is a complex biopsychosocial phenomenon that can have a profound impact on people’s lives. The condition persists beyond the normal time of healing and is conservatively defined as pain experienced every day for three months or more in the previous six months.” Chronic Pain Prevalence in Australia: Access Economics 2007
- 3. Persistent Pain is Common 1.. The High Price of Pain: The economic impact of persistent pain in Australia, Blyth et al, Access Economics Report 2007
- 5. Acute But .. Chronic? Rene Descartes (1644), L’Homme “Telestra” Old Thinking (1644-1965)
- 6. We “See” Structure … Not Pain MRI: Magnetic Resonance Imaging CT: Computer Tomography XR
- 7. The Gate Control Theory (1965) Nervous system Patrick Wall Ronald Melzack PAIN Disease, Injury
- 8. The gate control theory of pain S S = small fibres E E = excitatory inter-neuron L L = large fibres I = inhibitory inter-neuron I T Off On Brain CENTRAL CONTROL CENTRAL CONTROL
- 9. Implication of Gate Control The nervous system is NOT hard-wired = NEUROPLASTIC THE BRAIN CHANGES ITS OWN STRUCTURE!
- 10. Pain and Music fMRI: functional Magnetic Resonance Imaging [Blood Flow (not pain)]
- 12. Whole Person !! Stress sickness response IMMUNE NETWORK NEURAL NETWORK OTHER TISSUE CELLS SIGNALING MOLECULES STRESSED OR INJURED CELL SIGNALING MOLECULES SIGNALING MOLECULES SIGNALING MOLECULES ENDOCRINE SIGNALING MOLECULES SIGNALING MOLECULES
- 13. Acute versus Chronic .. Or.. “Simple” versus Complex Nociceptive Anxiety Fear Unknown ..Or … Pain versus Threat ARTIFICIAL GAP (time, definitions) !! INPUTS OUTPUTS Central Sensitisation, Activity Avoidance, Worry Nociception
- 14. Trick 1: Address all the inputs Nociceptive Anxiety Fear Unknown Reduce “threat” value of Pain INPUTS OUTPUTS Less: Central Sensitisation, Activity Avoidance, Worry Less: Nociception Non-catastrophic explanation, mindfulness, Patient control = active pain management skills Rx, Needles Pacing, Relax n TARGETS
- 15. Low Back Pain LBP is the most common MSK condition managed by GPs and is 26% of those people with persistent pain
- 16. Henschke BMJ (2008) ; Prof Christopher Maher APS 2009 N=973 (<3% drop out) Low Back Pain and ‘Load’ Sydney primary care Yellow flags (adverse prognostic factors): Courtesy of gPEP: GP Pain Education Program: SHRAC 2008-09
- 17. GUIDELINES “Less is More” http:// www.nzgg.org.nz/guidelines/acutenslbp http:// www.nhmrc.gov.au/nslbpguidelines http:// www.backpaineurope.org / © gPEP: GP Pain Education Program: SHRAC 2008-09
- 22. HOW ABOUT SPINAL INJECTIONS?
- 24. Sequence !! Active Strategies commenced prior to passive strategies Overview: Chou R et al. Interventional therapies, surgery, and interdisciplinary rehabilitation for low back pain: An evidence-based clinical practice guideline from the American Pain Society. Spine 2009;34:1066-1077. © STEPS @ Fremantle Pain Medicine Unit Procedure Subgroup NNT 50% relief Time Cervical RF 1 +ve Dx blocks only 2.0 7 months Lumbar TF RSI with epidural flow 2 Radicular pain 1.4 TNF 2.7 Steroid 2 6 months 8 weeks Lumbar Dorsal R neurotomies 3 +ve Dx Blocks only 4.4 8 weeks Facet Joint Injections 4,5 NSLBP 12 2-4 weeks Direct Epidurals 6 NSLBP, Sciatica 12 8 weeks
- 25. No Perfect ‘Fix’ ... yet © STEPS @ Fremantle Pain Medicine Unit Drug “ Rx” Condition NNT 50% relief NNH Opioids 1,2 Neuropathic pain 2.5 4.2 - 8.3 Tramadol 3,4 (100-150mg) Neuropathic pain Post-surgical 3.4 3 2.4 – 4.8 4 8.3 Tricylics 5 Neuropathic pain 3.6 5 6 (minor) 28 (major) Gabapentin 6,7 Pregabalin 8,9 ( > 300mg/day) Central Neuropathic Diabetic neuropathy PHN Fibromyalgia 5 8 2.9 - 5 6,8 3.9 8 13-22 9 3.7 (minor) Efexor 5 Duloxetine 10 Neuropathic pain 3.1 6 – 8 16.2 (major) 9.6 (minor) Panadol 11 (4 grams/day) Chronic arthritis pain 4-5 12 (GI SEs)
- 26. DRUGS (or PROCEDURES) ALONE NOT THE ANSWER ! Doctors pour drugs, of which they know little, for diseases of which they know less, into patients - of whom they know nothing. [Voltaire] STILL TRUE TODAY !! Deyo et al, Over-treating chronic back pain: time to back Off? J Am Board Fam Med 2009; 22:62-68
- 27. Tramadol - An Atypical Centrally Acting Analgesic 40% 40% 20% µ-agonist NA uptake inhibition 5HT uptake inhibition
- 29. Pain Detect: Nociceptive vs Neuropathic Pain © A/Prof Stephanie Davies
- 31. No Perfect ‘Fix’ ... yet © STEPS @ Fremantle Pain Medicine Unit Drug “ Rx” Condition NNT 50% relief NNH Opioids 1,2 Neuropathic pain 2.5 4.2 - 8.3 Tramadol 3,4 (100-150mg) Neuropathic pain Post-surgical 3.4 3 2.4 – 4.8 4 8.3 Tricylics 5 Neuropathic pain 3.6 5 6 (minor) 28 (major) Gabapentin 6,7 Pregabalin 8,9 ( > 300mg/day) Central Neuropathic Diabetic neuropathy PHN Fibromyalgia 5 8 2.9 - 5 6,8 3.9 8 13-22 9 3.7 (minor) Efexor 5 Duloxetine 10 Neuropathic pain 3.1 6 – 8 16.2 (major) 9.6 (minor) Panadol 11 (4 grams/day) Chronic arthritis pain 4-5 12 (GI SEs)
- 32. The Brain that Changes itself Norman Doige 2007 Dymocks- International BestSeller Explain Pain David Butler & Lorimer Moseley www.noigroup.com Light Reading Consumer websites: “APMA pain”- Google APMA: www.painmanagement.org.au then treatment – consumer – Fremantle Booklet & Triage Qs CPA: www.cpaaustralia.com.au APS: www.apsoc.org.au
- 34. TIME ACTIVITY BOOM – BUST is Non-Paced activity “ Over do – Under do” Cycle Pain contingent = Stop © A/Prof Stephanie Davies
- 36. Pacing = Timed Activity Management TIME ACTIVITY Time contingent = Stop Educators – Drs, OT, Physio, Psych, Nurse Baseline (below flare) and 10% rule © A/Prof Stephanie Davies
- 37. Address all the inputs !! Nociceptive Anxiety Fear Unknown Reduce “threat” value of Pain INPUTS OUTPUTS Less: Central Sensitisation, Activity Avoidance, Worry Less: Nociception Non-catastrophic explanation, mindfulness, Patient control = active pain management skills Rx, Needles Pacing, Relax n TARGETS
- 40. Team Work
- 42. The Brain that Changes itself Norman Doige 2007 Dymocks- International BestSeller Explain Pain David Butler & Lorimer Moseley www.noigroup.com Light Reading Consumer websites: “APMA pain”- Google APMA: www.painmanagement.org.au then treatment – consumer – Fremantle Booklet & Triage Qs CPA: www.cpaaustralia.com.au APS: www.apsoc.org.au
- 44. Opioid Worries © A/Prof Stephanie Davies Drug 100mg ME/day Morphine 100mg pre day Oxycontin 50-70mg per day Hydromorphone 16-20mg per day Methadone 30-40mg/day Tramadol 500mg/day Codeine 600mg/day Norspan 20mg patch (46-90mg morph) Fentanyl 25mcg/hr patch
- 47. Cognitive-Behavioural Model of Fear of Movement or (Re)Injury 1 Haythornthwaite JA. Assessment of pain beliefs, coping and function. Textbook of Pain. 5 th ed. 2006. p. 317. Painful experiences Catastrophising Fear of movement reinjury Avoidance Disability Disuse Depression Injury Non-catastrophising Confrontation Recovery
- 48. Low Back Pain LBP is the most common MSK condition managed by GPs and is 26% of those people with persistent pain
- 49. Henschke BMJ (2008) ; Prof Christopher Maher APS 2009 N=973 (<3% drop out) Low Back Pain and ‘Load’ Sydney primary care Yellow flags (adverse prognostic factors): Courtesy of gPEP: GP Pain Education Program: SHRAC 2008-09
- 50. GUIDELINES “Less is More” http:// www.nzgg.org.nz/guidelines/acutenslbp http:// www.nhmrc.gov.au/nslbpguidelines http:// www.backpaineurope.org / © gPEP: GP Pain Education Program: SHRAC 2008-09
- 54. Pain, pathology & radiology poorly correlated No help in ~ > 90% cases NSLBP 3 Red flags + High Index of Clinician Suspicion to be worth Radiation Dose !! www.DiagnosticImagingPathways.health.wa.gov.au
- 56. HOW ABOUT SPINAL INJECTIONS?
- 57. Sequence !! Active Strategies commenced prior to passive strategies Overview: Chou R et al. Interventional therapies, surgery, and interdisciplinary rehabilitation for low back pain: An evidence-based clinical practice guideline from the American Pain Society. Spine 2009;34:1066-1077. © STEPS @ Fremantle Pain Medicine Unit Procedure Subgroup NNT 50% relief Time Cervical RF 1 +ve Dx blocks only 2.0 7 months Lumbar TF RSI with epidural flow 2 Radicular pain 1.4 TNF 2.7 Steroid 2 6 months 8 weeks Lumbar Dorsal R neurotomies 3 +ve Dx Blocks only 4.4 8 weeks Facet Joint Injections 4,5 NSLBP 12 2-4 weeks Direct Epidurals 6 NSLBP, Sciatica 12 8 weeks
- 59. Chronic NSLBP: fMRI (assoc.) widespread changes in CNS
- 60. [Price, 2000] Location & intensity Affective responses etc. Early levels of pain localization processing Negative emotional valence to experience of pain Working memory, affect & attention Emotion Fear Anxiety Motor Planning Relay station 26 AREAS OF BRAIN INVOLVED IN PAIN (at the last count)
Hinweis der Redaktion
- WHO HAS HEARD OF THE GATE THEORY OF PAIN? TWO BRILLIANT PIONEERS - RONALD MELZACK, A CANADIAN PSYCHLOGIST, AND PATRICK WALL, A BRITISH NEUROSCIENTIST, USED THE OBSERVATION THAT MECHANICALLY STIMULATING THE SKIN IN REGION OF PAIN COULD RESULT IN PAIN REDUCTION. SUCH STIMULATION COULD BE RUBBING THE SKIN OR APPLYING AN ELECTRICAL CURRENT THROUGH A TENS MACHINE MELZACK AND WALL WERE AMONG THE FIRST PEOPLE TO TACKLE THE MYSTERIOUS BLACK BOX - THE NERVOUS SYSTEM THEIR THEORY HAS REVOLUTIONISED THE WAY WE THINK ABOUT PAIN.
- FINALLY, MESSAGES FROM THE BRAIN CAN TRIGGER EITHER THE ON OR THE OFF SWITCH - DEPENDING UPON THE CIRCUMSTANCES. THIS IS WHY FOOTBALLERS CAN KEEP ON PLAYING DESPITE INJURIES TO THEIR MUSCLES, KNEES OR ANKLES. AND WHY SOLDIERS CAN CONTINUE TO FIGHT EVEN WHEN WOUNDED OR MINUS A LIMB. AFTER THE GAME (OR THE BATTLE) THE “ON” SWITCH IS ACTIVATED AND MESSAGES OF TISSUE DAMAGE QUICKLY REACH THE BRAIN!
- THE IMPORTANT IMPLICATIONS OF GATE CONTROL THEORY ARE: FIRST - THE BRAIN CAN ENHANCE OR INHIBIT “PAIN” TRANSMISSION DEPENDING UPON THE CIRCUMSTANCES IN WHICH THE PERSON FINDS HIMSELF SECOND - THE NERVOUS SYSTEM IS PLASTIC - WHICH MEANS IT IS ADAPTABLE. NEW CONNECTIONS ARE FORMING ALL THE TIME! NERVE CELLS CAN ALSO TAKE ON NEW FUNCTIONS - SOME CAN REGENERATE. WHEN YOU THINK ABOUT IT, NEUROPLASTICITY IS A DOMINANT PRINCIPLE OF THE NERVOUS SYSTEM. WITHOUT IT, WE COULD NOT LEARN TO ADAPT TO OUR ENVIRONMENT!!! DNIC: classical counterirritation phenomenon (i.e. pain inhibits paineffect) might depend on diffuse noxious inhibitory controls (DNIC), which modulate the spinal transmission of nociceptive signals. With rare exception nerve impulses from the body all must come into the spinal cord. Here the nerves synapse with spinal nerves that form tracts that run to the brain. Where pain is concerned, these tracts run through the spine to the part of the brain known as the Thalamus. The Dorsal Horn is the part of the spinal cord that receives painful nerve impulses. Here nerve axon terminals synapse with nerve cell bodies. It is here where the battle against chronic pain begins. If this part of the nervous system fails, pain can be greatly increased and difficult to bring under control. Failure can occur with NMDA receptor based wind-up, neuropathic pain and/or brain based modulating.
- YOU SAW THIS SLIDE EARLIER. IT CONFIRMS THE OBSERVATION THAT BY LISTENING TO MUSIC, PAIN CAN BE REDUCED. PEOPLE IN PAIN TELL ME THAT THE SAME EFFECT IS PRODUCED WHEN THEY DO OTHER CREATIVE THINGS, SUCH AS PHOTOGRAPHY, PAINTING, READING, OR MEDITATING. THEY ARE USING IT (THE BRAIN) TO LOSE IT (THEIR PAIN). WHAT TECHNIQUES DO YOU USE TO MANAGE YOUR PAIN?
- Whenever tissues are damaged, many substances are released from the damaged cells and also from many other cells that congregate to mop up the damage. This is the process of inflammation. These substances excite nearby nerve endings which, in turn, release products that hasten the process of repair. Usually this is a finely tuned process. As you can see, when activated, the immune system talks to the nervous system and vice versa.
- [1] Lord SM, Barnsley L, Wallis BJ, McDonald GJ, Bogduk N. Percutaneous radio-frequency neurotomy for chronic cervical zygapophyseal-joint pain. N Engl J Med 1996;335:1721-1726 [2] Vad VB, Bhat AL, Lutz GE, Cammisa F. Transforaminal epidural steroid injections in lumbosacral radiculopathy: a prospective randomized study. Spine 2002;27:11-15. [3] van Kleef M, Barendse GA, Kessels A, Voets HM, Weber WE, de Lange S. Randomized trial of radiofrequency lumbar facet denervation for chronic low back pain. Spine 1999;24:1937-1942. [4] Carette S, Marcoux S, Truchon R, Grondin C, Gagnon J, Allard Y, Latulippe M. A controlled trial of corticosteroid injections into facet joints for chronic low back pain. N Engl J Med 1991;325:1002-1007. [5] Boswell MV, Colson JD, Sehgal N, Dunbar EE, Epter R. A systematic review of therapeutic facet joint interventions in chronic spinal pain. Pain physician 2007;10:229-253. [6] Price C, Arden N, Coglan L, Rogers P. Cost-effectivenss and safety of epidural steroids in the management of sciatica. Health Technol Asess 2005;9:1-58.
- [1] Eisenberg E, McNicol E, Carr DB. Opioids for neuropathic pain. Cochrane Database Syst Rev 2006;3:CD006146 [2] Chou R, Fanciullo GJ, Fine PG, Adler JA, Ballantyne JC, Davies P, Donovan MI, Fishbain DA, Foley KM, Fudin J, Gilson AM, Kelter A, Mauskop A, O'Connor PG, Passik SD, Pasternak GW, Portenoy RK, Rich BA, Roberts [3] Mattia C, Coluzzi F, Tramadol. Focus on musculoskeletal and neuropathic pain., Minerva Anestesiol, 2005, 71/10, 565-84, 16163147 [4] Moore R A, McQuay H J, Single-patient data meta-analysis of 3453 postoperative patients: oral tramadol versus placebo, codeine and combination analgesics., Pain, 1997, 69/3, 287-94, 9085303 In postsurgical pain tramadol 50, 100 and 150 mg had NNTs for > 50%maxTOTPAR of 7.1 (95% confidence intervals 4.6-18), 4.8 (3.4-8.2) and 2.4 (2.0-3.1), comparable with aspirin 650 mg plus codeine 60 mg (NNT 3.6 (2.5-6.3)) and acetaminophen 650 mg plus propoxyphene 100 mg (NNT 4.0 (3.0-5.7)). [5] Saarto T, Wiffen PJ. Antidepressants for neuropathic pain. Cochrane Database Syst Rev 2007;4:CD005454. [6] Wiffen PJ, McQuay HJ, Edwards JE, Moore R., Gabapentin for acute and chronic pain. Cochrane Database Syst Rev 2005;3:CD005452. [7] Finnerup NB, Otto M, McQuay HJ, Jensen TS, Sindrup SH. Algorithm for neuropathic pain treatment: An evidence based proposal. Pain 2005;118:289-305. [8] Moore R Andrew, Straube Sebastian, Wiffen Philip J, Derry Sheena, McQuay Henry J, Pregabalin for acute and chronic pain in adults., Cochrane Database Syst Rev, 2009, /3, CD007076, 20008756 [9] Straube Sebastian, Derry Sheena, Moore R Andrew, Paine Jocelyn, McQuay Henry J, Pregabalin in fibromyalgia--responder analysis from individual patient data., BMC Musculoskelet Disord, 2010, 11/, 150, 20602781 [1o] Lunn Michael Pt, Hughes Richard Ac, Wiffen Philip J, Duloxetine for treating painful neuropathy or chronic pain., Cochrane Database Syst Rev, 2009, /4, CD007115, 19821395 [11] Towhead T, Maxwell L, Judd M, Catton M, Hochberg MC, Wells GA. Acetaminophen for osteoarthritis. Cochrane Database of Syst Rev 2006;1:CD004257.
- THE ROMAN SAYING “TO RELIEVE PAIN IS DIVINE” IS AS APT TODAY AS IT WAS 2,000 YEARS AGO. ALTHOUGH WE DO A LOT BETTER THAN THE ANCIENT ROMAN DOCTORS, NONE OF US ON THE PAIN TEAM ARE GODS OR GODDESSES!!! WE STILL HAVE A LONG WAY TO GO!!! NEVERTHELESS, AS YOU HAVE SEEN (AND WILL SEE AGAIN TODAY) THE PATH TO PAIN RELIEF IS A LONG AND WINDING ROAD. TO SUM UP OUR SELF-MANAGEMENT APPROACH IN A FEW SIMPLE WORDS - USE IT TO LOSE IT!!
- [1] Eisenberg E, McNicol E, Carr DB. Opioids for neuropathic pain. Cochrane Database Syst Rev 2006;3:CD006146 [2] Chou R, Fanciullo GJ, Fine PG, Adler JA, Ballantyne JC, Davies P, Donovan MI, Fishbain DA, Foley KM, Fudin J, Gilson AM, Kelter A, Mauskop A, O'Connor PG, Passik SD, Pasternak GW, Portenoy RK, Rich BA, Roberts [3] Mattia C, Coluzzi F, Tramadol. Focus on musculoskeletal and neuropathic pain., Minerva Anestesiol, 2005, 71/10, 565-84, 16163147 [4] Moore R A, McQuay H J, Single-patient data meta-analysis of 3453 postoperative patients: oral tramadol versus placebo, codeine and combination analgesics., Pain, 1997, 69/3, 287-94, 9085303 In postsurgical pain tramadol 50, 100 and 150 mg had NNTs for > 50%maxTOTPAR of 7.1 (95% confidence intervals 4.6-18), 4.8 (3.4-8.2) and 2.4 (2.0-3.1), comparable with aspirin 650 mg plus codeine 60 mg (NNT 3.6 (2.5-6.3)) and acetaminophen 650 mg plus propoxyphene 100 mg (NNT 4.0 (3.0-5.7)). [5] Saarto T, Wiffen PJ. Antidepressants for neuropathic pain. Cochrane Database Syst Rev 2007;4:CD005454. [6] Wiffen PJ, McQuay HJ, Edwards JE, Moore R., Gabapentin for acute and chronic pain. Cochrane Database Syst Rev 2005;3:CD005452. [7] Finnerup NB, Otto M, McQuay HJ, Jensen TS, Sindrup SH. Algorithm for neuropathic pain treatment: An evidence based proposal. Pain 2005;118:289-305. [8] Moore R Andrew, Straube Sebastian, Wiffen Philip J, Derry Sheena, McQuay Henry J, Pregabalin for acute and chronic pain in adults., Cochrane Database Syst Rev, 2009, /3, CD007076, 20008756 [9] Straube Sebastian, Derry Sheena, Moore R Andrew, Paine Jocelyn, McQuay Henry J, Pregabalin in fibromyalgia--responder analysis from individual patient data., BMC Musculoskelet Disord, 2010, 11/, 150, 20602781 [1o] Lunn Michael Pt, Hughes Richard Ac, Wiffen Philip J, Duloxetine for treating painful neuropathy or chronic pain., Cochrane Database Syst Rev, 2009, /4, CD007115, 19821395 [11] Towhead T, Maxwell L, Judd M, Catton M, Hochberg MC, Wells GA. Acetaminophen for osteoarthritis. Cochrane Database of Syst Rev 2006;1:CD004257.
- Exercise interventions for cancer patients: systematic review of controlled trials; Stevinson Clare, Lawlor Debbie A, Fox Kenneth R, Cancer Causes Contro; 2004, 15/10, 1035-56 OBJECTIVE: To systematically review controlled trials investigating the effects of exercise interventions in cancer patients. METHODS: Studies were located through searching seven electronic databases (Medline, Embase, Cochrane Library, CancerLit, PsycInfo, Cinahl, SportDiscus), scanning reference lists of relevant articles, contacting experts (n = 20), and checking the contents lists of journals available through ZETOC (Electronic Table of Contents). To be included, trials had to be prospective, controlled, involve participants diagnosed with cancer and test an exercise intervention. Types of outcome were not restricted. Two reviewers independently applied the selection criteria. RESULTS: Thirty-three controlled trials (including 25 randomized trials) were included in the review. There was some evidence that physical function was increased among those who exercised. Furthermore, symptoms of fatigue did not appear to be increased and there were few adverse effects reported. There was insufficient evidence to determine effects on other outcomes, such as quality of life, with results hampered by the heterogeneity between studies as well as poor methodological quality. Data were also lacking on the long term effects of exercise relating to cancer recurrence or survival. CONCLUSIONS: There is preliminary evidence that exercise interventions for cancer patients can lead to moderate increases in physical function and are not associated with increased symptoms of fatigue. However, it is impossible from current evidence to determine whether exercise has long term beneficial effects on survival or quality of life
- OUR PATIENTS EXPECT US TO HAVE ALL THE ANSWERS AND ABLE TO DELIVER TREATMENT TO THEM (A QUICK FIX) IN AS SHORT A SPACE OF TIME AS POSSIBLE.
- Exercise interventions for cancer patients: systematic review of controlled trials; Stevinson Clare, Lawlor Debbie A, Fox Kenneth R, Cancer Causes Contro; 2004, 15/10, 1035-56 OBJECTIVE: To systematically review controlled trials investigating the effects of exercise interventions in cancer patients. METHODS: Studies were located through searching seven electronic databases (Medline, Embase, Cochrane Library, CancerLit, PsycInfo, Cinahl, SportDiscus), scanning reference lists of relevant articles, contacting experts (n = 20), and checking the contents lists of journals available through ZETOC (Electronic Table of Contents). To be included, trials had to be prospective, controlled, involve participants diagnosed with cancer and test an exercise intervention. Types of outcome were not restricted. Two reviewers independently applied the selection criteria. RESULTS: Thirty-three controlled trials (including 25 randomized trials) were included in the review. There was some evidence that physical function was increased among those who exercised. Furthermore, symptoms of fatigue did not appear to be increased and there were few adverse effects reported. There was insufficient evidence to determine effects on other outcomes, such as quality of life, with results hampered by the heterogeneity between studies as well as poor methodological quality. Data were also lacking on the long term effects of exercise relating to cancer recurrence or survival. CONCLUSIONS: There is preliminary evidence that exercise interventions for cancer patients can lead to moderate increases in physical function and are not associated with increased symptoms of fatigue. However, it is impossible from current evidence to determine whether exercise has long term beneficial effects on survival or quality of life
- Pain not attributable to pathology or neurological encroachment in about 85% of people. ~ 4% of people seen with low back pain in primary care have compression fractures and < 0.1% has a neoplasm. Ankylosing spondylitis and spinal infections are rarer Prevalence of prolapsed intervertebral disc is about 1% to 3%. (Waddell & Burton 2001)
- [1] Lord SM, Barnsley L, Wallis BJ, McDonald GJ, Bogduk N. Percutaneous radio-frequency neurotomy for chronic cervical zygapophyseal-joint pain. N Engl J Med 1996;335:1721-1726 [2] Vad VB, Bhat AL, Lutz GE, Cammisa F. Transforaminal epidural steroid injections in lumbosacral radiculopathy: a prospective randomized study. Spine 2002;27:11-15. [3] van Kleef M, Barendse GA, Kessels A, Voets HM, Weber WE, de Lange S. Randomized trial of radiofrequency lumbar facet denervation for chronic low back pain. Spine 1999;24:1937-1942. [4] Carette S, Marcoux S, Truchon R, Grondin C, Gagnon J, Allard Y, Latulippe M. A controlled trial of corticosteroid injections into facet joints for chronic low back pain. N Engl J Med 1991;325:1002-1007. [5] Boswell MV, Colson JD, Sehgal N, Dunbar EE, Epter R. A systematic review of therapeutic facet joint interventions in chronic spinal pain. Pain physician 2007;10:229-253. [6] Price C, Arden N, Coglan L, Rogers P. Cost-effectivenss and safety of epidural steroids in the management of sciatica. Health Technol Asess 2005;9:1-58.
- Mol Pain. 2007; 3: 25. Published online 2007 September 11. doi: 10.1186/1744-8069-3-25.PMCID: PMC2048498 Copyright © 2007 Borsook et al; licensee BioMed Central Ltd. Neuroimaging revolutionizes therapeutic approaches to chronic pain David Borsook, 1,2,3 Eric A Moulton,1 Karl F Schmidt,1,2 and Lino R Becerra1,2, Examples of CNS Functional Measures . A. Schematic of cortical areas involved with pain processing. The highlighted areas summarize areas found active in previous functional imaging studies. Color-coding reflects the hypothesized role of each area in processing the different psychological dimensions of pain. Numbers in parentheses indicate the relative involvement of these areas during different temporal stages of the pain experience. Areas displayed include insula, anterior cingulate cortex (ACC), posterior cingulate cortex (PCC), primary somatosensory cortex (SI), secondary somatosensory cortex (SII), inferior parietal lobe (Inf. Par), dorsolateral prefrontal cortex (DLPFC), pre-motor cortex (Pre-Mot), orbitofrontal cortex (OFC), medial prefrontal cortex (Med. PFC), posterior insula (P. Ins), anterior insula (A. Ins), hippocampus (Hip), entorhinal cortex (Ento). [Reprinted with permission from Casey and Tran, 2006]. For examples of brainstem involvement in pain processing, please refer to Tracey and Iannetti ([52]). B. Example of fMRI responses to painful phasic thermal stimulation to the forehead in a cohort of 12 subjects. (Moulton et al., unpublished observations). Schematic Examples of CNS Structural Changes. Red circles signify decreased gray matter density relative to controls. A. Subjects with chronic back pain show decreases in gray matter density in bilateral dorsolateral prefrontal cortex (DLPFC) and right anterior thalamus (adapted from [25]). At a macroscopic level, a number of papers have indicated changes in volume in brain regions in patients with chronic neuropathic pain [25], CRPS [26], and fibromyalgia [27]. These last two papers have been seminal in transforming our approach and thinking on chronic pain, since these changes indicate the potential of chronic pain being a neurodegenerative disease. At a microscopic level, changes in dendritic spine density or alterations in neuronal count have been observed in pain and stress [28]. Such changes also have implications for the development of co-morbid disease such as depression [29]. In chronic pain conditions, there is an altered internal milieu as a result of external inputs, altered endogenous processing, or both. Chronic pain resulting from physical (e.g., surgery, trauma) or emotional (abuse, torture, depression) events produce changes in gene function that result in alterations in neural circuits, neural integrity, and receptor function in the CNS. The result is the phenotypic expression of spontaneous pain and increased sensitivity to painful and normally non-painful stimuli (e.g., brush, pressure, thermal). In addition, the condition is sensitive to less obvious perturbations such as changes in barometric pressure, or exacerbated in generalized inflammatory conditions such as the flu. Neurochemical Changes Alterations in neurotransmitters have also been reported in chronic pain patients using magnetic resonance spectroscopy (MRS) [18]. Such approaches have been applied to migraine [19], back pain [20,21], and to spinal cord injury [22]. The approach can be used to define neuronal and axonal markers [23], including specific metabolites such as glutamate, aspartate, glycine, and GABA. Furthermore, the use of 19F-NMR as a non-invasive probe allows for measurements of pharmacokinetics of drugs at target sites as well as changes in patient disease state [24]. Neurochemical changes can define biomarkers that precede structural changes.
- IMAGING STUDIES (fMRI) OVER THE LAST 10 YEARS HAVE SHOWN THAT MANY AREAS OF THE BRAIN CAN CONTRIBUTE TO THE PAIN EXPERIENCE. HERE WE CAN SEE THAT THE THALAMAUS ACTS AS A RELAY STATION FOR INCOMING MESSAGES, THE AMYGDALA HAS A ROLE IN FEELINGS OF FEAR OR DREAD, THE PREFRONTAL CORTEX IN HOW WE FEEL ABOUT THE MESSAGES AND WHETHER WE PAY MUCH ATTENTION TO THEM, THE ANTERIOR CINGULATE CORTEX IN WHETHER OR NOT WE LIKE THE EXPERIENCE, THE SENSORY CORTEX IN DECIDING WHERE THE MESSAGES MIGHT BE COMING FROM, AND THE CEREBELLUM IN PLANNING THE APPROPRIATE ACTION. SCIENTISTS AND PHILOSOPHERS STILL PONDER UPON THE “HARD PROBLEM” - HOW BRAIN ACTIVITY PRODUCES OUR LIFE EXPERIENCES, INCLUDING PAIN. AS YOU CAN SEE, THERE AINT NO BELL IN THE BRAIN!!!