chronic pain – mechanisms and management principles · 2018. 12. 17. · chronic pain – pain...
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Chronic Pain – Mechanismsand Management principles
Dr Nick Shenker PhD FRCP
Addenbrooke’s Hospital
What is pain?International Association for the Study of Pain
(IASP)
‘An unpleasant sensory andemotional experience associated
with actual or potential tissuedamage, or described in terms of
such damage.’
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Pain pathways
Brain neuromatrix
Medulla
Spinal cord: dorsal horn
Nociceptive neurons
Nociception
ThermalMechanical
Chemical
Peripheralsensitisation
Centralsensitisation
Centralsensitisation
LearningNeuroplasticity
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Nociception: Transduction
Nociceptors
Mechanoreceptors Polymodal Receptors
Distortion Mechanical Injury ThermalIrritation
Chemical Stimulation
Sensitisation – development ofallodynia
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Nociception Transduction
Substance Source Effect on Nerve
Histamine Platelets, mast cells ActivatesBradykinin Plasma ActivatesSubstance P Nerve terminals SensitisesProstaglandins Damaged Cells SensitisesInterleukins Mast cells Activates, sensitisesLeukotrienes Damaged cells SensitisesTNF-α Macrophages Activates, sensitisesProtons Tissue damage Activates
Nociception Transmission
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Spinal cord Dorsal horn
Spinal cord Cartesian model
• Pain can be relieved bycounter-irritation
• Gross tissue damage not beaccompanied by pain
• Minor damage results inexquisite ‘burning’ pain
• Phantom limb pain
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Spinal cord Gate control
Ronald Melzack Patrick Wall
Gating at the spinal cord
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Spinal cord. Wind-up.
Neuroanatomy of Pain______________________________________________________________________________
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Acute pain neuromatrix
Acute pain neuromatrix
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Acute pain neuromatrix
Acute pain neuromatrix
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Acute pain neuromatrix
Acute pain neuromatrix
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Acute pain neuromatrix
Recap
• Nociception• Peripheral Sensitisation• Spinal gate• Brain pathways• Descending systems
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Spinal cord Descendingsystems
• Serotonergic
• Adrenergic
• Opioid– Diffuse Noxious
Inhibitory Control(DNIC)
Spinal cord Descendingsystems
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Development of chronic pain
• Acute pain– Usually obvious tissue damage– Protective function– Increased nervous system
activity1
– Pain resolves upon healing
1. Woolf CJ, Costigan M. Proc Natl Acad Sci U S A. 1999;96:7723-30. 2. Woolf CJ, Max MB. Anesthesiology.2001;95:241-9.
Chronic pain– Pain beyond expected period of
healing– Pain no longer serves a useful purpose– Changes in pain signalling and
detection2
– Degrades health and function
Chronic pain has systemicconsequences
Functional Domain Stress Responses to Pain Examples of Clinical Manifestations
Endocrine/metabolic Altered release of multiple hormones (e.g.,ACTH, cortisol, catecholamines, insulin) withassociated metabolic disturbances
Weight lossFeverIncreased respiratory and heart rateShockIncreased blood sugar
Cardiovascular Increased heart rateIncreased vascular resistanceIncreased blood pressureIncreased myocardial oxygen demandHypercoagulation
Unstable anginaMyocardial infarctionDeep vein thrombosis
Respiratory Decreased air flow due to involuntary (reflex musclespasm) and voluntary (“splinting”) mechanisms thatlimit respiratory effort
AtelectasisPneumonia
Gastrointestinal Decreased rate of gastric emptyingDecreased intestinal motility
Delayed gastric emptying, constipation,anorexia, ileus
Musculoskeletal Muscle spasmImpaired muscle mobility and function
ImmobilityWeaknessFatigue
Immune Impaired immune function Infection
Genitourinary Abnormal release of hormones that affect urineoutput, fluid volume, and electrolyte balance
Decreased urine outputHypertension (fluid retention)Electrolyte disturbances
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Brain neuromatrix
Medulla
Spinal cord: dorsal horn
Nociceptive neurons
Nociception
ThermalMechanical
Chemical
Anatomy
Structured approach to the patient in chronic painHague, Shenker, BERH, 2015
Brain neuromatrix
Medulla
Spinal cord: dorsal horn
Nociceptive neurons
Nociception
ThermalMechanical
Chemical
Peripheralsensitisation
Centralsensitisation
Centralsensitisation
LearningNeuroplasticity
Physiology Anatomy
Injury
Structured approach to the patient in chronic painHague, Shenker, BERH, 2015
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Brain neuromatrix
Medulla
Spinal cord: dorsal horn
Nociceptive neurons
Nociception
ThermalMechanical
Chemical
Peripheralsensitisation
Centralsensitisation
Centralsensitisation
LearningNeuroplasticity
Physiology Anatomy
Injury
Structured approach to the patient in chronic painHague, Shenker, BERH, 2015
Age <40
DepressionHigh anxiety traitLess perceived Social Support“Anger style” of emotional regulation>1 year duration
Pain report >4/10Altered body scheme (dysynchiria)>1 limb affected
Post-operative complicationsCold limb presentation
Leg affected (vs arm)Severity of injury
Brain neuromatrix
Medulla
Spinal cord: dorsal horn
Nociceptive neurons
Nociception
ThermalMechanical
Chemical
Peripheralsensitisation
Centralsensitisation
Centralsensitisation
LearningNeuroplasticity
Sleep, Depression, Anxiety
Alterations in body scheme, functional status
Allodynia, hyperalgesia, neuropathic paindescriptions
Signs of inflammation, altered structure
Physiology Anatomy Clinical Assessment
Figure 2. Structured approach to the patient in chronic pain
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Figure 3. Diagnoses associated with chronic pain
Sleep, Depression, Anxiety
Alterations in body scheme, functional status
Allodynia, hyperalgesia, neuropathic paindescriptions
Signs of inflammation, altered structure
Clinical Assessment
Degenerative and MSK diseaseincluding Immune mediatedinflammatory disease ( eg RA, AS etc)
Chronic infectionPost-surgicalPost-traumatic
Compression neuropathy(e.g. sciatica, CTS)
Peripheral neuropathy(e.g. diabetes)
Central nervous lesions(e.g. stroke,Parkinson’s, MS)
Central nervous dysfunction(e.g. fibromyalgia, CRPS, chronic low back pain,
phantom limb pain)
Endocrine dysfunction(e.g. Low vit D; thyroidabnormalities)
Figure 3. Diagnoses associated with chronic pain
Sleep, Depression, Anxiety
Alterations in body scheme, functional status
Allodynia, hyperalgesia, neuropathic paindescriptions
Signs of inflammation, altered structure
Clinical Assessment
Degenerative and MSK diseaseincluding Immune mediatedinflammatory disease (e.g. RA, AS, etc)
Chronic infectionPost-surgicalPost-traumatic
Compression neuropathy(e.g. sciatica, CTS)
Peripheral neuropathy(e.g. diabetes)
Central nervous lesions(e.g. stroke,Parkinson’s, MS)
Central nervous dysfunction(e.g. fibromyalgia, CRPS, chronic low back pain,
phantom limb pain)
Endocrine dysfunction(e.g. low vit D; thyroidabnormalities)
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Peripheralsensitisation
Centralsensitisation
Centralsensitisation
LearningNeuroplasticity
Physiology
Injury
Structured approach to the patient in chronic pain
Peripheralsensitisation
Centralsensitisation
Centralsensitisation
LearningNeuroplasticity
Physiology History
Injury
Structured approach to the patient in chronic pain
Psychosocial contributors
QuestionnairesHADNLSQ (depersonalisation)
BPI
Functional questionnairesUEFI/LEFIHAPTSS
Medications –Previously triedDosagesSide Effects
Fracture history
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Peripheralsensitisation
Centralsensitisation
Centralsensitisation
LearningNeuroplasticity
Physiology History
Injury
Structured approach to the patient in chronic pain
Psychosocial contributors
QuestionnairesHADNLSQ (depersonalisation)
BPI
Functional questionnairesUEFI/LEFIHAP
TherapiesMedications –
Previously triedDosagesSide Effects
Fracture history
58 year old ladyNormal relationships,money. Nolitigation/insurance workSleep disturbed11/21 Anx ; 4 / 21 Dep3.4/6
3-7/10, average of 5/10
38/80 Upper & 25 /80Lower57/94 Max; 34/94 adjusted
Physiotherapy
NSAID; Codeine;ParacetamolAmitriptyline 10mg
Peripheralsensitisation
Centralsensitisation
Centralsensitisation
LearningNeuroplasticity
Physiology
Injury
Structured approach to the patient in chronic pain
Mood assessmentGuarding / Distraction
Body scheme
AllodyniaHyperalgesia
Limb MovementActive/passive
Site assessmentSkinInflammation
Examination
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Peripheralsensitisation
Centralsensitisation
Centralsensitisation
LearningNeuroplasticity
Physiology
Injury
Structured approach to the patient in chronic pain
Mood assessmentGuarding / Distraction
Body scheme
AllodyniaHyperalgesia
Limb MovementActive/passive
Site assessmentSkinInflammation
Examination
Anxious, two crutchesPresent
Abnormal
Allodynia ++Hyperalgesia ++
Hip, knee, ankle OKToes much reduced
Colour and tempasymmetrySwellingNormal sweating, skin,nails
58 year old lady
Importance of early andeffective treatment of pain
• A lower degree of chronicity relates to abetter therapy result1
• Chronic pain is associated withmorphologicalchanges in the CNS 2,3
• Once present, it is often persistent andseldom totally resolves even withtreatment 4
• Chronic pain causes tremendous personalsuffering 5 and marked negative effects onwellbeing and quality of life 6
1 Schulte E et al. Eur J Pain 2010;14:308.e1-308.e10. 2 Tracey I, Bushnell MC. J Pain 2009;10:1113-20.3 Apkarian AV et al. J Neurosci 2004;24:10410-5. 4. Elliott AM et al. Lancet 1999;354:1248–1252. 5. Managementof Chronic pain in Adults, NHS Quality Improvement Scotland 2006. 6. Breivik H et al. Eur J Pain 2006;10:287-333.
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Biopsychosocial model
Social
Biological Psychological
Biopsychosocial model
Social
Biological Psychological
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Why is a biopsychosocialperspective important?
•
Edwards D et al. Pain Pract 2006;6:242-53.
4 pillars of care
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What is patient-centred care?• The term patient-centred care
meansthat healthcare professionals:
• Engage with patients at a deep level,which includes understanding boththeir illness and how it will affect theirlife1
• Take into account the patient’s desirefor information, share decision making,and respond appropriately2
1. Davies PG. J Epidemiol Community Health 2007;61:39. 2. Stewart M. BMJ 2001;322:444-5.
Education of the patient andtheir relatives
• Biopsychosocialpain model
• Basicpharmacology
• Basic anatomy• Weight
management• Information on
relevant painsyndromes
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Pharmacological approaches tochronic pain management
• Non-opioid analgesics (e.g. NSAIDs, paracetamol)• Opioid analgesics (e.g. tramadol, codeine, morphine, oxycodone)• Antidepressants (e.g. amytriptyline, duloxetine)• Anticonvulsants (e.g. gabapentin, pregabalin)• Topical analgesics (e.g. capsaicin, lidocaine 5% plaster)
Non-opioid analgesics: NSAIDS• E.g. aspirin, ibuprofen
1. Warner TD, Mitchell JA. FASEB J 2004;18:790-804.
Efficacy Mode of action Side effects
Mainly act onnociceptive pain1
Inhibition ofcyclooxygenase1
Prostaglandinsynthesisdecreases1
GI irritation/bleeding1
Renal toxicity1
Potential drug-druginteractions
Cardiovascularside-effects (Cox-2)1
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Other non-opioid analgesics:paracetamol
• Aniline derivative e.g. Panadol
Mattia A, Coluzzi F. Minerva Anestesiol. 2009;75:644-53.
Efficacy Mode of action Side effects
Analgesic andantipyretic effects
Noanti-inflammatoryaction
Inhibition ofcentralprostaglandinsynthesis
Not been fullyexplained
Risk of toxicliver damage
Opioid analgesics• Weak opioids: e.g. tramadol and codeine,
strong opioids: e.g morphine andoxycodone1
1. Hawthorn J & Redmond K (1998) Pain causes and management. Blackwell Science Ltd. 2. Furlan AD et al. CMAJ 2006;174:1589-94.3. Jacobsen R et al. J Opioid Manag 2007;3:207-14.
Efficacy Mode of action1 Side effects2,3
Mainly effectivein nociceptivepain
Less effective inchronic states
Only partiallyeffective inneuropathicpain
Activate theendogenousanalgesic system
- Stimulate receptorsin the limbic systemto eliminatethe subjectivefeeling pain
- Affect descendingpathways thatmodulate painperception
- Reduce ascendingpain signaltransmission in thespinal cord
Nausea
Vomiting
Constipation
Dizziness orvertigo
Somnolence
Dry skin,pruritus
Endogenous pain modulation
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Antidepressants: TCAs
• E.g. amytriptyline,imipramine
1. Dworkin RH et al. Arch Neurol. 2003;60:1524-34.
Efficacy Mode of action Side effects
Neuropathicpain1
Complexregional painsyndrome1
Tensionheadache
Inhibition ofneuronal reuptakeof noradrenalineand serotonin(5-HT)
Constipation1
Dry mouth1
Somnolence1
Abnormalitiesin heart rate orrhythm1
Insomnia
Increasedappetite
Antidepressants: Selective serotonin andnoradrenalin reuptake inhibitors (SSRIs & SNRIs)
• E.g. duloxetine, venlafaxine
1. Quilici S et al. BMC Neurol. 2009;9:6. 2. Attal N et al. Eur J Neurol. 2006;13:1153-69.
Efficacy Mode of action Side effects(duloxetine)
Neuropathicpain1,2
SNRIs are betteranalgesics thanSSRIs
Selectively inhibitreuptake ofnoradrenaline orserotonin or both
Provide analgesiaby intensifyingdescendinginhibition
Nausea &Vomiting2
Constipation2
Somnolence1,2
Dry mouth2
Increasedsweating2
Loss of appetite2
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Anticonvulsants• E.g. carbamazepine, gabapentin, pregabalin
1. Attal N et al. Eur J Neurol. 2006;13:1153-69. 2.Dworkin RH et al. Arch Neurol. 2003;60:1524-34.3. Ettinger AB, Argoff CE. Neurotherapeutics. 2007;4:75-83.
GabapentinEfficacy Mode of action Side effects
Neuropathicpain1,2
Different modesof action:
Gabapentin: bindsto presynapticvoltage-dependentcalcium channels1
Pregabalin:interacts withspecial N-typecalcium channels1
Carbamazepine:blocks Na+1 andCa2+ channels
Sedation1,2
Dizziness1,2
Ataxia1
Peripheraloedema1,2
Nausea1,2
Weight gain3
Carbamazepine
Pregabalin
Topical analgesics• Main categories of topical analgesics include:
– Rubefacients: traditional formulations based onsalicylate and nicotinate esters, capsaicin andcapsicum extracts and derivatives
– NSAIDs: diclofenac, felbinac, ibuprofen, ketoprofen,piroxicam, naproxen, flurbiprofen and other NSAIDs
– A miscellaneous group: including benzydamine,mucopolysaccharide polysulphate, salicylamideand cooling sprays
– Lidocaine 5% medicated plaster• Topical analgesics reduce pain impulses transmitted by:
– A-delta-fibres– C-fibres
• Main side effects are localised application site reactions, including:1-4
– Rash– Pruritus– Erythema
1. Boots Company PLC. Boots Pain Relief Heat Rub SmPC. January 2008. 2. Diomed DevelopmentsLimited. Ibuleve Gel SmPC. January 2009. 3. Meda Pharmaceuticals. Difflam Cream SmPC. March 2010.4. Grünenthal Ltd. Versatis 5% Medicated Plaster SmPC. September 2009.
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Main side effects ofpharmacological treatments
1. Furlan AD et al. CMAJ 2006;174:1589-94. 2. Jacobsen R et al. J Opioid Manag 2007;3:207-14. 3. Warner TD, MitchellJA. FASEB J 2004;18:790-804. 4. Ettinger AB, Argoff CE. Neurotherapeutics 2007;4:75-83. 5. Attal N et al. Eur J Neurol2006;13:1153-69. 6. Dworkin RH et al. Arch Neurol 2003;60:1524-34. 7. Quicili S et al. BMC Neurol 2009;9:6.
Opioids1,2 NSAIDs3
NauseaVomitingConstipationDizziness or vertigoSomnolenceDry skin, pruritus
Gastrointestinal irritation/bleedingRenal toxicityPotential drug-drug interactionsCardiovascular side effects (e.g.myocardial infarction, stroke andhypertension) with some selectiveCox-2 inhibitors
Anticonvulsants4,5,6 SNRIs5,7
SedationDizzinessAtaxiaPeripheral oedemaNauseaWeight gain
NauseaVomitingConstipationSomnolenceDry mouthIncreased sweatingLoss of appetite
Physiotherapy and strengthtraining
• Physiotherapy and strength training aim torelieve pain and improve mobility
• Various methods are used, including:–Massage–Joint mobilisations–Manipulation–Electrotherapy / US
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Peripheral stimulation andinterventional therapy
• Peripheral stimulation, e.g.– Transcutaneous electrical nerve
stimulation (TENS)– Acupuncture
• Interventional therapy, e.g.– Nerve blocks– Spinal stimulation– Surgical pain management
Complementary / alternativemedicine
• Some more establishedthan others
eg. Chiropracter, Osteopath, Acupuncture,Homeopathy, Herbal, Aryuvedic
VsBeauty therapy, Colonic hydrotherapy,Colour Breathing, Hopi Ear Candles,ReHarmonising
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Clinical assessment• Peripheral (tissue) driver
– OA, soft tissue, nerve damage, inflammation
• Peripheral sensitisation– Allodynia, hyperalgesia
• Central sensitisation– Sleep, systemic features, depersonalisation, body scheme
• Psychosocial– Mood, family, community, housing, benefits, litigation
Conclusions• Pain is complex• Treat tissue damage and pain will go but…
– Some damage is irreversible– Possible that pain exists with no damage
• Chronic pain approach helpful in parallel:– WHO Pain ladder– Adjuncts are useful– Biopsychosocial approach required– Palliate and counsel
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Chronic Pain – Mechanismsand Management principles
Dr Nick Shenker PhD FRCP
Addenbrooke’s Hospital
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