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Chronic PainManagement
Beverly Pearce-Smith, MDClinical Assistant Professor
Department of AnesthesiologyUPMC-McKeesport Hospital
July 2008
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IASP Definition of PainPain is an unpleasant sensory
and emotional experienceassociated with actual or potentialtissue damage or described in
terms of such damage.
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Acute vs Chronic Pain
Characteristic Acute Pain ChronicPain
Cause Generally known Often unknown
Duration of pain Short,
well-characterized
Persists after healing,
3 months
Treatment
approach
Resolution of
underlying cause,
usually self-limited
Underlying cause and pain
disorder; outcome is often
pain control, not cure
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What is Acute Pain? Physiologic response to tissue damage
Warning signals damage/danger
Helps locate problem source Has biologic value as a symptom
Responds to traditional medical model
Life temporarily disrupted (self limiting)
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What is Chronic Pain? Chronic pain is persistent or recurrent
pain, lasting beyond the usual course of
acute illness or injury, or more than 3 -6 months, and adversely affecting thepatients well-being
Pain that continues when it shouldnot
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What is Chronic Pain? Difficult to diagnose & perplexing to treat
Subjective personal experience
Cannot be measured except by behavior May originate from a physical source but
slowly it out-shouts and becomes the
disease It has no biologic value as a symptom
Life permanently disrupted (relentless)
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Domains of Chronic Pain
Social Consequences
Marital/familyrelations
Intimacy/sexual activity
Social isolation
Socioeconomic
Consequences
Healthcare costs
Disability
Lost workdays
Quality of LifePhysical functioning
Ability to performactivities of daily
livingWorkRecreation
PsychologicalMorbidity
DepressionAnxiety, angerSleep disturbancesLoss of self-esteem
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MixedTypeCaused by a
combination of bothprimary injury andsecondary effects
Nociceptive vs NeuropathicPain
NociceptivePain
Caused by activity inneural pathways in
response to potentially
tissue-damaging stimuli
NeuropathicPain
Initiated or caused byprimary lesion ordysfunction in the
nervous system
Postoperativepain
Mechanicallow back pain
Sickle cellcrisis
Arthritis
Postherpeticneuralgia
Neuropathiclow back pain
CRPS*
Sports/exerciseinjuries
*Complex regional pain syndrome
Central post-stroke pain
Trigeminal
neuralgia
Distalpolyneuropathy(eg, diabetic, HIV)
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Possible Descriptions
of Neuropathic Pain Sensations
numbness
tingling
burning
paresthetic
paroxysmal
lancinating
electriclike
raw skin
shooting
deep, dull, bonelike ache
Signs/Symptoms
allodynia: pain from astimulus that does not
normally evoke pain thermal
mechanical
hyperalgesia: exaggerated
response to a normallypainful stimulus
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Physiology of Pain Perception
Transduction
Transmission
Modulation Perception
Interpretation
Behavior
Injury
DescendingPathway
PeripheralNerve
DorsalRootGanglion
C-Fiber
A-beta Fiber
A-delta Fiber
AscendingPathways
DorsalHorn
Brain
Spinal Cord
Adapted with permission from WebMD Scientific American Medicine.10
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Pathophysiology of
Neuropathic Pain Chemical excitation of nonnociceptors
Recruitment of nerves outside of site of injury
Excitotoxicity Sodium channels
Ectopic discharge
Deafferentation
Central sensitization maintained by peripheral input
Sympathetic involvement
Antidromic neurogenic inflammation
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Multiple Pathophysiologies May
Be Involved in Neuropathic Pain More than one mechanism of action likely involved
Neuropathic pain may result from abnormalperipheral nerve function and neural processing ofimpulses due to abnormal neuronal receptor andmediator activity
Combination of medications may be needed tomanage pain: topicals, anticonvulsants, tricyclic
antidepressants, serotonin-norepinephrinereuptake inhibitors, and opioids
In the future, ability to determine the relationshipbetween the pathophysiology and symptoms/signs
may help target therapy
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Neuropathic Pain Pain initiated or caused by a primary lesion or
dysfunction in the nervous systemMerskey & Bogduk1994
Central & peripheral sites Acute & chronic pain states
CRPS I: consequent of acute, often minor trauma
CRPS II: consequence of nerve injury Sympathetically maintained Pain (SMP) or
independent of the SNS
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Neuropathic Pain Burning, stabbing, paraesthesia, allodynia, hyperalgesia
Threshold for activation of injured 1o afferents is lowered
Ectopic discharges may arise from the injury site or theDRG 2o to changes in Na+ channel expression
Central Sensitisation in the cord 2o to peripheral inputs
2o to central changes Reduced inhibition
Functional (neurotransmitter) & anatomical (sprouting)changes in A fibres tactile allodynia (pain induced by
light touch)
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Acute Neuropathic PainAcute causes
iatrogenic, traumatic, inflammatory,
infectiveAcute neuropathic pain = 1-3%
Based on cases referred to an acute painservice
Majority still present at 12 months May be a risk factor for chronic pain
Prompt diagnosis & Rx may prevent
chronic pain
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Examples of Acute NP Phantom Limb Pain (PLP)
Complex Regional Pain Syndrome (CRPS)
Spinal Cord Injury Pain Peripheral nerve injury
Post-surgical (eg thoracotomy,
mastectomy)
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NEUROPATHIC PAINLESION IN THE NERVOUS SYSTEM
EXPERIENCED IN PARTS OF BODY THATAPPEAR NORMAL
CHRONIC
SEVERE
RESISTANT TO OVER THE COUNTERANALGESICS
AGGRAVATED BY ALLODYNIA
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Chronic Pain Syndromes Neuralgias
Causalgia
Complex Regional Pain Syndrome (aka:RSD
Hyperesthesias
Myofascial pain syndromes Hemiagnosia
Phantom limb pain
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COMMON TYPES OF NEUROPATHIC PAIN
PERIPHERAL Polyradioculopathy
Alcoholic polyneuropathy Entrapment neuropathies
(carpal tunnel)
Nerve compression bytumor
Diabetic neuropathy
Phantom limb pain
Postherpetic neuralgia
Trigeminal neuralgia
CENTRAL Compressive myelopathy
from spinal stenosis HIV myelopathy
MS
Parkinson disease
Post ischemic myelopathy Poststroke pain
Posttraumatic spinalcordinjury
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CLINICAL EVALUATION OF PTS WITH
SUSPECTED NEUROPATHIC PAIN
HISTORY- pain intensity (0 to 10), sensorydescriptors, temporal variation, functional impact,attempted treatments, alcohol
PHYSICAL- gross motor, DTRs, skin, sensory-lighttouch, pin prick, vibration, dynamic /thermal
allodynia, hyperalgesia, tinel`s
SPECIAL TESTS- CT, MRI, EMG, nerve conduction,clinical biochemistry
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NEUROPATHIC PAIN
SPONTANEOUS- CONTINOUS OR
INTERMITTENT-Burning, Shooting, Shock-like
STIMULUS EVOKED- ALLODYNIA AND
HYPERALGESIA-Extension of allodynia above and below theoriginally affected dermatomes is a feature ofcentral sensitization.
Neuropathic pain arises following nerve
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Copyright 2006 Canadian Medical Association or its licensors
Gilron, I. et al. CMAJ 2006;175:265-275
Neuropathic pain arises following nerveinjury or dysfunction
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PATHOPHYSIOLOGY PERIPHERAL MECHANISMS
Peripheral nerve injury
1. Sensitization by spontaneous activity by neuron, loweredthreshold for activation, increased response to givenstimulus.
2. Formation of ectopic neuronal pacemakers along nerve andincreased expression of sodium channels and voltage gatedcalcium channels. ( 2 delta subunit- where gabapentin acts)
3. Adjacent demyelinated axons can have abnormal electricalconnections channels and increased neuronal excitability.
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PATHOPHYSIOLOGYCENTRAL MECHANISMS
Sustained painful stimuli results in spinal sensitization(neurons within dorsal horn)
1. Increased spontaneous activity of dorsal horn neurons,reduced activation thresholds and enhanced responsivenessto synaptic inputs.
2. Expansion of receptive fields, death of inhibitoryinterneurons (intrinsic modulatory systems).
3. Central sensitization mediated by NMDA receptors thatfurther release excitatory amino acids and neuropeptides.
4. Sprouting of sympathetic efferents into neuromas anddorsal root and ganglion cells.
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Pain Treatment ContinuumLeastinvasive
Mostinvasive
Psychological/physical approaches
Topical medications
*Consider referral if previous treatments were unsuccessful.
Systemic medications*
Interventional techniques*
Continuumnot related to
efficacy
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Nonpharmacologic Options Biofeedback
Relaxation therapy
Physical and occupational therapy Cognitive/behavioral strategies
meditation; guided imagery
Acupuncture Transcutaneous electrical nerve
stimulation
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Pharmacologic Treatment
Options Classes of agents with efficacy demonstrated
in multiple, randomized, controlled trials forneuropathic pain topical analgesics (capsaicin, lidocaine patch 5%)
anticonvulsants (gabapentin, lamotrigine,pregabalin)
antidepressants (nortriptyline, desipramine)
opioids (oxycodone, tramadol)
Consider safety and tolerability wheninitiating treatment
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FDA-Approved Treatments for
Neuropathic Pain Carbamazepine
trigeminal neuralgia
Duloxetine
peripheral diabetic neuropathy
Gabapentin
postherpetic neuralgia
Lidocaine Patch 5%
postherpetic neuralgia
Pregabalin*
peripheral diabetic neuropathy
postherpetic neuralgia
*Availability pending based upon controlled substance scheduling by the DEA.
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BRAIN
Pharmacologic Agents
Affect Pain DifferentlyDescending Modulation
Central Sensitization
PNS
Local Anesthetics
Topical Analgesics
Anticonvulsants
Tricyclic Antidepressants
Opioids
AnticonvulsantsOpioids
NMDA-Receptor AntagonistsTricyclic/SNRIAntidepressants
AnticonvulsantsOpioidsTricyclic/SNRIAntidepressantsCNS
SpinalCord
Peripheral
Sensitization
DorsalHorn
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Anticonvulsant Drugs for
Neuropathic Pain Disorders Postherpetic neuralgia
gabapentin*
pregabalin *
Diabetic neuropathy carbamazepine
phenytoin
gabapentin
lamotrigine
pregabalin *
HIV-associatedneuropathy
lamotrigine
Trigeminal neuralgia carbamazepine*
lamotrigine
oxcarbazepine
Central poststroke pain lamotrigine
*Approved by FDA for this use.HIV = human immunodeficiency virus.
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Gabapentin in Neuropathic
Pain Disorders FDA approved for postherpetic
neuralgia
Anticonvulsant: uncertain mechanism Limited intestinal absorption
Usually well tolerated; serious adverse
effects rare dizziness and sedation can occur
No significant drug interactions
Peak time: 2 to 3 h; elimination half-*Not approved by FDA for this use.
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Gabapentin Action: NT release from hyper-excited neurones
variable oral absorption, no interactions, completely renallyexcreted
Indication: Protective analgesia Neuropathic pain treatment (NNT = 4.7)
SE: sedation, dizziness, ataxia, tremor NNH minor = 4, NNH major =12-18 COST!
Doses: Pre-op: 600-1200mg (1-2 hours pre-op) Post-op prophylaxis: 100-300mg TDS (? 2 weeks) Post-op treatment: 100-900mg TDS (usu 300-600mg tds)
Dahl JB, Mathiesen O, Moiniche S. Protective premedication: an option with gabapentin and related drugs? Areview of gabapentin and pregabalin in the treatment of post-operative pain. Acta Anaesthesiol Scand2004; 48: 11301136
Hurley RW, Cohen SP, Williams KA, Rowlingson AJ, Wu CL. The Analgesic Effects of Perioperative Gabapentinon Postoperative Pain: A Meta-Analysis. Reg Anesth Pain Med 2006;31:237-247.
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PregabalinVery similar to gabapentin
More reliable oral absorption
Slightly different side effect profile Doses: 75-300mg BD
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Other Anticonvulsants Effective (NNT 2-3) but less user friendly
Most have uncommon but serious SE (eg.aplastic anaemia, hepatotoxicity, Stevens-Johnson syndrome etc) NNH minor = 3, NNH major = 16 - 24
Consider
Carbamazepine 100mg BD ( to 400mg bd/tds) Valproate 200mg BD ( to 1000-2000mg/d) Phenytoin 100mg nocte ( to 500mg/d)
Finnerup NB, Otto M, McQuay HJ, Jensen TS, Sindrup SH. Algorithm for neuropathic pain treatment: Anevidence based proposal. Pain 118 (2005) 289305
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Topical vs Transdermal
Drug Delivery Systems
Systemic activity
Applied away from painful site
Serum levels necessary
Systemic side effects
Peripheral tissue activity
Applied directly over painful site
Insignificant serum levels
Systemic side effects unlikely
Topical
(lidocaine patch 5%)
Transdermal
(fentanyl patch)
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Lidocaine Patch 5% Lidocaine 5% in pliable patch
Up to 3 patches applied once daily directly overpainful site
12 h on, 12 h off (FDA-approved label) recently published data indicate 4 patches (1824 h)
safe
Efficacy demonstrated in 3 randomized controlled trials
on postherpetic neuralgia Drug interactions and systemic side effects unlikely
most common side effect: application-site sensitivity
Clinically insignificant serum lidocaine levels
Mechanical barrier decreases allodynia
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Lidocaine Action: Na+ channel block
Indication: peripheral NP, ? others
Useful IV or topical (NNT = 4.4) No reliable oral equivalent (mexiletine NNT = 10)
SE: similar rates to placebo for sedation,N/V, pruritis etc
CNS toxicity at plasma levels > 5 mcg/ml Dose: IV 1-2 mg/kg/hr (??duration)
Patches available in USA, ?EMLA here
Challapalli V, Tremont-Lukats IW, McNicol ED, Lau J, Carr DB. Systemic administration of local anesthetic agents
to relieve neuropathic pain. Cochrane Database of Systematic Reviews 2005, Issue 4.
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Ketamine Action: NMDA receptor antagonist anti-hyperalgesic', 'anti-allodynic' and 'tolerance-
protective' agent
Indication: Protective analgesia, NP treatment, opioid-tolerant patients
SE: Dysphoria, nightmares, psychedelic effects
Dose: Low doses usually well tolerated
Intra-op: 0.5mg/kg bolus then 0.25-0.5 mg/kg/hr(beware prolonged recovery)
Post-op: 0.1-0.2 mg/kg/hr (?duration)
Himmelseher S, Durieux ME. Ketamine for Perioperative Pain Management. Anesthesiology 2005;102:21120
Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine. Acute PainManagement: Scientific Evidence, 2nd Ed. Australian and New Zealand College of
Anaesthetists, Melbourne, Australia, 2005; 143-144
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Principles of Opioid Therapy
for Neuropathic Pain Opioids should be titrated for therapeutic efficacy
versus AEs
Fixed-dose regimens generally preferred over prn
regimens Document treatment plan and outcomes
Consider use of opioid written care agreement
Opioids can be effective in neuropathic pain
Most opioid AEs controlled with appropriate specificmanagement (eg, prophylactic bowel regimen, use ofstimulants)
Understand distinction between addiction, tolerance,physical dependence, and pseudoaddiction
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OpioidsA select group of pain patients benefits
from opioids, with resultant pain
reduction and improved physical andpsychological functioning
They have minimal side effects & showincreased activity levels & less pain
Other patients do poorly with opioids,experiencing tolerance and side effects,especially with escalating doses
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Distinguishing Dependence,
Tolerance, and Addiction Physical dependence: withdrawal syndrome arises
if drug discontinued, dose substantially reduced,or antagonist administered
Tolerance: greater amount of drug needed tomaintain therapeutic effect, or loss of effect overtime
Pseudoaddiction: behavior suggestive of addiction;caused by undertreatment of pain
Addiction (psychological dependence): psychiatricdisorder characterized by continued compulsive useof substance despite harm
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Opioids Action: NT release, cell excitability Indications: Any NP
Oxycodone, morphine (NNT = 2.5)
Tramadol (NNT = 3.9)
SE: usual, and ?OIH
Doses: usual
? Stay below 100-200mg/d PO Morphineequivalent (ie. 30-60mg/d IV)
? methadone & buprenorphine less hyperalgesic
Finnerup NB, Otto M, McQuay HJ, Jensen TS, Sindrup SH. Algorithm for neuropathic paintreatment: An evidence based proposal. Pain 118 (2005) 289305
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Antidepressants in
Neuropathic Pain Disorders* Multiple mechanisms of action
Randomized controlled trials and meta-analysesdemonstrate benefit of tricyclic antidepressants
(especially amitriptyline, nortriptyline, desipramine)for postherpetic neuralgia and diabetic neuropathy
Onset of analgesia variable analgesic effects independent of antidepressant activity
Improvements in insomnia, anxiety, depression Desipramine and nortriptyline have fewer adverse
effects
*Not approved by FDA for this use.
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Tricyclic Antidepressants:
Adverse Effects Commonly reported AEs
(generally anticholinergic):
blurred vision
cognitive changes constipation
dry mouth
orthostatic hypotension
sedation sexual dysfunction
tachycardia
urinary retention
Desipramine
Nortriptyline
Imipramine
Doxepin
Amitriptyline
FewestAEs
MostAEs
AEs = adverse effects.
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Tricyclic Antidepressants Action: Mixed ( 5-HT &/ Norad at synapse) Indication:
All NP treatment (except SCI, PLP, HIV) NNT: overall = 3.1, central = 4.0, periph = 2.3
PHN prevention: 50% if used for 90days SE: dizzy, sedation, anticholinergic
NNH minor = 5, NNH major = 16
Doses Amitriptylline 10-25mg nocte, max 100mg Nortriptylline (?less sedating) same doses
Finnerup NB, Otto M, McQuay HJ, Jensen TS, Sindrup SH. Algorithm for neuropathic pain treatment: Anevidence based proposal. Pain 118 (2005) 289305
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Venlafaxine Action: SNRI
Indication: mastectomy pain prophylaxis,
peripheral NP treatment (NNT=5.5)
SE: sedation/insomnia, ataxia, BP, nausea NNH major = not significant
Doses Protective 75mg/d (pre-op then for 2wks)
Treatment: 37.5-375mg/d
Reuben SS, Makari-Judson G, Lurie SD. Evaluation of efficacy of the perioperative administration of venlafaxineXR in the prevention of postmastectomy pain syndrome. J Pain Symptom Manage. 2004; 27: 133-39.
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Calcitonin Action: uncertain
Indication: PLP, CRPS, ?other NP
SE: N/V, flushing, dizzy, allergy Skin prick test advised
Dose: 100 IU in 100ml saline over 1hr
Pre-treat with anti-emetics Repeat daily for 3 days
Visser EJ. A review of calcitonin and its use in the treatment of acute pain. Acute Pain 2005;7 :185-189.
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Interventional Treatments
for Neuropathic Pain Neural blockade
sympathetic blocks for CRPS-I and II(reflex sympathetic dystrophy and causalgia)
Neurolytic techniques
alcohol or phenol neurolysis
pulse radio frequency
Stimulatory techniques spinal cord stimulation
peripheral nerve stimulation
Medication pumps
CRPS = complex regional pain syndrome.
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Summary of Advances in
Treatments for Neuropathic Pain* Botulinum toxin: low back pain
Lidocaine patch 5%: low back pain, osteoarthritis,diabetic and HIV-related neuropathy, with gabapentin
CR oxycodone: diabetic neuropathy Gabapentin: HIV-related neuropathy, diabetic
peripheral neuropathy, others
Levetiracetam: neuropathic pain and migraine
Oxcarbazepine: neuropathic pain; diabeticneuropathy
Bupropion: neuropathic pain
Transdermal fentanyl: low back pain
*Applications not approved by FDA.
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CURRENT MANAGEMENTNON PHARMACOLOGIC
EXERCISE
TENS PENS
GRADED MOTOR IMAGERY
CBT
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World Health Organization
(WHO) Analgesic Ladder.
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INTERVENTIONAL PAIN
MANAGEMENT Epidural or Perineural injections of local
anesthetics or cortico steroids.
Implantations of epidural and intrathecal drugdelivery systems.
Neural ablative procedures.
Insertion of spinal cord stimulators.
Sympathetic nerve blocks.
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Treatment Goals - I Reduce and manage pain
Decreased subjective pain reports
Decreased objective evidence of disease Optimize medication use
Increase function & productivity
Restore life activities Increase psychological wellness
Reduce level of disability
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Treatment Goals - II Stop cure seeking
Reduce unnecessary health care
Prevent iatrogenic complications Improve self-sufficiency
Achieve medical stabilization
Prevent relapse / recidivism Minimize costs - maintain quality
Return to gainful employment
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Chronic Pain Evaluations Comprehensive multidisciplinary evaluations
offers a means of developing an appropriatetreatment plan
This can help identify factors which mayprolong complaints of pain and disabilitydespite traditional medical care
Such an evaluation can also identify whowould benefit from a more structured andintensive functional restoration program
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Measuring Opioid Usefulness Each individual with chronic pain should be
viewed as unique and the ultimate outcomeof the use of opioid medication must be
viewed in terms of Pain relief
Objective gains (function or increased activity)
Does taking an opioid allow the person to be
happier and do more things without unacceptableside effects or do the medications only createmore problems and no observable change inactivity level?
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Adjunctive TreatmentModalities
Joint, bursal & trigger point injections Botulinum toxin injections Nerve root and sympathetic blocks Peripheral and plexus blocks Facet and medial branch injections Lidocaine infusions
Epidurals Neuroablative techniques Chemical, Thermal, & Surgical
Neuromodulation Spinal cord stimulators & Implanted spinal pumps
Ph i l & O ti l
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Physical & OccupationalTherapy
Active
Improved body mechanics
Spine stabilization
Stretching & strengthening
Aerobic conditioning
Aquatics therapy Work hardening
Self-directed fitness program
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Psychological Approaches
Non-drug pain management skills Anxiety & depression reduction
Biofeedback, relaxation training, stress reduction skills,mindfulness meditation, & hypnosis
Cognitive restructuring
Improve coping skills
Learn activity pacing Habit reversal
Maintenance and relapse prevention
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Functional Restoration Locus of control issues
Timely and accurate diagnosis
Assessment of psychosocial strengths and weaknesses
including analysis of support system Evaluation of physical and functional capacity
Treatment planning and functional goal setting for returnto life and work activities
Active physical rehabilitation Cognitive behavioral treatment
Patient and family education
Frequent assessment of compliance and progress
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Facial Nerves and Pain Trigeminal nerve Largest of 12 cranial nerves Three major branches
Ophthalmic nerve Sensory information (tactile,
thermoception, nociception,proprioception) from green areas,nasal mucosa,and frontal sinuses
Maxillary nerve sensory information from pink
areas, nasal mucosa, palate,ethmoid and sphenoid sinuses
Mandibular nerve Sensory input from yellow areas,floor of the mouth, and anterior2/3 of tongue
Motor control of muscles involvedin biting, chewing, and swallowing
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Neural Mechanisms of Pain
Gate ControlTheory
Melzack and Wall
(1965)
Perception ofpain mediated bya gate located
in the dorsal hornof the spinal cord
SG-
SG+
T cell
L-fibers mediatingtactile perception(A-a and A-b)
S-fibers mediatingpain perception (A-
d and C)
PAIN
CentralControl
closesgate
opens gate
-
+
+
++
+
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Experimental Evidence for the Gate Selective
inactivation of L-fibers results ingreater pain
perception fromnoxious stimuli(Price, Hi, andDubner, 1977)
Phantom Limb Painmay result fromreduced L-fiberinput (Melzack,1970)
SG-
SG+
T cell
L-fibers mediatingtactile perception(A-a and A-b)
S-fibers mediatingpain perception (A-d and C
PAIN
CentralControl
closesgate
opens gate
-
+
+
+ +
+
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Endorphins and Pain Endorphins: neurotransmitters that act as endogenous
(naturally-occurring) morphine-like substances
Endorphins bind to same receptor sites in brain stem asopiates
SPA works best when endorphin sites are stimulatedmay release endorphins into the nervous system(Hosubuchi et al., 1977)
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Endorphins and Pain
Concentration of endorphins is generally less forpeople suffering from chronic pain (Akil et al., 1978)
Opiate inhibitors (e.g., naloxone) decrease theanalgesic effects of acupuncture, SPA, and placebos
Stress-induced analgesia may result from increased
release of endorphins during stress
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Nociceptors in Skin
Epidermis
Dermis
Free
NerveEndings
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Pain Pathways Lots of effort to id neural pathways
Found distinct categories of nerve fibres
A : mylinated, carry rapidly sharp pains (20-
30 ms-1)
C : unmylinated, carry slowly burning pain(0.5-2 ms-1)
Hence, short sharp, then delayed slow pain
Associated Area of Brain
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Associated Area of Brain
Fibres pass signals up spinal cord aselectrical impulses then onto the thalamus
Thalamus relays messages to cortex
Proved difficult to id. specific areaof the cortex that produce pain
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Gate Control Theory(Melzack & Wall, 1965)
A gate in the substantia gelatinosa of the dorsal horn can be openor closed, blocking pain information.
The gate can be closed by descending signals from the brain, or bythe balance of activity in A-beta fibres (large myelinated) and C
fibres (small non-myelinated) A-beta fibres produce touch sensations C fibres produce dull diffuse pain.Greater activity in A-beta fibres closes the gate, greater activity in
C fibres opens it. Other factors influencing the gate include
Attention Emotional & Cognitive factors Physical factors
Some forms of analgesia, e.g. TENS & acupuncture, might beaccommodated within gate control theory.
l h l k ll ( )
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Gate Control Theory - Melzack & Hall (1965)
Experience
Behaviour
Tissuedamage
Gate amplifies orattenuates signal
PainPerception
Emotion
O i & Cl i th G t
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Opening & Closing the GateFactor Opens Closes
Physical injury
agitationmedication
Emotional anxiety
stressfrustration
depressiontension
relaxation
optimismhappiness
Behavioural(Cognitive)
rumination
boredomenjoyable activities
complex tasksdistraction
social interaction
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Problems for Gate Control Theory
Evidence for propsed moderators, but nophysical evidence of gate
Still organic basis for pain (phantomlimb?)
Not truly integrative re: psyche & soma Still improvement on stimulus-response
paradigm
Subsequent Pain Theories
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Subsequent Pain Theories Reflect trends in general psychology
Fordyce (1976) - pain as behaviour
Reinforcement contingencies
+ve reinforcement (e.g. attention / affection for
pain behaviours)
-ve reinforcement (e.g. avoid unpleasant events
such as work, school)
Recently, growth in cognitive behaviour models
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Fear-Avoidance Theory (-ve) appraisals (catastrophising) fearof pain (illness cognitions) & re-injury
Fear of pain avoidance of potentiallypainful events (illness behaviour)
Little opportunity to disconfirm beliefs
Avoidance disuse syndrome & p(mood problems)
Disuse leads to p (painful experience)
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Treatments
Mirror pain theories
Medical (especially acute pain)
Non-anti-inflammatory non-steroid (paracetamol)
Anti-inflammatory non-steroids (eg ibprofen)
Opioids (eg morphine)
Psychological
Behavioural initially
Mostly cognitive behavioural now
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Treatment of Chronic Pain
Surgical procedures to block thetransmission of pain from the peripheralnervous system to the brain.
Synovectomy Removing membranesthat become inflamed in arthritic joints.
Spinal fusion joins two or more
adjacent vertebrae to treat chronic backpain.
Psychological Pain Control
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Psychological Pain ControlMethods
Biofeedback provides biophysiologicalfeedback to patient about some bodily
process the patient is unaware of (e.g.,forehead muscle tension).
Relaxation systematic relaxation of thelarge muscle groups.
Hypnosis relaxation + suggestion +distraction + altering the meaning of pain.
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Psychological Pain Methods
Acupuncture not sure how it works.Could include:
Counter-irritation may close the spinalgating mechanism in pain perception.
Expectancy
Reduced anxiety from belief that it will work.
Distraction
Trigger release of endorphins
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Phantom Limb pain Affects the majority of amputees
For most the sensation fades, but a minorityexperience lasting discomfort.
Theories Neuroma
Deafferented spinal neurons
Melzack (1992) Neuromatrix innate linkage between
sensation, emotion and self-recognition. Merzenich (1998) Cortical remapping & unmasking
Ramachandran (1992) phantom leg sensations oftenreferred from the chest, phantom arm sensationsfrom the face.
Phantom limb pain:during amputation under
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g pgeneral anesthesia the spinalcord can still experience theinsult produced by the
surgical procedure and centralsensitization occurs. To try toprevent it, local infiltration ofanesthetics in the site ofsurgery. But studies show also
rearrangement of corticalcircuits (cortical region of themissing limb receivesafferents from other site ofthe skin)
Phantom Painintensity as a functionof Cortical
Reorganization.
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Analgesia
Peripheral via prostaglandin synthesis inhibition(e.g. Asprin)
Central via receptors for endogenous opioids.
Bind to receptors in the periaqueductal gray,which activate descending serotoninergicfibres. These inhibit pain transmission
Endogenous opioids also underlie somepsychological influences. Naloxone blocks bothTENS and placebo analgesia
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PAIN TREATMENT CONTINUUMDiagnosis
Oral Medications
PT, Exercise, Rehabilitation
Behavioral Medicine
Corrective SurgeryTherapeutic Nerve Blocks
Oral Opiates
Implantable Pain Management DevicesNeurostimulation
Intrathecal Pumps
Neuroablation
M lti Di i li P i
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Multi-Disciplinary PainProgram Models
Pain Consultation Team
Multidisciplinary Programs Multidisciplinary Outpatient Programs
Multidisciplinary Inpatient Programs
Pain Service
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Pain Consultation Team
Multidisciplinary group
Provides consultation services only
not ongoing treatment
AnesthesiologyPsychology
NeurologyPharmacy
Nursing
Consultation Team Referral
Recommendation
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Multidisciplinary Clinics
Comprised of 2 or more disciplines
Goal is to provide coordinated and more
comprehensive care to patients for morecomplex chronic pain problems
3 general subtypes Psychoeducational clinic (mild and motivating)
Problem-based clinic (e.g. headache, LBP, FM) Comprehensive multidisciplinary clinic
Inpatient or outpatient
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Chronic Pain Disciplines and Roles(Core)
Anesthesiology nerve blocks
Kinesiotherapy pool therapy; activity
Neurology eval. treatmentNursing patient care
Physical Medicine exercise; modalities
Physical Therapy exercise; modalitiesPsychology eval. and treatment
Occupational Therapy UE eval and treatment
Vocational Rehab job eval and training Rheumatoid and Osteo-arthritis
Back painMenstrual Pain
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Labour PainPeripheral Nerve InjuriesShinglesHeadache and MigraineCancer PainTrigeminal NeuralgiaPhantom Limb PainSports InjuriesSciaticaAching JointsPost Operative PainMuscular PainWhiplash and Neck Injury and manyothers
Mechanistic Approach To Pain Therapy
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Decrease
InflammatoryResponse
NSAIDs,
Local Anesthetics,
Steroids
Decrease ConductionGabapentin,
Carbamazepine,
Local Anesthetics,
Opioids
Prevent
Centralization
COX 2,Opioids,
Ketamine,
a-2 Agonists.
Increase
Inhibition
TCAs, SSRIs,
Clonidine
Modify Expression
Anxiolytics
pp py
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Summary Chronic neuropathic pain is a disease, not a
symptom
Rational polypharmacy is often necessary
combining peripheral and central nervous systemagents enhances pain relief
Treatment goals include:
balancing efficacy, safety, and tolerability
reducing baseline pain and pain exacerbations
improving function and QOL
New agents and new uses for existing agentsoffer additional treatment options
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Further Reading
Rosenzweig et al. cover pain in thesecond half of chapter eight.
Horne, S. & Munafo, M. (1997). Pain,theory, research and intervention.Oxford University Press
Wall, P. & Melzack, R. (1988). The
challenge of Pain. Penguin.
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REFERENCES ReviewNeuropathic pain: a practical guide for the
clinician ; Ian Gilron, C. Peter N. Watson, CatherineM. Cahill and Dwight E. Moulin
Dworkin RH, Backonja M, Rowbotham MC, et al.Advances in neuropathic pain.Arch Neurol2003;60:1524-34.
Gilron I, Bailey JM, Tu D, et al. Morphine,gabapentin, or their combination for neuropathicpain. N Engl J Med2005;352:1324-34.
Stephen Macres, Understanding Neuropathic Pain Eisenberg E, McNicol ED, Carr DB. Efficacy and safetyof opioid agonists in the treatment of neuropathic
pain of nonmalignant origin. JAMA2005;293:3043-52.
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The end