Chronic Pain Management

Beverly Pearce-Smith, MD Clinical Assistant Professor Department of Anesthesiology UPMC-McKeesport Hospital

July 2008

IASP Definition of Pain

Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.

Acute vs Chronic Pain

Characteristic Cause Acute Pain Generally known Chronic Pain 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

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)

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 the patients well-being Pain that continues when it should not

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)

Domains of Chronic Pain

Quality of Life Physical functioning Ability to perform activities of daily living Work Recreation
Social Consequences Marital/family relations Intimacy/sexual activity Social isolation

Psychological Morbidity Depression Anxiety, anger Sleep disturbances Loss of self-esteem

Socioeconomic Consequences Healthcare costs Disability Lost workdays

Nociceptive vs Neuropathic Pain

Caused by activity in neural pathways in response to potentially tissue-damaging stimuli

Nociceptive Pain

Mixed Type
Caused by a combination of both primary injury and secondary effects

Initiated or caused by primary lesion or dysfunction in the nervous system CRPS*

Neuropathic Pain

Postoperative pain Mechanical low back pain

Arthritis Sickle cell crisis

Postherpetic neuralgia
Neuropathic low back pain

Trigeminal neuralgia Central poststroke pain

Sports/exercise injuries

Distal polyneuropathy (eg, diabetic, HIV)

*Complex regional pain syndrome

Possible Descriptions of Neuropathic Pain

Sensations

Signs/Symptoms

numbness tingling burning paresthetic paroxysmal lancinating electriclike raw skin shooting deep, dull, bonelike ache

allodynia: pain from a stimulus that does not normally evoke pain thermal mechanical hyperalgesia: exaggerated response to a normally painful stimulus

Physiology of Pain Perception

Injury Brain

Transduction Transmission Modulation Perception Interpretation Behavior

Peripheral Nerve Descending Pathway Dorsal Root Ganglion

Ascending Pathways
C-Fiber A-beta Fiber A-delta Fiber Dorsal Horn Spinal Cord

10

Adapted with permission from WebMD Scientific American Medicine.

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

Multiple Pathophysiologies May Be Involved in Neuropathic Pain

More than one mechanism of action likely involved Neuropathic pain may result from abnormal peripheral nerve function and neural processing of impulses due to abnormal neuronal receptor and mediator activity Combination of medications may be needed to manage pain: topicals, anticonvulsants, tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors, and opioids In the future, ability to determine the relationship between the pathophysiology and symptoms/signs may help target therapy

Neuropathic Pain

Pain initiated or caused by a primary lesion or dysfunction in the nervous system

Merskey & Bogduk 1994

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

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 the DRG o 2 to changes in Na+ channel expression Central Sensitisation in the cord o 2 to peripheral inputs o 2 to central changes

Reduced inhibition

Functional (neurotransmitter) & anatomical (sprouting) changes in A fibres tactile allodynia (pain induced by light touch)

Acute Neuropathic Pain

Acute causes

iatrogenic, traumatic, inflammatory, infective Based on cases referred to an acute pain service Majority still present at 12 months May be a risk factor for chronic pain

Acute neuropathic pain = 1-3%

Prompt diagnosis & Rx may prevent chronic pain

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)

NEUROPATHIC PAIN
LESION IN THE NERVOUS SYSTEM

EXPERIENCED IN PARTS OF BODY THAT APPEAR NORMAL CHRONIC SEVERE RESISTANT TO OVER THE COUNTER ANALGESICS AGGRAVATED BY ALLODYNIA

Chronic Pain Syndromes

Neuralgias Causalgia Complex Regional Pain Syndrome (aka: RSD Hyperesthesias Myofascial pain syndromes Hemiagnosia Phantom limb pain

COMMON TYPES OF NEUROPATHIC PAIN

PERIPHERAL Polyradioculopathy Alcoholic polyneuropathy Entrapment neuropathies (carpal tunnel) Nerve compression by tumor 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 spinalcord injury

CLINICAL EVALUATION OF PTS WITH SUSPECTED NEUROPATHIC PAIN

HISTORY- pain intensity (0 to 10), sensory descriptors, temporal variation, functional impact, attempted treatments, alcohol PHYSICAL- gross motor, DTRs, skin, sensory-light touch, pin prick, vibration, dynamic /thermal allodynia, hyperalgesia, tinel`s SPECIAL TESTS- CT, MRI, EMG, nerve conduction, clinical biochemistry

NEUROPATHIC PAIN

SPONTANEOUS- CONTINOUS OR INTERMITTENT -Burning, Shooting, Shock-like STIMULUS EVOKED- ALLODYNIA AND HYPERALGESIA -Extension of allodynia above and below the originally affected dermatomes is a feature of central sensitization.

Neuropathic pain arises following nerve injury or dysfunction

Gilron, I. et al. CMAJ 2006;175:265-275

Copyright 2006 Canadian Medical Association or its licensors

PATHOPHYSIOLOGY

PERIPHERAL MECHANISMS
Peripheral nerve injury

1. Sensitization by spontaneous activity by neuron, lowered threshold for activation, increased response to given stimulus. 2. Formation of ectopic neuronal pacemakers along nerve and increased expression of sodium channels and voltage gated calcium channels. ( 2 delta subunit- where gabapentin acts)

3. Adjacent demyelinated axons can have abnormal electrical connections channels and increased neuronal excitability.

PATHOPHYSIOLOGY
CENTRAL MECHANISMS
Sustained painful stimuli results in spinal sensitization (neurons within dorsal horn) Increased spontaneous activity of dorsal horn neurons, reduced activation thresholds and enhanced responsiveness to synaptic inputs. Expansion of receptive fields, death of inhibitory interneurons (intrinsic modulatory systems). Central sensitization mediated by NMDA receptors that further release excitatory amino acids and neuropeptides. Sprouting of sympathetic efferents into neuromas and dorsal root and ganglion cells.

1.

2.

3.

4.

Pain Treatment Continuum

Least invasive Most invasive

Continuum not related to efficacy Psychological/physical approaches Topical medications Systemic medications* Interventional techniques*

*Consider referral if previous treatments were unsuccessful.

Nonpharmacologic Options

Biofeedback Relaxation therapy Physical and occupational therapy Cognitive/behavioral strategies

meditation; guided imagery

Acupuncture Transcutaneous electrical nerve stimulation

Pharmacologic Treatment Options

Classes of agents with efficacy demonstrated in multiple, randomized, controlled trials for neuropathic pain

topical analgesics (capsaicin, lidocaine patch 5%) anticonvulsants (gabapentin, lamotrigine, pregabalin) antidepressants (nortriptyline, desipramine) opioids (oxycodone, tramadol)

Consider safety and tolerability when initiating treatment

FDA-Approved Treatments for Neuropathic Pain

Carbamazepine

trigeminal neuralgia peripheral diabetic neuropathy postherpetic neuralgia

Duloxetine

Gabapentin

Lidocaine Patch 5%

postherpetic neuralgia
peripheral diabetic neuropathy postherpetic neuralgia

Pregabalin*

*Availability pending based upon controlled substance scheduling by the DEA.

Pharmacologic Agents Affect Pain Differently

BRAIN
CNS
Spinal Cord

Descending Modulation
Anticonvulsants Opioids Tricyclic/SNRI Antidepressants

PNS
Peripheral Sensitization

Dorsal Horn
Local Anesthetics Topical Analgesics Anticonvulsants Tricyclic Antidepressants Opioids

Central Sensitization
Anticonvulsants Opioids NMDA-Receptor Antagonists Tricyclic/SNRI Antidepressants

Anticonvulsant Drugs for Neuropathic Pain Disorders

Postherpetic neuralgia

gabapentin* pregabalin *

HIV-associated neuropathy

lamotrigine

Diabetic neuropathy

Trigeminal neuralgia

carbamazepine phenytoin gabapentin lamotrigine pregabalin *

carbamazepine* lamotrigine oxcarbazepine

lamotrigine

Central poststroke pain

*Approved by FDA for this use. HIV = human immunodeficiency virus.

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

*Not approved by FDA for this use.

No significant drug interactions Peak time: 2 to 3 h; elimination half-

Gabapentin

Action: NT release from hyper-excited neurones variable oral absorption, no interactions, completely renally excreted 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? A review of gabapentin and pregabalin in the treatment of post-operative pain. Acta Anaesthesiol Scand 2004; 48: 11301136 Hurley RW, Cohen SP, Williams KA, Rowlingson AJ, Wu CL. The Analgesic Effects of Perioperative Gabapentin on Postoperative Pain: A Meta-Analysis. Reg Anesth Pain Med 2006;31:237-247.

Pregabalin

Very similar to gabapentin More reliable oral absorption Slightly different side effect profile Doses: 75-300mg BD

Other Anticonvulsants

Effective (NNT 2-3) but less user friendly Most have uncommon but serious SE (eg. aplastic anaemia, hepatotoxicity, StevensJohnson syndrome etc)

NNH minor = 3, NNH major = 16 - 24 Carbamazepine 100mg BD ( to 400mg bd/tds) Valproate 200mg BD ( to 1000-2000mg/d) Phenytoin 100mg nocte ( to 500mg/d)

Consider

Finnerup NB, Otto M, McQuay HJ, Jensen TS, Sindrup SH. Algorithm for neuropathic pain treatment: An evidence based proposal. Pain 118 (2005) 289305

Topical vs Transdermal Drug Delivery Systems

Topical (lidocaine patch 5%)

Transdermal (fentanyl patch)

Peripheral tissue activity Applied directly over painful site Insignificant serum levels Systemic side effects unlikely

Systemic activity Applied away from painful site Serum levels necessary Systemic side effects

Lidocaine Patch 5%

Lidocaine 5% in pliable patch Up to 3 patches applied once daily directly over painful 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

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.

Ketamine

Action: NMDA receptor antagonist anti-hyperalgesic', 'anti-allodynic' and 'toleranceprotective' agent Indication: Protective analgesia, NP treatment, opioidtolerant 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 Pain Management: Scientific Evidence, 2nd Ed. Australian and New Zealand College of Anaesthetists, Melbourne, Australia, 2005; 143-144

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 specific management (eg, prophylactic bowel regimen, use of stimulants) Understand distinction between addiction, tolerance, physical dependence, and pseudoaddiction

Opioids

A select group of pain patients benefits from opioids, with resultant pain reduction and improved physical and psychological functioning They have minimal side effects & show increased activity levels & less pain Other patients do poorly with opioids, experiencing tolerance and side effects, especially with escalating doses

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 to maintain therapeutic effect, or loss of effect over time Pseudoaddiction: behavior suggestive of addiction; caused by undertreatment of pain Addiction (psychological dependence): psychiatric disorder characterized by continued compulsive use of substance despite harm

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 Morphine equivalent (ie. 30-60mg/d IV) ? methadone & buprenorphine less hyperalgesic

Finnerup NB, Otto M, McQuay HJ, Jensen TS, Sindrup SH. Algorithm for neuropathic pain treatment: An evidence based proposal. Pain 118 (2005) 289305

Antidepressants in Neuropathic Pain Disorders*

Multiple mechanisms of action Randomized controlled trials and meta-analyses demonstrate 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.

Tricyclic Antidepressants: Adverse Effects

Commonly reported AEs (generally anticholinergic):

Fewest AEs

Desipramine Nortriptyline Imipramine

blurred vision cognitive changes constipation dry mouth orthostatic hypotension sedation sexual dysfunction tachycardia urinary retention

Doxepin
Amitriptyline

Most AEs

AEs = adverse effects.

Tricyclic Antidepressants

Action: Mixed ( 5-HT &/ Norad at synapse) Indication:

All NP treatment (except SCI, PLP, HIV)

SE: dizzy, sedation, anticholinergic

PHN prevention: 50% if used for 90days

NNH minor = 5, NNH major = 16

NNT: overall = 3.1, central = 4.0, periph = 2.3

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: An evidence based proposal. Pain 118 (2005) 289305

Venlafaxine

Action: SNRI Indication:

mastectomy pain prophylaxis, peripheral NP treatment (NNT=5.5) NNH major = not significant

SE: sedation/insomnia, ataxia, BP, nausea

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 venlafaxine XR in the prevention of postmastectomy pain syndrome. J Pain Symptom Manage. 2004; 27: 133-39.

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.

Interventional Treatments for Neuropathic Pain

Neural blockade

sympathetic blocks for CRPS-I and II (reflex sympathetic dystrophy and causalgia) alcohol or phenol neurolysis pulse radio frequency

Neurolytic techniques

Stimulatory techniques

spinal cord stimulation peripheral nerve stimulation

Medication pumps

CRPS = complex regional pain syndrome.

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; diabetic neuropathy Bupropion: neuropathic pain Transdermal fentanyl: low back pain

*Applications not approved by FDA.

CURRENT MANAGEMENT

NON PHARMACOLOGIC EXERCISE TENS PENS GRADED MOTOR IMAGERY CBT

World Health Organization (WHO) Analgesic Ladder.

INTERVENTIONAL PAIN MANAGEMENT

Epidural or Perineural injections of local anesthetics or cortico steroids.

Implantations of epidural and intrathecal drug delivery systems. Neural ablative procedures. Insertion of spinal cord stimulators. Sympathetic nerve blocks.

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

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

Chronic Pain Evaluations

Comprehensive multidisciplinary evaluations offers a means of developing an appropriate treatment plan This can help identify factors which may prolong complaints of pain and disability despite traditional medical care Such an evaluation can also identify who would benefit from a more structured and intensive functional restoration program

Measuring Opioid Usefulness

Each individual with chronic pain should be viewed as unique and the ultimate outcome of 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 unacceptable side effects or do the medications only create more problems and no observable change in activity level?

Adjunctive Treatment Modalities

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

Neuromodulation

Chemical, Thermal, & Surgical

Spinal cord stimulators & Implanted spinal pumps

Physical & Occupational Therapy

Active

Improved body mechanics Spine stabilization Stretching & strengthening Aerobic conditioning Aquatics therapy Work hardening Self-directed fitness program

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

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 return to life and work activities Active physical rehabilitation Cognitive behavioral treatment Patient and family education Frequent assessment of compliance and progress

Facial Nerves and Pain

Trigeminal nerve

Largest of 12 cranial nerves Three major branches Ophthalmic nerve

Maxillary nerve

Sensory information (tactile, thermoception, nociception, proprioception) from green areas, nasal mucosa,and frontal sinuses sensory information from pink areas, nasal mucosa, palate, ethmoid and sphenoid sinuses

Mandibular nerve

Sensory input from yellow areas, floor of the mouth, and anterior 2/3 of tongue Motor control of muscles involved in biting, chewing, and swallowing
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Neural Mechanisms of Pain

Gate Control Theory

L-fibers mediating tactile perception (A-a and A-b)

+

Central Control
-

Melzack and Wall (1965) Perception of pain mediated by a gate located in the dorsal horn of the spinal cord

SG- gate SG+

+

+ closes

PAIN T cell

opens gate

62

S-fibers mediating pain perception (Ad and C)

Experimental Evidence for the Gate

Selective inactivation of Lfibers results in greater pain perception from noxious stimuli (Price, Hi, and Dubner, 1977)
Phantom Limb Pain may result from reduced L-fiber input (Melzack, 1970)

L-fibers mediating tactile perception (A-a and A-b)

+

Central Control
-

SG- gate SG+

+

+ closes

PAIN
T cell

opens gate

63

S-fibers mediating pain perception (Ad and C)

Endorphins and Pain

Endorphins: neurotransmitters that act as endogenous (naturally-occurring) morphine-like substances

Endorphins bind to same receptor sites in brain stem as opiates SPA works best when endorphin sites are stimulated may release endorphins into the nervous system (Hosubuchi et al., 1977)

64

Endorphins and Pain

Concentration of endorphins is generally less for people suffering from chronic pain (Akil et al., 1978)

Opiate inhibitors (e.g., naloxone) decrease the analgesic effects of acupuncture, SPA, and placebos
Stress-induced analgesia may result from increased release of endorphins during stress

65

Nociceptors in Skin
Epidermi s Free Nerve Endings

Dermis

Pain Pathways

Lots of effort to id neural pathways

Found distinct categories of nerve fibres

A : mylinated, carry rapidly sharp pains (2030 ms-1) C : unmylinated, carry slowly burning pain (0.5-2 ms-1)

Hence, short sharp, then delayed slow pain

Associated Area of Brain

Fibres pass signals up spinal cord as electrical impulses then onto the thalamus

Thalamus relays messages to cortex

Proved difficult to id. specific area of the cortex that produce pain

Gate Control Theory (Melzack & Wall, 1965)

A gate in the substantia gelatinosa of the dorsal horn can be open or closed, blocking pain information. The gate can be closed by descending signals from the brain, or by the 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 be accommodated within gate control theory.

Gate Control Theory - Melzack & Hall (1965)

Pain Perception

Experience Emotion Behaviour Tissue damage

Gate amplifies or attenuates signal

Opening & Closing the Gate

Factor
Physical Emotional

Opens
injury agitation anxiety stress frustration depression tension rumination boredom

Closes
medication relaxation optimism happiness

Behavioural (Cognitive)

enjoyable activities complex tasks distraction social interaction

Problems for Gate Control Theory

Evidence for propsed moderators, but no physical evidence of gate Still organic basis for pain (phantom limb?) Not truly integrative re: psyche & soma Still improvement on stimulus-response paradigm

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

Fear-Avoidance Theory

(-ve) appraisals (catastrophising) fear of pain (illness cognitions) & re-injury

Fear of pain avoidance of potentially painful events (illness behaviour) Little opportunity to disconfirm beliefs Avoidance disuse syndrome & p (mood problems) Disuse leads to p (painful experience)

Treatments

Mirror pain theories Medical (especially acute pain)

Non-anti-inflammatory non-steroid (paracetamol) Anti-inflammatory non-steroids (eg ibprofen) Opioids (eg morphine) Behavioural initially Mostly cognitive behavioural now

Psychological

Treatment of Chronic Pain

Surgical procedures to block the transmission of pain from the peripheral nervous system to the brain. Synovectomy Removing membranes that become inflamed in arthritic joints. Spinal fusion joins two or more adjacent vertebrae to treat chronic back pain.

Psychological Pain Control Methods

Biofeedback provides biophysiological feedback to patient about some bodily process the patient is unaware of (e.g., forehead muscle tension). Relaxation systematic relaxation of the large muscle groups. Hypnosis relaxation + suggestion + distraction + altering the meaning of pain.

Psychological Pain Methods

Acupuncture not sure how it works. Could include:

Counter-irritation may close the spinal gating mechanism in pain perception. Expectancy Reduced anxiety from belief that it will work. Distraction Trigger release of endorphins

Phantom Limb pain

Affects the majority of amputees For most the sensation fades, but a minority experience 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 often referred from the chest, phantom arm sensations from the face.

Phantom limb pain:

during amputation under general anesthesia the spinal cord can still experience the insult produced by the surgical procedure and central sensitization occurs. To try to prevent it, local infiltration of anesthetics in the site of surgery. But studies show also rearrangement of cortical circuits (cortical region of the missing limb receives afferents from other site of the skin)

Phantom Pain intensity as a function of Cortical Reorganization.

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 serotoninergic fibres. These inhibit pain transmission Endogenous opioids also underlie some psychological influences. Naloxone blocks both TENS and placebo analgesia

PAIN TREATMENT CONTINUUM

Diagnosis Oral Medications PT, Exercise, Rehabilitation Behavioral Medicine Corrective Surgery Therapeutic Nerve Blocks Oral Opiates Implantable Pain Management Devices Neurostimulation Intrathecal Pumps Neuroablation

Multi-Disciplinary Pain Program Models

Pain Consultation Team Multidisciplinary Programs

Multidisciplinary Outpatient Programs Multidisciplinary Inpatient Programs

Pain Service

Pain Consultation Team

Multidisciplinary group Provides consultation services only

not ongoing treatment

Consultation Team Referral

Anesthesiology Neurology Psychology Pharmacy Nursing

Recommendation

Multidisciplinary Clinics

Comprised of 2 or more disciplines Goal is to provide coordinated and more comprehensive care to patients for more complex 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

Chronic Pain Disciplines and Roles (Core)

Anesthesiology nerve blocks Kinesiotherapy pool therapy; activity Neurology eval. treatment Nursing patient care Physical Medicine exercise; modalities Physical Therapy exercise; modalities Psychology eval. and treatment Occupational Therapy UE eval and treatment Vocational Rehab job eval and training

Rheumatoid and Osteo-arthritis Back pain Menstrual Pain Labour Pain Peripheral Nerve Injuries Shingles Headache and Migraine Cancer Pain Trigeminal Neuralgia Phantom Limb Pain Sports Injuries Sciatica Aching Joints Post Operative Pain Muscular Pain Whiplash and Neck Injury and many others

Mechanistic Approach To Pain Therapy

Modify Expression Anxiolytics Increase Inhibition TCAs, SSRIs, Clonidine

Decrease Inflammatory Response NSAIDs, Local Anesthetics, Steroids

Decrease Conduction Gabapentin, Carbamazepine, Local Anesthetics, Opioids

Prevent Centralization COX 2, Opioids, Ketamine, a-2 Agonists.

Summary

Chronic neuropathic pain is a disease, not a symptom Rational polypharmacy is often necessary

combining peripheral and central nervous system agents enhances pain relief balancing efficacy, safety, and tolerability reducing baseline pain and pain exacerbations improving function and QOL

Treatment goals include:

New agents and new uses for existing agents offer additional treatment options

Further Reading

Rosenzweig et al. cover pain in the second 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.

REFERENCES

Review Neuropathic pain: a practical guide for the

clinician ; Ian Gilron, C. Peter N. Watson, Catherine M. Cahill and Dwight E. Moulin Dworkin RH, Backonja M, Rowbotham MC, et al. Advances in neuropathic pain. Arch Neurol 2003;60:1524-34. Gilron I, Bailey JM, Tu D, et al. Morphine, gabapentin, or their combination for neuropathic pain. N Engl J Med 2005;352:1324-34. Stephen Macres, Understanding Neuropathic Pain Eisenberg E, McNicol ED, Carr DB. Efficacy and safety of opioid agonists in the treatment of neuropathic pain of nonmalignant origin. JAMA 2005;293:304352.

The end

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