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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%


Pregabalin*

peripheral diabetic neuropathy


*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
http://www.bodyshapers.com/htm/zoompics.htm

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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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