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 Acute Pain Chronic Pain

Cause Generally known Often unknown

Duration of pain Short, Persists after healing,

well-characterized 3 months

Treatment Resolution of Underlying cause and pain

approach underlying cause, disorder; outcome is often
usually self-limited 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 Psychological
Physical Morbidity
functioning Depression
Ability to Anxiety, anger
perform Sleep disturbances
activities of Loss of self-esteem
daily living
Work
Recreation
Social Consequences Socioeconomic
Marital/family Consequences
relations Healthcare costs
Intimacy/sexual Disability
activity Lost workdays
Social isolation
 Nociceptive vs
Neuropathic Pain
Nociceptive MixedType Neuropathic
Pain Caused by a
combination of both
Caused by activity in
neural pathways in
primary injury and Pain
secondary effects Initiated or caused by
response to potentially
tissue-damaging
primary lesion or
stimuli
dysfunction in the
nervous system CRPS*

Postherpeti
Postoperative
Arthritis c Trigeminal
pain
neuralgia neuralgia
Sickle cell Neuropathic
Mechanical crisis low back pain Central post-
low back pain
Distal stroke pain
Sports/exercise polyneuropathy
injuries (eg, diabetic, HIV)
*Complex regional pain syndrome
 Possible Descriptions

of Neuropathic
Sensations
Pain
Signs/Symptoms
numbness allodynia: pain from a
tingling stimulus that does not
burning normally evoke pain
paresthetic thermal

paroxysmal mechanical

lancinating hyperalgesia:
electriclike exaggerated response
raw skin to a normally painful
shooting stimulus
deep, dull, bonelike ache
 Physiology of Pain
Perception
Injury Brain

Transduction
Transmission
Modulation
Perception Descending
Pathway
Interpretation
Behavior
Dorsal
Peripheral Root
Nerve Ganglion

Ascending
Pathways
C-Fiber

A-beta Fiber Dorsal

Horn
A-delta Fiber
Spinal Cord
10 Adapted with permission from WebMD Scientific American
 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
More Pain
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
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)
 Acute Neuropathic Pain
Acute causes
iatrogenic, traumatic, inflammatory, infective
Acute neuropathic pain = 1-3%
Based on cases referred to an acute pain
service
Majority still present at 12 months
May be a risk factor for chronic pain
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 CENTRAL
Polyradioculopathy Compressive
Alcoholic polyneuropathy myelopathy from spinal
Entrapment neuropathies stenosis
(carpal tunnel) HIV myelopathy
Nerve compression by MS
tumor Parkinson disease
Diabetic neuropathy Post ischemic
Phantom limb pain myelopathy
Postherpetic neuralgia Poststroke pain
Trigeminal neuralgia 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)
1. Increased spontaneous activity of dorsal horn neurons,
reduced activation thresholds and enhanced
responsiveness to synaptic inputs.
2. Expansion of receptive fields, death of inhibitory
interneurons (intrinsic modulatory systems).
3. Central sensitization mediated by NMDA receptors that
further release excitatory amino acids and
neuropeptides.
4. Sprouting of sympathetic efferents into neuromas and
dorsal root and ganglion cells.
 Pain Treatment Continuum
Least Most
invasiv invasiv
e e
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
Carbamazepine
Pain

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.

 Pharmacologic Agents
Affect Pain
BRAIN
Differently
Descending
Modulation
Anticonvulsants
Opioids
Spinal Tricyclic/SNRI
CNS Cord Antidepressants

Dorsal Central
PNS Horn Sensitization
Anticonvulsants
Opioids
NMDA-Receptor
Peripheral Local Anesthetics Antagonists
Topical Analgesics Tricyclic/SNRI
Sensitization Antidepressants
Anticonvulsants
Tricyclic
Antidepressants
Opioids
 Anticonvulsant Drugs for
Neuropathic Pain Disorders
Postherpetic HIV-associated
neuralgia neuropathy
gabapentin* lamotrigine
pregabalin * Trigeminal neuralgia
Diabetic neuropathy carbamazepine*
carbamazepine lamotrigine
phenytoin oxcarbazepine
gabapentin Central poststroke
lamotrigine pain
pregabalin *
lamotrigine

*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
No significant drug interactions
Peak time: 2 to 3 h; elimination half-life: 5 to 7 h
Usual dosage range for neuropathic pain up to
3,600 mg/d (tidqid)*

*Not approved by FDA for this use.

 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, 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: An
evidence based proposal. Pain 118 (2005) 289305
 Topical vs Transdermal
Drug
Topical
Delivery Systems
Transdermal
(lidocaine patch 5%) (fentanyl patch)

Peripheral tissue activity Systemic activity

Applied directly over painful site Applied away from painful site
Insignificant serum levels Serum levels necessary
Systemic side effects unlikely 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

'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 Pain Management: Scientific Evidence, 2nd Ed. Australian and New Zealand
 Principles of Opioid
Therapy
forAEs Neuropathic Pain
Opioids should be titrated for therapeutic efficacy

versus
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
Fewest
Commonly reported AEs Desipramine
AEs
(generally anticholinergic):
blurred vision Nortriptyline
cognitive changes
Imipramine
constipation
dry mouth Doxepin
orthostatic hypotension
sedation Amitriptyline
sexual dysfunction
tachycardia Most
urinary retention AEs
AEs = adverse effects.
 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: An
evidence based proposal. Pain 118 (2005) 289305
 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
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)
Neurolytic techniques
alcohol or phenol neurolysis
pulse radio frequency
Stimulatory techniques
spinal cord stimulation
peripheral nerve stimulation
Medication pumps

CRPS = complex regional pain syndrome.

 Summary of Advances in
Treatments for Neuropathic

Pain* toxin: low back pain
Botulinum
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

 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
Chemical, Thermal, & Surgical
Neuromodulation
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

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
anterior 2/3 of tongue
Motor control of muscles
involved in biting, chewing,
and swallowing
61
 Neural Mechanisms of Pain
L-fibers Central
Gate Control mediating tactile Control
Theory perception (A-
Melzack and and A-)
+
+ closes
Wall (1965) -
SG- gate PAIN
Perception of
pain mediated T cell
by a gate +
SG+
located in the opens +
+
dorsal horn of gate
the spinal cord
S-fibers
mediating pain
62
perception (A-
 Experimental Evidence for the
Gate
Selective L-fibers Central
inactivation of L- mediating tactile Control
fibers results in perception (A-
greater pain
perception from and A-)
+
+ closes
noxious stimuli -
(Price, Hi, and SG- gate PAIN
Dubner, 1977)
T cell
+
Phantom Limb SG+
opens +
Pain may result +
from reduced L- gate
fiber input
(Melzack, 1970) S-fibers
63
mediating pain
perception (A-
 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

stimulatedmay 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

Epiderm
Free
is
Nerve
Endings

Dermis
 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

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
Experienc
e
Emotion

Behaviour

Tissue Gate amplifies

damage or attenuates
signal
Opening & Closing the Gate
Factor Opens Closes
Physical injury medication
agitation
Emotional anxiety relaxation
stress optimism
frustration happiness
depression
tension
Behavioural rumination enjoyable activities
(Cognitive) boredom 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)
Psychological

Behavioural initially
 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 Referra

l
AnesthesiologyNeurology

Psychology Pharmacy
Nursing Recommendati
on
 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 Increase
Anxiolytics Inhibition
TCAs, SSRIs,
Clonidine

Prevent
Decrease Centralization
Inflammatory Decrease Conduction COX 2,
Response Gabapentin, Opioids,
NSAIDs, Carbamazepine, Ketamine,
Local Anesthetics, Local Anesthetics, -2 Agonists.
Steroids Opioids
 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
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 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;293:3043-52.
 The end

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