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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,
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?
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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
patient’s well-being
Pain that continues when it should
not
What is Chronic Pain?
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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
Psychological
Morbidity
Depression
Anxiety, anger
Sleep disturbances
Loss of self-esteem
Social Consequences
 Marital/family
relations
 Intimacy/sexual activity
 Social isolation
Socioeconomic
Consequences
 Healthcare costs
 Disability
 Lost workdays
Nociceptive vs Neuropathic
Pain
Nociceptive
Pain
Mixed Type
Caused by activity in
neural pathways in
response to potentially
tissue-damaging stimuli
Caused by a
combination of both
primary injury and
secondary effects
Neuropathic
Pain
Initiated or caused by
primary lesion or
dysfunction in the
nervous system
CRPS*
Postoperative
pain
Arthritis
Mechanical
low back pain
Sickle cell
crisis
Sports/exercise
injuries
*Complex regional pain syndrome
Postherpetic
neuralgia
Trigeminal
neuralgia
Neuropathic
low back pain
Central poststroke pain
Distal
polyneuropathy
(eg, diabetic, HIV)
Possible Descriptions
of Neuropathic Pain
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Sensations
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numbness
tingling
burning
paresthetic
paroxysmal
lancinating
electriclike
raw skin
shooting
deep, dull, bonelike ache

Signs/Symptoms
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
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
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Transduction
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Transmission
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Modulation
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Perception
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Interpretation
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Behavior
Brain
Descending
Pathway
Peripheral
Nerve
Dorsal
Root
Ganglion
Ascending
Pathways
C-Fiber
A-beta Fiber
A-delta Fiber
10
Dorsal
Horn
Spinal Cord
Adapted with permission from WebMD Scientific American® Medicine.
Pathophysiology of
Neuropathic Pain
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Chemical excitation of nonnociceptors
Recruitment of nerves outside of site of injury
Excitotoxicity
Sodium channels
Ectopic discharge
Deafferentation
Central sensitization
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maintained by peripheral input
Sympathetic involvement
Antidromic neurogenic inflammation
Multiple Pathophysiologies May
Be Involved in Neuropathic Pain
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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
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“Pain initiated or caused by a primary lesion or
dysfunction in the nervous system”
Merskey & Bogduk 1994
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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
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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
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Reduced inhibition
Functional (neurotransmitter) & anatomical (sprouting)
changes in Aβ fibres  tactile allodynia (pain induced by
light touch)
Acute Neuropathic Pain
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Acute causes
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Acute neuropathic pain = 1-3%
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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
Prompt diagnosis & Rx may prevent
chronic pain
Examples of Acute NP
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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
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EXPERIENCED IN PARTS OF BODY THAT
APPEAR NORMAL
CHRONIC
SEVERE
RESISTANT TO OVER THE COUNTER
ANALGESICS
AGGRAVATED BY ALLODYNIA
Chronic Pain Syndromes
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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
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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
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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
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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. (α 2 delta subunit- where gabapentin acts)
3. Adjacent demyelinated axons can have abnormal electrical
connections channels and increased neuronal excitability.
PATHOPHYSIOLOGY
CENTRAL MECHANISMS
1.
2.
3.
4.
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.
Pain Treatment Continuum
Most
invasive
Least
invasive
Continuum not related to
efficacy
Psychological/physical approaches
Topical medications
Systemic medications*
Interventional techniques*
*Consider referral if previous treatments were unsuccessful.
Nonpharmacologic Options
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Biofeedback
Relaxation therapy
Physical and occupational therapy
Cognitive/behavioral strategies
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meditation; guided imagery
Acupuncture
Transcutaneous electrical nerve
stimulation
Pharmacologic Treatment
Options
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Classes of agents with efficacy demonstrated
in multiple, randomized, controlled trials for
neuropathic pain
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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
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Carbamazepine
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Duloxetine
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postherpetic neuralgia
Lidocaine Patch 5%
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peripheral diabetic neuropathy
Gabapentin
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trigeminal neuralgia
postherpetic neuralgia
Pregabalin*
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peripheral diabetic neuropathy
postherpetic neuralgia
*Availability pending based upon controlled substance scheduling by the DEA.
Pharmacologic Agents
Affect Pain Differently
BRAIN
CNS
PNS
Peripheral
Sensitization
Descending Modulation
Spinal
Cord
Dorsal
Horn
Local Anesthetics
Topical Analgesics
Anticonvulsants
Tricyclic Antidepressants
Opioids
Anticonvulsants
Opioids
Tricyclic/SNRI
Antidepressants
Central Sensitization
Anticonvulsants
Opioids
NMDA-Receptor Antagonists
Tricyclic/SNRI
Antidepressants
Anticonvulsant Drugs for
Neuropathic Pain Disorders
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Postherpetic neuralgia
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gabapentin*
pregabalin *
Diabetic neuropathy
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carbamazepine
phenytoin
gabapentin
lamotrigine
pregabalin *
*Approved by FDA for this use.
HIV = human immunodeficiency virus.
HIV-associated
neuropathy
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Trigeminal neuralgia
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lamotrigine
carbamazepine*
lamotrigine
oxcarbazepine
Central poststroke pain
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lamotrigine
Gabapentin in Neuropathic
Pain Disorders
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FDA approved for postherpetic
neuralgia
Anticonvulsant: uncertain mechanism
Limited intestinal absorption
Usually well tolerated; serious adverse
effects rare
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dizziness and sedation can occur
No significant drug interactions
Peak time: 2 to 3 h; elimination half-
*Not approved by FDA for this use.
Gabapentin
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Action:  NT release from hyper-excited neurones
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variable oral absorption, no interactions, completely renally
excreted
Indication:
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Protective analgesia
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Neuropathic pain treatment (NNT = 4.7)
SE: sedation, dizziness, ataxia, tremor
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NNH minor = 4, NNH major =12-18
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COST!
Doses:
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Pre-op: 600-1200mg (1-2 hours pre-op)
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Post-op “prophylaxis”: 100-300mg TDS (? 2 weeks)
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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: 1130—1136
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
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Very similar to gabapentin
More reliable oral absorption
Slightly different side effect profile
Doses: 75-300mg BD
Other Anticonvulsants
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Effective (NNT 2-3) but less “user friendly”
Most have uncommon but serious SE (eg.
aplastic anaemia, hepatotoxicity, StevensJohnson syndrome etc)
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NNH minor = 3, NNH major = 16 - 24
Consider
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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) 289–305
Topical vs Transdermal
Drug Delivery Systems
Topical
(lidocaine patch 5%)
Peripheral tissue activity
Applied directly over painful site
Insignificant serum levels
Systemic side effects unlikely
Transdermal
(fentanyl patch)
Systemic activity
Applied away from painful site
Serum levels necessary
Systemic side effects
Lidocaine Patch 5%
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Lidocaine 5% in pliable patch
Up to 3 patches applied once daily directly over
painful site
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Efficacy demonstrated in 3 randomized controlled trials
on postherpetic neuralgia
Drug interactions and systemic side effects unlikely
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12 h on, 12 h off (FDA-approved label)
recently published data indicate 4 patches (18–24 h)
safe
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
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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
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CNS toxicity at plasma levels > 5 mcg/ml
Dose: IV 1-2 mg/kg/hr (??duration)
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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
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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;
102:211–20
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
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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
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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
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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
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Oxycodone, morphine (NNT = 2.5)
Tramadol (NNT = 3.9)
SE: usual, and ?OIH
Doses: usual
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? 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) 289–305
Antidepressants in
Neuropathic Pain Disorders*
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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
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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
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Commonly reported AEs
(generally anticholinergic):
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blurred vision
cognitive changes
constipation
dry mouth
orthostatic hypotension
sedation
sexual dysfunction
tachycardia
urinary retention
AEs = adverse effects.
Fewest
AEs
Most
AEs
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Desipramine
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Nortriptyline
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Imipramine
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Doxepin
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Amitriptyline
Tricyclic Antidepressants
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Action: Mixed ( 5-HT &/ Norad at synapse)
Indication:
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All NP treatment (except SCI, PLP, HIV)
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PHN prevention: 50%  if used for 90days
SE: dizzy, sedation, anticholinergic
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NNT: overall = 3.1, central = 4.0, periph = 2.3
NNH minor = 5, NNH major = 16
Doses
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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) 289–305
Venlafaxine
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Action: SNRI
Indication:
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SE: sedation/insomnia, ataxia, BP, nausea

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mastectomy pain prophylaxis,
peripheral NP treatment (NNT=5.5)
NNH major = not significant
Doses
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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
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Skin prick test advised
Dose: 100 IU in 100ml saline over 1hr
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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
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Neural blockade
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Neurolytic techniques
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alcohol or phenol neurolysis
pulse radio frequency
Stimulatory techniques
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sympathetic blocks for CRPS-I and II
(reflex sympathetic dystrophy and causalgia)
spinal cord stimulation
peripheral nerve stimulation
Medication pumps
CRPS = complex regional pain syndrome.
Summary of Advances in
Treatments for Neuropathic Pain*
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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
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NON PHARMACOLOGIC
EXERCISE
TENS
PENS
GRADED MOTOR IMAGERY
CBT
World Health Organization
(WHO) Analgesic Ladder.
INTERVENTIONAL PAIN
MANAGEMENT
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
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.
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Sympathetic nerve blocks.
Treatment Goals - I
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Reduce and manage pain
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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
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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
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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

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
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
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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

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Chemical, Thermal, & Surgical
Neuromodulation

Spinal cord stimulators & Implanted spinal pumps
Physical & Occupational
Therapy

Active
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Improved body mechanics
Spine stabilization
Stretching & strengthening
Aerobic conditioning
Aquatics therapy
Work hardening
Self-directed fitness program
Psychological Approaches
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Non-drug pain management skills
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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
61
Neural Mechanisms of Pain

Gate Control
Theory


62
Melzack and Wall
(1965)
Perception of
pain mediated by
a “gate” located
in the dorsal horn
of the spinal cord
L-fibers mediating
tactile perception
(A-a and A-b)
+
Central
Control
+ closes
-
SG- gate
PAIN
T cell
SG+
+
+
opens gate
S-fibers mediating
pain perception (Ad and C)
+
Experimental Evidence for the Gate


63
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
+ closes
-
SG- gate
PAIN
T cell
SG+
+
+
opens gate
S-fibers mediating
pain perception (Ad and C)
+
Endorphins and Pain



64
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)
Endorphins and Pain



65
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
Nociceptors in Skin
Epidermi
s
Dermis
Free
Nerve
Endings
Pain Pathways

Lots of effort to id neural pathways

Found distinct categories of nerve fibres



A δ : 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)
Experience
Pain
Perception
Emotion
Behaviour
Tissue
damage
Gate – amplifies or
attenuates signal
Opening & Closing the Gate
Factor
Physical
Emotional
Behavioural
(Cognitive)
Opens
Closes
injury
agitation
anxiety
stress
frustration
depression
tension
rumination
boredom
medication
relaxation
optimism
happiness
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)
Psychological

Behavioural initially

Mostly cognitive behavioural now
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
Decrease
Inflammatory
Response
NSAIDs,
Local Anesthetics,
Steroids
Decrease Conduction
Gabapentin,
Carbamazepine,
Local Anesthetics,
Opioids
Increase
Inhibition
TCA’s, SSRI’s,
Clonidine
Prevent
Centralization
COX 2,
Opioids,
Ketamine,
a-2 Agonists.
Summary


Chronic neuropathic pain is a disease, not a
symptom
“Rational” polypharmacy is often necessary


Treatment goals include:




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
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.
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