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The perception of pain
Ching-Liang Lu
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What is pain?
• Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
IASP – International Association for the Study of Pain 2009
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What is pain?• Pain is
– subjective
• not a stimulus, but an experience
– protective (acute)
– modified by developmental, behavioural, personality and cultural factors
• Associated signs are crying, sweating, increased heart rate, blood pressure, behavioural changes etc
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Pain
• Dimensions of the ‘PAIN”
– Sensory-discriminative
– Affective-motivate
– Cognitive
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Nociceptive vs Neuropathic PainNociceptive
PainCaused by activity in
response to potentially tissue-damaging stimuli
Neuropathic Pain
Initiated or caused by primary lesion or dysfunction in the nervous system
Pospostoperative
pain
toperativepain
Mechanicallow arthritis, back pain
Sickle cellcrisis
Arthritis
Postherpeticneuralgia
Neuropathic low back pain
Phantom pain
Sports/e sports or exercise injuries xerciseinjuries
*Complex regional pain syndrome
Central post-stroke pain
Trigeminalneuralgia
Distalpolyneuropathy
(eg, diabetic, HIV)
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Nociceptive pain: Tissue injury/inflammation
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Postherpetic neuralgia
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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
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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)
Acute pain is not that bad.
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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 the patient’s well-being
• Pain that continues when it should not
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Domains of Chronic Pain
Social Consequences
• Marital/family relations
• Intimacy/sexual activity
• Social isolation
Socioeconomic
Consequences
• Healthcare costs
• Disability
• Lost workdays
Quality of LifePhysical functioningAbility to perform
activities of daily living
WorkRecreation
Psychological MorbidityDepressionAnxiety, angerSleep disturbancesLoss of self-esteem
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Pain measurement
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Nociceptors
• 3 classes of nociceptors
–Mechanical: pinch, punctate, squeeze
–Thermal: above 45C or below 5C
–Polymodal: mechanical, thermal, chemical
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Somatic receptor types
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Thermosensation
HeatDRG • 45% small- to medium-diameter neurons: threshold of ∼42°C heat-sensitive C and type II Aδ fibres TRPV-1 receptor• 5-10% medium- to large-diameter cells: threshold of ∼51°C type I Aδ TRPV-2 receptor• TRPV-3 TRPV -4: warm range 31∼39°C
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Thermosensation
Cold•TPRVM8 receptor: ∼26°C ; (cool to cold) express
in 10-20 % of small-diameter neuron• TRPA1: ∼17°C painful cold ?
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TRP channel family
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AFFERENT (SENSORY) NEURON
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Nociceptive afferents
Compound Action Potential
First pain: Sharp, faster A-delta fibers
Second pain: Dull, slower C-fibers
Blocking each nerve blocks the sensation
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Referred pain
• Signals from muscles and viscera can be felt as pain elsewhere
• Example: myocardial infarction and angina can be felt in chest and left arm
• Mechanism: convergence of afferents muscle/ viscera afferents and somatic afferents.
• Convergence on the same projection neurons in the dorsal horn
• The brain cannot tell the difference
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Neurotransmitters
• Excitatory neurotransmitters:glutamate, tachykinins
calcitonin gene-related peptide, vasoactive intestinal polypeptide, .
• Inhibitory neurotransmitters:gamma amino butyric acid (GABA)
• Neurotransmitters involved in Descending Pain Regulation:noradrenaline (norepinephrine)
serotonin
Opiates
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Substance P in dorsal horn
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Pain modulation below spinal level
1. PERIPHERAL
2. CENTRAL
1. Peripheral (Sensitization)
TISSUE INJURY
RELEASE OF SUBBSTANCE-P CHEMICAL MEDIATORS OF
AND GLUTAMATE INFLAMMATION
STIMULATE NOCICEPTORS IN
THE PERIPHERY
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Peripheral Sensitization
NSAID
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Peripheral sensitization
53C 30 sec at site A&D
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• “Wind-up”
– Response to second stimulus is stronger than the response to the first one in C fiber
• Change in temporal integration
Central sensitization for chronic pain:
wind-up
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40
30
20
10
0
0 10 20
ControlNMDA antagonist
Stimulus number
"Wind-up" is NMDA mediated. Response with and without an NMDA antagonist.
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Ascending pathwaysSpinal cord ThalamusCortex
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New pathway for visceral pain:
Dorsal column pathway
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Brain Pain perception
Rene Descartes (1596-1650)
No Brain, No Pain
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Lateral system: S1/2Discrimitive component
Thalamus
Medial system:Affective component
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Neuroimaging of acute painMuscle pain
Visceral pain
Niddam et al., 2002
Insula
Amygdala
ACC
PCC
Vermis
Thalamus
PPC
PFC
ACC
PCC
PCC
Vermis
PFC
PPC
PFC
Insula Insula
Lu et al., 2004
Chen et al.
Lin et al. (preliminary)
Tooth pain
Cutaneous pain
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Cortical neuronal correlates upon balloon distension in GI tract (volunteers)
Aziz Q. Gastroenerology 1997; 113:50
Lu CL Neurogastroenterol 2004;16:575Gastroenerology 2005; 128:1529
Esophagus Rectum Antrum Fundus
Mertz H. Gastroenerology2000; 118:8342
Ladabaum U. Gastroenerology 2001; 120:369
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Pain modulation (inhibition)
• Gate control theory
• Descending inhibition
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Gate control theory• P.D. Wall & R. Melzack (1965)
• “There is an interaction between pain fibres and touch fibre input at the spinal cord level in the form of a ‘gating mechanism’
Aβ fibres
Aδ, C fibres
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Gate control theory
When pain fibre is stimulated, gate will be opened & pain is felt
pain
pain is felt
+
gate is opened
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Gate control theory
When pain and touch fibres are stimulated together, gate will be closed & pain is not felt
pain is not felt
gate is closed
TOUCH
PAIN
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Gate control theory• This theory provided basis for various
methods of pain relief
– Massaging a painful area
– Applying irritable substances to a painful area (counter-irritation)
– Transcutaneous Electrical Nerve Stimulation (TENS)
– Acupuncture ?
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Descending inhibition
• Direct stimulation of PAG produces analgesia
– Inhibits firing of nociceptive neurons in lamina I and V
– Descending pathway recruited: PAG excites rostroventral medulla/nucleus raphe
magnus (5HT); Locus Ceruleus(NE)
• Role of Opioid receptor
– Opioid-induced analgesia via endogenous opioid receptors (-, δ-, κ-) in descending pathway (PAG, ventral medulla, superficial dorsal horn)
– Endogenous opioid peptide: enkephalins, β-endorphin, dynorphin
– Stress-Induced Analgesia (SIA)
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Key points
• The pain experienced by patients is a result of the interaction between sensory and emotional experiences.
• Afferent fibers– Aδ fibres transmit rapid, sharp, localized pain. – C fibres transmit slow, diffuse, dull pain.
• Ascending pathway– Spinothalamic, spinoreticular, spinomesencephalic tracts
• Pain modulation – Gate control at dorsal horn of the spinal cord – Descending inhibitory pathways.