The Science of Chronic Pain Management

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The Science of Chronic Pain Management

• Dr Alexander CrightonConsultant in Oral
  MedicineGlasgow Dental Hospital School

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What is Pain?

• Arrows shot by the Gods Homer
• Passion of the SoulAristotle
• Pain Pleasure arise from within the body
  Plato

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What is Pain?

• an unpleasant sensory and emotional experience
  associated with actual or potential tissue damage
  or described in terms of such damage
• International Association for the Study of Pain

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What is Pain?

• an unpleasant sensory and emotional experience
  associated with actual or potential tissue damage
  or described in terms of such damage
• International Association for the Study of Pain

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What is Pain?

• an unpleasant sensory and emotional experience
  associated with actual or potential tissue damage
  or described in terms of such damage
• International Association for the Study of Pain

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What is Pain?

• an unpleasant sensory and emotional experience
  associated with actual or potential tissue damage
  or described in terms of such damage
• International Association for the Study of Pain

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Why get pain when there is no obvious tissue
damage?

• Damaged nociception
• Damaged transmission of signal
• Central processing of signal defective

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Neuropathic Pain

• Somatic nerve damage
• Somatic nerve dysfunction
• Autonomic nerve damage/dysfunction
• Chronic Regional Pain Syndrome

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How do we feel pain?
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How do we feel pain?

• Nociception
• Peripheral Nerve Transmission
• Spinal Modulation
• Central Appreciation

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Peripheral Nociception
Tissue Damage
5-HT Bradykinin
Nociceptor
Spinal Cord
Substance PProstaglandins
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Peripheral Sensitisation
Tissue Damage
5-HT Bradykinin
Nociceptor
Spinal Cord
Substance PProstaglandins
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Peripheral Sensitisation

• Prostaglandins act directly on peripheral
  terminals of Ad C fibres to lower their
  thresholds
• Allodynia
• Hyperalgesia
• Preventative therapeutic role for NSAID!

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Spinal Cord
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Descartes

• Stimulus response model

Ascending pain

N
N
Spinal cord
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Gate control of Chronic Pain

• Melzak Wall

Touch A?
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Neuronal Plasticity

• Sprouting of Spinal Segment nerves

Pain fibre
Descending facilitation
N

Pain
Ascending pain C
N

-
Descendinginhibition
N
Sensory fibre
Sensation
Touch Ab
N
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The Spinal Cord

• 5 ascending tracts which are concerned in pain
  processing.
• These may show some specificity for
• Types of pain e.g. visceral or somatic
• Components of pain e.g. sensory, emotional
• Integration, orientation and reaction

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Receptors

• Nerve transmission CHEMICAL
• Drugs and other nerves can modify activity

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Receptors

• Nerve transmission CHEMICAL
• Drugs and other nerves can modify activity
• pre AND post synaptic
• excitatory inhibitory
• Chemical or Voltage Operated
• GABA, Adrenergic, NaN SNS SodiumProton,
  Opiate, Potassium, Calcium, ATP, Capsaicin, NMDA

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Receptors

• Nerve transmission CHEMICAL
• Drugs and other nerves can modify activity
• pre AND post synaptic
• excitatory
• inhibitory
• GABA, Adrenergic, NaN SNS SodiumProton,
  Opiate, Potassium, Calcium, ATP, Capsaican, NMDA
• Transmitters modulate activity
• Glutamate, Glycine, Norepinepherine, Adenosine,
  Opioids, Bradykinin, Eicosanoids, 5HT, H

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Receptors
NMDA
Opiate
Adrenergic
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Chronic Stimulation?

• NORMALRepeated stimulus REDUCES receptor
  sensitivity
• NMDARepeated Stimulus INCREASES receptor
  sensitivity

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Chronic Pain Summary

• Peripheral Sensitisation
• Tissue damage
• Neuronal Sprouting
• Tissue Damage
• Chronic Stimulation
• Tissue damage

Tissue Healing
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Chronic Pain Summary

• Peripheral Sensitisation
• Neuronal Sprouting
• Chronic Stimulation

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PAIN

• Pain is a complex feeling created in our brains,
  with affective cognitive components.
• Nociception
• Transmission
• Understanding

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Central Control of Chronic Pain
PAIN
Central Processes
Descending facilitation
N
Motor
Pain

M-A

• N

-
S-D
N
Descendinginhibition
Sensory fibre
Sensation
Effect
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The Cortex

• Somatosensory cortex
• spatial, temporal intensity discrimination
• Anterior Cingulate
• affective, motor and autonomic reactions.
• Insular
• visceral pain, homeostasis
• integrating pain memory
• BUT they all communicate discrete lesions dont
  produce discrete deficits

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Cognitive Deduction
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The Cortex
PAIN
Central Processes
Descending facilitation
N

Motor
Pain
M-A

• N

-
S-D
N
Descendinginhibition
Sensory fibre
Sensation
Effect
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Why Me?
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TreatmentsDo they fit the Science?

• Drug therapy
• Clinical Psychology
• TENS
• Acupuncture

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Drug therapy

• NSAID
• Local Anaesthetics
• Opioid drugs
• Tricyclic based drugs
• NMDA Blocking drugs
• Anti-epileptic drugs
• Membrane stabilising drugs

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Drug treatments

• Opioids
• tramadol
• MST
• Tricyclic based drugs
• amitriptyline
• dothiepin
• nortriptyline
• NMDA Blockers (GABA antagonists)
• ketamine
• amantadine
• dextropopoxyphene

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Drug treatments

• Anti-epileptic Drugs ( calcium channel
  blockers)
• gabapentin
• valproate
• topiramate
• vigabatrin
• carbamazepine
• Membrane stabilising drugs
• mexilitene
• tocainamide

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Clinical Psychology
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Clinical Psychology

• Cognitive Behavioural therapy
• Pain perception influences Mood
• Mood changes influence Pain perception
• Modulation of ONE will alter BOTH
• ATTENTION control is important

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Transcutaneous Electrical Nerve Stimulation -
TENS
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TENS

• High Frequency TENS
• Low Frequency TENS
• Burst TENS

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Acupuncture
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Acupuncture
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The future?

• Pregabalin 2004
• Membrane Stabilising drugs
• Gene therapy
• NMDA therapies
• AMPA therapies (NGX 424)