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The Science of Chronic Pain Management

The Science of Chronic Pain Management. Dr Alexander Crighton Consultant in Oral Medicine Glasgow Dental Hospital & School. What is Pain?. “Arrows shot by the Gods” Homer “Passion of the Soul” Aristotle “Pain & Pleasure arise from within the body” Plato. What is Pain?.

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The Science of Chronic Pain Management

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  1. The Science of Chronic Pain Management Dr Alexander CrightonConsultant in Oral MedicineGlasgow Dental Hospital & School

  2. What is Pain? “Arrows shot by the Gods” Homer “Passion of the Soul”Aristotle “Pain & Pleasure arise from within the body” Plato

  3. 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

  4. 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

  5. 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

  6. 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

  7. Why get pain when there is no obvious tissue damage? • Damaged nociception • Damaged transmission of signal • Central processing of signal defective

  8. Neuropathic Pain • Somatic nerve damage • Somatic nerve dysfunction • Autonomic nerve damage/dysfunction • Chronic Regional Pain Syndrome

  9. How do we feel pain?

  10. How do we feel pain? • Nociception • Peripheral Nerve Transmission • Spinal Modulation • Central Appreciation

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

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

  13. Peripheral Sensitisation • Prostaglandins act directly on peripheral terminals of Aδ & C fibres to lower their thresholds • Allodynia • Hyperalgesia • Preventative & therapeutic role for NSAID!

  14. Spinal Cord

  15. Descartes Stimulus response model Ascending pain + N N Spinal cord

  16. Pain fibre Descending facilitation N + Pain Ascending pain ‘C’ N - - Descendinginhibition N Sensory fibre Sensation N Gate control of Chronic Pain Melzak & Wall Touch ‘A’

  17. 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

  18. 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

  19. Receptors • Nerve transmission CHEMICAL • Drugs and other nerves can modify activity

  20. 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

  21. 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+

  22. Receptors NMDA Opiate Adrenergic

  23. Chronic Stimulation? • NORMALRepeated stimulus REDUCES receptor sensitivity • NMDARepeated Stimulus INCREASES receptor sensitivity

  24. Chronic Pain Summary • Peripheral Sensitisation • Tissue damage • Neuronal Sprouting • Tissue Damage • Chronic Stimulation • Tissue damage Tissue Healing

  25. Chronic Pain Summary • Peripheral Sensitisation • Neuronal Sprouting • Chronic Stimulation

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

  27. Central Control of Chronic Pain PAIN Central Processes N Descending facilitation N Motor Pain + M-A - S-D N Descendinginhibition Sensory fibre Effect Sensation

  28. 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 don’t produce discrete deficits

  29. Cognitive Deduction

  30. The Cortex PAIN Central Processes N Descending facilitation N + Motor Pain M-A - S-D N Descendinginhibition Sensory fibre Sensation Effect

  31. Why Me?

  32. TreatmentsDo they fit the Science? • Drug therapy • Clinical Psychology • TENS • Acupuncture

  33. Drug therapy • NSAID • Local Anaesthetics • Opioid drugs • Tricyclic based drugs • NMDA Blocking drugs • ‘Anti-epileptic’ drugs • Membrane stabilising drugs

  34. Drug treatments • Opioids • tramadol • MST • Tricyclic based drugs • amitriptyline • dothiepin • nortriptyline • NMDA Blockers (+GABA antagonists) • ketamine • amantadine • dextropopoxyphene

  35. Drug treatments • ‘Anti-epileptic’ Drugs (+ calcium channel blockers) • gabapentin • valproate • topiramate • vigabatrin • carbamazepine • Membrane stabilising drugs • mexilitene • tocainamide

  36. Clinical Psychology

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

  38. Transcutaneous Electrical Nerve Stimulation - TENS

  39. TENS • High Frequency TENS • Low Frequency TENS • Burst TENS

  40. Acupuncture

  41. Acupuncture

  42. The future? • Pregabalin 2004 • Membrane Stabilising drugs • ‘Gene therapy’ • NMDA therapies • AMPA therapies (NGX 424)

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